Objective To evaluate the effects of strict dietary salt restriction on blood pressure and proteinuria in chronic glomerulonephritis (CGN) patients. Methods From October 2007 to April 2009, 32 CGN inpatients were enrolled. Among them, 15 patients followed a strict dietary salt restriction menu (sodium 100 mmol/d, potassium 50 mmol/d, protein (0. 8-1. 0) g · kg~(-1) · d~(-1) , calorie (105-125) KJ · kg~(-1) · d~(-1) ) for 7 days, while the other 17 patients were fed freely offered by hospital as controls. 24 h urinary sodium excretion (24h-UNa) was used to monitor the salt intake. No changes of drug therapy were made during the study. Blood pressure was monitored every day. 24-hour urinary protein and serum biochemical parameter were measured before and after the study. Results There was no significant difference of baseline 24h-UNa between the two groups [(135.1 ±50.4) mmol/d vs (137.4 ±28.6) mmol/d) ]. During the study, the average 24h-UNa of patients with strict dietary intervention was (97. 2 ± 8.6) mmol/d. Both SBP [ (117. 7 ± 10. 0) mm Hg( 1 mm Hg=0. 133 kPa) vs (106.2 ±9.9) mm Hg] and DBP [ (76. 3 ± 6. 1 ) mm Hg vs (67. 5 ± 5. 5 ) mm Hg] decreased significantly ( P < 0. 001 ) . Proteinuria decreased significantly too [ 1. 57 (0. 3-3. 0) g/d vs 0. 57 (0. 16-2. 72) g/d,P = 0. 006]. The reduction of SBP was positively correlated with the reduction of 24h-UNa (r =0. 572, P =0. 026) , while the reduction of proteinuria correlated with both the reduction of SBP (r = 0. 568, P = 0. 027) and 24h-UNa (r =0. 525, P =0. 044). In the control group, only SBP decreased significantly [ ( 122. 6 ± 15. 5) mm Hg vs (115.8 ±10.4) mm Hg, P = 0.02] without significant changes of DBP and proteinuria When comparing the subgroups who took ACEI/ARB from both groups, the reduction of proteinuria wasmore prominent of those from the study group than the control group [ - 0. 4 ( -0. 95-0. 07) vs 0. 07 ( - 0. 39-0. 42), P = 0. 014 ]. Conclusion Strict dietary salt restriction is effective in reducing blood pressure and proteinuria in CGN patients.

Objective To explore the organic micro environmental effect of skeletal muscles on the proliferation of thoracic malignant cells, its significance in the rarity of metastases in skeletal muscles and the prospect for its clinical applications.Methods Primary culture of new born Wistar rat skeletal muscle cells was established.The murine skeletal muscle conditioned medium(MMCM)was prepared to test its effect on thoracic malignant cell lines of A549、Anip-973,PLA-801C,NCI-H466,Eca109 and benign cell line of BHK-21 by MTT assay.Results Proliferations of thoracic malignant cell lines of A549,Anip-973,PLA-801C,NCI-H466,and Eca109 were significantly restrained when cultured with MMCM,while the proliferation of benign renal cell line(BHK-21)was not affected.Conclusions The conditioned medium of new born Wistar rat skeletal muscle cells could selectively inhibit the proliferation of thoracic malignant cells in vitro.Moreover,it affects tumor cells only and has no apparent effect on normal cells,which differs from most of the chemotherapeutic agents.These findings suggest a sound mechanism in the rarity of metastases in skeletal muscles.A therapeutic agent could be generated from MMCM to complement surgery and/or chemotherapy.

Objective To study the effect of paeonol on the proliferation and apoptosis of A375 human melanoma cells and its mechanism.Methods Cell counting kit-8 (CCK8) was used to evaluate the proliferative activity of A375 cells treated with paeonol of 0.5,1,2,4,8 mmol/L for 24,48 and 72 hours respectively.Subsequently,A375 cells were treated with paeonol of 1.25,2.5 and 5 mmol/L for 24 hours followed by double staining with annexin V and propidium iodide for the detection of cell apoptosis,fluorometric assay for the estimation of caspase 3,caspase 8 and caspase 9 activity,and Western blot for the determination of the levels of p53,nuclear factor-κB proteins and some of their target proteins.The A375 cells receiving no treatment served as the blank control group.Statistical analysis was carried out by t test.Results Within the investigated concentration and time ranges,paeonol significantly inhibited the proliferative activity of A375 cells in a concentration-and timedependent manner.Compared with the blank control group,a significant increase was observed in the early apoptosis rate in A375 cells treated with paeonol of 1.25,2.5 and 5 mmol/L for 24 hours (13.74％-± 1.73％,25.95％ ± 0.57％ and 46.44％ ± 0.81％ vs.3.11％ ± 0.53％,P ＜ 0.05 or 0.01),as well as in the activity of caspase 3,8 and 9 in A375 cells treated with paeonol of 2.5 and 5 mmol/L for 24 hours (P ＜ 0.05 or 0.01).After 24-hour treatment,the protein levels of p53 and Bax were elevated,but those of nuclear factor-κB,Bcl-2 and Bcl-XL were decreased in A375 cells with the increase of paeonol concentration.Conclusions Paeonol can inhibit the proliferation but induce the apoptosis of A375 cells,and the apoptosis-inducing effect may be realized through intrinsic and extrinsic pathways by modulating nuclear factor-κB and p53 genes.

OBJECTIVE: To explore the molecular reasons of weak expression of B antigen on the red cell. METHODS: Serological test for blood group was carried out, including red cell and plasma grouping, and anti-A1 and anti-H testing, and confirming weak A or B antigens by adsorption and elution. Exons 1-7 were sequenced directly, and one of them was cloned and sequenced. RESULTS: All of the 23 samples showed the weak B antigen by serological method. The alleles of the subgroups were identified by DNA sequencing, including 2 Bel subgroup, 4 B3 subgroup, 14 Bw subgroup, 2 CisAB subgroup and a novel allele. The novel allele showed a nucleotide substitution 662G>A in the exon 7, and the sequence was submitted to Blood Group Antigen Gene Mutation Database, and the novel allele was named Bel10. CONCLUSION Nucleotide substitution in exon results in blood subgroup, which showed that the antigens were weakened, and Bw phenotype was the most frequently subgroup.
ABO Blood-Group System/genetics* ; Alleles ; Exons ; Genotype ; Humans ; Nucleotides ; Phenotype

Objective To investigate the role and mechanism of Rho-related GTP-binding protein F(RhoF)-mediated Th17 polarization in the development of severe acute pancreatitis(SAP).Methods RhoF transgenic mice were randomly divided into control group(n = 10),SAP group(n = 10)and SAP+Y-27632 group(n = 10),and WT mice were randomly divided into control group(n = 10),SAP group(n = 10)and SAP+Y-27632 group(n = 10).SAP models were established in all groups except the control group.The SAP+Y-27632 group was infused with Y-27632 via tail vein after model establishment.T cells in mouse blood samples were isolated for RhoF,p-MYPT1 protein detection and ROCK activity determination,and the percentage of lymphoid CD4+T cells producing IL-17 was analyzed by flow cytometry.Results The expression of RhoF and p-MYPT1 was increased in T cells in the SAP group compared with that in the control group(P<0.01),and the level of RhoF was closely correlated with that of p-MYPT1(P = 0.018).The expression of RhoF protein level in T cells of mice in the RhoF group increased by approximately 30%compared to that in the WT group,and the level of spontaneous IL-17 production by CD4+ T cells was significantly increased(P = 0.003).Compared with WT mice,the histological score of pancreatic injury,the expression of RhoF and p-MYPT1 in T cells,the number of IL-17+ T cells and serum IL-17 level in RhoF transgenic mice were significantly increased(P<0.05).The histological score,RhoF and p-MYPT1 expression of T cells,IL-17+ T cell numbers and serum IL-17 level were significantly lower in the SAP+Y-27632 group than those in the SAP group(P<0.05).Conclusion RhoF/ROCK signaling pathway-mediated polarization of Th17 cells is involved in the pathogenesis of SAP.

Objective This study aimed to investigate the neuroprotective effect of microglia polarization mediated by Raf kinase inhibitor protein(RKIP)intracerebral hemorrhage(ICH)model.Methods Forty-eight adult male Sprague-Dawley(SD)rats were randomly divided into three groups:the Sham+Vector group,the ICH+Vector group,and the ICH+RKIP group,with 16 rats in each group.The collagenase ICH model was established in ICH+Vector group and ICH+RKIP group.Before operation and 1,3,5,and 7 days after operation,8 animals in each group were tested for behavior.Apoptosis of neurons was detected by flow cytometry.Seven days after ICH,the expressions of RKIP,p-p65,and TRAF6 around hematoma were analyzed by protein blot.Results Compared with ICH+Vector group,rats in ICH+RKIP group need less time to find the platform,spend longer time in the target quadrant,and significantly reduce the times of crossing the platform(P<0.05).The number of Nissl corpuscles in ICH+RKIP group was significantly higher than that in ICH+Vector group(P<0.05).In addition,the number of neuronal apoptosis in ICH+RKIP group was significantly lower than that in ICH+Vector group(P<0.05).Compared with Sham group,rats receiving ICH showed a gradual decrease in RKIP expression,and reached the lowest value on the 7th day(P<0.05).Seven days after ICH,the expression of RKIP protein in hematoma of rats in ICH+RKIP group was significantly higher than that in ICH+Vector group(P<0.05),and the expression of p-p65 and TRAF6 protein was significantly lower than that in ICH+Vector group(P<0.05).Compared with ICH+Vector group,the number of iNOS+Ibal1+cells in ICH+RKIP group decreased significantly(P<0.05),while the number of Arg-1+Ibal1+cells increased significantly(P<0.05).Conclusion Up-regulation of RKIP promotes functional recovery after ICH,and its mechanism involves inhibiting TRAF6/NF-κB signaling pathway.

Objective To study the causes of two Chinese families with Branchio-oto syndrome.Methods The clinical data of two families were collected,and the pathogenic genes and variants of Branchio-oto syndrome were screened and verified by whole exome sequencing and Sanger sequencing.Results Two proband patients were diagnosed with Branchio-oto syndrome.Proband 1 presented with preauricular and anterior cervical fistulas,as well as congenital severe sensorineural hearing loss.On the other hand,proband 2 displayed a preauricular fistula and an anterior cervical cyst.At the age of 5,progressive deterioration of binaural hearing was observed,leadingtothe cur-rent diagnosis of severe mixed deafness.Genetic analysis showed that proband 1 and 2 carried nonsense variants of EYA1 gene:NM_000503.6:c.1408G＞T(p.Glu470Ter),and c.889C＞T(p.Arg297Ter).According to the guide-lines of the American College of Medical Genetics and Genomics(ACMG),the above variants were rated as patho-genic variants.After reviewing the literature,the c.1408G＞T variant had not been previously reported,and the c.889C＞T is a known variant.Conclusion The variants c.1408G＞T(p.Glu470Ter)and c.889C＞T(p.Arg297Ter)of EYA1 gene are the cause of these two families with Branchio-oto syndrome.The first report of c.1408G＞T broadens the mutational spectrum of EYA1 gene and provids a clinical reference for the diagnosis of Branchio-oto syndrome.

Objective:To explore application value of observed tumor enhancement characteristics by dynamic enhancement magnetic resonance imaging(MRI)in assessing blood supply of small hepatocellular cancer.Methods:The cases data of 80 patients with suspected small hepatocellular cancer who admitted to Yichang Central People's Hospital from January 2019 to January 2023 were retrospectively analyzed.The enhancement characteristics of tumors of all patients were real-timely observed by MRI scanner,which included the relative enhancement degree(RSI),enhancement mode,time-signal intensity curve,etc.The enhanced characteristics of the tumors were recorded,which were combined with a series of variables included disease history,tumor type,tumor size,the number of tumor,liver function status of patients to conduct analysis.The receiver operating characteristics(ROC)curve was adopted to analyze the application value of the observed tumor enhancement characteristics by dynamic enhancement MRI in assessing the status of blood supply of small hepatocellular cancer.Results:There were statistically significant differences in the RSI(F=40.151,P＜0.05),enhancement degree(x2=27.374,P＜0.05),and time-signal intensity curve(x2=20.950,P＜0.05)of dynamic enhanced MRI among different stages of small hepatocellular cancer.The differences in medical history(F=17.844,P＜0.05),tumor type(x2=11.219,P＜0.05),tumor size(x2=14.081,P＜0.05),and the number of tumor(x2=74.310,P＜0.05)among different enhancement degrees of arterial phase were also statistically significant.With the enhancement degree increased,the asymptomatic period increased,and the number of malignant tumors increased,and tumor size increased.The differences in liver function status among different time-signal intensity curves were statistically significant(F=330.182,325.872,216.689,P＜0.05).The area under curve(AUC)value of the ROC of the RSI of observed tumor enhancement characteristics by dynamic enhancement MRI was 0.582(95％CI:0.493-0.670)in assessing blood supply of small hepatocellular cancer.Conclusion:Dynamic enhancement MRI can observe the vascular generation and hemodynamic changes of small hepatocellular cancer,which has a certain application value in assessing blood supply of small hepatocellular cancer,and it can help doctors to choose appropriate treatment plan and assess treatment effect.

BACKGROUND:Animal models of diabetic encephalopathy that have been studied mainly include streptozotocin-induced model,high-sugar and high-fat diet-induced model and spontaneous animal model.Establishing a simple,easy,short-cycle,safe and effective model of diabetic encephalopathy can help to explore the subsequent pathogenesis and screen therapeutic drugs. OBJECTIVE:To further explore and evaluate the method of building diabetic encephalopathy rat models. METHODS:Twenty Sprague-Dawley rats were randomly divided into control(n=10)and model(n=10)groups.Rats in the model group were given a single injection of 45 mg/kg streptozotocin in the left lower abdominal cavity,and those in the control group were given the same amount of citrate buffer.During the experiment,the body mass,feed intake,water intake and blood glucose were measured.After 8 weeks,the glucose tolerance and oxidative stress levels were measured,and the pathological changes of brain tissue and the expression of apoptotic proteins were compared between groups. RESULTS AND CONCLUSION:Compared with the control group,the food intake,water intake,encephalization quotient,blood glucose and area under the blood glucose curve were significantly increased in the model group,while the body mass decreased significantly(P<0.01).Histopathological examination of the brain showed that compared with the control group,the number of surviving nerve cells was significantly reduced in the model group(P<0.01),with more significant pathological damage of nerve cells.Compared with the control group,the activities of serum superoxide dismutase,catalase and glutathione in the model group were significantly decreased(P<0.01),and the content of oxidative malondialdehyde was significantly increased(P<0.05).The expression levels of apoptosis-related proteins Bax and Caspase-3 in brain tissue increased in the model group compared with the control group,while the expression of Bcl-2 decreased(P<0.01).In conclusion,an 8-week injection of 45 mg/kg streptozotocin can cause obvious pathological damage to the brain tissue of diabetic rats,to successfully establish the rat model of diabetic encephalopathy.