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Biomedical subjects

C L Yang

Publications and source records attributed to C L Yang.

At least 37 records · Page 2Linked to original sources
PubMed1999

Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice.

NHE3 is the predominant isoform responsible for apical membrane Na(+)/H(+) exchange in the proximal tubule. Deletion of NHE3 by gene targeting results in an NHE3(-/-) mouse with greatly reduced proximal tubule HCO(-)(3) absorption compared with NHE3(+/+) animals (P. J. Schultheis, L. L. Clarke, P. Meneton, M. L. Miller, M. Soleimani, L. R. Gawenis, T. M. Riddle, J. J. Duffy, T. Doetschman, T. Wang, G. Giebisch, P. S. Aronson, J. N. Lorenz, and G. E. Shull. Nature Genet. 19: 282-285, 1998). The purpose of the present study was to evaluate the role of other acidification mechanisms in mediating the remaining component of proximal tubule HCO(-)(3) reabsorption in NHE3(-/-) mice. Proximal tubule transport was studied by in situ microperfusion. Net rates of HCO(-)(3) (J(HCO3)) and fluid absorption (J(v)) were reduced by 54 and 63%, respectively, in NHE3 null mice compared with controls. Addition of 100 microM ethylisopropylamiloride (EIPA) to the luminal perfusate caused significant inhibition of J(HCO3) and J(v) in NHE3(+/+) mice but failed to inhibit J(HCO3) or J(v) in NHE3(-/-) mice, indicating lack of activity of NHE2 or other EIPA-sensitive NHE isoforms in the null mice. Addition of 1 microM bafilomycin caused a similar absolute decrement in J(HCO3) in wild-type and NHE3 null mice, indicating equivalent rates of HCO(-)(3) absorption mediated by H(+)-ATPase. Addition of 10 microM Sch-28080 did not reduce J(HCO3) in either wild-type or NHE3 null mice, indicating lack of detectable H(+)-K(+)-ATPase activity in the proximal tubule. We conclude that, in the absence of NHE3, neither NHE2 nor any other EIPA-sensitive NHE isoform contributes to mediating HCO(-)(3) reabsorption in the proximal tubule. A significant component of HCO(-)(3) reabsorption in the proximal tubule is mediated by bafilomycin-sensitive H(+)-ATPase, but its activity is not significantly upregulated in NHE3 null mice.

Absorption↗
PubMed1999

[Relationship between the familial nonrandom chromosome loss (NCL) and leukomogenesis].

By using R-banding karyotypic analysis technique, the bone marrow (BM) cells were performed in 223 hematopoietic malignacies and 105 diopathic throbocytopenic purpura (ITP), which served as control. The following results were obtained: (1) Nonrandom chromosome loss (NCL), such as, -11, -14, -21, etc, which were found in the affected members of leukemia families, were found in about 30% sporadic ANLL, MDS and about 50% ALL, espedislly in 100% (5/5) CLL, but not found in ITP (P < 0.001). These results indicated that the familial nonrandom chromosome loss were associated with leukomogenesis. (2) Because most of BM cells are hypodiploed and have the same kinds of NCL in each cases of CLL, which can develop into ALL, ANLL and also cancers, ALL BM hypo- and hyper-diploid and/or polyploid cells might be origin of hypodiploid cells. (3) 28% (6/21) of pediatric patients with AL, MDS, or FA (Fanconi Anemia) have one parent, who have up to 30% BM hypodiploid cells and similar kinds of NCL and also have the rearrangement of C-erbB and abnormal proliferation of BM. The NCL were found in the three consecutive generations of a family with 5 ALL among 10 members of third generation. It indicated that the familial NCL might be inherited and be coded by a unknown gene alteration, which might be related to leukomo and carcinogenesis, because there are genes or their candidates for leukemia in the chromosomes 11, 14 and 21. (4) Based on the works of my colleages and I, the model of leukomo and carcinogenesis was proposed and the relationship between chromosome monosomy, deletion, translocations and leukomogenesis were showed elswhere. The significance of monosomy 11, 14 and 21 etc. were discussed briefly.

Bone Marrow Cells↗
PubMed1998

Role of neuropeptide Y in cold stress-induced hypertension.

Chronic cold stress (4 degrees C) produced a sustained increase in mean arterial pressure in both normotensive and borderline hypertensive rats (BHR). The high blood pressure in BHRs was significantly reversed by a neuropeptide Y (NPY) Y1 receptor antagonist suggesting that NPY is involved in mediating stress-induced hypertension. Corresponding increases in adrenal NPY messenger RNA and NPY immunoreactivity were found during the stress; furthermore, chronic cold stress also potentiated the pressor response of rats to a subsequent acute stress test in which NPY has been shown to play a role. These results suggest that chronic cold stress-induced hypertension is mediated by elevated NPY release and vascular tone as a result of increased NPY gene expression and storage.

Adrenal Glands↗
PubMed1998

Characterization of recombinant type II collagen: arthritogenicity and tolerogenicity in DBA/1 mice.

Recombinant human type II collagen (rhCII) was produced using both the HT1080 mammalian cell expression system (rhCIIht) and a baculovirus expression system (rhCIIbac). The biosynthesis of CII requires extensive post-translational modifications, such as the hydroxylation of prolyl and lysyl residues and glycosylation of hydroxylysyl residues. Amino acid analyses indicated that the rhCIIbac was adequately hydroxylated at prolyl residues but underhydroxylated at lysyl residues and underglycosylated compared with tissue-derived hCII, while rhCIIht was hyperhydroxylated and hyperglycosylated at lysyl residues. When the murine collagen-induced arthritis (CIA) model was used to investigate the immunological properties of the two forms of recombinant CII, each induced a high incidence of arthritis following immunization of susceptible mice when emulsified with complete Freund's adjuvant (CFA). However, the severity of the arthritis, as assessed by the number of affected limbs, was significantly higher in mice immunized with rhCIIht than in mice immunized with rhCIIbac. These data indicate that the degree of hydroxylysine glycosylation may play a role in the induction of the arthritogenic response to CII. Each of the recombinant collagens was comparable to tissue-derived hCII in their ability to induce tolerance and suppress arthritis when given as intravenous or oral tolerogens. Taken together, our data suggest that recombinant CII can be prepared in adequate amounts for therapeutic uses and that the material is immunologically comparable to tissue-derived hCII when used to induce tolerance.

Administration, Oral↗
PubMed1998

Direct evidence for the role of neuropeptide Y in sympathetic nerve stimulation-induced vasoconstriction.

Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter with norepinephrine (NE) in sympathetic nerve terminals and is thought to be involved in sympathetic nerve stimulation (SNS)-induced vasoconstriction. Using BIBP-3226, a Y1 receptor selective antagonist, we examined this hypothesis in the isolated and perfused mesenteric vascular bed. SNS produced a frequency-dependent increase in perfusion pressure and concomitant overflow of NPY immunoreactivity in the perfusate. [Leu31,Pro34]NPY potentiated NE-induced and ATP-induced vasoconstriction, indicating the presence and biological action of Y1 receptors in this vascular bed. The potentiation effect of [Leu31,Pro34]NPY of the increase in perfusion pressure by NE, ATP, or SNS was prevented by BIBP-3226. In addition, SNS-induced vasoconstriction at both high and low frequencies was significantly attenuated by BIBP-3226 at a concentration that completely blocked the [Leu31,Pro34]NPY-induced potentiation of the NE- or ATP-induced vasoconstrictor effect. These results suggest that approximately 30% of vasoconstriction produced by SNS depends on NPY in the mesenteric vascular bed.

Animals↗
PubMed1998

Rosai-Dorfman disease with primary cutaneous manifestations--a case report.

Rosai-Dorfman disease (sinus histiocytosis with massive lymphadenopathy) is a benign systemic proliferative disorder of histiocytes resembling the sinus histiocytes of lymph nodes. The typical clinical features of this disease include bilateral painless lymphadenopathy, fever, and polyclonal hyperglobulinaemia. The condition may present with extranodal involvement in 43% of cases, and cutaneous lesions are the most common form of extranodal diseases. However, purely cutaneous Rosai-Dorfman diseases occur rarely, particularly among Orientals. We describe a 48-year-old female presenting with an erythematous dermal nodule on the abdomen. Complete physical examinations and laboratory tests demonstrated that the lesion was only limited to the skin. Histologically, the lesion consisted of proliferative large histiocytes frequently exhibiting emperipolesis. Immunohistochemical and ultrastructural studies were also performed. The former showed characteristic cytoplasmic staining of histiocytes against S-100 protein. Because cutaneous Rosai-Dorfman disease may be unfamiliar to most pathologists, cases limited to the skin are probably underestimated.

Abdomen↗
PubMed1997

Sodium/hydrogen exchanger gene defect in slow-wave epilepsy mutant mice.

The "housekeeping" sodium/hydrogen exchanger, NHE1, mediates the electroneutral 1:1 exchange of Na+ and H+ across the plasma membrane. NHE1 is ubiquitous and is studied extensively for regulation of pHi, cell volume, and response to growth factors. We describe a spontaneous mouse mutant, slow-wave epilepsy, (swe), with a neurological syndrome including ataxia and a unique epilepsy phenotype consisting of 3/sec absence and tonic-clonic seizures. swe was fine-mapped on Chromosome 4 and identified as a null allele of Nhe1. Mutants show selective neuronal death in the cerebellum and brainstem but otherwise are healthy. This first example of a disease-causing mutation in an Nhe gene provides a new tool for studying the delicate balance of neuroexcitability and cell survival within the CNS.

Animals↗
PubMed1996

Overexpression of the natural recO sequence and its effects on DNA repair of Escherichia coli.

The recO gene is required for the RecF pathway of recombination and the repair of DNA daughter-strand gaps in Escherichia coli. In this work, the structural portion of recO was synthesized by the polymerase chain reaction (PCR) and cloned onto expression vectors at their Nco1 fusion cloning site, to eliminate the presence of mRNA leader sequence. While the plasmid carrying a Ptac promoter failed to overproduce RecO, the plasmid carrying a T7O10 promoter overproduced RecO in large quantity, indicating that the natural recO may be overexpressed. An increase of intracellular RecO, which may be due to the increased recO gene copies or to the induction of RecO synthesis, increased the UV resistance of recA, recF, and ssb cells, but did not increase the UV resistance of uvrB, uvrB recF, uvrB recA and uvrB ssb cells. We suggest that an increase of intracellular RecO may allow some recombination-deficient cells to perform more excision repair, thus increasing the survival. The possible causes for RecO overproduction on excision repair, and for the differential expression of recO by the Ptac and T7 promoter plasmids are discussed.

Bacterial Proteins↗
PubMed1996

Neuropeptide Y-ATP interactions and release at the vascular neuroeffector junction.

1. The ability of neuropeptide Y (NPY) to potentiate the contractile effect of ATP was examined using the perfused mesenteric arterial bed as a model of the vascular neuroeffector junction. 2. NPY (10(-9)-10(-7) M) and the NPY-Y1 selective agonist, Leu31Pro34 NPY (10(-9)-10(-7) M) both produced a concentration dependent potentiation of the ATP (1 and 3 mM) induced increase in perfusion pressure while the NPY-Y2 selective agonist, NPY 14-36 did not. 3. The NPY-Y1 selective antagonist BIBP 3226 (10-100 nM) produced a significant concentration dependent blockade of the Leu31Pro34 NPY (30 nM) induced potentiation of the ATP (3 mM) induced increase in perfusion pressure. These results are consistent with the NPY-induced potentiation of ATP effect being due to activation of the NPY-Y1 receptor subtype. 4. Periarterial nerve stimulation (supramaximal voltage, 8 and 16 Hz, 30s caused a release of ATP, as well as metabolites, from the perfused mesenteric arterial bed. KCl evoked (50 mM, 5 min) release of ATP from nerve growth factor (NGF) differentiated PC12 cells. 5. Endothelin-1 (ET-1) produced a concentration dependent (10(-15)-10(-8) M) inhibition of the K-1-evoked release of ATP from NGF-differentiated PC12 cells. This effect was mimicked by the selective ETB agonists, BQ 3020, STX-6C and IRL 1620. The ETA/ETB antagonist PD142893 blocked the inhibitory effect of ET-1. These results are consistent with the ET-1 induced inhibition of the evoked release of ATP being due to activation of ETB receptors.

Adenosine Triphosphate↗
PubMed1995

Effects of lipids on intestinal adaptation following 60% resection in rats.

The effects of long-chain triglycerides (LCT) and of medium-chain triglycerides (MCT) on intestinal adaptation in rats were compared following a 60% resection of intestine. Sixty Long-Evans rats were divided into four groups: control (sham-operated) rats fed an MCT-enriched diet, control rats fed an LCT-enriched diet, experimental rats fed an MCT-enriched diet, and experimental rats fed an LCT-enriched diet. In the MCT-enriched diet, 90% of the fat was MCT; in the LCT diet, 90% was LCT. In each diet, 31-32% of daily caloric intake came from fat. All diets were isocaloric and isonitrogenous. Following the 60% intestinal resection from the mid-portion of the small intestine, there were significant increases in mucosal height, villous height, villous width, and crypt depth (P < 0.05). Gut weight, mucosal weight, protein and DNA content, and DNA synthetic rate also increased. In the ileum, rats receiving the LCT diet showed greater increases in gut weight, mucosal weight, crypt depth, protein and DNA content, and DNA synthetic rate than the MCT rats did (P < 0.05). In the jejunum, however, the differences were not statistically significant. In both the jejunum and the ileum, the response of the intestine was greater closer to the anastomotic site (P < 0.05). Results of these studies demonstrated that LCT had a better effect than MCT on intestinal response both structurally and functionally.

Adaptation, Physiological↗
PubMed1995

Synergy between signal transduction pathways is obligatory for expression of c-fos in B and T cell lines: implication for c-fos control via surface immunoglobulin and T cell antigen receptors.

Expression of the protooncogene c-fos is controlled by three main regulatory pathways involving kinase C, cAMP, and calcium. Kinase C mediates its effects via phosphorylation of serum response factor (SRF) which interacts with the serum response element (SRE); cAMP and calcium mediate their effects via phosphorylation of CREB (cAMP regulatory element binding protein) presumably by activation of a protein kinase A or calmodulin-regulated kinase. We have examined the function of these elements in Burkitt's lymphoma cells (Ramos and Daudi) as well as a T lymphocytic cell line (Jurkat). We have found that stimulation of any one of these pathways alone has little or no effect on c-fos induction. However, kinase C activation (PMA stimulation) combined with either cAMP (forskolin plus MIX) or calcium stimulation (ionophore) leads to greatly enhanced c-fos induction. By contrast, cAMP in the presence of calcium shows no synergy in c-fos induction. Okadaic acid augments PMA- as well as calcium-mediated activation of c-fos, and has little or no effect when combined with cAMP. The main difference between Ramos (B cells) and Jurkat (T cells) in the regulation of c-fos is that cAMP plus calcium is strongly synergistic in Jurkat and is without effect in Ramos. Analysis of AP-1 activity using gel mobility shift assays confirms that the requirements for synergy in c-fos mRNA induction are paralleled by requirements for synergy in induction of AP-1 activity. Signaling in B cells due to anti-Ig stimulation involves both kinase C activation and release of intracellular calcium, and results in c-fos mRNA induction. Our results indicate that synergy between the kinase C activation and calcium is needed for efficient c-fos induction since neither of these two alone induces c-fos well. That synergy of signaling pathways is relevant for the anti-Ig induction of c-fos is supported by the fact that cAMP-inducing agents and okadaic acid further enhance anti-Ig induction of c-fos. These results suggest that cell-specific patterns of synergy are an essential feature for c-fos induction and may be relevant for c-fos control through B and T cell antigen receptors.

Antibodies, Anti-Idiotypic↗
PubMed1995

Neuropeptide-Y-ATP interactions at the vascular sympathetic neuroeffector junction.

Neuropeptide Y (NPY) and ATP are considered cotransmitters with norepinephrine (NE) in sympathetic neurons innervating some blood vessels, including those of the mesentery. A prominent action of NPY is to potentiate the postjunctional contractile effect of NE as well as that of other vasoactive agents. We wished to investigate whether NPY also potentiates the contractile effect of ATP and, if so, to determine which receptor subtype mediates such an effect. The effect of NPY, the NPY-Y1-selective agent Leu31Pro34 NPY, and the NPY-Y2-selective fragment NPY 14-36 on the increase in perfusion pressure produced by ATP was examined in rat perfused mesenteric arterial bed. Results demonstrated that both NPY and Leu31Pro34 NPY but not NPY 14-36 potentiated the increase in perfusion pressure produced by ATP. These results suggest that NPY acts on Y1 receptors to enhance the postjunctional response of ATP. The putative NPY antagonist PYX2, but not the putative antagonists benextramine or PYX1, attenuated the effect of NPY, indicating that PYX2 acts as an NPY antagonist in this system. A major action of NPY is to enhance the postjunctional response of both cotransmitters, ATP and NE at the vascular sympathetic neuroeffector junction in the mesenteric arterial bed, and this may be mediated by NPY-Y1 receptors.

Adenosine Triphosphate↗
PubMed1995

Renal cortical mitochondria are the source of oxygen free radicals enhanced by gentamicin.

Rat renal cortical mitochondria were isolated from Wistar male rats weighing 80 to 120 g to investigate whether the source of oxygen free radicals was renal cortical mitochondria enhanced by gentamicin. In renal cortical mitochondria with or without the addition of gentamicin, DMSO, DFO, CAT, SOD, and MT1 were added separately, then incubated at 37 degrees C for 90 min. Superoxide anions and hydroxyl radicals were then determined. The results showed that superoxide anions and hydroxyl radicals generated in mitochondria were enhanced by the addition of in vitro gentamicin (12.4 mg/mL) when compared to those without the addition of gentamicin. Dimethylsulfoxide (DMSO), catalase (CAT), and deferoxamine (DFO) significantly inhibited hydroxyl radicals enhanced by gentamicin, but superoxide dismutase (SOD) and metallothionein-1 (MT1) did not. SOD significantly inhibited the production of superoxide anions. Our data indicated that renal cortical mitochondria are the source of oxygen free radicals and that production is enhanced by gentamicin. This provides more insight on the pathogenetic role of hydroxyl radicals and superoxide anions in gentamicin-induced nephrotoxicity in vitro.

Animals↗
PubMed1995

[Preliminary observation on the destructive effect of chemical disinfectants in serum markers of hepatitis B and C].

Chloroform, 40% formaldehyde, 3% hydrogen peroxide solution and 75% alcohol were used to act on hepatitis B surface antigen (HBeAg), hepatitis B e antigen (HBaAg) and anti-hepatitis C virus antibody (Anti-HCV) positive serum for 5, 15, 30 and over 60 minutes. They were examined by enzyme-linked immunosorbent assay and observed for the effect. The destructive effect of chloroform on HBsAg and anti-HCV positive derum was marked. It was discovered that 40% formaldehyde solution destroyed HBsAg, HBeAg, and anti-HCV positive serm, while 75% alcohol also showed destructive effect on HBsAg, HBeAg and anti-HCV positive serum.

Chloroform↗
PubMed1994

Zinc-induced metallothionein synthesis could protect from gentamicin nephrotoxicity in suspended proximal tubules of rats.

We have reported that preinjection of zinc could ameliorate gentamicin-induced nephrotoxicity in vivo via the induction of metallothionein. The present project was designed to study whether preinjection of zinc could protect from the harmful effects of gentamicin on DNA synthesis, Na(+)-K(+)-ATPase activity, and free radical production in rat renal proximal tubules (PT) in vitro. PT were prepared and cultured from normal, saline-preinjected, and Zn-preinjected (Zn 10 mg/k/day s.c. 5 days) Wistar male rats weighing 80-120 g. The results showed that DNA synthesis and Na(+)-K(+)-ATPase activity were significantly suppressed in the normal and saline-preinjected rats' PT by addition of gentamicin to the media in the concentration of 12.4 mg/mL; however, these reactions were not suppressed by gentamicin in Zn-preinjected rats' PT, and malondialdehyde and hydroxyl radical production in Zn-preinjected rats' PT were significantly lower than those in the normal and saline-preinjected rats' PT (p < .01). On the other hand, the metallothionein in Zn-preinjected rats' PT was very significantly higher than that in the normal and saline-preinjected rats' PT (p < .001). Our data indicate that gentamicin-induced suppression of DNA synthesis and Na(+)-K(+)-ATPase activity in rat PT, which lead to renal injury, may be relevant to free radicals generated by gentamicin; and that preinjection of zinc could ameliorate gentamicin-induced nephrotoxicity via the induction of the metallothionein synthesis in rat PT to scavenge free radicals generated by gentamicin.

Animals↗
PubMed1994

Mechanism of gentamicin nephrotoxicity in rats and the protective effect of zinc-induced metallothionein synthesis.

We examined the role of reactive oxygen metabolites and the protective effect of zinc-induced metallothionein (MT) synthesis on gentamicin nephrotoxicity both in vivo and in vitro. In vivo study we found that the MT content of renal cortex of the zinc preinjected rats was significantly increased, and proximal tubular necrosis and acute renal failure caused by injection of gentamicin were ameliorated. In suspended proximal tubules (PT), Na(+)-K(+)-ATPase activity and DNA synthesis were suppressed by the addition of gentamicin, but in zinc-pretreated rats' PT, these were not suppressed by the addition of gentamicin. Meanwhile MDA and hydroxyl radicals were significantly less in zinc-pretreated rats' PT compared to that in the control. Finally, we found that gentamicin enhanced superoxide anion and hydroxyl radical productin in renal cortical mitochondria. Superoxide anion could be suppressed by SOD and hydroxyl radical could be scavenged by DMSO, DFO and CAT. Our data confirm that hydroxyl radicals play a role in the pathogenesis of gentamicin nephrotoxicity, gentamicin can induce suppression of Na(+)-K(+)-ATPase activity and DNA synthesis in rats' proximal tubules leading to renal injury; this injury may be relevant to reactive oxygen metabolites generated by gentamicin. Renal cortical mitochondria is the source of reactive oxygen metabolites, which induces renal injury, and zinc-induced metallothionein synthesis could ameliorate gentamicin nephrotoxicity via scavenging reactive oxygen metabolites.

Acute Kidney Injury↗
PubMed1994

Inhibitory effects of high molecular weight substances from CAPD dialysate on mouse bone marrow progenitor cells and lymphocyte transformation.

The isolation and purification of F A1 (MW 23-64 KD), F B1 (MW 24-54 KD), F A2 and F B2 (both MW 67 KD) of high molecular weight substances (HMS) from continuous ambulatory peritoneal dialysis (CAPD) dialysate of 2 end staged renal disease (ESRD) patients (A and B) were carried out by precipitation, desalting, gradient elution, chromatography and concentration. 0.1ml of tris-buffer, 0.2ml of uremic serum. 0.1ml of F A1, F B1, 0.2ml of F A2 were separately added to mouse bone marrow culture medium and lymphocyte culture medium, then colony-forming unit of erythroid (CFU-E), burst-forming unit of erythroid (BFU-E), colony-forming unit of granulocyte-macrophage (CFU-GM) and lymphocyte transformation (LT) were measured. We found that the uremic serum and F A1, F B1 could inhibit CFU-E, BFU-E very significantly (P < 0.001) compared to the tris-buffer control, but could not inhibit CFU-GM. The uremic serum and F A1 could inhibit LT significantly (P < 0.01) compared to the tris-buffer control, while F A2 could inhibit neither CFU-E nor BFU-E. If the dosage of erythropoietin (EPO) added to mouse bone marrow progenitor cell culture medium increased 3-6 times. F A1 could not express its inhibitory effect on CFU-E or BFU-E.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗