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Biomedical subjects

T Wang

Publications and source records attributed to T Wang.

At least 397 records · Page 22Linked to original sources
PubMed1998

Increased peritoneal permeability is associated with decreased fluid and small-solute removal and higher mortality in CAPD patients.

BACKGROUND: Recent studies suggest that increased peritoneal membrane permeability is associated with higher morbidity and mortality in peritoneal dialysis patients. It is not known, however, whether the difference in clinical outcome among different peritoneal transport groups is due to differences in peritoneal fluid and solute removal. In the present study, we compared the peritoneal fluid and solute transport and clinical outcome in CAPD patients with high (H), high-average (H-A), low-average (L-A) and low (L) peritoneal transport patterns. DESIGN: A 6-h dwell study was performed in 46 patients with frequent dialysate and plasma samples using 2 l of 3.86% glucose dialysate with 131I albumin as an intraperitoneal volume marker. The patients were divided into four transport groups according to their D/P of creatinine at 240 min. RESULTS: The results showed that high transporters had significantly lower peritoneal fluid and small-solute removal but high glucose absorption and high protein loss during a 6-h exchange. The serum albumin was lower and blood pressure and triglycerides were higher in high transporters compared with the other groups. Two-year patient survival from the start of CAPD treatment was significantly lower for high transporters (64, 85, 90 and 100% for H, H-A, L-A and L respectively, P < 0.01). The 1-year patient survival from the dwell study was also significantly lower in high transporters (16, 63, 90 and 100% for each group, P<0.01). CONCLUSION: Our results suggest that high transporters remove less fluid and small solutes and have higher protein loss and increased glucose absorption. These alterations may contribute to fluid overload, malnutrition and lipid abnormalities that perhaps contribute to the increased mortality among the high transporters.

Adult↗
PubMed1998

Reduction of hepatic ischemia/reperfusion injury by a soluble P-selectin glycoprotein ligand-1.

OBJECTIVE: The authors' goal was to determine the effects of specific binding and blockade of P- and E-selectins by a soluble P-selectin glycoprotein ligand-1 (PSGL-1) in rat models of hepatic in vivo warm ischemia and ex vivo cold ischemia. The authors also sought to determine the effect of selectin blockade on isograft survival in a syngeneic rat orthotopic liver transplant model. SUMMARY BACKGROUND DATA: Ischemia/reperfusion (I/R) injury is a major factor in poor graft function after liver transplantation, which may profoundly influence early graft function and late changes. It is hypothesized that I/R injury leads to the upregulation of P-selectin, which is then rapidly translocated to endothelial cell surfaces within 5 minutes of reperfusion of the liver, initiating steps leading to tethering of polymorphonuclear neutrophil leukocytes to the vascular intima. Local production by leukocytes of interleukin-1, tumor necrosis factor-alpha, or both induces P-selectin expression on the endothelium and continues the cascade of events, which increases cell adherence and infiltration of the organ. METHODS: To examine directly the effects of selectins in a warm hepatic I/R injury model, 100 microg of PSGL-1 or saline was given through the portal vein at the time of total hepatic inflow occlusion. The effects of PSGL-1 in cold ischemia were assessed using an isolated perfused rat liver after 6 hours of 4 degrees C storage in University of Wisconsin (UW) solution, with or without the instillation of PSGL-1 before the storage. To evaluate the effect of selectin blockade on liver transplant survival, syngeneic orthotopic liver transplants were performed between inbred male Sprague-Dawley rats after 24 hours of cold ischemic storage in UW solution. A separate group of animals received two doses of 100 microg of PSGL-1 through the portal vein before storage and before reperfusion of the transplanted liver. Recipient survival was assessed at 7 days, and the Kaplan-Meier product limit estimate method was used for univariate calculations of time-dependent recipient survival events. RESULTS: In an in vivo warm rat liver ischemia model, perfusion with PSGL-1 afforded considerable protection from I/R injury, as demonstrated by decreased transaminase release, reduced histologic hepatocyte damage, and suppressed neutrophil infiltration, versus controls (p < 0.05). When cold stored livers were reperfused, PSGL-1 reduced the degree of hepatocyte transaminase release, reduced neutrophil infiltration, and decreased histologic hepatocyte damage (p < 0.05 vs. UW-only controls). On reperfusion, livers treated with PSGL-1 demonstrated increased portal vein blood flow and bile production (p < 0.05 vs. UW-only controls). In addition, 90% of the rats receiving liver isografts stored in UW solution supplemented with PSGL-1 survived 7 days versus 50% of those whose transplanted syngeneic livers had been stored in UW alone (p < 0.05). CONCLUSIONS: Selectins play an important role in I/R injury of the liver. Early modulation of the interaction between P-selectin and its ligand decreases hepatocyte injury, neutrophil adhesion, and subsequent migration in both warm and cold rat liver ischemia models. In addition, the use of PSGL-1 before ischemic storage and before transplantation prevents hepatic injury, as documented by a significant increase in liver isograft survival. These findings have important clinical ramifications: early inhibition of alloantigen-independent mechanisms during the I/R damage may influence both short- and long-term survival of liver allografts.

Animals↗
PubMed1998

Functional recovery and timing of hospital discharge after primary total hip arthroplasty.

BACKGROUND: Early discharge programmes in hospitals are encouraged to increase financial efficiency and bed availability, but standards of clinical care must not be compromised. Criteria for safe hospital discharge must be established and objective data are needed to assess how rapidly patients can achieve these discharge criteria. METHODS: A prospective study was performed on 65 patients (mean age = 71 years) scheduled for primary total hip arthroplasty (THA). The Modified Barthel Index (MBI) was measured pre-operatively and postoperatively at set intervals to asses recovery of function after THA. A score of 90 out of a possible 100 was used as a discharge criterion and indicated that the patient was functionally independent for safe hospital discharge. In addition, a combined score for thigh flexion and extension isokinetic peak strength was recorded for each patient before and after surgery. The number and nature of comorbidities and complications were also recorded. RESULTS: The length of hospital stay in this sample varied from 5 to 39 days. The MBI scores increased rapidly between days 3 and 5, then began to plateau from day 8 onwards. Based on the MBI, 58% of patients were fit for discharge at or before day 8. The remainder were fit for discharge from day 10 onwards (mean = 14.2 days). The latter group who required an extended hospital stay were older (P = 0.003), had more identified comorbidities (P = 0.01) and were weaker in their hip musculature prior to surgery (P = 0.001), compared to those who were discharged by day 8. A logistic regression analysis indicated that the pre-operative MBI score and hip strength score were strong predictors of timing for hospital discharge. CONCLUSIONS: A clinical pathway with functional milestones laid out over 8 days would be an appropriate criterion for the discharge of the majority of patients. However, approximately 40% of the patients presented in this study required a longer hospital stay before the criteria for safe discharge could be achieved. These patients can be identified pre-operatively by screening their MBI and composite hip strength scores.

Aged↗
PubMed1998

Detection of grlA and gyrA mutations in 344 Staphylococcus aureus strains.

Mutations in the grlA and gyrA genes of 344 clinical strains of Staphylococcus aureus isolated in 1994 in Japan were identified by combinations of single-strand conformation polymorphism analysis, restriction fragment length analysis, and direct sequencing to identify possible relationships to fluoroquinolone resistance. Five types of single-point mutations and four types of double mutations were observed in the grlA genes of 204 strains (59.3%). Four types of single-point mutations and four types of double mutations were found in the gyrA genes of 188 strains (54.7%). Among them, the grlA mutation of TCC-->TTC or TAC (Ser-80-->Phe or Tyr) and the gyrA mutation of TCA-->TTA (Ser-84-->Leu) were principal, being detected in 137 (39.8%) and 121 (35.9%) isolates, respectively. The grlA point mutations of CAT-->CAC (His-77 [silent]), TCA-->CCA (Ser-81-->Pro), and ATA-->ATT (Ile-100 [silent]) were novel, as was the GAC-->GGC (Asp-73-->Gly) change in gyrA. A total of 15 types of mutation combinations within both genes were related to ciprofloxacin resistance (MIC > or = 3.13 microg/ml) and were present in 193 mutants (56.1%). Strains containing mutations in both genes were highly resistant to ciprofloxacin (MIC at which 50% of the isolates are inhibited [MIC50] = 50 microg/ml). Those with the Ser80-->Phe or Tyr alteration in grlA but wild-type gyrA showed a lower level of ciprofloxacin resistance (MIC50 < or = 12.5 microg/ml). Levofloxacin was active against 68 of 193 isolates (35.2%) with mutations at codon 80 of grlA in the presence or absence of a concomitant mutation at codon 73, 84, or 88 in gyrA (MIC < or = 6.25 microg/ml). The new fluoroquinolone DU-6859a showed good activity with 186 of 193 isolates (96.4%) for which the MIC was < or = 6.25 microg/ml.

4-Quinolones↗
PubMed1998

Carbon dioxide transport in alligator blood and its erythrocyte permeability to anions and water.

Deoxygenation of alligator red blood cells (RBCs) caused binding of two HCO3- equivalents per hemoglobin (Hb) tetramer at physiological pH. At lowered pH, some HCO3- binding also occurred to oxygenated Hb. The erythrocytic total CO2 content was large, and Hb-bound HCO3-, free HCO3-, and carbamate contributed about equally in deoxygenated cells. The nonbicarbonate buffer values of RBCs and Hb were high, and the Hb showed a significant fixed acid Haldane effect. Binding of HCO3- on deoxygenation occurred without a change in RBC intracellular pH, revealing equivalence between oxylabile HCO3- and H+ binding. Erythrocyte volume, plasma pH, and plasma HCO3- concentration also varied little with the degree of oxygenation. Diffusional water permeability was higher in oxygenated than deoxygenated RBCs. The RBCs have rapid band 3-mediated Cl- and HCO3- transport, which was not affected by degree of oxygenation, but net fluxes of Cl- and HCO3- via the anion exchanger are small during blood circulation at rest. Most of the CO2 taken up into the blood as it flows through tissue capillaries is carried within the erythrocytes as Hb-bound HCO3- until CO2 is excreted when blood flows through pulmonary capillaries.

Acid-Base Equilibrium↗
PubMed1998

Effect of metabolic acidosis on NaCl transport in the proximal tubule.

In metabolic acidosis, the capacity of the proximal tubule for bicarbonate absorption is enhanced, whereas NaCl reabsorption is inhibited. Recent evidence indicates that transcellular NaCl absorption in the proximal tubule is mediated by apical membrane Cl/formate exchange and Cl/oxalate exchange, in parallel with recycling of these organic anions. We evaluated whether the effect of metabolic acidosis to inhibit NaCl reabsorption in the proximal tubule is due at least in part to inhibition of organic anion-dependent NaCl transport in this nephron segment. Absorption rates of bicarbonate (JHCO3), chloride (JCl), and fluid (Jv) were measured in rat proximal tubule segments microperfused in situ. We confirmed that metabolic acidosis stimulates JHCO3 in tubules microperfused with 25 mM HCO3, pH 7.4. For measurements of JCl, tubules were microperfused with a low-bicarbonate (5 mM), high-chloride solution, simulating conditions in the late proximal tubule. Under these conditions, baseline JCl and Jv measured in the absence of formate and oxalate were not significantly different between control and acidotic rats. However, whereas addition of 50 ¿M formate or 1 ¿M oxalate to luminal and capillary perfusates markedly stimulated JCl and Jv in control rats, formate and oxalate failed to stimulate JCl and Jv in acidotic rats. We conclude that metabolic acidosis markedly downregulates organic anion-stimulated NaCl absorption, thereby allowing differential regulation of proximal tubule NaHCO3 and NaCl transport.

Absorption↗
PubMed1998

A tyrosine-based signal regulates H-K-ATPase-mediated potassium reabsorption in the kidney.

Isoforms of the H-K-ATPase participate in active K resorption in the renal collecting tubule. The cytoplasmic tail of the beta-subunit of the gastric H-K-ATPase includes a 4 amino acid motif which is highly homologous to tyrosine-based endocytosis signals. We have generated transgenic mice expressing an H-K-ATPase beta-subunit in which the tyrosine residue in this sequence has been mutated to alanine. Mice expressing the mutated protein manifest constitutive hypersecretion of gastric acid, demonstrating that the beta-subunit tyrosine-based motif is required for the regulated endocytosis of the H-K pump and hence the cessation of gastric acid output. To test the possibility that the tyrosine-based sequence in the tail of the H-K-ATPase beta-subunit plays a role in regulating the function of renal H-K-ATPases, we examined renal K clearance in normal and in transgenic mice. Blood pressure, urine volume, glomerular filtration rate (GFR), plasma Na, and Na excretion are similar in control and transgenic mice. However, plasma K concentrations are significantly higher in transgenic mice (4.76 +/- 0.13 meq/l in transgenic and 4. 12 +/- 0.04 meq/l in control; n = 9, P < 0.05) and K excretion is lower in the transgenic animals (fractional excretion of K was 26.2 +/- 3.62% in transgenic and 50.1 +/- 4.78% in control; n = 9, P < 0. 01). These data suggest that the tyrosine-based signal in the cytoplasmic tail of the H-K-ATPase beta-subunit functions in the kidney as it does in the stomach to internalize H-K pump and thus inactivate pump function. Its elimination may result in the constitutive presence of the pump at the cell surface and lead to excessive urinary K reabsorption.

Animals↗
PubMed1998

Factors contributing to catabolism in end-stage renal disease patients.

End-stage renal disease (ESRD) patients, whether they are treated with hemodialysis or continuous ambulatory peritoneal dialysis, frequently suffer from protein-energy malnutrition, which is associated with increased morbidity and mortality. The protein requirements in dialysis patients are increased compared to those of healthy individuals and nondialyzed patients with chronic renal failure. The intake of protein and energy is frequently reduced because of the underlying disease, comorbidity, psychosocial factors, and uremic anorexia (underdialysis). There are several factors in ESRD patients that may enhance protein catabolism and increase protein requirements, such as low energy intake, amino acid abnormalities, metabolic acidosis, endocrine abnormalities (insulin resistance, hyperglucagonemia, hyperparathyroidism, insensitivity to growth hormone and insulin-like growth factor-1, cardiac failure, infection and inflammation, anemia, and physical inactivity. The dialytic procedures per se may enhance protein catabolism due to dialytic losses of protein and amino acids and, in hemodialysis, an inflammatory response to blood-dialyzer interaction. The relative importance of the various factors which cause anorexia and stimulate protein catabolism is still not well understood.

Acidosis↗
PubMed1998

Expression of Mel-CAM in implantation site intermediate trophoblastic cell line, IST-1, limits its migration on uterine smooth muscle cells.

An immortalized implantation site intermediate trophoblastic cell line, IST-1, was established from a human placenta of 7 weeks gestation. IST-1 cells phenotypically resembled the implantation site intermediate trophoblastic cells in situ and expressed Mel-CAM (MUC 18 or CD146). Mel-CAM is a cell adhesion molecule belonging to the immunoglobulin gene superfamily. It is involved in heterophilic cell-cell adhesion and plays a role in several biological processes including tumor progression. We have previously shown that Mel-CAM was highly expressed in the intermediate (extravillous) trophoblast in the human implantation site. In this study we determined the function of Mel-CAM in the interaction of trophoblast and uterine smooth muscle in the implantation site. IST-1 cells failed to adhere to immobilized recombinant Mel-CAM in solid phase whereas the uterine smooth muscle cells did. The presence of the putative Mel-CAM ligand in smooth muscle cells was further supported by the finding that Mel-CAM-transfected but not the mock-transfected U937 leukemia cells bind to the confluent monolayer of uterine smooth muscle cells. IST-1 cells attached efficiently to the monolayer of the uterine smooth muscle cells and acquired a spindle-shaped morphology simulating smooth muscle cells. The cell binding was only marginally affected by Mel-CAM blocking antibodies. However, Mel-CAM blocking antibodies and recombinant Mel-CAM promoted cell migration from IST-1 cell spheroids on the smooth muscle monolayer. Taken together, our results suggest that IST-1 cells express Mel-CAM but not the putative Mel-CAM ligand. In contrast, the uterine smooth muscle cells express the putative Mel-CAM ligand which binds to Mel-CAM on the surface of the IST-1 cells. The interaction between Mel-CAM and its putative ligand confers a stationary phenotype for trophoblastic cells. These observations are consistent with an important role for Mel-CAM in limiting trophoblastic migration within the myometrium in the implantation site.

Animals↗
PubMed1998

Hypoxia elicits an increase in pulmonary vasculature resistance in anaesthetised turtles (Trachemys scripta).

In mammals and birds, low oxygen levels in the lungs cause a constriction of the pulmonary vasculature. This response is locally mediated and is considered to be important for local matching of perfusion and ventilation. It is not known whether reptiles respond in a similar fashion. The present study describes the effects of altering lung oxygen levels (at a constant FCO2 of 0.03) on systemic and pulmonary blood flows and pressures in anaesthetised (Nembumal, 50 mg kg-1) and artificially ventilated turtles Trachemys scripta. During severe hypoxia (1.5-3 kPa PO2), pulmonary blood flow decreased in all animals; systemic blood flow increased, resulting in an increased net right-to-left shunt blood flow. The redistribution of blood flows was associated with reciprocal changes in the vascular resistances within the pulmonary and the systemic circulations (Rpul and Rsys, respectively). At 1.5 kPa O2, Rpul increased from 0.09 0.01 to 0.15 0.03 kPa ml-1 min kg during normoxia (means 1 s.e.m., N=5). Concurrently, Rsys tended to decrease from a normoxic value of 0.12 0.01 to 0.09 0.02 kPa ml-1 min kg (P=0.08). The effects of hypoxia on the haemodynamic variables persisted following atropinisation (1 mg kg-1) and cervical vagotomy, suggesting that the increased Rpul during hypoxia is locally mediated. This study therefore demonstrates that turtles exhibit hypoxic pulmonary vasoconstriction, although the threshold is low compared with that of mammals.

Adrenal Medulla↗
PubMed1998

Immunotherapy of colon cancer using chimeric mAb 31.1.

We have produced two monoclonal antibodies specific for membranes of colon carcinoma cells that demonstrate minimal if any cross reactivity with normal colon tissue. The antigen of one of the two antibodies (mAb 33.28) is extremely immunogenic eliciting both cell mediated and humoral immunity. The monoclonal antibodies developed in in vitro studies suggested strong antibody dependent cell cytotoxicity (ADCC) for both antibodies, but somewhat stronger for the mAb 31.1. The murine version of mAb 31.1 produced approximately 90% tumor cell destruction in the same period of time. Nude mice with LS174T xenografts (human colon carcinoma) were challenged with 1 x 10(6) cells given subcutaneously in the thigh. By day 10, well animals were incapacitated by tumor growth. Among those animals receiving 400 micrograms of intraperitoneal chimeric 31.1 at day one, all were protected and remained free of disease. Those challenged with chimeric antibody and human effector cells at day 7 demonstrated regression of established tumor nodules among 80% of the animals so treated. Therapy of patients with extensive primary as well as metastatic colon cancer may be found to respond to the above form of therapy post surgery, when employed alone or in combination with an effective cytotoxic (chemotherapeutic) agent.

Animals↗
PubMed1998

Detection and utilization of single genes without DNA assays.

Quantitative traits are often assumed to be controlled by a large number of loci that each have a small effect. Under this assumption, the distribution of genotypic and phenotypic values can be adequately modeled by a multivariate normal distribution. Thus, most genetic analyses are based on mixed linear models. Evidence is accumulating, however, for the presence of loci that have large effects on traits of economic importance. If the genotypes for such loci can be observed without error, then--conditional on these observed genotypes--genotypic and phenotypic values follow a multivariate normal distribution, and data from very large pedigrees can be analyzed using a mixed linear model that includes the genotypic effects for these loci as fixed effects. However, when the major genotype is not observed, the genotypic and phenotypic values follow a mixture of multivariate normal distributions, and analyses based on fitting a mixed linear model may not be optimum, especially for populations undergoing selection and nonrandom mating. Several approaches are discussed for the genetic analysis of data when the major genotypes are not known.

Algorithms↗
PubMed1998

Glucagon-like peptide-1 (7-36) amide administered into the third cerebroventricle inhibits water intake in rats.

Intracerebroventricular (icv) injection of glucagon-like peptide-1 (7-36) amide (GLP-1) has been shown to reduce food intake in rats. In these studies, we confirmed that injection of 10 microg of GLP-1 into the third cerebroventricle suppressed food intake. Moreover, we observed a reduction in water intake associated with the decreased food intake. We further examined whether GLP-1 injected icv in rats has a specific inhibitory effect on water intake. It was found that GLP-1 reduced water deprivation-induced drinking. Furthermore, the same dose of GLP-1 (10 microg) was sufficient to condition taste aversion. Finally, when 2 microg of GLP-1 were injected into the third ventricle, it only suppressed water deprivation-induced water intake and failed to influence spontaneous food and water intakes or induce conditioned taste aversion. These observations indicate that GLP-1 is a potent inhibitor of water intake in the rat and may play a role in the control of fluid homeostasis.

Animals↗
PubMed1998

[Clinical application of the reversed digital artery island flap containing palmar digital vein].

In order to introduce a novel reversed digital artery island flap, it was used in 13 cases involving 17 digital skin defects since 1993, in which digital skin defects were covered by a reversed digital artery island flap, a comparative study was made between the flaps with or without a palmar digital vein. The results showed that the 17 island flaps were all survived, and during the early stage after operation, the incidence of venous crisis in the flaps without palmar digital vein was 87.5% (7/8) while that in the flaps with the vein was only 11.1% (1/9), so, it was concluded that the reversed digital artery island flap containing a palmar digital vein could obviously reduce the incidence of venous crisis and improve the survival of the flap.

Adolescent↗
PubMed1998

New developments in automated PrepLCMS extends the robustness and utility of the method for compound library analysis and purification.

New developments in the high throughput purification of combinatorial libraries by automated preparative LC-MS is presented. To facilitate high speed purifications at the multimilligram level, short columns operated at ultra high flow rates were incorporated. In order to match the linear velocity of the short analytical columns for high speed separations (operated at 4.0 mL/min), it was required to operate the preparative columns at flow rates in excess of 70 mL/min. For chromatographically well-behaved compounds, analytical LC-MS analyses and preparative LC-MS analyses could be achieved in as little as 5 min. For compounds exhibiting poor chromatographic peak shapes and/or for compound mixtures requiring higher resolution separations, slightly longer preparative LC-MS analysis times were required (8-10 min/sample).

Chemistry, Pharmaceutical↗