More and more studies suggest that endocrine-metabolic diseases and liver diseases influence each other. Endocrine-metabolic diseases may lead to abnormal liver function, and liver diseases are found also to cause disturbance of endocrine-metabolic system.

OBJECTIVE:To investigate the effect of Cyslosorus acuminatus flavonone glycoside (CAF) on kidney epitheli-al-mesenchymal transition(EMT)in rats with diabetic kidney disease(DKD). METHODS:Rats were randomly divided into nor-mal group(normal saline),model group(normal saline),positive group [rosiglitazone,0.4 mg/(kg·d)],CAF high-dose and low-dose groups [12.5,25 mg/(kg·d)],10 in each group. Except for normal group,other groups were intraperitoneally injected strepto-zotocin(60 mg/kg)+high fat diet to induce DKD,and intragastrically administrated related medicines in 13-16 weeks. After the ex-perimental period,fasting blood glucose level and serum creatinine(Scr),blood urea nitrogen(BUN)contents of rats were detect-ed,collagen deposition and basement membrane thickening in kidney tissue were observed. Immunohistochemistry was used to de-tect α-smooth muscle actin(α-SMA),fibronectin,epithelial cadherin(E-cadherin)expressions in kidney tissue,and Western blot was used to determine the glycogen synthase kinase 3β(GSK-3β),phosphorylated GSK-3β(p-GSK-3β),β-catenin expressions in kidney tissue. RESULTS:Compared with normal group,fasting blood glucose level,Scr and BUN contents in model group were significantly increased (P<0.01);kidney tissue showed obvious collagen deposition and basement membrane thickening;theα-SMA,fibronectin,β-catenin expression levels and GSK-3β phosphorylation degree in kidney tissue were significantly increased (P<0.01),while E-cadherin expression levels was significantly decreased(P<0.01). Compared with model group,fasting blood glucose level,Scr and BUN contents in each administration group were significantly reduced(P<0.05 or P<0.01);collagen depo-sition and basement membrane thickening in kidney tissue were significantly improved;the α-SMA,fibronectin,and β-catenin ex-pression levels and GSK-3β phosphorylation degree in kidney tissue were significantly decreased (P<0.05 or P<0.01),while E-cadherin expression levels in positive group and CAF high-dose group were significantly increased(P<0.01). CONCLUSIONS:CAF can inhibit the kidney EMT of rats with DKD,the molecular mechanism may be associated with downregulating β-catenin ex-pression and inhibiting GSK-3βphosphorylation inactivation.

Objective To study the effects of aminoguanidine (AG), a selective inhibitor of inducible nitric oxide synthase (iNOS) on the pathological changes of liver tissues and ultrastructural changes of liver cells in rodent model of endotoxic shock. Methods Twenty-four male Wistar rats were randomly divided into normal control group,lipopolysaccharide (LPS) control group and AG treatment group, each group had 8 rats. Rats were challenged by E.coli LPS to set up the model of endotoxic shock, AG group were treated by aminoguanidine. The pathological and ultrastructural changes of liver tissues and plasma NO contents of three groups were observed and compared. Results Light microscopy revealed that many tiny abscesses scattered in liver tissue in LPS group, accompanied by necrosis of liver cells and neutrophils infiltration, while liver injuries of AG group were much slighter than that in LPS group. Electron microscopy revealed that there were dissolved plaques in hepatocyte nuclears, swelling of mitochondria, decreasing in number of mitochondrial ridges, while AG play a protective role to nuclears and mitochondria of hepatocytes. The plasma NO levels of LPS control group were higher than that of normal control group, and plasma NO levels decreased significantly after AG treatment, but still higher than that of normal control group. Conclusion Aminoguanidine selectively inhibits iNOS activity and prevents the overproduction of NO induced by iNOS, thus attenuates the damages of liver structure induced by NO. This method has potential value in clinical application, which deserves more deep research.

Through various common domestic and foreign electronic sphygmomanometers to test blood pressure, we find that when measuring high blood pressure or low blood pressure, there is a mismatch between the maximum inflation pressure and the blood pressure measurement, which often results in repeatedly inflating and deflating as well as the problem of high inflation pressure. In order to solve these problems and find a suitable maximum inflation pressure, two intelligent pneumatic solutions based on identifying of pulse wave are suggested and 700 groups of blood pressure experiments are done, then the two solutions are verified by experiments. The experiment proved that these solutions proposed have good stability and accuracy, they can solve the problems appeared in measuring blood pressure effectively, at the same time, the second solution that estimate the maximum inflation pressure during inflation is considered as the best one.
Blood Pressure ; Blood Pressure Determination ; instrumentation ; Heart Rate ; Humans ; Hypertension ; Sphygmomanometers

Objective To obtain more information concerning polymorphism of the thyrotropin (TSHR) in Graves diseases(GD). Methods (1)A family of GD was studied (including 3 patients and 9 healthy family members)to examine SNPs of TSHR through direct sequencing of all 10 exons and part of introns. (2)In the current case-control study, 30 patients with familiar GD, 48 sporadic patients and 96 healthy control individuals were used to assess whether SNP of TSHR was associated with GD. Genomic DNA was extracted from peripheral leukocytes isolated from ACD-anticoagulated blood. Ten exons were amplified by PCR, using primers designed by ourselves. After purifying, the products were sequenced. Results Eight polymorphisms were found. There was a novel polymorphism in exon 8. There were no significant differences between patients and controls. Conclusions These findings suggested that the novel and other polymorphisms of the TSHR gene may not be responsible for GD. There are racial differences in the distribution of polymorphisms of TSHR gene.

Objective To investigate the molecular defects of CYPl7A1 gene in a pedigree with two 46,XY patients suffering from 17α-hydroxylase deficiency (17-OHD) and explore the steroid biosynthetic difference in carriers of 17-OHD before and after adrenocorticotrophic hormone (ACTH) test.Methods Clinical data and hormone profiles were collected from the members of the pedigree.CYPl7A1 genotyping was performed in the patients and family members with PCR-direct sequencing.A short ACTH test was evaluated in some cases.Results The CYP17 genes of the patients were proved to hold a homozygous mutation with a base deletion and a base transversion (TAC/AA) in exon 6,which produced a missense mutation of Tyr→ Lvs at codon 329 and changed the open reading frame following this codon.The hormone response of the carriers after ACTH stimulation was abnormal between the patients and normal controls.Conclusion 17-OHD in this family was caused by CYP17A1 mutation (TAC329AA):some hormonal response to ACTH stimulation Was abnormal in carriers.

Breast imaging reporting and data system (BI-RADS) is a standardized system for reporting breast pathology covered mammography,ultrasound and MRI.BI-RADS improves the standardization in interpretation of medical imaging and reduces the confusion of breast imaging interpretation.It is a widely accepted risk assessment and quality assurance tool in mammography,ultrasound and MRI.The development history,clinical applications,limitations of BI-RADS,as well as the clinical applications combined with other imaging techniques were reviewed in this article.

Objective To discuss Bushen Huoxue Prescription mechanism of action on follicular granulosa cell apoptosis of premature ovarian failure (POF) mice. Methods The mouse zona pellucida 3 as the antigen, multi-point injection of subcutaneous immunization BALB/c to female mice was used to establish autoimmune POF model. Forty clean female mice were randomly divided into blank group, model group, Estradiol Valerate group and Bushen Huoxue Prescription group. All medicine groups were given relevant medicine for gavage, while model and blank groups were given normal saline with the same amount for gavage for 15 days. After the treatment, ovary, uterus, and thymus were weighed, and the viscera index was calculated. An ovarian slice was taken and HE staining was used to observe granulosa cell apoptosis. The levels of E2, LH, and FSH were detected by using the radioimmunoassay method. RT-PCR was used to analyze Fas and Fas-L mRNA expressions in ovarian granulosa cells. Results Compared with blank group, the weight of ovary, thymus, and uterus decreased significantly (P<0.05, P<0.01);Serum E2 level dropped (P<0.01);levels of FSH and LH, and expressions of Fas and Fas-L mRNA increased significantly (P<0.01). Compared with model group, granulosa cell apoptosis significantly decreased, and ovary index, uterus index, and thymus index increased (P<0.05);serum E2 level increased (P<0.01);levels of FSH and LH, and expressions of Fas and Fas-L mRNA significantly decreased (P<0.05). Conclusion Bushen Huoxue Prescription can decrease expressions of Fas and Fas-L mRNA to inhibit cell apoptosis by adjusting the hormone level of hypothalamus-pituitary-ovarianaxis.

To investigate the clinical features, genetic diagnosis, and treatment of a patient with Prader-Willi syndrome(PWS). For a case with clinically suspected PWS, methylation specific PCR(MSPCR)amplification was applied to CpG islands of SNRPN(exon α)gene locus in the 15q11-q13. Furthermore, the diagnosis was comfirmed by the method of bisulfite sequencing PCR(BSPCR). Metabolic status before and after the operation of sleeve gastrectomy were compared. Absence of amplification of paternal allele on chromosome 15q11-q13 was detected in the case by MSPCR, different from the normal control. Results of BSPCR further proved a full methylation of CpG islands in the SNRPN gene locus. Four months after sleeve gastrectomy, systemic metabolic status and ventricular function were improved. MSPCR and BSPCR were both consistent with genetic diagnosis of PWS. Weight loss surgery is expected to be a major therapy of this disease.

Objective To analyze CYP17A1 gene mutation in a patient with 46,XY disordered sex development and to explore the possible influence on the phenotype of the patient.Methods Eight exons of CYP17AI gene in the patient and her parents were amplified and directly sequenced.In order to construct Mini-gene system,PCR fragments containing wildtype and mutant splicing sites were inserted in expression vector,and then transfected into cells.RT-PCR was used to observe the influence of splicing site mutation.Wildtype and aberrant splicing CYP17A1 cDNA expression plasmids were constructed and transfected into cells respectively,and CYP17A1 enzyme activity was tested in vitro.Results Mutation analysis revealed compound heterozygous CYP17A1 mutations,with Y329fs in one allele and a synonymous substitution( c.1263G＞A:GCG＞GCA) in another allele.In vitro analysis showed that the synonymous substitution induced a novel splicing site,which resulted in aberrant splicing of CYP17A1 mRNA and lacked six or seven amino acids after 415 in splicing product.In vitro transfection and enzyme activity experiment showed that the aberrant splicing product abolished the enzyme activity completely.However,this mutation did not completely influence splicing.The patient also had a part of normal splicing product,which was a coincidence to the phenotype of the patient.Conclusion This is the first description of an exonic splicing mutation in CYP17A1 relevant to the 17ot-hydroxylase deficiency phenotype.The functional study of the aberrant splicing variant has been initiated.