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
Immune-mediated necrotizing myopathy (IMNM) is a type of autoimmune myopathy characterized by relatively severe proximal weakness with high serum muscle enzyme levels, myofiber necrosis with minimal inflammatory cell infiltrate on muscle biopsy, and infrequent extra-muscular involvement. The mechanism of necrotizing myopathy remains unclear. The new European Neuromuscular Centre criteria divides IMNM into three distinct subtypes according to different autoantibodies, which reminds us antibodies may be involved in the pathogenesis of IMNM and different subtypes may have different pathogenesis. This review summarizes the current understanding of the pathogenesis of IMNM.
With the surged prevalence of myopia, the pathogenic mechanism underlying myopia has attracted attention. At present, it is generally believed in the flied that the reduced blood perfusion in the choroid is crucial for myopigenesis. Then, in the process of myopigenesis, how are the blurred visual signals transmitted to the choroidal blood vessels through the retina and retinal pigment epithelium, leading to the reduced choroidal blood perfusion. The cellular and molecular mechanisms underpinning this process remain elusive. In recent years, the theory of scleral hypoxia has attracted much attention. Popular signaling molecules in current research include dopamine, epidermal growth factor, retinoic acid, cholinergic molecules and adenosine, etc. These factors are likely to participate in signal transduction in retina and RPE, thus causing changes in choroidal blood flow and affecting the occurrence and development of myopia. Therefore, these signaling factors and their downstream pathways may provide new ideas for the prevention and control of myopia targets.
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.
Objective To study the preventive measure of the subambient temperature burn by analysing the pathogenesis feature. Methods The cl inical data were analysed from 351 cases of subambient temperature burn between February 2004 and February 2009, including age, sex, burn season, burn factors, burn position, burn area, burn degree, treatment way, and wound heal ing. Results Subambient temperature burn occurred in every age stage. The susceptible age stages included infant, children, and the elderly. Female patients were more than male patients. The common burn reasons werehot-water bottle burn, honey warm keeper burn, and heating device burn. The peak season was winter. Lower l imb was the most common site of the subambient temperature burn. The deep II degree to III degree were the most common level, and the burn area was always small, often 1% of total body surface area. Most of patients were treated with changing dressings at cl inic and few patients needed hospital ization. Though the surface of wound could heal finally, and the wound healed well with no obvious scar in patients who received operation. Conclusion Subambient temperature burn is the frequently encountered disease in winter. Use of the warming articles should be cautious, at the same time safety awareness should be strengthened so as to decrease the incidence rate of subambient temperature burn and the injury degree.
Objective To review the research progress of alcohol-induced osteonecrosis of the femoral head (ONFH). Methods Recent literature concerning alcohol-induced ONFH was reviewed and summarized. Results Alcohol-induced ONFH accounte for approximately 1/3 of total ONFH. Alcohol intake and the incidence of ONFH has a significant dose-effect relationship. There are some correlations between alcohol-induced ONFH and lipid metabolism, secretion of corticosteroid, and some gene of alcohol or lipid metabolism. Conclusion The relationships between alcohol and lipid metabolism, and between alcohol and steroid are still the main direction of the research of ONFH. Gene level researches can not demonstrate the pathogenesis, therefore further research should be carried on.
Objective To explore the clinical features and prognosis related factors of severe drug eruption. Methods The clinical data of 48 patients with drug eruption treated between January 2010 and August 2015 were retrospectively analyzed. Results The major type of drug eruption was Stevens-Johnson syndrome (58.3%), followed by toxic epidermal necrolysis (TEN) (27.1%) and hypersensitivity syndrome (14.6%). The major allergenic drug which might cuase drug eruption was antimicrobial agent (25.0%), followed by antipyretic analgesic drug (22.9%) and antigout drug (18.8%). Carbamazepine and allopurino were the common drugs caused TEN. Conclusion It is important to give sufficient corticosteroid earlier combined with intravenous immunoglobulin for reducing mortalities of severe drug eruption.
The pathogenesis of Vogt-Koyanagi Harada disease (VKH) has not yet been fully defined. Current studies mainly suggest that VKH is actually an autoimmune disease, especially related to the immune response mediated by various signal transduction pathways involved in the function of T cells. In recent years, the influence of the balance imbalance of various T cell subsets in cellular immunity on the pathogenesis of VKH has been a hot research direction. Currently, T helper cell 17/T regulatory cells, balance is the focus of clinical research, meanwhile, new discoveries and potential clinical treatment schemes have been made for related cellular pathways, particularly the Janus kinase/signal transducers and activators of transcription pathway and NF-kappa B pathway. The exploration of B cells in the pathogenesis of VKH has also achieved initial results through the successful application of various targeted drugs. In the future, further screening and localization of genes or proteins that are abnormally regulated or expressed in VKH, for which early comprehensive and in-depth exploration will be helpful, thus improve the efficacy of clinical treatment programs and develop new therapeutic targets.
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.
Bacterial biofilm is the key problem of chronic wound infection and difficult healing. How to prevent and control bacterial biofilm and improve the prognosis of chronic wound has become a research hotspot in the field of wound care. This paper will summarize from the following aspects: four major stages in the process of chronic wound bacteria biofilm formation (surface adhesion, formation of small colonies, biofilm maturation, and dispersion and separation); characteristics of host immune response in the presence of biofilms; morphological, microbiological, and molecular detection methods for biofilms; and progress in in vitro trials, animal trials, clinical trials, and new therapeutic methods of biofilm. The purpose of this review is to provide evidence for the treatment of biofilms for chronic wounds.