Objective: to study the effect of valsartan combined with amlodipine in the treatment of three high diseases. Methods: a total of 100 patients in our hospital from 2019 to date were randomly divided into two groups. T...Objective: to study the effect of valsartan combined with amlodipine in the treatment of three high diseases. Methods: a total of 100 patients in our hospital from 2019 to date were randomly divided into two groups. The patients in the first group were treated with valsartan, and the patients in the second group were treated with amlodipine while valsartan. After the treatment was completed, the physical conditions of the two groups were compared, including whether there was any adverse reaction. Results: the physical condition of patients in the second group after treatment was lower than that in the first group (P < 0.05). No obvious adverse reactions were observed in the two groups during the treatment, and the treatment effects were relatively good. P > 0.05. Conclusion: valsartan combined with amlodipine in the treatment of hypertension can obtain better effect, which is very good for improving patients' physical condition, improving patients' life quality and ensuring the safety in the treatment process.展开更多
Background:Overexpression of inducible nitric oxide synthase(iNOS)has been reported in diabetic retinopathy(DR).The kinin B1 receptor(B1R)is also overexpressed in DR,and can stimulate iNOS via Gαi/ERK/MAPK pathway.We...Background:Overexpression of inducible nitric oxide synthase(iNOS)has been reported in diabetic retinopathy(DR).The kinin B1 receptor(B1R)is also overexpressed in DR,and can stimulate iNOS via Gαi/ERK/MAPK pathway.We previously showed that the topical administration of a B1R antagonist,LF22-0542,significantly reduces leukocyte infiltration,increased vascular permeability and overexpression of several inflammatory mediators,including iNOS in DR.Thus,the aim of this study was to determine whether the pro-inflammatory effects of B1R are attributed to oxidative stress caused by the activation of iNOS pathway in order to identify new therapeutic targets for the treatment of DR.iNOS and B1R being absent in the normal retina,their inhibition is unlikely to result in undesirable side effects.The approach will be no invasive by eye application of drops.Methods:Diabetes was induced in male Wistar rats(200-230 g)by a single intraperitoneal injection of streptozotocin(STZ,65 mg/kg b.w).One week later,rats were randomly divided into four groups(N=5)and treated for one week as follows:Gr 1:control rats treated with the selective iNOS inhibitor(1,400 W,0.06μM twice a day by eye-drops×7 days),Gr 2,STZ-diabetic rats treated with 1,400 W,Gr 3:control rats received a selective B1R agonist[Sar(D-Phe8)-des-Arg9-BK,100μg twice a week]by intravitreal injections(itrv)and treated with 1,400 W,Gr 4:STZ-diabetic rats+B1R agonist+1,400 W.At the end of treatment and two weeks post-STZ,three series of experiments were carried out to measure vascular permeability(by Evans blue dye method)and the expression of vasoactive and inflammatory mediators,including iNOS,VEGF-A,VEGF-R2,IL-1β,Cox-2,TNF-α,bradykinin 1 and 2 receptors and carboxypeptidase M/kininase 1(by Western Blotting and qRT-PCR).The nitrosative stress(nitrosylation of proteins)was also assessed by Western Blotting.One-way Anova test with Bonferroni post hoc was used for statistical analysis.Results:STZ-diabetic rats showed a significant increase in retinal vascular permeability(22.8μg/g Evans blue dye per g of fresh retinas,P=0.016)compared with control rats and control treated rats(17.2 and 16.8μg/g respectively).The injections of B1R agonist amplified the increase of vascular permeability which was normalized by the 1,400 W.The overexpression of inflammatory markers was also normalized by the 1,400 W in STZ-diabetic rats received or not the B1R agonist.Conclusions:These results support a contribution of iNOS in the deleterious effects of B1R in this model of diabetic retinopathy.Hence,iNOS inhibition by ocular application of 1,400 W may represent a promising and non-invasive therapeutic approach in the treatment of diabetic retinopathy.展开更多
玻璃体切除术(pars plana vitrectomy,PPV)为增殖性糖尿病视网膜病变(proliferative diabeticretinopathy,PDR)常用治疗手段,但手术难度大、出血量多,难以有效控制,会延长手术时间、增加手术失败风险。采取有效措施优化治疗,降低手术风...玻璃体切除术(pars plana vitrectomy,PPV)为增殖性糖尿病视网膜病变(proliferative diabeticretinopathy,PDR)常用治疗手段,但手术难度大、出血量多,难以有效控制,会延长手术时间、增加手术失败风险。采取有效措施优化治疗,降低手术风险是近年来的研究热点。展开更多
Hepatocyte nuclear factor 1-β(HNF1B)defects cause renal cysts and diabetes syndrome(RCAD),or HNF1B-maturity-onset diabetes of the young.However,the hepatic phenotype of HNF1B variants is not well studied.We present a...Hepatocyte nuclear factor 1-β(HNF1B)defects cause renal cysts and diabetes syndrome(RCAD),or HNF1B-maturity-onset diabetes of the young.However,the hepatic phenotype of HNF1B variants is not well studied.We present a female neonate born small for her gestational age[birth weight 2360 g;-2.02standard deviations(SD)and birth length 45 cm;-2.40 SD at the 38th gestational week].She developed neonatal cholestasis due to biliary atresia and required surgical intervention(portoenterostomy)when 32-d old.Following the operation,icterus resolved,but laboratory signs of liver dysfunction persisted.She had hyperechogenic kidneys prenatally with bilateral renal cysts and pancreatic hypoplasia postnatally that led to the diagnosis of an HNF1B deletion.This represents the most severe hepatic phenotype of an HNF1B variant recognized thus far.A review of 12 published cases with hepatic phenotypes of HNF1B defects allowed us to distinguish three severity levels,ranging from neonatal cholestasis through adult-onset cholestasis to noncholestatic liver impairment,all of these are associated with congenital renal cysts and mostly with diabetes later in life.We conclude that to detect HNF1B variants,neonates with cholestasis should be checked for the presence of renal cysts,with special focus on those who are born small for their gestational age.Additionally,patients with diabetes and renal cysts at any age who develop cholestasis and/or exocrine pancreatic insufficiency should be tested for HNF1B variants as the true etiological factor of all disease components.Further observations are needed to confirm the potential reversibility of cholestasis in infancy in HNF1B mutation/deletion carriers.展开更多
糖尿病（Diabetes）
Pharmacist：Hello!What can I do for you？
药师：您好,请问您需要什么帮助？
Client：I want to ask you about general in-structions on how to take medication for diab etes.
顾客：我想咨询一下有关糖...糖尿病（Diabetes）
Pharmacist：Hello!What can I do for you？
药师：您好,请问您需要什么帮助？
Client：I want to ask you about general in-structions on how to take medication for diab etes.
顾客：我想咨询一下有关糖尿病的用药常识。展开更多
To pursue insulin and islet transplantation replacement therapy for type 1 diab etes based on engineered human non β cells which secrete mature insulin Methods Human proinsulin cDNA was cloned from its genomic ge...To pursue insulin and islet transplantation replacement therapy for type 1 diab etes based on engineered human non β cells which secrete mature insulin Methods Human proinsulin cDNA was cloned from its genomic gene and mutated by overlap e xtension PCR, introducing furin consensus cleavage sequences (Arg Xaa Lys/Arg Arg) An expression vector encoding a genetically modified human proinsulin c DNA was generated and transduced to Hela, 293, and L02 cells by lipofectin medi ated DNA transfection Following G418 screening, the surviving L02 cells were s elected and enriched Insulin levels in the supernatant and cells were evaluate d using radioimmunoassay and immunofluorescence staining Results Three sites in the insulin gene were mutated simultaneously Insulin gene m odified cells were able to express insulin at different levels: 8 45-188 00? μIU/24 h/2 0×10 6 Hela cells and 159 88-242 14?μIU/24 h/2 0×10 6 293 cells for transient expression, and 2 56-61 95?μIU/24 h/2 0×10 6 from se veral L02 clones screened with G418 No insulin was released by control cells Furthermore, immunofluorescence staining confirmed that proinsulin was stored a s vacuoles in the cytoplasm of L02 cells Conclusion A correctly mutated human proinsulin cDNA was obtained successfully, transfected and expressed efficiently in non beta cells, lending support to the study of s omatic gene therapy in diabetes mellitus展开更多
文摘Objective: to study the effect of valsartan combined with amlodipine in the treatment of three high diseases. Methods: a total of 100 patients in our hospital from 2019 to date were randomly divided into two groups. The patients in the first group were treated with valsartan, and the patients in the second group were treated with amlodipine while valsartan. After the treatment was completed, the physical conditions of the two groups were compared, including whether there was any adverse reaction. Results: the physical condition of patients in the second group after treatment was lower than that in the first group (P < 0.05). No obvious adverse reactions were observed in the two groups during the treatment, and the treatment effects were relatively good. P > 0.05. Conclusion: valsartan combined with amlodipine in the treatment of hypertension can obtain better effect, which is very good for improving patients' physical condition, improving patients' life quality and ensuring the safety in the treatment process.
文摘Background:Overexpression of inducible nitric oxide synthase(iNOS)has been reported in diabetic retinopathy(DR).The kinin B1 receptor(B1R)is also overexpressed in DR,and can stimulate iNOS via Gαi/ERK/MAPK pathway.We previously showed that the topical administration of a B1R antagonist,LF22-0542,significantly reduces leukocyte infiltration,increased vascular permeability and overexpression of several inflammatory mediators,including iNOS in DR.Thus,the aim of this study was to determine whether the pro-inflammatory effects of B1R are attributed to oxidative stress caused by the activation of iNOS pathway in order to identify new therapeutic targets for the treatment of DR.iNOS and B1R being absent in the normal retina,their inhibition is unlikely to result in undesirable side effects.The approach will be no invasive by eye application of drops.Methods:Diabetes was induced in male Wistar rats(200-230 g)by a single intraperitoneal injection of streptozotocin(STZ,65 mg/kg b.w).One week later,rats were randomly divided into four groups(N=5)and treated for one week as follows:Gr 1:control rats treated with the selective iNOS inhibitor(1,400 W,0.06μM twice a day by eye-drops×7 days),Gr 2,STZ-diabetic rats treated with 1,400 W,Gr 3:control rats received a selective B1R agonist[Sar(D-Phe8)-des-Arg9-BK,100μg twice a week]by intravitreal injections(itrv)and treated with 1,400 W,Gr 4:STZ-diabetic rats+B1R agonist+1,400 W.At the end of treatment and two weeks post-STZ,three series of experiments were carried out to measure vascular permeability(by Evans blue dye method)and the expression of vasoactive and inflammatory mediators,including iNOS,VEGF-A,VEGF-R2,IL-1β,Cox-2,TNF-α,bradykinin 1 and 2 receptors and carboxypeptidase M/kininase 1(by Western Blotting and qRT-PCR).The nitrosative stress(nitrosylation of proteins)was also assessed by Western Blotting.One-way Anova test with Bonferroni post hoc was used for statistical analysis.Results:STZ-diabetic rats showed a significant increase in retinal vascular permeability(22.8μg/g Evans blue dye per g of fresh retinas,P=0.016)compared with control rats and control treated rats(17.2 and 16.8μg/g respectively).The injections of B1R agonist amplified the increase of vascular permeability which was normalized by the 1,400 W.The overexpression of inflammatory markers was also normalized by the 1,400 W in STZ-diabetic rats received or not the B1R agonist.Conclusions:These results support a contribution of iNOS in the deleterious effects of B1R in this model of diabetic retinopathy.Hence,iNOS inhibition by ocular application of 1,400 W may represent a promising and non-invasive therapeutic approach in the treatment of diabetic retinopathy.
文摘玻璃体切除术(pars plana vitrectomy,PPV)为增殖性糖尿病视网膜病变(proliferative diabeticretinopathy,PDR)常用治疗手段,但手术难度大、出血量多,难以有效控制,会延长手术时间、增加手术失败风险。采取有效措施优化治疗,降低手术风险是近年来的研究热点。
基金Supported by Grants No.NT11457 and No.NT11402(to IGA MZ CR)grant from Research project(Ministry of Health Care,Czech Republic)of the conceptual development of research organization,No.00064203(to FN Motol)
文摘Hepatocyte nuclear factor 1-β(HNF1B)defects cause renal cysts and diabetes syndrome(RCAD),or HNF1B-maturity-onset diabetes of the young.However,the hepatic phenotype of HNF1B variants is not well studied.We present a female neonate born small for her gestational age[birth weight 2360 g;-2.02standard deviations(SD)and birth length 45 cm;-2.40 SD at the 38th gestational week].She developed neonatal cholestasis due to biliary atresia and required surgical intervention(portoenterostomy)when 32-d old.Following the operation,icterus resolved,but laboratory signs of liver dysfunction persisted.She had hyperechogenic kidneys prenatally with bilateral renal cysts and pancreatic hypoplasia postnatally that led to the diagnosis of an HNF1B deletion.This represents the most severe hepatic phenotype of an HNF1B variant recognized thus far.A review of 12 published cases with hepatic phenotypes of HNF1B defects allowed us to distinguish three severity levels,ranging from neonatal cholestasis through adult-onset cholestasis to noncholestatic liver impairment,all of these are associated with congenital renal cysts and mostly with diabetes later in life.We conclude that to detect HNF1B variants,neonates with cholestasis should be checked for the presence of renal cysts,with special focus on those who are born small for their gestational age.Additionally,patients with diabetes and renal cysts at any age who develop cholestasis and/or exocrine pancreatic insufficiency should be tested for HNF1B variants as the true etiological factor of all disease components.Further observations are needed to confirm the potential reversibility of cholestasis in infancy in HNF1B mutation/deletion carriers.
文摘糖尿病（Diabetes）
Pharmacist：Hello!What can I do for you？
药师：您好,请问您需要什么帮助？
Client：I want to ask you about general in-structions on how to take medication for diab etes.
顾客：我想咨询一下有关糖尿病的用药常识。
基金agrantfromtheShanghaiMunicipalGovernment (No 9841190 2 4)
文摘To pursue insulin and islet transplantation replacement therapy for type 1 diab etes based on engineered human non β cells which secrete mature insulin Methods Human proinsulin cDNA was cloned from its genomic gene and mutated by overlap e xtension PCR, introducing furin consensus cleavage sequences (Arg Xaa Lys/Arg Arg) An expression vector encoding a genetically modified human proinsulin c DNA was generated and transduced to Hela, 293, and L02 cells by lipofectin medi ated DNA transfection Following G418 screening, the surviving L02 cells were s elected and enriched Insulin levels in the supernatant and cells were evaluate d using radioimmunoassay and immunofluorescence staining Results Three sites in the insulin gene were mutated simultaneously Insulin gene m odified cells were able to express insulin at different levels: 8 45-188 00? μIU/24 h/2 0×10 6 Hela cells and 159 88-242 14?μIU/24 h/2 0×10 6 293 cells for transient expression, and 2 56-61 95?μIU/24 h/2 0×10 6 from se veral L02 clones screened with G418 No insulin was released by control cells Furthermore, immunofluorescence staining confirmed that proinsulin was stored a s vacuoles in the cytoplasm of L02 cells Conclusion A correctly mutated human proinsulin cDNA was obtained successfully, transfected and expressed efficiently in non beta cells, lending support to the study of s omatic gene therapy in diabetes mellitus
