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Biomedical subjects

D Wang

Publications and source records attributed to D Wang.

At least 685 records · Page 38Linked to original sources
PubMed1997

Suicide in three ethnic groups in Huhhot, Inner Mongolia.

Suicide was examined in three ethnic groups in Huhhot, Inner Mongolia, for the period 1986-1991. The influence of the different cultures on suicide was studied. The Han have the most tolerant views toward suicide and were found also to have the highest suicide rate. The Hui follow Islam, which condemns suicide, and were found to have the lowest suicide rate. The Meng expect to suffer in life and are thus not prone to suicide, though as they move to the cities and become more educated, they tend to adopt Han cultural values so that their suicide rate is now moderately high.

Adult↗
PubMed1997

Suicide and meteorological factors in Huhhot, Inner Mongolia.

The authors investigated the relationship between the incidence of suicide and meteorological factors in Huhhot, Inner Mongolia, for the period 1986-1991. Suicide rates were higher during the days of each month with extreme temperature and atmospheric pressure.

Adult↗
PubMed1997

Role of the CD40 and CD95 (APO-1/Fas) antigens in the apoptosis of human B-cell malignancies.

Ligation of CD40 inhibits apoptosis and stimulates proliferation of normal B cells, whereas ligation of CD95 (APO-1/Fas) induces apoptosis of activated lymphocytes. Aberrant signalling through the CD40 and CD95 antigens could thus participate in the pathogenesis of lymphoid malignancies. The expression and function of CD40 and CD95 on neoplastic B cells from patients with acute lymphoblastic leukaemia (ALL), chronic lymphocytic leukaemia (CLL) and non-Hodgkin's lymphoma (NHL) were examined. CD40 was expressed by all 30 B-cell tumours, whereas CD95 was detected on neoplastic B cells in only one of 10 cases of ALL, two of 10 cases of CLL, and three of 10 cases of NHL. Incubation with an agonistic CD95 monoclonal antibody (MoAb) did not augment apoptosis in any of the unstimulated B-cell neoplasms. CD40 triggering did not consistently inhibit spontaneous apoptosis, but ultimately stimulated the growth of neoplastic B cells in most cases. Furthermore, CD40 activation led to up-regulation of the CD95 antigen in all 30 B-cell neoplasms. Ligation of CD95 on CD40-activated tumour cells augmented apoptosis in five of 10 ALL, three of 10 CLL, and nine of 10 NHL cases. The degree of apoptosis induced by CD95 triggering was greater for NHL cells than for ALL cells or CLL cells. Bcl-2 expression by ALL and NHL cells was substantially decreased after in vitro culture, whereas Bcl-2 expression by CLL cells was not significantly changed. However, there was no correlation between the level of Bcl-2 expression and sensitivity to CD95-mediated apoptosis. Thus, factors other than levels of CD95 and Bcl-2 determine susceptibility of malignant B cells to apoptosis after CD95 triggering. CD40-activated lymphoma cells appear to be very sensitive to CD95-mediated apoptosis, suggesting potential strategies for treatment of NHL. Elucidation of the mechanisms underlying resistance of ALL and CLL cells to CD95 triggering may facilitate the development of novel therapeutic approaches to these diseases as well.

Apoptosis↗
PubMed1997

Mutation and downregulation of the transforming growth factor beta type II receptor gene in primary squamous cell carcinomas of the head and neck.

In the present study, we analyzed 28 squamous cell carcinomas of the head and neck (SCCHN) for mutations in the coding region of TbetaR-II using 'Cold' SSCP and automatic DNA sequencing analyses. Twenty-one percent (6/28) of the SCCHN examined contained TbetaR-II mutations compared with patient-matched normal tissues. These alterations included five missense mutations (A:T-->G:C transitions in codons 250, 401, 448 and 488, and a G:C-->T:A transversion in codon 373), and a 38-bp deletion between nucleotides 1825 to 1862. In addition to these code-altering mutations, one case exhibited a silent mutation (A:T-->G:C transition in codon 451) and three cases contained one of two potential population polymorphisms (codons 354 and 389). In contrast to colon and gastric cancers exhibiting microsatellite instability (MI) or replication errors (RER+), no 'indirect' frameshift mutations were identified within a 10-bp polyadenine repeat present in the TbetaR-II coding sequence. All of the mutations in the present study occurred within the highly conserved serine/threonine kinase domain and represent the first report of such 'direct' TbetaR-II mutations in primary human tumors. In addition, we analyzed a subset of SCCHN and corresponding normal samples for TbetaR-II mRNA expression using semi-quantitative multiplex RT-PCR. Expression of TbetaR-II was decreased by 24% to 74% in 20 of 23 SCCHN (87%) compared with patient-matched normal tissues. Taken together, the results from this study suggest that alterations in the nucleic acid sequence and mRNA expression of TbetaR-II are prevalent events in the development of SCCHN, which may deregulate cell cycle control.

Carcinoma, Squamous Cell↗
PubMed1997

Frequent occurrence of identical heavy and light chain Ig rearrangements.

Single-cell PCR analyses of expressed Ig H and L chain sequences presented here show that certain rearrangements occur repeatedly and account for a major segment of the well-studied repertoire of B-1 cell autoantibodies that mediate the lysis of bromelain-treated mouse erythrocytes, i.e. antibodies reactive with phosphatldyicholine (PtC). We repeatedly isolated at least 10 different types of VH region rearrangements, involving three distinct germline genes, among FACS-sorted PtC-binding B-1 cells from three strains of mice (C57BL/6J, BALB/c and C.B-17). The predominant rearrangement, VH11-DSP-JH1 (VH11 type 1), has been previously found in anti-PtC hybridomas in several studies. We show that within each of six mice from two strains (C57BL/6J and BALB/c), unique instances of IgH/IgL pairing arose either from different B cell progenitors prior to IgH rearrangement or from pre-B cells which expanded after IgH rearrangement but prior to IgL rearrangement. Together with other recurrent rearrangements described here, our findings demonstrate that clonal expansion of mature B cells cannot account for all repeated rearrangements. As suggested by initial studies of dominant idiotype expression, these findings confirm that clonal expansion is only one of the mechanisms contributing to the establishment of recurrent rearrangements.

Amino Acid Sequence↗
PubMed1997

The pathogenesis of hypertension in autosomal dominant polycystic kidney disease.

BACKGROUND: Hypertension is a common and serious complication of autosomal dominant polycystic kidney disease (ADPKD), often occurring early in the disease before the renal function starts to decrease. The pathogenesis of this early hypertension is controversial. OBJECTIVE: To review studies on the pathogenesis of early and late hypertension in ADPKD. STUDY SELECTION: Studies on ADPKD and hypertension were retrieved from Medline from the last 20 years, with an emphasis on the last 10 years. These studies, together with selected published abstracts from recent hypertension and nephrology meetings, were reviewed critically. RESULTS: Cyst growth, renal handling of sodium, activation of the renin-angiotensin-aldosterone system, volume expansion, an elevated plasma volume, and increased plasma atrial natriuretic peptide and plasma endothelin levels have all been found to be associated with hypertension in ADPKD. In some studies an inappropriate activity of the renin-angiotensin-aldosterone system that could be related to cyst growth and intrarenal ischemia was found. An increase in renal vascular resistance has been demonstrated and might be caused by intrarenal release of angiotensin II. Interestingly, the protective effect of angiotensin converting enzyme inhibitors on the renal function could not be demonstrated in ADPKD patients with a moderately decreased renal function. The importance, if any, of endothelial vasodilatory factors is not known. Sympathetic nervous activity seems to be increased in ADPKD, but the importance of this for the blood pressure level is not known. CONCLUSION: The pathogenesis of hypertension in ADPKD is complex and likely to be dependent on the interaction of hemodynamic, endocrine and neurogenic factors.

Atrial Natriuretic Factor↗
PubMed1997

An approach to the understanding of the nasal early-phase reaction induced by nasal allergen challenge.

Quantitative determinations of the inflammatory mediators in nasal secretions were performed and correlated with the objective nasal symptoms within 1 h after nasal allergen challenge (NAC). Twenty-six patients with seasonal allergic rhinitis were enrolled outside the pollen season. All measurements were performed before (as a baseline control) and at 1, 5, 10, 30, and 60 min after NAC. This study aimed to clarify the pathogenic mechanism of the early-phase reaction (EPR) by monitoring the evolution of early-phase mediators in nasal secretions and the presence of nasal symptoms during this period. The results showed that, after NAC, the maximal mediator concentration was already reached after 1 min for histamine (124 ng/g), 5 min for tryptase (56 microU/g), and 5-10 min for leukotriene C4 (40 ng/g). Itching and sneezing started as early as 20-30 s, and they were predominant symptoms within 5 min. Rhinorrhea and nasal obstruction started a few minutes after NAC and lasted until more than 1 h after NAC. There was no significant correlation between any single mediator and nasal symptoms during the sampling period. In conclusion, this study demonstrated that during the EPR the presence of nasal symptoms involves a complex mechanism, reflecting the interaction between the mediators released by inflammatory cells, and the receptors on different target organs. When evaluating symptoms during the EPR, one must consider not only the severity of these symptoms but also the time period within which these symptoms occur. For the symptoms of nasal obstruction and rhinorrhea, the early-phase reaction often lasted more than 1 h.

Adult↗
PubMed1997

Molecular analysis of the SNF2/SWI2 protein family member MOT1, an ATP-driven enzyme that dissociates TATA-binding protein from DNA.

MOT1 is an essential Saccharomyces cerevisiae protein and a member of the SNF2/SWI2 family of ATPases. MOT1 functions by removing TATA-binding protein (TBP) from DNA, and as a consequence, MOT1 can regulate transcription both in vitro and in vivo. Here we describe the in vivo and in vitro activities of MOT1 deletion and substitution mutants. The results indicate that MOT1 is targeted to TBP both in vitro and in vivo via amino acids in its nonconserved N terminus. The conserved C-terminal ATPase of MOT1 appears to contribute to TBP-DNA complex recognition in the absence of ATP, but it appears to function primarily during the actual ATP-dependent dissociation reaction. Chimeric proteins in which homologous portions of SNF2/SWI2 have been substituted for the MOT1 ATPase can bind to TBP-DNA complexes but fail to dissociate these complexes in the presence of ATP, suggesting that the specificity of action of MOT1 is also conferred by the C-terminal ATPase. ATPase assays demonstrate that the MOT1 ATPase is activated by TBP. Thus, MOT1 undergoes at least two conformational changes: (i) an allosteric effect of TBP that mediates the activation of the MOT1 ATPase and (ii) an ATP-driven "power stroke" that causes TBP-DNA complex dissociation. These results provide a general framework for understanding how members of the SNF2/SWI2 protein family use ATP to modulate protein-DNA interactions to regulate many diverse processes in cells.

Adenosine Triphosphatases↗
PubMed1997

Mechanisms underlying the chronotropic effect of angiotensin II on cultured neurons from rat hypothalamus and brain stem.

The chronotropic effect of angiotensin II (Ang II) was studied in cultured neurons from rat hypothalamus and brain stem with the use of the patch-clamp technique. Ang II (100 nM) increased the neuronal spontaneous firing rate from 0.8 +/- 0.3 (SE) Hz in control to 1.3 +/- 0.4 Hz (n = 7, P < 0.05). The amplitude of threshold stimulation was decreased by Ang II (100 nM) from 82 +/- 4 pA to 62 +/- 5 pA (n = 4, P < 0.05). These actions of Ang II were reversed by the angiotensin type 1 (AT1) receptor antagonist losartan (1 microM). In the presence of tetrodotoxin, Ang II (100 nM) significantly increased the frequency and the amplitude of the Cd2+-sensitive subthreshold activity of the cultured neurons. Ang II also stimulated the subthreshold early afterdepolarizations (EADs) to become fully developed action potentials. Similar to the action of Ang II, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA, 100 nM) increased the firing rate from 0.76 +/- 0.3 Hz to 2.3 +/- 0.5 Hz (n = 6, P < 0.05) and increased the neuronal subthreshold activity. After neurons were intracellularly dialyzed with PKC inhibitory peptide (PKCIP, 5 microM), PMA alone, Ang II alone, or PMA plus Ang II no longer increased the action potential firing initiated from the resting membrane potential level. However, superfusion of PMA plus Ang II or Ang II alone increased the number of EADs that reached threshold and produced action potentials even in the presence of PKCIP (5 microM, n = 4). The actions of Ang II could also be mimicked by depolarizing pulse and K+ channel blockers (tetraethylammonium chloride or 4-aminopyridine). These results indicate that Ang II by activation of AT1 receptors increases neuronal excitability and firing frequency, and that this may involve both PKC dependent and -independent mechanisms.

4-Aminopyridine↗
PubMed1997

A-type K+ current in neurons cultured from neonatal rat hypothalamus and brain stem: modulation by angiotensin II.

The regulation of A-type K+ current (I(A)) and the single channel underlying I(A) in neonatal rat hypothalamus/brain stem cultured neurons were studied with the use of the patch-clamp technique. I(A) had a threshold of activation between -30 and -25 mV (n = 14). Steady-state inactivation of I(A) occurred between -80 and -70 mV and had a membrane voltage at which I(A) was half-maximum of -52.2 mV (n = 14). The mean values for the activation and inactivation (decay) time constants during a voltage step to +20 mV were 2.1 +/- 0.3 (SE) ms (n = 8) and 13.6 +/- 1.9 ms (n = 8), respectively. Single-channel recordings from outside-out patches revealed A-type K+ channels with voltage-dependent activation, 4-aminopyridine (4-AP) sensitivity, and inactivation kinetics similar to those of I(A). The single-channel conductance obtained from cell-attached patches was 15.8 +/- 1.3 pS (n = 4) in a physiological K+ gradient and 41.2 +/- 3.7 pS (n = 5) in symmetrical 140 mM K+. Angiotensin II (Ang II, 100 nM) reduced peak I(A) by approximately 20% during a voltage step to +20 mV (n = 8). Similarly, Ang II (100 nM) markedly reduced single A-type K+ channel activity by decreasing open probability (n = 4). The actions of Ang II on I(A) and single A-type K+ channels were reversible either by addition of the selective angiotensin type 1 (AT1) receptor antagonist losartan (1 microM) or on washout of the peptide. Thus the activation of AT1 receptors inhibits a tetraethylammonium-chloride-resistant, 4-AP-sensitive I(A) and single A-type K+ channels, and this may underlie some of the actions of Ang II on electrical activity of the brain.

4-Aminopyridine↗
PubMed1997

In vitro plasticity of the direct feedback pathway in the electrosensory system of Apteronotus leptorhynchus.

We have used field and intracellular recording from pyramidal cells in an in vitro preparation of the electrosensory lateral line lobe (ELL) of Apteronotus leptorhynchus to investigate synaptic plasticity of a direct feedback pathway: the (StF). Tetanic stimulation of the StF enhanced the StF-evoked synaptic response by 145% in field and the excitatory postsynaptic potential (EPSP) 190% in intracellular recordings. Maximal enhancement occurred at 5 s and lasted for approximately 120 s. Tetanic frequencies of 100-300 Hz produced enhancement; lower or higher frequencies failed to produce statistically significant changes in EPSP amplitude. Rates of 100-200 Hz occur in vivo in the cells of origin of the StF, suggesting that this form of plasticity may be operative under natural conditions. We could not elicit either long-term potentiation or depression by any stimulation protocol of the StF; in the case of long-term potentiation, this held even when excitatory transmission was enhanced by application of bicuculline, a gamma-aminobutyric acid-A antagonist. When tetanic stimulation of the StF was paired with hyperpolarization of pyramidal cells, subsequent StF-evoked EPSPs were increased by 146% (5 min posttetanus); this anti-Hebbian synaptic enhancement lasted for approximately 10 min. Neither tetanic stimulation alone, hyperpolarization alone, nor tetanic stimulation paired with pyramidal cell depolarization altered StF-evoked EPSP amplitudes on this time scale. Anti-Hebbian synaptic enhancement was not blocked by the N-methyl--aspartate-receptor antagonist D. L-aminophosphovalerate. The in vitro demonstration of anti-Hebbian plasticity at StF synapses replicates similar in vivo results. Anti-Hebbian synaptic plasticity of the StF may be responsible in part for the ability of gymnotiform fish to reject redundant electrosensory signals.

Animals↗
PubMed1997

Effect of topical applications of budesonide and azelastine on nasal symptoms, eosinophil count and mediator release in atopic patients after nasal allergen challenge during the pollen season.

We studied the activity of a topical form of a corticosteroid (budesonide) and an antihistamine (azelastine) in the treatment of seasonal allergic rhinitis by including an assessment of mediator concentrations and the percentage of eosinophils in the nasal secretions before and after the treatment. Nasal allergen challenge (NAC) during the season was performed to mimic an acute attack of allergic rhinitis and to objectively evaluate the effect of the drugs on the early-phase reaction. The study compared in a randomized way (2 parallel groups) the effect of budesonide (Rhinocort Aqua) and azelastine (Allergodil nasal spray) in a group of 14 patients during the pollen season. The study showed that azelastine significantly reduced sneezing, total nasal resistance and increased nasal airflow even when significant increases in histamine, tryptase and leukotriene C4 (LTC4) concentrations in nasal secretions were evidenced immediately after NAC. Budesonide showed a strong (p<0.05) decrease in infiltration and activation of eosinophils, and on tryptase and LTC4 release after NAC. These effects (not for LTC4) lasted at least for 1 week after therapy. Azelastine is a powerful topical antihistamine, while budesonide appears to be a potent long-acting anti-inflammatory agent.

Adolescent↗
PubMed1997

Eotaxin protein and gene expression in guinea-pig lungs: constitutive expression and upregulation after allergen challenge.

Eotaxin is an eosinophil-specific chemoattractant originally identified in bronchoalveolar lavage fluid after allergen challenge of sensitized guinea-pigs. We have determined and quantified for the first time the cellular sources of guinea-pig lung eotaxin and localized gene expression in structural cells of large and small airways and in alveolar macrophages. We used anti-guinea-pig eotaxin monoclonal and polyclonal antibodies and a complementary ribonucleic acid (cRNA) probe to detect eotaxin protein and cytoplasmic messenger ribonucleic acid (mRNA) transcripts by the techniques of immunohistochemistry and in situ hybridization in: 1) naive; 2) ovalbumin-sensitized/ saline-exposed; and 3) ovalbumin-sensitized/ovalbumin-challenged animals (n = 5 for each group). Compared with the naive animals, there was a fivefold increase of eotaxin protein and a 25 fold upregulation of eotaxin gene expression in the airway epithelium 3 h after ovalbumin challenge of sensitized animals (p < 0.001). The average percentages of alveolar macrophages staining for eotaxin protein and mRNA in the naive animals were approximately 30 and 10% respectively: both increased significantly in the sensitized/ovalbumin-challenged animals to 78 and 57%, respectively (p < 0.0001). Compared with the naive animals, the procedure of sensitization and saline exposure significantly increased eotaxin gene expression in both bronchial epithelium and alveolar macrophages (p < 0.01): the upregulation at these two sites showed a strong positive association (rcorr = 0.95; p < 0.0001). The results indicate that there are multiple cellular sources of guinea-pig lung-derived eotaxin, including bronchial and bronchiolar epithelial cells, airway smooth muscle, bronchial vascular endothelium, and chondrocytes and alveolar macrophages, and that there are relatively rapid and marked increases of eotaxin protein and gene expression in airway epithelium and alveolar macrophages following allergen challenge.

Allergens↗
PubMed1997

[Expression and antagonist role of endothelin and nitric oxide synthase in atherosclerotic plaque].

OBJECTIVE: To study the pathogenetic mechanism of atherosclerotic plaque, the action of mediation and antagonism of endothelin (ET) and nitric oxide synthase (NOS) was investigated. METHODS: In situ hybridization, RT-PCR on endothelin and NOS, cytochemistry on NOS were measured using the rabbit atherosclerosis model and cultured vascular smooth muscle cells (VSMC) from normal rabbit. RESULTS: Transcription of endothelin mRNA increased and transcription of NOS mRNA decreased in astherosclerotic plaque: compared with normal aorta, expression of ET gene in plaque was increased by 1.2 times and the expression of NOS gene was decreased by 22.2%; cytochemistry combined with image pattern analysis showed that ET could inhibit NOS protien synthesis in VSMC; type A receptor antagonist of ET could inhibit the role of ET which causes a decrease of NOS protein in VSMC. CONCLUSION: The imbalance between NOS and ET, namely abnormal increase of ET and/or obvious decrease of NOS, is related to atherosclerotic plaque formation.

Animals↗
PubMed1997

[A study on the loss of heterozygosity at 17p13.3 and abnormal expression of p53 protein in gastric carcinoma].

OBJECTIVE: To evaluate the role of 17p13.3 loss and abnormal expression of p53 in the development and progress of gastric carcinoma. METHODS: The loss of heterozygosity (LOH) at 17p13.3 and abnormal expression of p53 gene were examined with PCR-RFLP and immunohistochemical methods in 51 surgical specimens of gastric carcinoma. RESULTS: LOH at 17p13.3 was detected in 16/31 cases (51.6%) and positive staining for p53 protein was found in 19/51 cases (37.3%). No significant correlation was found between LOH at 17p13.3 and abnormal expression of p53 or between these two events in any clinicopathological parameters. LOH was found in one cases of early gastric cancer. CONCLUSIONS: These results suggest that LOH at 17p and abnormal expression of p53 protein are frequently found in gastric carcinoma and may play an important role in the carcinogenesis and progress of both intestinal and gastric types of gastric cancer.

Adenocarcinoma↗