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Biomedical subjects

D Cheng

Publications and source records attributed to D Cheng.

At least 91 records · Page 5Linked to original sources
PubMed1998

[Therapeutic effects of ultrashort wave and He-Ne laser on experimental infection in skin flaps of rabbits].

In order to investigate the therapeutic effects of ultrashort wave and He-Ne laser on experimentally infected skin flaps, 24 lower abdominal skin flaps on 24 rabbits were established, under each flap 1 ml of S. aureus (9 x 10(8) bacterials/ml) was injected respectively. Then, ultrashort wave and He-Ne laser were utilized respectively in 2 groups once a day for 6 days, with on treatment in two another two groups as control groups. After the period of treatment, the 4 groups were evaluated in the bacterial amounts, thickness of skin flaps and degree of infection. The results showed that the skin flaps in the treatment groups were much better than those in the control groups. It suggested that both the ultrashort wave and He-Ne laser are helpful in the treatment of infection of S. aureus in skin flaps.

Animals↗
PubMed1998

[Cromakalim inhibits endothelin-1 induced pulmonary hypertension in rats].

There is evidence that endothelin-1 (ET-1) and potassium channel may play an important role in the development of pulmonary hypertension. To evaluate the effect of ATP-sensitive K+ channel opener on pulmonary hypertension induced by ET-1, catheter was inserted into the pulmonary artery in ten male Wistar rats which had had pulmonary hypertension established by infusion of ET-1 (1.5 micrograms/kg), and then cromakalim were injected with a dose of 150 micrograms/kg. The mean pulmonary arterial pressure (mPAP), cardiac output (CO) monitored before and after infusion of ET-1, and 1 min, 5 min, 10 min after cromakalim injection, and pulmonary vascular resistance (PVR) were calculated. It was found that the mPAP was significantly increased, from 2.36 +/- 0.24 kPa to 3.32 +/- 0.49 kPa(P < 0.01), and PVR also increased, by infusion of ET-1. After cromakalim injection, mPAP were decreased to 2.50 +/- 0.62 kPa in 1 min, 1.14 +/- 0.18 kPa in 5 min and 2.33 +/- 0.52 kPa in 10 min, PVR decreased significantly. It is suggested that there is interaction between ET-1 and potassium Channel, and Cromakalim decreases mPAP in part by inhibiting the response of pulmonary artery to ET-1.

Animals↗
PubMed1998

[Changes of the gene expression of vascular endothelial growth factor in the lung of rats with chronic hypoxic pulmonary hypertension].

To observe the effect of chronic hypoxia on the gene expression of vascular endothelial growth factor (VEGF) in rat's lung, and the role of VEGF in the pathogenesis of hypoxic pulmonary hypertension, thirteen male Wistar rats were exposed to isobaric hypoxia for 3 weeks. The pulmonary artery pressure was measured by right cardiac catheterization. The serum level of VEGF was measured by Elisa. The VEGF cRNA was labeled with digoxigenin-UTP by in vitro transcription. The expression of VEGF mRNA in the lung was examined by hybridization in situ. The pulmonary artery pressure was significantly increased after hypoxic exposure. The serum level of VEGF in rats treated with hypoxia (420.3 +/- 73.1 pg/ml) was significantly increased in comparison with that of normal rats (322.2 +/- 58.1 pg/ml). The VEGF hybridization signals on the wall of pulmonary arteriole were significantly increased in rats with pulmonary hypertension. Chronic hypoxia can markedly increase expression of VEGF mRNA in the pulmonary arteriole and hence stimulate VEGF synthesis and secretion. The increase of VEGF may play a role in the developing process of hypoxic pulmonary hypertension.

Animals↗
PubMed1998

[Changes of level and distribution of vascular endothelial growth factor in the lungs of rats with hypoxic pulmonary hypertension].

This study was designed to elucidate whether the level and distribution of vascular endothelial growth factor (VEGF) are changed in the lungs of rats with hypoxic pulmonary hypertension. 13 male Wistar rats were exposed to isobaric hypoxia for 3 weeks. The pulmonary artery pressure was measured by right cardiac catheterization. The level of VEGF in pulmonary homogenate was measured by Elisa method. The distribution of VEGF in the rat lung was examined by immunohistochemistry. The results showed that the pulmonary artery pressure was significantly increased after hypoxic exposure. The level of VEGF in pulmonary homogenate of rats treated with hypoxia (466.9 +/- 75.5 pg/g) were significantly increased as compared with taht of normal rats (376.2 +/- 47.1 pg/g). The contents of VEGF in the wall of pulmonary arteriole were significantly increased in rats with pulmonary hypertension. So we suggest that chronic hypoxia can strongly stimulate VEGF secretion, and VEGF may mediate the process of hypoxic pulmonary vascular remodeling and pulmonary hypertension.

Animals↗
PubMed1998

[Isolation and identification of smooth muscle cells from pulmonary artery in rats].

To explore the method of isolating acutely the smooth muscle cells from pulmonary artery in rats, small pulmonary arteries (700-200 microns, ID) were dissected free of connective tissue and were allowed to digest in a N-2-hydroxyethyl-piperazine-N'-2-ethanesulfonic acid(HEPES)-buffered physiological saline solution (HPSS) containing collagenase, papain and bovine serum albumin. The tissue was then triturated to disperse smooth muscle cells. The isolated cells in suspension were identified and photographed with film on electron microscope (EM). We succeeded in isolating the single smooth muscle cell, which appeared compressed typically. 90% cells in suspension were identified smooth muscle cells on EM. We conclude that the method for isolation of pulmonary arterial smooth muscle cells is simple, stable and effective and is recommanded for use.

Animals↗
PubMed1998

[The change of plasma level of endothelin in patients with acute attack of asthma].

In order to assess the interaction of endothelin (ET) and acute attack of asthma, the plasma levels of ET in 23 patients with acute attack of asthma and 12 normal controls were measured by radioimmunoassay. The partial pressure of oxygen in arterial blood (PaO2) and peak flow (PEF) were measured synchronously. The results showed that the plasma ET level in asthmatic patients (89.2 +/- 8.4 ng/L) was much higher than that in normal controls (52.2 +/- 6.5 ng/L), P < 0.001. There was a significant negative correlation between the plasma level of ET and the PaO2 (r = -0.7893, P < 0.01) or PEF (r = -0.7124, P < 0.01). The results suggest that ET may play a role in acute attack of asthma, and its level may stand for the degree of the disease.

Adolescent↗
PubMed1998

[The inhibition effect of acute hypoxia on K+Ca-ATP channels of pulmonary artery smooth muscle cells of rats].

OBJECTIVE: To explore the possible mechanism underlying hypoxic pulmonary vasoconstriction, we evaluated the effect of acute hypoxia on potassium channels in pulmonary artery smooth muscle cells. METHOD: The single smooth muscle cell was freshly isolated from pulmonary artery (phi 700-200 microns) of Wistar rats with acute enzymatic digestion method. In symmetrical high K+ solution, we separated one outward K+ current from the patch of smooth muscle cells with inside-out configuration using patch-clamp technique. According to the electrophysiological response to the patch channel, this current was identified as the Ca2+, ATP activated potassium channel (K+Ca-ATP). The hypoxic solution was obtained by aeration with 5% CO2-balance N2 mixture. RESULT: The currents of K+Ca-ATP in the patch of smooth muscle cells was much inhibited while the oxygen tension of solution was reduced from normoxic (PO2 > or = 13.33 kPa) to hypoxic (PO2 < or = 2.67 kPa) levels (P < 0.01). Cromakalim (10 nmol/L), an opener of potassium channel, could activate the currents of K+Ca-ATP decreased by acute hypoxia (P < 0.01). CONCLUSION: Acute hypoxia has an inhibition role on K+Ca-ATP currents in pulmonary artery smooth muscle cells, causes the membrane potentional depolarization, leads to pulmonary vasoconstriction, increases pulmonary vascular resistance and artery pressure. The decrease of K+Ca-ATP contributes to development of hypoxic pulmonary vasoconstriction. Cromakalim is one of effective antagonists for hypoxic pulmonary vasoconstriction.

Animals↗
PubMed1998

[Effect of tetrandrine on the collagen contents of lungs in rats with chronic hypoxia].

OBJECTIVE: To investigate the effect of tetrandrine (Tet) on the collagen contents of lung tissues in rats with chronic hypoxic pulmonary hypertension. METHOD: Using colorimetric method after oxidized by chloramine T to determine hydroxyproline contents of lung tissues and extrapulmonary arteries, using Masson method, image pattern analysis technique and gray scale scanning to observe the changes of collagen distribution in extrapulmonary arteries and lung tissues in rats with hypoxia and the effect of treatment with Tet. RESULT: Tet could remarkably reduce the mean pulmonary arterial pressure and pulmonary vascular resistance in rats with hypoxic pulmonary hypertension and could inhibit the increase of collagen contents in lung tissues and extrapulmonary arterial wall. CONCLUSION: Tet may be used as one of the main drugs in the treatment of chronic hypoxic pulmonary hypertension due to its action of reducing mPAP and collagen contents.

Alkaloids↗
PubMed1998

[Inhibition of potassium channel by chronic hypoxia on pulmonary artery smooth muscle cells in rats].

OBJECTIVE: To explore the possible effect of potassium channel in chronic hypoxic pulmonary hypertension. METHOD: Male Wistar rats were placed in the identical normobaric or hypoxic environmental chamber. In one chamber, rats were maintained in 10% +/- 0.5% O2(by displacement with N2) for 3 weeks, whereas in the other, rats were maintained in air. The single smooth muscle cell was isolated from pulmonary artery (phi 200-700 microns) of Wistar rats with acute enzymatic digestion method. Using patch-clamp technique, we recorded the outward K+ currents in pulmonary artery smooth muscle cells and identified a Ca2+.ATP activated K+ channel (K+Ca-ATP) and a delayed rectifier K+ channel among the outward K+ currents. We compared the activities of Ca2+.ATP activated K+ channel (K+Ca-ATP) or delayed rectifier K+ channel in smooth muscle cells isolated from pulmonary artery of chronic hypoxic and normoxic rats. RESULT: The activities of Ca2+.ATP activated K+ channel (K+Ca-ATP) and delayed rectifier K+ channel in chronic hypoxic group are much lower than that in normal group (T test, P < 0.01). Cromakalim (10 mmol) caused a marked enhancement of activity of the reduced K+Ca-ATP but not the delayed rectifier K+ channel in rats of hypoxic group. CONCLUSION: The persistent decrease of potassium channel activity may contribute to setting the development of chronic hypoxic pulmonary hypertension. Cromakalim, one of potassium channel openers, can decrease the pulmonary hypertension induced by chronic hypoxia and may be a new effective drug for treatment of hypoxic pulmonary hypertension.

Animals↗
PubMed1997

Identification of complexes between the COOH-terminal domains of sterol regulatory element-binding proteins (SREBPs) and SREBP cleavage-activating protein.

SREBP cleavage-activating protein (SCAP) stimulates the proteolytic cleavage of membrane-bound SREBPs, thereby initiating the release of NH2-terminal fragments from cell membranes. The liberated fragments enter the nucleus and stimulate transcription of genes involved in synthesis and uptake of cholesterol and fatty acids. Sterols repress cleavage of SREBPs, apparently by interacting with the membrane attachment domain of SCAP. In the present studies we show that SCAP, like the SREBPs, is located in membranes of the endoplasmic reticulum and nuclear envelope. The COOH-terminal domain of SCAP, like that of the SREBPs, is located on the cytosolic face of the membranes. Co-immunoprecipitation experiments show that SCAP and SREBP-2 form a complex that can be precipitated with antibodies to either component. Complex formation occurs when cells express only the COOH-terminal domain of either SREBP-2 or SCAP, indicating that the complex forms between the two COOH-terminal domains. Truncation of SREBP-2 at its COOH terminus prevents the formation of complexes with SCAP and simultaneously reduces proteolytic cleavage. We conclude that proteolytic cleavage of SREBPs requires the formation of a complex with the COOH-terminal domain of SCAP and that SCAP is therefore a required element in the regulation of sterol and fatty acid metabolism in animal cells.

Animals↗
PubMed1997

Differentiation and death of premyelinating oligodendrocytes in developing rodent brain.

Previous studies have indicated that newly formed oligodendrocytes are dynamic cells whose production, survival, and differentiation depend upon axonal influences. This study has characterized the appearance and fate of newly formed oligodendrocytes in developing rat brain. Oligodendrocytes appear in predictable locations and radially extend DM-20-positive processes that cover 80-microm domains in the cortex and 40-microm domains in the corpus callosum. These premyelinating oligodendrocytes have one of two fates: they myelinate axons or degenerate. Between 7 and 21 d after birth, approximately 20% of premyelinating oligodendrocytes identified in the cerebral cortex were degenerating. Oligodendrocytes that ensheathed axons expressed and selectively targeted proteolipid protein to compact myelin and did not degenerate. These observations support the hypothesis that axonal influences affect oligodendrocyte survival, differentiation, and expression of proteolipid protein gene products.

Animals↗
PubMed1997

Undifferentiated U937 cells transfected with chemoattractant receptors: a model system to investigate chemotactic mechanisms and receptor structure/function relationships.

Transfection of either the C5a receptor or the formyl peptide receptor into undifferentiated U937 cells generated continuously growing cell lines that stably expressed these receptors. The transfected cells displayed significant numbers of cell surface receptors that had ligand binding properties similar to fully differentiated U937 cells. Undifferentiated transfected U937 cells were capable of a ligand-specific calcium flux and showed migratory responses that were qualitatively and quantitatively similar to differentiated cells and were specific for each chemoattractant. Moreover, the chemotactic response could be desensitized by preincubating the cells in a high concentration of ligand and could be blocked by pertussis toxin. These results demonstrate that undifferentiated U937 cells possess the subcellular signaling apparatus and machinery necessary to generate a motile response and that the only missing component for chemotaxis is expression of a chemoattractant receptor. In addition, the results demonstrate that undifferentiated U937 cells transfected with chemoattractant receptors provide a defined model system to study receptor structure/function relationships and may be used to investigate receptor-mediated chemotactic responses in a relevant human myeloid cell.

Antigens, CD↗
PubMed1997

Routine chest roentgenography on admission to intensive care unit after heart operations: is it of any value?

The need for routine immediate postoperative chest roentgenography after heart operations has recently been questioned. In this study we investigated the impact of routine postoperative chest roentgenography on treatment instituted in the cardiovascular intensive care unit immediately after heart operations done via median sternotomy. A total of 404 random patients admitted to the cardiovascular intensive care unit underwent clinical (positioning of endotracheal tube, nasogastric tube, and pulmonary artery catheter) and laboratory (oxygenation) assessment by a cardiovascular intensive care unit physician according to a strict protocol. After clinical assessment, chest roentgenography was done for all admitted patients and the findings reviewed by the same physician. Pathologic conditions noted were recorded on the study form together with any required treatment. Eighteen patients (4.5%) out of 404 required intervention because of abnormalities detected by the chest x-ray film but not predicted by the initial physical and laboratory assessment. None of the pathologic conditions detected was life threatening. We conclude that chest roentgenography done on admission to the cardiovascular intensive care unit should be done only if clinical and laboratory assessment indicate the possibility of underlying pathologic conditions that can only be confirmed or diagnosed by chest roentgenography.

Aged↗
PubMed1997

Determinants of reluctance to perform CPR among residents and applicants: the impact of experience on helping behavior.

BACKGROUND: Though mouth-to-mouth resuscitation (MMR) is widely endorsed as a useful lifesaving technique, studies have shown that health care professionals are reluctant to perform it. To characterize the circumstances which facilitate this reluctance among physicians, we have surveyed current and future residency trainees regarding attitudes toward providing ventilation by this method to strangers experiencing arrest in the community. METHODS: A total of 280 categorical emergency medicine (EM) and internal medicine (IM) house officers and respective program applicants at a 655 bed Brooklyn, New York teaching hospital were anonymously surveyed regarding their willingness to attempt resuscitation in five hypothetical scenarios of cardiopulmonary arrest. RESULTS: A direct relationship was observed between residency training level and reluctance to perform MMR in each scenario. Applicants expressed greater overall willingness to perform MMR than all residents (56 versus 34%, P < 0.00001). Willingness among experienced residents was lower than for junior-level residents (29 versus 40%, P = 0.01). EM and IM physicians were statistically indifferent in their responses. There were no differences in willingness to perform MMR by age in MD applicant or resident groups. CONCLUSIONS: Many physicians and future doctors are reluctant to perform MMR on arrest victims in the community, a trend that increases in prevalence among those with more residency training. These data support the hypothesis that diminished helping behavior occurs gradually over the training period and may occur as a direct consequence of the training experience. A model for characterizing the elements that make up a rescuer's decision process is proposed.

Accidents, Traffic↗
PubMed1997

Acyl-coenzyme A:cholesterol acyltransferase.

Due to its presumed role in regulating cellular cholesterol homeostasis, and in various pathophysiological conditions, acyl-coenzyme A:cholesterol acyltransferase (ACAT) has attracted much attention. Cloning the ACAT gene provides the necessary tool to advance molecular studies of this enzyme. The topics reviewed in this chapter include the pathophysiological roles of ACAT, the biochemistry and molecular biology of the ACAT protein and the ACAT gene, and the mode of regulation by sterol or nonsterol agents in mammalian cells. In addition, we present a working model linking the presumed allosteric property of ACAT with cholesterol trafficking into and out of the endoplasmic reticulum.

Amino Acid Sequence↗
PubMed1997

[Expression and distribution of bFGF in rat lung tissue of chronic hypoxic pulmonary hypertension].

OBJECTIVE: To evaluate the role of bFGF in the development of hypoxic pulmonary hypertension. METHOD: Rat models with chronic hypoxia induced pulmonary hypertension were established, the pulmonary hemodynamics were measured and the pulmonary arterioles change were studied with morphometric analysis under light microscopes, immunohistochemical staining with monoclonal antibody against human recombinant bFGF was performed in the paraffin section of rat lung. RESULT: (1) The mean pulmonary artery pressure (mPAP), and the ratio of the thickness of pulmonary arteriolar wall to external diameter of pulmonary arterioles (MT%) were 3.96 +/- 0.47 kPa and 33.8% +/- 3.5% in rats exposed to hypoxia for 3 weeks respectively, both were significant higher than those in normal control group, P < 0.01. (2) The positive staining for bFGF in the wall of pulmonary arterioles in hypoxic rats was stronger than that of control group (P < 0.01), there was a statistical relationship between increase of staining for bFGF and MT% in rats exposed to hypoxia. CONCLUSION: (1) Hypoxia can induce formation of pulmonary hypertension and structual remodeling of pulmonary arterioles. (2) bFGF may modulate the structure remodeling of pulmonary arterioles in chronic hypoxic pulmonary hypertension.

Animals↗