Academic literature on the topic '945/.632'

Résumé Cet article procède à l’analyse des sources narratives traitant d’un phénomène unique dans les débuts de l’islam, le passage d’une partie du groupe arabophone des Iyād au service des Romains. Les auteurs d’époque abbasside (132/750-333/945) situent les transfuges dans le contexte des conquêtes (futūḥ) arabo-musulmanes du Moyen-Orient romain et sassanide (v. 10/632-20/642). En mettant en évidence les contradictions, incohérences et anachronismes de ces versions, notamment leur propension à traiter en réalité plus de la migration de l’Irak vers la Syrie du Nord, nous proposons un scénario alternatif : les Iyād s’installèrent progressivement dans le nord du district militaire (ǧund) de Homs, du Nord de la Syrie-Mésopotamie ex-romaine. Compte tenu du contexte des migrations, ralliements et transfuges au cours de la période omeyyade (40/661-132/750) ainsi que des fréquents déplacements de la frontière dans la zone des confins (ṯuġūr), nous suggérons que les Iyād, comme beaucoup d’ethnies chassées et enrôlées dans la région par les deux empires, passèrent peut-être à plusieurs reprises du service des Byzantins à celui des Omeyyades. Finalement, la rigidification des frontières géographiques, politiques et confessionnelles transforma de tels déplacements opportunistes ou forcés, bien qu’encore attestés, en apostasies contre-nature. Or ce contexte prévalut à la rédaction des sources narratives sur leur fuite primordiale au « pays des Romains ».

Bursaphelenchus piceae sp. n. is described from the bark of Norway spruce, Picea abies. Adults and propagative juveniles of the nematode are found in larval galleries of the six-toothed spruce bark beetle, Pityogenes chalcographus, while its dauer juveniles aggregate in Malpighian tubules of older larvae, pupae and adult beetles. The new species is characterised by the body length of 719 (530-945) μm in female and 632 (474-808) μm in male, its moderately slender body (a = 41.4 (35.4-50.2) and 42.6 (35.1-47.2) in female and male, respectively), and small spicules (16.0 (14.0-18.3) μm along arc and 13.7 (12.2-15.5) μm along chord). The extended anterior vulval lip in female, lateral fields with four incisures, long post-uterine sac extending for 67-91% of vulva-anus distance, and number (7) and arrangement of male caudal papillae suggest that B. piceae sp. n. is closely related to the xylophilus-group yet it differs by the relatively small, claw-like spicules with no cucullus at the tip. The close relation of B. piceae sp. n. to the xylophilus-group has been confirmed by DNA sequencing and phylogenetic analysis. Morphologically B. piceae sp. n. most closely resembles B. tokyoensis and B. fagi but can be separated from both by the unique shape of the spicules. The taxonomic separation of the new species is also confirmed by the unique molecular profile of the ITS region (ITS-RFLP). The presence of dauer juveniles of B. piceae sp. n. in Malpighian tubules of adult P. chalcographus may lead to extensive damage to this organ as shown by local expansion of the tubule basement membrane and degradation of its cellular epithelium. Detailed phylogenetic analysis revealed that B. piceae sp. n. together with five other bark beetle-associated Bursaphelenchus species, namely B. trypophloei, B. masseyi, B. tiliae, B. tokyoensis and B. fagi, constitutes a small phylogenetic clade that is most closely located to, but separate from, the xylophilus-group.

ImportanceThe Sepsis Prediction Model (SPM) is a proprietary decision support tool created by Epic Systems; it generates a predicting sepsis score (PSS). The model has not undergone validation against existing sepsis prediction tools, such as Systemic Inflammatory Response Syndrome (SIRS), Sequential Organ Failure Assessment (SOFA), or quick Sepsis-Related Organ Failure Asessement (qSOFA).ObjectiveTo assess the validity and timeliness of the SPM compared with SIRS, qSOFA, and SOFA.Design, Setting, and ParticipantsThis retrospective cohort study included all adults admitted to 5 acute care hospitals in a single US health system between June 5, 2019, and December 31, 2020. Data analysis was conducted from March 2021 to February 2023.Main Outcomes and MeasuresA sepsis event was defined as receipt of 4 or more days of antimicrobials, blood cultures collected within ±48 hours of initial antimicrobial, and at least 1 organ dysfunction as defined by the organ dysfunction criteria optimized for the electronic health record (eSOFA). Time zero was defined as 15 minutes prior to qualifying antimicrobial or blood culture order.ResultsOf 60 507 total admissions, 1663 (2.7%) met sepsis criteria, with 1324 electronic health record–confirmed sepsis (699 [52.8%] male patients; 298 [22.5%] Black patients; 46 [3.5%] Hispanic/Latinx patients; 945 [71.4%] White patients), 339 COVID-19 sepsis (183 [54.0%] male patients; 98 [28.9%] Black patients; 36 [10.6%] Hispanic/Latinx patients; and 189 [55.8%] White patients), and 58 844 (97.3%; 26 632 [45.2%] male patients; 12 698 [21.6%] Black patients; 3367 [5.7%] Hispanic/Latinx patients; 40 491 White patients) did not meet sepsis criteria. The median (IQR) age was 63 (51 to 73) years for electronic health record–confirmed sepsis, 69 (60 to 77) years for COVID-19 sepsis, and 60 (42 to 72) years for nonsepsis admissions. Within the vendor recommended threshold PSS range of 5 to 8, PSS of 8 or greater had the highest balanced accuracy for classifying a sepsis admission at 0.79 (95% CI, 0.78 to 0.80). Change in SOFA score of 2 or more had the highest sensitivity, at 0.97 (95% CI, 0.97 to 0.98). At a PSS of 8 or greater, median (IQR) time to score positivity from time zero was 68.00 (6.75 to 605.75) minutes. For SIRS, qSOFA, and SOFA, median (IQR) time to score positivity was 7.00 (−105.00 to 08.00) minutes, 74.00 (−22.25 to 599.25) minutes, and 28.00 (−108.50 to 134.00) minutes, respectively.Conclusions and RelevanceIn this cohort study of hospital admissions, balanced accuracy of the SPM outperformed other models at higher threshold PSS; however, application of the SPM in a clinical setting was limited by poor timeliness as a sepsis screening tool as compared to SIRS and SOFA.

ImportanceProcess-based quality measures are generally intended to promote evidence-based practices that have been proven to improve outcomes. However, due to lack of standardized implementation of diagnostic codes in dentistry, assessing the association between process and oral health outcomes has been challenging.ObjectiveTo estimate the association of adhering to dental quality measures with patient oral health outcomes.Design, Setting, and ParticipantsUsing a target trial emulation, a causal inference framework, this retrospective cohort study estimated the difference in the risk of developing tooth decay between US children who adhered to process-based dental quality measures (receiving topical fluoride and sealant [treated groups]) and those who did not (control groups). Electronic health records of US children and adolescents aged 0 to 18 years from January 1, 2014, to December 31, 2020, were used. To emulate random treatment assignment based on baseline confounders, coarsened exact matching was used to produce covariate balance between the treated and control groups. A time-to-event regression model produced effect estimates, adjusting for time-varying covariates. Near-far matching was used to account for unmeasured confounders as a sensitivity analysis. Data were analyzed from May 1 to August 7, 2023.ExposuresAdherence to dental quality measures.Main Outcomes and MeasuresIncidence of tooth decay.ResultsAmong 69 212 US children aged between 0 and 18 years (mean [SD] age, 10.2 [5.0] years; 49.5% male, 50.4% female, and 0.1% unknown or transgender), 1930 (2.8%) were Asian, 2038 (2.9%) were Black, 8667 (12.5%) were Hispanic, 33 632 (48.6%) were White, and 22 945 (33.2%) were multiracial, other, or missing racial and ethnic group identification. Relative to control individuals, treated individuals were more likely to be at elevated risk of caries (fluoride measure: 16 453 [76.5%] vs 15 236 [39.8%]; sealant measure: 2264 [54.6%] vs 997 [44.0%]) and have regular dental visits (fluoride measure: 21 498 [100%] vs 13 741 [35.9%]; sealant measure: 1623 [39.2%] vs 871 [38.4%]). Adherence to quality measures was associated with reduced risk of tooth decay with adjusted hazard ratios of 0.82 (95% CI, 0.78- 0.86) for fluoride and 0.86 (95% CI, 0.76-0.97) for sealant in the matched cohort. Benefits of adhering to quality measures were greater among children at elevated vs low risk and with public vs commercial insurance for both measures.ConclusionsIn this cohort study, adhering to dental quality measures was associated with reduced risk of tooth decay, and benefits were greater among children at elevated risk and with public insurance. These findings provide insights in facilitating targeted application of quality measures or developing more tailored quality improvement initiatives.

Abstract Purpose To characterize T1 relaxation times of the pancreas, liver, and spleen in children with and without abdominal pathology. Methods This retrospective study included pediatric patients (< 18-years-old). T1 mapping was performed with a Modified Look-Locker Inversion Recovery sequence. Patients were grouped based on review of imaging reports and electronic medical records. The Kruskal–Wallis test with Dunn’s multiple comparison was used to compare groups. Results 220 participants were included (mean age: 11.4 ± 4.2 years (1.5 T); 10.9 ± 4.5 years (3 T)). Pancreas T1 (msec) was significantly different between subgroups at 1.5 T (p < 0.0001). Significant pairwise differences included: normal (median: 583; IQR: 561–654) vs. acute pancreatitis (731; 632–945; p = 0.0024), normal vs. chronic pancreatitis (700; 643–863; p = 0.0013), and normal vs. acute + chronic pancreatitis (1020; 897–1099; p < 0.0001). Pancreas T1 was also significantly different between subgroups at 3 T (p < 0.0001). Significant pairwise differences included: normal (779; 753–851) vs. acute pancreatitis (1087; 910–1259; p = 0.0012), and normal vs. acute + chronic pancreatitis (1226; 1025–1367; p < 0.0001). Liver T1 was significantly different between subgroups only at 3 T (p = 0.0011) with pairwise differences between normal (818, 788–819) vs. steatotic (959; 848–997; p = 0.0017) and normal vs. other liver disease (882; 831–904; p = 0.0455). Liver T1 was weakly correlated with liver fat fraction at 1.5 T (r = 0.39; 0.24–0.52; p < 0.0001) and moderately correlated at 3 T (r = 0.64; 0.49–0.76; p < 0.0001). There were no significant differences in splenic T1 relaxation times between subgroups. Conclusion Pancreas T1 relaxation times are higher at 1.5 T and 3 T in children with pancreatitis and liver T1 relaxation times are higher in children with steatotic and non-steatotic chronic liver disease at 3 T.

A osteoporose é responsável por causar condições devastadoras no tecido ósseo elevando o risco de fraturas, constituindo uma problemática importante de saúde pública. É comum o uso de medicamentos, como os bifosfonatos para o controle dessa patologia. Contudo, a associação do uso desse medicamento com a osteonecrose dos maxilares vem sendo amplamente discutido na literatura, assim como a dificuldade da reabilitação desses pacientes como implantes e do protocolo de tratamento dessa condição. Assim sendo, o objetivo do presente trabalho foi realizar uma revisão de literatura para discutir as principais falhas associadas a instalação de implantes em pacientes portadores de osteonecrose dos maxilares associada ao uso de bifosfonatos (OMAB), assim como as possibilidades de tratamento, e relatar um caso clínico. As informações obtidas na revisão nos permitiu concluir que o uso de bifosfonatos orais, como o alendronato, é capaz de levar ao desenvolvimento da OMAB sendo necessária bastante precaução na reabilitação oral com implantes dentários, tanto em pacientes que fazem uso, como pacientes que apresentam risco de futura utilização de bifosfonatos para o tratamento de desordens esqueléticas. Descritores: Osteoporose; Alendronato; Osteonecrose; Implantes Dentários.ReferênciasEsposito M, Hirsch JM, Lekholm U, Thomsen P. Biological factors contributing to failures of osseointegrated oral implants. (I). Success criteria and epidemiology. Eur J Oral Sci. 1998;106(1):527-51.Quirynen M, De Soete M, Van Steenberghe D. Infectious risks for oral implants: a review of the literature. Clin Oral Implants Res. 2002;13(1):1-19.Van Steenberghe D, Jacobs R, Desnyder M, Maffei G, Quirynen M. The relative impact of local and endogenous patient‐related factors on implant failure up to the abutment stage. Clin Oral Implants Res. 2002;13(6):617-22.Migliorati CA. Bisphosphanates and oral cavity avascular bone necrosis. J Clin Oncol. 2003;21(22)4253-54.Migliorati CA, Casiglia J, Epstein J, Jacobsen PL, Siegel MA, Woo SB. Managing the care of patients with bisphosphonate-associated osteonecrosis: an American Academy of Oral Medicine position paper. J Am Dent Assoc. 2005;136(12):1658-68.Madrid C, Sanz M. What impact do systemically administrated bisphosphonates have on oral implant therapy? A systematic review. Clin Oral Implants Res. 2009;20(Suppl 4):87-95.Black DM, Schwartz AV, Ensrud KE, Cauley JA, Levis S, Quandt SA et al. Effects of continuing or stopping alendronate after 5 years of treatment: the Fracture Intervention Trial Long-term Extension (FLEX): a randomized trial. JAMA. 2006;296(24):2927-38.Schwartz AV, Bauer DC, Cummings SR, Cauley JA, Ensrud KE, Palermo L et al. Efficacy of continued alendronate for fractures in women with and without prevalent vertebral fracture: the FLEX trial. J Bone Miner Res. 2010;25(5):976-82.Marx RE. Pamidronate (Aredia) and zoledronate (Zometa) induced avascular necrosis of the jaws: a growing epidemic. J Oral Maxillofac Surg. 2003;61(9):1115-17.Ruggiero SL, Mehrotra B, Rosenberg TJ, Engroff SL. Osteonecrosis of the jaws associated with the use of bisphosphonates: a review of 63 cases. Journal of oral and maxillofacial surgery, 2004;62(5):527-34.Ruggiero SL. Guidelines for the diagnosis of bisphosphonate-related osteonecrosis of the jaw (BRONJ). Clin Cases Miner Bone Metab.2007;4(1):37-42.Ruggiero SL, Dodson TB, Assael LA, Landesberg R, Marx RE, Mehrotra B et al. American Association of Oral and Maxillofacial Surgeons position paper on bisphosphonate-related osteonecrosis of the jaws—2009 update. J Oral Maxillofac Surg. 2009;67(5 Suppl):2-12.Ruggiero SL, Drew SJ. Osteonecrosis of the jaws and bisphosphonate therapy. J Dent Res. 2007;86(11):1013-21.Otto S, Abu-Id MH, Fedele S, Warnke PH, Becker ST, Kolk A et al. Osteoporosis and bisphosphonates-related osteonecrosis of the jaw: not just a sporadic coincidence–a multi-centre study. J Craniomaxillofac Surg. 2011;39(4):272-77.Yarom N, Yahalom R, Shoshani Y, Hamed W, Regev E, Elad S. Osteonecrosis of the jaw induced by orally administered bisphosphonates: incidence, clinical features, predisposing factors and treatment outcome. Osteoporos Int. 2007;18(10):1363-70.Sambrook P, Cooper C. Osteoporosis. Lancet. 2006;367(9527):2010-18.Cranney A, Guyatt G, Griffith L, Wells G, Tugwell P, Rosen C. Meta-analyses of therapies for postmenopausal osteoporosis. Endocr Rev. 2002;23(4):570-78.Close P, Neuprez A, Reginster JY. Developments in the pharmacotherapeutic management of osteoporosis. Expert Opin Pharmacother. 2006;7(12):1603-15.Rodan GA, Fleisch HA. Bisphosphonates: mechanisms of action. J Clin Invest. 1996;97(12): 2692-96.Dannemann C, Grätz KW, Riener MO, Zwahlen RA. Jaw osteonecrosis related to bisphosphonate therapy: a severe secondary disorder. Bone. 2007;40(4):828-34.Kos M, Luczak K, Godzinski J, Klempous J. Treatment of monostotic fibrous dysplasia with pamidronate. J Craniomaxillofac Surg. 2004;32(1):10-15.Pastor-Zuazaga D, Garatea-Crelgo J, Martino-Gorbea R, Etayo-Pérez A, Sebastián-Lopez C. Osteonecrosis of the jaws and bisphosphonates. Report of three cases. Med Oral Patol Oral Cir Bucal. 2006;11(1):E76-9.Sato M, Grasser W, Endo N, Akins R, Simmons H, Thompson DD et al. Bisphosphonate action. Alendronate localization in rat bone and effects on osteoclast ultrastructure. J Clin Invest. 1991;88(6):2095-2105.Sahni M, Guenther HL, Fleisch H, Collin P, Martin TJ. Bisphosphonates act on rat bone resorption through the mediation of osteoblasts. J Clin Invest.1993;91(5):2004-11.Merigo E, Manfredi M, Meleti M, Corradi D, Vescovi P. Jaw bone necrosis without previous dental extractions associated with the use of bisphosphonates (pamidronate and zoledronate): a four‐case report. J Oral Pathol Med. 2005;34(10):613-17.Olson KB, Hellie CM, Pienta KJ. Osteonecrosis of jaw in patient with hormonerefractory prostate cancer treated with zoledronic acid. Urology. 2005;66(3):658.Graziani F, Cei S, La Ferla F, Cerri E, Itro A, Gabriele M. Association between osteonecrosis of the jaws and chronic high-dosage intravenous bisphosphonates therapy. J Craniofac Surg. 2006;17(5):876-79.Greenberg MS. Comment in. Intravenous bisphosphonates and osteonecrosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004;98(3):259-60.Gibbs SD, O'Grady J, Seymour JF, Prince HM. Bisphosphonate-induced osteonecrosis of the jaw requires early detection and intervention. Med J Aust. 2005;183(10):549-50.Marx RE, Sawatari Y, Fortin M, Broumand V. Bisphosphonate-induced exposed bone (osteonecrosis/osteopetrosis) of the jaws: risk factors, recognition, prevention, and treatment. J Oral Maxillofac Surg. 2005;63(11)1567-75.Melo MD, Obeid G. Osteonecrosis of the jaws in patients with a history of receiving bisphosphonate therapy: strategies for prevention and early recognition. J Am Dent Assoc. 2005;136(12):1675-81.Purcell PM, Boyd IW. Bisphosphonates and osteonecrosis of the jaw. Med J Aust. 2005;182(8)417-18.Vannucchi AM, Ficarra G, Antonioli E, Bosi A. Osteonecrosis of the jaw associated with zoledronate therapy in a patient with multiple myeloma. Br J Haematol. 2005;128(6):738.Bilezikian JP. Osteonecrosis of the jaw - do bisphosphonates pose a risk? N Engl J Med. 2006;355(22):2278-81.Van Poznak C, Estilo C. Osteonecrosis of the jaw. J Oncol Pract. 2006;2(1):3-4.Santini D, Vincenzi B, Avvisati G, Dicuonzo G, Battistoni F, Gavasci M et al. Pamidronate induces modifications of circulating angiogenetic factors in cancer patients. Clin Cancer Res. 2002;8(5):1080-84.Wood J, Bonjean K, Ruetz S, Bellahcène A, Devy L, Foidart JM et al. Novel antiangiogenic effects of the bisphosphonate compound zoledronic acid. J Pharmacol Exp Ther. 2002;302(3):1055-61.Badros A, Weikel D, Salama A, Goloubeva O, Schneider A, Rapoport A et al. Osteonecrosis of the jaw in multiple myeloma patients: clinical features and risk factors. J Clin Oncol. 2006;24(6):945-52.Woo SB, Hellstein JW, Kalmar JR. Narrative [corrected] review: bisphosphonates and osteonecrosis of the jaws. Ann Intern Med.2006;144(10):753-61.Cafro AM, Barbarano L, Nosari AM, D'avanzo G, Nichelatti M, Bibas M et al. Osteonecrosis of the jaw in patients with multiple myeloma treated with bisphosphonates: definition and management of the risk related to zoledronic acid. Clin Lymphoma Myeloma. 2008;8(2):111-16.Mavrokokki T, Cheng A, Stein B, Goss A. Nature and frequency of bisphosphonate-associated osteonecrosis of the jaws in Australia. J Oral Maxillofac Surg. 2007;65(3):415-23.Odvina CV, Zerwekh JE, Rao DS, Maalouf N, Gottschalk FA, Pak CY. Severely suppressed bone turnover: a potential complication of alendronate therapy. J Clin Endocrinol Metab. 2005;90(3):1294-301.Bedogni A, Blandamura S, Lokmic Z, Palumbo C, Ragazzo M, Ferrari F et al. Bisphosphonate-associated jawbone osteonecrosis: a correlation between imaging techniques and histopathology. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008;105(3):358-64.Khan AA, Sándor GK, Dore E, Morrison AD, Alsahli M, Amin F et al. Canadian consensus practice guidelines for bisphosphonate associated osteonecrosis of the jaw. J Rheumatol. 2008;35(7):1391-97.Hoff AO, Toth BB, Altundag K, Johnson MM, Warneke CL, Hu M et al.Frequency and risk factors associated with osteonecrosis of the jaw in cancer patients treated with intravenous bisphosphonates. J Bone Miner Res. 2008;23(6):826-36.Assael LA. Oral bisphosphonates as a cause of bisphosphonate-related osteonecrosis of the jaws: clinical findings, assessment of risks, and preventive strategies. J Oral Maxillofac Surg. 2009;67(5 Suppl):35-43.Lazarovici TS, Yahalom R, Taicher S, Schwartz-Arad D, Peleg O, Yarom N. Bisphosphonate-related osteonecrosis of the jaw associated with dental implants. J Oral Maxillofac Surg. 2010;68(4):790-96.Jacobsen C, Metzler P, Rössle M, Obwegeser J, Zemann W, Grätz KW. Osteopathology induced by bisphosphonates and dental implants: clinical observations. Clin Oral Investig. 2013;17(1):167-75.López-Cedrún JL, Sanromán JF, García A, Peñarrocha M, Feijoo JF, Limeres J, Diz P. Oral bisphosphonate-related osteonecrosis of the jaws in dental implant patients: a case series. Br J Oral Maxillofac Surg. 2013;51(8):874-79.Kwon TG, Lee CO, Park JW, Choi SY, Rijal G, Shin HI. Osteonecrosis associated with dental implants in patients undergoing bisphosphonate treatment. Clin Oral Implants Res. 2014;25(5):632-40.Ramalho-Ferreira G, Faverani LP, Prado FB, Garcia IR, Okamoto R. Raloxifene enhances peri-implant bone healing in osteoporotic rats. Int J Oral Maxillofac Surg. 2015;44(6):798-805.Bone HG, Hosking D, Devogelaer JP, Tucci JR, Emkey RD, Tonino RP. Ten years' experience with alendronate for osteoporosis in postmenopausal women. N Engl J Med. 2004;350(12):1189-99.Lerner UH. Bone remodeling in post-menopausal osteoporosis. J Dent Res. 2006;85(7):584-95.Ettinger B, Black DM, Mitlak BH, Knickerbocker RK, Nickelsen T, Genant HK et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial. JAMA. 1999;282(7):637-45.Gallacher SJ, Dixon T. Impact of treatments for postmenopausal osteoporosis (bisphosphonates, parathyroid hormone, strontium ranelate, and denosumab) on bone quality: a systematic review. Calcif Tissue Int. 2010;87(6)469-84.