Adult ; Hemoperfusion ; Humans ; Male ; Paraquat ; blood ; poisoning

Objective:To explore the effect of the methanol extract of Macrothelypteris oligophlebia on chronic non-bacterial prosta-titis ( CNP) in rats to confirm the active fractions. Methods:The powdered rhizomes of M. oligophlebia were soaked in methanol. The methanol extract was suspended in water and then extracted successively with chloroform and ethyl acetate to obtain chloroform fraction, ethyl acetate fraction and water fraction. Carrageenan-induced CNP in rats was established. The rats were randomly divided into the sham-operated control group, model group, positive control group, methanol extract group, ethyl acetate fraction group, chloroform fraction group and water fraction group. The anti-prostatitis effect was evaluated by the prostate index, and the pathological examination of prostate was performed using HE staining. The levels of interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), cyclooxyge-nase-2 (COX-2) and prostaglandin E2(PGE2) were analyzed using ELISA kits. Results:The ethyl acetate fraction group and metha-nol extract group with high flavonoid content could significantly decrease prostate index (P<0. 01) and the levels of IL-10, TNF-α, COX-2 and PGE2(P<0. 05 or P<0. 01), and improve the prostate morphology when compared with the model group, especially with the ethyl acetate fraction group. Conclusion:The rhizomes of M. oligophlebia show promising therapeutic effect on CNP, and the ethyl acetate fraction is the active fraction.

Objective To investigate the effect of hepatitis B virus core protein (HBc) dimer interfaces amino acids mutation on nucleocapsid assembly and HBV DNA replication. Methods Based on HBc three dimension structure, four HBc dimer interfaces domain mutation plasmids, pHBc14-18M,pHBc120-135M,pHBc23-39M and pHBc122-139M were constructed in pcDNA3.1 vector by PCR site-directed mutagenesis, there was a flag-tag at the C-terminal of all mutants for easy detection. Wild type core protein plasmid 1-183flag was also constructed as a positive control. The 4 mutants were cotransfected HepG2 cells with pHBV1.2 core negative plasmid (pHBV1.2-core-) ,which contained 1.2 copies of HBV whole genome but the core protein would not express due to a stop codon. The capsid formation, HBV pregenome(pgRNA) and HBV DNA replication mediate were analyzed by native agarose gel electrophoresis and Western blot, Northern blot and Southern blot , respectively. The 4 mutants were also cotransfected HepG2 cells with HBV wild type plasmid pHBV1.2 and examined by Southern blot. Virions in the medium were determined by native agarose gel electrophoresis and Western blot. Results Cotransfecting HepG2 cells with pHBV1.2-core- plasmid, pHBc14-18M,pHBc120-135M and pHBc122-139M mutant groups formed nucleocapsid-like structure but pHBc23-39M could not, Northern and Southern blot displayed no signal in all mutants except 1-183flag conrol group. In pHBV1.2 cotransfection experiment, HBV DNA replication was blocked in pHBc14-18M, pHBc120-135M and pHBc122-139M mutant groups, sharply decreased in pHBc120-135M and pHBc122-139M groups, correspondingly virons production in medium were also inhibited. pHBc23-39M mutant exerted no influence on HBV replication. Conclusion pHBc23-39M mutant can neither form nucleocapsid-like structure nor interact with wild type HBc dimmer to interfere HBV replication.On the contrast, pHBc14-18M, pHBc120-135M and pHBc122-139M mutants can form nucleocapsid-like structure by themselves, but this structure does not support HBV DNA synthesis. Besides, they can effectively inhibit wild type HBV DNA replication by contacting with wild HBc dimmers resulting in nucleocapsid dysfunction.

OBJECTIVETo study the effect of Modified Dachengqi Decoction (MDD) as whole course therapy on mediators of inflammation in severe acute pancreatitis (SAP) model rats, and to compare interventional advantages over intestinal mucosal barrier (IMB) of SAP rats between whole course therapy of MDD and early stage therapy of MDD.

METHODSTotally 190 SD rats were divided into five groups according to random digit table, i.e., the sham-operation group, the model group, the octreotide (OT) group, the early stage MDD treatment group, the whole course MDD treatment group, 38 in each group. SAP models were established with retrograde injection of 5% sodium taurocholate into the pancreaticobiliary duct. Three hours after modeling normal saline (NS) was administered to rats in the sham-operation group and the model group by gastrogavage, once per 12 h.1.35 µg/100 g OT was subcutaneously injected to rats in the OT group, once every 8 h. 0.4 mL/100 g MDD was administered to rats in the early stage MDD treatment group, and 6 h later changed to NS (once per 12 h).0.4 mL/100 g MDD was administered to rats in the whole course MDD treatment group, once every 12 h. The accumulative survival rate and morphological manifestations of pancreas and small intestine were observed under microscope 48 h after modeling. Pathologic scores of the pancreas and small intestine were conducted at 4, 6, 24, and 48 h after modeling. Contents of serum amylase (AMY), alanine transaminase (ALT), and TNF-α were also detected. The expression of high mobility group box protein 1 (HMGB1) in the small intestine tissue was also detected by Western blot. The positive rate of bacterial translocation in mesenteric lymph nodes (MLNs) was observed within 48 h. Correlations between serum TNF-α or HMGB1 in small intestinal tissue and pathological scores of the pancreas or the small intestine were analyzed.

RESULTSThe accumulative survival rate was 100. 0% in the sham-operation group, 79. 2% in the whole course MDD treatment group, 70. 8% in the OT group, 45. 8% in the early stage MDD treatment group, and 37.5% in the model group. At 6 h after modeling, pathological scores decreased more in the whole course MDD treatment group, the early stage MDD treatment group, the OT group than in the model group (P < 0.05). At 24 and 48 h after modeling, pathological scores of the pancreas and the small intestine decreased more in the whole course MDD treatment group and the OT group than in the early stage MDD treatment group (P <0. 05). At 6, 24, and 48 h after modeling, serum contents of AMY and ALT both decreased more in the whole course MDD treatment group, the early stage MDD treatment group, the OT group than in the model group (P < 0.05). At 48 h after modeling serum contents of AMY and ALT both decreased more in the whole course MDD treatment group and the OT group than in the early stage MDD treatment group (P < 0.05). At 6 h after modeling serum TNF-α levels decreased more in the whole course MDD treatment group, the early stage MDD treatment group, the OT group than in the model group (P < 0.05). At 6, 24, and 48 h after modeling the level of HMGB1 in the small intestinal tissue decreased more in the whole course MDD treatment group, the early stage MDD treatment group, the OT group than in the model group (P < 0.05). Of them, HMGB1 levels at 24 and 48 h were lower in the whole course MDD treatment group and the OT group than in the early stage MDD treatment group (P < 0.05). The number of MLNs bacterial translocation at 48 h after modeling was lower in the whole course MDD treatment group and the OT group than in the early stage MDD treatment group and the model group (P < 0.05). Serum TNF-α contents within 6 h were positively correlated with pathological scores of pancreas (r = 0.579, P < 0.01). ROC curve showed that serum TNF-α contents could predict the severity of SAP (ROC = 0.990, 95% Cl: 0.971 to 1.000). HMGB1 in the small intestine was positively correlated with pathological scores of the small intestine (r = 0.620, P < 0.01).

CONCLUSIONSEarly stage use of MDD could effectively reduce the release of TNF-α, while whole course use of MDD could effectively inhibit the expression of HMGB1. The latter could preferably attenuate injuries of the pancreas and the small intestine, lower MLNs bacterial translocation, and elevate the survival rate.

Animals ; Bacterial Translocation ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; HMGB1 Protein ; Intestinal Mucosa ; drug effects ; Octreotide ; Pancreas ; Pancreatitis ; drug therapy ; Plant Extracts ; pharmacology ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Taurocholic Acid ; Tumor Necrosis Factor-alpha

Aged ; Drug-Related Side Effects and Adverse Reactions ; blood ; therapy ; Emergency Treatment ; Female ; Hemoperfusion ; Humans ; Hypnotics and Sedatives ; poisoning ; Male ; Middle Aged ; Serum ; chemistry

OBJECTIVETo explore the effect of hemoperfusion(HP) about the patients of methamidophos poisoning.

METHODSOn the basis of comprehensive treatment,15 cases of severe acute methamidophos poisoning patients were treated with HP, Blood samples were collected at 7 time points, before and 5, 15, 30, 45, 60mins following the beginning and the end of hemoperfusion. Blood samples were used for measuring the concentration of methamidophos and perfusion devices were used for measuring the volume of methamidophos adsorbed by the device after hemoperfusion.

RESULTS15 patients live in 12 cases, 3 cases of death. HP (former) blood Cholinesterase vigor were 662.60 + 632.05, HP (after) blood cholinesterase vigor were 2577.52 + 920.38 IU/L; The difference of blood Cholinesterase vigor between the before and after HP was statistically significant (P < 0.01). The patients' methamidophos concentration of blood when HP treated 45, 60, 120 min were respectively (851 + 672), (680 + 529), (587 + 520) microg /ml, there were significantly lower than that the patients' methamidophos concentration of blood who were before HP (1659 + 1105) microg/ml, a statistically significant difference (P < 0.01).

CONCLUSIONHP can be cut down obviously methamidophos poisoning patients serum concentrations of toxic, the experimental method directly prove the clinical application of carbon HP can really adsorption methamidophos.

Adult ; Cholinesterases ; metabolism ; Female ; Hemoperfusion ; methods ; Humans ; Insecticides ; poisoning ; Male ; Middle Aged ; Organothiophosphorus Compounds ; poisoning ; Treatment Outcome ; Young Adult

OBJECTIVETo study the clinical and pathological features of drug-induced liver injury (DILI).

METHODSLiver specimens were obtained through needle biopsies from 100 patients with DILI. The histological preparations of the specimens were stained with haematoxylin eosin, several histochemistry methods, and immunohistochemistry stains. The pathological changes of the livers were analyzed together with the patients's clinical data. The patients were divided into two groups, an acute DILI group (n=39) and a chronic DILI group (n=61), based on their clinical courses and histological changes in their livers. In the chronic DILI group, the clinical courses were longer than 6 months and/or fibrosis or cirrhosis occurred in their liver tissues.

RESULTSAmong our cases the leading cause of DILI was Chinese herb medicine, accounting for 21% of the 100 cases; steroids induced cases were 11% of the total. 78% of the patients presented elevated serum transaminases and/or jaundice. The degree of transaminases elevation and the frequency of jaundice happening in the acute group were significantly higher than those in the chronic group (P less than 0.05). The histopathological liver changes in these DILI cases included: (1) necrosis commonly occurred in acinar zone 3, (2) abundant neutrophil and/or eosinophil infiltrations, (3) hepatocytic and/or canalicular cholestasis with little or no inflammation, (4) microvesicular steatosis mixed with macrovesicular steatosis, and (5) presentation of epitheloid cell granuloma. There were no significant differences in liver histopathology between the acute and the chronic DILI groups, except that the fibrosis and the ductular proliferation were different.

CONCLUSIONDILI has become a notable liver disease in mainland China, and the use of Chinese herbal medicine must be improved, standardized and regulated more closely.

Adolescent ; Adult ; Aged ; Chemical and Drug Induced Liver Injury ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Liver ; pathology ; Male ; Middle Aged ; Young Adult

OBJECTIVETo explore the effect of hemoperfusion (HP) on tylenol poisoned patients.

METHODSUrgently established the blood access by transfemoral catheterization of femoral vein, we used charcoal hemoperfusion by blood pump and dynamically monitored the plasma concentration of tylenol active ingredients for the 2 patients and the content of tylenol active ingredients in the charcoal was determined.

RESULTSPlasma concentration of tylenol active ingredients of the 2 patients was declined gradually during and after the HP management. The acetaminophen serum concentration of the case 1 was declined from the 13.4 µg/L at the start of HP to the 5.81 µg/L at the end of HP; and the case 2 was declined from 51.1 µg/L to 22.3 µg/L. The adsorption amount of acetaminophen in the blood perfusion device are respectively 119 542 µg of case 1 and 33 2154 µg of case 2.

CONCLUSIONEarly hemoperfusion should be carried out for acute tylenol poisoning patients if there were indications, hemoperfusion can clear the tylenol active ingredients and this is an effective measure to eliminate tylenol active ingredients.

Acetaminophen ; blood ; pharmacokinetics ; poisoning ; Adult ; Anti-Inflammatory Agents, Non-Steroidal ; blood ; pharmacokinetics ; poisoning ; Drug Overdose ; therapy ; Drug-Related Side Effects and Adverse Reactions ; blood ; Female ; Hemoperfusion ; Humans ; Metabolic Clearance Rate ; Young Adult

In this study,the current status for breast diseases in a region with high-incidence of cervical cancer were epidemiologically investigated.From March to August,2009,17618 women,from Wufeng area of Hubei province,China,were recruited to screen breast diseases by using breast infrared diagnostic apparatus.Other diagnostic methods,such as B-mode ultrasound,X-ray mammography,needle biopsy and pathological examination were,if necessary,used to further confirm the diagnosis.The screening showed that 5990 of 17618 cases (34.00％) had breast diseases,5843 (33.16％) had mammary gland hyperplasia,48 (0.27％) had breast fibroadenoma,ll (0.06％) had breast carcinoma,and 88 (0.50％) had other breast diseases.The peak morbidity of breast cancer was found in the women aged 50-0 ages.The morbidity of breast cancer was significantly increased in women elder than or equal to 50 years old (n=8,0.157％) in comparison with that in the subjects younger than 50 years old (n=3,0.024％) (u=2.327,P＜0.05).It was shown that the occurrence of breast diseases was concentrated in women aged 20-40 years,while the total morbidity reached its peak at the age of 30 years and then decreased sharply after age of 40.Compared with the patients elder than or equal to 40 years old (n=3289,27.46％),the morbidity rate of breast diseases was significantly increased in women less than 40 years old (2648 cases,47.18％; P＜0.001).However,there was no significant difference in the morbidity of breast diseases between the age group of 20-29 years and that of 30-39 years (P=0.453),and both of them were high.There was no significant association between the morbidity of breast diseases and cervical cancer.Since the morbidity of breast diseases was higher among young women,more attention should be paid to the screening of breast diseases among young women for early diagnosis.

Mammalian pancreatic β-cells play a pivotal role in development and glucose homeostasis through the production and secretion of insulin. Functional failure or decrease in β-cell number leads to type 2 diabetes (T2D). Despite the physiological importance of β-cells, the viability of β-cells is often challenged mainly due to its poor ability to adapt to their changing microenvironment. One of the factors that negatively affect β-cell viability is high concentration of free fatty acids (FFAs) such as palmitate. In this work, we demonstrated that Yes-associated protein (Yap1) is activated when β-cells are treated with palmitate. Our loss- and gain-of-function analyses using rodent insulinoma cell lines revealed that Yap1 suppresses palmitate-induced apoptosis in β-cells without regulating their proliferation. We also found that upon palmitate treatment, re-arrangement of F-actin mediates Yap1 activation. Palmitate treatment increases expression of one of the Yap1 target genes, connective tissue growth factor (CTGF). Our gain-of-function analysis with CTGF suggests CTGF may be the downstream factor of Yap1 in the protective mechanism against FFA-induced apoptosis.
Actins ; metabolism ; Adaptor Proteins, Signal Transducing ; antagonists & inhibitors ; genetics ; metabolism ; Animals ; Apoptosis ; drug effects ; physiology ; Bridged Bicyclo Compounds, Heterocyclic ; pharmacology ; Cell Line, Tumor ; Connective Tissue Growth Factor ; genetics ; metabolism ; pharmacology ; Cytochalasin D ; pharmacology ; Fatty Acids, Nonesterified ; pharmacology ; HEK293 Cells ; Humans ; Immunohistochemistry ; Insulin-Secreting Cells ; cytology ; drug effects ; metabolism ; Mice ; Microscopy, Fluorescence ; Palmitic Acid ; pharmacology ; Phosphoproteins ; antagonists & inhibitors ; genetics ; metabolism ; RNA Interference ; RNA, Small Interfering ; metabolism ; Rats ; Recombinant Proteins ; genetics ; metabolism ; pharmacology ; Thiazolidines ; pharmacology