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R Huang

Publications and source records attributed to R Huang.

At least 181 records · Page 10Linked to original sources
PubMed1993

Expression of a mast cell tryptase in the human monocytic cell lines U-937 and Mono Mac 6.

Expression of a mast cell tryptase mRNA was detected in two human monocytic cell lines, the U-937 and the Mono Mac 6, and in normal human peripheral blood (PB) monocytes. In the U-937 cell line but not in normal PB monocytes, the tryptase expression was upregulated 3-50 fold following phorbol ester (PMA)-induced differentiation, but no such induction was seen after retinoic acid, interferon-gamma or vitamin D3 exposure. The tryptases expressed in PMA-induced and non-induced U-937 and in Mono Mac 6 were characterized by PCR amplification and nucleotide sequence analysis. The U-937 cell line was found to express a tryptase identical to one of the previously cloned mast-cell beta tryptases (Tryptase I), and the tryptase expressed in Mono Mac 6 was found to be nearly identical to the previously cloned alpha tryptase. By northern blot analysis with oligonucleotide probes specific for the alpha and beta tryptases both cell lines were found to express only one type of tryptase. Densitometric quantifications of tryptase mRNA levels, in the two cell lines, showed approximately 80 times higher mRNA levels in Mono Mac 6 compared to non-induced U-937. Immunohistochemical staining for tryptase showed a marked heterogeneity in the Mono Mac 6 cell line. Only one out of 10 cells were positive for the protein but the levels in these cells were very high, equivalent, or even higher than the levels seen in the human mast cell line HMC-1. This shows that the expression of a single tryptase, in this case the alpha tryptase, is sufficient for the production of a stable protein and probably also a stable proteolytically active tetramer. The family of human mast-cell tryptases has been considered to represent a class of proteases specifically expressed in mast cells and basophilic leucocytes. The expression of tryptases in two monocytic cell lines and in normal PB monocytes indicate that in humans, the lineage specificity of these serine proteases is less restricted than earlier expected. The cloning of a full length cDNA for the murine counterpart to the human mast cell tryptases, the MMCP-6, is presented. No expression of the MMCP-6 was detected in a panel of mouse monocyte or macrophage cell lines indicating a species difference in the lineage specificity of the 'mast cell tryptases'.

Animals↗
PubMed1993

Glutamate and glutamine metabolism and compartmentation in astrocytes.

Metabolism of glutamate and glutamine in cultured mouse cerebral cortical astrocytes has been investigated using either radioactively labelled (14C) amino acids or 13C-labelled amino acids combined with NMR spectroscopy of cell extracts and lyophilyzed incubation media. Using [U-13C]glutamate it has been shown that in astrocytes exogenously supplied glutamate is primarily (70%) metabolized oxidatively through the tricarboxylic acid (TCA) cycle and to a lesser extent (30%) directly to glutamine. Glutamate metabolized in the TCA cycle is to a large extent recovered as lactate showing that the astrocyte-specific enzyme, malic enzyme is functionally active. Incubation with [U-14C]glutamine led to a higher specific radioactivity in glutamate than in glutamine. It could also be shown that glutamate and glutamine were metabolized differently to aspartate and alanine. These results taken together strongly suggest that glutamate/glutamine metabolism in astrocytes is compartmentalized and a model with multiple cytoplasmic and mitochondrial compartments of these amino acids is proposed.

Animals↗
PubMed1993

Utilization of glutamine and of TCA cycle constituents as precursors for transmitter glutamate and GABA.

In the present review evidence is presented that (1) glutamine synthesis in astrocytes is essential for synthesis of GABA in neurons; (2) alpha-ketoglutarate in the presence of alanine (as an amino group donor) can replace glutamine as a precursor for synthesis of transmitter glutamate, but maybe not as a precursor for transmitter GABA; (3) differences exist in the intraneuronal metabolic pathways for utilization of alpha-ketoglutarate plus alanine and of glutamine, and (4) alanine also functions as a substrate for oxidative metabolism in glutamatergic neurons. It should be emphasized that the supply of precursors for transmitter glutamate and GABA in glutamatergic and GABAergic neurons depends on metabolic processes in astrocytes regardless whether glutamine or alpha-ketoglutarate plus L-alanine function as the transmitter precursors. The key reason that an interaction with astrocytes is essential is that both pyruvate carboxylase, the major enzyme in the brain for net synthesis of tricarboxylic acid cycle intermediates, and glutamine synthetase, the enzyme forming glutamine from glutamate, are specifically located in astrocytes, but not in neurons.

Animals↗
PubMed1993

A study of changes in the marital pattern of Chinese women in the past 40 years.

"There has been a considerable amount of research on changes in the pattern of first marriage among Chinese women and its impact on [the] fertility rate since 1950. This paper attempts to establish several indexes for measuring various dimensions subsumed in the status of 'being married'...to expound the inter-relationships between the number and structure of marriages and the index of first marriage in the population."

Asia↗
PubMed1992

Phenotypic characterization of KU812, a cell line identified as an immature human basophilic leukocyte.

The knowledge about the differentiation of basophilic leukocytes is fragmentary. This report discusses a detailed phenotypic characterization of molecular markers for hematopoietic differentiation in a basophilic leukemia cell line, KU812. The expression of markers for lymphoid, erythroid, neutrophil, eosinophil, monocytic, megakaryocytic, mast cell and basophil differentiation was analyzed at the mRNA level by Northern blots in the KU812 cells, and for reference, in a panel of human cell lines representative of the different hematopoietic differentiation lineages. KU812 was found to express a number of mast cell and basophil-related proteins, i.e. mast cell tryptase, mast cell carboxypeptidase A, high-affinity immunoglobulin (IgE) receptor alpha and gamma chains and the core protein for heparin and chondroitin sulphate synthesis. We found no expression of a number of monocyte/-macrophage or neutrophil leukocyte markers except for lysozyme. From earlier studies, it has been shown that lysozyme is not expressed in murine mucosal mast cell lines. This finding, together with the expression of the mast cell carboxypeptidase in KU812 might distinguish the phenotype of this cell line from that typical of mucosal mast cell lines in rodents. We found a low level of expression of the eosinophil and basophil marker, major basic protein, which might indicate a relationship between basophils and eosinophils. No expression is, however, detected with the eosinophil-specific markers eosinophil cationic protein, eosinophil-derived neurotoxin or eosinophil peroxidase. We also report an extensive screening for inducers of basophilic differentiation of the KU812 cells. The most efficient protocol of induction included serum starvation which led to a dramatic increase in a number of markers specific for mast cells and basophils such as tryptase, carboxypeptidase A and the heparin core protein. Finally, diisopropylfluorophosphate analysis of total protein extracts from KU812 show four labeled protein bands with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, indicating that this cell line expresses at least three previously undescribed serine proteases of which one or more could be a potential basophil-specific marker(s).

Basophils↗
PubMed1992

Prospective analysis of mental status progression in ethanol-intoxicated patients.

Distinguishing patients with uncomplicated ethanol intoxication from intoxicated patients with other causes of mental status depression is a common clinical dilemma. The authors serially tested mental status in a group of ethanol-intoxicated patients to determine the interval over which mental status changes could be attributed to uncomplicated intoxication. Study patients were identified by (1) admission breath ethanol greater than or equal to 100 mg/dL; (2) ethanol-related impairment necessitating further observation or treatment; and (3) not critically ill or exhibiting focal neurologic signs. Mental status scores (sums of specific indices of alertness, orientation, and agitation) were determined initially, 1 hour after arrival, then every 2 hours. Causes of mental status depression other than acute intoxication were diagnosed in 16 patients, while another 18 failed to completely normalize mental status by the time of emergency department discharge or hospital admission. The remaining 71 with uncomplicated ethanol intoxication required (mean +/- SD) 3.2 +/- 3.6 hours to normalize mental status scores. A large proportion, however, took considerably longer to normalize mental status: 15 (21%) took 7 or more hours, and three (4%) took as long as 11 hours. Although patients with ethanol-associated depression of mental status lasting 3 hours after emergency department admission should be carefully evaluated for other causes of mental status abnormalities, the authors' observations indicate considerable individual variation in the duration of mental status depression caused by uncomplicated ethanol intoxication.

Alcoholic Intoxication↗
PubMed1992

Effect of body locale and addition of epinephrine on the duration of action of a local anesthetic agent.

STUDY OBJECTIVE: Little information exists relating body locale to the duration of action of local anesthetics. We tested the duration of action of a local anesthetic with and without epinephrine at different body locales. PARTICIPANTS: Twenty healthy volunteers aged 27 to 48 years (mean, 32.0 years). INTERVENTIONS: In the first of two experiments (L), 20 subjects had 1 mL buffered 1% lidocaine injected intradermally on the forehead, hand, forearm, and calf. In the second experiment (LE), ten subjects were injected at the same sites with lidocaine containing epinephrine. METHODS: Subjects ranked anesthesia by reaction to pinprick from 0 (complete) to 20 (none) on a scale with testing done every 15 (L) or 30 (LE) minutes and continued until no anesthetic effect was present. Duration of effective and of any anesthesia were times until score of more than 5 and of more than 19, respectively. Mean duration of anesthesia was compared by analysis of variance (between body areas) and paired two-tailed t-test (L vs LE). Significance was taken as P less than or equal to .05. RESULTS: Anesthesia was significantly briefer for the face than for all other body locales by both indexes of duration and for both plain lidocaine and lidocaine with epinephrine (P less than .001 to P less than .05). Anesthesia with epinephrine lasted significantly longer than with lidocaine alone at all body locales and for duration of both effective or any anesthesia (P = .0001 to P = .001). Based on 95% confidence interval limits, the duration of anesthesia at other body locales is predicted to be 1.3- to 3.2-fold that on the face. Confidence interval analysis indicated that addition of epinephrine to lidocaine increases the duration of anesthetic action by 1.3- to 13.0-fold that of lidocaine alone. CONCLUSION: The duration of action of local anesthesia is considerably shorter for the face than for other body areas. Epinephrine significantly increases the duration of action of lidocaine at all body locales.

Adult↗
PubMed1991

Antiviral activity of some natural and synthetic sugar analogues.

A number of natural and synthetic sugar analogues have been tested for their antiviral activity, using an influenza virus strain as a model. Hemagglutinating titres (HA) and cytopathic effect (CPE) were surveyed to estimate the virus production. It was found that introduction of the benzyl group into these sugars generally causes them to become antivirally active. Substitution with methyl, acetyl, uridyl and thiocyanyl groups or derivatization with azido, isopropylidene and benzylidene groups were without effect. All sugars containing the 2-deoxy-2-acetamido group were inactive.

Animals↗
PubMed1991

Elevated cytosolic Ca2+ activates phospholipase D in human platelets.

We have examined the activation of phospholipase D in human platelets treated with alpha-thrombin. When incubated with 1-O-[9,10-3H2]hexadecyl-2-lysophosphatidylcholine (PtdCho) and 1-alkyl-[32P]lysoPtdCho for 2 h, platelets formed 3H/32P-labeled PtdCho in a ratio of 11:1. After incubation of such labeled platelets with alpha-thrombin for 5 min, increased accumulation of 3H/32P-labeled phosphatidic acid (PtdOH) was detected in the same ratio, indicating the action of phospholipase D. The Ca2+ ionophore A23187 and alpha-thrombin each stimulated the formation of labeled PtdOH as above in a time- and concentration-dependent manner, with only minor changes in labeled diglyceride. A23187 was able to cause increases in labeled PtdOH comparable to those observed with alpha-thrombin. beta-Phorbol 12,13-dibutyrate, an activator of protein kinase C, only slightly stimulated the accumulation of labeled PtOH. The protein kinase C inhibitor, staurosporine, totally blocked these changes but only slightly inhibited the increases in labeled PtdOH promoted by alpha-thrombin. These results suggest that an increase in intracellular Ca2+, rather than protein kinase C activity, is a major factor regulating phospholipase D in platelets exposed to alpha-thrombin. We have also examined the relative contributions of phospholipase D and diglyceride kinase (following phospholipase C action) to PtdOH accumulation in [32P]Pi-labeled platelets by comparing the 32P-specific radioactivities of PtdOH, PtdCho, and metabolic gamma-ATP in control and alpha-thrombin-exposed platelets. Based on these determinations, we conclude that 13 and 87% of incremental PtdOH in human platelets exposed to alpha-thrombin arises via phospholipase D acting on PtdCho and phospholipase C/diglyceride kinase, respectively.

Alkaloids↗
PubMed1991

Cytokines regulating human B cell growth and differentiation.

Utilizing a model system of anti-CD3-stimulated T cells, we have identified a potent B cell differentiation factor (BCDF) in the supernatant of these cells. This factor, 446-BCDF, appears to act on SAC-activated B cells inducing a 10- to 100-fold increase in Ig secretion. 446-BCDF has an apparent MW of 32 kDa and a pI of 6.0. Its activity cannot be inhibited by an anti-IL-6 antiserum, and activity is enhanced after passage over an anti-IL-6 affinity column. 446-BCDF activity is detected in the 50 mM salt fraction eluted from a Mono Q column. This 50 mM fraction has the only activity detected after passage over an anti-IL-6 affinity column and migrates with an apparent pI of 6.0. Taken together these data suggest that 446-BCDF is a unique potent polyclonal human BCDF which may be a predominant factor regulating terminal B cell differentiation.

Antibodies, Monoclonal↗
PubMed1991

[Acid-base imbalance in acute cerebrovascular diseases].

Ninety cases of cerebral hemorrhage or infarction confirmed with CT scans were reported. Blood specimens were taken within 4 to 24 hours after the onset of the strokes for blood gas analysis. The results showed that respiratory alkalosis occurred in all patients with cerebral hemorrhage or embolism, while the metabolic acidosis accompanied only those with severe cerebral infarctions or intracerebral hematomas rupturing into the ventricles small local infarcts caused only hypoxemia or no changes at all. It seemed likely that the blood acid-base changes were closely related to the nature and the size of the lesions. It was suggested that since hyperventilation caused by cerebral lesions might be the main factor that give rise to respiratory alkalosis, it would be of great importance to maintain the acid base balance in the acute stage of the stroke with proper dehydration therapy and oxygen administration.

Acid-Base Imbalance↗
PubMed1991

Anti-PPD antibodies in Chinese Behçet's disease.

Anti-PPD antibody determinations were carried out by the ELISA method using extracted PPD of tubercle bacillus H37RV as the target antigen. The positive rates of anti-PPD antibodies in patients with active tuberculosis, inactive tuberculosis, Behçet's disease, or non-tubercular disease and in a village population were 97.5%, 77.4%, 48.9%, 33.6% and 13.9%, respectively. Although the average titer of anti-PPD antibodies in Behçet's disease was lower (2.168 +/- 0.854) than that in active tuberculosis (3.126 +/- 1.182), it was about the same as that in inactive tuberculosis (2.336 +/- 1.250). In comparison with the village community population surveyed, the average titer of anti-PPD antibodies in Behçet's disease patients was distinctly higher (P less than 0.001). These results indicate that tuberculosis may be etiologically related to Behçet's disease.

Antibodies, Bacterial↗