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Biomedical subjects

Z Zhou

Publications and source records attributed to Z Zhou.

At least 487 records · Page 27Linked to original sources

Differences in arterial and arteriolar endothelial structure during endotoxin shock.

Previous studies of physiological and ultrastructural assessment changes in the walls of the femoral artery and A1, A2, and A3 arterioles in the rat cremaster muscle after infusion of Escherichia coli endotoxin (ENDT) (6 mg/kg-1 hr. period) indicate there may be a difference in the alteration of the endothelial structure of arteries and arterioles. Functionally, ENDT has been shown to abolish acetylcholine (ACh)-induced relaxation in the femoral artery [Zhou, PhD dissertation, University of South Florida, Tampa, 1992]. Dilations of A1 arterioles were shown to be reduced, but dilations of A2 and A3 arterioles were not significantly changed from control [Baker and Sutton, Am J Physiol, 264:H 1118-H 1123, 1993]. In the current study, ultrastructural evaluation of femoral arterial tissue post-ENDT at the mean arterial pressure (MAP) of 100 mm Hg revealed partially destroyed endothelial cells. The MAP decreased as the animal progressed into shock. At 80 mm Hg, 60 mm Hg and 40 mm Hg, essentially all endothelial cells were destroyed, with the internal elastic lamina denuded. In contrast, endotoxin damage in the A1, A2, and A3 arterioles was minimal even at a MAP of 40 mm Hg. Endothelial cells of A1 arterioles post-ENDT had more vacuoles than at control. Therefore, arteriolar endothelium was functionally and anatomically relatively undamaged, consequent to endotoxin administration, in contrast to femoral arteries where the endothelium was destroyed in a short time.

Animals↗

Mesangioproliferative glomerulonephritis in mink with encephalitozoonosis.

Renal specimens from 6 mink with encephalitozoonosis were studied by light and electron microscopy and immunohistochemistry. The glomeruli of affected kidneys had a mesangioproliferative glomerulonephritis which was characterized by an increase in mesangial cells and matrix in most glomeruli. Some glomeruli were partially or completely sclerosed. There were protein or granular casts in the cortical and medullary tubules. Interstitial nephritis, vasculitis and tubular cysts were found. Electron microscopy demonstrated extensive matrix and increased cellularity in the mesangial areas. Glomeruli showed segmentally thickened or wrinkled capillary basement membranes. Electron dense deposits were found in the glomerular basement membranes and mesangium. Peroxidase-anti-peroxidase immunohistochemistry demonstrated that IgG and IgM positive material was present as granular deposits in the glomerular basement membrane and occasionally in the mesangium.

Animals↗

Na(+)-Ca2+ exchange current in latent pacemaker cells isolated from cat right atrium.

1. Single latent pacemaker cells were isolated from cat right atrium, and studied in a whole-cell configuration using a nystatin-perforated patch recording method. The nystatin method avoids alterations in intracellular Ca2+, cellular constituents and run-down of ionic currents. 2. Depolarizing voltage clamp pulses from -40 mV elicited L-type Ca2+ current (ICa) that exhibited an initial rapid phase of inactivation followed by a secondary slower inward current component that decayed over about 100 ms. The secondary inward component appeared as a slowly decaying inward tail current following short (10-40 ms) depolarizing clamp steps. 3. Slowly decaying inward currents were abolished by internally dialysing pacemaker cells with 2 mM EGTA using a ruptured patch recording method. Inward tail currents were also abolished by exposure to 1 microM ryanodine and significantly decreased by replacing 85% of external Na+ with lithium, without effect on peak ICa. These findings identify a Na(+)-Ca2+ exchange current (INa-Ca) that is mediated by sarcoplasmic reticulum (SR) Ca2+ release. 4. Properties of INa-Ca and ICa differed significantly: (i) ICa exhibited a bell-shaped voltage dependence that peaked at 0 mV and decreased at more positive voltages. INa-Ca was maximal at -10 mV and remained relatively constant at more positive voltages; (ii) a paired pulse protocol showed that the time course of INa-Ca recovery (5 s) was significantly longer than that of ICa (2 s); (iii) cadmium (50 microM) induced an inhibition of ICa that did not correlate in time with changes in INa-Ca. 5. The duration of depolarizing steps between 10 and 120 ms had no effect on the time course of INa-Ca tail currents. 6. Isoprenaline > or = 5 x 10(-8) M significantly increased peak ICa amplitude, peak INa-Ca amplitude, accelerated INa-Ca rate of decay and decreased the absolute time of INa-Ca decay. 7. Free-running pacemaker action potentials were clamped during diastole at either -40 or -70 mV (maximum diastolic potential) for variable periods of time. At times between 0.2 and 1 s, INa-Ca exhibited a voltage-dependent increase in amplitude over time, i.e. INa-Ca recovered more rapidly from -70 mV than from -40 mV. At times > 2 s, INa-Ca exhibited a voltage-dependent decline in amplitude over time, i.e. from -40 mV INa-Ca decreased by 10% of maximum whereas from -70 mV INa-Ca decreased by 60% of maximum.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

Clinical and experimental studies on shallow needling technique for treating childhood diarrhea.

Treatment of diarrhea in children by shallow needling and by drugs was studied in 3 separate groups for comparison. For Group I, the lateral line II of the forehead was taken, i.e. the upper, middle and lower points of the line staring from Toulinqi (UB 15) vertically downwards to the place 1 cm below the hairline were selected. For Group II, shallow needling was done on body acupoints, the main points selected being Qihai (Ren 6), Shuifen (Ren 9), bilateral Tianshu (St 25), and bilateral Zusanli (St 36); the adjuvant acupoints were Taibai (Sp 3) and Gongsun (Sp 4). The depth of shallow needling was merely puncturing the skin. For Group III the drugs used were Liteling, Berberine, Gentamycin, Ampicillin, and SMZ Co. The results of treatment in Group I and II differed insignificantly, while both were significantly superior to drugs in Group III. Experimental studies also showed that shallow needling enhanced the humoral and cellular immunity and promoted the intestinal peristaltic function.

Acupuncture Therapy↗

Preparation and evaluation in vitro and vivo of copoly (lactic/glycolic) acid microspheres containing norethisterone.

Poly (lactic/glycolic) acid (PLGA) microspheres containing 20% norethisterone (NET) were prepared and the preparation methodology was optimised. The microspheres showed a slow and steady release pattern up to more than 96 hours in 27.5 wt% ethanol solution. In vivo performance of the microspheres indicated that a single intramuscular injection of 80 mg of microspheres could significantly prolong the duration of estrus suppression up to 45 days in rats. In addition, the studies on the stability of microspheres showed that there was no significant change both in the NET content of microspheres and the NET release rate in vitro after storage for one year.

Animals↗

Abolition with chloramine-T of inactivation in barnacle muscle fibers results in stimulation of the ouabain-insensitive sodium efflux.

The hypothesis that chloramine-T stimulates the basal Na+ efflux in barnacle fibers as the result of the entry of trigger Ca2+ into the myoplasm from the bathing medium was examined in this study. Two reasons for doing so can be given. One is that the oxidant is known to abolish inactivation in sodium and potassium channels. The other is that L-type Ca2+ channels are present in barnacle fibers, and an increase in internal free Ca2+ in these fibers is known to stimulate the Na+ efflux, particularly in ouabain-poisoned fibers. The results of the experiments are as follows: (i) Chloramine-T exerts a biphasic effect on the Na+ efflux: inhibition is followed by stimulation, the threshold concentration being 10(-5) M. This is also found to be the threshold concentration for shortening of these fibers. (ii) The kinetics of the inhibitory effect resemble those of ouabain. (iii) Ouabain is without effect on the stimulatory phase caused by chloramine-T. (iv) Application of chloramine-T after the full effect of 10(-4) M-ouabain is reached elicits solely a stimulatory response. (v) The dose-response curves for the stimulatory action of chloramine-T in unpoisoned and ouabain-poisoned fibers are alike except that the threshold concentration is less than 10(-5) M in poisoned fibers. (vi) Basal light emission from unpoisoned and ouabain-poisoned fibers loaded with the photoprotein, aequorin, some 60 min beforehand increases as soon as they are exposed to 10(-4) M chloramine-T. The response recorded in unpoisoned fibers is monophasic and usually transitory, whereas it is multiphasic and usually sustained in ouabain-poisoned fibers. (vii) The dose-response curve for chloramine-T shows a shift to the left in poisoned fibers. (viii) The magnitude of the rise in light emission depends on the external Ca2+ concentration. A rise fails to take place in the nominal absence of external Ca2+. Taken together, these results support the above hypothesis that chloramine-T causes the entry of trigger Ca2+ into the myoplasm from the outside and provide evidence that stimulation of the Na+ efflux is associated not only with this event but also with a reduced Na+ gradient resulting from inhibition of the membrane Na+/K(+)-ATPase system by the oxidant. Thus, the suggestion put forward is that this oxidant promotes reverse Na+/Ca2+ exchange and is able to exert multiple effects on membrane transport.

Animals↗

Influence of recombinant human interleukin (IL)-7 on disease progression in mice infected with Friend virus complex.

Recombinant human (rhu) IL-7 was evaluated for its influence on disease progression in mice infected with the polycythemia-inducing strain of the Friend virus complex (FVC). DBA/2 mice were injected i.v. with FVC, and then treated s.c. with rhuIL-7. IL-7 significantly prolonged survival time and decreased spleen focus-forming virus (SFFV) levels, expression of SFFV mRNA and SFFV protein production in FVC-infected mice. IL-7 did not appear to directly inactivate SFFV. Although both splenic weight and cellularity in FVC-infected mice treated with IL-7 were higher than those of normal mice, they were respectively 58% and 66% lower than those of the untreated FVC-infected mice. NK-cell activity was substantially lower in FVC-infected mice than in normal mice, while IL-7 restored NK-cell activity to normal levels. IL-6 and IFN-gamma levels were markedly reduced in FVC-infected mice compared to normal mice, but treatment of FVC-infected mice with IL-7 restored these cytokine levels. While the actual mechanisms of these effects are not yet known, the results suggest the potential therapeutic efficacy of IL-7 for certain hematopoietic and viral disorders, possibly mediated through an action on accessory cells and cytokine production.

Animals↗

The gene for human eosinophil Charcot-Leyden crystal protein directs expression of lysophospholipase activity and spontaneous crystallization in transiently transfected COS cells.

Expression of the gene encoding human eosinophil lysophospholipase, the Charcot-Leyden crystal (CLC) protein, was studied in transiently transfected COS cells. Recombinant CLC (rCLC) protein expression was demonstrated both by Western blot and radioimmunoassay inhibition analyses of transfected COS cell extracts and by immunofluorescent staining and ultrastructural immunogold analyses of intact cells. The rCLC protein was immunochemically indistinguishable from native eosinophil-derived CLC protein, and each transfected COS cell expressed approximately 11 pg of rCLC protein as determined by radioimmunoassay and assessment of transfection efficiency. Immunofluorescent microscopy and ultrastructural immunogold analyses localized rCLC protein to the nucleus, cytoplasm, and plasma membrane of COS cells. Lysates from transfected COS cells producing CLC protein expressed significant lysophospholipase activity. Furthermore, rCLC protein expressed in COS cells spontaneously formed the distinctive intracytoplasmic and intranuclear hexagonal bipyramidal crystals characteristic of the native eosinophil and basophil-derived protein. Expression of the CLC gene confirms the authenticity of the CLC cDNA, the expression of lysophospholipase activity by this unique eosinophil and basophil constituent, and will facilitate the routine purification of the active enzyme for in vitro and animal model studies of its role (or roles) in eosinophil and basophil associated allergic inflammation and eosinophil-parasite interactions.

Animals↗

Ribonucleotide reductase: regulation, regulation, regulation.

Ribonucleotide reductase (RNR) catalyses the rate limiting step in the production of deoxyribonucleotides needed for DNA synthesis. It is composed of two dissimilar subunits, R1, the large subunit containing the allosteric regulatory sites, and R2, the small subunit containing a binuclear iron center and a tyrosyl free radical. Recent isolation of the mammalian and yeast RNR genes has shown that, in addition to the well documented allosteric regulation, the synthesis of the enzyme is also tightly regulated at the level of transcription. The mRNAs for both subunits are cell-cycle regulated and, in yeast, inducible by DNA damage. Yeast encode a second large subunit gene, RNR3, that is expressed only in the presence of DNA damage. This regulation is thought to provide a metabolic state that facilitates DNA replicational repair processes.

Animals↗

Isolation of crt mutants constitutive for transcription of the DNA damage inducible gene RNR3 in Saccharomyces cerevisiae.

Ribonucleotide reductase is an essential enzyme that catalyzes the rate limiting step for production of the deoxyribonucleotides required for DNA synthesis. It is encoded by three genes, RNR1, RNR2 and RNR3, each of which is inducible by agents that damage DNA or block DNA replication. To probe the signaling pathway mediating this DNA damage response, we have designed a general selection system for isolating spontaneous trans-acting mutations that alter RNR3 expression using a chromosomal RNR3-URA3 transcriptional fusion and an RNR3-lacZ reporter plasmid. Using this system, we have isolated 202 independent trans-acting crt (constitutive RNR3 transcription) mutants that express high levels of RNR3 in the absence of DNA damaging agents. Of these, 200 are recessive and fall into 9 complementation groups. In some crt groups, the expression of RNR1 and RNR2 are also elevated, suggesting that all three RNR genes share a common regulatory pathway. Mutations in most CRT genes confer additional phenotypes, among these are clumpiness, hydroxyurea sensitivity, temperature sensitivity and slow growth. Five of the CRT genes have been identified as previously cloned genes; CRT4 is TUP1, CRT5 is POL1/CDC17, CRT6 is RNR2, CRT7 is RNR1, and CRT8 is SSN6. crt6-68 and crt7-240 are the first ts alleles of RNR2 and RNR1, respectively, and arrest with a large budded, cdc terminal phenotype at the nonpermissive temperature. The isolation of crt5-262, an additional cdc allele of POL1/CDC17, suggests for the first time that directly blocking DNA replication can provide a signal to induce the DNA damage response. crt2 mutants show a defect in basal level expression of RNR1-lacZ reporter constructs. These are the first mutants isolated in yeast that alter the regulation of DNA damage inducible genes and the identification of their functions sheds light on the DNA damage sensory network.

Alleles↗

Properties of the pacemaker current (If) in latent pacemaker cells isolated from cat right atrium.

1. Single latent pacemaker cells were isolated from the Eustachian ridge of cat right atrium using Langendorff perfusion and enzyme dispersion techniques. Whole-cell patch-clamp techniques were used to study the hyperpolarization-activated inward current (I(f)). 2. All cells studied beat rhythmically. Pacemaker activity was recorded in the voltage range -68 +/- 1 to -54 +/- 2 mV and its cycle length was 901 +/- 67 ms (72 +/- 5 beats min-1) at 34-36 degrees C. Cells were elongated with tapered ends, and appeared bent or crinkled without obvious striations. Mean cell diameter and length were 7.4 +/- 0.5 microns and 93.1 +/- 5.9 microns, respectively (n = 15). Input resistance and total membrane capacitance were 2.2 +/- 0.2 G omega and 27.8 +/- 3.1 pF, respectively. 3. Hyperpolarizing clamp steps more negative than -50 mV elicited a time-dependent increasing inward current that was maximally activated at -120 mV. Activation of I(f) was well within the pacemaker voltage range. Half-maximal activation voltage and slope factor were calculated, using a Boltzmann function, to be -80.5 mV and 8.4, respectively. 4. The fully activated current-voltage (I-V) relationship was approximately linear at voltages more negative than -30 mV and showed outward rectification at more positive voltages. The reversal potential of I(f) was -26 mV and the fully activated conductance was 1.75 +/- 0.14 nS (n = 21). Caesium (2 mM) blocked I(f) at voltages more negative than the reversal potential. Reducing extracellular Na+ or K+ shifted the reversal potential more negative, and increasing extracellular K+ exerted the opposite effect. Reducing extracellular Na+ decreased I(f) amplitude and the slope of the fully activated I-V relationship, and elevated extracellular K+ increased I(f) amplitude and the slope of the fully activated I-V relationship. 5. Some pacemaker cells exhibited a short delay in the onset of I(f) activation whereas other pacemaker cells exhibited little, if any, delay in activation. I(f) currents exhibiting no delay in activation were best fitted by a single exponential function with a mean time constant of 3.20 +/- 1.03 s at -70 mV (n = 4). 6. A nystatin-permeabilized patch recording method was used to record spontaneous pacemaker action potentials and I(f) from the same pacemaker cell. Caesium (2 mM) inhibited I(f) by more than 90% (at -70 mV), and decreased the slope of diastolic depolarization, resulting in a 48 +/- 5% decrease in spontaneous rate.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

[An epidemiological investigation of outbreak of measles among temporarily living people in Shenyang].

This paper reported an outbreak of measles occurred in a factory of Heping District in Shenyang in March 1989. All of the six diagnosed cases were temporarily workers, which represented 15 percent (6/40) of total workers. No secondary cases were detected. The results of epidemiological and laboratory analysis showed that this outbreak was caused by an imported case, and only spread in temporarily workers. Furthermore, we discussed that under the condition that measles incidence was limited under control level, even imported cases could not cause epidemic of measles. So, it is indicated that the flowing people can easily cause accumulation of susceptible people in cities, which may result in outbreak of some infectious diseases.

Adult↗

Effects of human HSS on hepatocyte and hepatoma cell proliferation and D-GAL induced acute liver failure.

Human hepatic stimulator substance (HSS), an organ-specific and heat-stable factor which differs from insulin, glucagon and EGF, has been partially purified from aborted human fetal livers. It was found to stimulate DNA synthesis of human hepatocytes. AH22 hepatoma cells responded dose-dependently. HSS was also found to enhance the survival of D-GAL intoxicated rats as compared to control (62.5% vs. 26.1%). Our results suggest that human HSS is very similar to that in animals.

Animals↗

Calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) levels are elevated in plasma and decreased in vena cava during endotoxin shock in the rat.

Calcitonin gene-related peptide (CGRP), a potent vasodilator, and neuropeptide Y (NPY), a potent vasoconstrictor and potentiator of norepinephrine-induced vasoconstriction, were examined in an animal model of endotoxin shock. Gram-negative bacterial endotoxin (lipopolysaccharide B from Salmonella enteritidis) was administered as a bolus (16.7 mg/kg, i.v.) to conscious, unrestrained rats, previously cannulated for blood pressure measurements and blood withdrawal. At 30 min, endotoxin caused 35-40 mm Hg drop in mean arterial pressure and significant increases in heart rate and plasma levels of glucose and lactate. By 3 hr, blood pressure had returned to near normal levels and remained normal until cardiovascular collapse at 4-6 hr (approximately 70% of the rats). Endotoxin elevated plasma CGRP levels by fourfold at 30 min and 22-fold at 3 hr. Of the organs tested, only vena cava showed significant decreases in CGRP levels. Endotoxin also elevated plasma NPY levels by 67% and decreased NPY levels in adrenal gland and vena cava at 30 min and 3 hr. The data suggest that both CGRP and NPY are released into the circulation during development of endotoxin shock in the rat. NPY may contribute to the compensatory mechanism, tending to bring arterial pressure back to normal levels during intermediate stages of endotoxemia. CGRP, because of its extremely high potency as a hypotensive agent, may contribute to the hypotension at both early and late stages during pathogenesis of endotoxin shock.

Animals↗

Fluorescence spectroscopy studies of the effects of pyrethroids on the DPPC vesicles.

The interactions of pyrethroids with membrane lipids have been studied by means of fluorescent membrane probe DPH. Pyrethroids located in the interior hydrophobic regions of the lipid bilayer, differed in their effectiveness of lowering the phase transition temperature and in their ability to broaden the temperature range of this transition. With the increase in the concentrations of pyrethroids, the effects of disordering hydrocarbon packing were increased by pyrethroids. Fluorescence polarizations (P) were decreased in gel state, but not changed in fluid state by permethrin. The pyrethroids containing a cyano substituent could not only disturb the hydrocarbon packing in the bilayer core, but also cause collisional quenching of DPH fluorescence in gel state, P were decreased, then were increased and at last were decreased slightly again as the concentrations were increased, in fluid state P were not changed substantially at low concentrations and were increased obviously when the concentrations were higher.

1,2-Dipalmitoylphosphatidylcholine↗

Identification of cell surface receptors for murine macrophage inflammatory protein-1 alpha.

We have produced recombinant proteins for a cytokine, L2G25BP (macrophage inflammatory protein-1 alpha) (MIP-1 alpha). By using the recombinant protein (rMIP-1 alpha), receptors for MIP-1 alpha were identified on Con A-stimulated and unstimulated CTLL-R8, a T cell line, and LPS-stimulated RAW 264.7, a macrophage cell line. The 125I-rMIP-1 alpha binds to the receptor in a specific and saturable manner. Scatchard analysis indicated a single class of high affinity receptor, with a Kd of approximately 1.5 x 10(-9) M and approximately 1200 binding sites/Con A-stimulated CTLL-R8 cell and a Kd of 0.9 x 10(-9) M and approximately 380 binding sites/RAW 264.7 cell. 125I-rMIP-1 alpha binding was inhibited by unlabeled rMIP-1 alpha in a dose-dependent manner, but not by IL-1 alpha or IL-2. rMIP-1 alpha inhibited the proliferation of unstimulated CTLL-R8 cells. Rabbit anti-rMIP-1 alpha antibodies blocked the growth-inhibitory effect of the rMIP-1 alpha on CTLL-R8 cells.

Animals↗