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Journal articles on the topic 'Intact sibling'
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Rohner, Ronald P., Azmi Varan, and Nicholas Koberstein. "RELATIVE CONTRIBUTIONS OF ELDER SIBLINGS’ VERSUS PARENTS’ ACCEPTANCE AND BEHAVIORAL CONTROL TO THE PSYCHOLOGICAL ADJUSTMENT OF YOUNGER SIBLINGS IN TURKEY." International Journal of Child, Youth and Family Studies 4, no. 2 (April 10, 2013): 209. http://dx.doi.org/10.18357/ijcyfs42201312208.
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This study explores the differential contribution of elder siblings' versus parents' acceptance and behavioral control to the psychological adjustment of younger siblings in Turkey. One hundred eighty younger siblings (<em>M</em> = 12.38 years) in intact nuclear families with at least one older sibling (<em>M </em>= 15.79 years) responded to four self-reports. Results of simple regression analyses showed that younger siblings' perceptions of odler siblings, mothers', and fathers' acceptance (but not behavioral control) each made a unique contribution to the psychological adjustment of the younger siblings. Hierarchical regression analyses, however, showed that younger brothers' perceptions of older sisters' acceptance did not make a unique contribution to the boys' adjustment. But all other sibling pairs did contribute uniquely to the adjustment of younger siblings.
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Albert, Vicky N., and William C. King. "Survival Analyses of the Dynamics of Sibling Experiences in Foster Care." Families in Society: The Journal of Contemporary Social Services 89, no. 4 (October 2008): 533–41. http://dx.doi.org/10.1606/1044-3894.3819.
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The present study compares reunification for sibling groups in foster care under alternate placement conditions, including placement with kin and entering care within the same month. The findings suggest siblings placed completely or partially together reunify at a faster rate than those placed apart. The gap between siblings placed completely or partially together and those placed completely apart increases over time, in particular after the first year in care. Fewer of those placed together remain in care during the first 8 months than those placed apart. Efforts to place siblings together should be strengthened. Monetary incentives might encourage more foster parents to provide homes to keep siblings together. Training foster parents about sibling issues may lead to more intact placements.
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Cassidy, Tony, Elizabeth Noon, and Elizabeth Wright. "Sibling constellations and wellbeing in intact and non-intact families." Journal of Adolescent Psychology and Psychiatry 1 (October 10, 2015): 2. http://dx.doi.org/10.18482/1132.
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Moser, Richard P., and Theodore Jacob. "Parental and Sibling Effects in Adolescent Outcomes." Psychological Reports 91, no. 2 (October 2002): 463–79. http://dx.doi.org/10.2466/pr0.2002.91.2.463.
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This study examined the differential effects of parenting and sibling influences (and the interaction between the two) in predicting adolescents' problem behaviors. The reliability and validity of the Sibling Relationship Questionnaire was also assessed. Subjects were 99 intact families from the San Francisco Bay area, all of whom contained both parents and at least one target child between 10 and 18 years of age still living in the home. Analysis indicated that sibling behavior was a significant predictor of deviant behavior, as measured by the Child Behavior Checklist, even when parenting effects were statistically controlled. Parenting effects had a separate effect on adolescents' positive behaviors. The analysis of the Sibling Relationship Questionnaire indicated adequate test-retest and internal consistency reliability, and construct validity. Findings are discussed in terms of the larger literature on socialization on the different ways that siblings and parents influence adolescent outcomes.
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Lacy, Eva L., and Timothy J. Bartness. "Effects of white adipose tissue grafts on total body fat and cellularity are dependent on graft type and location." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (August 2005): R380—R388. http://dx.doi.org/10.1152/ajpregu.00116.2005.
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Surgical removal of body fat (lipectomy) triggers compensatory increases in nonexcised white adipose tissue (WAT), thus restoring adiposity levels in many species, including Siberian hamsters. In Siberian hamsters, when their lipectomized WAT is transplanted to another site (autologous grafts, no net change in body fat), healthy grafts result, but the lipectomy-induced compensatory increases in nonexcised WAT masses are exaggerated, an effect that apparently occurs only when the grafts contact intact WAT. When WAT is added to nonlipectomized hamsters to increase body fat, native WAT pads do not decrease. Thus WAT addition or removal-replacement does not induce compensatory WAT responses consistent with total body fat regulation as does WAT subtraction. Therefore, we tested whether the exaggerated response to lipectomy occurring with autologous WAT transplantation is dependent on graft site placement and whether the donor graft source [inguinal or epididymal WAT (IWAT, EWAT), sibling vs. nonsibling] affected body fat responses to WAT additions in nonlipectomized hamsters. Lipectomized hamsters received subcutaneous autologous EWAT grafts placed remotely from other WAT (ventrum) or in contact with intact WAT (dorsum), whereas intact hamsters received EWAT or IWAT grafts from sibling or nonsibling donors. The exaggerated response to lipectomy only occurred when grafts were in contact with intact WAT. EWAT, but not IWAT, additions to nonlipectomized siblings or nonsiblings increased native IWAT and retroperitoneal WAT mass but not EWAT mass compared with controls. Collectively, WAT transplantation to either lipectomized or nonlipectomized hamsters increased body fat contingent on graft contact with intact or native WAT.
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Mack, Kristin Y. "The Effects of Early Parental Death on Sibling Relationships in Later Life." OMEGA - Journal of Death and Dying 49, no. 2 (October 2004): 131–48. http://dx.doi.org/10.2190/btuq-011v-anew-v7rt.
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The present study draws on elements of kinship and life course perspectives to examine the influence of parental death during childhood on adult sibling contact and closeness. Using data from the National Survey of Families and Households ( N = 3,684), comparisons are made between adults who experienced early parental death and those with no history of childhood family disruptions, and between adults who experienced early maternal death and those who experienced paternal death during childhood. Results from Ordinary Least Squares (OLS) regression analyses indicate that adults who experienced parental death during childhood do not have more sibling contact, but are closer to their siblings in adulthood than adults who grew up in intact families. In addition, adults who experienced maternal death during childhood have less sibling contact than adults who experienced paternal death, but there are not differences between these two groups in terms of closeness. These findings indicate that it is important to assess the long-term impact of early parental death on adult outcomes and that gender of the deceased parent may have more significant implications for some dimensions of adult sibling relationships than others.
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Pantaleo, Valeria, Paolo D’Ettorre, Marco Caldin, and Aldo Vezzoni. "Metaphyseal osteopathy-like disease in two sibling kittens." Veterinary and Comparative Orthopaedics and Traumatology 29, no. 01 (January 2016): 94–97. http://dx.doi.org/10.3415/vcot-15-03-0054.
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SummaryThis report describes the diagnosis and treatment of a growth plate disturbance resembling canine metaphyseal osteopathy in two, two-month-old, sibling, intact, female Domestic Shorthair cats. Clinical signs and radiographic lesions resolved spontaneously after three months. Follow-up examination at six months of age showed complete recovery and no radiographic abnormalities.
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Summers, Marcia, Carl R. Summers, and Frank R. Ascione. "A Comparison of Sibling Interaction in Intact and Single-Parent Families." Journal of Divorce & Remarriage 20, no. 1-2 (March 7, 1994): 215–27. http://dx.doi.org/10.1300/j087v20n01_12.
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HINTON, VERONICA J., DARRYL C. DE VIVO, NANCY E. NEREO, EDWARD GOLDSTEIN, and YAAKOV STERN. "Selective deficits in verbal working memory associated with a known genetic etiology: The neuropsychological profile of Duchenne muscular dystrophy." Journal of the International Neuropsychological Society 7, no. 1 (January 2001): 45–54. http://dx.doi.org/10.1017/s1355617701711058.
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Forty-one boys diagnosed with Duchenne muscular dystrophy (DMD) were each compared to an unaffected sibling on a battery of neuropsychological tests. Verbal, visuospatial, attention/memory, abstract thinking, and academic achievement skills were tested. Results indicated the boys with DMD performed similarly to their siblings on the majority of measures, indicating intact verbal, visuospatial, long-term memory, and abstract skills. However, the DMD group did significantly more poorly than their siblings on specific measures of story recall, digit span, and auditory comprehension, as well as in all areas of academic achievement (reading, writing, and math). This profile indicates that verbal working memory skills are selectively impaired in DMD, and that that likely contributes to limited academic achievement. The association between the known impact of the genetic mutation on the development of the central nervous system and boys' cognitive profile is discussed. (JINS, 2001, 7, 45–54.)
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Björklund, Andreas T., Marie Schaffer, Cyril Fauriat, Olle Ringdén, Mats Remberger, Christina Hammarstedt, A. John Barrett, Per Ljungman, Hans-Gustaf Ljunggren, and Karl-Johan Malmberg. "NK cells expressing inhibitory KIR for non–self-ligands remain tolerant in HLA-matched sibling stem cell transplantation." Blood 115, no. 13 (April 1, 2010): 2686–94. http://dx.doi.org/10.1182/blood-2009-07-229740.
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Abstract Natural killer (NK)–cell alloreactivity in recipients of hematopoietic stem cell grafts from HLA-identical siblings is intriguing and has suggested breaking of NK-cell tolerance during the posttransplantation period. To examine this possibility, we analyzed clinical outcomes in a cohort of 105 patients with myeloid malignancies who received T cell–replete grafts from HLA-matched sibling donors. Presence of inhibitory killer cell immunoglobulin-like receptors (KIRs) for nonself HLA class I ligands had no effect on disease-free survival, incidence of relapse, or graft-versus-host disease. A longitudinal analysis of the NK-cell repertoire and function revealed a global hyporesponsiveness of NK cells early after transplantation. Functional responses recovered at approximately 6 months after transplantation. Importantly, NKG2A− NK cells expressing KIRs for nonself HLA class I ligands remained tolerant at all time points. Furthermore, a direct comparison of NK-cell reconstitution in T cell–replete and T cell–depleted HLA-matched sibling stem cell transplantation (SCT) revealed that NKG2A+ NK cells dominated the functional repertoire early after transplantation, with intact tolerance of NKG2A− NK cells expressing KIRs for nonself ligands in both settings. Our results provide evidence against the emergence of alloreactive NK cells in HLA-identical allogeneic SCT.
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Wakahara, Masami. "Kin Recognition among Intact and Blinded, Mixed-Sibling Larvae of a Cannibalistic Salamander Hynobius retardatus." Zoological Science 14, no. 6 (December 1997): 893–99. http://dx.doi.org/10.2108/zsj.14.893.
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Tsamparli, Anastasia, and Helias Halios. "Quality of sibling relationship and family functioning in Greek families with school-age children." Journal of Psychologists and Counsellors in Schools 29, no. 2 (June 4, 2019): 190–205. http://dx.doi.org/10.1017/jgc.2019.9.
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AbstractThe aim of the current study is to examine the quality of sibling relationships in relation to family functioning in Greek families with typically developing school-age children. The sample: 251 intact Greek families with two children (251 parents — 1 parent participated from each family — and 251 children). Research instruments: (a) the Family Adaptability and Cohesion Evaluation Scales III (FACES III; Olson, 1986), administered to both parents and children), (b) the Sibling Relationship Questionnaire (SRQ; Furman& Buhrmester, 1985); and (c) the family constellation: number of children, birth order, gender and socioeconomic level. According to the findings, the quality of a sibling relationship is associated with family cohesion and adaptability. Regarding children’s gender, the Warmth/Closeness scale is lower in families with children of different gender compared to families with children of the same gender. Regarding birth order, first-born children report higher levels of cohesion (ideal and actual), as well as higher Warmth/Closeness (children and parents), in comparison to the second-born children. Regarding parental educational level, parents and children report a higher level when it comes to ideal family and cohesion type (ideal level), as well as higher Warmth/Closeness (parents) when at least one of the parents has a university education background.
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Sprenkeler, Evelien G. G., Stefanie S. V. Henriet, Anton T. J. Tool, Iris C. Kreft, Ivo van der Bijl, Cathelijn E. M. Aarts, Michel van Houdt, et al. "MKL1 deficiency results in a severe neutrophil motility defect due to impaired actin polymerization." Blood 135, no. 24 (June 11, 2020): 2171–81. http://dx.doi.org/10.1182/blood.2019002633.
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Abstract Megakaryoblastic leukemia 1 (MKL1) promotes the regulation of essential cell processes, including actin cytoskeletal dynamics, by coactivating serum response factor. Recently, the first human with MKL1 deficiency, leading to a novel primary immunodeficiency, was identified. We report a second family with 2 siblings with a homozygous frameshift mutation in MKL1. The index case died as an infant from progressive and severe pneumonia caused by Pseudomonas aeruginosa and poor wound healing. The younger sibling was preemptively transplanted shortly after birth. The immunodeficiency was marked by a pronounced actin polymerization defect and a strongly reduced motility and chemotactic response by MKL1-deficient neutrophils. In addition to the lack of MKL1, subsequent proteomic and transcriptomic analyses of patient neutrophils revealed actin and several actin-related proteins to be downregulated, confirming a role for MKL1 as a transcriptional coregulator. Degranulation was enhanced upon suboptimal neutrophil activation, whereas production of reactive oxygen species was normal. Neutrophil adhesion was intact but without proper spreading. The latter could explain the observed failure in firm adherence and transendothelial migration under flow conditions. No apparent defect in phagocytosis or bacterial killing was found. Also, monocyte-derived macrophages showed intact phagocytosis, and lymphocyte counts and proliferative capacity were normal. Nonhematopoietic primary fibroblasts demonstrated defective differentiation into myofibroblasts but normal migration and F-actin content, most likely as a result of compensatory mechanisms of MKL2, which is not expressed in neutrophils. Our findings extend current insight into the severe immune dysfunction in MKL1 deficiency, with cytoskeletal dysfunction and defective extravasation of neutrophils as the most prominent features.
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Reese-Weber, Marla, and Jeffrey H. Kahn. "Familial predictors of sibling and romantic-partner conflict resolution: comparing late adolescents from intact and divorced families." Journal of Adolescence 28, no. 4 (August 2005): 479–93. http://dx.doi.org/10.1016/j.adolescence.2004.09.004.
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Yao, Yao, Xiaoli Li, Liangjing Xu, Bin Liu, Yue Han, Xiaopeng Tian, Chengcheng Fu, et al. "The Association of KIR2DS4 and Its Variant KIR1D with CMV Infection after HLA-Matched Sibling Hematopoietic Stem Cell Transplantation." Blood 124, no. 21 (December 6, 2014): 2555. http://dx.doi.org/10.1182/blood.v124.21.2555.2555.
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Abstract Objective To expolore the association of KIR2DS4 and its variant KIR1D with cytomegalovirus(CMV) infection after HLA-matched sibling hematopoietic stem cell transplantation. Methods Polymerase chain reaction with sequence-specific primers (PCR-SSP) method was used to genotype KIR genes in 267 donor-recipient pairs from Oct 2005 to Apr 2014. Posttransplant monitoring for CMV infection was performed by immune histochemically assays .165 donor-recipient pairs who belong to KIR gene haplotype AA were analyzed for the presence of KIR2DS4 and its variant KIR1D and then further subdivided into the following groups: 2DS4-/1D+ (homozygous for the deletion variant KIR1D), 2DS4+/1D+ (heterozygous), 2DS4+/1D- (two intact KIR2DS4 alleles). Furthermore, we investigated the influence of the KIR2DS4 variants on CMV infection of 165 patients receiving Sibling related HLA matched transplantation. Results There were no significant differences in frequency of KIR2DS4 or KIR1D between donors and recipients in the haplotype AA group. The ratio of 2DS4+ and KIR1D in haplotype AA group was 2:1.There was no difference on neutrophil engraftment and platelet recovery among the three groups after hematopoietic stem cell transplantation. The CMV infection rate was significantly higher in 2DS4+/1D- group compared with 2DS4+/1D+ group (44.0% vs 19.0%，P=0.002)．In 2DS4-/1D+ group ，the CMV infection rate was higer than that in 2DS4+KIR1D+ group (50.0% vs 19%，P=0.028). However，there was no difference in CMV infection rate between 2DS4+/1D-group and 2DS4-/1D+ group. Conclusion KIR2DS4 and its variant KIR1D are associated with CMV infection after HLA-matched sibling hematopoietic stem cell transplantation Disclosures No relevant conflicts of interest to declare.
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Williamson, Josh, and Kristy Howells. "The Influence of Siblings on Young Children’s Understanding of Fluid Intake." International Journal of Nutrition 6, no. 3 (February 20, 2021): 13–20. http://dx.doi.org/10.14302/issn.2379-7835.ijn-21-3709.
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Background Children need to drink enough water (1.1-1.3 litres) throughout the day to stay hydrated and for health benefits1. Wellbeing and cognitive function benefits have been identified for children who are hydrated2. Yet there is a dearth of research focusing specifically on children’s perceptions of their own fluid intake levels and who helps support them in ensuring they are drinking enough water, this is a novel area to investigate. Previous research3 identified that 44.2% of young children’s fluid intake were influenced the strongest by a family member. This paper will explore in further detail the influence of siblings on children’s fluid intake, in particular older versus younger siblings. Methods 130 children (67 girls and 63 boys, of which 45 had a younger sibling (s) and 85 having an elder sibling(s), from 4 primary schools in the South East of England, were questioned between January and April 2019 using an adapted version of Coppinger and Howells’ (2019)4 questionnaire, on their understanding of fluid intake, how much they perceived they drank and who supported them in prompting them to drink. Physical visual representations were used to aid question comprehension and to ensure the questions were appropriate for young children. The data was analysed using SPSS 24.0 using MANOVAs (P < 0.05) to consider statistical variance in gender and older sibling status. Results The most significant results were linked to elder siblings influence younger siblings in drinking too little fluids within a school day (F=0.530, p<0.05), whilst those without an elder sibling, thought they drank beyond the daily recommended guidelines and reported they drank over 2 litres. This illustrates that children misunderstand fluid intake recommendations regardless of whether they have an elder sibling or not. Children named adults, both parents and teachers as well as elder siblings as the key influencers of them drinking (F=3.67, p<0.05) and the data indicated that girls were more influenced by siblings than boys, whilst twins were not influenced by each other. Conclusion It is concluded that siblings do have an influence on the consumption of water, as siblings act as role models and other siblings follow their habits, therefore the whole family unit is important to ensure that the right fluid intake is consumed. It is recommended that further education, curriculum and community development is needed to continue to support young children’s knowledge and understanding of fluid intake.
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Leichtentritt, Judy. "“It is difficult to be here with my sister but intolerable to be without her”: Intact sibling placement in residential care." Children and Youth Services Review 35, no. 5 (May 2013): 762–70. http://dx.doi.org/10.1016/j.childyouth.2013.01.022.
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O'Connor, Thomas G., Judy Dunn, Jennifer M. Jenkins, Kevin Pickering, and Jon Rasbash. "Family settings and children's adjustment: differential adjustment within and across families." British Journal of Psychiatry 179, no. 2 (August 2001): 110–15. http://dx.doi.org/10.1192/bjp.179.2.110.
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BackgroundChildren in stepfamilies and single-parent families exhibit elevated levels of behavioural and emotional problems compared with children in intact (biological) families, but there is variation within and across these family types.AimsTo examine the sources of variation in children's behavioural and emotional problems across diverse family settings.MethodLevels of behavioural and emotional problems in children from diverse stepfamilies and single-parent families were compared with children living with both biological parents. Psychosocial risks were measured at the individual child and family levels.ResultsBehavioural and emotional problems were elevated in children in stepmother/complex stepfamilies and single-parent families, but not in simple stepfather families, relative to ‘biological’ families. Psychopathology associated with family type was explained by compromised quality of the parent–child relationship, parental depression and socio-economic adversity. Sibling similarity in behavioural and emotional problems was most pronounced in high-risk family settings.ConclusionsFamily type is a proxy for exposure to psychosocial risks; the extent of family-wide influence on children's development may be strongest in high-stress settings.
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Ramadhana, Maulana Rezi, Ravik Karsidi, Prahastiwi Utari, and Drajat Tri Kartono. "Role of Family Communications in Adolescent Personal and Social Identity." Journal of Family Sciences 4, no. 1 (July 2, 2019): 1–11. http://dx.doi.org/10.29244/jfs.4.1.1-11.
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This study examines the relationship between family communication patterns (involving two dimensions of conversation and conformity) and the personal-social identity of adolescents. This study uses a survey technique involving 214 adolescents from intact families and single-parent families in one school in Bandung, by providing two scales of the Family Communication Pattern Revised (FCPR) from Ritchie and the scale of Social Identity-Personal Identity (SIPI) from Nario-Redmond. Data analysis to test three hypotheses in this study using Pearson product-moment correlation and regression analysis to find moderation of the measured variables. The findings indicate that the dimensions of the conversation are significantly positively related to social identity and personal identity. While the dimensions of conformity are negatively associated with social identity and positively associated with personal identity. After controlling for family status and sibling position in the family, the dimensions of conformity moderate significantly positive relationships between dimensions of conversation and social identity.
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Kendler, K. S., H. Ohlsson, K. Sundquist, and J. Sundquist. "The causes of parent–offspring transmission of drug abuse: a Swedish population-based study." Psychological Medicine 45, no. 1 (May 14, 2014): 87–95. http://dx.doi.org/10.1017/s0033291714001093.
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BackgroundWhile drug abuse (DA) is strongly familial, we still have limited knowledge about the causes of its cross-generational transmission.MethodWe examined DA ascertained from national registers in offspring of three family types from the Swedish population [intact (n = 2 111 074), ‘not-lived-with’ (n = 165 315, where biological parents never lived with their offspring) and ‘step’ (n = 124 800 offspring)], which reflected, respectively, the effects of genes + rearing, genes only and rearing only. We replicated these results in three high-risk co-relative designs.ResultsCombined across mothers and fathers, the hazard ratio (HR) for DA in offspring given DA in parents was 3.52 in intact, 2.73 in ‘not-lived-with’ and 1.79 in stepfamilies. In 968 biological full or half-sibling pairs one of whom was reared by and the other never lived with their parent with DA, the HR for DA was greater in the reared than ‘not-lived-with’ child (HR 1.57). In 64 offspring pairs of a parent with DA, the HR for DA was greater in a reared biological v. step-parented non-biological child (HR 3.33). In 321 pairs of offspring of a parent with DA one of whom was a not-lived-with biological child and the second a step-parented non-biological child, the HR for DA was greater in the biological v. stepchild (HR 1.80).ConclusionsBoth genetic and environmental factors contribute substantially to parent–offspring resemblance for DA. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent–offspring resemblance.
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Bourne, H., N. Richings, DY Liu, GN Clarke, O. Harari, and HW Baker. "Sperm preparation for intracytoplasmic injection: methods and relationship to fertilization results." Reproduction, Fertility and Development 7, no. 2 (1995): 177. http://dx.doi.org/10.1071/rd9950177.
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Sperm preparation for intracytoplasmic sperm injection (ICSI) is described and the effect of high speed centrifugation during preparation on fertilization rate is evaluated. No significant differences were found in the 2-pronuclear or abnormal fertilization rates between sibling oocytes injected with sperm prepared by swim-up or mini-Percoll combined with high speed centrifugation. The high fertilization rate obtained with both methods indicates that high speed centrifugation is not necessary to prepare sperm for ICSI. Fertilization rates were also compared for sperm obtained from ejaculates, fresh and frozen epididymal aspirates, and testicular biopsies. High fertilization rates were obtained from all groups but they were significantly higher in those oocytes injected with epididymal sperm (78% per oocyte surviving injection). The high fertilization rate with epididymal sperm may reflect sperm quality or may result from the method of sperm preparation for injection. Fertilization after the injection of sperm from which the tail was dislodged during immobilization was compared with that obtained using intact sperm. A significantly lower rate of 2-pronuclear fertilization was found in those oocytes injected with sperm heads only (55%) compared with intact sperm (68%), although cleavage rates between the two groups were similar. The use of hypo-osmotic medium to select potentially live sperm from an immotile sample is also described and fertilization was obtained after the injection of sperm with a structural defect which were selected using this technique. These results indicate that high fertilization rates can be obtained with ejaculated, epididymal and testicular sperm without special treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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Merriman, P. J., C. D. Grimes, J. Ambroziak, D. A. Hackett, P. Skinner, and M. J. Simmons. "S elements: a family of Tc1-like transposons in the genome of Drosophila melanogaster." Genetics 141, no. 4 (December 1, 1995): 1425–38. http://dx.doi.org/10.1093/genetics/141.4.1425.
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Abstract The S elements form a diverse family of long-inverted-repeat transposons within the genome of Drosophila melanogaster. These elements vary in size and sequence, the longest consisting of 1736 bp with 234-bp inverted terminal repeats. The longest open reading frame in an intact S element could encode a 345-amino acid polypeptide. This polypeptide is homologous to the transposases of the mariner-Tc1 superfamily of transposable elements. S elements are ubiquitous in D. melanogaster populations and also appear to be present in the genomes of two sibling species; however, they seem to be absent from 17 other Drosophila species that were examined. Within D. melanogaster strains, there are, on average, 37.4 cytologically detectable S elements per diploid genome. These elements are scattered throughout the chromosomes, but several sites in both the euchromatin and beta heterochromatin are consistently occupied. The discovery of an S-element-insertion mutation and a reversion of this mutation indicates that S elements are at least occasionally mobile in the D. melanogaster genome. These elements seem to insert at an AT dinucleotide within a short palindrome and apparently duplicate that dinucleotide upon insertion.
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Kernan, NA, C. Bordignon, G. Heller, I. Cunningham, H. Castro-Malaspina, B. Shank, N. Flomenberg, J. Burns, SY Yang, and P. Black. "Graft failure after T-cell-depleted human leukocyte antigen identical marrow transplants for leukemia: I. Analysis of risk factors and results of secondary transplants." Blood 74, no. 6 (November 1, 1989): 2227–36. http://dx.doi.org/10.1182/blood.v74.6.2227.bloodjournal7462227.
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Risk factors for graft failure were analyzed in 122 recipients of an allogeneic T-cell-depleted human leukocyte antigen (HLA)-identical sibling marrow transplant as treatment for leukemia. In each case pretransplant immunosuppression included 1,375 to 1,500 cGy hyperfractionated total body irradiation and cyclophosphamide (60 mg/kg/d x 2). No patient received immunosuppression prosttransplant for graft-versus-host disease (GVHD) prophylaxis. Nineteen patients in this group experienced graft failure. The major factors associated with graft failure were transplants from male donors and the age of the patient (or donor). Among male recipients of male donor-derived grafts a low dose per kilogram of nucleated cells, progenitor cells (colony forming unit-GM) and T cells was also associated with graft failure. Additional irradiation to 1,500 cGy, high dose corticosteroids posttransplant, and additional peripheral blood donor T cells did not decrease the incidence of graft failure. In addition, type of leukemia, time from diagnosis to transplant, an intact spleen, or the presence of antidonor leukocyte antibodies did not correlate with graft failure. To ensure engraftment of secondary transplants, further immunosuppression was necessary but was poorly tolerated. However, engraftment and survival could be achieved with an immunosuppressive regimen in which antithymocyte globulin and high dose methylprednisolone were administered both before and after infusions of secondary partially T- cell-depleted marrow grafts.
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Kernan, NA, C. Bordignon, G. Heller, I. Cunningham, H. Castro-Malaspina, B. Shank, N. Flomenberg, J. Burns, SY Yang, and P. Black. "Graft failure after T-cell-depleted human leukocyte antigen identical marrow transplants for leukemia: I. Analysis of risk factors and results of secondary transplants." Blood 74, no. 6 (November 1, 1989): 2227–36. http://dx.doi.org/10.1182/blood.v74.6.2227.2227.
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Abstract Risk factors for graft failure were analyzed in 122 recipients of an allogeneic T-cell-depleted human leukocyte antigen (HLA)-identical sibling marrow transplant as treatment for leukemia. In each case pretransplant immunosuppression included 1,375 to 1,500 cGy hyperfractionated total body irradiation and cyclophosphamide (60 mg/kg/d x 2). No patient received immunosuppression prosttransplant for graft-versus-host disease (GVHD) prophylaxis. Nineteen patients in this group experienced graft failure. The major factors associated with graft failure were transplants from male donors and the age of the patient (or donor). Among male recipients of male donor-derived grafts a low dose per kilogram of nucleated cells, progenitor cells (colony forming unit-GM) and T cells was also associated with graft failure. Additional irradiation to 1,500 cGy, high dose corticosteroids posttransplant, and additional peripheral blood donor T cells did not decrease the incidence of graft failure. In addition, type of leukemia, time from diagnosis to transplant, an intact spleen, or the presence of antidonor leukocyte antibodies did not correlate with graft failure. To ensure engraftment of secondary transplants, further immunosuppression was necessary but was poorly tolerated. However, engraftment and survival could be achieved with an immunosuppressive regimen in which antithymocyte globulin and high dose methylprednisolone were administered both before and after infusions of secondary partially T- cell-depleted marrow grafts.
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Kubiak, Adam. "Narrative Interfaces, Identity of The Game and The Integrity of The Interfaces." Panoptikum, no. 24 (October 20, 2020): 80–101. http://dx.doi.org/10.26881/pan.2020.24.02.
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The paper aims to address an issue of the game’s identity in the context of narrative interfaces and their integrity. Following the approach of Jenkins (2002), Bizzocchi (2007, 2011) and Koenitz (2015, 2018) I propose there to address said topic by attention paid to the integrity of the narrative interfaces design and their role in the presentation and experience of “the game” as particular “that game”. Especially in the context of attempts to recreate specific experience (remake/revival, sequel and sibling identity), for which main example is the game Planescape Torment and its revival (Enhanced Edition) and “spiritual successor” Tides of Numenera. The short study on said example, as I argue, shows that the main issue has a multilayered nature (including technology, studio politics, artistic design, license legal limitations and such), and the integrity of the interfaces, especially these which may be identified as the “core” ones, is an important part of them and seemingly small and mere changes, may break it completely. And while the storytelling may deliver literally “the same” story, a changed (or broken) integrity of narrative interface’s design cannot be restored. Creating in effect a different experience, and in essence: a different game. However, keeping said core integrity intact allows to sustain the game identity (and its experience) allowing extending existing mechanics, additional layers of gameplay etc.
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Garcia, Jacqueline S., Jozef Madzo, Devin Cooper, Sarah A. Jackson, Kenan Onel, Richard A. Larson, Andrew Artz, and Lucy A. Godley. "Pre-Donor Evaluation of an HLA Matched Sibling Identifies a Novel Inherited RUNX1 Mutation Encoding a Missense Mutation Found Outside of the RUNT Domain in Familial Platelet Disorder." Blood 116, no. 21 (November 19, 2010): 2709. http://dx.doi.org/10.1182/blood.v116.21.2709.2709.
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Abstract Abstract 2709 Introduction: RUNX1 is a critical transcription factor in the regulation of normal hematopoiesis. Inherited RUNX1 mutations have been identified as the culprit genetic lesion in Familial Platelet Disorder (FPD; OMIM 601399), a rare autosomal dominant condition with a propensity to myeloid malignancy. The spectrum of RUNX1 mutations causing the FPD/acute myeloid leukemia (AML) syndrome includes frameshift and termination mutations detected throughout the gene, and missense mutations clustered within the highly conserved RUNT homology domain (RHD), which is responsible for both DNA binding and heterodimerization with CBFβ/PEBP2β, the non-DNA binding regulatory subunit. We present a new FPD/AML pedigree with a novel missense mutation leading to a single amino acid change, L56S. This L56S mutation is the first reported point mutation in this syndrome to be found outside of the RHD. Patients and Methods: Our new pedigree involves a 41-year-old man (proband) diagnosed with myelodysplastic syndrome (MDS, specifically refractory anemia with excess blasts type-2) with a normal karyotype. He was initiated on azacitidine, which was administered on a seven-day treatment schedule every four weeks. Bone marrow biopsy analysis after six monthly cycles of azacitidine showed persistent MDS, with similar findings after a total of ten monthly cycles. Given his lack of a clinical response, his young age and good performance status, he was referred to The University of Chicago for allogeneic hematopoietic stem cell transplantation (HCT). Routine pre-transplant evaluation revealed mild thrombocytopenia (platelets = 123,000 K/μl) in his HLA-matched brother. In addition, his father was reported to have thrombocytopenia. Clinical concern for an inherited condition initiated the investigation for a RUNX1 mutation in the family. Results: We sequenced full-length cDNA synthesized from leukocyte-derived RNA collected from the proband's sibling with thrombocytopenia, and detected a novel missense germline mutation in exon 4 at nucleotide position 371, causing a T to C mutation leading to a single amino acid change in the RUNX1 protein, L56S. This amino acid substitution is located N-terminal to the RHD (aa 76–209). RUNX1 sequencing of the proband with MDS demonstrated the same mutation. The RUNX1 RHD and the transactivation domain remain intact in this mutant. Initial transactivation assays using a luciferase reporter assay performed in triplicate demonstrated similar levels of activation as wild-type RUNX1. Corresponding Western blot analysis showed similar levels of protein expression of both wild-type RUNX1 and mutant RUNX1 transfected cell lines using an anti-RUNX1-antibody. Current studies include determination of the transactivation ability of mutant RUNX1 with its heterodimerization partner, CBFβ/PEBP2β, testing the DNA binding ability of this RUNX1 mutant by electrophoretic mobility shift assay, and analysis of the RUNX1 cDNA for an acquired biallelic mutation in leukocytes collected from the proband's bone marrow aspirate at the time of diagnosis of bone marrow malignancy. Conclusions: FPD/AML is likely an underreported condition. Clinical suspicion for this inherited syndrome may be raised by the presence of mild to moderate thrombocytopenia in healthy siblings, and should lead to prompt screening for germline RUNX1 mutations to confirm an inherited predisposition and to prevent siblings carrying RUNX1 mutations from being selected as HCT donors. In vitro studies of identified RUNX1 mutations may elucidate potential mechanisms involved in the pathogenesis of the FPD/AML syndrome. Disclosures: No relevant conflicts of interest to declare.
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Nishioka, Tomohiro, Katsuya Onishi, Naoshi Shimojo, Yuka Nagano, Hidenori Matsusaka, Masaki Ikeuchi, Tomomi Ide, et al. "Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 3 (March 2010): H1072—H1078. http://dx.doi.org/10.1152/ajpheart.00255.2009.
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Tenascin-C (TN-C) is an extracellular matrix glycoprotein with high bioactivity. It is expressed at low levels in normal adult heart, but upregulated under pathological conditions, such as myocardial infarction (MI). Recently, we (Ref. 34 ) reported that MI patients with high serum levels of TN-C have a greater incidence of maladaptive cardiac remodeling and a worse prognosis. We hypothesized that TN-C may aggravate left ventricular remodeling. To examine the effects of TN-C, MI was induced by ligating coronary arteries of TN-C knockout (KO) mice under anesthesia and comparing them with sibling wild-type (WT) mice. In WT+MI mice, TN-C expression was upregulated at day 1, peaked at day 5, downregulated and disappeared by day 28, and the molecule was localized in the border zone between intact myocardium and infarct lesions. The morphometrically determined infarct size and survival rate on day 28 were comparable between the WT+MI and KO+MI groups. Echocardiography and hemodynamic analyses demonstrated left ventricular end-diastolic diameter, myocardial stiffness, and left ventricular end-diastolic pressure to be significantly increased in both WT+MI and KO+MI mice compared with sham-operated mice. However, end-diastolic pressure and dimension and myocardial stiffness of KO+MI were lower than those of the WT+MI mice. Histological examination revealed normal tissue healing, but interstitial fibrosis in the residual myocardium in peri-infarcted areas was significantly less pronounced in KO+MI mice than in WT+MI mice. TN-C may thus accelerate adverse ventricular remodeling, cardiac failure, and fibrosis in the residual myocardium after MI.
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Fagan, John, Leena Naughton, and Bobby Smyth. "Opiate-dependent adolescents in Ireland: a descriptive study at treatment entry." Irish Journal of Psychological Medicine 25, no. 2 (June 2008): 46–51. http://dx.doi.org/10.1017/s0790966700010934.
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AbstractObjectives: To describe the drug history and co-existing psycho-social problems among under-19 year olds accessing treatment for opiate dependency, including methadone maintenance, and examine for any gender differences.Method: A descriptive study of under-19 years assessed at the largest drug treatment clinic in Dublin, Ireland, between October 2000 and September 2006. Data was obtained through review of case notes, assessment questionnaires and urine drug screens.Results: Eighty-six young people were included. Their mean age was 16.8 years. Forty-six (54%) were female. Only 26 (30%) reported an intact family of origin. Twenty-three (27%) had been in care. Mean age for first use of any illicit drug was 12.4 years, and for heroin was 14.8 years. The mean age of leaving school was 14.4 years; 42 (49%) first tried heroin after leaving school. Forty-one (48%) had a history of homelessness. Forty-four (51%) had previously injected; 26 (30%) were currently injecting. Fifty-six (65%) had not been screened for blood-borne diseases; twenty-one (24%) subsequently tested positive for hepatitis C. Thirty-eight (48%) had previous convictions; 33 (38%) were facing charges. Forty-five (52%) had previously seen a psychiatrist; nine (11%) had received inpatient psychiatric treatment. Boys were more likely to leave school early, have a substance-abusing sibling, and to have a past conviction. Girls were more likely to have a partner, and have taken a deliberate overdose.Conclusions: This study highlights the multiple and complex needs of teenagers abusing opiates. Services seeking to meet their needs will require a broad range of interventions and excellent interagency co-operation.
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Russo, M., T. E. Van Rheenen, M. Shanahan, K. Mahon, M. M. Perez-Rodriguez, A. Cuesta-Diaz, E. Larsen, A. K. Malhotra, and K. E. Burdick. "Neurocognitive subtypes in patients with bipolar disorder and their unaffected siblings." Psychological Medicine 47, no. 16 (June 7, 2017): 2892–905. http://dx.doi.org/10.1017/s003329171700143x.
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BackgroundOur previous work revealed substantial heterogeneity in the cognitive profile of bipolar disorder (BD) due to the presence of three underlying cognitive subgroups characterized as: globally impaired, selectively impaired, or cognitively intact. In an effort to determine whether these subgroups are differentially related to genetic risk for the illness, we investigated whether cognitive deficits were more pronounced in unaffected siblings (UAS) of BD probands within identified clusters.MethodsCluster analysis was used to identify cognitive clusters in BD (N = 60). UAS (N = 49) were classified into groups according to their proband sibling's cluster assignment; comparisons were made across all clusters and healthy controls (HCs; N = 71).ResultsThree cognitive clusters in BD emerged: a globally impaired (36.7%), a selectively impaired (30%), and a cognitively intact cluster (33.3%). UAS showed a qualitatively similar pattern to their BD siblings; UAS of the globally impaired BD cluster showed verbal memory and general cognitive impairments relative to HCs. In contrast, UAS of the other two clusters did not differ from HCs.ConclusionsThis study corroborates findings from prior work regarding the presence of cognitive heterogeneity in BD. UAS of subjects in the globally impaired BD cluster presented with a qualitatively similar cognitive profile to their siblings and performed worse than all other BD clusters and UAS groups. This suggests that inherited risk factors may be contributing to cognitive deficits more notably in one subgroup of patients with BD, pointing toward differential causes of cognitive deficits in discrete subgroups of patients with the disorder.
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Wirth, Julie J., Li Chen, and Michele M. Fluck. "Systemic Polyomavirus Genome Increase and Dissemination of Capsid-Defective Genomes in Mammary Gland Tumor-Bearing Mice." Journal of Virology 74, no. 15 (August 1, 2000): 6975–83. http://dx.doi.org/10.1128/jvi.74.15.6975-6983.2000.
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ABSTRACT BALB/c mice that developed tumors 7 to 8 months following neonatal infection by polyomavirus (PYV) wild-type strain A2 were characterized with respect to the abundance and integrity of the viral genome in the tumors and in 12 nontumorous organs. These patterns were compared to those found in tumor-free mice infected in parallel. Six mice were analyzed in detail including four sibling females with mammary gland tumors. In four of five mammary gland tumors, the viral genome had undergone a unique deletion and/or rearrangement. Three tumor-resident genomes with an apparently intact large T coding region were present in abundant levels in an unintegrated state. Two of these had undergone deletions and rearrangements involving the capsid genes and therefore lacked the capacity to produce live virus. In the comparative organ survey, the tumors harboring replication-competent genomes contained by far the highest levels of genomes of any tissue. However, the levels of PYV genomes in other organs were elevated by up to 1 to 2 orders of magnitude compared to those detected in the same organs of tumor-free mice. The genomes found in the nontumorous organs had the same rearrangements as the genomes residing in the tumors. The original wild-type genome was detected at low levels in a few organs, particularly in the kidneys. The data indicate that a systemic increase in the level of viral genomes occurred in conjunction with the induction of tumors by PYV. The results suggest two novel hypotheses: (i) that genomes may spread from the tumors to the usual PYV target tissues and (ii) that this dissemination may take place in the absence of capsids, providing an important path for a virus to escape from the immune response. This situation may offer a useful model for the spread of HPV accompanying HPV-induced oncogenesis.
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Soiffer, RJ, L. Bosserman, C. Murray, K. Cochran, J. Daley, and J. Ritz. "Reconstitution of T-cell function after CD6-depleted allogeneic bone marrow transplantation." Blood 75, no. 10 (May 15, 1990): 2076–84. http://dx.doi.org/10.1182/blood.v75.10.2076.2076.
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Abstract Patients who undergo allogeneic bone marrow transplantation (BMT) are clinically immunodeficient for a prolonged period after engraftment. In the present study, we examined immune function after BMT in a series of patients who had received HLA compatible sibling marrow grafts purged of T cells with anti-CD6 monoclonal antibody and complement. None of the patients in this analysis received immunomodulating agents and none had developed graft-versus-host disease (GVHD). Initially after BMT, natural killer (NK) cells are the predominant cell type, giving way to CD3+, CD5+ T cells after 4 to 8 weeks. Despite the return of normal numbers of T lymphocytes post-BMT phenotypic analysis reveals several long-term abnormalities, including an inverted T4:T8 ratio and a significant fraction of CD3+ T cells that do not co-express CD6. In mitogenic assays, stimulation by either nonspecific lectin (phytohemagglutinin; PHA) or antibodies to the CD2 surface structure (anti-T11(2) + anti-T11(3)) results in decreased levels of T-cell proliferation compared with controls for over 18 months post-BMT. In contrast, the ability of unstimulated peripheral blood mononuclear cells (PBMC) to respond to recombinant interleukin-2 (rIL-2) is relatively intact, most likely reflecting early functional reconstitution of the NK cell population. To further characterize the prolonged abnormalities in T-cell proliferation after PHA or CD2 stimulation, we examined more proximal events in T-cell activation such as induction of IL-2 receptor expression and stimulus-induced intracellular calcium flux. We found that the induction of IL-2 receptor (p55) after in vitro activation, although initially abnormal, recovers completely by 6 months post-BMT. We also found that, after CD2 stimulation, calcium flux in T cells was normal immediately after engraftment. In contrast, after stimulation with anti-CD3 antibodies, a large population of T cells do not develop intracellular calcium flux compared with controls. We conclude that despite the recovery of normal numbers of T lymphocytes early after engraftment of CD6-depleted marrow, these T cells exhibit several physiologic and functional abnormalities that persist for varying intervals post-BMT. At present, it is unclear which of these specific defects is most closely associated with increased susceptibility to infectious agents after BMT.
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Soiffer, RJ, L. Bosserman, C. Murray, K. Cochran, J. Daley, and J. Ritz. "Reconstitution of T-cell function after CD6-depleted allogeneic bone marrow transplantation." Blood 75, no. 10 (May 15, 1990): 2076–84. http://dx.doi.org/10.1182/blood.v75.10.2076.bloodjournal75102076.
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Patients who undergo allogeneic bone marrow transplantation (BMT) are clinically immunodeficient for a prolonged period after engraftment. In the present study, we examined immune function after BMT in a series of patients who had received HLA compatible sibling marrow grafts purged of T cells with anti-CD6 monoclonal antibody and complement. None of the patients in this analysis received immunomodulating agents and none had developed graft-versus-host disease (GVHD). Initially after BMT, natural killer (NK) cells are the predominant cell type, giving way to CD3+, CD5+ T cells after 4 to 8 weeks. Despite the return of normal numbers of T lymphocytes post-BMT phenotypic analysis reveals several long-term abnormalities, including an inverted T4:T8 ratio and a significant fraction of CD3+ T cells that do not co-express CD6. In mitogenic assays, stimulation by either nonspecific lectin (phytohemagglutinin; PHA) or antibodies to the CD2 surface structure (anti-T11(2) + anti-T11(3)) results in decreased levels of T-cell proliferation compared with controls for over 18 months post-BMT. In contrast, the ability of unstimulated peripheral blood mononuclear cells (PBMC) to respond to recombinant interleukin-2 (rIL-2) is relatively intact, most likely reflecting early functional reconstitution of the NK cell population. To further characterize the prolonged abnormalities in T-cell proliferation after PHA or CD2 stimulation, we examined more proximal events in T-cell activation such as induction of IL-2 receptor expression and stimulus-induced intracellular calcium flux. We found that the induction of IL-2 receptor (p55) after in vitro activation, although initially abnormal, recovers completely by 6 months post-BMT. We also found that, after CD2 stimulation, calcium flux in T cells was normal immediately after engraftment. In contrast, after stimulation with anti-CD3 antibodies, a large population of T cells do not develop intracellular calcium flux compared with controls. We conclude that despite the recovery of normal numbers of T lymphocytes early after engraftment of CD6-depleted marrow, these T cells exhibit several physiologic and functional abnormalities that persist for varying intervals post-BMT. At present, it is unclear which of these specific defects is most closely associated with increased susceptibility to infectious agents after BMT.
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Hohman, Emily E., Jennifer S. Savage, Leann L. Birch, and Ian M. Paul. "The Intervention Nurses Start Infants Growing on Healthy Trajectories (INSIGHT) Responsive Parenting Intervention for Firstborns Affects Dietary Intake of Secondborn Infants." Journal of Nutrition 150, no. 8 (May 15, 2020): 2139–46. http://dx.doi.org/10.1093/jn/nxaa135.
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ABSTRACT Background Although previous work has shown that children with older siblings tend to have poorer diet quality, no study has directly compared diets of infant siblings. Objective The goals of this analysis were to examine birth-order differences in dietary intake between firstborn (FB) and secondborn (SB) siblings, and to determine whether a responsive parenting (RP) intervention modified birth-order effects on diet. Methods The Intervention Nurses Start Infants Growing on Healthy Trajectories (INSIGHT) study randomly assigned first-time mothers to an RP intervention, which included guidance on feeding, sleep, soothing, and interactive play, or control. INSIGHT mothers who delivered a second child enrolled in an observation-only study of their SB infant (SIBSIGHT). Mothers completed FFQs for both children at ages 6 (n = 97 sibling pairs) and 12 (n = 100) mo. FB compared with SB intake of food groups of interest were compared, and the moderating effect of the RP intervention on birth-order differences was tested using generalized linear mixed models. Results Though FBs and SBs had similar diets, more FBs than SBs consumed 100% fruit juice at both 6 (13.8 compared with 3.2%, P = 0.006) and 12 mo (46.0 compared with 32.0%, P = 0.01). SBs consumed fruit more frequently (FB 2.8 compared with SB 3.2 times/d, P = 0.01), and were more likely to consume fried potatoes (FB 38.4 compared with SB 57.6%, P = 0.0009) and processed meats (FB 43.0 compared with SB 58.0%, P = 0.02) than FBs at 12 mo. There were no differences by birth order in intake of sweets, snacks, or sugar-sweetened beverages at 12 mo. At 12 mo, RP-group SBs ate vegetables more times per day (3.2) than control SBs (2.2, P = 0.01). RP-SBs also consumed a greater variety of vegetables (10.2) than control-SBs (7.9, P = 0.01). Conclusions Birth order is not consistently associated with healthy or unhealthy infant dietary intake. However, an RP intervention delivered to first-time mothers may benefit subsequent infants’ vegetable intake. This trial was registered at clinicaltrials.gov as NCT01167270.
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Osai, Keith V., and Shawn D. Whiteman. "Family Relationships and Youth Sport: Influence of Siblings and Parents on Youth's Participation, Interests, and Skills." Journal of Amateur Sport 3, no. 3 (November 28, 2017): 86–105. http://dx.doi.org/10.17161/jas.v3i3.6518.
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Taking a family systems perspective, the present study investigated how older siblings’ and parents’ (mothers’ and fathers’) interests, skills, and participation in sports predicted younger siblings’ attitudes and behaviors in those same domains. Testing social learning principles, we further examined whether family members’ influence was stronger when they shared warmer relationships and siblings shared the same gender. Participants included mothers, fathers, and adolescent-aged first and second-born siblings from 197 maritally intact families. Families participated in home interviews as well as a series of 7 nightly phone calls during which participants reported on their daily activities. Across dependent variables, results revealed that parents’ and (with one exception) older siblings’ qualities were predictive of younger siblings’ interests, skills, and participation in sports. Inconsistent with hypotheses, however, family members’ influence was not moderated by relational warmth. Discussion highlights the need to examine the socialization processes by which siblings shape each other’s sport-related attitudes and activities.
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Richter, Alex G., Stephen Harding, Steve Rimmer, Guy Pratt, Aarnoud Huissoon, and Mark Drayson. "Biclonal Multiple Myeloma with Monoclonal Free IgG3 Heavy Chain and kappa Free Light Chains." Blood 110, no. 11 (November 16, 2007): 4768. http://dx.doi.org/10.1182/blood.v110.11.4768.4768.
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Abstract Background: Heavy chain disease (HCD) is a rare lymphoproliferative disorder characterized by a monoclonal heavy chain (HC) unattached to a light chain (LC). IgGHCD or γHCD typically presents as a lymphoproliferative disorder with lymphadenopathy and hepatosplenomegaly. Myeloma has been described associated with γHCD but only with a second intact Ig paraprotein. This report describes a unique presentation of multiple myeloma with monoclonal free γ3HC and kappa free light chains. Case: A 34 year old gentleman presented with mild persistent neutropenia following two episodes of pneumonia, 18 months previously. He admitted to persistent night sweats but no other significant history. Baseline investigations revealed a mild anaemia, neutropenia and a large IgG paraprotein with no associated light chain. Bone marrow aspirate and trephine confirmed myeloma. The patient was treated with cyclophosphamide, thalidomide and dexamethasone and has had a very good partial remission. He is awaiting a sibling allogeneic peripheral blood stem cell transplant. Investigations and results: Serum Electrophoresis confirmed a large IgG paraprotein (23g/l) with no associated light chain in the serum and identified as γ3 subclass by radial immunodiffusion. Western blot showed the γ3HC was truncated with a large deletion. Markedly elevated free kappa (κ) LC (503.58 mg/l [3.30–19.4]) were found in the serum with gross skewing of the kappa/lambda ratio. Urine electrophoresis revealed separate γHC and κ LC paraproteins. Western blot of the fractionated urine protein demonstrated different sized κLC aggregates. Flow cytometry of the marrow aspirate revealed an unusual staining pattern; CD5,19,38,45+ve and CD20,22,23,34,56,138 –ve plasma cells. Cytoplasmic staining revealed 2 distinct populations of plasma cells, the first producing γ3HC and the second only free κLC. Cytogenetics and FISH analysis for 14q, p53 and c-myc abnormalities were normal. Discussion: This is the first description of a Biclonal Myeloma with separate plasma cell populations producing γ3HC and κLC paraproteins. The biclonality confirms the free HC occurs as a result of abnormal synthesis not cleavage. The clinical and immunological findings are clearly different to typical findings in both γ3HCD and Myeloma. HCD has an appalling prognosis and this case is likely to have been ‘smouldering’ for 18 months, evidenced by the 2 pneumonias and persistent night sweats. There is no lymphadenopathy or organomegaly associated with γ3HCD. The immunophenotype of the malignant plasma cells is unique. Other atypical features include frank proteinuria, with a HC in the urine, but normal renal function and no radiological or biochemical evidence of bone involvement. We propose that this unique biclonal myeloma has distinct immunological and clinical features.
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Liu, Yin, David Michelson, Robin Clark, and June-Anne Gold. "Child Neurology: Siblings with infantile epilepsy and developmental delay." Neurology 91, no. 3 (July 16, 2018): 143–47. http://dx.doi.org/10.1212/wnl.0000000000005815.
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ObjectiveChromosome 14q11-q22 deletion syndrome (OMIM 613457) is a rare genomic disorder with a variable phenotype.MethodsWe report 2 full siblings, a brother and sister, with a unique familial 2.4 Mb microdeletion at 14q13.1–14q13.3 by microarray (first identified in the brother, Mayo Clinical Laboratories, 2010).ResultsBoth children presented with infantile spasms that evolved to intractable epilepsy and profound developmental delay. They share distinctive dysmorphic features: long expressionless facies, full cheeks, flattened midface, full lips, and generalized hypotonia. Only the sister has hemophagocytic lymphohistiocytosis (HLH). Testing in the brother revealed 3 variants of unknown significance (VUS) (Greenwood Genetics, epilepsy/seizure panel, 145 genes, 2015). The sister had normal results with a different gene panel (GeneDx, infantile epilepsy panel, 75 genes, 2016) but it did not include the 3 genes in which VUS were identified in her brother. Whole exome sequencing in the mother, father, and both siblings was negative without VUS (GeneDx, XomeDx, 2016). There were no variants within the deleted interval in the intact allele for both children. Parental fluorescent in situ hybridization studies for 14q13.1–14q13.3, done in 2017, were normal. Haplotype analysis of the intact chromosome 14 in the sister supported paternal origin for the deletion and likely germline mosaicism in the father. Haploinsufficiency of genes in the deleted region has not been associated with an abnormal phenotype.ConclusionsThese children have a specific, recognizable neurodevelopmental phenotype and 14q13 microdeletion. This report highlights the challenges of coordinating and interpreting genetic testing in syndromic epilepsy.
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Jiang, Wei, Emily Blyth, Peter J. Shaw, Leighton Edward Clancy, Kenneth P. Micklethwaite, Abir Bhattacharyya, Elissa Atkins, et al. "Donor-Derived T-Cells Specific for WT1 and PRAME in Combination with T-Cells Specific for Multiple Pathogens for Prevention of Relapse and Infection after Haemopoietic Stem Cell Transplant (HSCT) for Acute Myeloid Leukaemia (AML) or High-Risk Myelodysplasia (MDS) - (The INTACT Trial)." Blood 136, Supplement 1 (November 5, 2020): 38. http://dx.doi.org/10.1182/blood-2020-143136.
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Introduction Disease relapse and infection cause significant morbidity and mortality after allogeneic HSCT for AML and MDS. Wilms' tumour 1 (WT1) and preferentially expressed antigen in melanoma (PRAME) are both commonly overexpressed in these conditions, and are attractive targets for immunotherapy. We have assessed the safety of a novel combination of tumour associated antigen (TAA) specific and multipathogen (MP) specific T cells administered prophylactically after HSCT in a phase 1 trial. Methods Patients were eligible for the study if WT1 or PRAME gene expression was elevated as determined by droplet digital PCR on diagnostic tumour samples. TAA and MP specific T cells were generated from stem cell donors by stimulating apheresis-derived mononuclear cells with autologous antigen presenting cells expressing tumour, viral or fungal antigens. T cells specific for CMV, EBV and Aspergillus antigens were produced separately and pooled in equal parts into a MP product. Patients received 1 infusion of MP specific T cells and up to 4 infusions of TAA specific T cells at 4-weekly intervals dosed at 2x107/m2, from 28 days post HSCT. Results Seven HSCT recipients have received a total of 26 T cell infusions to date. Median age was 49 years (range 26-67), disease AML (n=4) or high risk MDS (n=3), conditioning myeloablative (n=6) or reduced-intensity (n=1), donor source sibling (n=4) or matched unrelated (n=3). Median expression of WT1 on diagnostic bone marrow tissue was 1464 copies/104 copies of ABL (0-3870), PRAME 131 copies/104 copies of ABL (4-1670). Mean tumour antigen specificity in the TAA product was 2.2% of CD3+ cells for WT1 and 7.3% of CD4+ cells for PRAME. Mean total pathogen specificity in the MP product was approximately 15% (CMV=4.7% and EBV=5.4% of CD3+ cells, Aspergillus=5.3% of CD4+ cells). Patients received WT1 specific (n=3), PRAME specific (n=3) or both WT1 and PRAME specific T cells (n=1). All patients received MP specific T cells. No immediate infusion-related adverse events were reported. At the time of report, at a median of 375 days post-transplant (80-847), 5 out of 7 patients remain alive. Four patients remain in complete disease remission without graft versus host disease (GVHD). One patient did not proceed after 3 of 5 planned infusions after developing chronic lung GVHD but remains in disease remission. There have been 2 deaths (progressive disease and multiorgan failure). The patient with progressive disease had MDS with complex cytogenetics with evidence of persistent disease pre and post-HSCT, prior to T cell infusions. The patient with multiorgan failure had multiple post-transplant complications including bacterial sepsis, hepatic venoocclusive disease and grade 3 acute GVHD of the gut prior to infusion. Patients had low level viral reactivation (CMV n=3, EBV n=5, BKV n=3, HHV6 n=2), however none required treatment and there were no cases of viral tissue disease or EBV post-transplant lymphoproliferative disorder. There were no invasive fungal infections. Conclusion Prophylactic infusions of donor derived WT1/PRAME specific and multipathogen specific T cells post HSCT are well-tolerated and associated with low rates of infection and relapse in patients treated to date. Disclosures No relevant conflicts of interest to declare.
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McFarland, Janice G., James B. Bussel, Richard H. Aster, and Brian R. Curtis. "Diagnostic Yield Of Serologic Evaluation For Neonatal Alloimmune Thrombocytopenia (NAIT) In Cases With Fetal Abnormalities Without Documented Thrombocytopenia." Blood 122, no. 21 (November 15, 2013): 3660. http://dx.doi.org/10.1182/blood.v122.21.3660.3660.
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Abstract NAIT, in which mothers are sensitized to a paternally derived fetal platelet antigen, is known to be a major cause of fetal in utero intracranial hemorrhage (ICH). The diagnosis can be serologically confirmed by demonstrating a platelet antigen (HPA) incompatibility between the parents (or between mother and fetus or neonate) and detection of maternal antibody with matching specificity. An increasing number of NAIT serologic evaluations are being referred based on a clinical presentation of a fetal hemorrhage or an abnormality thought to be due to such a hemorrhage, usually without a fetal platelet count. We sought to compare the diagnostic yield of our laboratory’s standard NAIT evaluation in cases referred because of in utero ICH without known fetal platelet counts with the yield in a previously reported series of cases that were referred usually because of documented fetal or neonatal thrombocytopenia. Between July 2000 and April 2013, we were consulted by referring physicians on 33 cases in which a fetal abnormality had been detected (usually by ultrasound or MRI) that was either a frank hemorrhage or could have been caused by hemorrhage. No fetal platelet counts had been done. In all cases, no previous sibling had been recognized to have had thrombocytopenia. Of the 33 evaluations performed, 18 were done during an affected pregnancy and 15 were performed after an affected pregnancy had occurred. There were 25 frank ICH, 4 porencephalic cysts (PEC), 2 hydrocephalus only, 1 fetal stroke and in 1 case the abnormality was not specified. The abnormalities were detected between 20 weeks and 35 weeks gestation, median 24 weeks. 15 were detected at 24 weeks or earlier, 11 between 25 and 31 weeks and 2 at 32 weeks or later. In 5 cases (all in the previous pregnancy group) the week in gestation when the abnormality was detected was not known. The standard NAIT evaluation involved testing of maternal serum for antibody to intact platelets, pooled class I HLA, and platelet glycoproteins (GP) including GPIIb/IIIa, GPIa/IIa, GPIb/IX and GPIV derived from blood group O panel platelets of known HPA phenotype. Panel platelets were known to express both alleles (-a and –b) of HPA-1 to 5 and -15. In addition, maternal serum was tested against intact paternal platelets and paternal platelet GPIIb/IIIa. Genotyping was performed on genomic DNA from both parents for HPA -1 to 6, -9 and -15 alleles. In only 2 of the 33 cases (6.4%) was a diagnosis of NAIT serologically confirmed: 1 due to an HPA-15a antibody detected during a current affected pregnancy complicated by a fetal PEC discovered at 20 weeks; and another due to an HPA-5b antibody detected 4 months after a pregnancy complicated by a fetal ICH discovered at 21 weeks gestation. In our previously reported series (Transfusion 44:1220, 2004) NAIT was serologically diagnosed in 31% of 1162 suspected cases, almost all of which were referred based on known fetal or neonatal thrombocytopenia. Moreover, the severity of the fetal abnormalities in these cases (PEC and ICH) occurring prior to 21 weeks gestation is unusual in non-HPA-1a related NAIT, leading to some uncertainty as to whether the HPA antibodies detected in these 2 cases were causal. Although the diagnostic yield of a serologic NAIT evaluation is lower when the clinical indication is either a frank fetal hemorrhage or an abnormality that is likely caused by hemorrhage and no fetal platelet count is available Vs in cases in which fetal or neonatal thrombocytopenia is documented (6.4% Vs 31%), testing may still be reasonable to pursue, given the potential importance for managing subsequent pregnancies in such families. Disclosures: Bussel: Cangene: Research Funding; GlaxoSmithKline: Equity Ownership, Membership on an entity’s Board of Directors or advisory committees, Research Funding; Amgen: Equity Ownership, Membership on an entity’s Board of Directors or advisory committees, Research Funding; Genzyme: Research Funding; IgG of America: Research Funding; Immunomedics: Research Funding; Ligand: Membership on an entity’s Board of Directors or advisory committees, Research Funding; Eisai: Membership on an entity’s Board of Directors or advisory committees, Research Funding; Shionogi: Membership on an entity’s Board of Directors or advisory committees, Research Funding; Sysmex: Research Funding; Symphogen: Membership on an entity’s Board of Directors or advisory committees.
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Sigal, John J., Jana Meislova, Joseph Beltempo, and Daniel Silver. "Some Determinants of Individual Differences in the Behaviour of Children of Parentally Deprived Parents." Canadian Journal of Psychiatry 33, no. 1 (February 1988): 51–56. http://dx.doi.org/10.1177/070674378803300112.
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Parents who had been placed in an orphanage as children rated the behaviour of all their children who were between the ages of 6–18 years on a children's behaviour survey instrument. All families were intact and the parents had not requested professional help for marital problems. A significant number of relationships were found between parental background variables and higher reported levels of conflict with siblings and with parents, dependent-unassertive behaviour, and undemandingness in the children. Although sampling difficulties preclude generalization, the results suggest that repercussion of events in the lives of the first and second generation that are usually pathogenic may be seen in the third generation, even when the second generation may not be grossly adversely affected. These events most frequently related to individual differences in the third generation in the area of undercontrol of aggression directed toward parents and siblings.
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Shimoni, Avichai, Marjory Hertz, Moshe Yeshurun, Orit Portnoy, Izhar Hardan, Michal Amitai, Arnon Nagler, and Sara Apter. "Abdominal CT in the Clinical Evaluation of Acute Graft-Versus-Host Disease of the Gastrointestinal Tract: Diffuse Small Intestine Involvement Is Associated with Severity and Outcome." Blood 104, no. 11 (November 16, 2004): 5073. http://dx.doi.org/10.1182/blood.v104.11.5073.5073.
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Abstract Acute graft-versus-host disease (GVHD) is the major treatment-related complication after allogeneic stem-cell transplantation. Acute GVHD of the gastrointestinal (GI) tract is a clinical diagnosis supported by histo-pathological findings. The presenting symptom is most often large volume diarrhea.The volume of diarrhea determines disease stage and prognosis, however its assessment is inconvenient and inaccurate due to low compliance. Moreover, patients (pts) may present with atypical symptoms such as abdominal pain and vomiting. Also, biopsies of the GI-tract may be falsely negative due to patchy involvement or may be contraindicated in pts with severe thrombocytopenia. This study was designed to determine the CT features associated with acute GI GVHD and to evaluate its role in the assessment of severity and prognosis. Thirty-four consecutive pts with symptoms suggestive of acute GI GVHD were evaluated early after presentation by abdominal CT. The median age was 52 years (range, 20–66). Diagnoses included AML (n=10), ALL (n=5), multiple myeloma (n=8), NHL (n=5), CLL (n=4) and others (n=2). The donors were HLA-matches sibling (n=21), 1-Ag mismatched relative (n=2) or matched unrelated (n=11). Nine pts had myeloablative conditioning and 25 had reduced-intensity regimens. None had infectious etiology by standard evaluation. Eighteen pts had clinical stage I–II of GI-GVHD and 14 had clinical stage III–IV by the Glucksberg criteria. Thirty-two pts had pathological finding in CT. The most consistent finding was thickening of the bowel wall, which was limited to the small (n=11) or large bowel (n=5) or involved both (n=16). Involvement was diffuse or segmental. Other manifestations included intestinal dilatation (n=11), mucosal enhancement (n=3) and gastric wall thickening (n=7). Extra-intestinal findings were also common and included mesenteric stranding (n=22), ascites (n=13) and biliary systems abnormalities (n=11). Ten pts had urinary excretion of orally administered gastrografin which is not normally absorbed by an intact intestine. Diffuse thickening of the small bowel wall and/or any involvement of the large intestine were patterns associated with severe clinical presentation. Eleven and 14 of the 16 patients with clinical stage III–IV GI-GVHD had these patterns, respectively, compared to 5 and 7 of the 18 pts with stage I–II disease (p=0.03). Overall, nineteen pts responded to immunesuppressive therapy. Nine pts are alive; 25 died, 13 of complications directly related to GVHD. Diffuse small bowel disease was associated with poor prognosis. Only six of 16 pts showing this pattern responded to immunosuppressive therapy compared to thirteen of 18 pts without this pattern (p=0.05). The cumulative incidence of GVHD-related death was and 56% (95% CI, 37–87) and 25% (95% CI 11–58), respectively (p=0.05), however overall survival was not significantly different in the two groups. In conclusion, abdominal CT may have an important role in the diagnosis of GVHD in atypical presentations and in the prognostic evaluation. Diffuse small intestinal disease and any colon disease are associated with severe clinical disease. Diffuse small intestinal disease is also associated with poor response to therapy and GVHD-related mortality. CT findings may direct the clinician in determining the therapeutic approach.
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Vinciguerra, Patrizia, Susana Godinho, Kalindi Parmar, David Pellman, and Alan D'Andrea. "Cytokinesis Failure in Fanconi Anemia Pathway Deficient Murine Hematopoietic Stem Cells." Blood 114, no. 22 (November 20, 2009): 495. http://dx.doi.org/10.1182/blood.v114.22.495.495.
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Abstract Abstract 495 Fanconi Anemia (FA) is a rare recessive chromosomal-instability disorder characterized by congenital malformations, a high predisposition to cancer, and progressive bone marrow failure. FA is genetically heterogeneous and, to date, thirteen FA genes have been identified (FANCA, -B, -C, -D1, -D2, -E, -F, -G, -I, -J, -L, -M, -N). The thirteen encoded FA proteins cooperate in a common DNA repair pathway active during the Synthesis (S) phase of the cell cycle. DNA damage detected during replication results in the monoubiquitination of two FA proteins, FANCD2 and FANCI, that translocate into chromatin-associated DNA repair foci where they colocalize with downstream components of the pathway. Partial colocalization with BLM, the RecQ helicase mutated in Bloom's syndrome, has also been described. How disruption of this pathway leads to bone marrow failure is a critical unanswered question. Interestingly, FA cells also have abnormalities that suggest a defect in mitosis, including micronuclei and multinucleation. The objectives of this study were to 1) investigate the role of the FA pathway in normal mitosis and 2) determine whether defects in this function underlie the bone marrow failure of FA patients. For this study, we used HeLa cells transiently or stably knocked down for FA genes, FA patient derived cell lines and hematopoietic stem cells from Fanconi mice models generated in our laboratory (Fancd2-/- and Fancg-/-). First, a polyclonal antibody was raised against FANCI and, together with an anti-FANCD2 antibody, used to investigate the localization of the FANCD2-I complex throughout the cell cycle by immunostaining. FANCI and FANCD2 colocalized to discrete foci on condensed chromosomes in a population of cells in Mitosis (M) phase, consistent with results of Chan et al. (Replication stress induces sister-chromatid bridging at fragile site loci in mitosis. Nat Cell Biol. 2009;11:753-760), Naim and Rosselli (The FANC pathway and BLM collaborate during mitosis to prevent micro-nucleation and chromosome abnormalities. Nat Cell Biol. 2009;11:761-768). These foci were dependent on an intact FA pathway, but did not localize at centromeres and did not increase when the spindle assembly checkpoint was challenged. By immunofluorescence, we showed an increase in the presence of Hoechst positive DNA bridges and PICH positive / BLM positive DNA bridges (Hoechst positive and negative) in anaphase and telophase of FA deficient cells compared to FA proficient cells. This increase of DNA bridges between separating sister chromatids in FA deficient cells correlated with an increase of multinucleated cells. Multinuclearity, scored by immunostaining for microtubules and Hoechst staining for DNA, was the result of cytokinesis failure as observed by live cell imaging. Furthermore, inhibition of apoptosis increased the number of binucleated cells, suggesting that cytokinesis failure led to apoptosis. Importantly, an increase in binucleated cells was also observed in the hematopoietic stem cells population from Fancd2-/- and Fancg-/- mice, compared to wild-type sibling mice, and this increase correlated with elevated apoptosis in those cells. Based on these new findings, we conclude that the Fanconi pathway is required for normal mitosis and hypothesize that apoptosis induced by cytokinesis failure of hematopoietic stem cells may cause the bone marrow failure commonly found in FA patients. Disclosures: No relevant conflicts of interest to declare.
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Callicott, Joseph H., Michael F. Egan, Venkata S. Mattay, Alessandro Bertolino, Ashley D. Bone, Beth Verchinksi, and Daniel R. Weinberger. "Abnormal fMRI Response of the Dorsolateral Prefrontal Cortex in Cognitively Intact Siblings of Patients With Schizophrenia." American Journal of Psychiatry 160, no. 4 (April 2003): 709–19. http://dx.doi.org/10.1176/appi.ajp.160.4.709.
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Shi, Haichun, Yang Yu, Ronghuan Gu, Chenxi Feng, Yu Fu, Xuejie Yu, Jichao Yuan, Qun Sun, and Yongpei Ke. "Male sterile 305 Mutation Leads the Misregulation of Anther Cuticle Formation by Disrupting Lipid Metabolism in Maize." International Journal of Molecular Sciences 21, no. 7 (April 3, 2020): 2500. http://dx.doi.org/10.3390/ijms21072500.
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The anther cuticle, which is mainly composed of lipid polymers, functions as physical barriers to protect genetic material intact; however, the mechanism of lipid biosynthesis in maize (Zea mays. L.) anther remains unclear. Herein, we report a male sterile mutant, male sterile 305 (ms305), in maize. It was shown that the mutant displayed a defective anther tapetum development and premature microspore degradation. Three pathways that are associated with the development of male sterile, including phenylpropanoid biosynthesis, biosynthesis of secondary metabolites, as well as cutin, suberine, and wax biosynthesis, were identified by transcriptome analysis. Gas chromatography-mass spectrometry disclosed that the content of cutin in ms305 anther was significantly lower than that of fertile siblings during the abortion stage, so did the total fatty acids, which indicated that ms305 mutation might lead to blocked synthesis of cutin and fatty acids in anther. Lipidome analysis uncovered that the content of phosphatidylcholine, phosphatidylserine, diacylglycerol, monogalactosyldiacylglycerol, and digalactosyldiacylglycerol in ms305 anther was significantly lower when compared with its fertile siblings, which suggested that ms305 mutation disrupted lipid synthesis. In conclusion, our findings indicated that ms305 might affect anther cuticle and microspore development by regulating the temporal progression of the lipidome in maize.
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Carpenter, Thomas O., John M. Pettifor, Robert M. Russell, Josef Pitha, Sohrab Mobarhan, Mervyn S. Ossip, Stephen Wainer, and Constantine S. Anast. "Severe hypervitaminosis A in siblings: Evidence of variable tolerance to retinol intake." Journal of Pediatrics 111, no. 4 (October 1987): 507–12. http://dx.doi.org/10.1016/s0022-3476(87)80109-9.
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Hunt, Pamela S., Ginger M. Lant, and Christine A. Carroll. "Enhanced intake of ethanol in preweanling rats following interactions with intoxicated siblings." Developmental Psychobiology 37, no. 2 (2000): 90–99. http://dx.doi.org/10.1002/1098-2302(200009)37:2<90::aid-dev4>3.0.co;2-d.
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Kelishadi, R., M. Hashemipour, N. Ahmadi, and F. Haj Sadeghi. "P1080 COMPARISON OF FOOD INTAKE AND ENERGY EXPENDITURE AMONG OBESE AND NON-OBESE SIBLING ADOLESCENTS." Journal of Pediatric Gastroenterology and Nutrition 39, Supplement 1 (June 2004): S467—S468. http://dx.doi.org/10.1097/00005176-200406001-01204.
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Houle, Janie, François Chagnon, Denis Lafortune, Réal Labelle, and Katherine Belleville Paquette. "Correlates of Help-Seeking Behaviour in Adolescents Experiencing a Recent Negative Life Event." Canadian Journal of Family and Youth / Le Journal Canadien de Famille et de la Jeunesse 5, no. 1 (February 12, 2013): 39–63. http://dx.doi.org/10.29173/cjfy18947.
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This study examines the psychological factors associated with formal and informal help-seeking behaviour after a recent negative life event in adolescents 14-17 years old. A sample of 126 adolescents attending secondary schools completed the Life Events Questionnaire (Newcomb), the Beck Depression Inventory, the Temperament and Character Inventory (Cloninger) and the Impulsivity Scale (Barratt). The results indicate that informal help-seeking is more frequent than formal. The factors associated with seeking help from the informal network (friends, parents, siblings, relatives) after the life event were the female gender, living in an intact nuclear family, and reward dependence. Formal help seeking is associated with having sought help from the mother and cognitive impulsivity. Recommendations for increasing adolescents’ help-seeking behaviour are suggested.
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Hunt, Pamela S., Jennifer L. Holloway, and Elka M. Scordalakes. "Social interaction with an intoxicated sibling can result in increased intake of ethanol by periadolescent rats." Developmental Psychobiology 38, no. 2 (2001): 101–9. http://dx.doi.org/10.1002/1098-2302(200103)38:2<101::aid-dev1002>3.0.co;2-4.
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Papadopoulou, Eleni, Jérémie Botton, Ida Henriette Caspersen, Jan Alexander, Merete Eggesbø, Margaretha Haugen, Nina Iszatt, et al. "Maternal seafood intake during pregnancy, prenatal mercury exposure and child body mass index trajectories up to 8 years." International Journal of Epidemiology 50, no. 4 (March 13, 2021): 1134–46. http://dx.doi.org/10.1093/ije/dyab035.
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Abstract Background Maternal seafood intake during pregnancy and prenatal mercury exposure may influence children’s growth trajectories. Methods This study, based on the Norwegian Mother, Father and Child Cohort Study (MoBa), includes 51 952 mother-child pairs recruited in pregnancy during 2002–08 and a subsample (n = 2277) with maternal mercury concentrations in whole blood. Individual growth trajectories were computed by modelling based on child’s reported weight and length/height from 1 month to 8 years. We used linear mixed-effects regression analysis and also conducted discordant-sibling analysis. Results Maternal lean fish was the main contributor to total seafood intake in pregnancy and was positively but weakly associated with child body mass index (BMI) growth trajectory. Higher prenatal mercury exposure (top decile) was associated with a reduction in child’s weight growth trajectory, with the estimates ranging from -130 g [95% Confidence Intervals (CI) = -247, -12 g] at 18 months to -608 g (95% CI = -1.102, -113 g) at 8 years. Maternal fatty fish consumption was positively associated with child weight and BMI growth trajectory, but only in the higher mercury-exposed children (P-interaction = 0.045). Other seafood consumption during pregnancy was negatively associated with child weight growth compared with no intake, and this association was stronger for higher mercury-exposed children (P-interaction = 0.004). No association was observed between discordant maternal seafood intake and child growth in the sibling analysis. Conclusions Within a population with moderate seafood consumption and low mercury exposure, we found that maternal seafood consumption in pregnancy was associated with child growth trajectories, and the direction of the association varied by seafood type and level of prenatal mercury exposure. Prenatal mercury exposure was negatively associated with child growth. Our findings on maternal seafood intake are likely non-causal.
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Davis, Zachary, Martin Felices, Todd R. Lenvik, Sujan Badal, Peter Hinderlie, Bruce R. Blazar, Daniel A. Vallera, and Jeffrey S. Miller. "PD-1 Is Expressed at Low Levels on All Peripheral Blood Natural Killer Cells but Is a Significant Suppressor of NK Function Against PD-1 Ligand Expressing Tumor Targets." Blood 134, Supplement_1 (November 13, 2019): 621. http://dx.doi.org/10.1182/blood-2019-127261.
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Checkpoint blockade has become a promising immunotherapy for the treatment of a variety of malignancies. In particular, the receptor programmed death-1 (PD-1) has become a focus of intense study due to its expression on and negative regulation of T-cell function. The ligand for PD-1, PD-L1, is upregulated on many tumors and, as a result, can suppress antigen-specific T-cells thereby limiting their anti-tumor response. Pharmacological PD-1/PD-L1 axis disruption can occur with either Pembrolizumab and Nivolumab (PD-1 antagonists) and Avelumab and Atezolizumab (PD-L1 antagonists). These antibodies (mAbs) are being used to treat melanoma, non-small cell lung cancer, kidney, bladder and head and neck cancer with varying degrees of success. Like T-cells, natural killer cells (NK) also have potent antitumor cytolytic properties. The expression and functional effects of PD-1 on NK cells remain unclear due to difficulties in receptor detection and efficacy of receptor blockade by available commercial reagents. While some studies have been unable to detect PD-1 on resting NK cells, others have identified PD-1 expression only on specific NK populations under certain conditions (e.g. Cytokine stimulation or virus infection). Here, we identify PD-1 expression on peripheral blood NK cells. Using commercial reagents (Figure 1A) and a FITC-labeled clinical mAb (Pembrolizumab, Pembro), we detect low yet consistent PD-1 expression on all circulating, resting NK cells. Since FITC-Pembro mean fluorescent intensity was low and a high proportion of FITC labeled NK cells overlapped with the isotype control (Figure 1B), we designed a short-chain variable fragment (scFv) of the mAb to determine whether the smaller scFv molecule has better binding and functional activity than the intact mAb. The Pembro scFv bound to resting NK cells with a distinct fluorescent peak compared to the native Prembro from which the scFv was derived (Figure 1B). Compared to intact Prembro, use of the Pembro scFv as a PD-1 antagonist resulted in a 2-fold increase of NK cell cytolytic activity and a 3-4 fold increase in cytokine production against the PD-L1 expressing CML target, K562 (Figure 1C-D) and the AML target, THP-1 (Figure 1E-F). While PD-1 blockade enhanced NK cell degranulation and target cell killing, a greater functional enhancement was seen for interferon-γ production. PD-1 signaling inhibits PI3K induced pAkt and NK function. PD-1/PD-1 ligand blockade by the Pembro scFv resulted in increased NK cell pAKT in the presence of PD-L1 and NK activating NKG2D-ligand-expressing THP-1 cells. In addition to natural cytotoxicity, NK-mediated ADCC was also enhanced with PD-1 blockade. CD33 mAb immunoconjugates have been used to treat AML. Combined anti-CD33 mAb and PD-1 blockade against THP-1 cells resulted in a small but significant increase in NK cell degranulation and a 4-fold increase in cytokine production compared to anti-CD33 mAb without PD-1 blockade (Figure 1G-H). Since stimulation with IL-15, a cytokine that effectively lowers the NK activation threshold, abrogated the benefits of Pembro scFv in diminishing PD-1 inhibitory effects on NK cells, PD-1 control of NK function appears limited to be mostly relevant to resting NK cells. To understand the physiologic expression of PD-1 in vivo, we studied samples taken from AML patients receiving matched sibling donor transplantation at the University of Minnesota. Increased PD-1 on reconstituting NK cells in BMT recipients up to day 100 post-transplant was shown by both flow-cytometric (Figure 2A) and mass-cytometric (CyTOF) analyses (Figure 2B). Blockade of PD-1 on these cells significantly enhanced both NK degranulation (Figure 2C) and cytokine production (Figure 2D) against K562 targets. A similar increase in NK function was observed with PD-1 blockade in AML patients receiving umbilical cord transplants (not shown). These data indicate that PD-1 is present on human NK cells and PD-1 ligation negatively regulates NK function against PD-L1 expressing tumor targets. The observation that functional PD-1 is expressed on NK cells under resting conditions strongly suggests that the use of a PD-1 antagonist, in combination with NK cell therapy, should be clinically effective for treatment of cancer. Disclosures Felices: GT Biopharma.: Other: consulting funds, Research Funding. Blazar:Kamon Pharmaceuticals, Inc: Membership on an entity's Board of Directors or advisory committees; Tmunity: Other: Co-Founder; BlueRock Therapeutics: Membership on an entity's Board of Directors or advisory committees; Regeneron Pharmaceuticals: Membership on an entity's Board of Directors or advisory committees; Five Prime Therapeutics Inc: Co-Founder, Membership on an entity's Board of Directors or advisory committees; KidsFirst Fund: Research Funding; Childrens' Cancer Research Fund: Research Funding; Leukemia and Lymphoma Society: Research Funding; Abbvie Inc: Research Funding; Alpine Immune Sciences, Inc.: Research Funding; RXi Pharmaceuticals: Research Funding; Fate Therapeutics, Inc.: Research Funding; Magenta Therapeutics and BlueRock Therapeuetics: Membership on an entity's Board of Directors or advisory committees. Vallera:GT Biopharma, Inc.: Consultancy, Research Funding. Miller:Fate Therapeutics, Inc: Consultancy, Research Funding; GT BioPharma: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; CytoSen: Membership on an entity's Board of Directors or advisory committees; OnKImmune: Membership on an entity's Board of Directors or advisory committees; Dr. Reddys Laboratory: Membership on an entity's Board of Directors or advisory committees; Moderna: Membership on an entity's Board of Directors or advisory committees. OffLabel Disclosure: Keytruda. PD-1 blockade on NK cells for tumor immunotherapy