Objective To investigate the effect of the comprehensive rehabilitation on shoulder hand syndrome after stroke.Methods 181 patients with shoulder hand syndrome after stroke were divided into the comprehensive rehabilitation group(observed group,96 cases)and control group(85 cases).All the patients were treated with routine rehabilitation training,while those of the observed group accepted normal limbs in good position,air pressure,cold/warm water alternate dip in,motor imagery,etc.in addition.Results The shoulder pain,range of motor,dropsy of the observed group obviously improved to that of the control group(P<0.05).Conclusion The comprehensive rehabilitation is more effective on shoulder hand syndrome after stroke.

Primary biliary cholangitis (PBC) is an autoimmune liver disease with unclear pathogenesis.The amino acid composition and sequence in the complementarity-determining region 3 of T cell receptor (TCR) and B cell receptor (BCR) are highly diverse, which forms a large antigen recognition receptor repertoire, i.e., immune repertoire.In recent years, second-generation sequencing techniques combined with multiplex PCR or amplicon rescue multiplex PCR have been used to study the features of immune repertoire in PBC patients, and it has been found that PBC patients have clonal expansion of specific CD4+ T lymphocytes, clonal diversity of B lymphocytes, somatic hypermutation, and reduction in class switch, as well as increase in clonal diversity after treatment with ursodeoxycholic acid.These findings need to be confirmed by large-scale in vivo and in vitro studies and different immune repertoire research strategies.

The innervation and distribution of 5-HT cells in gastric wall of rabbit and rat were studied by means of histochemical techniques of monoamine fluorescence and cholinesterase. And the morphological relation between them was investigated using the consecutive method for demonstrating the fluorescence and ChE on the same section. At the fundic gland, 5-HT cells were in contact with both the adrenergic and cholinergic axonal terminals. There are adrenergic and cholinergic terminals to innervate the gland cells of fundic gland, partial fundic gland the dual axonal terminal are identical in their localization and morphological outline. The loyer of muscle and smooth muscles surrounding the arteriole in various stomach layers were innervated by both adrenergic and cholinergic terminals, some of them are superimposed at the samelocalization. There are a lot of nsChE nerve ending network in gastric lamina propria beneath epithelium of gastric mucous membrane, it was discussed about their sensory nature in this paper.

AIM:to investigate the effects of extract of ginkgo biloba (EGB) on human tubular epithelial-mesenchymal transition induced by transforming growth factor-?1.METHODS: HK2 cells were induced to epithelial-mesenchymal transition by transforming growth factor-?1 (TGF-?1, 10 ?g/L). EGB was added into the medium of HK2 cells 2 h before TGF-?1 was added. The expressions of E-cadherin, ?-smooth muscle actin (?-SMA), NADPH oxidase p67phox and superoxide dismutase (SOD) were determined by Western blotting. Malondialdehyde (MDA) in the mediums of HK2 cells was detected. RESULTS: EGB significantly attenuated the downregulation of E-cadherin, the upregulation of ?-SMA and p67phox, the downregulation of SOD and the upregulation of MDA in HK2 cells induced by TGF-?1.CONCLUSION: EGB significantly attenuates human tubular epithelial-mesenchymal transition induced by TGF-?1, and its underlying mechanism is that EGB attenuates the upregulation of p67phox and the downregulation of SOD induced by TGF-?1.

Tubulointerstitial fibrosis (TIF) is a common pathological feature of end-stage kidney disease. Previous studies showed that upregulation of TGFbeta1 notably contributed to the chronic renal injury and irbesartan halted the development of TIF in rats with 5/6 renal mass reduction. This study was to investigate the effects of irbesartan on chronic TIF and the mechanism involved TGFbeta1 in the rodent model of chronic renal failure involving 5/6 nephrectomy. The results showed that irbesartan significantly attenuated the rise in blood pressure and tubulointerstitial injury observed in this model. Masson staining of the renal tissue revealed that there appeared severe renal tubule atrophy and fibrosis in operation group, but the lesion was attenuated mostly in irbesartan-treated group. Immunohistochemistry showed that irbesartan treatment apparently decreased the protein expression of TGFbeta1 which was up-regulated in operation groups. Western blot showed that irbesartan treatment down-regulated the expression of TGFbeta1, phosphorylated smad2 (p-smad2), AT1R and phosphorylated p38 (p-p38) MAPK, but significantly up-regulated the protein expression of smad6 as compared with operation group. These findings suggest that irbesartan attenuates hypertension and reduces the development of TIF in rats with 5/6 renal mass reduction via changes in the expression of these proteins at least including smad6, TGF-beta1, p-smad2, AT1 and p-p38 MAPK.

Objectives The present study aimed to investigate the associations between genetic polymorphism of methylenetetrahydrofolate reductase ( MTHFR) G1793A, plasma homocysteine (Hcy) levels, vitamin status and ulcerative colitis ( UC) in a cohort of patients in Hubei Han nationality. Methods Two hundred and ninty-nine UC patients and 764 age- and sex-matched healthy controls were recruited in this study. Polymorphism of MTHFR G1793A was examined using a PCR-RELP method.Plasma levels of Hcy, folate and vitamin B12 were determined by enzymatic cycling assay and corpuscle immune chemiluminescence assay, respectively.Results Both variant allele and genotype frequencies in MTHFR G1793A gene were significantly higher in the UC patients compared to the controls (22.24% vs 14.20% , P<0.001 ;42.81% vs 26.97%, P < 0.001, respectively).Plasma Hcy levels were increased in UC patients compared to the controls [(20.67 ±6.42)mmol/L vs (13.21 ±5.11)mmol/L, P <0.001] while folate and vitamin B12 concentrations were significantly decreased [(11.37±6.34) nmol/L vs (14.89±7.21) nmol/L, P < 0.001; (324.15±127.53 ) pmol/L vs (421.54±128.45 ) pmol/L, P < 0.001, respectively].Furthermore, hyperhomocysteinaemia (HHcy) and folate deficiency were also more prevalent in the UC patients (32.44% vs 25.78% , P = 0.029; 23.41% vs 17.01%, P =0.016, respectively).Conclusions Genetic polymorphism of MTHFR G1793A Wag strongly associated with UC.HHcy,folate deficiency and low vitamin B12 concentration were common phenomena in the UC patients of Hubei Han nationality.Our findings demonstrate that the genes relmed to Hey metabolism may play an important role in the pathogenesis of UC.

[ ABSTRACT] AIM:To investigate the preventive effects of Clostridium butyricum ( C.butyricum) on the type of pylorus ligated gastric ulcer ( GU) in mice and the underlying mechanisms.METHODS:ICR mice were randomly divided into 4 groups:sham operation group, model group, C.butyricum pretreatment group and omeprazole pretreatment group. Gastric pyloric ligation was adopted to establish GU model in mice.The gastric juice was collected to measure the content of gastric free mucus, the pH of gastric juice and the activity of pepsin.The gastric tissues were collected for routine HE stai-ning to observe the pathological changes.The content of glycogen was detected by PAS staining.The protein expression of Bax and Bcl-2 in the gastric mucosa was also assessed by immunohistochemical staining.RESULTS: The HE and PAS staining showed that the C.butyricum pretreatment obviously attenuated the mucosa lesion induced by ligation.Compared with model group, the pH of gastric juice was significantly raised.The activity of pepsin fell off in C.butyricum group, which was lower than that in omeprazole group.In comparison with model group, the content of gastric free mucus was dra-matically increased and PAS staining showed a significant rise in C.butyricum group, but not in omeprazole group.The protein expression of Bax was decreased and the protein expression of Bcl-2 was upgraded in C.butyricum group than those in model group.CONCLUSION:C.butyricum protects gastric mucosa against the challenge of pylorus ligation in mice and its mechanism may be related to inhibiting gastric acid secretion and the activation of pepsin, increasing the production of gastric free mucus, strengthening the expression of bcl-2 gene and inhibiting the expression of bax gene.

Background and Objectives: Dental pulp stem cells (DPSCs) play an important role in the repair of tooth injuries. Electrogenic sodium bicarbonate cotransporter 1 (NBCe1) is a Na＋ -coupled HCO3− transporter encoded by the solute carrier 4A4 (SLC4A4) gene and plays a crucial role in maintaining the pH of DPSCs. Our previous research confirmed that NBCe1 is highly expressed in odontoblasts during the development of the tooth germ. Therefore, in this study, we aimed to investigate the effect of NBCe1 on odontogenic differentiation of DPSCs and further clarify the underlying mechanisms. Methods: and Results: DPSCs were isolated and identified, and the selective NBCe1 inhibitor S0859 was used to treat DPSCs. We used a cell counting Kit-8 assay to detect cell proliferative ability, and intracellular pH was assessed using confocal microscopy. Odontogenic differentiation of DPSCs was analyzed using real-time PCR and Alizarin Red S staining, and the NF-κB pathway was assessed using western blotting. Our results indicated that 10 μM S0859 was the optimal concentration for DPSC induction. Intracellular pH was decreased upon treatment with S0859. The mRNA expressions of DSPP, DMP1, RUNX2, OCN, and OPN were upregulated in the NBCe1 inhibited group compared to the controls. Moreover, NBCe1 inhibition significantly activated the NF-κB pathway, and a NF-κB inhibitor reduced the effect of NBCe1 on DPSC differentiation. Conclusions NBCe1 inhibition significantly promotes odontogenic differentiation of DPSCs, and this process may be regulated by activating the NF-κB signaling pathway.

Objective To investigate the effect of improving immunity in the treatment of chronic brucellosis,and to analyze and evaluate its clinical curative effect.Methods A patient with chronic brucellosis was treated with Mongolian medicine combined with chemical drugs to enhance immunity.The clinical symptoms,serological antibodies,Brucella DNA and immune function were compared before and after treatment.The specific antibody against Brucella in serum was detected by tube agglutination test (SAT) and tiger red plate agglutination test (RBPT).Brucella DNA in serum and blood cells was detected by PCR,and the peripheral blood lymphocyte subsets were detected by flow cytometry.Immuno-luminescence technique was used to detect serum immunoglobulin and complement components.Results After treatment,the clinical symptoms such as cold back,fatigue,and joint pain disappeared completely,and the results of serum specific antibodies against Brucella were SAT 1 ∶ 50 (++)and RBPT (+) with no changes before and after treatment,and the results of cells and serum were both negative after treatment though the results of DNA detection of Brucella were cell positive and seronegative before treatment.The results of immunological function test showed that γδT cells decreased to 9.50％ after treatment compared to 14.00％ before treatment,and the percentage of monocytes and Treg cells were 5.59％ and 7.33％ after treatment,which were higher than 3.35％ and 4.72％ of before treatment,and the level of complement C3 was 0.79 g/L before treatment and 0.91 g/L after treatment that was returned to normal reference range (0.88 ～ 2.01 g/L).Conclusion The patients with chronic brucellosis can improve their clinical treatment by improving immunity.

Tubulointerstitial fibrosis(TIF)is a common pathological feature of end-stage kidney disease.Previous studies showed that upregulation of TGFβ1 notably contributed to the chronic renal injury and irbesartan halted the development of TIF in rats with 5/6 renal mass reduction.This study was to investigate the effects of irbesartan on chronic TIF and the mechanism involved TGFβ1 in the rodent model of chronic renal failure involving 5/6 nephrectomy.The results showed that irbesartan significantly attenuated the rise in blood pressure and tubulointerstitial injury observed in this model.Masson staining of the renal tissue revealed that there appeared severe renal tubule atrophy and fibrosis in operation group,but the lesion was attenuated mostly in irbesartan-treated group.Immunohistochemistry showed that irbesartan treatment apparently decreased the protein expression of TGFβ1 which was up-regulated in operation groups.Western blot showed that irbesartan treatment down-regulated the expression of TGFβ1,phosphorylated smad2(p-smad2),AT1R and phosphorylated p38(p-p38)MAPK,but significantly up-regulated the protein expression of smad6 as compared with operation group.These findings suggest that irbesartan attenuates hypertension and reduces the development of TIF in rats with 5/6 renal mass reduction via changes in the expression of these proteins at least including smad6,TGF-β1,p-smad2,AT1 and p-p38 MAPK.