Dislocation of the proximal tibiofibular joint in association with a tibial shaft fracture: two case reports and a literature review.

Dislocation of the proximal tibiofibular joint (PTFJ) in association with a displaced tibial shaft fracture and an intact fibula is an exceedingly rare injury. We present 2 cases of tibia fractures associated with an intact fibula and a PTFJ dislocation. The first case involves a man who sustained a closed spiral fracture of the distal tibial shaft, with an intact fibula, an anterolaterally dislocated PTFJ, and a partial tear of the lateral collateral ligament. The tibia was percutaneously plated, and the PTFJ was reduced and then stabilized with temporary screw fixation. The second case involves a woman who sustained a closed fracture of the tibia in association with a PTFJ dislocation. The tibia was fixed with an intramedullary nail, and the PTFJ was similarly reduced and fixed with a temporary screw. We also provide a brief literature review focusing on classification of PTFJ dislocations, mechanism of injury, associated injuries, and treatment options.     

广州市至灵学校167名学员智残原因的调查分析

本文以广州市至灵学校（智低）167名学员为研究对象，完成智力测验、体格检查和染色体分析．并且追溯围产期和出生后的种种异常．询查智力低下的家族史。综合分析有关资料，显示围产期的某些不利因素、遗传与先天疾病，以及婴幼儿中枢神经系统疾病是主要的发病原因。从而指出，加强优生咨询、重视围产期保健、提高产前诊断和产程中的监护水平、早期防治胎婴儿中枢神经系统损伤和疾病等，是降低智残儿发生率的重要措施。     

Anterior Crackles: A Neglected Sign?

We report on a man, aged 83 years, with chronic heart failure, atrial fibrillation, right ventricular pacing, and worsening exertional dyspnea who was referred for cardiac resynchronization therapy. Detection by anterior chest auscultation of pulmonary crackles during comfortable supine breathing in the context of documented low filling pressures led to the realization that unrecognized pulmonary fibrosis, not congestion, was the principal cause of his shortness of breath. We propose that the incidental finding in chronic heart failure of diffuse anterior crackles during comfortable supine breathing initiate a workup for alternate disorders such as occult pulmonary fibrosis.     

Minocycline attenuates HIV‐1 infection and suppresses chronic immune activation in humanized NOD/LtsZ‐scidIL‐2Rγnull mice

More than a quarter of a century of research has established chronic immune activation and dysfunctional T cells as central features of chronic HIV infection and subsequent immunodeficiency. Consequently, the search for a new immunomodulatory therapy that could reduce immune activation and improve T‐cell function has been increased. However, the lack of small animal models for in vivo HIV study has hampered progress. In the current study, we have investigated a model of cord blood haematopoietic progenitor cells (CB‐HPCs) ‐transplanted humanized NOD/LtsZ‐scidIL‐2Rγ^null mice in which progression of HIV infection is associated with widespread chronic immune activation and inflammation. Indeed, HIV infection in humanized NSG mice caused up‐regulation of several T‐cell immune activation markers such as CD38, HLA‐DR, CD69 and co‐receptor CCR5. T‐cell exhaustion markers PD‐1 and CTLA‐4 were found to be significantly up‐regulated on T cells. Moreover, increased plasmatic levels of lipopolysaccharide, sCD14 and interleukin‐10 were also observed in infected mice. Treatment with minocycline resulted in a significant decrease of expression of cellular and plasma immune activation markers, inhibition of HIV replication and improved T‐cell counts in HIV‐infected humanized NSG mice. The study demonstrates that minocycline could be an effective, low‐cost adjunctive treatment to regulate chronic immune activation and replication of HIV.