Fibrous dysplasia of the jaws: Integrating molecular pathogenesis with clinical,radiological, and histopathological features

Fibrous dysplasia is a non‐neoplastic developmental process that affects the craniofacial bones, characterized by painless enlargement as a result of bone substitution by abnormal fibrous tissue. Postzygotic somatic activating mutations in the GNAS1 gene cause fibrous dysplasia and have been extensively investigated, as well as being helpful in the differential diagnosis of the disease. Fibrous dysplasia may involve one (monostotic) or multiple bones (polyostotic), sporadically or in association with McCune‐Albright syndrome, Jeffe‐Lichenstein syndrome, or Mazabreud syndrome. This review summarizes the current knowledge on fibrous dysplasia, emphasizing the value of integrating the understanding of its molecular pathogenesis with the clinical, radiological, and histopathological features. In addition, we address important aspects related to the differential diagnosis and patient management.     

Primary epidural lumbar Ewing sarcoma presenting as cauda equina syndrome in an adult patient who underwent surgical decompression: A case report

Ewing sarcoma (ES) is a rare primary neoplasm in the lumbar adult spine and may mimic a benign tumor. In this case, after a patient's three-month history of lower back pain and rapidly progressing leg numbness and weakness, magnetic resonance imaging (MRI) showed a mass in the third lumbar vertebra. At a two-month follow-up, imaging showed a fracture, compression and lesion enlargement. Decompression and fixation confirmed ES, and the patient began combined radiotherapy and chemotherapy. Two months postoperatively, residual ES was suspected on MRI. The patient underwent a second surgery, and histopathology confirmed necrosis. A six-month follow-up after the first surgery showed no tumor recurrence. This case supports the inclusion of ES in the differential diagnosis of pathologic spinal fracture. Early decompression and spinal fixation are critical for preserving neurologic and spinal functions in ES complicated by a compression fracture. Combined adjuvant radiotherapy and chemotherapy remain the standard therapeutic strategy.     

后路枕骨髁螺钉技术研究进展

正枕骨、寰椎和枢椎共同构成了枕颈部活动的结构功能单位,即枕颈交界区~([1-2])。炎症、创伤、肿瘤及畸形等因素会导致枕颈交界区失稳,从而引起颈脊髓或神经根的损伤、麻痹及难以忍受的疼痛,甚至危及生命~([3-4])。后路内固定融合技术是治疗枕颈部失稳的重要手段,目前常用术式为枕骨螺钉技术,该技术较钢丝固定技术有更好的生物力学稳定     

新型管理模式在护理实习教学管理中的应用探讨

目的探讨在进行护理实习教学管理期间新型管理模式应用可行性。方法选择我院2018年1月-2019年2月102例实习护生作为试验对象;数字奇偶法分组后探究每组教学管理模式;对照组(51名):选择传统护理教学管理模式展开;试验组(51名):选择新型护理教学管理模式展开;比较两组护实习护生行为规范合格率、平均业务学习出勤率以及教学满意度评分结果。结果试验组实习护生规范合格率(98.04%)高于对照组(64.71%)(P<0.05);试验组实习护生平均业务学习出勤率(98.04%)高于对照组(62.75%)(P<0.05);试验组实习护生各项教学满意度评分均高于对照组(P<0.05)。结论医院实习护生在接受新型护理实习教学管理后,对于规范合格率的提升,平均业务学习出勤率的提升以及教学满意度评分的提升,均获得显著效果,最终为医院实习护生的学习效率以及护理安全提升奠定了基础。     

Clinical and subclinical cardiovascular disease in female SLE patients: Interplay between body mass index and bone mineral density

Background and aims

Since accelerated atherosclerosis has been reported in systemic lupus erythematosus (SLE), predictive biomarkers of cardiovascular disease (CVD) are needed. Among non-traditional risk factors, bone mineral density (BMD) has been related to CVD. However, its role in SLE remains controversial. This study aims to analyze the associations of subclinical atherosclerosis with traditional and non-traditional CV risk factors.

Host MyD88 signaling protects against acute graft-versus-host disease after allogeneic bone marrow transplantation

Recent experimental strategies to reduce graft-versus-host disease (GVHD) have focused largely on modifying innate immunity. Toll-like receptor (TLR)-driven myeloid differentiation primary response 88 (MyD88)-dependent signalling pathways that initiate adaptive immune function are also critical for the pathogenesis of GVHD. This study aimed to delineate the role of host MyD88 in the development of acute GVHD following fully major histocompatibility complex-mismatched allogeneic bone marrow transplantation (BMT). When myeloablated BALB/c MyD88 knock-out recipients were transplanted with C57BL/6 (B6) donor cells, they developed significantly more severe GVHD than wild-type (WT) BALB/c hosts. The increased morbidity and mortality in MyD88^–/– mice correlated with increased serum levels of lipopolysaccharide and elevated inflammatory cytokines in GVHD target organs. Additionally, MyD88 deficiency in BMT recipients led to increased donor T cell expansion and more donor CD11c⁺ cell intestinal infiltration with apoptotic cells but reduced proliferation of intestinal epithelial cells compared with that in WT BMT recipients. Decreased expression of tight junction mRNA in epithelial cells of MyD88^–/– mice suggested that MyD88 contributes to intestinal integrity. Cox-2 expression in the GVHD-targeted organs of WT mice is increased upon GVHD induction, but this enhanced expression was obviously inhibited by MyD88 deficiency. The present findings demonstrate an unexpected role for host MyD88 in preventing GVHD after allogeneic BMT.