Metal sulfides are chemically attacked by Fe~ 3+ and H~+, resulting in the formation of elemental sulfur via polysulfides or thiosulfate pathway. Elemental sulfur may aggregate and even form a layer on the metal sulfide surface, which will inhibit leaching metals from the sulfides minerals. Elimination of inert elemental sulfur in a typical acidic environment can exclusively be by way of oxidation of acidophilic sulfur-oxidizing bacteria, such a way includes the attachment, transport and oxidation process of elemental sulfur by acidophilic sulfur-oxidizing bacteria. On the basis of analysis on the pertinent researches, the molecular mechanism of sulfur elimination by the acidophilic bacteria is far away from elucidated, and to attain that target, there are still much work to be done for elucidating the molecular mechanism on the attachment, transport and oxidation process of elemental sulfur by the acidophilic sulfur-oxidizing bacteria.

OBJECTIVETo study the effects of Dihydromyricetin (DMY) on antilipid-peroxidation.

METHODThe antilipid-peroxidation of DMY on heart, liver, brain tissue homogenate and mitochondria was measured by the determination of malondiadehyde (MDA) induced by Fe2+ -Vit C, Fe2+ -H2O2, Fe-Cys with TBA spectrometric method.

RESULTDMY could inhibit the lipid peroxidation of homogenate and mitochondria. The inhibition exhibited concentration-dependent manner.

CONCLUSIONDMY has good antilipid-peroxidation effect, which is worth studing further.

Ampelopsis ; chemistry ; Animals ; Antioxidants ; isolation & purification ; pharmacology ; Brain ; metabolism ; Dose-Response Relationship, Drug ; Flavonols ; isolation & purification ; pharmacology ; Lipid Peroxidation ; drug effects ; Liver ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mitochondria ; metabolism ; Mitochondrial Swelling ; drug effects ; Myocardium ; metabolism ; Plants, Medicinal ; chemistry ; Rats

OBJECTIVETo investigate the phenotypes and functions of cord blood dendritic cells of fetuses whose mothers are patients with chronic hepatitis B.

METHODSPeripheral blood and cord blood mononuclear cells (PBMC) were isolated from whole blood by density gradient centrifugation with Ficoll-Hypaque. The adherent cells were cultured in AIM-V medium containing recombinant human IL-4, TNF-alpha and GM-CSF. On day 9, mature DCs (mDC) were harvested and used for phenotype analysis. The amounts of IL-12 which dendritic cells produced were measured. The dendritic cells that were studied and compared were from cord blood of fetuses of both CHB positive and negative mothers and from CHC adult peripheral blood.

RESULTSThe expression rate of CD80 and CD83 of chronic hepatitis B mother cord blood dendritic cells was low compared with that of the healthy cord blood, healthy adult peripheral blood, and chronic hepatitis B adult peripheral blood, P < 0.05. The amount of IL-12 produced by chronic hepatitis B mother cord blood dendritic cells was lower than that of healthy cord blood, healthy adult peripheral blood, chronic hepatitis B adult peripheral blood (P < 0.05). The T lymphocyte proliferation inducing ability of dendritic cells of healthy adult peripheral blood was higher in inducing cord blood T lymphocytes proliferation, which was greater than that of the healthy adult peripheral blood in inducing adult T lymphocytes and was greater than that of the healthy cord blood dendritic cells in inducing cord blood T lymphocytes, which was greater than that of the healthy cord blood in inducing adult T lymphocytes, which was greater than that of chronic hepatitis B mothers in inducing cord blood T lymphocytes, which was greater than that of chronic hepatitis B mother cord blood in inducing adult T lymphocytes.

CONCLUSIONThe maturation and functioning of CHB mother cord blood dendritic cells were lower than those of healthy cord blood, healthy adult peripheral blood and CHB adult peripheral blood.

Adult ; Cells, Cultured ; Dendritic Cells ; cytology ; immunology ; Female ; Fetal Blood ; immunology ; Hepatitis B, Chronic ; immunology ; Humans ; Phenotype ; Pregnancy ; Pregnancy Complications, Infectious ; immunology ; T-Lymphocytes ; immunology

Objective To investigate the characteristics and distribution of human eehinococcosis in Hobukesar Mongolian Autonomous County (HMAC) in Xinjiang. Methods Using cluster sampling methods, the 2 counties (Tiebukenwusa and Narenhebuke) in HMAC were chosen as focusing areas for investigation. A survey of human echinococcosis including questionnaire, serological test and abdominal ultrasonic scan was carried out. Results The prevalence of human echinococcosis was 9.0% (64/712) by ultrasound and surgical history, including 8.7% (62/712) for cystic eehinococcosis(CE), 0.3%(2/712) for alveolar echinococcosis(AE) and 15.6%(111/712) for total of serological positives in HMAC. CE prevalence rate of different occupations, age, family slaughtering livestock and drinking water source had significant differences(P<0.05). Herdsmen as the highest risk group showed a CE prevalence of the 13.4% (27/201) in comparison with other occupations. The ages between 20 to<40 year-old were at the highest risk stage with 12.8% incidence. But CE prevalence rate of different gender, ethnic and education groups had not significant differences(P>0.05). Conclusions HMAC could be considered as a high endemic human CE region in Xinjiang. The current study reported the main risk factors may include occupations, age difference and drinking water source.

OBJECTIVETo induce the differentiation of K562/MDR1 cells into dendritic cells (DC) with multidrug resistance property.

METHODSK562/MDR1 cells and K562 cells were cultured in the presence of GM-CSF and IL-4 to generate DC and matured by TNF-α. On d14 K562/MDR1-DC and K562-DC cells were harvested and the expressions of CD1a, CD83, CD80, CD86, HLA-ABC and HLA-DR were assessed by flow cytometry (FCM). The antigen presentation function of K562/MDR1-DC and K562-DC was determined by allogenic mixed lymphocyte reaction (Allo-MLR). The expression of P-glycoprotein and the intracellular accumulation of daunorubicin (DNR) were detected by FCM. The sensitivity of K562/MDR1-DC and K562-DC cell to vincristine, adriamycin was measured using MTT assay.

RESULTSBoth K562/MDR1 and K562 cells were differentiated into dendritic cells in the presence of cytokine cocktails, showing the morphologic and immunophenotypic characteristics of DC. K562/MDR1-DC more markedly enhanced proliferation of allogeneic lymphocytes in MLR than K562-DC. High level expression of P-glycoprotein and efflux of DNR were demonstrated in K562/MDR1-DC. K562/MDR1-DC showed multidrug resistance property, with higher IC(50) to VCR and ADM than that of K562-DCs.

CONCLUSIONK562/MDR1 cells can be differentiated into DC with the presence of cytokines, the induced K562/MDR1-DC cells express high level of P-glycoprotein and acquire the multidrug resistance property.

ATP-Binding Cassette, Sub-Family B, Member 1 ; genetics ; Cell Differentiation ; drug effects ; Dendritic Cells ; cytology ; Drug Resistance, Multiple ; Granulocyte-Macrophage Colony-Stimulating Factor ; pharmacology ; Humans ; Interleukin-4 ; pharmacology ; K562 Cells ; cytology ; Transfection ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo analyze the relationship between hepatorenal syndrome (HRS) and plasma ammonia.

METHODSPlasma ammonia, liver and renal function of 465 patients with liver cirrhosis in our hospital, from June 2007 to March 2009, were analyzed. 80 renal dysfunction patients and 80 healthy controls were recruited in the control group. In addition, 40 patients with HRS were followed up.

RESULTSUsing urea as the diagnosis standard of HRS, the morbidity rate of HRS was 39.6%, which was higher than that using creatinine as the diagnosis standard of HRS (Chi-square test = 97.33, P less than 0.01). using urea and creatinine as the diagnosis standard of HRS, the ammonia level of HRS groups was (57.39+/-48.83)mumol/L, (64.80+/-47.25)mumol/L, which were higher than that in the non-HRS groups (t = -3.07, t = -3.67, P less than 0.01). The ammonia level of patients with renal dysfunction was (26.59+/-14.34)mumol/L, which was lower than that in HRS group, non-HRS group (P less than 0.01), but there was no statistical significance between the patients with renal dysfunction and the healthy peoples [(22.36+/-8.72)mumol/L] (t = 1.52, P more than 0.05). The followed-up analysis of 40 patients with HRS indicated that plasma ammonia level was positively correlated with urea and creatinine, and correlation coefficients were 0.874 and 0.834 (P less than 0.05).

CONCLUSIONHepatic encephalopathy is liver-kidney-intestine-brain syndrome. HRS plays an important role in the development of hepatic encephalopathy.

Adult ; Aged ; Ammonia ; blood ; Biomarkers ; blood ; Blood Urea Nitrogen ; Case-Control Studies ; Creatinine ; blood ; Female ; Hepatic Encephalopathy ; etiology ; prevention & control ; Hepatorenal Syndrome ; blood ; diagnosis ; epidemiology ; Humans ; Liver Cirrhosis ; blood ; complications ; Liver Function Tests ; Male ; Middle Aged ; Retrospective Studies

BACKGROUNDEpidermal growth factor (EGF), a mitogenic polypeptide that binds to cell surface receptors, is an important regulator of cell differentiation and fetal lung surfactant synthesis. We investigated the preventive and therapeutic effects of EGF in respiratory distress syndrome, by administering EGF and dexamethasone (Dex) to mother rat before delivery.

METHODSSix female Sprague-Dawley (SD) rats were assigned to three groups (2 rats each); EGF or Dex was given to pregnant rats (EGF group and Dex group, respectively) from gestational day 16 to day 18 by intraperitoneal injection, while the group with normal saline injection was used as negative controls. Fetal rats were taken out of womb by hysterotomy on day 19 of pregnancy, then 24 fetal rats were randomly chosen from each group. Their body weights were measured, and pulmonary surfactant protein-A and -B (SP-A and SP-B) antigens were determined by immunohistochemical staining in each group. The histologic structure was examined under a light microscope, a light microscopic image system or an electron microscope.

RESULTSThe expressions of SP-A and SP-B could be detected in each group. A significant difference was observed for SP-A and SP-B in the EGF and Dex groups compared with the control group (P < 0.01). Image analysis showed that the relative values of air space area and interalveolar septa area in the EGF and Dex groups were significantly greater than those in the control group (P < 0.01), while no significant difference was found between the two groups (P > 0.05). The ultrastructural features of fetal lungs showed that the number of alveolar type II cells containing lamellar bodies in the EGF and Dex groups was apparently increased compared with that in the control group. The mean body weight of fetus from the Dex group was smaller than that from the control group ((1.3192 +/- 0.0533) g, (1.3863 +/- 0.0373) g), but there was no significant difference between the EGF group and the control group ((1.3986 +/- 0.0730) g, (1.3863 +/- 0.0373) g).

CONCLUSIONSMaternal treatment with EGF and Dex on days 16 - 18 of gestation could promote morphogenesis and increase the surfactant levels in premature fetal lung. However, maternal treatment with Dex, not EGF, decreased the body weight.

Animals ; Dexamethasone ; pharmacology ; Epidermal Growth Factor ; pharmacology ; Female ; Immunohistochemistry ; Lung ; drug effects ; embryology ; ultrastructure ; Microscopy, Electron, Transmission ; Pregnancy ; Pulmonary Surfactant-Associated Protein A ; metabolism ; Pulmonary Surfactant-Associated Protein B ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the variation of specific antibody among convalescent of severe acute respiratory syndrome (SARS) patients through a three-year program.

METHODSSera samples were collected from SARS cases in the 5th, 20th and 35th month after onset of the illness. The SARS-CoV specific antibody was detected for all of them by ELISA and neutralized test simultaneously. The titer of neutralizing antibodies was calculated using Reed-Muench method, and the comparison between different time groups was analyzed regarding the variance of data on repeated measures after logarithm conversion.

RESULTS13, 17 and 13 sera samples were collected in the 5th, 20th and 35th month after onset. Results showed that despite the fact that the positive rates of ELISA antibody were 100%, 82.4% and 84.6% respectively,the neutralizing antibody was still positive for all the samples. The average neutralizing antibody titers were 1:43 (1:16-1:203), 1:36 (1:17-1:59) and 1:21 (1:10-1:39) on the 5th, 20th and 35th month after onset, and the differences were statistically significant (F = 60.419, P < 0.001). On the 35th month after the onset, 30.8% (4/13) of the patients were still having the neutralizing antibody level of above 1:36, but the neutralizing antibody level in another 30.8% (4/13) of the patients had decreased to as low as 1:10, when the cut-off level was set as 1:8.

CONCLUSIONResults of the study indicated that the neutralizing antibody of SARS cases could last for at least three years, but the sera specific antibody in SARS cases decreased gradually when time went by. However, neutralizing antibody in some of the cases decreased to a lower level on the 35th month. Further follow-up study was worthwhile to observe the long-lasting profile of antibody existence on SARS cases.

Antibodies, Neutralizing ; analysis ; Enzyme-Linked Immunosorbent Assay ; Follow-Up Studies ; Humans ; Severe Acute Respiratory Syndrome ; immunology

OBJECTIVEMultiple genetic and environmental factors contribute to the onset of many human diseases, such as neonatal hyperbilirubinemia. OATP 1B1 is an important polymorphism gene which transmembrane transports unconjugated bilirubin(UCB). Genetic polymorphisms that affect the functionality of the protein may potentially lead to altered transport characteristics. The T521C/A388G polymorphism of this gene has been reported to considerably reduce the transporting property of drugs like pravastatin, and may be involved in the membrane translocation of bilirubin. Some studies have shown that OATP 1B1 mediates bilirubin uptake from blood into the liver, and the OATP 1B1 polymorphism is a likely mechanism explaining the differences of bilirubin level in peripheral blood. The aim of this study was to evaluate the relationship between OATP 1B1 polymorphisms and neonatal hyperbilirubinemia.

METHODSA total of 220 newborn infants with hyperbilirubinemia were recruited from Hunan Children Hospital from November 2008 to December 2009 according to the diagnostic criteria. Age and sex matched control subjects comprised of 200 unrelated, hyperbilirubinemia-free newborns. Biochemical and clinical data were collected from the case history. One ml venous blood samples in EDTA vials were taken from each subject and DNA was isolated from peripheral leukocytes by standard methods, preserved in 4°C. 1 - 2 ml venous blood samples were also taken for detecting the serum total bilirubin and direct bilirubin level by chemical oxidation method. OATP 1B1 T521C/A388G polymorphisms were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Allele and genotype frequencies were compared between patients and control. The gene polymorphism and risk of disease were also analyzed. Serum total bilirubin, conjugated bilirubin and unconjugated bilirubin levels were compared between different OATP 1B1 T521C/A388G genotypes.

RESULTSAllele frequencies in patients and control population were in Hardy-Weinberg equilibrium (P > 0.05). Allele and genotype frequencies of the OATP 1B1 T521C polymorphism in patients were significantly different from the controls. The OATP 1B1 521C allele frequency was only 8.2% in patients, while reached 14.0% in the control group which was very close to the frequency of common Chinese people. However, the proportion of wild type genotypes was significantly higher than those of the controls, reached 84.1%. The 521 C allele and genotypes carrying 521 C allele illustrated low risk for neonatal hyperbilirubinemia (OR = 0.530, 95%CI = 0.328 - 0.857; OR = 0.541, 95%CI = 0.344 - 0.851). However, the frequencies of alleles and genotypes of SLCO1B1 A388G did not differ significantly from those of the controls, and this polymorphism did not influence susceptibility to such disease. Among the three OATP 1B1 A388G genotypes, the level of total serum bilirubin (TSB), direct bilirubin (DB) and unconjugated bilirubin (UCB) were significantly different. Values of TSB, DB and UCB were the highest in wild type subjects, lower in heterozygotes, and the lowest in mutant homozygotes. TSB and UCB in patients with wild type genotypes reached 602.5 µmol/L and 585.0 µmol/L respectively, nearly twice the average value of homozygous patients. While the TSB and UCB in homozygotes were below the average value of all patients, only 351.7 µmol/L and 338.8 µmol/L respectively.

CONCLUSIONSOur findings indicated that OATP 1B1 A388G polymorphism has a notable influence on the serum bilirubin level in neonatal hyperbilirubinemia patients. The OATP 1B1 521T allele may be a potential risk factor of such disease. OATP 1B1 T521C/A388G was an important polymorphism gene which related with neonatal hyperbilirubinemia. Future study should involve other polymorphisms of OATP 1B1, more candidate genes and environmental risk factors. It is also necessary to investigate their association with the severity and prognosis of this disease in order to elucidate the genetic pathogenesis of neonatal hyperbilirubinemia as a complex disease. This study should be repeated in a larger population and different ethnic groups.

Bilirubin ; blood ; Case-Control Studies ; Female ; Humans ; Hyperbilirubinemia, Neonatal ; genetics ; Infant, Newborn ; Male ; Organic Anion Transporters ; genetics ; Polymorphism, Restriction Fragment Length ; Solute Carrier Organic Anion Transporter Family Member 1b1

BACKGROUNDIslet transplantation is an effective way of reversing type I diabetes. However, islet transplantation is hampered by issues such as immune rejection and shortage of donor islets. Mesenchymal stem cells can differentiate into insulin-producing cells. However, the potential of human umbilical cord mesenchymal stem cells (huMSCs) to become insulin-producing cells remains undetermined.

METHODSWe isolated and induced cultured huMSCs under islet cell culture conditions. The response of huMSCs were monitored under an inverted phase contrast microscope. Immunocytochemical and immunofluorescence staining methods were used to measure insulin and glucagon protein levels. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect gene expression of human insulin and PDX-1. Dithizone-staining was employed to determine the zinc contents in huMSCs. Insulin secretion was also evaluated through radioimmunoassay.

RESULTSHuMSCs induced by nicotinamide and β-mercaptoethanol or by neurogenic differentiation 1 gene (NeuroD1) transfection gradually changed morphology from typically elongated fibroblast-shaped cells to round cells. They had a tendency to form clusters. Immunocytochemical studies showed positive expression of human insulin and glucagon in these cells in response to induction. RT-PCR experiments found that huMSCs expressed insulin and PDX-1 genes following induction and dithizone stained the cytoplasm of huMSCs a brownish red color after induction. Insulin secretion in induced huMSCs was significantly elevated compared with the control group (t = 6.183, P < 0.05).

CONCLUSIONSHuMSCs are able to differentiate into insulin-producing cells in vitro. The potential use of huMSCs in β cell replacement therapy of diabetes needs to be studied further.

Cell Differentiation ; genetics ; physiology ; Cells, Cultured ; Cellular Reprogramming ; genetics ; physiology ; Female ; Humans ; Immunohistochemistry ; Insulin-Secreting Cells ; cytology ; metabolism ; Mesenchymal Stromal Cells ; cytology ; Pregnancy ; Reverse Transcriptase Polymerase Chain Reaction ; Umbilical Cord ; cytology ; Wharton Jelly ; cytology