Quantum versus stochastic or hidden-variable fluctuations in two-photon interference effects.
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Biomedical subjects
Publications and source records attributed to C Su.
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Hb Westmead or alpha 2 122(H5)His----Gln beta 2 is one of the most common hemoglobin variants in Guangxi, a province in Southern China. The alpha 2-globin DNA sequence of a carrier for this variant was selectively amplified by the polymerase chain reaction and analyzed with the restriction enzyme Stu I. We found that this mutant globin was encoded at the alpha 2 locus and that the CAC----CAG mutation at codon 122 created a new Stu I restriction site. It is easy to detect this mutation by these methods.
Three cases of rare chronic hypophysitis found by surgery are reported, with a review of the related literature. Two main types of inflammatory lesions of the pituitary gland are described: lymphocytic hypophysitis (LCH) and giant-cell granulomatous hypophysitis (GGH). These present clinically as a pituitary tumor but are characterized by distinct hypopituitarism with a slightly enlarged sella turcica. Only a few cases present as hyperprolactinemia. The inflammatory process may be resolved with hormonal replacement alone for LCH, while surgical intervention is proposed for GGH.
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Because vibrational frequencies are sensitive to structure, RR spectroscopy can provide structural information about kinetic steps in protein transformations when carried out in a time-resolved mode. UVRR spectroscopy has shown that the aromatic groups of the HbCO photoproduct respond with a delay of 20 microseconds and has provided direct structural evidence that the 20-microseconds kinetic step is the R-T quaternary re-arrangement of the subunits. RR bands of the porphyrin ring show that the core relaxes via a 0.1-microsecond protein motion, which probably allows the Fe atom to attain its full out-of plane displacement. The Fe-His stretching frequency has an elevated value immediately after CO photolysis, in part, perhaps, because of the protein constraint on the Fe displacement. It relaxes on both the 0.1- and 1-microsecond time scales to its value in R-state Hb and then decreases further to its T-state value. These changes may be connected with reorientation of the proximal His side chain. At very early times after a photolysis pulse, heating effects may be an important aspect of the protein dynamics, but further experiments are needed to understand the RR response.
A comparison of bacteriostatic ability has been carried out among oleum of Perilla frutescens and Cinnamomum cassia, benzoic acid and nipagin A. The result shows that the inhibiting effect of Perilla frutescens and Cinnamomum cassia on microorganisms inoculated and spontaneously contaminated is similar to or obviously superior to nipagin A and benzoic acid.
The effects of beta-adrenoceptor agonists and antagonists on pressor responses of the isolated perfused mesenteric arteries to periarterial nerve stimulation (PNS) in the prehypertensive 4-week-old spontaneously hypertensive rat (SHR) and the age-matched Wistar Kyoto rats (WKY) were examined. The systolic arterial blood pressure (SBP) of SHR and WKY were not significantly different at this young age. The pressor responses of the mesenteric arteries to PNS at various stimulating frequencies, however, were significantly greater in SHR than WKY. Cocaine, isoproterenol (a nonselective beta-adrenoceptor agonist) and salbutamol (a selective beta 2-adrenoceptor agonist) significantly enhanced the pressor responses to PNS in SHR and WKY, with significantly greater increase in SHR than WKY. The nonselective beta-adrenoceptor antagonist (propranolol) and the selective beta 2-adrenoceptor antagonist (ICI 118,551) significantly inhibited the pressor response to PNS in SHR without affecting that in WKY. The selective beta 1-adrenoceptor antagonist (practolol) was without effect on the PNS-induced pressor responses in both SHR and WKY. These results demonstrate that the presynaptic beta 2-adrenoceptor-mediated facilitation of neurogenic pressor response in mesenteric arteries already are enhanced in 4-week-old SHR. In view of the higher concentration of circulating epinephrine (Epi) in prehypertensive SHR, the enhanced facilitatory modulation via presynaptic beta 2-adrenoceptors in prehypertensive SHR may be involved in development of hypertension.
The effects of angiotensin III (des-Asp1-angiotensin II) on the pressor responses of the perfused mesenteric vascular bed to periarterial nerve stimulation (PNS) and exogenously administered noradrenaline (NA) of spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared. Angiotensin III (10, 20, 30 and 50 ng/ml) induced a marked potentiation of the pressor response to PNS (8 Hz) in a concentration-dependent manner with a slight elevation of the basal perfusion pressure in both SHR and WKY. The facilitatory effect of angiotensin III was blocked by [Sar1,Ile8]angiotensin II (200 ng/ml) and did not significantly differ for SHR and WKY. Angiotensin III also potentiated the pressor response to infusion of NA (50 ng) to the same extent in SHR and WKY. The degree of potentiation of the response to NA was similar to that to PNS in both WKY and SHR. Perfusion of angiotensin III (50 ng/ml) did not alter the increase in the 3H-efflux evoked by PNS (8 Hz) in the perfused mesenteric vascular bed prelabelled with [3H]NA, whereas the peptide potentiated significantly the pressor response to PNS in WKY and SHR to the same extent. These results suggest that angiotensin III postsynaptically facilitates the adrenergic neurotransmission of the mesenteric vascular bed to the same extent in WKY and SHR.
Detailed data are presented concerning the relative amounts of Hb A and two alpha chain variants (Hb Duan with alpha 75 Asp----Ala, and Hb Westmead with alpha 122 His----Gln), and the occurrence of an alpha-thalassemia-2 heterozygosity in five members of a small Chinese family. The three children who have the three abnormalities inherited the alpha-Duan and alpha-thalassemia-2 heterozygosities from their father, and the alpha-Westmead heterozygosity from their mother. The base substitution which leads to the synthesis of the alpha-Duan chain occurred at codon 75 of the alpha 1 globin gene of the chromosome which also carried the alpha-thalassemia-2 deletion; the concentration of alpha-Duan (37% of total alpha) is similar to that observed for other alpha chain variants, linked to an alpha-thalassemia-2 condition.
The effects of angiotensin I (AI) and angiotensin II (AII) on ring segments of femoral arteries from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were studied. AI and AII elicited significantly greater direct contractile response in arteries from SHR than those from WKY. These peptides also potentiated the contractile response to transmural adrenergic nerve stimulation (TNS) in both preparations, but to a greater extent in those of WKY than SHR, without potentiating the contractile response to exogenous norepinephrine (NE). The potentiation of the TNS response and direct contraction caused by AI were markedly attenuated by captopril, an AI-converting enzyme inhibitor. Destruction of endothelium failed to alter the contractile response to AI in both WKY and SHR but augmented that to AII in WKY. Isoproterenol and salbutamol produced significant potentiation of TNS response only in arteries of SHR. Yohimbine and prostaglandin F2 alpha potentiated TNS response to a similar extent in arteries of WKY and SHR. These results suggest that AII locally generated from AI can act postsynaptically to cause contraction and presynaptically to promote adrenergic neurotransmission in the isolated rat femoral artery. The AI to AII conversion appears to take place mainly at sites other than endothelial cells. The postsynaptic effect of AII is greater in SHR than WKY, but its presynaptic effect is diminished in SHR unlike some other agents which facilitate adrenergic neurotransmission, and unlike that in mesenteric arteries of SHR.
The role of endothelial cells in the constrictor and dilator responses of mesenteric arteries to infused drugs was evaluated. Fifteen- to seventeen-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were used. Periarterial sympathetic nerve stimulation (PNS, 6 Hz, 30 sec) elicited greater pressor responses in SHR than WKY. Acetylcholine (ACh, 1.0 microM) lowered the perfusion pressure elevated by norepinephrine (NE, 0.1 microM) significantly more in SHR than WKY. Angiotensin I and II (AI and AII, 1.0 nM) markedly potentiated the PNS-induced constriction in both animals. Collagenase perfusion (Type 1A, 2 mg/ml, 5 ml/min intermittently, for 23 min) significantly diminished the ACh-induced dilation, indicative of endothelium destruction. However, it greatly increased the constrictor effect of NE and AI and AII in SHR and the potentiating effects of AI and AII on PNS-evoked construction in both SHR and WKY, especially in SHR. These results suggest that, while endothelial cells mediate the dilator response to ACh, they are unnecessary for the constrictor and potentiating effects of NE, AI and AII and, in fact, counteract the latter two effects, particularly in the hypertensive rats. Furthermore, the endothelial cell functions promoting the effect of ACh or countering those of NE, AI and AII are in general greater in SHR than WKY.
The inhibitory effect of leupeptin on [3H]dexamethasone binding to the glucocorticoid receptor from lactating goat mammary cytosol has been studied. Leupeptin (10 mM) caused a significant (about 35%) inhibition of [3H]dexamethasone binding to glucocorticoid receptor. Binding inhibition is further increased following filtration of unlabeled cytosolic receptor through a Bio-Gel A 0.5-m column. Binding inhibition was partially reversed by monothioglycerol at 10 mM concentration. A double reciprocal plot revealed that leupeptin appears to be a competitive inhibitor of [3H]dexamethasone binding to the glucocorticoid receptor. Low salt sucrose density gradient centrifugation revealed that the leupeptin-treated sample formed a slightly larger (approximately 9 S) receptor complex (leupeptin-free complex sediments at 8 S).
Accumulations of serotonin (5-HT) and norepinephrine (NE) were compared in control and 6-hydroxydopamine (6-OHDA) pretreated rat aorta, mesenteric and tail arteries. The distribution of these amines was corrected by subtracting tissue uptake of tritiated sorbitol in the extracellular space. 5-HT greatly accumulated both in control and 6-OHDA pretreated arteries. In contrast, NE accumulation in mesenteric and tail arteries was substantially decreased after 6-OHDA treatment. In the aorta 6-OHDA pretreatment did not affect the accumulation of both amines. These findings suggest that 5-HT accumulation in these arteries is mainly extraneuronal, and NE mainly neuronal. Since the accumulation of 5-HT in the aorta was not influenced by pretreatment with 10 microM NE, the extraneuronal uptake mechanisms for 5-HT and NE appear to be different.
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The effects of adenosine on stimulation-evoked 3H-efflux from perfused mesenteric arteries pretreated with 3H-norepinephrine and on norepinephrine-induced contractile responses of the thoracic aorta before and after mechanical removal of endothelial cells were examined in spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto rats (WKY). Adenosine inhibited the stimulation-evoked 3H-efflux; this inhibitory effect was smaller in young and adult SHR than age-matched WKY. Mechanical removal of endothelial cells rendered the SHR aorta much less responsive to adenosine, while in the WKY aorta endothelial removal had no influence on the relaxation response to adenosine. These results support the hypothesis that pre-synaptic factors are contributory whereas endothelial factors are compensatory to hypertension in SHR.
Blood vessel responses to relaxant drugs have been reported to change with aging and with the development of hypertension. In view of the requirement of endothelial cells for the activity of many relaxant drugs, we examined the role of the endothelium in the relaxation response of vascular tissue. Aortic and mesenteric ring segments from normotensive and hypertensive rats, ages 5 to 6, 15 to 18 and 30 to 31 weeks, were examined for relaxation to sodium nitroprusside, sodium nitrite, atrial natriuretic factor and 8-bromo-cyclic GMP. Relaxation responses to the nitrovasodilators were reduced progressively with aging in ring segments of Wistar-Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) with intact endothelium; however, intact SHR ring preparations displayed less relaxation to nitrovasodilators at 15 to 18 and 30 to 31 weeks than those of WKYs. Rubbed (endothelium denuded) ring preparations displayed greatest relaxation to nitrovasodilators with no difference being observed between SHR and WKY preparations at any age tested. Relaxation to atrial natriuretic factor and 8-bromo-cyclic GMP was not different between rubbed and unrubbed ring segments or between SHRs and WKYs, indicating no detectable impairment of the overall relaxation response in the vascular smooth muscle of SHRs. These results suggest that the total functional capacity of vascular smooth muscle to relax to nitrovasodilators is not changed with aging or hypertension. However, the endothelial cells exert modulatory influences upon the vascular smooth muscle to reduce overall responsiveness to nitrovasodilators, an effect that is enhanced with aging and the development of genetic hypertension.
The mechanisms of extraneuronal serotonin (5-HT) uptake in the rat aorta were studied. Aortic strips were pretreated with 0.1 mM pargyline and incubated with 0.1 to 9.1 microM 5-HT (5-HT, 0.02-1.60 microgram/ml including [3H]-5-HT, 0.02 microgram/ml) for 1, 2, 3 and 5 min at 37 degrees C. Accumulation of [3H]sorbitol was used to correct for extracellular distribution of this amine. The initial rate of 5-HT uptake was related linearly to the substrate concentration within the tested range. Cocaine, imipramine, desipramine (10 microM each), Na+-free solution and cooling (0 degrees C) inhibited markedly both the 1- and 5-min uptake of 5-HT. Removal of the endothelium did not affect the 5-HT uptake for 1 min but reduced slightly that for 5 min. Corticosterone (10 microM), norepinephrine (10 microM) and 6-hydroxydopamine pretreatment did not affect the uptake of 5-HT. Autoradiography demonstrated that uptake of 5-HT for 5 min in the rat aorta occurs primarily at the smooth muscle cells near the lumen. These results suggest that the rat aorta has a large capacity of cocaine-sensitive extraneuronal uptake of 5-HT. This uptake appears to occur primarily in the muscle layers adjacent to the lumen, suggesting that the muscle cells of the luminal side function differently from those from the adventitial side. The mechanism of the extraneuronal uptake of 5-HT appears to be different from that of norepinephrine and the extraneuronal uptake of 5-HT occurs initially in a nonsaturable mode and later through a Na-dependent, carrier-mediated transport.