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Biomedical subjects

C Han

Publications and source records attributed to C Han.

172 records · Page 10Linked to original sources
PubMed1988

An investigation of the effects of cadmium exposure on human health.

An epidemiological survey of the effects of cadmium (Cd) exposure on the population living near Cd industries, carried out in five provinces of China, revealed that the critical value of urinary Cd excretion was 15 micrograms/liter. Both the average amount of Cd excreted and the incidence of low-molecular-weight protein in urine were positively correlated with the total intake of Cd. The incidence of low-molecular-weight protein excreted in urine was elevated significantly in the exposed group, with a total Cd intake of 133 micrograms per capita per day. It is suggested that the acceptable daily intake (ADI) of Cd be 100 micrograms per capita or 1.67 micrograms/kg body wt.

Adult↗
PubMed1987

Neuropeptide Y potentiates contraction and inhibits relaxation of rabbit coronary arteries.

The effects of neuropeptide Y (NPY) on contraction and relaxation of isolated rabbit coronary arteries were studied. NPY alone caused a weak contraction of coronary arteries with a mean EC50 value of 29 +/- 2.0 nM. Following exposure of coronary arteries to 30 nM NPY, the potencies of norepinephrine (in the presence of 3 microM timolol) and histamine in causing contraction were increased twofold, with no change in maximal contraction. After half-maximal contraction of coronary arteries with histamine and addition of 30 nM NPY, relaxation produced by norepinephrine (in the presence of 3 microM phentolamine), adenosine, and acetylcholine was inhibited. Concentration-response curves for all vasodilators were shifted to the right 10-22-fold by 30 nM NPY. Maximal relaxation caused by adenosine and norepinephrine was not changed by NPY, whereas the maximal response to acetylcholine was 37% less in the presence of NPY. Correlation of the tension produced by NPY with the shift in agonist contraction or relaxation concentration-response curves indicated that NPY-induced increases in baseline tone had no effect on the degree of shift in agonist concentration-response curves. These results show that NPY causes a modest potentiation of agonist-induced contraction and a dramatic blockade of vasodilator-induced relaxation of rabbit coronary arteries.

Acetylcholine↗
PubMed1987

Heterogeneity of alpha 1-adrenergic receptors revealed by chlorethylclonidine.

Chlorethylclonidine (CEC) has previously been shown to inactivate only a subpopulation of the alpha 1-adrenergic receptor binding sites in rat brain. We compared alpha 1-adrenergic receptors in different tissues to determine whether such selective inactivation might reveal the presence of distinct receptor subtypes. Pretreatment of broken cell preparations with 10 microM CEC for 10 min caused a 70-80% decrease in the density of specific 125IBE 2254 binding sites in rat liver and spleen, a 25% decrease in neocortex, but no significant loss in kidney, hippocampus, heart, vas deferens, or caudal artery. The effect of CEC in liver was not reversed by extensive washing, suggesting irreversible inactivation. The selectivity between different tissues was due to differences in the efficacy of CEC inactivating the binding sites and not due to differences in binding affinity. To determine whether the effects on 125IBE 2254 binding reflected selective inactivation of functional receptors, contractile responses of rat spleen and vas deferens were examined. Pretreatment of intact tissues with 100 microM CEC for 30 min caused a large decrease in the potency and maximal contraction to norepinephrine in spleen but had no effect in vas deferens. Inhibition of specific 125IBE 2254 binding by various agonists and antagonists was determined in CEC-sensitive (liver, spleen) and insensitive (hippocampus, vas deferens) tissues. Although many drugs had similar affinities in all tissues, others were substantially less potent in the CEC-sensitive tissues. These experiments suggest that there are at least two subtypes of alpha 1-adrenergic receptors with different pharmacological properties in mammalian tissues, only one of which is inactivated by CEC.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Alpha 1-adrenoceptor subtypes linked to different mechanisms for increasing intracellular Ca2+ in smooth muscle.

Receptor-mediated increases in intracellular Ca2+ levels can be caused by release from intracellular organelles and/or influx from the extracellular fluid. Noradrenaline (NA) released from sympathetic nerves acts on alpha 1-adrenoceptors to increase cytosolic Ca2+ and promote smooth muscle contraction. In many cells activation of alpha 1-adrenoceptors causes formation of inositol 1,4,5-trisphosphate which promotes Ca2+ release from intracellular stores. The mechanism by which receptor activation opens cell surface Ca2+ channels is not known, although in some cases it may be secondary to formation of inositol phosphates or release of stored intracellular Ca2+ (ref. 3). However, alpha 1-adrenoceptors have recently been shown to have different pharmacological properties in different tissues, and it has been proposed that different alpha 1-adrenoceptor subtypes may control mobilization of intracellular Ca2+ and gating of extracellular Ca2+ influx. We here report evidence for two subtypes of alpha 1-adrenoceptors which cause contractile responses through different molecular mechanisms. One subtype stimulates inositol phosphate (InsP) formation and causes contractions which are independent of extracellular Ca2+, and the other does not stimulate inositol phosphate formation and causes contractions which require the influx of extracellular Ca2+ through dihydropyridine-sensitive channels. These results suggest that neurotransmitters and hormones may control Ca2+ release from intracellular stores and influx through voltage-gated membrane channels through distinct receptor subtypes.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Haemopoietic origin of myofibroblasts formed in the peritoneal cavity in response to a foreign body.

This study utilized both in vivo and in vitro techniques to investigate whether cells of bone marrow origin can differentiate into smooth muscle-like cells (myofibroblasts) with contractile filaments and proteins. Female C57BL/6 mice expressing the Ly5.2 antigen on the surface of their haemopoietic cells had four pieces of silastic tubing (3 x 0.5 mm outer diameter) or boiled blood clot (2-3 mm diameter) placed in their peritoneal cavity. After 3, 5, 7 and 14 days (n = 4/group) the implants were removed and those that had remained free-floating were processed for light microscopy, immunohistochemistry and electron microscopy. In the first 3-5 days, rounded cells adhered to the entire surface of the tubing then flattened. These cells stained with fluoresceinated antibodies to Ly5.2 showing that they were derived from haemopoietic cells. By 14 days the cells had become elongated and multilayered in a collagen matrix, forming a thick tissue capsule around the tubing or boiled clot. They contained contractile filaments and stained with antibodies to alpha-smooth muscle actin but no longer stained for Ly5.2. A separate set of female C57BL/6 Ly5.2 mice were X-irradiated to destroy bone marrow then immediately transfused with 10(6) nucleated bone marrow cells taken from the femur and tibia of a congenic strain of male mice expressing the Ly5.1 allele. Eight of the female mice with successful engraftment (80-99%) had silastic tubing implanted in the peritoneal cavity. After 14 days, in situ hybridization with Y chromosome probe confirmed the male donor, and thus bone marrow, origin of the elongated cells that formed the capsule. In vitro studies showed that cells of the murine macrophage cell lines RAW 264.7 and J774 express alpha-smooth muscle actin after exposure to the cytokine gamma-interferon in vitro. These data show that bone marrow-derived cells can differentiate into smooth muscle-like cells and raises the possibility that blood-derived cells may contribute to the development of fibro-proliferative vascular diseases such as atherosclerosis.

Actin Cytoskeleton↗
PubMedDate not supplied

Diagnosis of pit and fissure caries using frequency-domain infrared photothermal radiometry and modulated laser luminescence.

Non-intrusive, non-contacting frequency-domain photothermal radiometry (FD-PTR or PTR) and frequency-domain luminescence (FD-LUM or LUM) have been used with 659- and 830-nm laser sources to assess the pits and fissures on the occlusal surfaces of human teeth. Fifty-two human teeth were examined with simultaneous measurements of PTR and LUM and were compared to conventional diagnostic methods including continuous (dc) luminescence (DIAGNOdent), visual inspection and radiographs. To compare each method to the others, sensitivities and specificities were calculated by using histological observations as the gold standard. With the combined criteria of four PTR and LUM signals (two amplitudes and two phases), it was found that the sensitivity of this method was much higher than any of the other methods used in this study, whereas the specificity was comparable to that of dc luminescence diagnostics. Therefore, PTR and LUM, as a combined technique, has the potential to be a reliable tool to diagnose early pit and fissure caries and could provide detailed information about deep lesions. Using the longer wavelength (830-nm) laser source, it has been shown that detection of deeper subsurface lesions than the 659-nm probe provides is possible.

Body Temperature↗
PubMedDate not supplied

beta-Adrenoceptors in endothelium of rabbit coronary artery and alteration in atherosclerosis.

The existence of beta-adrenoceptor (beta-AR) in endothelium of rabbit coronary artery and its alteration in atherosclerosis (AS) were determined by relaxation experiments in isolated preparations and in situ hybridization with a digoxigenin-labelled beta 2-AR cDNA probe. The concentration-relaxing response curves for isoproterenol (ISO) and norepinephrine (NE) in the presence of phentolamine were shifted to the right, and the maximal relaxations were reduced by removing the endothelium. Nitric oxide synthase inhibitor L-NG-nitro-arginine reduced the maximal relaxation induced by ISO, while the cyclooxygenase inhibitor indomethacin showed no effect on relaxation. In situ hybridization showed that mRNA for beta-AR was detected not only in smooth muscles, but also in endothelial cells. Coronary artery AS was created by high cholesterol feeding and was confirmed histologically under light microscopy. The relaxation response to acetylcholine (ACh) was abolished or significantly diminished in AS preparations. The relaxation responses to ISO or NE, however, were potentiated in AS arteries, especially in those which showed diminished (but not abolished) ACh response. The relaxation induced by sodium nitroprusside was reduced significantly in the AS arteries. Those results suggest that beta-AR are present in endothelium of rabbit coronary artery, and that endothelium beta-AR-mediated vasorelaxation is potentiated in AS.

Animals↗