ObjectiveTo systematically review the clinical features of chronic fatigue syndrome (CFS) cases with pathogens infection. MethodsWe electronically searched databases including VIP, WanFang Data, CNKI, CBM, PubMed, MEDLINE, EMbase, The Cochrane Library, Web of Science, Elsevier and Google Scholar from 1994 to 2014 for CFS-related studies. Two reviewers independently screened literature and extracted data. Then we systematically reviewed and analyzed the information on demographic characteristics, clinical manifestations, types of infected pathogens, and results of some biochemical examinations. ResultsA total of 84 studies (case reports and case series) involving 2 565 CFS cases from 18 countries were included. The major infected pathogens of included CFS cases were mycoplasma, EB virus, intestinal virus, Bernat rickettsia, human-herpes virus, and Gram-negative intestinal bacteria. Fifty-seven studies reported that there might be associations between the pathogenic infection and CFS pathogenesis. Although there were different types of CFS-related pathogens, almost all the studies inferred that pathogens infection linked with immune dysfunction, which might cause CFS symptoms. ConclusionThere may be associations between the pathogenic infection and CFS pathogenesis.
Knee osteoarthritis (KOA) is one of the common degenerative joint diseases, which is more common in the middle-aged and elderly population. It shows significant gender differences, with a significantly higher incidence rate in women than in men, seriously affecting the quality of life of patients. However, there are few research reports on the correlation between gender differences and the incidence of KOA both domestically and internationally. Therefore, this article will summarize and analyze the potential causes of gender differences related to the incidence of KOA from five aspects: hormone levels, anatomical biomechanical characteristics, genes, obesity, and exercise-muscle factors. Through a comprehensive review of research progress, the aim is to provide a theoretical basis for gender based personalized treatment of KOA in clinical practice.
Objective Glucocorticoid is the main cause of non-traumatic avascular necrosis of femoral head. To explore the changes of reactive oxygen species (ROS) in the bone microvascular endothel ial cells treated with glucocorticoid so as to investigate the pathogenesis of steroid-induced avascular necrosis of femoral head. Methods The cancellous bone of femoral head was harvested from voluntary donators undergoing total hip arthroplasty, and then the bone microvascular endothel ial cells were isolated by enzyme digestion. The cells at passage 3 were cocultured with different concentrations of hydrocortisone (0, 0.03, 0.10, 0.30, and 1.00 mg/mL) for 24 hours. MTT assay was used for the inhibitory rate of cell prol iferation, flow cytometry for apoptosis rate, and fluorescence probe for the production of ROS and xanthine oxidase (XOD). Results At 2-3 days primary culture, the cells were spindle and arranged l ike cobbles and they reached confluence after 1 week. The inhibitory rates of cell prol iferation in 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 20.22% ± 2.97%, 22.94% ± 4.52%, 43.98% ± 3.35%, and 78.29% ± 3.85%, respectively; and 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 2 low-concentration groups (0.03 and 0.10 mg/mL groups). The apoptosis rates in 0, 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 0.10% ± 0.01%, 0.23% ± 0.02%, 1.83% ± 0.04%, 6.34% ± 0.11%, and 15.33% ± 0.53%, respectively; 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 0 mg/mL group. In 0, 0.30, and 1.00 mg/ mL groups, the ROS levels were 57.35 ± 7.11, 120.47 ± 15.68, and 166.15 ± 11.57, respectively, and the XOD levels were 0.017 9 ± 0.000 9, 0.028 3 ± 0.001 7, and 0.067 7 ± 0.004 1, respectively; there were significant differences in the levels of ROS and XOD among 3 groups (P lt; 0.05). Conclusion Increasing of ROS production in bone microvascular endothel ial cells can be induced by high concentration glucocorticoid, and it can result in cell injury
Objective To study the etiology， pathogenesis， and diagnosis of small bowel volvulus in adults. Method The clinical data of 43 cases of small bowel volvulus admitted to HassanⅡHospital of Settat from October 2009 to October 2012 were analyzed retrospectively. Results There were 11 cases of spontaneous small bowel volvulus.There were 32 cases of secondary small bowel volvulus， of which 19 cases due to postoperative abdominal adhesions. Clinical manifestation：early persistent severe abdominal pain was in 40 cases， frequent vomiting was in 29 cases， intestinalpattern or abdominal mass was in 28 cases. All 43 patients were received surgery， 22 （51.2%） cases were diagnosed by preoperative ultrasonography， small bowel necrosis was found in 16 cases during operation， 37 （86.0%） patients were cured and 6 （14.0%） patients died. Conclusions Secondary small bowel volvulus is main small bowel volvulus， post-operative abdominal adhesion is major causes of small bowel volvulus， the value of abdominal X-ray in diagnosing is limited. However， ultrasonography and CT are helpful in diagnosing these diseases. Small bowel volvulus and intestinal obstruction can reinforce each other. Early small bowel volvulus is characterized by clinical conditions such as severe abdominal pain， early vomiting signs， and signs not matching the symptoms. Acute onset and rapid progression are the features of small bowel volvulus， surgery should be intervened in early stage.
ObjectiveTo understand the pathogenesis and the research progress of comprehensive treatment of primary retroperitoneal liposarcoma (PRLPS) and to provide evidence for clinical diagnosis and treatment.MethodThe recent literatures on the pathological classification, pathogenesis of PRLPS, and comprehensive treatment including the surgery, radiotherapy, chemotherapy, and molecular targeted therapy were reviewed.ResultsThe pathological types of PRLPS were highly differentiated, dedifferentiated, mucoid/round cell, polymorphic, and mixed. The main molecular pathogenesis was the synergistic effect of MDM2 with related genes, abnormal expressions of c-myc gene and microRNAs, Prune-nm23-H1 mechanism, and abnormal protein products of FUS-CHOP fusion gene which regulated the growth of tumor. The treatment of PRLRS included the radical resection, extended resection, and palliative resection combined with radiotherapy, chemotherapy, and molecular targeted therapy.ConclusionsPRLPS is a rare malignant tumor with high recurrence rate, but early diagnosis and treatment are difficult. With the further study of the molecular mechanism of PRLPS, the treatment of PRLPS has been transformed into a comprehensive treatment based on surgery, adjuvant radiotherapy and chemotherapy, and molecular targeted therapy.