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Biomedical subjects

S C Wang

Publications and source records attributed to S C Wang.

At least 109 records · Page 6Linked to original sources
PubMed1996

Nuclear medicine training in china.

There are diverse approaches to the teaching of nuclear medicine in China: (1) Nuclear medicine is taught as part of the clinical curriculum in most medical schools. (2) Three medical schools undertake undergraduate training in nuclear medicine. (3) Four medical schools train nuclear medicine specialists to graduate level. (4) Eight medical schools have been authorized to provide a postgraduate programme in nuclear medicine leading to an M.S. degree. Among them, four are also permitted to offer Ph.D. degrees. (5) No less than 20 medical schools offer a course in "Isotope techniques and their biomedical applications" for graduate students in various fields of medicine. (6) Many departments of nuclear medicine in medical schools offer short-term training courses or continuing education workshops on specific topics in nuclear medicine. (7) Some schools of pharmacy offer radiopharmacy courses. (8) Members of staff undergo in-service training in computer science, foreign languages, radiology, etc. (9) Graduate students and more senior scientists or physicians are sent abroad to pursue advanced training. (10) Foreign students have been admitted to our nuclear medicine centres for further training. (11) Exhibitions, summer camps and radio broadcasts have been used to inform the community of the usefulness of nuclear medicine.

China↗
PubMed1996

The relaxivity of Gd-EOB-DTPA and Gd-DTPA in liver and kidney of the Wistar rat.

The NMR relaxivities of Gd-EOB-DTPA and Gd-DTPA were determined in the kidney and liver of intact male Wistar rats immediately following sacrifice and in vitro in solutions and gels, at 1.5 T using a clinical MR scanner, T1 and T2 values of tissue samples were derived from spin-echo image sequences. Tissue gadolinium concentrations were determined by radioassay of Gd153, Gd-EOB-DTPA T1 and T2 relaxivities, R1 and R2 (s-1 mmole-1 kg), were found to be 10.7 +/- 0.5 and 22.5 +/- 3.2 respectively, for liver, 2.4 +/- 0.2 and 12.1 +/- 1.7 for kidney cortex, 2.7 +/- 0.2 and 14.5 +/- 1.9 for kidney outer medulla, 2.0 +/- 0.2 and 11.4 +/- 2.1 for kidney inner medulla. Gd-DTPA R1 and R2 were found to be 4.8 +/- 0.4 and 14.5 +/- 3.7 for liver, 1.2 +/- 0.1 and 7.9 +/- 0.8 for kidney cortex, 1.6 +/- 0.1 and 10.2 +/- 1.4 for kidney outer medulla, 1.3 +/- 0.1 and 10.2 +/- 1.2 for kidney inner medulla. Gd-EOB-DTPA and Gd-DTPA R1 was increased in liver compared to agarose gets at 38 degrees C (4.49 +/- 0.03 and 3.47 +/- 0.06), but reduced in kidney tissues. All R2 were elevated compared to agarose gels at 38 degrees C (5.72 +/- 0.12 and 4.12 +/- 0.03). Elevated R2 and R1 (expressed in terms of the concentration of gadolinium per kg of tissue) can be accounted for in part by the lower water content of tissues compared with gels or solutions increased microviscosity and binding to macromolecules. In addition, susceptibility effects may give rise to further increases in R2. By contrast, the reduced R1 observed in kidney may be the result of compartmentalization of the magnetopharmaceuticals. Statistically improved fits were obtained for T1 recovery curves for liver in the presence of Gd-EOB-DTPA when a dual exponential model was used. Assuming in vitro values for the relaxivities of these artificial contrast agents will lead to inaccuracies when relating observed signal enhancement factors to tissue gadolinium concentration.

Animals↗
PubMed1996

Expression of an oncofetal 65-kDa phosphoprotein in lymphocytic and granulocytic leukemias.

We examined the expression of an oncofetal 65-kDa phosphoprotein, termed p65, in patients with lymphocytic and granulocytic leukemia. This protein was previously identified in rat fetal tissues and in epithelial cancers of rat and human origin. Using the anti-p65 monoclonal antibodies MB2 and MF11 in a double-antibody sandwich enzyme-linked immunosorbent assay (ELISA), we analyzed the expression of the protein in sera of 80 normal, healthy controls and in 61 patients with benign, nonneoplastic diseases. We established that the upper level of normal p65 concentration is 115 U/ml p65 (mean plus two standard deviations above the mean in a control group). We also analyzed p65 levels in sera of 71 patients with leukemia in different stages of development. The level of p65 was well above normal in 95% of acute lymphocytic leukemia (ALL; 19 cases), 83% of acute myeloblastic leukemia (AML; 23 cases), 37% of chronic lymphocytic leukemia (CLL; 19 cases), and 30% of chronic myelogenous leukemia (CML; 10 cases). MB2 monoclonal antibodies were used for immunocytochemical staining of isolated lymphocytes from normal peripheral blood and from blood of leukemic patients (in 12 CLL patients, the p65 positivity was 83%, in 2 ALL patients, 100%, and in 4 AML patients, 75%). Our data suggest that p65 protein may be of use as a tumor marker in leukemia.

Adult↗
PubMed1996

Blunt force injury of the abdominal aorta.

OBJECTIVE: To review the clinical presentation, diagnosis, and management of injury to the abdominal aorta after blunt force trauma. DESIGN: This study was a retrospective review. RESULTS: A total of 5,676 patients were admitted to the University of Michigan Medical Center with traumatic injury. Seven had injuries to the abdominal aorta after a blunt force mechanism. Five patients had operative repair of the aortic injury, of which four involved orthotopic graft placement and one had an extra-anatomic bypass. Two patients had the aortic injury repaired by endovascular stent placement in the angiography suite. One patient died, and lower extremity amputations were performed in three patients. CONCLUSIONS: Surgical repair of abdominal aortic injury is preferable for the unstable patient or those with threatened extremities. In the stable patient with viable limbs, treatment with radiologic placement of endovascular stents may provide a nonoperative option for management.

Adult↗
PubMed1996

[Experimental study of R plasmid eliminating action of Coptis chinensis on E. coli].

The R plasmid curing experiment was performed in vitro with E. coli strain E. 102 bearing R plasmid as target bacteria and Coptis chinensis as elimination agent. The influence of different time on R plasmid elimination was also observed. Results showed that when the acting time was 24 hours, the cure rate of R plasmid was 2.42% and when the acting time increased to 48 hours, the cure rate elevated to 22.57%. The Missing patterns of R plasmid might be occurred in disappearence of either multiple or single resistance.

Drugs, Chinese Herbal↗
PubMed1996

Decreased tubular reabsorption of zinc in rats with chronic uremia.

Effect of chronic uremia on tubular reabsorption of zinc was studied in rats with different zinc nutritional status. Using inulin clearance to represent glomerular filtration rate and plasma ultrafiltrate to imitate glomerular filtrate in vivo, the glomerular filtered load of zinc was estimated in each rat. The amount of tubular reabsorption of zinc equals the amount of zinc filtered minus the amount of zinc excreted into the urine. Proportion of filtered zinc excreted was estimated to be 2.8-8.7% in control rats and 17.3-29.8% in uremic rats induced by five-sixths nephrectomy. Similarly, proportion of filtered zinc reabsorption decreased significantly from 91.3-97.3% in control rats to 70.1-82.7% in uremic rats. Zinc deficiency increased fractional reabsorption of zinc in uremic rats but not in control rats. Fractional excretion of zinc correlated with both urine flow rate and urinary excretion of protein. The results suggest that uremia toxins may influence tubular reabsorption of zinc even in the presence of renal adaptation to zinc deficiency.

Animals↗
PubMed1995

The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain.

STUDY DESIGN: A prospective cross-sectional analytic study. OBJECTIVES: To assess in patients with chronic low back pain whether the presence or absence of pain originating from the lumbar zygapophysial joints correlates with changes seen on computed tomography. SUMMARY OF BACKGROUND DATA: Results of studies have been divided as to whether or not radiologic imaging is able to predict those patients with pain originating from the zygapophysial joints. METHODS: Sixty-three patients with low back pain lasting for longer than 3 months underwent computed tomography and blocks of the zygapophysial joints at L5-S1, L4-L5, and L3-L4. The zygapophysial joints of all images were scored by three independent, masked radiologists. RESULTS: Interobserver agreement was poor with intraclass correlation coefficients of 0.34-0.66 using total joint scores for all three assessors. Using the results of a repeat assessment with two radiologists there was no statistically significant difference in joint scores between those with and those without pain originating from the zygapophysial joint. CONCLUSIONS: Computed tomography has no place in the diagnosis of lumbar zygapophysial joint pain.

Adult↗
PubMed1995

Cytokine mRNA profiles in mouse orthotopic liver transplantation. Graft rejection is associated with augmented TH1 function.

Although mouse liver allografts are spontaneously accepted without immunosuppression in many strain combinations, rejection can be induced by presensitization with a donor skin graft two weeks prior to transplantation. In this study, the semiquantitative reverse transcription polymerase chain reaction (RTPCR) was used to assess the involvement of T helper (TH) cell subsets in liver allograft acceptance by determining cytokine mRNA in the graft and spleen of recipients with (A) spontaneously accepting allografts (B) rejecting liver allografts after previous skin sensitization, and (C) syngeneic controls. Spontaneously accepted liver allografts showed upregulation of TH1 (IL-2, IFN-gamma) and TH2 (IL-4, IL-10) intragraft cytokine mRNA, which peaked at day 6 and tapered off thereafter, when compared with levels in syngeneic grafts, but both IFN-gamma and IL-10 mRNA persisted up to day 30. This cytokine mRNA profile correlated with the transient intragraft inflammation associated with spontaneously resolving rejection. Presensitized recipients that rejected their grafts revealed marked upregulation of TH1 (IL-2 and IFN-gamma) and TH2 (IL-4, IL-6) intragraft cytokine mRNAs compared with spontaneously accepting recipients, although IL-10 mRNA levels showed no differences between the two groups. The most striking difference was seen in IFN-gamma levels, which correlated well with the preferential deposition of IgG2a antibody isotype in the rejecting compared with the spontaneously accepting liver allograft recipients. These results suggested an association between liver allograft rejection and enhanced TH1 cytokine immune response. The ability to reject liver allografts by the adoptive transfer of splenocytes, but not serum, from a sensitized mouse ruled out preformed antibodies alone as a cause of rejection. However, spleen cytokine mRNA profiles showed no differences or trends in TH1 or TH2 expression in spontaneously accepting versus rejecting recipients, which suggested that the spleen is not a major site of alloreactive immune expansion. These data suggest that spontaneous acceptance of mouse liver allografts is associated with an insufficient intragraft TH1 cytokine response, the cause of which is currently under investigation.

Animals↗
PubMed1995

Cyclic GMP and guanylate cyclase mediate lipopolysaccharide-induced Kupffer cell tumor necrosis factor-alpha synthesis.

Tumor necrosis factor-alpha (TNF-alpha) is an important mediator in sepsis and septic shock. Kupffer cells (KCs) are the resident macrophages of the liver and are potent producers of TNF-alpha in response to inflammatory stimuli such as bacterial endotoxin or lipopolysaccharide (LPS). Although the effects of exogenous cytokines such as interferon-gamma on TNF-alpha production by macrophages have been fairly well studied, the intracellular pathways regulating KC TNF-alpha synthesis are largely unknown. We investigated the role of guanylate cyclase and cGMP in LPS-induced KC TNF-alpha synthesis. Exogenous 8-BrcGMP and dbcGMP increased LPS-stimulated TNF-alpha synthesis but had no effect on KC TNF-alpha in the absence of LPS. Sodium nitroprusside (SNP), a nitric oxide-releasing substance that stimulates guanylate cyclase, increased TNF-alpha synthesis in response to LPS, whereas methylene blue and LY83583, guanylate cyclase inhibitors, decreased KC TNF-alpha synthesis. The inhibitory effect of methylene blue could be overcome with exogenous dbcGMP or SNP. Our results demonstrate that guanylate cyclase and cGMP mediate LPS-induced KC TNF-alpha synthesis and suggest that agents that alter cyclic nucleotide metabolism in KCs may affect the response of these cells to inflammation and inflammatory stimuli.

Aminoquinolines↗
PubMed1995

Evidence for LFA-1/ICAM-1 dependent stimulation of protein tyrosine phosphorylation in human B lymphoid cell lines during homotypic adhesion.

JK32.1 and SKW6.4 are Epstein-Barr virus (EBV)-positive human B cell lines that undergo spontaneous, lymphocyte function-associated antigen 1 (LFA-1) dependent homotypic adhesion in culture. This process is associated with induction of tyrosine phosphoproteins of molecular mass 90, 106, and 120 kDa and could be reproduced when these cells were centrifugationally aggregated. Antibodies to the beta 2 (CD18) chain of LFA-1 interfered with induction of p120, p106, and p90 during cellular aggregation. Response induction was abrogated when cells were incubated with protein tyrosine kinase (PTK) inhibitors (erbstatin, genistein, and geldanomycin) or cytochalasin B prior to aggregation. An in vitro kinase assay did not reveal activation of focal adhesion kinase. Although the role of LFA-1-dependent tyrosine phosphorylation in B cells is uncertain, patients with the leukocyte adhesion defect (LAD) exhibit humoral abnormalities. Moreover, aggregation did not induce specific tyrosine phosphoproteins in an EBV-transformed B cell line from a LAD patient. These results suggest that an LFA-1-dependent PTK pathway may play an important role in human B cell function.

Antibodies, Monoclonal↗
PubMed1995

Role of lipopolysaccharide (LPS), interleukin-1, interleukin-6, tumor necrosis factor, and dexamethasone in regulation of LPS-binding protein expression in normal hepatocytes and hepatocytes from LPS-treated rats.

Lipopolysaccharide (LPS)-binding protein (LBP) has been reported to be an acute-phase protein. LBP binds to LPS with a high affinity; LPS-LBP complexes then interact with the receptor CD14, resulting in increased expression of LPS-inducible genes. Hepatocytes represent a major source of LBP, but little is known about the regulation of rodent hepatocyte LBP synthesis. In these studies, undertaken to characterize hepatocyte LBP expression, we show that greater-than-20-fold increases in LBP mRNA levels in hepatocytes occurred following injection of LPS or turpentine in rats. In primary cultures of rat hepatocytes, the addition of interleukin-6 (IL-6) and LPS led to 4.5- and 3.2-fold stimulation in LBP mRNA levels, respectively. The induction of LBP by IL-6 or LPS was attenuated by dexamethasone. In contrast to IL-6 and LPS, in the presence of 10(-6) M dexamethasone, IL-1 and tumor necrosis factor (TNF) led to maximal LBP mRNA induction levels, 4.7- and 3.8-fold, respectively, suggesting that IL-6 and LPS stimulate LBP expression by mechanisms different from those of IL-1 and TNF. Similar induction levels of LBP mRNA were seen in rat H35 hepatoma cells for all four stimuli, and dexamethasone inhibited these responses. Dexamethasone alone increased the spontaneous induction in primary hepatocytes at early time points but suppressed induction at later time points. Furthermore, hepatocytes from rats treated with LPS in vivo exhibited a > 10-fold increase in mRNA expression in response to LPS and enhanced responses to TNF and IL-1. As with the normal hepatocytes, dexamethasone inhibited the LPS-dependent induction in the LPS-treated rat hepatocytes. These data suggest that LBP synthesis by hepatocytes is under the control of LPS, IL-1, TNF, IL-6, and glucocorticoids and that the LPS treatment primes hepatocytes for subsequent responses to LPS, TNF, and IL-1 for LBP synthesis.

Acute-Phase Proteins↗
PubMed1995

Prevalence and clinical features of lumbar zygapophysial joint pain: a study in an Australian population with chronic low back pain.

OBJECTIVES: To determine the prevalence of pain arising from the zygapophysial joint in patients with chronic low back pain and to determine whether any clinical features could distinguish patients with and without such pain. METHODS: Sixty three patients with chronic low back pain were studied prospectively. All patients underwent a detailed history and physical examination as well as a series of intra-articular zygapophysial joint injections of 0.5% bupivacaine starting at the symptomatic level to a maximum of three levels or until the pain was abolished. They also received injections of normal saline into paraspinal muscles to act as controls. RESULTS: All patients proceeded with the injections. Twenty (32%; 95% confidence interval (CI) 20 to 44%) obtained greater than 50% relief of their pain following the administration of saline. Fifty seven patients completed the study; 23 of them (40%; 95% CI 27 to 53%) failed to obtain relief following the injection of saline but obtained relief following one or more intra-articular injections of local anaesthetic. None of the historical features or clinical tests could discriminate those patients with and those without zygapophysial joint pain. CONCLUSION: Pain originating from the zygapophysial joint is not uncommon, but this study failed to find any clinical predictors in patients with such pain.

Aged↗
PubMed1995

Induction of lipopolysaccharide-binding protein gene expression in cultured rat pulmonary artery smooth muscle cells by interleukin 1 beta.

Lipopolysaccharide (LPS)-binding protein (LBP) binds with high affinity to LPS, and the LBP-LPS complex enhances cellular inflammatory responses to LPS. Although it is present in normal serum, LBP is also induced as part of the acute phase response. Synthesis of LBP is though to be limited to the liver, but we have recently reported significant extrahepatic (including pulmonary) LBP mRNA expression in in vivo rat models of sepsis and inflammation. In the present study, we tested the hypothesis that a cellular source of pulmonary LBP in the rat may be vascular smooth muscle, by exposing cultured rat pulmonary artery smooth muscle cells (RPASMC) to cytokines and LPS. Treatment of RPASMC for 4 and 24 h with a combination of tumor necrosis factor alpha, interleukin 1 beta (IL-1 beta), interferon gamma, and LPS resulted in significant LBP mRNA expression. Of this mixture, IL-1 beta alone was sufficient to induce LBP mRNA expression in both a time- and dose-dependent manner. The effects of IL-beta on LBP mRNA expression were significantly antagonized by IL-1 receptor antagonist protein. Furthermore, supernatants from RPASMC treated with IL-1 beta enhanced the binding of [125I]ASD-LPS by the macrophage cell line RAW 264.7, indicative of LBP bioactivity. We conclude that pulmonary artery smooth muscle cells stimulated with IL-1 beta produce a transcript for LBP or a homologous product in vitro. Local production of LBP could play an important role in the pulmonary response to inflammation and sepsis.

Acute-Phase Proteins↗
PubMed1995

Lipopolysaccharide binding protein participation in cellular activation by LPS.

Lipopolysaccharide binding protein (LBP) is a plasma protein that plays an important intermediary role in host-endotoxin (LPS) interactions. LBP binds with high affinity to the lipid A portion of LPS and then interacts with the monocytic differentiation antigen CD14 to markedly up-regulate TNF-alpha production by mononuclear phagocytes. In the presence of LBP, 100-fold less LPS is required to trigger this cytokine response. LBP has been implicated in the interaction of LPS with both CD14+ (monocytes, macrophages, neutrophils) and CD14-cells (endothelial and epithelial cells) to promote such varying responses as secretion of cytokines and nitric oxide (NO), expression of adhesion molecules, production of tissue factor, and activation of neutrophils. Non-CD 14-bearing cells, such as endothelial cells, can also respond to LPS through this pathway via the soluble form of CD14, an interaction that is similarly enhanced by LBP. Recently, it has been proposed that LBP cannot only potentiate host responses to LPS but can also facilitate the neutralization of LPS under certain conditions. LBP has been described as acting as a lipoprotein transfer protein facilitating the transfer of LPS both to the target receptor (CD14) and lipoprotein (HDL).

Acute-Phase Proteins↗
PubMed1994

Molecular cloning, characterization, and tissue distribution of rat lipopolysaccharide binding protein. Evidence for extrahepatic expression.

LPS binding protein (LBP) is a glycoprotein present in normal serum that becomes markedly elevated during acute phase responses. LBP has been reported to greatly potentiate host responses to endotoxin or LPS. Therefore, LBP may play a critical role in the body's response to injury and infection. Little is known about the factors regulating production of LBP. To investigate the regulation of LBP expression, we have cloned the full-length cDNA for rat LBP. The deduced amino acid sequence of rat LBP was highly homologous with that reported for rabbit and human LBP. The sequence of rat LBP further refines the conserved regions found within the family of proteins that bind LPS; this family is comprised of bactericidal permeability-increasing protein and LBP from multiple species. Use of the rat LBP cDNA clone for Northern blot analysis reveals that LBP mRNA levels are markedly up-regulated in liver during acute phase responses. However, in contrast to previous reports, we also find evidence of extrahepatic expression of LBP under these induced conditions. The presence of LBP mRNA in activated tissues other than liver suggests that LBP may play a larger role in local tissue responses to LPS than previously appreciated.

Acute-Phase Proteins↗
PubMed1994

Activation of a novel serine/threonine kinase that phosphorylates c-Fos upon stimulation of T and B lymphocytes via antigen and cytokine receptors.

Ligation of Ag receptors in T and B lymphocytes initiates signal transduction cascades which alter the expression of genes that regulate cellular proliferation and differentiation. The transmission of signals from the membrane to the nucleus is mediated principally through the action of protein tyrosine and serine/threonine kinases. We have identified and characterized a novel serine/threonine kinase that phosphorylated the proto-oncogene product, c-Fos, and is termed Fos kinase. Fos kinase was rapidly activated after ligation of the CD3 and CD2 receptors in Jurkat and normal human T lymphocytes and in response to IL-6 and anti-IgM in the human B cell lines AF10 and Ramos, respectively. The phorbol ester, PMA, was also a potent inducer of Fos kinase activity in all of the above populations, suggesting that PKC plays a role in the regulation of this enzyme. Fos kinase phosphorylates c-Fos at a site near the C-terminus, as well as a peptide derived from this region (residues 359-370, RKGSSSNEPSSD), and Fos peptide competitively inhibited c-Fos phosphorylation. Fos kinase was shown to be distinct from other identified serine/threonine kinases, including protein kinase A, protein kinase C, casein kinase II, MAP kinases, p70S6K and p90RSK. Fos kinase was purified by anion exchange chromatography and exhibited an apparent M(r) = 65,000 and isoelectric point = 6.1. Fos kinase may play a role in transcriptional regulation through its capacity to phosphorylate c-Fos at a site required for expression of the transcriptional transrepressive activity of this molecule. Moreover, its rapid activation suggests it may have a wider role within signal transduction cascades in lymphocytes.

Amino Acid Sequence↗
PubMed1994

Differential induction of nitric oxide synthase in hepatocytes during endotoxemia and the acute-phase response.

OBJECTIVE: Nitric oxide (NO) is a potent biologic mediator produced by hepatocytes following exposure to cytokines and lipopolysaccharide (LPS). These cytokines are also known to regulate induction of the hepatic acute-phase response. The objective of this study was to determine whether inducible nitric oxide synthase (iNOS), the enzyme that produces NO, is expressed as part of the hepatic acute-phase response. DESIGN: The gene expression for inducible NOS (iNOS) as well as alpha 1-acid glycoprotein (AGP), an established acute-phase reactant, was measured by Northern blot analysis in rat hepatocytes in vivo during endotoxemia (LPS injection) and during the acute-phase response produced by hindlimb turpentine injection. Hepatocyte iNOS messenger RNA (mRNA) levels were correlated with iNOS activity and circulating plasma nitrite and nitrate levels. In vitro, iNOS and AGP mRNA levels were determined in cultured hepatocytes stimulated with interleukin 6 (IL-6), interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), or dexamethasone. RESULTS: The AGP mRNA levels were increased in vivo following both LPS and turpentine injection, while iNOS expression was induced only by LPS injection. Hepatocyte iNOS activity and plasma nitrite and nitrate levels also increased after LPS treatment. In vitro, the cytokine combination IL-6, IL-1 beta, and TNF-alpha induced hepatocyte iNOS expression but had minimal effects on AGP in the absence of dexamethasone. Addition of dexamethasone alone markedly increased AGP mRNA levels, with further increases seen with TNF-alpha or IL-1 beta addition. In contrast, dexamethasone decreased iNOS expression. CONCLUSION: The results show that hepatocyte iNOS expression is not part of the acute-phase response induced by remote inflammation and indicates that iNOS is differentially regulated from the acute-phase reactant, AGP.

Acute-Phase Reaction↗