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Biomedical subjects

A Tang

Publications and source records attributed to A Tang.

At least 73 records · Page 4Linked to original sources
PubMed1998

Regulation of the anaphase-promoting complex/cyclosome by bimAAPC3 and proteolysis of NIMA.

Surprisingly, although highly temperature-sensitive, the bimA1(APC3) anaphase-promoting complex/cyclosome (APC/C) mutation does not cause arrest of mitotic exit. Instead, rapid inactivation of bimA1(APC3) is shown to promote repeating oscillations of chromosome condensation and decondensation, activation and inactivation of NIMA and p34(cdc2) kinases, and accumulation and degradation of NIMA, which all coordinately cycle multiple times without causing nuclear division. These bimA1(APC3)-induced cell cycle oscillations require active NIMA, because a nimA5 + bimA1(APC3) double mutant arrests in a mitotic state with very high p34(cdc2) H1 kinase activity. NIMA protein instability during S phase and G2 was also found to be controlled by the APC/C. The bimA1(APC3) mutation therefore first inactivates the APC/C but then allows its activation in a cyclic manner; these cycles depend on NIMA. We hypothesize that bimAAPC3 could be part of a cell cycle clock mechanism that is reset after inactivation of bimA1(APC3). The bimA1(APC3) mutation may also make the APC/C resistant to activation by mitotic substrates of the APC/C, such as cyclin B, Polo, and NIMA, causing mitotic delay. Once these regulators accumulate, they activate the APC/C, and cells exit from mitosis, which then allows this cycle to repeat. The data indicate that bimAAPC3 regulates the APC/C in a NIMA-dependent manner.

Anaphase↗
PubMed1998

A double-blind placebo-controlled evaluation of the human electrophysiologic effects of zatebradine, a sinus node inhibitor.

The purpose of this study was to evaluate the electrophysiologic effects of zatebradine, a sinus node inhibitor, in human subjects. Patients without structural heart disease were randomized to receive intravenous zatebradine (23 patients) or placebo (12 patients). Electrophysiologic measures were obtained at baseline and repeated at 40 and 70 min after drug administration. In the placebo group, there were no significant changes in any parameter over time. After zatebradine, sinus node function changed significantly at 40 min, with no further change at 70 min; sinus cycle length was prolonged by 16 and 17% (p < 0.001), and corrected sinus node recovery time was prolonged by 30 and 22% (p = 0.008). Similarly, atrioventricular node function changed significantly at 40 min, with no further change at 70 min; atrio-His interval was prolonged by 15 and 15% (p = 0.02), atrioventricular node effective refractory period was prolonged by 12 and 11% (p = 0.01), and Wenckebach cycle length was prolonged by 15 and 11% (p = 0.002). Atrial refractoriness, His-Purkinje conduction, ventricular refractoriness, and action-potential duration were not affected by zatebradine. Zatebradine, a sinus node inhibitor, alters the conduction and refractory properties of the human atrioventricular node, in addition to the expected effect on sinus node function.

Action Potentials↗
PubMed1998

The use and cost of HIV service provision in England in 1996. National Prospective Monitoring System (NPMS) Steering Group and NPMS Working Party on Costs.

OBJECTIVE: The aim of the study was to measure the use and estimate the cost of HIV service provision in England. DESIGN AND SETTING: Standardised activity and case-severity data were collected prospectively in 10 English HIV clinics (5 London and 5 non-London sites) for the periods 1 January 1996 to 30 June 1996 and 1 July 1996 to 31 December 1996 and linked to unit cost data. In total, 5440 patients with HIV infection attended during the first 6 months and 5708 during the second 6 months in 1996. MAIN OUTCOME MEASURES AND RESULTS: The mean number of inpatient days per patient-year for patients with AIDS was 19.7 [95% confidence interval (CI): 13.7 to 25.7] for January to June and 20.8 (95% CI: 15.3 to 26.4) for July to December 1996. The mean number of outpatient visits for asymptomatic patients with HIV infection was 14.8 (95% CI: 11.9 to 17.6) and 13.3 (95% CI: 10.8 to 15.7) for the respective periods and 16.1 (95% CI: 13.21 to 18.97) and 15.7 (95% CI: 11.2 to 20.2), respectively, for patients with symptomatic non-AIDS (i.e. symptomatic patients with HIV infection but without AIDS-defining conditions). Substantial centre-to-centre variation was observed, suggesting that many clinics can continue the shift from an inpatient- to an outpatient-based service. Cost estimates per patient-year for HIV service provision for 1996 varied from 4695 Pounds (95% CI: 3769 Pounds to 5648 Pounds) for asymptomatic patients, to 7605 Pounds (95% CI: 6273 Pounds to 8909 Pounds) for symptomatic non-AIDS patients to 20,358 Pounds (95% CI: 17,681 Pounds to 23,206 Pounds) for patients with AIDS. CONCLUSIONS: Different combinations of antiretroviral therapy affect the cost estimates of HIV service provision differently. Anticipated reduction in inpatient-related activity through the increased use of combination antiretroviral therapy will further shift service provision from an inpatient- to outpatient-based service and reduce costs per patient-year. The extent and duration of such effects are currently unknown. The long term effects of combination treatment on the morbidity and mortality patterns of individuals infected with HIV are also currently unknown, as are their implications on the use and cost of HIV service provision. Multicentre databases like the National Prospective Monitoring System (NPMS) will provide healthcare professionals with information to improve existing services and anticipate the impact of new developments.

Acquired Immunodeficiency Syndrome↗
PubMed1998

[The effects of hypertonic saline/mannitol resuscitation on the myocardiac contractility and blood pressure of rabbits with hemorrhagic shock].

Eighteen healthy adult male rabbits were hemorrhaged to shock and treated with hypertonic-hyperoncotic solutions in 3 groups (6 per group): hypertonic saline/dextran(HSD), hypertonic saline/mannitol(HSM) and hypertonic acetate/mannitol(HAM). The results showed that HSM. HAM and HSD could raise the left ventricular pressure(LVP), maximum change rate of LVP (+/- dp/dt max) and the arterial blood pressure of hemorrhagic shock rabbits quickly at small dose. The efficiency of HSM was better than that of HSD and HAM (P < 0.05), and the time of blood pressure rise was in accordance with that of LVP and +/- dp/dt max, which may partly explain the mechanism of shock resuscitation by hypertonic-hyperoncotic solution.

Animals↗
PubMed1998

[Protection of hypertonic saline/mannitol to thymic cell apoptosis induced by endotoxin (LPS) in mice].

To observe the effect of HSM (hypertonic saline/mannitol) on thymic cell apoptosis induced by endotoxin (LPS) in mice, twenty-four mice were divided into three groups (8 mice/each group): 1. Control group, each mouse was intraperitonealy injected with normal saline; 2. LPS group, each mouse was intraperitonealy injected with LPS; 3. LPS + HSM group, each mouse was intraperitonealy injected with HSM before and after injection of LPS. The results showed that the percentage of apoptosis of HSM + LPS group was lower than that of LPS group (P < 0.01); the ladder of nucleosomal DNA fragments by agarose gel eletrophoresis of HSM group was not typical as compared with that of LPS group. It is suggested that HSM might protect the apoptosis of mouse thymic cell induced by LPS and may improve the immune function.

Adjuvants, Immunologic↗
PubMed1998

[Determination of tryptophan in human serum by high-performance liquid chromatography].

In this paper a high-performance liquid chromatographic(HPLC) method has been developed to determine the concentration of tryptophan(Trp) in human serum. Serum sample was precipitated with trichloroacetic acid solution(0.6 mol.L-1) to remove protein and centrifuged and assayed by HPLC. The operating conditions were NOVA-PAK C18 column(3.9 mm x 150 mm), KH2PO4(0.1 mol.L-1) mobile phase with flow rate of 0.7 ml.min-1, and detective wave-length at 295 nm. The linear range was 1.223-2447.381 mumol.L-1. The detection limit was 0.612 mumol.L-1. The average recovery was 96.3%. Intra-assay CV is less than 4% and inter-assay less than 5%. The concentration of Trp in normal adult serum was 46.603 +/- 5.108 mumol.L-1. The detection time of serum Trp was within 5 min. The results suggest that this method is simple, fast, accurate, and convenient.

Adult↗
PubMed1998

Hepatic lipase activity is lower in African American men than in white American men: effects of 5' flanking polymorphism in the hepatic lipase gene (LIPC).

Plasma high density lipoprotein cholesterol (HDL-C) concentrations are higher in African American men than in white men, but the mechanism(s) responsible for this ethnic difference has not been elucidated. This study examined the relationship between hepatic lipase activity, plasma HDL-C concentrations, and a hepatic lipase polymorphism (-514T) in African American and white American men. Consistent with previous reports, plasma HDL-C concentrations were significantly higher in African American men than in white American men. Mean post-heparin plasma hepatic lipase activity was significantly lower in African American than in white American men (27 +/- 12 vs. 44 +/- 17 mmol x h(-1) x l(-1), P < 0.001). The -514T hepatic lipase allele was associated with low hepatic lipase activity in both populations, and was 3-fold more common among African Americans than white Americans. Taken together, these data suggest that genetic differences in hepatic lipase activity contribute to the differences in plasma HDL-C concentrations between African American men and white American men.

Adult↗
PubMed1998

Body mass index and hepatic lipase gene (LIPC) polymorphism jointly influence postheparin plasma hepatic lipase activity.

The -514 polymorphism in the hepatic lipase gene (LIPC) is associated with decreased hepatic lipase activity. In the present study, the interaction between body mass index (BMI), the -514 polymorphism, and hepatic lipase activity was examined in 118 white men and in 51 African American men. BMI was significantly positively correlated with hepatic lipase activity in both populations. BMI was similar in men with genetic differences in hepatic lipase activity, indicating that high hepatic lipase activity did not cause increased BMI. The data therefore suggest that high BMI leads to increased hepatic lipase activity. The actions of BMI and the -514 polymorphism on hepatic lipase activity appear to be additive and independent, rather than synergistic. This finding indicates that hepatic lipase activity is a multifactorial trait, determined in part by polymorphism within the LIPC gene as well as by factors that influence BMI.

Adolescent↗
PubMed1998

CT findings in splenic tuberculosis.

Splenic tuberculosis is rare and delay in diagnosis is common. We present two cases of splenic tuberculosis with their appearance on CT. The CT findings were multiple, round or ovoid, low-density lesions without calcification. Except for non-specific lymphadenopathy no abnormality nor history suggestive of tuberculosis was revealed prior to laparotomy. Although CT does not confirm a diagnosis of splenic tuberculosis, it would be a valuable examination to define the extent of disease and guide aspiration biopsy.

Abscess↗
PubMed1998

Three polymorphisms associated with low hepatic lipase activity are common in African Americans.

We have shown previously that a hepatic lipase allele (designated -514T) is common among African Americans and contributes to low hepatic lipase activity in this population. To identify other hepatic lipase alleles associated with low hepatic lipase activity in this population, the coding region and intron-exon boundaries of the hepatic lipase gene were sequenced in 20 African American men with low hepatic lipase activity. Two polymorphisms (N193S and L334F) were associated with low post-heparin plasma hepatic lipase activity and were much more common in African Americans than in whites. This finding, together with our previous data on the -514T allele, indicates that at least three different hepatic lipase polymorphisms associated with low hepatic lipase activity are common among African Americans. Analysis of hepatic lipase haplotypes revealed that 97% of African Americans have at least one hepatic lipase allele that is associated with low hepatic lipase activity.

Adult↗
PubMed1997

Proteolysis and tyrosine phosphorylation of p34cdc2/cyclin B. The role of MCM2 and initiation of DNA replication to allow tyrosine phosphorylation of p34cdc2.

Previously, it has been shown that Aspergillus cells lacking the function of nimQ and the anaphase-promoting complex (APC) component bimEAPC1 enter mitosis without replicating DNA. Here nimQ is shown to encode an MCM2 homologue. Although mutation of nimQMCM2 inhibits initiation of DNA replication, a few cells do enter mitosis. Cells arrested at G1/S by lack of nimQMCM2 contain p34(cdc2)/cyclin B, but p34(cdc2) remains tyrosine dephosphorylated, even after DNA damage. However, arrest of DNA replication using hydroxyurea followed by inactivation of nimQMCM2 and bimEAPC1 does not abrogate the S phase arrest checkpoint over mitosis. nimQMCM2, likely via initiation of DNA replication, is therefore required to trigger tyrosine phosphorylation of p34(cdc2) during the G1 to S transition, which may occur by inactivation of nimTcdc25. Cells lacking both nimQMCM2 and bimEAPC1 are deficient in the S phase arrest checkpoint over mitosis because they lack both tyrosine phosphorylation of p34(cdc2) and the function of bimEAPC1. Initiation of DNA replication, which requires nimQMCM2, is apparently critical to switch mitotic regulation from the APC to include tyrosine phosphorylation of p34(cdc2) at G1/S. We also show that cells arrested at G1/S due to lack of nimQMCM2 continue to replicate spindle pole bodies in the absence of DNA replication and can undergo anaphase in the absence of APC function.

Amino Acid Sequence↗
PubMed1997

The G2/M DNA damage checkpoint inhibits mitosis through Tyr15 phosphorylation of p34cdc2 in Aspergillus nidulans.

It is possible to cause G2 arrest in Aspergillus nidulans by inactivating either p34cdc2 or NIMA. We therefore investigated the negative control of these two mitosis-promoting kinases after DNA damage. DNA damage caused rapid Tyr15 phosphorylation of p34cdc2 and transient cell cycle arrest but had little effect on the activity of NIMA. Dividing cells deficient in Tyr15 phosphorylation of p34cdc2 were sensitive to both MMS and UV irradiation and entered lethal premature mitosis with damaged DNA. However, non-dividing quiescent conidiospores of the Tyr15 mutant strain were not sensitive to DNA damage. The UV and MMS sensitivity of cells unable to tyrosine phosphorylate p34cdc2 is therefore caused by defects in DNA damage checkpoint regulation over mitosis. Both the nimA5 and nimT23 temperature-sensitive mutations cause an arrest in G2 at 42 degrees C. Addition of MMS to nimT23 G2-arrested cells caused a marked delay in their entry into mitosis upon downshift to 32 degrees C and this delay was correlated with a long delay in the dephosphorylation and activation of p34cdc2. Addition of MMS to nimA5 G2-arrested cells caused inactivation of the H1 kinase activity of p34cdc2 due to an increase in its Tyr15 phosphorylation level and delayed entry into mitosis upon return to 32 degrees C. However, if Tyr15 phosphorylation of p34cdc2 was prevented then its H1 kinase activity was not inactivated upon MMS addition to nimA5 G2-arrested cells and they rapidly progressed into a lethal mitosis upon release to 32 degrees C. Thus, Tyr15 phosphorylation of p34cdc2 in G2 arrests initiation of mitosis after DNA damage in A. nidulans.

Aspergillus nidulans↗
PubMed1997

Blockade of CD40-CD40 ligand pathway induces tolerance in murine contact hypersensitivity.

Interactions between CD40 on antigen-presenting cells and its ligand (CD40L) on T cells has been implicated in T cell-mediated immune responses. Previously, we have shown that contact hypersensitivity (CHS), a cell-mediated cutaneous immune response in reaction to haptens, could be subclassified based on whether the hapten primed for Th1 or Th2 cytokines in cells isolated from draining lymph nodes. We also found that tolerance to a Th2-priming hapten could be induced only by simultane blockade of the CD40-CD40L and B7-CD28 at the time of sensitization. Here we demonstrate that blockade of CD40-CD40L signaling alone induces long-lasting unresponsiveness to the Th1 hapten 2,4-dinitrofluorobenzene (DNFB), and inhibits antigen-specific T cell proliferation in vitro. We find that CD40-CD40L signaling is required in the sensitization but not elicitation phase of DNFB-induced CHS, as treatment of mice with anti-CD40L monoclonal antibody (mAb) does not affect the response to hapten challenge in previously sensitized and untreated animals. Examination of cytokine production shows that anti-CD40L mAb decreases interferon-gamma production by draining lymph node cells from DNFB-sensitized mice, and reciprocally increases interleukin (IL)-4 production. Consistent with this Th1 to Th2 immune deviation, anti-CD40L mAb prevents the induction of IL-12 mRNA in regional lymph nodes, an event which is normally seen within 12 h following hapten sensitization. In contrast, suppression of CHS by CTLA4Ig decreased the production of all cytokines by draining lymph node cells. Together, these data show that blockade of the CD40-CD40L pathway by itself is sufficient to induce tolerance to DNFB-induced CHS, and that this is associated with blockade of IL-12 induction and Th1 to Th2 immune deviation.

Animals↗
PubMed1997

Fibromuscular dysplasia of small coronary arteries and fibrosis in the basilar ventricular septum in mitral valve prolapse.

The mechanism of sudden cardiac death in patients with mitral valve prolapse is poorly understood. Twenty-four hearts from patients with mitral valve prolapse who suddenly died (mean age 34 +/- 8 years) and 16 trauma control hearts (mean age 30 +/- 7 years) were histologically studied. Dysplasia of the atrioventricular nodal artery was present in 18 of 24 hearts with mitral valve prolapse and four of 16 controls hearts (p = 0.003). The degree of luminal narrowing, as morphometrically measured, was significantly greater in hearts with mitral valve prolapse (p = 0.003). The degree of fibrosis in the base of the ventricular septum, as calculated by computerized morphometry, was greater in hearts with mitral valve prolapse (p = 0.0002) and independent of age, sex, and heart weight (p = 0.005). We conclude that arterial dysplasia in mitral valve prolapse may contribute to sudden cardiac death mediated by ventricular fibrosis.

Adult↗
PubMed1997

[Respiratory monitoring and high frequence jet ventilation (HFJV) in the treatment of severe chest injuries].

Twenty-eight patients with severe chest injuries were classified into 3 groups: fractures of rib, hemopneumothorax and lung injured. Their respiratory rate (RR), SpO2 and blood gas were analysed. The results showed that SpO2 and PaO2 in lung-injured group were the lowest and RR was the highest in the 3 groups. After HFJV, there was a significant rise in PaO2 and SpO2 (P < 0.05) and a gradual recovery of respiratory and pulse rates in lung-injured group. The results suggest that respiratory monitoring is important for patients with chest injuries and HFJV may be used as an effective ventilation method for treating patients with severe chest injuries.

Adult↗