Objective To investigate the hepatitis B liver cirrhosis complicated with hepatic encephalopathy (HE),relevant risk factors in the development of strategies for the prevention and treatment of the disease,and make for the clinical experience accumulation.Methods A retrospective analysis of 64 cases of liver cirrhosis patients complicated with HE,for the observation group.In addition,53 patients of hepatitis B cirrhosis without HE patients were selected as control group.The two groups of patients with objective physiological indicators were recorded and compared.Results (1) Compared with the control group,blood ammonia,serum total bilirubin,blood urea nitrogen level and infection,incidence of digestive tract hemorrhage of the study group increased,blood sodium,alanine amin otrans ferase,decrease the serum albumin level,the differences were statistically significant (t =3.0 8 5,5.5 2 8,x2 =9.174,7.126,t =4.102,4.337,8.675,5.323,all P ＜0.05).(2) For the patients in the study group,age,more than 3 kinds of incentives and C grade of liver function were the high risk factors of death.(3) In the cause of deaths in the study group,the infection was the most common,the incidence rate was 75.9%,the second above digestive rare tract hemorrhage,the incidence rate was 65.5%.Conclusion The elderly,the number of risk factors and severity of liver function are the occurrence and development of related risk factors of hepatitis B related cirrhosis with hepatic encephalopathy,to remove the incentive is the key of HE with prevention and treatment of hepatitis B cirrhosis.

Transcuataneous electrical nerve stimulation (TENS) analgesia as a non-drug method has received people's more and more attention recently. Considering problems of existing products, such as unstable performance and unsatisfied effectiveness, we developed a new analgesia therapy system for delivery based on bio-feedback TENS in our laboratory. We proposed a new idea for stimulation signal design, that is, we modulated a middle frequency signal by a traditional low frequency TENS wave in the new system. We designed different prescription waves for pain relief during a uterine contraction or massage between contractions. In the end, a bio-feedback TENS method was proposed, in which the waveforms of stimulation signals were selected and their parameters were modified automatically based on feedback from uterine pressure, etc. It was proved through quality tests and clinical trials that the system had good performance and satisfied analgesia effectiveness.
Analgesia ; methods ; Biofeedback, Psychology ; methods ; Female ; Humans ; Pain Management ; Transcutaneous Electric Nerve Stimulation ; methods ; Uterine Contraction

AIM: To establish an HPLC method for determining sophocarpine,sophoridine and oxymatrine in Sophora flavescens Ait,so as to investigate their contents in different years and different parts. METHODS: An Elite Hypersil NH2 column(250 mm ? 4. 6 mm,5 ?m) was used with the mobile phase being acetonitrile-absolute alcohol-3% phosphoric acid solution(82 ∶ 10 ∶ 8),flow rate being 1 mL/min,determinating wavelength being 220 nm,the column temperature being 26 ℃,The injection volume was 5 ?L. RESULTS: The calibration curves of sophocarpine,sophoridine and oxymatrine were in good linearity over the ranges of 0. 004 99 - 0. 149 7 ?g(r = 0. 999 9),0. 025 08 - 0. 752 25 ?g(r = 0. 999 9),0. 075 38 - 2. 261 25 ?g(r = 0. 999 9); and the average recovery of sophocarpine,sophoridine and oxymatrine was 99. 91% ,99. 26% ,100. 27% with RSD of 1. 11% , 0. 82% ,2. 18% respectively. CONCLUSION: The HPLC method shows a good separation,reproducibility and accuracy,there are obvious differences in the contents of three alkaloids in different years and different parts of Sophora flavescens Ait. The results provide important data for quality evaluation and utilization of Sophora flavescens materials.

ObjectiveTo observe the effects of Jintong capsule on model rats of Tourette syndrome (TS) and explore its probable pharmacological mechanisms.MethodsSD rats were randomly divided into six groups: blank control, TS model, haloperidol and three Jintong capsule treated groups. Model rats were copied by intraperitoneal injection of iminodipropionitrile (IDPN). The stereotyped behaviors of model rats were recorded. Open field test was used to detect ability of space recognition of rats, high performance liquid chromatography was used to detect content of monoamines, and flow cytometry was used to detect the ratio of T lymphocyte.ResultsJintong capsule can ameliorate the stereotyped behaviors of model rats, decrease content of dopamine in striatum and increase the ratio of CD4/CD8.ConclusionJintong capsule can improve behaviors of model rats. The potential mechanism of Jintong capsule maybe: it can affect the dopaminergic system of model rats, and Jintong can enhance the immune system of model rats.

ObjectiveTo observe the influence of mitochondrial cytochrome c oxidase(COX) decrease on cholinergic and dopaminergic system in brain of model rats.MethodsRats were administrated with 1mg/kg/h or 2mg/kg/h subcutaneously via an Alzet minipump for 30 days. Choline-acetyl-transfertase(ChAT) and acetylcholinesterase(AChE) activity in hippocampus and cortex of rats were measured by radiochemical method and hydroxylamine colorimetry separately. The contents of Norepinephrine(NE), dopamine, 5-hydroxytryptamine(5-HT) and their metabolic products in striatum were measured by HPLC.ResultsChAT activity was significantly inhibited in hippocampus and cortex of model rats, however, the activity of AChE increased in hippocampus and was not affected at the cortex. Therefore, the ratio of ChAT/AChE decreased in model rats. The content of NE, dopamine, 5-HT and their metabolic products in striatum were not different among all groups.ConclusionsCOX deficiency can induce abnormality of ChAT and AChE activity in model rats. Dysfunction of neurotransmitter-acetylcholine would be account for learning-memory deficiency. Model rats indicated cholinergic system deficit without any dopaminergic system abnormality, so chronic infusion of sodium azide via minipump may specially serve as a tool for developing the experimental model of Alzheimer's disease.

Tau protein, a kind of microtubule-associated protein, plays an important role in the pathogenesis of Alzheimer's disease (AD) and other tauopathies, and has drawn more and more attention of scientific researchers. Appropriate animal models of mutated tau protein are important in the studies of the pathogenesis and drug therapy of tauopathies. So far, some transgenic animal models expressing human tau protein have been established, among which the transgenic animal model overexpressing P301L mutated form of tau protein has been widely used because of its obvious pathological changes. In this review, we will review the research progress in the pathological manifestations of the P301L tau transgenic animal model and its applications in pharmacological studies.

OBJECTIVETo explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC).

METHODSForty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08 ± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively.

RESULTSThe serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ(2)=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ(2)=6.146, P=0.046 and χ(2)=1.017, P>0.05; respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ(2)=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085).

CONCLUSIONSerum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and -negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.

Antiviral Agents ; therapeutic use ; DNA, Viral ; blood ; Hepatitis B Surface Antigens ; blood ; Hepatitis B, Chronic ; blood ; Humans ; Liver Cirrhosis ; blood ; virology ; Viral Load

Objective To explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC). Methods Forty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively. Results The serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=6.146, P=0.046 andχ2=1.017, P>0.05;respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ2=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085). Conclusion Serum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and-negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.

Objective To explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC). Methods Forty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively. Results The serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=6.146, P=0.046 andχ2=1.017, P>0.05;respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ2=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085). Conclusion Serum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and-negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.

Objective:To investigate the relationship between inherited dysplasminogenemia and cerebral infarction (CI) by phenotype and gene mutation analysis of 2 inherited dysplasminogenemia pedigrees.Methods:Retrospective analysis was carried out on clinical data of 2 patients diagnosed with CI who were treated in the Department of Neurology, the First Affiliated Hospital of Wenzhou Medical University in January and March 2021, and peripheral venous blood samples were collected from proband 1 and his family members (8 subjects, 4 generations in total) and proband 2 and her family members (5 subjects of 3 generations in total), and their plasminogen (PLG) activity (PLG:A), protein C activity, protein S activity, antithrombin activity and the content of PLG antigen (PLG: Ag), fibrinogen, D-dimer and fibrinogen degradation products were measured for definite diagnosis. All 19 exons,5′ and 3′ untranslated regions of PLG were amplified with polymerase chain reaction, and the amplification products were analyzed by direct DNA sequencing. The results were compared with human PLG reference sequences published in the National Center for Biotechnology Information database using Chromas software to find the mutation sites, and confirmed by reverse sequencing.Results:Both of the 2 patients with confirmed CI had a young onset, and PLG: A was reduced to 21% in the proband 1 and to about 50% in 4 family members; PLG: A was reduced to about 50% in the proband 2 and 2 family members; PLG:Ag and the above tests were essentially normal in both probands and family members. Gene analysis showed that the proband 1 had the homozygous mutation of c.1858G>A in exon 15, the 4 family members of the proband 1, proband 2 and her 2 family members had the heterozygous mutation of c.1858G>A in exon 15, which resulted in a mutation of alanine at position 620 in PLG to threonine (p.Ala620Thr).Conclusions:The decrease of PLG:A was caused by the p.Ala620Thr missense mutation of PLG gene. Proband having CI may be related to the inhibition of fibrinolytic function in the organism due to the p.Ala620Thr missense mutation.