Surface phase transition and interface interaction in the alpha -Sn/InSb{111} system.
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Biomedical subjects
Publications and source records attributed to T Osaka.
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Responses of sleep-related neurons in the preoptic area (POA) to stimulation of the locus coeruleus (LC) and the ventrolateral medulla (VLM), components of the reticular activating system, were recorded in the unanesthetized, head-restrained rat. Single-pulse stimulation of the LC and the VLM, respectively, inhibited 50% and 54% of 30 sleep-active neurons and excited 47% and 67% of 34 waking-active neurons. The remaining neurons were mostly unaffected. Seventy-three neurons that were not related to a sleep-wake state were mostly (i.e., 73-80%) unresponsive to stimulation. The high incidence of responses by sleep-related neurons suggests that neural inputs from the LC and VLM regulate the hypnogenic mechanisms in the POA. Stimulation of the LC antidromically activated 15% of sleep-active neurons and 11% of waking-active neurons. Thus, some of the sleep-related neurons in the POA may regulate LC neurons. In a later stage of the experiment, we used isoflurane-anesthetized rats that had been used for recording sleep-related neurons. Antagonists for adrenoceptors at a concentration of 10 microM were applied to neurons through a multibarrel micropipette to examine the involvement of noradrenaline in the responses as a neurotransmitter. Application of the alpha 2-blocker, yohimbine, attenuated the inhibitory responses in all 7 neurons tested. The beta-blocker, timolol, and the alpha 1-blocker, prazosin, did not alter any of the inhibitory responses. On the other hand, timolol attenuated the excitatory responses in 4 of 7 neurons, and prazosin attenuated the excitatory responses in 5 of 12 neurons. Yohimbine did not affect the excitatory responses. Thus, the LC and the VLM probably inhibit sleep-active neurons through alpha 2-adrenoceptors and excite waking-active neurons through either beta- or alpha 1-adrenoceptors.
BACKGROUND: The healing process of rat chronic colitis was investigated to evaluate the role of fibronectin produced by fibroblasts in the healing tissue. METHODS: Chronic colitis was produced by intrarectal instillation of 2,4,6-trinitrobenzene sulfonic acid. The healing process was observed by light and electron microscopy and immunocytochemistry. Time course of fibronectin mRNA expression was measured by Northern blot hybridization. RESULTS: By light and electron microscopy, an abundance of young fibroblasts had gathered at the healing tissue and were involved in incorporation into the endothelium of the preexisting vessels, as vasoformative cells, and in transformation to new muscle cells in muscular regeneration. Such processes became pronounced from day 3 and persisted for 6 weeks. Immunocytochemical data showed that fibronectin, produced in the rough endoplasmic reticulum of the fibroblasts and released to the extracellular surface, played inductive roles in the movement and aggregation of such cells and in their contacts with neighboring endothelial cells of the preexisting capillaries. Northern hybridization showed that mRNA coding for fibronectin rapidly reached maximum on day 3 and gradually decreased almost to the control level at 6 weeks. CONCLUSIONS: These observations elucidate the role of young fibroblasts, as multipotent cells, and of fibronectin in acceleration of the healing process in this model of chronic colitis.
Kainic acid (KA) and muscimol were injected into the lateral preoptic area (LPO) of the rat to study their effects on drinking behavior. A low dose (5 ng) of KA, which stimulates neurons, decreased the amount of water intake induced by hypertonic saline (IP) and angiotensin II (SC). Injection of 2 ng muscimol, a potent GABAA receptor agonist that suppresses neurons, facilitated drinking responses induced by hypertonic saline, but did not affect angiotensin II-induced drinking. Rats injected with a high dose (150 ng) of KA, which destroys neurons, showed marked polydipsia accompanied by increased urination. One week after the KA lesion, drinking and urine output recovered to normal. During the polydipsia, a small volume of concentrated urine could be excreted if water intake was restricted. After recovery, excessive drinking responses followed water deprivation and hypertonic saline load. The rats normally drank water in response to angiotensin II and to polyethylene glycol solution. The results show that activation of LPO neurons inhibits water intake, and that suppression of LPO neurons facilitates osmotically induced water intake. Therefore, LPO neurons are probably involved in the inhibition of thirst.
We have studied developmental changes in the muscarinic cholinergic modulation of L-type Ca2+ current (ICa) in enzymatically isolated adult and newborn (1-4 days old) rabbit ventricular cells using the whole-cell patch-clamp method. Carbachol (10 microM) caused a 2.8-fold increase in the half-maximal concentration (EC50) for isoproterenol to stimulate ICa for adult cells compared with the control with little effect on the maximal ICa density (Imax), whereas the stimulatory effect of isoproterenol on newborn ICa was completely eliminated by 10 microM of carbachol and was decreased by 40% at 0.1 microM carbachol. Carbachol increased the EC50 for forskolin to stimulate ICa 2.9-fold for adult cells and 7.3-fold for newborn cells with little effect on the Imax for either group. 5'-Guanylyl imidodiphosphate [Gpp(NH)p; 100 microM] reduced the stimulatory effect of 0.1 microM isoproterenol on adult ICa (percent increase over predrug level) by a factor of 1.8 compared with the control (400 microM guanosine triphosphate), whereas the isoproterenol effect on newborn ICa was completely eliminated by Gpp(NH)p. The isoproterenol effect on adult ICa persisted after the washout of isoproterenol in the presence of Gpp(NH)p. Gpp(NH)p also reduced the stimulatory effect of 1 microM of forskolin by a factor of 2.0 and 8.2 for adult and newborn cells, respectively, in comparison to the control. Carbachol caused no additional effect on forskolin-stimulated ICa for either adult or newborn ICa in the presence of Gpp(NH)p. Pretreatment with pertussis toxin completely eliminated the inhibitory effect of carbachol on forskolin-stimulated ICa for both groups. In addition, the effect of forskolin on ICa was markedly enhanced by the pertussis toxin pretreatment in newborn cells, whereas the enhancement was relatively small for adult cells. We conclude that the muscarinic cholinergic influence on L-type ICa decreases after birth in rabbit ventricular cells, presumably through a diminishing influence of an inhibitory G protein on regulating adenylyl cyclase during the postnatal period.
To investigate the nutritional condition in a hilly village (Kotyang) and a suburban village (Bhadrakali) in Nepal and to clarify the possible cause of the difference in total serum cholesterol level between the two groups of villagers habitually eating low fat diets, we carried out a nutrition survey using the 24-h recall method and blood sampling in 403 subjects (204 men and 199 women) in the hilly village and 466 (244 men and 222 women) in the suburban village. Total serum cholesterol was statistically significantly lower in the hilly villagers than in the suburban villagers for both sexes, but HDL-cholesterol was not. In both villages, 82% of the total energy was taken from carbohydrate, 7-8% from fat and 10% from protein. Energy, protein, fiber, potassium, magnesium, monounsaturated fatty acid, polyunsaturated fatty acid, and vitamin A in the hilly villagers were significantly higher than those in the suburban villagers. Total serum cholesterol was significantly associated with age and body fat percentage, suggesting that total serum cholesterol level was not directly associated with total fat intake in these Nepalese people.
The relation between BP and the factors influencing an increase in BP with age were investigated in the inhabitants of two representative hilly (Kotyang: 206 men and 212 women) and suburban (Bhadrakali: 265 and 244) villages in Nepal. BP for both sexes was statistically significantly higher in Bhadrakali than in Kotyang. Neither hypertension nor elevation of BP with age for men and very few women (1.4%) with hypertension were observed in Kotyang, while 10.9% of men and 4.9% of women were found to be hypertensive in Bhadrakali. Average urinary Na excretion was 183-221 mEq/day in both villages. Urinary Na/K ratio, percentage body fat (%Fat), total protein, total cholesterol and serum Ca were statistically significantly higher in Bhadrakali than in Kotyang, and maximal oxygen uptake and serum Mg were higher in Kotyang. In spite of high salt consumption, there was no increase in BP with age in Kotyang's males, suggesting that the BP may be influenced by physical activity, fat-free mass and nutrient consumption in addition to the high sodium intake, and that extremely high physical activity and very low %Fat could serve to mute the influence of high sodium intake.
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Decrease in water intake after intraperitoneal injection of interleukin-1 beta (IL-1 beta) was studied in the rat. Administration of IL-1 beta at a dose of 20 micrograms/kg attenuated osmotic thirst induced by intraperitoneal injection of hypertonic saline, but did not affect hypovolemic thirst induced by subcutaneous injection of either polyethylene glycol or angiotensin II. Interleukin-1 beta also decreased spontaneous intake of water but not that of 1.8% saline. The results suggest that the decrease in water intake by IL-1 beta is caused, at least in part, by suppression of osmotic thirst but not by general suppression of behavior. The effects of IL-1 beta were not secondary responses accompanied by feeding behavior, since food supply was removed during the experiments. Pretreatment with indomethacin blocked the decrease in water intake by IL-1 beta, suggesting the involvement of production of prostaglandins.
The structure of the mannan of Candida albicans NIH A-207 strain (serotype A) was investigated by adopting mild acetolysis followed by enzymolysis with an Arthrobacter GJM-1 exo-alpha-mannosidase. The resultant oligosaccharides, from pentaose to octaose (where manp = D-mannopyranose), were identified as manp beta (1----2)manp alpha (1----2)manp alpha (1----2)manp alpha (1----2)manp, manp beta (1----2)manp beta (1----2)manp alpha (1----2)manp alpha (1----2)- manp alpha (1----2)manp, manp beta (1----2)manp beta (1----2)manp beta (1----2)manp alpha (1----2)manp alpha (1----2)manp alpha (1----2)manp and manp beta (1----2)manp beta (1----2)manp beta (1----2)manp beta (1----2)manp alpha (1----2)manp alpha (1----2)manp alpha (1----2)manp, respectively. Analyses of alpha-linked oligosaccharides obtained by acetolysis under conventional conditions gave the same oligosaccharides, from biose to heptaose, as those obtained from the mannans of C. albicans NIH B-792 (serotype B) and J-1012 (serotype A, formerly serotype C).
Extracellular recordings were made from 467 anti-dromically identified neurosecretory neurons and 148 non-neurosecretory neurons in the paraventricular nucleus of the hypothalamus of hemispherectomized cats under pentobarbital anesthesia. Stimulation of the dorsal, median, and pontine raphe nuclei excited 31%, 26%, and 12% of neurosecretory neurons tested, respectively, and inhibited 9%, 7%, and 8%. The excitatory responses in 13 of 14 neurons tested were blocked by either of two intravenously administered 5-HT2 antagonists, cyproheptadine or methysergide. The 5-HT1A antagonist, (-)pindolol, partially blocked the excitatory responses elicited by raphe stimulation in three of five neurons tested. The inhibitory responses to raphe stimulation were not affected by application of these antagonists. More non-neurosecretory neurons than neurosecretory neurons were excited in response to raphe stimulation and these excitatory responses were also blocked by these antagonists. We conclude that most electrically stimulated synaptic inputs from the midbrain raphe nuclei to the hypothalamic paraventricular nucleus are excitatory and are mainly mediated by 5-HT2 receptors.
Action potentials were recorded extracellularly from single neurons in the subfornical organ (SFO) of the pentobarbital-anesthetized cat following stimulation of the regions surrounding the anteroventral third ventricle (AV3V). Of 328 SFO neurons studied, 103 were antidromically activated, showing direct projections from the SFO to the AV3V. However, the major effects of stimulations of the AV3V on SFO neurons were orthodromic inhibition; almost 30% of SFO neurons were inhibited by various sites in the AV3V, while a smaller proportion of cells were excited. Local application of bicuculline, an antagonist for GABA, attenuated the inhibitory responses induced by stimulation of the AV3V in seven out of eight neurons tested. Application of GABA inhibited 16 out of 24 neurons, while that of bicuculline alone excited 11 out of 26 neurons, suggesting the tonic inhibitory action of GABA on some SFO neurons. On the other hand, application of kynurenic acid, a nonspecific antagonist for the excitatory amino acids, did not affect the excitatory responses induced by stimulation of the AV3V, but kynurenic acid itself inhibited 6 out of 18 neurons tested. Application of glutamate excited most SFO neurons. This suggests that the excitatory amino acids may be the transmitter(s) of interneurons in the SFO but may not mediate the excitation from the AV3V.
We studied the developmental changes in the beta-adrenergic modulation of L-type calcium current (ICa) in enzymatically isolated adult (AD) and newborn (NB, 1-4-day-old) rabbit ventricular cells using the whole-cell patch-clamp method. ICa was measured as the peak inward current at a test potential of +15 mV by applying a 180-450-msec pulse from a holding potential of -40 mV with Cs(+)-rich pipettes and a K(+)-free bath solution at room temperature. In control, ICa density (obtained by normalizing ICa to the cell capacitance) was significantly higher in AD cells (5.5 +/- 0.2 [mean +/- SEM] pA/pF, n = 65) than in NB cells (2.6 +/- 0.1 pA/pF, n = 60). Isoproterenol (ISO, 1 nM-30 microM) increased ICa in a dose-dependent manner for both groups. The maximal effect (Emax) of ISO, expressed as percent increase in ICa over control levels, and the concentration for one half of the maximal effect (EC50) were 203% and 51 nM, respectively, for AD cells and 111% and 81 nM, respectively, for NB cells. The effect of ISO (1 microM) on ICa was decreased as the test potential was increased from -10 to +40 mV. However, the ratio of the percent increase in ICa for AD versus NB cells was almost constant (2.09-2.45) at each test potential. Dose-response curves of forskolin (FOR, 0.3-50 microM) gave Emax and EC50 of 268% and 0.74 microM, respectively, for AD cells and 380% and 1.15 microM, respectively, for NB cells. After stimulating ICa by 10 microM ISO, the addition of 10 microM FOR produced a further increase in ICa of only 12 +/- 2% in AD cells (n = 4) but a further increase of 140 +/- 41% in NB cells (n = 6). FOR (10 microM) did not produce any increase in ICa for AD and NB cells after stimulating ICa by intracellular application of 200 microM cAMP. ICa density stimulated by 10 microM ISO (17.8 +/- 1.1 pA/pF, n = 7), 10 microM FOR (21.0 +/- 1.3 pA/pF, n = 8), or 200 microM cAMP (18.0 +/- 1.3 pA/pF, n = 5) was equivalent in AD cells, whereas ICa density stimulated by 10 microM ISO (5.8 +/- 0.6 pA/pF, n = 9) was significantly lower than that stimulated by either 10 microM FOR (13.8 +/- 1.5 pA/pF, n = 7) or 200 microM cAMP (13.4 +/- 0.7 pA/pF, n = 7) in NB cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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Strikingly discrepant values were obtained by two commercial precipitating reagents for serum HDL cholesterol determination in three patients with cholestatic liver diseases (two patients with primary biliary cirrhosis and one patient with chronic hepatitis). An abnormal alpha 2-migrating lipoprotein (slow alpha-lipoprotein) was observed in agarose gel electrophoresis for each serum. The slow alpha-lipoprotein was partly recovered in the supernatant by precipitation with polyethylene glycol, and was completely precipitated with a polyanion-containing reagent, which well explains the discrepancy. The slow alpha-lipoprotein isolated from one of the cases is notable for (1) having an intermediate particle size between normal LDL and normal HDL, (2) containing apo E as the major apolipoprotein, and (3) being enriched with cholesterol (esterified and free) and phospholipid. Cholesterol accumulation was also found in another HDL subclass, alpha 1-migrating HDL. A severe impediment in the clearance of cholesterol-loaded HDL particles from plasma was implied. Electrophoresis of serum lipoproteins and/or the measurement of serum apo E concentrations are necessary to avoid an erroneous estimation of HDL cholesterol in patients with hepatobiliary diseases.
It is well established that ventricular tissue, under some conditions, exhibits the phenomenon of postrepolarization refractoriness (PRR) in which the tissue excitability is depressed after an action potential. We have done parallel experiments on rabbit papillary muscles and on isolated rabbit ventricular cells to explain the cellular basis of this phenomenon, using elevated extracellular K+ concentration ([K+]o) (8 mM) to depolarize the tissue and the isolated cells. For isolated cells, we could separately measure cellular excitability (the inverse of the cellular current threshold) and the cellular responsiveness (the ability of the cell to generate inward current after excitation has occurred). We present two hypotheses that could explain the magnitude and time course of tissue PRR in terms of either changes in cellular excitability or changes in cellular responsiveness. We show that, although small changes in cellular excitability do occur, the predominant cellular mechanism for tissue PRR is the time course of recovery of the cellular responsiveness.