Biomedical subjects
Publications and source records attributed to Z J Yu.
A 23-year-old man sustained traumatic loss of both hands. His left defective forearm underwent lengthening with a 3-cm segment of the ipsilateral radius; this was immediately followed by an ipsilateral second toe microvascular transfer to the stump of the radius to provide pinch. Two years after the procedure the reconstructed hand had recovery of both motion and sensibility.
As has been demonstrated, infusion of hydrochloric acid (HCl) and pepsin into the human esophageal lumen, which mimics the natural gastroesophageal reflux, results in a significant increase in salivary volume, salivary bicarbonate and epidermal growth factor. However, the impact of intraluminal acid/pepsin solution on salivary prostaglandin E2 (sPGE2), the major protective factor of the upper alimentary tract, has never been explored. Therefore, using the newly developed esophageal perfusion model, the impact of both mechanical and chemical stimuli of the esophagus on sPGE2 secretion in humans was studied. Salivary PGE2 was assessed in saliva collected during basal conditions, chewing of parafilm, placement of intraesophageal tubing, inflation of intraesophageal balloons, and perfusion with sodium chloride, HCl, or HCl/pepsin solutions. The concentration of sPGE2 was measured using the RIA kit from Amersham (Arlington Heights, IL) after the solid-phase extraction and derivatization. The concentration of sPGE2 in the basal saliva was (mean +/- standard error of mean) 186 +/- 31 pg/mL and was similar during the chewing of parafilm (171 +/- 32 pg/mL). The placement of intraesophageal tubing, however, resulted in a significant decline of sPGE2 concentration to the value of 91 +/- 22 pg/mL (P < 0.01). This decline was maintained when intraesophageal balloons, which compartmentalized a 7.5 cm perfused segment of the esophagus, were inflated (86 +/- 17 pg/mL; P < 0.01). This decline was potentiated further when subsequent perfusion with saline was implemented to reach the lowest value of 46 +/- 17 pg/mL (P < 0.001 versus basal and P < 0.05 versus tubing and balloon evoked values) at the end of the perfusing procedure. Esophageal perfusion with acid and acid/pepsin solution, however, partly restored the significant decline in sPGE2 concentration observed during prolonged perfusion with saline. The sPGE2 output during basal conditions was 89 +/- 13 pg/min and increased dramatically during stimulation by placement of intraesophageal tubing (241 +/- 48 pg/min; P < 0.01) and inflation of intraesophageal balloons (244 +/- 48 pg/min; P < 0.01). Subsequent esophageal perfusion with saline resulted in a gradual decline of sPGE2 output evoked by mechanical stimuli that reached the final value of 178 +/- 39, which was not significantly different from that observed in the basal condition (P < 0.1 versus basal value). Introduction of HCl and pepsin into the perfusing solution significantly prevented the decline of sPGE2 output observed during perfusion with saline (252 +/- 36 pg/min; P < 0.01 versus basal). The modulatory impact of mechanical and chemical stimulation on sPGE2, demonstrated for the first time in humans, may suggest the potential contribution of salivary prostanoids to the maintenance of the integrity of the esophageal mucosa.
Northern blot analysis determined whether multiple alpha 4 transcripts for neuronal nicotinic receptors in rat brain could be detected as distinct bands. When poly(A)+ RNA was isolated from brain regions and hybridized with a Hinfl fragment of alpha 4-1 cDNA containing a sequence shared by both alpha 4-1 and alpha 4-2, but little homology with other alpha or beta subunits, bands at 6.0, 4.6, and 2.6 kb were obtained. When a Taql fragment with selectivity for alpha 4-1 was used, a single band was present at 6.0 kb. The 6.0-kb band was least abundant in all brain regions; the 2.6-kb band was most abundant in frontal cortex, hippocampus, striatum, basal forebrain, and thalamus, whereas the 4.6-kb band was most abundant in midbrain and cerebellum. Nicotine (3.6 mumol/kg, a.c., twice daily) increased the abundance of the 4.6-kb transcript in frontal cortex significantly by 28% following 2.5 days of injections; the 6.0- and 2.6-kb transcripts were unchanged. Nicotine did not affect alpha 4 transcripts in other brain regions. Results suggest that increased mRNA levels may mediate the nicotine-induced up-regulation of receptors in cerebral cortex.
100 labouring women were selected in the hospital and divided into psychological support group and control group randomly (50 in each group) in this study. The former was given psychological education and support by special staff and the later was managed in routine methods. The result showed that the serious pain rate of the psychological support group was lower than that of the control group in the first stage of labour (P < 0.01). There was a significant difference between the pain levels in two groups in the second stage of labor (P < 0.05). The time of the first stage, the second stage, and total labor course in the psychological support group was shorter than that of the control group (P < 0.05). The normal labor rate of the psychological support group was much higher than that of the control group (P < 0.001). This study indicated that providing psychological support to the parturients may reduce the pain level during delivery and decrease the difficult labor rate.
The present study is undertaken to investigate the effects of NO, its inhibitor L-NNA and its procursor L-Arg on the status of myocardial tissue during ischemia (hypoxia) and reperfusion (reoxygenation) in two different models, i.e. Langendorff heart and cultured heart cells of rat. The results were as follows: (1) When heart perfusion was stopped for 30 min and reinstitued for 20 min with K-H buffer containing NO, the coronary flow rate (CFR), left ventricular pressure (LVP) and +/- dp/dtmax increased significantly. When NO was replaced by L-NNA opposite effects were observed. L-Arg alone was without effect on CFR, LVP and +/- dp/dtmax, but attenuated the decreasing effect of L-NNA on CFR. NO decreased MDA and NAGase content of myocardium while L-NNA increased them. (2) When cultured ventricular myocytes were subjected to hypoxia for 30 min and reoxygenated for 20 min, none of the substances under investigation showed any effects on Ca2+ content of heart cells, but all of them decreased MDA, NAGase content of the culture tissue after reoxygenation. The above findings show that NO plays an important role in protecting myocardium from ischemic and reperfused injury by improving blood supply of reperfused myocardium and attenuation of oxygen free radical injury.
Reoxygenation is more serious for hypoxic myocardial cells because of the subsequent calcium overload. The calcium overload is known due to augmentation of H(+)-Na+, Na(+)-Ca2+, exchange during pH paradox. But the present experiment showed that, when H(+)-Na+, Na(+)-Ca2+ exchange was inhibited, calcium could still enter myocardial cells after hypoxia or reoxygenation. Similar result was observed after using Na(+)-Free solution, suggesting that calcium entrance into the cell was unrelated to Na+ channel. It was further shown that calcium accumulation was related to pH gradient across the myocardial cell membrane, i.e., being increased with increase of H+ concentration in the cell. Therefore, it appears that, besides H(+)-Na+, Na(+)-Ca2+ exchange, H(+)-Ca2+ exchange is one of the reasons of calcium overload during intracellular pH paradox.
The objective of these experiments was to determine whether the chronic administration of nicotine, at a dose regimen that increases the density of nicotine binding sites, alters the nicotine-induced release of [3H]-dopamine ([3H]DA), [3H]norepinephrine ([3H]NE), [3H]-serotonin ([3H]5-HT), or [3H]acetylcholine ([3H]ACh) from rat striatal slices. For these experiments, rats received subcutaneous injections of either saline or nicotine bitartrate [1.76 mg (3.6 mumol)/kg, dissolved in saline] twice daily for 10 days, and neurotransmitter release was measured following preloading of the tissues with [3H]DA, [3H]NE, [3H]5-HT, or [3H]choline. Chronic nicotine administration did not affect the accumulation of tritium by striatal slices, the basal release of radioactivity, or the 25 mM KCl-evoked release of neurotransmitter. Superfusion of striatal slices with 1, 10, and 100 microM nicotine increased [3H]DA release in a concentration-dependent manner, and release from slices from nicotine-injected animals was significantly (p < 0.05) greater than release from saline-injected controls; release from the former increased to 132, 191, and 172% of release from the controls following superfusion with 1, 10, and 100 microM nicotine, respectively. Similarly, [3H]5-HT release increased in a concentration-related manner following superfusion with nicotine, and release from slices from nicotine-injected rats was significantly (p < 0.05) greater than that from controls. [3H]5-HT release from slices from nicotine-injected rats evoked by superfusion with 1 and 10 microM nicotine increased to 453 and 217%, respectively, of release from slices from saline-injected animals. The nicotine-induced release of [3H]NE from striatal slices was also concentration dependent but was unaffected by chronic nicotine administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wistar-Kyoto and spontaneously hypertensive rats received i.v. infusions of cocaine hydrochloride (60 mg/kg per day) for 3, 7, and 14 days, or saline for 7 days. Acute cocaine challenge (40 mg/kg, s.c.) was given to treated and control rats 24 hr after the termination of each infusion period. There were no strain differences in brain levels of cocaine during cocaine infusion, nor after cocaine challenges. There were no strain differences in resting levels of [3H]dopamine release. Release of [3H]dopamine decreased in nuclei accumbens of 7- and 14-day cocaine-infused animals. Release of [3H]dopamine was maximal in both brain regions 2 hr after acute cocaine challenge. After 14 days of cocaine infusion, cocaine challenge in both strains reduced [3H]dopamine release in the nucleus accumbens, but not in the striatum; the reduction being greater in Wistar-Kyoto rats. The behavioral tolerance which accompanies similar cocaine infusion regimens may be related to striatal "tolerance" to cocaine-induced dopamine release.
Transcatheter arterial embolization (TAE) using hydroxycamptothecin, cantharidin and cisplatin which were mixed thoroughly with lipiodol, combined with large doses interferon and interleukin-2 as adoptive immunotherapy were carried out in the treatment of 48 patients with unresectable advanced stage primary hepatoma, evaluation of therapeutic effect showed that partial remission rate was 54.2%, significantly higher than that of embolization group using chemotherapeutic agents alone (cisplatin, adriamycin and mitomycin), the partial remission rate was 32.1% (P < 0.01). The side effects of camptothecin and cantharidin including hematuria, urodynia were also successfully eliminated.
Large soft tissue defects of the lower extremity of 8 children was repaired with latissimus dorsi myocutaneous flaps. The age of the children ranged from 6 to 9 years. Both functional recovery and cosmetic appearance of the repaired limbs were satisfactory. Cross-bridge vascular anastomoses were used in four cases because no vessels were available for anastomosis at the recipient site. No significant functional impairments have been noted at the donor site. Operative techniques, indications for this procedure and related problems are discussed.
Effects of acute and subacute cocaine administration on dopamine (DA) and its metabolites in striata and nucleus accumbens of nine week-old Wistar-Kyoto and spontaneously hypertensive rats were studied. Levels of DA,3,4-dihydroxphenylacetic acid (DOPAC) and homovanillic acid (HVA) were determined by HPLC-EC. There were no differences in DA levels in striata and nucleus accumbens between control WKY and SHR. Levels of DA in two brain regions were unaffected in groups treated acutely with cocaine. Both strains showed a significant increase in striatal HVA 2 hr after cocaine injection. Seven day treatment declined DA levels in striatum of WKY and in nucleus accumbens of SHR. However, only WKY treated subacutely with cocaine showed significantly increased HVA either with or without changes in DOPAC in nucleus accumbens and striatum, respectively. Increased DOPAC/DA and HVA/DA ratios appeared only in striatum of WKY and in nucleus accumbens of SHR following subacute treatment. These results suggest that subacute cocaine administration affects DA levels in striata and nucleus accumbens differently between WKY and SHR.
The characteristics of D-1 and D-2 dopamine receptors after acute and subacute cocaine administration were determined in striata and nuclei accumbens from WKY and SHR. In striata from acutely treated rats, significant increases in D-2 receptor density were observed at 30 min, 2 or 24 h following cocaine injection in both strains without changes in affinities. The density of D-1 receptors was significantly decreased 30 min after the injection in WKY, but not in SHR. In striata from subacutely treated rats, the density of D-1 receptors was significantly increased in 3- and 7-day treated WKY, but not in SHR. The affinities of both binding sites remained unchanged. In nuclei accumbens, the change in both D-1 and D-2 receptors after cocaine administration were similar to those observed in the striatum. The results suggest that cocaine administration alters dopamine receptor binding characteristics. Furthermore, D-1 and D-2 dopamine receptors appear to be differently regulated.
The characteristics of dopamine uptake after acute and subacute cocaine administration were determined in striata from WKY and SHR. In acutely-treated (40 mg/kg, s.c.) rats, significant increases in the Vmax of dopamine uptake were observed 30 min after the cocaine injection in both strains, without changes in Km values. The in vitro IC50 for cocaine was significantly decreased at 30 min in WKY and at 2 h in SHR. However, the in vitro IC50 for GBR-12909 was significantly increased at 30 min and at 2 h in both strains following cocaine administration. In both strains, the density (Bmax) of the [3H]GBR-12935 binding site was significantly increased at 30 min and at 2 h with no changes in Kd. In subacutely-treated (20 mg/kg, twice daily for 3 or 7 days) rats, a significant increase in the Km for dopamine uptake was observed in 7 day treated SHR. The in vitro IC50 for GBR-12909 was significantly increased in 3 day treated WKY. The results suggest that cocaine administration alters dopamine uptake and characteristics of dopamine uptake sites in the rat brain.
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Protective effects of continuous administration of physostigmine alone, or in addition to scopolamine, against soman-induced toxicity were studied in guinea pigs. The results clearly demonstrated that treatment with physostigmine continuously via implanted mini-osmotic pumps for 4 or 7 days prior to soman exposure significantly protected from soman-induced mortality. In vehicle-infused guinea pigs, tremors, convulsions and loss of righting reflex occurred prior to their deaths induced by soman. Although all of the guinea pigs which received physostigmine pretreatment for 4 days prior to soman administration also displayed soman-induced tremors and convulsions, the onsets of these symptoms were significantly delayed. When animals continuously treated with physostigmine received injections of scopolamine 10 min prior to soman injections, there was a decreased incidence of all three toxicity symptoms as well as an increase in the latency to onset of tremors. Scopolamine was also able to reverse toxicity symptoms when soman was administered earlier. In animals which had been continuously treated with physostigmine via mini-osmotic pumps, the protective action against soman-induced toxicity was still apparent. On the contrary, acute physostigmine administration failed to protect against soman lethality. The present results suggest that the prophylactic uses of physostigmine via mini-osmotic pumps might be more useful than the acute bolus administration of physostigmine.
Large soft tissue lower leg defects in children, especially those around joints, can cause severe secondary and progressive deformity and can interfere with growth of the affected limb. If function is to be restored and possible amputation prevented, repair procedures are necessary. Eight children with such defects, ranging from six to nine years of age, have been treated successfully, using bilateral latissimus dorsi myocutaneous flaps. All the flaps survived, and both functional recovery and cosmetic improvement of the repaired limbs have been satisfactory. Cross-bridge flaps from the contralateral leg were used in four of the cases because no vessels were available for anastomosis at the recipient site. No significant functional impairments at the donor site have been noted. Operative techniques, indications for the procedure, and related problems are discussed.
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