Acquired Immunodeficiency Syndrome ; blood ; complications ; diagnosis ; Antibodies, Viral ; blood ; Child ; Cough ; complications ; Fatal Outcome ; Fever ; complications ; HIV-1 ; immunology ; Humans ; Male

Objective Hepatitis-associated aplastic anemia( HAAA) is a rare and severe disease that can be fatal,if left untreated. In the childhood,it is a syndrome in which marrow failure follows the develop-ment of hepatitis. The aim of this study was to summary clinical characteristic of children with HAAA. Methods We retrospectively reviewed the hospital records of 7 children with HAAA from 2001 to 2010,and summarized and classified the clinical features of HAAA,the laboratory characteristics in 7 patients with com-bined aplastic anemia and severe hepatits,the immune status of those patients,the pathogen of those patients and the results of treatment. Results The average age of patients was 11. 1 years old(8~14 years old). The clinical features were similar in all cases. The early stage of disease,all the children had markedly elevated liver enzyme levels and peripheral blood count was normal. After symptomatic treatment,the hepatic function began to recover but appeared pancytopenia. Bone marrow biopy showed hypoplasia. The median time from onset of hepatic symptoms until diagnosis of aplasic anemia was 43. 3 days. All the children had immune dis-order. Only one boy showed parovirus B19-IgM positive and another girl was diagnosed as acute HAV hepati-tis,the pathogen results of other children were negative. All the patients were treated by immunosuppressive therapy,one patient gave up due to some reasons and others had completed remission. Conclusion HAAA is a life-threatening hematologic disorder in which an episode of hepatitis precedes AA by a period of weeks or months. Characteristically,the HAAA syndrome is more prevalent among young men. It is reported that it is in a higher frequency of patients with non-A,non-B hepatitis. Clincal features and experimental results strong-ly suggest a central role for an immune-mediated pathogenesis. The main treatment is immunosuppressive therapy,which include hormone,antithymocyte glubulin and cyclosporine.

ObjectiveTo investigate the effect of cerebroprotein hydrolysate on diabetic peripheral neuropathy.Methods105 diabetic patients were randomly divided into the treatment group (34 cases, treated with intravenous injection of cerebroprotein hydrolysate), standard control group (38 cases, treated with intramuscular injection of Metrycobal combined with intravenous injection of Actovegin) and blank control group (33 cases, treated with oral vitamin B1, B6, B12). Curative effects of three groups were evaluated.ResultsIt was shown that intravenous injection of cerebropotein hydrolysate could improve patients' symptoms, raised speed of nerve conduction and its curative effect was as same as intramuscular injection of Metrycobal combined with intravenous injection of Actovegin.ConclusionIntravenous injection of cerebropotein hydrolysate has a curation effect on diabetic peripheral neuropathy.

Humans ; Infant ; Male ; Mycobacterium tuberculosis ; Otitis Media ; microbiology ; Tuberculosis

BACKGROUND: Umbilical cord blood-mesenchymal stem cells (UCB-MSCs) following differentiation into cardiomyocytes were transplanted into ischemic myocardium. The transplanted cells can build connection with host cells and repair the infarct myocardium. OBJECTIVE: To detect the cell-cell junction after transplantation of the cardiac-like cell derived from the canine umbilical cord blood stem cells. DESIGN, TIME AND SETTING: A randomized controlled animal study was performed from July 2006 to October 2007 at the Animal Experimental Center of Xinhua Hospital Affiliated to School of Medicine, Shanghai Jiao Tong University. MATERIALS: A total of 2 full-term pregnant canines were used for isolation of UCB-MSCs. A total of 36 adult mongrel canines were divided into cell transplantation group and model control group (n=18) according to the rule of random digits table. METHODS: The MSCs at passage 4 were transfected by Laz-Z. After 3-day culture, MSCs were induced by 10 μmol/L 5-azacytidine (5-aza). The canine models of myocardium infarction were established following 3 weeks of culture. 2 mL (1 ×107)MSCs were transplanted into dogs with acute myocardium infarction by coronary artery infusion and local injection in cell transplantation group. An equal volume of saline was used in the model control group. The specimens were harvested and detected at 2, 4 and 8 weeks, respectively. Cell junction was determined using immunohistochemistry. MAIN OUTCOME MEASURES: The following parameters were measured: gene trensfection, myogenic induction and differentiation results of UCB-MSCs; junction of transplanted cells and host cardiomyocytes. RESULTS: Following 72 hours of transfaction, mass of cells expressed LacZ gene, synthetized galactosidase, and stained blue using X-gal staining. Following 3 weeks of 5-aza induction, the antigen a-Actin, Desmin and Connexin43 were all been positively expressed, but before induction they were all negative. From the myocardial section of 8 weeks after transplantation, the junction was formed between the transplanted cells and the host myocardium as formed between the transplanted cells. In the junction, green-fluorescence positive expression of cadherin and connexin43 could be seen. However, in the model control group, only cadherin and connexin43 expressed positively, but the transplanted UCB-MSCs with red fluorescence could not been observed. CONCLUSION: The UCB-MSCs is able to differentiate into cardiac-like cell in vitro and form cell-cell junction in vivo to communicate with surrounding cells.

Alcoholic liver disease ( ALD ) , a chronic progres-sive disease, threatens human health seriously. An increasing number of studies have shown that gut flora dysbiosis plays an important role in the development of ALD. Intestinal microbiota maintains a steady state under normal conditions, regulating gut flora normal physiological function. However, chronic alcohol consumption produces intestinal bacteria overgrowth and dysbio-sis, including the alteration of the composition of intestinal mi-croflora, the increment of gut permeability and bacterial translo-cation. Subsequently, the host immune is activated, promoting the production of inflammatory cytokines in liver, which plays a central role in the development of ALD. Notably, the supple-ment of prebiotics or probiotics reverses the intestinal flora disor-der,ameliorating the clinical symptoms effectively in ALD pa-tients. The evidence impies that the modulation of dysbiosis may be effective in the prevention and treatment of ALD. This review summarizes the research progress on the mechanism of the devel-opment of dysbiosis-mediated ALD, to provide a theoretical basis for the research on intestinal flora and ALD.

Objective Inflammatory bowel disease is an important chronic gastrointestinal disease of childhood and adolescence.Intestinal mucosa barrier damage plays an important role in its pathogenesis.This study attempts to use IL-1β stimulating Caco-2 cell monolayer simulates inflammatory intestinal epithelial barrier in vitro,provides the basis for studying the pathogenesis and treatment of IBD.Methods Caco-2 cells were cultivated in vitro until the 21st day to simulate intestinal epithelial cell monolayer barrier.The cells of inflammation group one were disposed with IL-1β for 2 h since the 5th day and detected TEER every other day until the 21st day.The cells of inflammation group two were disposed with IL-1 β at the 18th day for 0,12,24,48,72h, and detected TEER respectively.Normal control group cells were cultured with common medium and detected TEER at the corresponding time point.Results The TEER of Caco-2 cells gradually increased from the 5th to 15th days,reached 600Ω·cm2 in the 15th day of a plateau until to the 21st day.Since the 5th day,the TEER of inflammation group one were all lower than normal group,and still to the 21st day ＜ 500Ω·cm2.Inflammation group two shows the time dependence TEER gradually reduce,peaked at 48 hours,then a slight increase in 72 hours.Conclusion The Caco-2 cells cultured for 2 ～ 3 weeks can form intestinal epithelial monolayer barrier with polarity,then treated with IL-1 β can manufacture inflammatory intestinal epithelial barrier model in vitro.

BackgroundThe favorable effect of bone marrow mesenchymal stem cells (BMSCs) on the reconstruction of injured corneas have been reported,but the mechanism remains unclear.ObjectiveThis study was to evaluate the anti-inflammatory and antiangiogenic effect after transplantation of BMSCs in chemically burned corneas.Methods BMSCs were isolated and extracted from the bone marrow.The cells were cultured and passaged and then were seeded on the amniotic membrane.Corneal alkali injury models were created in 18 clean SD rats by sticking the filter paper containing 1 mol/L NaOH at the central cornea for 40 seconds.The rats were then randomized into 3 groups.Amniotic membrane with BMSCs or amniotic membrane without BMSCs were transplanted in 1 week after the establishment of models,and the rats without transplantation were used as the control group.The severity of corneal lesion was graded,and angiogenesis area was measured 2 weeks after the transplantation.The expression of interleukin-2 ( IL-2 ),interferon-γ(IFN-γ),IL-10 and transforming growth factor-β ( TGF-β ) were examined by ELISA,and the mRNA of the matrix metalloproteinase-2 ( MMP-2 ),vascular endothelial growth factor (VEGF),epidermal growth factor(EGF) and basic fibroblast growth factor(bFGF) were analyzed by real-time PCR.ResultsThe positive rates of the cells were 99.78％ and 99.79％ for CD90 and CD29,7.90％,1.16％ and 1.28％ for CD34,CD45 and CDllba.The cells grew well on the amniotic membrane.The corneal inflammatory score and neovascularization area were similar among the three groups ( F =0.021,P-- 0.979 ; F =0.076,P =0.927 ).However,the corneal inflammatory score was significantly reduced and neovascularization area was significantly less in the amniotic membrane group compared with the BMSCs group and control group(P=0.011,0.001 ;P=0.005,0.000).The levels of IL-2 and IFN-γ secreted by Th1 cells were decreased (P =0.000,0.002;P =0.003,0.045 ) and the levels of IL-10 and TGF-β secreted by Th2 cells were increased in the BMSCs group compared with the amniotic membrane and control group ( P =0.000,0.000 ; P =0.000,0.021 ).No significant difference was found in VEGF expression among three groups( F=4.880,P =0.056).But the mRNA of the MMP-2 and bFGF were lower in the BMSCs group than the amniotic membrane group(P=0.009,0.003 ) and control group(P＜0.01 ).Conclusions BMSCs modulate the expression of inflammatory-related and angiogenic-related cytokines and therefore play the antiinflammatory and anti-angiogenic effects in the chemically burned cornea.

Migraine is one of the common and frequently encountered diseases. The study proves that 5-hydroxytryptamine (5-HT) receptor, plays an important role in the occurrence of migraine. Rat striatum was used for preparation of the cell membrane stationary phase (CMSP) in our experiments. The cell membrane chromatography (CMC)-offline-HPLC system was applied to specifically recognize the components from the drug pair of Chuanxiong Rhizoma and Angelicae Dahuricae Radix, which interact with the receptors on CMSP. The dissociation equilibrium constant (KD) was measured in a rat striatum/CMC system, performed by continuously pumping sumatriptan, a 5-HT1D agonist, ranging from 2.42 x 10(-8) to 4.84 x 10(-7) mol · L(-1) through a CMC column, and the capacity factors (k') were recorded. The KD value obtained from the model was (4.59 ± 0.33) x 10(-6) mol · L(-1) for imperatorin, and the rat model of migraine induced by nitroglycerin was applied to validate the pharmacological effects of the drug pair. The results indicated that the CMC method could be a quick and efficient way for characterizing the drug-receptor interactions in vitro.
Angelica ; chemistry ; Animals ; Cell Membrane ; chemistry ; Chromatography, High Pressure Liquid ; methods ; Drug Evaluation, Preclinical ; methods ; Drugs, Chinese Herbal ; chemistry ; Male ; Migraine Disorders ; drug therapy ; Rats ; Rats, Sprague-Dawley ; Receptor, Serotonin, 5-HT1D ; chemistry ; Serotonin Receptor Agonists ; analysis

Background and purpose:P38 mitogen-activated protein kinase (P38MAPK) signal transduction pathway is involved in occurrence, development and transfer process in a wide variety of tumors. Urokinase-type plasminogen activator (uPA) plays an important role in tumor invasion and metastasis. This study aimed to explore the clinical signiifcance of the P38MAPK signaling pathway and the expression of uPA in ovarian cancer.Methods:The expressions of uPA, P38MAPK, ERK and AKT were detected in 49 cases of cervical adenocarcinoma by immunohistochemistry. The expressions of uPA and P38MAPK were detected by Western blot in ovarian cancer cell lines HO8910, HO-8910PM, SKOV3 and CAOV3. The changes of uPA and P38MAPK were detected by SB203580, a speciifc inhibitor of P38MAPK signal transduction pathway.Results:The result of immunohistochemical method showed that positive expression rates for uPA, P38MAPK, ERK and AKT were 61.22%, 57.14%, 53.06% and 55.10%, respectively. The expression of the uPA was positively correlated with the P38MAPK (r=0.865,P=0.001), and related with clinicopathologic stage, differentiated degree, lymph node metastasis, but not related with age and histologic type (P>0.05). The expressions of AKT and ERK were related with the lymph node metastasis and greater omentum metastasis(P<0.05), but not related with age and histologic type (P>0.05). The expression of uPA in HO-8910PM was higher than that in ovarian cancer cell lines HO8910, SKOV3 and CAOV3, and the expression of uPA reduced when the P38MAPK signal transduction pathway was cut off by the SB203580. The expressions of P38MAPK and uPA were negatively correlated with the prognosis of ovarian cancer (Log-rank=3.897 and 11.044,P=0.048 and 0.001). Conclusion:The P38MAPK signal transduction pathway was activated in ovarian cancer. The activated P38MAPK signal transduction pathway can raise the expression of uPA, which may contribute to the development of ovarian cancer. The result indicates that the P38MAPK signal transduction pathway and uPA might play an important role in the invasion and metastasis of ovarian cancer. P38MAPK and uPA might be useful markers for evaluating prognosis of ovarian cancer.