Asymmetric impurity modes in nonlinear lattices.
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Journal Article↗
Biomedical subjects
F Zhang
Publications and source records attributed to F Zhang.
Critical-current characteristics of c-axis-oriented (Bi,Pb)2Sr2Ca2Cu3Ox silver-sheathed tapes from 10 K to Tc0.
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Journal Article↗
Experimental microvenous thrombosis following anastomosis with a knotted suture.
An experimental model for producing venous thrombosis was developed in end-to-end anastomoses of femoral veins in rats. The anastomoses were performed using a suture (9-0 suture-70 microns needle) with a knot 1 cm from the needle. The knot was formed by making either six or eight half-hitches in one throw of the suture. Vessel patency was assessed through the direct "milking test" at 20 min and 24 hrs. The incidence of thrombosis when using one knot with six half-hitches ranged from 20% to 40% and with eight half-hitches, from 50% to 70%. The incidence of femoral vein thrombosis varied directly with the presence and size of the knot. In this model, thrombosis was induced by exaggerating vessel injuries that may occur when performing routine microvascular anastomoses. This study demonstrates a reproducible thrombogenic model which mimics clinical practice and may be used to study the effects of local and systemic antithrombogenic agents.
Anastomosis, Surgical↗
Microvenous thrombosis rates following anastomosis with vein grafting and a knotted suture.
An experimental microvenous thrombosis model was developed combining vein grafting in femoral vein defects with exaggerated vessel injuries using a knotted suture in the vessel repair. The rat femoral vein grafts were separately subjected to injuries caused by an anastomosis performed with a suture knotted with eight half-hitches at the distal anastomosis (upstream), the proximal anastomosis (downstream), and both anastomotic sites. These groups were compared to vein grafting done with a standard suture. Vessel patency was assessed at 20 min and 24 hr, and the thrombus component was histologically analyzed at 24 hr after the procedures. One hundred percent of control vein grafts were patent at 24 hr. All experimental groups had significantly decreased patency at 24 hr (P < 0.001). Among the experimental groups, knotted suture anastomoses at both anastomoses produced significantly lower patency (13.3%, P < 0.05) than knotted suture anastomoses at distal anastomoses. Histological analyses of thrombosed grafts showed that a large amount of thrombocyte deposition and inflammatory cells were noted at both anastomotic sites in the vein grafts with a knotted suture at the distal anastomosis and in the grafts with a knotted suture at both anastomoses. Thrombocyte deposition and inflammatory cells were seen only at the site of proximal anastomosis when using a knotted suture at the proximal anastomosis site alone. This study demonstrated that quantified microvenous thrombosis can be produced by exaggerating vessel injuries with a knotted suture in a vein graft model. This thrombosis model can be used to study the effects of antithrombogenic agents.
Anastomosis, Surgical↗
Comparison of nylon and polypropylene sutures in a microvenous thrombosis model.
Thrombosis rates of femoral end-to-end microvenous anastomoses with nylon and polypropylene sutures (9-0 suture, 70 mu needle) were compared in a microvenous thrombosis model. The vessel injuries were produced during anastomosis by using a suture with a knot 1 cm from the needle. Anastomotic thrombosis rates were assessed by visual inspection and strip test at 24 hr postoperatively. Low thrombosis rates (0% and 20%, respectively) of anastomoses with both unknotted nylon and unknotted polypropylene sutures were obtained. Anastomoses with knotted nylon and polypropylene sutures resulted in 65% and 45% thrombosis rates, respectively. Statistical analyses showed that there were no significant differences between thrombosis rates, both in anastomosis performance with unknotted nylon and polypropylene sutures (P > 0.05) and with knotted nylon and polypropylene sutures (P > 0.05), while there were significant differences between the thrombosis rate using unknotted sutures and knotted sutures (P < 0.01). It was concluded that vascular injury, not suture material, is the main factor leading to thrombosis in this model.
Anastomosis, Surgical↗
Rheumatoid arthritis in the northeastern area of the People's Republic of China and western Japan.
The clinical features of 134 consecutive hospitalized patients with rheumatoid arthritis in the northeastern area of the People's Republic of China and 251 consecutive hospitalized patients from western Japan were compared. A total of 91.8% of the Chinese patients were of Han nationality, while all of the patients from Japan were Japanese. The patients in the People's Republic of China showed more inflammatory articular disease and more frequent subcutaneous nodules than did the Japanese patients in the presence of a less elevated ESR value and less radiographic joint destruction. The clinical features of the patients of Han nationality and the Japanese did not change even after adjusting the patients' age and disease duration. The reasons for the contradictory features in the Chinese patients still remain to be clarified. This study is hopefully a first step in promoting more precise studies on rheumatoid arthritis in the People's Republic of China.
Adult↗
Homolateral cerebrocortical changes in neuropeptide and receptor expression after minimal cortical infarction.
A cortical infarct of 2 mm diameter was obtained in the parietal cortex after a craniotomy, disruption of the dura mater and topical application of 3 M KCl. It has been shown previously that the presence of a small cortical infarct induces an increase in immediate early gene messenger RNA expression followed by an increase in neuropeptide and glutamic acid decarboxylase messenger RNA expression. Glutamate, acting at N-methyl-D-aspartate receptors, is held responsible for these changes, since they are blocked by pretreatment with dizocilpine. In the present study, we have analysed the consequences of the dramatic changes in messenger RNA expression on the level of immediate early gene products c-fos and zif 268, and on that of neuropeptides by using immunohistochemistry. After just 1 h, an increase in c-fos- and zif 268-like immunoreactivity is observed in the entire cortical hemisphere homolateral to the infarct, and is no longer detected after 6 h. An increase in cholecystokinin octapeptide-, substance P-, neuropeptide Y- and somatostatin-like immunoreactivity is observed in the entire cortical hemisphere homolateral to the infarct after three days, and is no longer detected after 30 days. To investigate if these dramatic increases in neuropeptide immunoreactivities may have functional consequences, we studied the level of cholecystokinin receptors by autoradiographic binding using [125I]cholecystokinin-8S and in situ hybridization for the detection of cholecystokinin-b receptor messenger RNA. A decrease in cholecystokinin binding sites and cholecystokinin-b receptor messenger RNA is observed in the entire cortical hemisphere homolateral to the infarct after three days, and is no longer detected after nine days. This study shows that a topical stimulation has diffuse effects, reaching regions far from the site of the lesion, and some of them are still strongly present after nine days. The increase in neuropeptide messenger RNAs is followed by an increase in the protein products of these genes, which may modify the neurotransmission. As a corollary to this, a decrease in cholecystokinin binding sites occurs. This may have further consequences on signal transduction pathways. This decrease in cholecystokinin binding sites is associated with a decrease in the cholecystokinin-b receptor messenger RNA, and this is the first example of a decrease in messenger RNA levels in this experimental model.
Animals↗
Role of nitric oxide and acetylcholine in neocortical hyperemia elicited by basal forebrain stimulation: evidence for an involvement of endothelial nitric oxide.
We examined the role of acetylcholine and nitric oxide in the increases in cerebrocortical blood flow elicited by stimulation of a region of the basal forebrain from which the major cholinergic projection to the cerebral cortex originates. In halothane-anesthetized rats a 3 x 3 mm area of the parietal cortex was exposed and the site was superfused with Ringer (37 degrees C; pH 7.3-7). Cortical blood flow was monitored at the site of superfusion by laser-Doppler flowmetry. The basal forebrain was stimulated electrically (100 microA; 50 Hz) and stimulated sites were histologically verified at the end of the experiment. With Ringer superfusion (n = 8), basal forebrain stimulation increased neocortical flow by 185 +/- 9% (mean +/- S.E.M.). The flow increase was attenuated (-38 +/- 6%; n = 5) by superfusion with the muscarinic cholinergic antagonist atropine (100 microM). Superfusion with atropine plus the nicotinic antagonist mecamylamine (100 microM) did not attenuate the response further (P > 0.05 from atropine alone; n = 6). Superfusion with the nitric oxide synthase inhibitor nitro-L-arginine, but not with the inactive isomer nitro-D-arginine (n = 6), attenuated the vasodilation in a dose-dependent fashion (-43 +/- 4% at 1 mM; n = 7) and reduced nitric oxide synthase catalytic activity at the site of superfusion by 95 +/- 4%. Co-application of nitro-L-arginine and atropine did not attenuate the vasodilation further (P > 0.05 from nitro-L-arginine alone; n = 6). Administration of the somewhat selective inhibitor of neuronal nitric oxide synthase 7-nitroindazole (50 mg/kg, i.p.) attenuated the increases in flow produced by topical application of N-methyl-D-aspartate (40 microM; n = 5) or by hypercapnia (n = 7), but did not affect the vasodilation produced by basal forebrain stimulation (n = 5) and by topical application of acetylcholine (10 microM; n = 5). 7-nitroindazole reduced constitutive nitric oxide synthase enzymatic activity in forebrain by 72 +/- 3% (n = 8). The data suggest that the neocortical vasodilation elicited by basal forebrain stimulation is, in part, mediated by local release of acetylcholine which, in turn, leads to increased nitric oxide synthesis in endothelial cells.
Acetylcholine↗
Localization of the two protein kinase C beta-mRNA subtypes in cat visual system.
Protein kinase C (PKC) consists of a family of different subtypes encoded by different PKC genes. We investigated the distribution of PKC beta 1 and PKC beta 2 in the visual system of the adult cat by in situ hybridization using oligonucleotide probes complementary to the PKC beta 1 and PKC beta 2 mRNAs, two splicing variants of the same gene transcript. In the primary visual cortex PKC beta 1 and PKC beta 2 were both present. The laminar distribution patterns found for the two PKC subtypes were identical. A remarkable finding was the difference between the laminar distribution of the PKC beta s in areas 17 and 18 when compared with area 19. In all three areas the highest expression levels were found in layer VI, moderately high levels were found in layers II, III and V, while layer I was devoid of signal. In area 17 and 18 layer IV stood out by its low PKC beta signal. In sharp contrast, layer IV of area 19 was indiscernible from the superficial layers because of an evenly high signal. In the dLGN of the adult cat PKC beta 1 and PKC beta 2 mRNAs were distributed rather homogeneously over the different layers, but the expression levels for PKC beta 1 were clearly higher than those for PKC beta 2.
Animals↗
Inducible nitric oxide synthase gene expression in brain following cerebral ischemia.
Cerebral ischemia is followed by a local inflammatory response that is thought to participate in the extension of the tissue damage occurring in the postischemic period. However, the mechanisms whereby the inflammation contributes to the progression of the damage have not been fully elucidated. In models of inflammation, expression of the inducible isoform of nitric oxide synthase (iNOS) is responsible for cytotoxicity through the production of large amounts of nitric oxide (NO). In this study, therefore, we sought to establish whether iNOS is expressed in the ischemic brain. Rats were killed 6 h to 7 days after occlusion of the middle cerebral artery. iNOS expression in the ischemic area was determined by reverse-transcription polymerase chain reaction. Porphobilinogen deaminase mRNA was detected in the same sample and used for normalization. In the ischemic brain, there was expression of iNOS mRNA that began at 12 h, peaked at 48 h, and returned to baseline at 7 days (n = 3/time point). iNOS mRNA expression paralleled the time course of induction of iNOS catalytic activity, determined by the citrulline assay (17.4 +/- 4.4 pmol citrulline/micrograms protein/min at 48 h; mean +/- SD; n = 5 per time point). iNOS immunoreactivity was seen in neutrophils at 48-96 h after ischemia. The data provide molecular, biochemical, and immunocytochemical evidence of iNOS induction following focal cerebral ischemia. These findings, in concert with our recent demonstration that inhibition of iNOS reduces infarct volume in the same stroke model, indicate that NO production may play an important pathogenic role in the progression of the tissue damage that follows cerebral ischemia.
Amino Acid Oxidoreductases↗
Marked induction of calcium-independent nitric oxide synthase activity after focal cerebral ischemia.
We studied the effect of focal cerebral ischemia on inducible (iNOS) and constitutive (cNOS) nitric oxide synthase enzymatic activities in the affected brain. The middle cerebral artery (MCA) was occluded in spontaneously hypertensive rats. Animals were killed 1, 2, 4, and 7 days later. cNOS and iNOS enzymatic activities were determined in the infarcted cortex using the assay of Bredt and Snyder. cNOS was assayed in the presence of calcium, whereas iNOS was assayed in the absence of calcium and in the presence of tetrahydrobiopterin. The validity of the iNOS assay was verified in rats treated with bacterial lipopolysaccharide. In these animals, the magnitude of the induction of iNOS enzymatic activity in lung, spleen, and brain paralleled the expression of iNOS mRNA, assessed by reverse-transcription polymerase chain reaction. After MCA occlusion, calcium-dependent (cNOS) activity was markedly reduced only in lesioned cerebral cortex at days 1-7 (p < 0.001; analysis of variance and Tukey's test). In contrast to cNOS, calcium-independent (iNOS) activity was induced substantially in the infarct (p < 0.005) but not in the contralateral intact cortex (p > 0.05). iNOS activity peaked at day 2 and was not different from baseline at day 7 (p > 0.05). No NADPH diaphorase-positive neurons were observed in the area of the lesion at days 1-7. Macrophages appeared at day 2 and invaded the infarcted tissue by day 7. At this time, numerous glial fibrillary acidic protein-positive astrocytes were observed within the lesion. The results suggest that the decline in calcium-dependent (cNOS) activity reflects loss of NOS neurons within the lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Oxidoreductases↗
Time dependence of effect of nitric oxide synthase inhibition on cerebral ischemic damage.
Nitric oxide, a potent vasodilator and an inhibitor of platelet aggregation, may be beneficial in the early stages of focal cerebral ischemia as it may facilitate collateral blood flow to the ischemic territory. Accordingly, the effect of inhibition of nitric oxide synthesis on cerebral ischemic damage may vary depending on the timing of the inhibition relative to the induction of ischemia. We therefore studied the time course of the effect of nitric oxide synthesis inhibition on focal cerebral ischemic damage. The middle cerebral artery was permanently occluded in spontaneously hypertensive rats and the nitric oxide synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME) was administered systemically (3 mg/kg) < 5 min or 2, 3, or 6 h later. Arterial pressure, rectal temperature, plasma glucose, and hematocrit were monitored. Infarct volume was determined on thionin-stained sections 24 h after induction of ischemia. NOS activity was determined in cerebellum from the conversion of L-[3H]arginine to L-[3H]citrulline. Administration of L-NAME < 5 min after arterial occlusion increased the infarct volume by 23 +/- 14% (mean +/- SD; p < 0.05, analysis of variance), while administration of L-NAME at 2 or 6 h did not affect the size of the infarct (p > 0.05). L-NAME administration 3 h after induction of ischemia reduced neocortical infarct size by 14 +/- 11% (p < 0.05). L-NAME decreased cerebellar NOS activity comparably in all groups (range 16-25%). We conclude that the effects of inhibition of nitric oxide synthesis on focal cerebral ischemic damage are time dependent.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Oxidoreductases↗
Effect of the calcium antagonist amlodipine on the two phases of hypoxic pulmonary vasoconstriction in rat large and small isolated pulmonary arteries.
Calcium antagonists inhibit hypoxic pulmonary vasoconstriction (HPV), which was recently shown to be biphasic in isolated vessels, but the sensitivity of the two phases to calcium antagonism is unknown. We studied HPV in rat isolated large pulmonary arteries (PA) and resistance pulmonary arteries (PRV), using a small vessel myograph. Two phases of acute hypoxic pulmonary vasoconstriction were confirmed to occur in both sizes of vessel. The first phase was short-lived and was followed by a more persistent phase of gradual onset. The magnitude of the first phase of contraction was greater than the second (p < 0.01). The first phase was reproducible, but the second was variable. Tension generated per square millimeter of vessel during both phases of hypoxic contraction was significantly greater in PRV than in PA (p < 0.05). Amlodipine caused dose-dependent inhibition of the first phase of HPV (p = 0.01), with a greater effect in PRV (p < 0.01). The second phase was not significantly inhibited. These results confirm that HPV is biphasic in isolated large and small PA, with a greater sensitivity of the first phase to calcium antagonism. Therefore, the first phase may represent HPV as observed in vivo.
Amlodipine↗
Kinks and conformational defects in nonlinear chains.
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Journal Article↗
Model simulations of DNA dynamics.
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Journal Article↗
Inhibition of inducible nitric oxide synthase ameliorates cerebral ischemic damage.
We sought to determine whether expression of the inducible, calcium-independent isoform of nitric oxide synthase (iNOS) contributes to the tissue damage produced by focal cerebral ischemia. The middle cerebral artery was occluded in halothane-anesthetized spontaneously hypertensive rats. Twenty-four hours later rats received intraperitoneal injections of the iNOS inhibitor aminoguanidine (100 mg/kg twice per day; n = 10) or of aminoguanidine + L-arginine (300 mg/kg four times per day; n = 7), aminoguanidine + D-arginine (n = 7), arginine alone (n = 6), or vehicle (n = 9). Drugs were administered for 3 consecutive days. Infarct volume was determined by image analysis in thionin-stained brain sections 4 days after induction of ischemia. Administration of aminoguanidine reduced infarct volume by 33 +/- 4% (P < 0.05 from vehicle; analysis of variance and Tukey's test), a reduction that was antagonized by coadministration of L- but not D-arginine. Administration of L-arginine alone did not affect infarct size (P > 0.05 vs. vehicle). In separate rats (n = 10), aminoguanidine attenuated calcium-independent NOS activity in the infarct (P < 0.05 vs. vehicle) without affecting calcium-dependent activity (P > 0.05). Aminoguanidine did not affect resting cerebral blood flow or the cerebrovascular vasodilation elicited by hypercapnia, as determined by laser-Doppler flowmetry (n = 4). We conclude that aminoguanidine selectively inhibits iNOS activity in the area of infarction and reduces the volume of the infarct produced by middle cerebral artery occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Oxidoreductases↗
Fluoresein diacetate uptake to determine the viability of human fetal cerebral cortical cells.
We investigated the accuracy of fluorescein diacetate uptake as an indicator of the viability of human fetal cerebral cortical cells. Cortical cells from 16-26-week-old normal fetuses were studied. The cortices were dissociated mechanically with normal saline to make a suspension. Fluorescein diacetate uptake and trypan blue exclusion were compared as methods for examining cell viability. Our results show that fluorescein diacetate uptake is a simple and sensitive method for examining human fetal cortical cell viability.
Cell Survival↗
In vivo facilitation of Tetrahymena group I intron splicing in Escherichia coli pre-ribosomal RNA.
The observation that the large ribosomal RNA intron of Tetrahymena is spliced 20-50-fold more rapidly in vivo than in vitro (Brehm SL, Cech TR, 1983, Biochemistry 22:2390-2397; Bass BL, Cech TR, 1984, Nature 308:820-826) suggests facilitation of RNA folding in vivo. To determine whether a specific group I splicing factor is required in Tetrahymena, the intron was inserted into the analogous position of the Escherichia coli 23S rRNA. We report that the intron is rapidly excised from pre-rRNA in bacteria and that the magnitude of the in vivo rate enhancement is similar to that in Tetrahymena. These results demonstrate that a species-specific protein is not required. Instead, a common mechanism of assisting RNA folding is sufficient to accelerate the removal of self-splicing introns from ribosomal RNA.
Animals↗