[Histopathological improvement in chronic hepatitis B patients after treatment of marin solution].
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Adolescent↗
Biomedical subjects
Ling Zhang
Publications and source records attributed to Ling Zhang.
Reestablishment of second hepatic hilum: a new technique for the treatment of Budd-Chiari syndrome.
OBJECTIVE: To assess a new intervention for reestablishing the second hepatic hilum by means of puncturing and stenting the liver tissue between the intrahepatic vena cava and a hepatic vein for the treatment of Budd-Chiari syndrome (BCS). METHODS: Two patients with BCS, in which no second hepatic hilum structure was found in transhepatic venography, underwent an interventional procedure of canalizing and stenting the parenchyma tract between the intrahepatic vena cava and a hepatic vein. The procedures were performed in the percutaneous transhepatic and right jugular vein, respectively. A metallic stent with a 10 mm diameter was implanted to maintain tract patency. RESULTS: The free hepatic vein pressure (FHVP) of both patients decreased from 37 mm Hg to 5 mm Hg and from 28 mm Hg to 4 mm Hg, respectively, after the procedure. The complication of hemorrhage due to puncture was observed in one patient. Both patients maintained hepatic improvements in 3-year follow-up. Both clinical conditions and laboratory values were significantly improved after the procedure. Furthermore, the stented canals (the reestablished second hepatic hilum) maintained patent with normal FHVP, which was confirmed by control venography. CONCLUSION: The new technique provides a simple, safe, effective, and relatively inexpensive treatment of Budd-Chiari syndrome. Long-lasting effectiveness is expected.
Adult↗
[Cloning the genes differently expressed in human hepatocellular carcinoma by suppression subtractive hybridization].
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Carcinoma, Hepatocellular↗
[Effect of Zingiber OfficinaleRosc on lipid peroxidation in hyperlipidemia rats].
Zingiber Officinale Rosc(ginger) is the food of rhizoma species as well as Chinese traditional medicine and has various pharmacological effects. The last researches showed that ginger not only reduced plasma lipid levels but also the mouse atherosclerotic lesion areas. The ginger antioxidative effect maybe pay an important role in attenuation of development of atherosclerosis. Antioxidative effect of Zingiber Officinale Rosc on hyperlipidemia rats have been studied and the changes of GSH-Px and LPO in their blood have been observed in this paper. Male adult Wistar rats were grouped into control, preventive and curative teams. The experimental teams were respectively fed on the test diet containing 2% ginger and 5% ginger, in order to measure the changes of plasma lipid peroxides (LPO) and glutathione (GSH-Px) after the experiment. The results show that ginger increased GSH-Px and reduced LPO in the rats' blood. Ginger could inhibit and/or scaving radicals of rat body in different degrees.
Animals↗
[Gene clone and its characteristics on band 7-like protein in Plasmodium falciparum FCC1/HN].
OBJECTIVE: To identify and clone the gene named pfstom gene which encoding the protein belonging to band 7 family and to do primary research on its function. METHODS: Based on the finished data in international public malaria database, coding sequence of pfstom cDNA was obtained by RT-PCR from FCC1/HN. Its phylogenetic profiles and the homogeny were analyzed by some softwares. After Prokaryotic expression, C terminal of Pfstom protein was expressed by Pet30a system. Recombinant Pfstom protein was used to immol/Lunize rabbit and then serum was harvested and the IgG was purified for Western blot. RESULTS: The coding sequence of pfstom is 1,125 bp which encoding 374 amino acids with C-terminal fragment being homogenous to stomatin-like protein which belongs to band 7 family. Phylogenetic profiles analysis revealed its homogeny to stomatin. Western blot showed its stage-specific expression in trophozoite. CONCLUSION: Pfstom belongs to band-7 family. It was expressed specifically in trophozoite in erythrocyte stage of plasmodium falciparum. It was not expressed in ring stage. And it is membrane-related protein. All these results provided the foundation for further research on pfstom.
Amino Acid Sequence↗
[Investigation on reproductive tract infection among floating married women of childbearing age in Fengtai district in Beijing].
OBJECTIVE: In order to develop plans for effective intervention measures, prevalence and health-seeking behavior related to reproductive tract infection among floating married women of childbearing age in Fengtai district in Beijing were studied. METHODS: Cross-sectional study was carried out. Two thousand and sixty-nine eligible women were randomly selected from strata based on their home provinces. From June to July 2001, the subjects were given face-to-face interview at the Fengtai family planning clinic in Beijing using standard questionnaire followed by gynecologic examination and laboratory tests. RESULTS: Thirty point three percent of the subjects were found to have reproductive tract infections (RTI) by laboratory tests. Prevalence rates of bacterial vaginosis, candida and trichomonas vaginitis were 22.2%, 4.9% and 2.1% respectively. Prevalence rates of chlamydia, gonorrhea, condyloma acuminatum and syphilis were 2.2%, 1.6%, 0.5% and 0.2% respectively. Of these infected women, only 43.1% (270/626) were symptomatic, and 61.5% (166/270) of these women with symptoms had sought treatment. CONCLUSION: Compared to other results in the literature, we found a relatively high prevalence of RTI in our study population. Only a small proportion of these infected women were symptomatic but only few of them sought treatment. We suggested that the provision of more family planning service and promotion of RTI knowledge to the floating women of childbearing age.
Adolescent↗
[Construction of N-LMP1 transgenic mice with the specific regulation region in nasopharynx].
In order to elucidate the role of EBV-LMP1 in the nasopharyngeal carcinogenesis, the expression vector was constructed with subjecting the N-LMP1 gene to double regulation of two specific regulators: EDL-2 and PLUNC-p. The N-LMP1 related transgenic mice model has been constructed successfully by pronucleus microinjection. 58 founder mice were born, 4 of which were founded to be positive by PCR and Southern blot. Immunohistochemistry assay showed that N-LMP1 protein was expressed in the nasopharynx, tongue and forestomach of transgenic mice.
Animals↗
[The effects of the Smad3-knockout on the hematopoiesis of mouse].
The effects of the Smad3- knockout on the hematopoiesis of mouse were investigated in this work. Five pairs of wild type and Smad3- null mice were studied. White blood cell(WBC), red blood cell(RBC) and platelet (PLT) counting of peripheral blood cells were performed with blood obtained from tails. And white blood cells were classified by their morphology. Bone marrow nucleated cells (BMNCs) were counted and classified. The CFU-GM, BFU-E, CFU-GEMM yields were measured in each pair of mice. CFU-S yield of each mouse was measured by injecting bone marrow cells into lethally irradiated 8-10 weeks old wild type female mice. And the pathomorphism of their bone marrows, spleens and livers were observed. As a result, WBC and PLT of Smad3- null mice were significantly higher than those in wild type mice. Smad3- null mice had much more proportion of granulocytes in classification. There wasn't any difference in RBC counting and BFU-E measurement. The yield of CFU-GM increased, while the yields of CFU-GEMM and CFU-S markedly reduced. Bone marrows are actively proliferative, with granulocytosis. The granulocyte/erythrocyte ratio increased. There were no obviously alterative in spleen and liver. Thus Smad3- knockout results in a decreased number of stem and progenitor cells. Moreover hematopoietic differentiation is abnormal with a tendency to forming more granulocytes and platelets. The effect of Smad3 on hematopoiesis is correlative to that of TGF-beta.
Animals↗
[Study on high-expression of soluble hbFGF in Escherichia coli].
The formation of inclusion body is correlated with the overexpression of foreign proteins in Escherichia coli. Controlling of the expression level seems to be critical to increase the soluble component. With the prerequisite of no alterations in amino acid sequence, the wobble bases of the first 3 codons downstream the initiation codon ATG of a hbFGF high-expression mutation, established previously, were changed into the bases of the native hbFGF sequences. Seven primers were synthesized for retro-mutations, after PCR were undertaken, the products were cloned into pET-3c, and recombinants were transformed into BL21 (DE3) plysS for expression. One strain with high solubility and bioactivity were identified, indicating that restriction of the expression level of recombinant protein is helpful for high-solubility.
Codon↗
Complete SHOX deficiency causes Langer mesomelic dysplasia.
The SHOX (short-stature homeobox-containing) gene encodes isoforms of a homeodomain transcription factor important in human limb development. SHOX haploinsufficiency has been implicated in three human growth disorders: Turner syndrome, idiopathic short stature, and Leri-Weill dyschondrosteosis. Langer mesomelic dysplasia is thought to be the homozygous form of dyschondrosteosis. However, complete SHOX deficiency has not been demonstrated for any postnatal patient with the classic Langer phenotype. We studied four adults and one child with Langer mesomelic dysplasia. SHOX abnormalities were detected in all five probands. One was a homozygote or hemizygote and two were compound heterozygotes. The homozygous or hemizygous mutation was in exon 6a, implying that the SHOXa isoform is essential for normal skeletal development. These findings confirm clinical inferences that Langer mesomelic dysplasia is the homozygous form of Leri-Weill dyschondrosteosis and add to our understanding of genotype/phenotype relationships in SHOX deficiency disorders.
Adult↗
Control of myeloid-specific integrin alpha Mbeta 2 (CD11b/CD18) expression by cytokines is regulated by Stat3-dependent activation of PU.1.
Granulocyte colony-stimulating factor (G-CSF) plays an essential role in regulating multiple aspects of hematopoiesis. To elucidate the role of G-CSF in controlling hematopoietic cell migration capabilities, we studied inducible expression of the myeloid-specific marker, integrin alpha(M)beta(2) (CD11b/CD18, Mac-1), in the myeloid cell line, 32D. We found that G-CSF stimulates the synthesis and cell surface expression of alpha(M) and beta(2) integrin subunits. Induction of both alpha(M) and beta(2) is dependent on Stat3, a major G-CSF-responsive signaling protein. However, the kinetics of expression suggested the involvement of an intermediate protein regulated by Stat3. Our results demonstrate that Stat3 signaling stimulates the expression of PU.1, a critical regulator of myelopoiesis. Furthermore, we show that PU.1 is an essential intermediate for the inducible expression of alpha(M)beta(2) integrin. Thus, Stat3 promotes alpha(M)beta(2) integrin expression through its activation of PU.1. These findings indicate that G-CSF-dependent Stat3 signals stimulate the changes in cell adhesion and migration capabilities that occur during myeloid cell development. These data also demonstrate a link between Stat3 and PU.1, suggesting that Stat3 may play an instructive role in hematopoiesis.
Animals↗
Efficiency of Iε promoter-directed switch recombination in GFP expression-based switch constructs works synergistically with other promoter and/or enhancer elements but is not tightly linked to the strength of transcription.
One key unresolved issue in immunoglobulin class switch recombination (CSR) is how the accessibility of the switch region for CSR is controlled. To better understand the nature of accessibility control for human Ig CSR, we developed a novel inducible switch recombination assay based on expression of green fluorescence protein (GFP) from switch constructs undergoing substrate switch recombination (SSR). Efficient SSR depends on the cytokine-inducible Iepsilon promoter and co-stimulation with IL-4+anti-CD40. Characterization of SSR reveals that both S-S deletional recombination and S-S inversion occur. We show that the IL-4-inducible Iepsilon promoter (pIepsilon) selectively determines the efficiency of the accessibility for SSR. However, the pIepsilon-induced transcription, by itself,is not sufficient to direct efficient SSR. For efficient SSR, both pIepsilon-driven transcriptional activity and an additional promoter/enhancer-derived activity are required. The efficiency of SSR is not tightly correlated with the strength of the combined transcriptional activity. Our results suggest that the mechanism(s) underlying the transcriptional activity, e.g. DNA modification is important for controlling the accessibility for efficient switch recombination.
Animals↗
Mechanism of norepinephrine-mediated inhibition of human NK cytotoxic functions: inhibition of cytokine secretion, target binding, and programming for cytotoxicity.
Norepinephrine (NE) has been shown to inhibit human peripheral blood-derived natural-killer (NK) cell cytotoxicity (NKCC) in vitro. We demonstrate in this study that NE not only inhibits IL-2-activated NKCC but antibody-dependent cellular cytotoxicity (ADCC) as well. NK cytotoxicity by purified NK cells against K562 (NKCC) and against Raji cells (ADCC) were inhibited by NE (1-100 microM) by more than 50% in a 4-h (51)Cr release assay. The mechanism underlying the inhibition has been examined. NK cytotoxicity is dependent on target recognition and formation of NK-target conjugates, and activation by IL-2 is dependent on the secretion of cytokines (such as TNF-alpha) by NK cells. We hypothesized that the inhibition of NK functions by NE may be due to disruption of NK-target conjugation, blocking programming for lysis, and/or inhibition of cytokine secretion. Pretreatment of human peripheral blood mononuclear cells (PBMC) with NE for 15 min significantly reduced the binding to K562 cells by CD16(+) NK lymphocytes. In the presence of K562 cells, NE down-regulated the expression of CD16 (FcgammaRIII) by human PBMC, an NK cell receptor responsible and necessary for ADCC and cytokine secretion. We also demonstrate that NE inhibited the IL-2-mediated up-regulation of the activation marker CD69. At concentrations of 10(-6) to 10(-5) M, NE inhibited TNF-alpha, IFN-gamma, and GM-CSF secretion by NK cells, which are essential for IL-2-driven NK maturation and functions. In addition, using single-cell analysis, NE pretreatment of lymphocytes reduced the frequency of killer cells in the NK-K562 conjugate population in a concentration-dependent manner, indicating an inhibition of the programming for lysis by NK cells. In summary, these data demonstrate that NE-induced inhibition of NK cytotoxicity is manifested at multiple levels, including a modification of NK cell receptor ligation to target cells, blockade of NK cytokine secretion necessary for NK maturation and differentiation, and inhibition of the target-induced activation of the cytotoxic mechanism(s) in NK cells. Thus, sympathetic activation, as often induced experimentally, may profoundly impair natural cellular immunity through varied measurable pathways.
Antigens, CD↗
D1 dopamine receptor regulation of cell cycle in FGF- and EGF-supported primary cultures of embryonic cerebral cortical precursor cells.
In the mammalian fetus, proliferation of the majority of cells destined for the cerebral cortex takes place within the transient proliferative zones of the cerebral wall. Recent investigations have demonstrated that cell of these zones express high levels of D1 dopamine receptors (D1Rs). However, the specific roles of these receptors have not been investigated. The present study tests the hypothesis that D1Rs are capable of regulating the cell cycle of cerebral cortical precursor cells. For this purpose, primary cultures of cells of the proliferative zones from the cerebral wall of 14-day-old mouse fetuses were generated and maintained in the presence of either fibroblast growth factor-2 (FGF2) or epidermal growth factor (EGF). These growth factors were chosen as supporting two distinct populations of precursor cells in the fetal cortical proliferative matrix. The involvement of D1Rs in the regulation of proliferative activity was examined by the addition of a range of concentrations of the D1R-specific agonist, SKF82958, to the culture media. Bromodeoxyuridine incorporation assays demonstrated that exposure to this agonist led to a dose-dependent reduction of DNA synthesis in both FGF2- and EGF-supported cultures. Flow cytometric cell cycle assays further revealed that this was due to prevention of the transition of cells from the G1 phase to the S phase of the cell cycle. The D1R specificity of the effects of SKF82958 was supported in that they were blocked by the addition of the D1R antagonists, SCH23390 or NNC010756. We also found that D1R stimulation induced stronger suppression of proliferative activity in EGF-supported than in FGF2-supported cultures. Our observations suggest that D1Rs are capable of regulating the cell cycle during corticogenesis. Furthermore, they raise a possibility that these receptors may display different efficacies in affecting proliferative activity in FGF2-supported versus EGF-supported cerebral cortical precursor cells.
Animals↗
CD40-mediated p38 mitogen-activated protein kinase activation is required for immunoglobulin class switch recombination to IgE.
BACKGROUND: Signaling through CD40 activates multiple kinases and signal pathways that drive diverse CD40-mediated biologic functions. The specific pathways activated by CD40 signaling involving CD40-dependent Ig class switch recombination (CSR) have not been defined. OBJECTIVE: We sought to dissect CD40-activated signaling required for CD40-mediated Ig CSR by using the specific signal pathway inhibitors, with the emphasis on CD40-activated p38 mitogen-activated protein kinase (p38 MAPK) signaling in CD40-mediated CSR to IgE. METHODS: Human B cells were costimulated with IL-4 plus anti-CD40 in the presence or absence of specific signal pathway inhibitors. Ig production, kinase phosphorylation, IgH epsilon germline transcripts and Smu-Sepsilon recombination were examined, and their relationships were analyzed. RESULTS: CD40-dependent IgE induction was inhibited by the specific p38 MAPK inhibitor SB203580 but not by the extracellular signal-regulated protein kinase-specific inhibitor PD98059 or the phosphatidylinositol 3-kinase-specific inhibitor LY294002. CD40 activation of p38 MAPK correlated with CD40-dependent IgE production, and IgE suppression by SB203580 correlated with the inhibition of CD40-activated p38 MAPK phosphorylation. Suppression of IgE production by SB203580 was not due to inhibition of cell proliferation because SB203580 did not suppress IL-4 plus alpha-CD40-induced cell proliferation. SB203580, but neither PD98059 nor LY294002, inhibited CD40-dependent Smu-Sepsilon recombination, as determined by using a digestion circularization PCR assay. The inhibitory effects of SB203580 on IgE production and Smu-Sepsilon recombination were directly related to its ability to suppress production of Ig epsilon germline transcripts. CONCLUSION: These results demonstrate that p38 MAPK is required for CD40-mediated class switching to IgE.
B-Lymphocytes↗
Interdisciplinary meetings: investigating the collaboration between persons with brain injury and treatment teams.
The purpose of this study was to gain an understanding of the collaboration that occurs in interdisciplinary team meetings (ITMs) at a post-acute brain injury rehabilitation centre. A qualitative descriptive case study was chosen for its interpretative and naturalistic approach. The study included participant observation of 51 meetings, five interviews, document review of charts and memos, and inductive analyses. Four themes emerged: (1) the ITM transformation ritual (the meetings themselves); (2) the ITM shapers (the case managers); (3) the ITM collaborators (the professional interdisciplinary team members); and (4) the ritual ghosts (surprisingly, the clients). Several patterns of interactions were documented, including subservient clients, lengthy meetings, and client transformation. These findings are discussed within the context of client-centred practice. The results indicate that inclusion of the client in interdisciplinary meetings does not necessarily lead to collaboration. Clinical implications and future research are discussed.
Adult↗
Comparison of the Community Integration Questionnaire, the Craig Handicap Assessment and Reporting Technique, and the Disability Rating Scale in traumatic brain injury.
OBJECTIVE: To examine the concurrent validity of the Community Integration Questionnaire (CIQ) in assessing outcomes in traumatic brain injury (TBI) by comparing it with two widely used and well-validated measurements of rehabilitation outcome. DESIGN: A retrospective relational study of the concurrent validity of the CIQ, Craig Handicap Assessment and Reporting Technique (CHART), and Disability Rating Scale (DRS). SETTING: A postacute rehabilitation facility. PARTICIPANTS: Seventy patients with a medical diagnosis of TBI admitted between April 1996 and October 1998 participated in the study. RESULTS: CIQ and CHART provide ratings that are similar in several areas to those provided by the DRS. Correlation (r) among total scores and subscales for all three instruments ranged from 0.021 to 0.671 (P <.01). Correlation between CIQ and CHART is stronger than that between CIQ and DRS or between CHART and DRS, and the correlation between CHART and DRS is stronger than that between CIQ and DRS. CONCLUSION: The CIQ appears to be the most appropriate instrument in quantifying rehabilitation outcome in patients with TBI at the participatory (handicap) level. The findings of this study can help clinicians gain a greater understanding of the nature, redundancy, and gaps among functional outcome measures. Monitoring outcomes can also help clinicians better understand the effectiveness of interventions.
Adolescent↗
Sex-specific acute effect of estrogen on endothelium-derived contracting factor in the renal artery of hypertensive Dahl rats.
OBJECTIVE: To determine whether estrogen rapidly affects endothelium-derived contracting factor (EDCF) in the renal artery of hypertensive Dahl rats, and whether factors other than nitric oxide (NO) contribute to the effect of estrogen. DESIGN: Acute effects of estrogen on the acetylcholine-induced vasomotor responses and on prostaglandin H2/thromboxane A2 mimetic, U46619,-induced contraction were examined in isolated arterial rings. METHODS AND RESULTS: Dahl salt-sensitive male and female rats were fed an 8% NaCl diet for 4 weeks. The blood pressure increased more rapidly and to a greater extent in males than in females. Renal arterial rings were prepared for isometric tension recording. 17beta-Estradiol, but not the biologically less active stereoisomer, 17alpha-estradiol, improved the relaxation response to acetylcholine in renal arteries from females. Estrogen also rapidly decreased the contraction evoked by acetylcholine (10(-6) to approximately 10(-4) mol/l) in renal arteries from females and it was effective at a physiological concentration (10(-9) mol/l) in the presence of Nomega-nitro-l-arginine methyl ester (an NO synthase inhibitor). The estrogen receptor antagonist, ICI 182,780, abolished the effect of estrogen, whereas the cytochrome P450 inhibitor, miconazole, had no effect. The contraction induced by U46619 was also suppressed by estrogen, without any contribution from NO. Estrogen had no effect on either relaxation or contraction responses in renal arteries from males. CONCLUSION: 17beta-Estradiol antagonizes increases in vascular tone in hypertensive females by enhancing NO-dependent relaxation, and by suppressing EDCF-mediated mechanisms in an NO-independent manner.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗