Academic literature on the topic 'Multifactorial disorder'
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Journal articles on the topic "Multifactorial disorder"
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Surushkina, S. Yu, E. A. Yakovenko, L. S. Chutko, and M. D. Didur. "Dyslexia as a Multifactorial Disorder." Neuroscience and Behavioral Physiology 51, no. 3 (March 2021): 303–8. http://dx.doi.org/10.1007/s11055-021-01072-8.
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Rieux-Laucat, F., and A. Magerus-Chatinet. "Autoimmune lymphoproliferative syndrome: a multifactorial disorder." Haematologica 95, no. 11 (October 31, 2010): 1805–7. http://dx.doi.org/10.3324/haematol.2010.030395.
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Drossman, Douglas A. "Irritable Bowel Syndrome: A Multifactorial Disorder." Hospital Practice 23, no. 9 (September 15, 1988): 119–33. http://dx.doi.org/10.1080/21548331.1988.11703538.
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Coentre, R., D. Barrocas, and P. Levy. "Low Bone Mineral Density and Psychosis: A Multifactorial Relation." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70491-2.
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Aims:Low bone mineral density (BMD) is a major public health issue leading to fractures, pain and disability. The association between psychosis and low bone density has been suggested in the last years.Method:The authors review the literature in Medline database using the words ‘bone mineral density’, ‘psychosis’, ‘antipsychotic’, ‘schizophrenia’, ‘bipolar disorder’ and ‘psychiatry disorders’.Results:Some studies show elevated prevalence of changes in BMD in patients with psychiatry disorders, namely psychosis. These changes are multifactorial, due to therapeutic factors and/or to the disorder per se. The low BMD induced by some antipsychotic drugs has been attributed mostly to hyperprolactinaemia and its consequences. Lithium, carbamazepine, sodium valproate and the use of thyroid-stimulating hormone-suppressive doses of L-thyroxin used in bipolar disorder also have a negative impact on bone health. Patients with psychosis could be vulnerable to bone abnormalities even without treatment, environmental factors like smoking, sedentary lifestyle, decreased exposure to sunlight, alcoholism, dietary deficiencies and polydipsia are partially responsible for that. Also genetic factors (vitamin D receptor gene, estrogen receptor gene etc.) and biological factors (gender, decreased of peak bone mass, abnormalities in immune-inflammatory mechanisms, hypercortisolemia stress-induced etc.) contribute to the abnormalities in bone dynamics in psychosis.Conclusion:The association between low BMD and psychosis has been demonstrated in literature, understanding all the factors involved in this process will help the development of preventive and treatment strategies. A large study including first psychotic episode patients could be useful to distinguish between disorder and drug induced factors of low BMD in psychosis.
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Hernandez, Diana, and Elizabeth M. C. Fisher. "Down syndrome genetics: unravelling a multifactorial disorder." Human Molecular Genetics 5, Supplement_1 (September 1996): 1411–16. http://dx.doi.org/10.1093/hmg/5.supplement_1.1411.
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Lee, Stella, and Andrew P. Lane. "Chronic Rhinosinusitis as a Multifactorial Inflammatory Disorder." Current Infectious Disease Reports 13, no. 2 (February 1, 2011): 159–68. http://dx.doi.org/10.1007/s11908-011-0166-z.
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Iqbal, Khalid, and Inge Grundke-Iqbal. "Alzheimer's disease, a multifactorial disorder seeking multitherapies." Alzheimer's & Dementia 6, no. 5 (September 2010): 420–24. http://dx.doi.org/10.1016/j.jalz.2010.04.006.
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Scheinberg, P. "Dementia due to vascular disease--a multifactorial disorder." Stroke 19, no. 10 (October 1988): 1291–99. http://dx.doi.org/10.1161/01.str.19.10.1291.
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Benarroch, Eduardo E. "Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder." Mayo Clinic Proceedings 87, no. 12 (December 2012): 1214–25. http://dx.doi.org/10.1016/j.mayocp.2012.08.013.
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Simmons-Alling, Susan, and Sandra Talley. "Bipolar Disorder and Weight Gain: A Multifactorial Assessment." Journal of the American Psychiatric Nurses Association 13, no. 6 (January 2008): 345–52. http://dx.doi.org/10.1177/10783903080130060401.
Full textDissertations / Theses on the topic "Multifactorial disorder"
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Zhang, Feng. "Investigating schizophrenia as a complex multifactorial disorder." Thesis, University of Aberdeen, 2005. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU197547.
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Schizophrenia has a complex aetiology involving both genetic and environmental factors. In this thesis, I describe my research into maternal malnutrition as a potential environmental risk factor and three candidate genetic risk factors for schizophrenia. I examined maternal malnutrition as a potential environment risk factor to schizophrenia in a large cohort dataset collected from a population in China (Wuhu region, Anhui Province) exposed to famine in 1960-1961. Our study shows that prenatal exposure to famine appears to approximately double the risk of schizophrenia, and has no significant effect on the rate of positive family history. Gene-environment interaction is proposed as a possible mechanism. I also carried out DNA association studies on a large Scottish case control sample set to investigate association between three candidate genes, namely DTNBP1, RGS4 and DISC1, and schizophrenia. Despite some modestly significant results from DTNBP1 and RGS4, our results essentially failed to replicate the initial reports. By contrast, DISC1 study showed significant association with schizophrenia for two markers in 5' end of the gene at allele, genotype and haplotype levels. The significant distributions of risk allele and haplotype are similar to the results from an earlier Finnish study.
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Campbell, Margaret. "Balance disorder after traumatic brain injury : a multifactorial observational study." Thesis, Sheffield Hallam University, 2007. http://shura.shu.ac.uk/20637/.
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This research was undertaken to improve the assessment and treatment of balance disorder after Traumatic Brain Injury (TBI). It had three aims: to identify factors that have shaped healthcare practice concerning balance disorder and describe barriers to improved practice; to develop understanding of the nature of TBI balance disorder; to establish proposals for an improved healthcare response for those with balance disorder following TBI. TBI is a significant cause of disability in the young adult population and problems with balance are consistently reported. A mixed methods approach was employed to address the aims within a common framework. This comprised a series of subject reviews, an observational study and a systematic analysis of emergent findings. Topics for the subject reviews were chosen for their relevance to TBI physiotherapy practice. The observational study involved 27 participants in the recovery and rehabilitation phase after TBI and was structured using a new comprehensive assessment protocol developed from first principles. Findings were explored using frequency analysis and thematic analysis generated from the development of individual participant narratives. Emergent topics were then considered with reference to the literature, existing theories and concepts of postural control. Different conceptualisations of balance were identified, influenced by discipline tradition, their evidence base, the evolution of ideas, and past and current purpose. Practice development was constrained by the lack of a comprehensive conceptualisation of human balance, inconsistent and fragmented service response and limited knowledge concerning the nature and prevalence of impairments affecting balance function after TBI. Balance disorder was found to be highly prevalent and multifactorial in nature. New sensorimotor characteristics of TBI balance disorder were identified, including observations of importance to the contentious debate concerning symptomatic minor TBI. Issues of key importance in the structure and process of assessment were also identified. Balance disorder is prevalent in the rehabilitation and recovery phase following TBI and is multifactorial in nature. Assessment and treatment of suspected balance disorder could be enhanced by the adoption of a single comprehensive conceptualisation of human balance, a systematic approach to assessment and formulation of causal hypotheses and a service process focused on the functional requirements of individuals. Research for the enhanced development of assessment and intervention strategies should also be pursued in the same context.
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Sayers, Laurie A. "Osteoporosis : a model for cross-cultural investigation of a multifactorial disorder." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1124873.
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The purpose of this paper is the development of a model to investigate possible causal relationships among some of the commonly reported risk factors for the development of osteoporosis and consequential hip fracture. Comparison of hip fracture incidence between women of primarily European descent, referred to in the literature as Caucasians, and Japanese women is made. Studies report the incidence of hip fractures among Japanese women is lower than among Caucasian women. Numerous factors related to the development of osteoporosis are significantly different between Japan and the United States. The model helps explain the interrelationships among the variables involved in this observed geographical variation in hip fracture incidence.Department of Anthropology
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Adaralegbe, Adeleye Ayinde. "Multifactorial Determinants of Change in Mental Disorder and Happiness among Older Americans." Thesis, University of North Texas, 2020. https://digital.library.unt.edu/ark:/67531/metadc1707369/.
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Mental health is an intrinsic capability that constitute an essential component of healthy aging. Mental health is constituted by positive constructs such as happiness and negative constructs (mental disorders) such as depression. As people grow older, they become more prone to developing mental disorders which are linked to poorer quality of life, increased disability, increased utilization and cost of health services, and higher rates of suicide. This dissertation involved three studies that focused on factors that predict change in mental disorders and happiness of older Americans over a period of five years. Two waves of publicly available national representative data from the National Social Life Health and Aging Project (NSHAP) collected in 2010 and 2015 were used. A total of 2210 older adults within the ages 62-90 years were used in the analyses. Mental health measures were CES-Depression scale, HADS anxiety scale, and self-rated happiness. Essay 1 aimed to identify the important aspects of older adults' interaction with their neighborhood that predict the presence of mental disorder and happiness. Essay 2 evaluated the psychosocial factors that predict change in mental disorder and happiness of older adults, whereas essay 3 investigated the multifactorial determinants of change in mental disorder and happiness of older adults. These three essays provide insight into the impact of mental health in old age and the role of environmental, social, and demographic factors in successful aging. It also provides gaps for future research in the field of mental health and aging.
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Cottrell, Catherine Elise. "Genetic variation and complex disease the examination of an X-linked disorder and a multifactorial disease /." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1196182829.
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Cottrell, Catherine E. "Genetic variation and complex disease: the examination of an X-linked disorder and a multifactorial disease." The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1196182829.
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Chikhani, Sherin. "The Potential Role of GATA4, ESR1, GRIA3 and SCN1A Genes in Migraine Susceptibility." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/366267.
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Migraine is a common and painful neurological disorder, with genetic and environmental components. The prevalence of migraine varies between different racial groups, being higher in Caucasian populations (12%). Several conditions have been shown to be comorbid with migraine. One heart disorder that has been associated with migraine is a cardiac malformation affecting the interatrial septum and leading to patent foramen ovale (PFO), resulting from an incomplete anatomic fusion of the atrial septum primum and secundum. Mutations in the development regulatory gene GATA-4, located on human chromosome 8p23.1-p22, have been found to be responsible for some cases of congenital heart defects including PFO. To determine whether the GATA-4 gene is involved in migraine, the present study performed an association analysis of a common GATA-4 variant that results in a change of amino acid (S377G), in a large case/control population (275 unrelated Caucasian migraineurs versus 275 control individuals). Samples were genotyped for the single nucleotide polymorphism (SNP) using FACSArray flow cytometer and frequencies for this variant compared in migraine cases and age, sex and ethnicity matched controls...Thesis (Masters)
Master of Philosophy (MPhil)
School of Medical Science
Griffith Health
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Tajouri, Lotfi, and n/a. "Gene Expression Analysis and Genetic Studies in Multiple Sclerosis." Griffith University. School of Health Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060111.123933.
Full textAbstract:
Multiple Sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS). As part of this disorder the myelin sheath undergoes degeneration, leading to alterations in the conductivity of axons, and impaired function. The onset of the disease occurs in young adults and clinical pathology is characterised by varying severity. These include i) Relapsing Remitting MS (RR-MS), ii) Secondary Progressive MS (SP-MS) and iii) Primary Progressive MS (PP-MS). MS is more prevalent in women and accounts for more than two thirds of all MS sufferers. MS is considered to be a multifactorial disorder with both genetic and environmental components. The prevalence of MS is dependent on geographical localisation, with lower sunlight exposure linked to higher prevalence. Also, studies show an increased risk in close relatives, or in identical twins, indicating a significant genetic component to the disorder. There are a number of genes that may plausibly be involved in MS pathophysiology. These include myelin-related genes, such as the myelin basic protein (MBP), immune-related genes, such FC receptor and osteopontin, and heat shock proteins such as xb crystallin. These candidate genes have been implicated in a variety of ways but usually through immunological and/or genetic studies. One of the most consistent findings in recent years has been the association of disease with alterations in the specific major histocompatibility complex (MHC) localised to chromosome 6p21.3, and includes MHC I, II, III. Genome wide screens have permitted the identification of loci in the genome, which are associated with MS susceptibility. The number of genes involved in MS is unknown and several case-control association studies have been undertaken to reveal the involvement of potential candidate genes. In general terms, current research is aimed at determining allelic variation of candidate genes. Such genes have been implicated in MS because they reside within susceptible regions of the chromosome associated with MS or they have a plausible potential pathophysiological role in MS. Candidate loci investigated in this study, for association with MS susceptibility, include members of the nitric oxide synthase family of metabolic proteins (inducible NOS, iNOS/NOS2A and neuronal NOS, nNOS), methylenetetrahydrofolate reductase (MTHFR), catechol-O-methyl transferase (COMT), and vitamin D receptor (VDR). The MS population used in all studies consisted of over 100 MS cases and gender, age and ethnicity matched controls. In our study of inducible and neuronal NOS genes, PCR based assays were developed to amplify a region of both promoters that contained known microsatellite variation. Supporting phyisological data suggests that the neuroinflammatory aspects of MS are associated with aberrant NO production, which may be due to aberrant regulation of NOS activity. Specific amplified products were identified by fluorescent capillary electrophoresis and allele frequencies were statistically compared using chi-squared analysis. In the nNOS and iNOS study, no association was identified with allele frequency variation and MS susceptibility (nNOS: ?2=5.63, P=0.962; iNOS: ?2=3.4; P=0.082). Similarly, no differences in allele frequencies were observed for gender or clinical course for both markers (Pvalue greater than 0.05). In short, results from this study indicate that the NOS promoter variations studied do not play a significant role in determining susceptibility to MS in the tested population. The COMT and MTHFR genes are localised at 22q12-13 and 1p36.3 respectively, regions of the genome that have been found to be positively associated with MS susceptibility. In our research, we set out to examine the G158A change in the 4th exon of the COMT gene. This functional mutation leads to an amino acid change (valine to methionine) that is directly associated with changes in the activity of COMT. The MTHFR enzyme plays a role in folate metabolism, and can be implicated in the turnover of homocysteine. Previous investigations have shown that high levels of homocysteine are encountered in MS patients, where it is also linked to demyelination in the CNS. In our study the aim was to examine the C677T variation (alanine to valine amino acid change) in the exon 4 coding region of the MTHFR gene and the G158A variation in the COMT gene. Restriction fragment length polymorphism (RFLP) analysis and gel electrophoresis was used to identify specific alleles for both COMT and MTHFR. However, as with the NOS study, no specific association was identified between MS susceptibility and variation for either of the tested COMT or MTHFR (Pvalue greater than 0.05) variants. In a final genomic investigation of the MS population, three variations in the VDR gene were analysed for association with MS susceptibility and pathology. Using RFLP analysis, three VDR variants were investigated with genotypes detected using the Taq I, Apa I and Fok I restriction enzymes. In contrast to previous genotypic analyses, this study did show a positive association, specifically between the functional variation in exon 9 of the VDR gene and MS (Taq I, 2= 7.22, P= 0.0072). Interestingly, the Apa I variant of VDR was also found to be associated with MS ( 2=4.2, P=0.04). The Taq I and Apa I variants were also found to be in very strong and significant linkage disequilibrium (D'=0.96, Pvalue less than 0.0001) and their associations were more prominent with the progressive forms of MS (SP-MS and PP-MS). In addition to genotypic analysis of a clinical population, additional research was undertaken to identify novel targets for MS susceptibility studies. Global gene expression analysis was undertaken using comparative subtractive fluorescent microarray technology to examine differences in gene activity (expression) in age and sex matched MS plaque tissue and anatomically matched normal white matter (NWM). MS plaques were obtained post mortem from MS sufferers with no drug history in the last two months before death and matched anatomically to healthy white matter from donors with no previous neurological disorders. Target arrays consisted of 5000 cDNAs and analysis was conducted using the Affymetrix 428 scanner. In this way, 139 genes were shown to be differentially regulated in MS plaque tissue compared to NWM. Of these, 69 genes showed a common pattern of expression in the chronic active and acute plaque tissues investigated (Pvalue less than 0.0001, a=0.73); while 70 transcripts were uniquely differentially expressed ( 1.5-fold) in either acute or chronic active lesions. To validate the gene expression profile results, quantitative real time reverse transcriptase (RT) PCR (Q-PCR) analysis was performed. 12 genes were selected because they were shown to be differentially expressed by array analysis in this study, or because of their involvement in MS pathology. These included transferrin (TF), superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPX1), glutathione S-transferase pi (GSTP1), crystallin, alpha-B (CRYAB), phosphomannomutase 1 (PMM1), tubulin beta-5 (TBB5), inositol 1,4,5-trisphosphate 3-kinase B (ITPKB), calpain 1 (CAPNS1), osteopontin (SPP1 or OPN), as well as the signal transducer and activator of transcription 1 (STAT1) and protein inhibitor of activated STAT1 (PIAS1). Both absolute (copy number) and comparative differences in the relative levels of expression in MS lesions and NWM were determined for each gene. The results from this study revealed a significant correlation of real time PCR results with the microarray data, while a significant correlation was also found between comparative and absolute determinations of fold. As with the results of array analysis, a significant difference in gene expression patterning was identified between chronic active and acute plaque pathologies. For example, a up to 50-fold increase in SPP1 and ITPKB levels in acute plaques contrasted with the 5-fold or less increase in chronic active plaques (P less than 0.0.1, unpaired t-Test). Of particular note, gamma-amino butyric acid receptor ?2 (GABG2), integrin ?5 (ITGB5), complement component 4B (C4B), parathyroid hormone receptor 1 (PTHR1) were found up-regulated in MS and glial derived neurotropic factor ?2 (GDNFA2), insulin receptor (INSR), thyroid hormone receptor ZAKI4 (ZAKI4) were found down-regulated in MS. Data also revealed a decreased expression of the immune related genes STAT1 and PIAS1 in acute plaques. In conclusion, this research used both genomic analysis and technologies in gene expression to investigate both known and novel markers of MS pathology and susceptibility. The study developed tools that may be used for further investigation of clinical pathology in MS and have provided interesting initial expression data to further investigate the genes that play a role in MS development and progression.
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Tajouri, Lotfi. "Gene Expression Analysis and Genetic Studies in Multiple Sclerosis." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/366467.
Full textAbstract:
Multiple Sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS). As part of this disorder the myelin sheath undergoes degeneration, leading to alterations in the conductivity of axons, and impaired function. The onset of the disease occurs in young adults and clinical pathology is characterised by varying severity. These include i) Relapsing Remitting MS (RR-MS), ii) Secondary Progressive MS (SP-MS) and iii) Primary Progressive MS (PP-MS). MS is more prevalent in women and accounts for more than two thirds of all MS sufferers. MS is considered to be a multifactorial disorder with both genetic and environmental components. The prevalence of MS is dependent on geographical localisation, with lower sunlight exposure linked to higher prevalence. Also, studies show an increased risk in close relatives, or in identical twins, indicating a significant genetic component to the disorder. There are a number of genes that may plausibly be involved in MS pathophysiology. These include myelin-related genes, such as the myelin basic protein (MBP), immune-related genes, such FC receptor and osteopontin, and heat shock proteins such as xb crystallin. These candidate genes have been implicated in a variety of ways but usually through immunological and/or genetic studies. One of the most consistent findings in recent years has been the association of disease with alterations in the specific major histocompatibility complex (MHC) localised to chromosome 6p21.3, and includes MHC I, II, III. Genome wide screens have permitted the identification of loci in the genome, which are associated with MS susceptibility. The number of genes involved in MS is unknown and several case-control association studies have been undertaken to reveal the involvement of potential candidate genes. In general terms, current research is aimed at determining allelic variation of candidate genes. Such genes have been implicated in MS because they reside within susceptible regions of the chromosome associated with MS or they have a plausible potential pathophysiological role in MS. Candidate loci investigated in this study, for association with MS susceptibility, include members of the nitric oxide synthase family of metabolic proteins (inducible NOS, iNOS/NOS2A and neuronal NOS, nNOS), methylenetetrahydrofolate reductase (MTHFR), catechol-O-methyl transferase (COMT), and vitamin D receptor (VDR). The MS population used in all studies consisted of over 100 MS cases and gender, age and ethnicity matched controls. In our study of inducible and neuronal NOS genes, PCR based assays were developed to amplify a region of both promoters that contained known microsatellite variation. Supporting phyisological data suggests that the neuroinflammatory aspects of MS are associated with aberrant NO production, which may be due to aberrant regulation of NOS activity. Specific amplified products were identified by fluorescent capillary electrophoresis and allele frequencies were statistically compared using chi-squared analysis. In the nNOS and iNOS study, no association was identified with allele frequency variation and MS susceptibility (nNOS: ?2=5.63, P=0.962; iNOS: ?2=3.4; P=0.082). Similarly, no differences in allele frequencies were observed for gender or clinical course for both markers (Pvalue greater than 0.05). In short, results from this study indicate that the NOS promoter variations studied do not play a significant role in determining susceptibility to MS in the tested population. The COMT and MTHFR genes are localised at 22q12-13 and 1p36.3 respectively, regions of the genome that have been found to be positively associated with MS susceptibility. In our research, we set out to examine the G158A change in the 4th exon of the COMT gene. This functional mutation leads to an amino acid change (valine to methionine) that is directly associated with changes in the activity of COMT. The MTHFR enzyme plays a role in folate metabolism, and can be implicated in the turnover of homocysteine. Previous investigations have shown that high levels of homocysteine are encountered in MS patients, where it is also linked to demyelination in the CNS. In our study the aim was to examine the C677T variation (alanine to valine amino acid change) in the exon 4 coding region of the MTHFR gene and the G158A variation in the COMT gene. Restriction fragment length polymorphism (RFLP) analysis and gel electrophoresis was used to identify specific alleles for both COMT and MTHFR. However, as with the NOS study, no specific association was identified between MS susceptibility and variation for either of the tested COMT or MTHFR (Pvalue greater than 0.05) variants. In a final genomic investigation of the MS population, three variations in the VDR gene were analysed for association with MS susceptibility and pathology. Using RFLP analysis, three VDR variants were investigated with genotypes detected using the Taq I, Apa I and Fok I restriction enzymes. In contrast to previous genotypic analyses, this study did show a positive association, specifically between the functional variation in exon 9 of the VDR gene and MS (Taq I, 2= 7.22, P= 0.0072). Interestingly, the Apa I variant of VDR was also found to be associated with MS ( 2=4.2, P=0.04). The Taq I and Apa I variants were also found to be in very strong and significant linkage disequilibrium (D'=0.96, Pvalue less than 0.0001) and their associations were more prominent with the progressive forms of MS (SP-MS and PP-MS). In addition to genotypic analysis of a clinical population, additional research was undertaken to identify novel targets for MS susceptibility studies. Global gene expression analysis was undertaken using comparative subtractive fluorescent microarray technology to examine differences in gene activity (expression) in age and sex matched MS plaque tissue and anatomically matched normal white matter (NWM). MS plaques were obtained post mortem from MS sufferers with no drug history in the last two months before death and matched anatomically to healthy white matter from donors with no previous neurological disorders. Target arrays consisted of 5000 cDNAs and analysis was conducted using the Affymetrix 428 scanner. In this way, 139 genes were shown to be differentially regulated in MS plaque tissue compared to NWM. Of these, 69 genes showed a common pattern of expression in the chronic active and acute plaque tissues investigated (Pvalue less than 0.0001, a=0.73); while 70 transcripts were uniquely differentially expressed ( 1.5-fold) in either acute or chronic active lesions. To validate the gene expression profile results, quantitative real time reverse transcriptase (RT) PCR (Q-PCR) analysis was performed. 12 genes were selected because they were shown to be differentially expressed by array analysis in this study, or because of their involvement in MS pathology. These included transferrin (TF), superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPX1), glutathione S-transferase pi (GSTP1), crystallin, alpha-B (CRYAB), phosphomannomutase 1 (PMM1), tubulin beta-5 (TBB5), inositol 1,4,5-trisphosphate 3-kinase B (ITPKB), calpain 1 (CAPNS1), osteopontin (SPP1 or OPN), as well as the signal transducer and activator of transcription 1 (STAT1) and protein inhibitor of activated STAT1 (PIAS1). Both absolute (copy number) and comparative differences in the relative levels of expression in MS lesions and NWM were determined for each gene. The results from this study revealed a significant correlation of real time PCR results with the microarray data, while a significant correlation was also found between comparative and absolute determinations of fold. As with the results of array analysis, a significant difference in gene expression patterning was identified between chronic active and acute plaque pathologies. For example, a up to 50-fold increase in SPP1 and ITPKB levels in acute plaques contrasted with the 5-fold or less increase in chronic active plaques (P less than 0.0.1, unpaired t-Test). Of particular note, gamma-amino butyric acid receptor ?2 (GABG2), integrin ?5 (ITGB5), complement component 4B (C4B), parathyroid hormone receptor 1 (PTHR1) were found up-regulated in MS and glial derived neurotropic factor ?2 (GDNFA2), insulin receptor (INSR), thyroid hormone receptor ZAKI4 (ZAKI4) were found down-regulated in MS. Data also revealed a decreased expression of the immune related genes STAT1 and PIAS1 in acute plaques. In conclusion, this research used both genomic analysis and technologies in gene expression to investigate both known and novel markers of MS pathology and susceptibility. The study developed tools that may be used for further investigation of clinical pathology in MS and have provided interesting initial expression data to further investigate the genes that play a role in MS development and progression.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
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Percelay, Solenn. "Validation d'un modèle murin de schizophrénie pour améliorer la recherche de nouveaux traitements : approche psychopharmacologique, en imagerie et en électrophysiologie A new 3-hit mouse model of schizophrenia built on genetic, early and late factors Functional dysregulations in CA1 hippocampal networks of a 3-hit mouse model of schizophrenia Olfactory laterality is valence-dependent in mice Assessing olfactory laterality in mice: new tool in preclinical psychiatric study Combination of MAP6 deficit, maternal separation and MK801 in female mice: a 3-hit animal model of neurodevelopmental disorder with cognitive deficits Antipsychotic lurasidone: Behavioural and pharmacokinetic data in C57BL/6 mice." Thesis, Normandie, 2021. http://www.theses.fr/2021NORMC403.
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La schizophrénie est une maladie psychiatrique très invalidante qui concerne près de 1% de la population. Bien que son étiologie soit toujours inconnue, elle est certainement multifactorielle et comprend une interaction entre prédisposition génétique et facteurs environnementaux. Il existe des traitements médicamenteux mais ils ne sont pas totalement efficaces, particulièrement pour la prise en charge des symptômes négatifs et des déficits cognitifs. Le développement de nouveaux traitements plus efficaces passe par l’amélioration des modèles animaux prenant en compte le caractère multifactoriel de l’étiologie de cette pathologie.Nous avons développé un modèle murin multifactoriel de schizophrénie innovant (modèle 3-hit) présentant une forte validité de construction. Pour cela, nous avons combiné une modification génétique (1er hit : délétion partielle du gène MAP6) avec un stress environnemental précoce (2nd hit : séparation maternelle de 24h au 9ème jour de vie) et une exposition tardive au THC durant l’adolescence (3ème hit : administration quotidienne de tétrahydrocannabinol à 8mg/kg du 32ème au 52ème jour).Dans un premier temps, nous avons montré une bonne validité d’apparence de ce modèle à travers des études comportementale, en imagerie et en électrophysiologie. En effet, au niveau comportemental les souris 3-hit présentent des symptômes de type négatif, des déficits cognitifs et une altération de la latéralité olfactive. Nous avons aussi montré un déficit d’inhibition du réflexe de sursaut, qui est un élément comportemental clef dans les modèles animaux de schizophrénie, car il est également utilisé en recherche clinique. Nous avons également observé certaines altérations morphologiques et fonctionnelles cérébrales caractéristiques de la schizophrénie comme une réduction du volume de l’hippocampe, une altération des fibres du corps calleux et un dysfonctionnement des systèmes de neurotransmission glutamatergique et GABAergique. Certains dimorphismes sexuels ont été également montrés dans nos études.Dans un deuxième temps, nous avons comparé les déficits des animaux 3-hit avec ceux d’autres modèles de schizophrénie développés au laboratoire. La caractérisation des effets de chaque facteur, indépendamment et en association, nous a permis de mettre en évidence un phénomène de synergie entre les facteurs et non une simple addition des déficits induits par chacun d’entre eux.Le modèle de schizophrénie 3-hit présente de bonnes validités de construction et d’apparence, il est maintenant nécessaire afin de parfaire sa caractérisation de tester sa validité pharmacologiqueAffecting 1% of worldwide population, schizophrenia is a debilitating pathology. Whether the aetiology of schizophrenia remains unknown, its multifactorial aspect is conversely now well admitted, and certainly gathers genetic vulnerability and environmental factors. Actual treatments are still unmet, particularly for negative and cognitive symptoms. For a better translation from treatments design of schizophrenia to clinical efficiency, there is a crucial need to refine preclinical animal models that considers the multifactorial aspects of this disease.We developed a new murine multifactorial model of schizophrenia (3-hit), that possesses a strong construct validity. To this, we combined a genetic predisposition (1st hit: partial deletion of MAP-6) with an early postnatal stress (2nd hit: 24 h maternal separation at postnatal day 9), and a late cannabinoid exposure during adolescence (3rd hit: tetrahydrocannabinol THC from post-natal day 32 to 52; 8 mg/kg/day).First, we characterised a promising face validity through behavioural, imaging and electrophysiological studies. At behavioural level, we demonstrated that 3-hit mice displayed negative-like symptoms, cognitive deficits and altered olfactory laterality. Moreover, we showed a sensory motor gating deficit, that is a major translational clue for animal models of schizophrenia. Additionally, 3-hit mice displayed some characteristic morphological and functional impairments of the disease: reduced hippocampal volume, altered callosal fibres, glutamatergic and GABAergic neurotransmission dysfunctions. We moreover highlighted some sexual dimorphisms.Second, we compared deficits of 3-hit mice to those of others models of schizophrenia developed in our laboratory. Deficits induced by one factor, or combination of several factors, evidenced a synergistic effect, and not a simple addition between each of them.The 3-hit model therefore presents strong construct validity and promising face validity, encouraging to assess the pharmacological validity
Books on the topic "Multifactorial disorder"
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Vlassakova, Bistra G. Anesthesia for the Child with Autism Spectrum Disorder. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0063.
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Autism spectrum disorder (ASD) is the fastest growing neurodevelopmental disorder. Approximately 1% of the world’s population is affected. Patients with ASD have impairment in social interactions and communication and exhibit repetitive and restrictive behaviors and interests. The exact etiology of the condition is unknown, and it is believed to be multifactorial in origin—genetic predisposition and environmental factors have been implicated. Patients with ASD can be highly intelligent or severely developmentally delayed. The wide variety of clinical presentations poses serious challenges to the anesthesiologist. Common clinical manifestations include difficulties with changing daily routines and stereotyped behavior as well as hypersensitivity to light, noise, and unfamiliar people. Patients with ASD are therefore susceptible to behavioral outbursts during the perioperative period. Assuring a smooth perioperative course for this patient population can be achieved by a multidisciplinary team approach and good communication between caregivers and team members.
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Prasad, Supritha, and Edwin H. Cook. Novel Approaches for Treating Pediatric Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0067.
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Multifactorial mechanisms, including varying degrees of polygenic risk, contribute to most child onset psychiatric disorders. Methods to better understand the biological impact of inherited low-risk variation are emerging, and these studies may be useful to develop novel treatments for childhood onset psychiatric disorders. In some neurodevelopmental disorders, specifically autism spectrum disorder (ASD) and intellectual disability (ID), recurrent spontaneously mutated genes have been identified. This leads to the current focus on individual, high-risk targets (e.g., SHANK3, FMR1, MECP2, CHD8) for development of novel treatments. This chapter summarizes and begins to compare neurobiological data from several distinct single gene disorders as a means to guide further therapeutic development based on overlapping pathways of interest.
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Pezzini, Alessandro. Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0011.
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Ischaemic stroke is a heterogeneous multifactorial disorder. Although epidemiological data from twin and family studies provide substantial evidence for a genetic basis for stroke, the contribution of genetic factors identified so far is small. Large progress has been made in single-gene disorders associated with ischaemic stroke, particularly at young age. By contrast, little is known about the genes associated with multifactorial stroke. The reported genome-wide association studies of ischaemic stroke have shown that no single common genetic variant imparts major risk, but data on early-onset disease are scarce in this regard. Larger studies with samples numbering in the thousands are ongoing to identify common variants with smaller effects on risk. This approach, in addition with new analytic techniques, will likely contribute to the identification of additional genes, novel pathways, and eventually novel therapeutic approaches to cerebrovascular disorders in the near future. The aims of this review are to summarize data on clinical, genetic, and epidemiologic aspects of monogenic conditions associated with juvenile ischaemic stroke, to discuss recent findings and methodological limitations regarding the genetics of sporadic ischaemic stroke in this age category, and to provide a brief overview of the potential future approaches to stroke genetics.
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Timothy, Bishop D., and Sham Pak, eds. Analysis of multifactorial disease. Oxford: BIOS, 2000.
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(Editor), T. Bishop, and P. Sham (Editor), eds. Analysis of Multifactorial Diseases (Human Molecular Genetics). Academic Press, 2000.
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Giuseffi, Jennifer, John McPherson, Chad Wagner, and E. Wesley Ely. Acute cognitive disorders: recognition and management of delirium in the cardiovascular intensive care unit. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0074.
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Delirium is the most common acute cognitive disorder seen in critically ill patients in the cardiovascular intensive care unit. It is defined as a disturbance of consciousness and cognition that develops suddenly and fluctuates over time. Delirious patients can become hyperactive, hypoactive, or both. The occurrence of delirium during hospitalization is associated with increased in-hospital and long-term morbidity and mortality. The cause of delirium is multifactorial and may include imbalances in neurotransmitters, inflammatory mediators, metabolic disturbances, impaired sleep, and the use of sedatives and analgesics. Patients with advanced age, dementia, chronic illness, extensive vascular disease, and low cardiac output are at particular risk of developing delirium. Specialized bedside assessment tools are now available to rapidly diagnose delirium, even in mechanically ventilated patients. Increased awareness of delirium risk factors, in addition to non-pharmacological and pharmacological treatments for delirium, can be effective in reducing the incidence of delirium in cardiac patients and in minimizing adverse outcomes, once delirium occurs.
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McPherson, John, Jennifer Giuseffi, Chad Wagner, and E. Wesley Ely. Acute cognitive disorders: recognition and management of delirium in the cardiovascular intensive care unit. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0074_update_001.
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Delirium is the most common acute cognitive disorder seen in critically ill patients in the cardiovascular intensive care unit. It is defined as a disturbance of consciousness and cognition that develops suddenly and fluctuates over time. Delirious patients can become hyperactive, hypoactive, or both. The occurrence of delirium during hospitalization is associated with increased in-hospital and long-term morbidity and mortality. The cause of delirium is multifactorial and may include imbalances in neurotransmitters, inflammatory mediators, metabolic disturbances, impaired sleep, and the use of sedatives and analgesics. Patients with advanced age, dementia, chronic illness, extensive vascular disease, and low cardiac output are at particular risk of developing delirium. Specialized bedside assessment tools are now available to rapidly diagnose delirium, even in mechanically ventilated patients. Increased awareness of delirium risk factors, in addition to non-pharmacological and pharmacological treatments for delirium, can be effective in reducing the incidence of delirium in cardiac patients and in minimizing adverse outcomes, once delirium occurs.
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Cohen, Mary Ann, Anna L. Dickerman, and Harold W. Goforth. Distress in Persons with HIV and AIDS. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0022.
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Persons with HIV have multifactorial and multidimensional sources of distress. Distress has a profoundly negative impact on persons with HIV and their loved ones. While the term distress is more acceptable to patients and does not carry with it the stigma of a specific psychiatric diagnostic disorder, the anguish and suffering associated are still painful. This chapter explores the sources for distress utilizing a comprehensive biopsychosocial approach and presents ways to recognize distress. Related tools in assessing HIV-related distress include the Distress Thermometer (DT), Hospital Anxiety and Depression Scale (HADS), and HIV Symptom Distress Scale (SDS). An overview of the symptoms and illnesses associated with distress include biological, psychological, and social aspects including HIV stigma. Evidence-based approaches to alleviate distress in persons with HIV/AIDS are also presented in the chapter.
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Abbott, Richard. Gait disorders. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0046.
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Gait problems can arise from a number of different causes ranging from primary neurological to locomotor conditions. Prevalence increases with age, and causation is often multifactorial. Falls are a frequent consequence. This chapter covers the diagnosis of gait disorders and therapies.
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Thomas, David F. M. Disorders of sex development. Edited by David F. M. Thomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0124.
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The aetiology of disorders of sex development (DSD) is multifactorial and includes chromosomal defects, developmental abnormalities of the gonads, and defects of hormonal synthesis and expression. Infants born with ambiguous genitalia require urgent investigation because of the risk of hyponatraemia associated with congenital adrenal hyperplasia (CAH) and to permit an informed decision on gender assignment. CAH is the commonest form of DSD, accounting for around 80% of all infants born with ambiguous genitalia. Despite controversy regarding timing and consent, feminizing genitoplasty in early childhood remains the accepted management for girls with significant clitoromegaly. Surgical reconstruction for 46XY DSD is guided by several factors, notably the size of the phallus and gonadal phenotype. The majority of individuals with disorders of sex development will require ongoing specialist care and long-term multidisciplinary follow-up and support.
Book chapters on the topic "Multifactorial disorder"
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Riess, Olaf, and R. Krüger. "Parkinson’s disease — a multifactorial neurodegenerative disorder." In Journal of Neural Transmission. Supplementa, 113–25. Vienna: Springer Vienna, 1999. http://dx.doi.org/10.1007/978-3-7091-6360-3_6.
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Richardson, Rita, William D. Rumbaugh, and Hanna Zembrzuska. "The Multifactorial Approach to PTSD in the Active Duty Military Population." In Posttraumatic Stress Disorder and Related Diseases in Combat Veterans, 225–31. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22985-0_16.
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Lavorato, Elisabetta, Antonio Rampino, and Valentina Giorgelli. "Gender Dysphoria: Overview and Psychological Interventions." In Practical Clinical Andrology, 263–72. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11701-5_20.
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AbstractIn the DSM V, the condition known as “Gender Identity Disorder” becomes “Gender Dysphoria” in order to avoid the stigma of being labeled as carriers of psychopathology. Gender Dysphoria (GD) refers to mental discomfort deriving by incongruence between the expressed gender and the assigned one. The term Transgender refers to identities or gender expressions that differ from social expectations typically based on the birth assigned sex. Not all people living “Gender Variance” express psychological or physic discomfort. The personal gender identity develops influenced by emotionally significant relationships and by socialeducational environment, based on predisposing biological characteristics. Most of clinical and psycho-social studies agree on multifactorial nature of this process, focusing on the combined action of biological, psychological, social and cultural factors. The first symptoms of gender dysphoria may appear from first years of life and then they may persist in puberty and adulthood. The causes of Gender Dysphoria are still unclear.Both psychosocial and biological factors have been called into question to explain the onset. The Gender Dysphoria Treatment aims to reduce, or to remove, suffering of person with GD and it is based on teamwork of psychologists, psychiatrists, endocrinologists and surgeons. The cure is, firstly, psychological and is provided by mental health experts. Hormone therapy can be prescribed to all people with persistent and well documented Gender Dysphoria if there are no medical contraindications; lastly, sex reassignment surgery. The formation and definition of transgender and transsexual identity obviously represents a specific complexity, to which is added an environmental, cultural and consequently individual and conditioning stigmatization.
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Sweet, Kevin M., and Ron C. Michaelis. "Other Multifactorial Disorders for Which Genetic/Genomic Testing Is Providing Insights." In The Busy Physician’s Guide To Genetics, Genomics and Personalized Medicine, 173–98. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1147-1_7.
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Beckmann, Jacques S., and Stylianos E. Antonarakis. "Lessons from the Genome-Wide Association Studies for Complex Multifactorial Disorders and Traits." In Vogel and Motulsky's Human Genetics, 287–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-37654-5_10.
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Van Loey, Nancy E. E. "Psychological Impact of Living with Scars Following Burn Injury." In Textbook on Scar Management, 429–34. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_48.
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AbstractLiving with scars in a society that highly values beauty can be challenging for a burn survivor. Particularly in the current society in which there are signals that increasing demands of beauty are becoming normalized, health care providers should be aware of this changing notion of normality that may increase the call for cosmetic and plastic surgery interventions and, at the same time, may decrease the acceptance of visible differences. This chapter describes psychological problems that may occur in burn survivors with visible differences. The adjustment process that follows after burn injury is complex and multifactorial. A changed appearance can elicit diminished self- and body-esteem and can hamper encounters with others. Knowledge on most frequent psychological disorders and its symptoms are reviewed and the multifaceted process of adjusting to visible differences involving personal and societal factors is described. It outlines risk factors for psychological problems associated with burn scars and how psychological problems can influence the perception of the scars. It also briefly describes psychological interventions that can be applied in this field.
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Dredla, Brynn K., and Vichaya Arunthari. "Circadian Disorders, Insomnia, and Parasomnias." In Mayo Clinic Neurology Board Review, edited by Kelly D. Flemming, 1208–16. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197512166.003.0134.
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Circadian rhythm disorders have misalignment between the desired sleep schedule and the circadian (24-hour) sleep-wake rhythm. Many persons experience this misalignment with jet lag. Other common circadian rhythm disorders include delayed sleep-phase disorder, advanced sleep-phase disorder, and shift-work sleep disorder. Insomnia is one of the most common medical concerns, and its prevalence increases with age. Patients may have difficulty initiating sleep or maintaining sleep and generally have a poor quality of sleep. Causes of insomnia are multifactorial.
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Langley, Kate, and Anita Thapar. "Genetics of attention-deficit/hyperactivity disorder." In New Oxford Textbook of Psychiatry, edited by John R. Geddes, Nancy C. Andreasen, and Guy M. Goodwin, 327–34. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0034.
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Studies have demonstrated that attention-deficit/hyperactivity disorder (ADHD) is a highly heritable disorder. The evidence for this and the investigation into specific genetic risk factors associated with the disorder are discussed in this chapter. Both common and rare genetic risk variants have been identified for the disorder, although sample sizes have limited the discovery of such risk factors to date. Identification of additional risk factors, as well as further investigation to understand the role of these factors in the pathophysiology of ADHD, are now under way. As with other multifactorial disorders, there are both genetic and environmental risks associated with ADHD, and the interplay of these different risk types, as well as how they have been studied, is discussed. ADHD is a phenotypically heterogenous disorder, and the influences of comorbid conditions and developmental age on the genetic risk factors for the disorder are considered, as well as the genetic overlap between ADHD and other psychiatric conditions.
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Kirupa, Kadarkarai, R. Rajashri, Kamali Raman, Aishwarya Balaji, Pavithra Elango, and Swetha Karupaiah. "Temporomandibular Joint Pain." In Temporomandibular Joint - Surgical Reconstruction and Managements [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104842.
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Temporomandibular joint (TMJ) is a synovial articulation between mandibular condyle and glenoid fossa in the temporal bone. Any structural and/or functional changes can affect the TMJ and related structures. Temporomandibular disorder (TMD) is a heterogeneous group of musculoskeletal disorders mainly characterised by regional pain in the facial and preauricular area and/or limitations/interference of jaw movement. TMD has multifactorial aetiology, which includes biology, and environmental social, emotional, and cognitive factors. TMD is more common orofacial pain condition and nondental origin. Factors associated with TMD include other pain condition, auto-immune disorder and psychiatric illness. The clinical conditions may present with limitation in opening and closing mouth, pain and articular noise. So this chapter mainly deals with the classification of TMJ disorder, diagnosis and management particularly TENS and ultrasound therapy for TMJ disorder.
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Kubota, Takeo. "Biological Understanding of Neurodevelopmental Disorders Based on Epigenetics, a New Genetic Concept in Education." In Learning Disabilities [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99867.
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Neurodevelopmental disorders, such as autism spectrum disorder, attention deficit hyperactive disorder, and learning disabilities, are heterogeneous conditions that are thought to have a multifactorial etiology including congenital genetic abnormalities and acquired environmental factors. Epigenetics is a biological mechanism that controls gene expression based on chemical modifications of DNA and chromosomal histone proteins. Environmental factors, such as severe mental stress, have been demonstrated to alter gene expression by changing epigenetic chemical modifications in the brain. Therefore, epigenetics is not only involved in congenital autism spectrum disorder-like conditions (e.g., Prader-Willi syndrome and Rett syndrome) but may also be involved in acquired attention deficit hyperactive disorder-like conditions (e.g., via child abuse and neglect). In this chapter, we introduce the basis of the epigenetic mechanism and the recent biological understanding of neurodevelopmental disorders based on epigenetics, which is a new genetic concept not only in medicine but also in education, which bridges internal brain mechanisms and external environmental factors.
Conference papers on the topic "Multifactorial disorder"
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Jallah, Zegbeh C., Laura Skoczylas, Suzan Stein, Naoki Yoshimura, Pamela Moalli, and Steven D. Abramowitch. "Maternal Childbirth Injury Alters Vaginal Smooth Muscle Contractility." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53798.
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Pelvic organ prolapse (POP) is a multifactorial disorder, characterized by the descent of the pelvic organs into the vaginal canal. POP is associated with decreased quality of life, and even depression, yet 50% of women over the age of fifty are living with this disorder. The estimated direct cost for POP surgeries is over one billion dollars annually, in the United States alone. This rather exorbitant figure includes the cost of surgery performed for symptom management, but does not include strategies which address the underlying cause of the disorder. It is not surprising then, that within a few years over 10% of repairs will require a second procedure. Thus, more studies are needed to understand the pathophysiology of POP.
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Ipsen, Brian J., John L. Williams, Michael J. Harris, and Thomas L. Schmidt. "Shear Strength of the Pig Capital Femoral Epiphyseal Plate: An Experimental Model for Human Slipped Capital Femoral Epiphysis Fixation Studies." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32611.
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Slipped capital femoral epiphysis (SCFE) is the most common hip disorder affecting adolescent children [1]. The etiology is not fully understood but thought to be multifactorial, related to both biological and biomechanical factors [2]. SCFE occurs when the epiphysis of the proximal femur slips in relation to the metaphysis through the growth plate, causing pain, disability and potential long-term sequellae from joint incongruity. The treatment for SCFE typically involves some form of stabilization procedure using pins, screws, bone grafting, osteotomy, or casting.
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Jallah, Zegbeh C., Pamela Moalli, Andrew Feola, William Barone, Stacy Palcsey, Naoki Yoshimura, and Steven D. Abramowitch. "The Impact of Mesh Implantation on Vaginal Smooth Muscle Innervation and Contraction." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14008.
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Pelvic organ prolapse (POP) is a multifactorial disorder characterized by the descent of the pelvic organs into the vaginal canal. This disorder is associated with decreased quality of life, and even depression, yet 50% of women over the age of fifty are living with POP. The cost associated with the repair of POP exceeds one billion dollars annually, in the United States alone. This rather exorbitant figure includes the cost of surgery performed for symptom management, but does not include strategies which address the underlying cause of the disorder for which there are none. Because failure rates of native tissue repairs are as high as 30%, vaginal mesh is increasingly used in the surgical repair of POP. The procedure aims to reinforce the fibromuscular layer of the vagina and the paravaginal attachments, thus providing structural integrity to the weakened native tissues. However, the use of mesh is limited by mesh-related complications including exposure, erosion, pain contraction and infection.
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Tessaro, Camila Lorenzini, Renata Dal-Prá Ducci, Cláudia Suemi Kamoi Kay, Otto Jesus Hernandez Fustes, Lineu César Werneck, Paulo José Lorenzoni, and Rosana Hermínia Scola. "Clinical and electrophysiological characteristics of the peripheral polyneuropathies from a single specialized center in the Southern Brazil." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.359.
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Background: The peripheral polyneuropathies have etiological heterogeneity, with more than a hundred known causes. In addition, they have a lack of information related to their epidemiology. Objectives: The aim of this study is to determine the prevalence of each etiology of polyneuropathy in a single specialized center from Southern Brazil and to correlate main clinical manifestations and electrophysiological aspects. Design and setting: Observational cross-sectional study. Neuromuscular disorder center from a tertiary service. Methods: This study comprised individuals with electrodiagnostic tests compatible with polyneuropathy from a neuromuscular disorder center. Selected patients were those who underwent nerve conduction studies between 2008 and 2017. Through analysis of medical records, polyneuropathies were classified according to etiology and neurophysiological aspect. Results: The sample population consisted of 380 patients who has a male predominance (59.5%), with a median age of 43 years (26-57). The main etiologies were inflammatory (23.7%), hereditary (18.9%), idiopathic (13.7%), multifactorial (11.1%) and diabetes (10.8%). The main electrophysiological patterns were Axonal Sensorimotor Polyneuropathy (36.1%) and Demyelinating- Axonal Sensorimotor Polyneuropathy (27.9%). Idiopathic, diabetic, and multifactorial polyneuropathies had predominantly axonal pattern, while inflammatory and hereditary polyneuropathies had mainly demyelinating pattern. Conclusions: The frequency of inflammatory etiology was higher than previously described and frequency of diabetic polyneuropathy was lower. There may be a change in epidemiology of polyneuropathy in specialized centers, with a tendency to decrease idiopathic polyneuropathy. Electrodiagnostic testing is useful for etiological diagnosis since electrophysiological patterns correlate with specific etiologies.
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Innocencio, Giovanna de Camargo, Paulo Roberto Hernandes Júnior, Patrick de Abreu Cunha Lopes, Juliana de Souza Rosa, and Jhoney Francieis Feitosa. "Epidemiological analysis, risk factors and therapeutic plan for post-stroke depression." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.176.
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Background: the stroke is defined by the OMS as the rapid development of neurological symptoms and/or focal signs that last for more than 24 hours, resulting from the sudden change in blood flow to the region. Major depressive disorder is one of the main complications that exist after a stroke. Objectives to correlate the occurrence of depression and stroke, to analyze the risk factors and the best therapeutic approach for the condition. Methods: a literature review was carried out from the Scielo and PubMed database, using as descriptors “Stroke”, “Depression” and “Post-stroke depression”, where 13 articles between 2003 and 2018 were selected. Results: the major depressive disorder is the most common psychiatric complication after strokes. A meta-analysis identified a cumulative incidence of depression from 29% to 52% in the first five years after stroke, although several studies have shown that post-stroke depression is diagnosed in only 10% of cases. When not diagnosed or treated, it is associated with a reduction in the patient’s active participation in the rehabilitation process, a decrease in quality of life and an increase in mortality. Risk factors include previous functional and cognitive impairment, history of depressive disorder, sex, age, previous stroke, hypercortisolemia, poor social support network, neuroanatomical characteristics of the stroke and high serum levels of IL-6. The pharmacological management can be carried out prophylactically or therapeutically, with selective serotonin reuptake inhibitors being the most indicated and tricyclic antidepressants as an alternative. Conclusion: the frequency of depressive disorder after stroke is relatively high and characterized as a predictor of poor prognosis. The importance of attention to the multifactorial context in which depression arises and the early treatment of psychiatric comorbidities in post-stroke individuals should be reinforced, since this strategy may reflect on better quality of life and reduction in morbidity and mortality rates that occur after the condition.
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Al-Qeraiwi, Maha, Manar Al-Rashid, Nasser Rizk, Abdelrahman El Gamal, and Amena Fadl. "Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0214.
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Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.
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Rakitko, Alexander. "Multifactorial Dimensionality Reduction for Disordered Trait." In International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and and Technology Publications, 2015. http://dx.doi.org/10.5220/0005285302320236.
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Rogers, Ian, and Ranjan Srivastava. "Using ensemble modeling to determine causes of multifactorial disorders." In GECCO '18: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3205651.3205686.
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Siqueira, Fernando, Vanessa Siqueira, Lucas Falcão, Arthur Bezerra, and Carlos Silva. "THE INFLUENCE BETWEEN ALZHEIMER’S DISEASE AND HEALTHY EATING: A SYSTEMATIC REVIEW." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda062.
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Background: Alzheimer’s Disease (AD) is a neurodegenerative disease responsible for neuronal losses that affect mainly the cortex and hippocampus, which begin to shrink in size, damaging cognitive functions. This process affects cholinergic neurons, influencing acetylcholine (ACH) levels, a memoryrelated neurotransmitter. Glucose metabolism and low thiamine levels appear to be affected by AD. Consequently, diabetes becomes a disease associated with AD and the thiamine deficiency levels depress the use of glucose by the brain. Thus, nutrition may have a role in preventing dementia through the treatment and prevention. Objective: To summarize the knowledge about this topic by reviewing articles and analyzing if healthy eating influences the development of AD. Methods: Selection of articles from the Scielo database. Results: Inflammation contributes to the pathogenesis of AD. The effect observed in patients with adherence to the Mediterranean diet translates into a decrease in inflammatory markers at the plasma level. One of the symptoms, memory loss, can be prevented by a micronutrient named thiamine, a precursor of ACH, it is found in the leguminous. The Mediterranean diet has been shown to attribute a neuroprotective activity which goes with its anti-inflammatory effect. Conclusion: AD starts by its multifactorial etiology that consists of genotype and phenotype. Nutrition would be efficient as a preventive and a therapeutic alternative among other.
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Rangel, Elen de Souza, Julio Cezar Albuquerque da Costa, Ana Carolina Soares Marinho, Laís Rosa e. Silva Oliveira Santos, Letícia Emanuelle de Almeida Lima, and Leogildo Alves Freires. "The risks of sleep fragmentation on cognitive skills: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.098.
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Background: The sleep fragmentation may conduct to breakdown in neutral networks, which tends to affect cognitive abilities or cognitive skills (CS) and bring notable deficits to the subject’s typical neuronal functioning. Objectives: Analyze the academic discussion of this theme and how this sleep deprivation can incapacitate the CS elemental to properly functioning circadian rhythm, as well as its multifactorial causes may be related to the subject’s complaint. Methods: To this article, it has been accomplished a systematic review on PubMed and Virtual Health Library database, using the descriptors “Sleep” and “ Cognitive abilities”, using articles from the last two years. Nine articles were used to guide this study. Results: It was possible to analyze that there are multifactorial complements related to sleep disturbance - neurodegenerative disorders, lack of sleep, prescription stimulants. The studies show that it is essential to elaborate a therapeutic plan, to define which CS is affected and what is going to be done about it, since the existing especifities may be present in neural correlates or in different CS, which makes indispensable the therapeutic plan. Conclusion: After all, it is indispensable the continuity of studies that research affected neural correlates in front of sleep deprivation, in order to understand sleep dysregulation for cognitive skills and provide an effective therapy for society, which permeates, consequently, a better quality of life.