Objective To investigate the effect of stoma skin care powde combined with skin protective mem-brane in prevention and treatment of secondary eczema after anal fistula surgery. Methods Eighty-three patients after anal fistula operation were divided into test group and control group. On the basis of routine treatment,the pa-tients in test group were used stoma skin care powder combined with skin protective membrane to protect the peri-anal skin. While the patients in control group were treated routinely. The degree of pruritus,the onset time,the number of skin lesions,the area of eczema and the healing time of eczema were observed in two groups 4 d,14 d and 24 d post-operation. Results Patients in test group had lowerdegree of pruritus,later onset time after dressing, less skin lesions,samller area of eczemaand shorter healing time of eczema than patients in control group in the 3 time nodes (all P<0.05). Conclusion Stoma skin care powder combined with skin protective membrane could effec-tively isolatepostoperative wound secretions and anus polyrrhea,and have preventive and therapeutic effects on sec-ondary perianal eczema after anal fistula surgery.

Urinary excretions of transforming grow th factor-? 1 (TGF-? 1), laminin (LN) and type Ⅳ collagen were determined i n 182 type 2 diabetic patients. Urinary excretions of TGF-? 1, LN and type Ⅳ collagen were increased in type 2 diabetic patients, and these findings were fa irly well correlated with severity of diabetic nephropathy (DN). Urinary TGF-? 1 seems to be the early index of DN, urinary LN and type Ⅳ collagen appear to be the indices of DN severity.

AIM: To investigate the effect of losartan on the mRNA expression of type 2 angiotensin II receptor and cytokines in diabetic rat kidney.METHODS: SD rats were randomly divided by following groups: control rats(group C),diabetic rats(group D) and diabetic rats treated with losartan (30(mg?kg~(-1)?d~(-1)),by gavage,group DT).At the end of 8-weeks study,mRNA expressions of the type 2 angiotensin II receptor(AT_2),transforming growth factor-?_1(TGF-?_1),platelet-derived growth factor-B(PDGF-B),tumor necrosis factor-?(TNF-?) and collagen Ⅳ in rats renal cortex were measured by RT-PCR,respectively.In addition,angiotensin Ⅱ level in renal cortex was determined by the radioimmunoassay.RESULTS: In group D,urine protein excretion(P

AIM: To investigate the molecular mechanism of amylin in inducing apoptosis of human pancreatic islet ?-cells. METHODS: Human pancreatic islet cells were isolated and cultured. The cells were treated with amylin or amylin and aminoguanidine (AG group) for 24 h, respectively. Apoptosis of pancreatic islet ?-cells was studied by in situ TUNEL method combined with double staining for insulin and ELISA. The levels of insulin, NO 2 -/NO 3 - and glutathione (GSH), p53 mRNA and bcl-2 mRNA were also detected. RESULTS: (1) The enrichment factor and the apoptosis rate of pancreatic islet ?-cells in amylin group were markedly higher than that in control group and AG group ( P

Objective To explore the effects of applied course reform of emergency critical care nursing on self-directed learning ability of nursing students. Methods From September 2016 to January 2017, a total of 180 nursing undergraduates from Xi'an Peihua University of grade 2014 were selected as the research subjects. 86 students from 3 classes were randomly recruited into control group, and 94 students from other 3 classes to observation group. Control group was treated with traditional teaching methods, while experimental group adopted the applied course reform of emergency critical nursing. Nursing students' self-directed learning ability was compared between the two groups before and after the course. Results After the whole course, the total score of students' self-directed learning, learning motivation,planning and implementation,self management and interpersonal communication dimensions were(78.31±8.15), (23.94±3.06),(23.09±2.77), (15.51±2.13) and (15.78±2.04) , which were all higher than (73.37±9.91), (22.79±3.61), (21.72±3.38), (14.28±2.38), (14.58±2.59) in the control group respectively. The differences were statistically significant(t=-3.611, -2.301, -2.970, -3.661, -3.458; P< 0.05). The final exam score of the experimental group was (84.57±8.21), which was higher than that in the control group (81.40±8.07), with a statistically significant difference (t=2.616, P=0.007).Conclusions Applied course reform of emergency critical nursing care can enhance nursing undergraduates' self-directed learning ability.

OBJECTIVE To explore the anti-liver fibrosis effect and mechanism of Atractylenolide Ⅲ-induced hepatic stellate cell(HSC)senescence.METHODS ASCT2 siRNA and Atractylenolide Ⅲ(40 μmol·L-1)acted on human hepatic stellate cells LX2 respectively to inhibit ASCT2,MTT was used to evaluate cell viability,EdU method was used to detect cell proliferation,and se-nescence associated-β-galactosidase(SA-β-Gal)staining was used to detect cell senescence;Western blot was used to detect chan-ges in the LC3-Ⅱ/Ⅰ ratio in LX2 cells,laser confocal detection was used to detect changes in LC3 autophagy flow and error protein accumulation,and the fluorescence of the lysosomal marker LAMP1 was also observed to detect lysosomal function and quantity;kits were applied to detect ROS and MDA levels as well as SOD activity in LX2 cells,and flow cytometry was used to analyze mitochondrial ROS levels and membrane potential.A CCl4-induced mouse liver fibrosis model was constructed.Atractylenolide Ⅲ was administered at 20,30,or 40 mg·kg-1.HE,Masson,and Sirius Red staining were used to observe liver tissue damage and collagen deposition.Western blot was used to detect the expression levels of P21 and P16 in mice in each group,and SA-β-Gal staining and immunohistochemistry were used to analyze the situation and origin of senescent cells.RESULTS After inhibiting ASCT2,the viabil-ity of LX2 cells decreased and senescence increased(P<0.01).Meanwhile,the autophagy function was enhanced and the number of lysosomes was increased but the function was weakened.After adding chloroquine(CQ)to clear lysosomes,the cell viability and auto-phagy function increased(P<0.01).After inhibiting ASCT2,the levels of MDA and ROS in LX2 cells increased,and the activity of SOD decreased(P<0.01).Among them,the level of mitochondrial ROS increased and the membrane potential decreased(P<0.01).After adding rotenone,the cellular redox homeostasis was improved,and the number of lysosomes was restored(P<0.01).In vivo experimental results showed that compared with the model group,Atractylenolide Ⅲ improved liver tissue structural damage and collagen deposition,induced HSC senescence in liver tissue of mice with liver fibrosis,and inhibited HSC activation marker α-smooth muscle actin(α-SMA),promoted the expression of senescence indicators P16 and P21(P<0.01).CONCLUSION Atractylenol-ide Ⅲ induces an increase in mitochondrial ROS and a decrease in membrane potential by inhibiting ASCT2,which further promotes the enhancement of HSC autophagy function,increases the number of lysosomes and weakens their function,thereby inducing the se-nescence of activated HSCs.

Objective To compare the safety and efficacy of insulin degludec (IDeg) with those of insulin glargine (IGlar) in insulin-naive subjects with type 2 diabetes (T2DM).Methods This was a 26-week,randomized,open-label,parallel-group,treat-to-target trial in 560 Chinese subjects with T2DM (men/women:274/263,mean age 56 years,mean diabetes duration 7 years) inadequately controlled on oral antidiabetic drugs (OADs).Subjects were randomized 2:1 to once-daily IDeg (373 subjects) or IGlar(187 subjects),both in combination with metformin.The primary endpoint was changes from baseline in glycosylated hemoglobin(HbA1c) after 26 weeks.Results Mean HbA1c decreased from 8.2％ in both groups to 6.9％ in IDeg and 7.0％ in IGlar,respectively.Estimated treatment difference (ETD) of IDegIGlar in change from baseline was-0.10％ points (95％ CI-0.25-0.05).The proportion of subjects achieving HbA1c ＜ 7.0％ was 56.3％ and 49.7％ with IDeg and IGlar,respectively [estimated odds ratio of IDeg/IGlar:1.26 (95 ％ CI 0.88-1.82)].Numerically lower rateof overall confirmed hypoglycaemia and statistically significantly lower nocturnal confirmed hypoglycemia were associated with IDeg compared with IGlar,respectively [estimated rateratio of IDeg/IGlar 0.69 (95％ CI 0.46-1.03),and 0.43 (95％ CI 0.19-0.97)].No differences in other safety parameters were found between the two groups.Conclusions IDeg was non-inferior to IGlar in terms of glycaemic control,and was associated with a statistically significantly lower rate of nocturnal confirmed hypoglycaemia.IDeg is considered to be suitable for initiating insulin therapy in Chinese T2DM patients on OADs requiring intensified treatment.Clinical trail registration Clinicaltrials.gov,NCT01849289.

AIM:To investigate the antagonism mechanism of benazepril on renal fibrosis of unilateral uretreal obstructire (UUO).METHODS:Fiftyfour Sprague-Dawley (SD) rats were randomly divided into three groups:sham operation group,model group,benazepril group.All the other groups were treated with surgery method of unilateral ureteral ligation to establish a rat model of renal fibrosis except the sham operation group.The pathological changes were observed by Masson staining;the positive staining expression of TGF-β1,Col-Ⅳ,Wnt1,Wnt4 in frozen sections were observed by immunofluorescence staining;the expressions TGF-β1,Col-Ⅳ,Wnt1 and Wnt4 mRNA in renal tissues were detected by real time fluorescence quantitative PCR.RESULTS:Masson staining results:compared with the sham group,the parts of blue dye collagen fiber and the degree of renal fibrosis increased significantly in all modeled groups;compared with the model group,the parts of blue dye collagen fiber and the degree of renal fibrosis decreased significantly in benazepril group.Immunofluorescence and PCR results:compared with the model group,the positive expression of Wnt1,Wnt4,TGF-β1,Col-Ⅳ and mRNA in the benazepril group decreased significantly.CONCLUSION:Benazepril can improve renal fibrosis by inhibiting the expression of TGF-β1,Col-Ⅴ,Wnt1,Wnt4 and ameliorating the level of renal fibrosis.

Objective To discuss the genotype and phenotype features of 187 patients with spinocerebellar ataxia type 3 (SCA3) and analyze their genotype-phenotype relationship.Methods A total of 187 patients genetically diagnosed as having SCA3 from 160 families were enrolled from our hospital from 2005 to 2015.Detailed medical histories were collected.SPSS 22.0 was conducted to statistically analyze the genotypes and pathogenic CAG expansions of A TXN3 gene in the patients.Results One hundred males and 87 females suffered SCA3.Mean age at onset was 35.43±11.17 years.The ranges of pathogenic CAG expansion were 65-86 repeats,with mean pathogenic CAG expansion of 74.11±3.56 repeats.A negative correlation was found between number of CAG repeats and age of onset (r=-0.815,P=0.000).Frequencies of the patients with tendon hyporeflexia were 28.9％ and 6.0％,respectively,in the smaller pathogenic CAG expansion group (≤74) and larger pathogenic CAG expansion group (＞74),with significant difference (P＜0.05).Frequencies of patients with rigidity were 27.8％ and 49.4％,respectively,in the smaller pathogenic CAG expansion group and larger pathogenic CAG expansion group,with significant difference (P＜0.05).Conclusions SCA3 is neurodegenerative disorder with high clinical and genetical heterogeneity.There are distinct correlations between number of pathogenic CAG expansion and age of onset,frequency ofhyporeflexia and rigidity.

Background: and PurposeHyperekplexia (HPX), a rare neurogenetic disorder, is classically characterized by neonatal hypertonia, exaggerated startle response provoked by the sudden external stimuli and followed by a shortly general stiffness. Glycine receptor alpha 1 (GLRA1) is the major pathogenic gene of the disease. We described the clinical manifestations of genetically confirmed HPX patients and made a literature review of GLRA1-related HPX to improve the early recognition and prompt the management of the disorder. Methods: Extensive clinical evaluations were analyzed in 4 Chinese HPX patients from two unrelated families. Next generation sequencing was conducted in the probands. Sanger sequence and segregation analysis were applied to confirm the findings. Results: All four patients including 3 males and 1 female presented with excessive startle reflex, a cautious gait and recurrent falls. Moreover, startle episodes were dramatically improved with the treatment of clonazepam in all cases. Exome sequencing revealed 2 homozygous GLRA1 mutations in the patients. The mutation c.1286T>A p.I429N has been previously reported, while c.754delC p.L252* is novel. Conclusions HPX is a treatable disease, and clonazepam is the drug of choice. By studying and reviewing the disorder, we summarized the phenotype, expanded the genotype spectrum, and discussed the possible pathogenic mechanisms to enhance the understanding and recognition of the disease. Early awareness of the disease is crucial to the prompt and proper administration, as well as the genetic counseling.