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Biomedical subjects

T Ohta

Publications and source records attributed to T Ohta.

At least 1,063 records · Page 59Linked to original sources

Effects of spinal cord compression on repetitive impulse conduction of the ascending fibers of the dorsal column.

The effects of spinal cord compression on conduction of compound action potentials (CAPs) in the dorsal column fibers at various stimulus frequencies were analysed in pentobarbital anesthetised cats. The L 6 posterior root was given 1 to 500 Hz stimuli, and the CAPs were recorded from the L 2 posterior column. The 100th CAP was recorded at 100, 200 and 500 Hz. The L 4 cord segment was compressed by stepped increments (0.5 mm/5 min.) with a plastic plate (4 x 10 mm) until the responses at 1 Hz disappeared, then the compression was released. Before compression, each CAP at all frequencies showed almost uniform amplitudes and latencies. During compression, the CAPs were not altered significantly at any frequency until the spinal cord was compressed 2.5-4.0 mm. Further compression produced a progressive decrease in amplitude and increase in latency of the CAPs. At 500 Hz, however, the conduction block (amplitude loss, latency increase) was much severer than that produced at lower frequencies. After release of compression, the CAPs at all frequencies recovered progressively, and became almost stable after about 1 hour. The recovery rate of amplitude was only about 30% compared to the amplitude before compression at 500 Hz, and about 50% at 1 and 200 Hz. However, the recovery rate of amplitude at 100 Hz (65%) exceeded those at 1 and 200 Hz. To observe the difference in recovery rates among them, all the trains of CAPs were analyzed. Before compression, the amplitudes were almost uniform at stimulus frequencies as high as 500 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

The spread and prognosis of carcinoma in the region of the pancreatic head.

Tumor infiltration and prognosis were studied in 73 patients who underwent surgery for carcinoma in the region of the pancreatic head, in order to evaluate the grade of malignancy of pancreatic cancer. Twenty three patients had carcinoma of the head of the pancreas, 16 had carcinoma of the intrapancreatic bile duct and 34 had carcinoma of the papilla of Vater. It was found that the prognosis in carcinoma of the head of the pancreas was not related to tumor size, but to lymph node metastasis and the pancreatic capsular or perineural invasion of the tumor. The poorer prognosis seen in carcinoma of the head of the pancreas could be attributed to the fact that lymph node metastasis and invasion of the pancreatic capsule or nerve plexus occurred much more frequently in this carcinoma than in carcinoma of the other two areas. The 5-year survival rate of the patients with carcinoma of the head of the pancreas was 12.5 per cent, this being significantly lower than that of the patients with either carcinoma of the papilla of Vater (50.0 per cent) or carcinoma of the intrapancreatic bile duct (44.4 per cent). These findings suggest that lymph node metastasis and pancreatic capsular or perineural invasion closely correlate with the prognosis of patients with pancreatic carcinoma.

Ampulla of Vater↗

Extrahepatic portal venous obstruction of different pathogenesis in pancreatic diseases: reports of 4 autopsy cases with chronic pancreatitis and pancreatic carcinoma.

Four autopsy cases of extrahepatic portal venous obstruction associated with pancreatic diseases, 1 case of pancreatitis and 3 cases of pancreatic carcinoma, are presented. The pathogenesis of portal obstruction was different in each case; old thrombosis with recanalization due to chronic pancreatitis with pseudocysts formation in 1 case, fresh thrombosis due to intraportal venous catheterization for pancreatic carcinoma in 1 case, fresh thrombosis probably due to pancreatitis accompanying pancreatic carcinoma in 1 case, and direct invasion of pancreatic carcinoma into the portal vein in the remaining 1 case. Morphologic evidence for portal hypertension was present in each case. In the pancreatitis case and one pancreatic carcinoma case with portal tumor invasion, both of which had chronic portal obstruction, there were many thin-walled vascular channels (cavernous transformation) around the occluded portal vein. Their endothelia were positive for factor VIII-related antigen and Ulex europaeus lectin I, implying that these vessels were hepatopetal blood vascular collaterals. It was shown that pancreatic diseases resulted in portal venous obstruction by several different mechanisms and chronic portal obstruction in pancreatic diseases led to the formation of hepatoperal blood vascular collaterals.

Adenocarcinoma↗

Quantitative and qualitative changes of apolipoprotein AI-containing lipoproteins in patients on continuous ambulatory peritoneal dialysis.

Using immunoaffinity chromatography, two species of apo-AI containing lipoproteins (AILp); lipoprotein containing apo-AI and apo-AII (Lp-AI/AII), and lipoprotein containing apo-AI, but no apo-AII (Lp-AI) were isolated from 13 female patients on continuous ambulatory peritoneal dialysis (CAPD), then characterized. The results were compared with findings obtained in agematched normolipidemic (control I) and mild hypertriglyceridemic (control II) female subjects. In comparison with control I: In AILp, the levels of total cholesterol (TC), cholesteryl ester (CE) and phospholipid (PL), and the levels of apoE were significantly lower in the CAPD patients while the levels of triglyceride (TG) and apo-CIII were significantly higher in these patients. The levels of apo-AI and apo-AII did not differ between the CAPD and control subjects. In Lp-AI/AII, changes of TC, CE, PL, TG, and apolipoproteins were similar to those of AILp, except for the ratio of apo-AI/apo-AII and the level of apo-CII, which was higher in the CAPD patients. In Lp-AI, changes of TC, CE, PL, and TG were also similar to those of AILp and Lp-AI/AII, but the apo-AI level was significantly lower in the CAPD patients. In comparison with control II: In AILp, the levels of PL, apo-AI, apo-AII, and apo-E were significantly lower in CAPD patients, but the apo-CIII levels were significantly higher. In Lp-AI/AII, the levels of PL and apo-E were significantly lower in CAPD patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Suppressing effect of tannic acid on the frequencies of mutagen-induced sister-chromatid exchanges in mammalian cells.

The effects of tannic acid (m-galloyl gallic acid) and 7 of its analogues on the frequencies of sister-chromatid exchanges (SCEs) were investigated in cultured Chinese hamster cells. SCEs induced by UV-light or mitomycin C (MMC) were suppressed by post-treatment with tannic acid and 5 of its analogues. These effects were independent of the extension of the cell cycle. The compounds which showed an SCE-suppressing effect have a common structure of 3 neighboring hydroxy or methoxy groups substituted on the phenyl group in benzoic acid or ester. These decreasing effects of tannic acid were observed in the G1 phase but not in the S or G2 phase of the cell cycle and a greater decline of the frequencies of UV-induced SCEs during liquid holding was seen in the presence of tannic acid. However, cells irradiated with X-rays were not influenced by tannic acid. In cells from a xeroderma pigmentosum (XP) patient, a Fanconi's anemia (FA) patient, and a normal human embryo, MMC-induced SCEs were also decreased by post-treatment with tannic acid. Tannic acid reduced the SCE frequencies in UV-irradiated FA and normal human cells but not in UV-irradiated XP cells. Our results suggest that tannic acid modifies DNA-excision repair and that the decrease in the amount of unrepaired DNA damage might cause the reduction of induced SCEs.

Animals↗

Modifying effects of components of plant essence on the induction of sister-chromatid exchanges in cultured Chinese hamster ovary cells.

The influence of 21 kinds of components of plant essence on sister-chromatid exchanges (SCEs) induced by mitomycin C was investigated in cultured Chinese hamster CHO K-1 cells. Posttreatment with scopoletin, jasmone, caffeic acid and ferulic acid significantly increased the frequency of SCEs. Further investigation of the SCE-enhancing effect of analogues of caffeic acid and ferulic acid revealed that an alpha,beta-unsaturated carbonyl group may be necessary for SCE-enhancing effects. The influence of caffeic acid and ferulic acid on X-ray- or UV-induced SCEs was also studied. The frequencies of SCEs induced by UV were increased by treatment with these compounds. This increasing effect was observed in the S phase of the cell cycle. On the contrary, X-ray-induced SCEs were reduced by the treatment with these compounds. The decreasing effect was observed in the G1 phase but not in the S or G2 phase. To explain these contradictory results, we assumed that caffeic acid and ferulic acid may modify the repair of DNA strand breaks.

Animals↗

Histamine directly acts on beta-adrenoceptors as well as H1-histaminergic receptors, and causes positive inotropic effects in isolated ventricular muscles of carp heart (Cyprinus carpio).

1. The mechanism for positive and negative inotropic effects of histamine was studied in electrically stimulated ventricular strips of carp heart. 2. A high concentration of histamine (1 mM) caused a transient negative, and subsequent positive inotropic effects. The positive effect was significantly reduced by pyrilamine, diphenhydramine or dl-propranolol, but was not affected by cimetidine or d-propranolol. 3. Prior treatment with reserpine significantly decreased epinephrine and norepinephrine contents in ventricular muscles, and also almost completely abolished the positive inotropic effect caused by tyramine; however, this treatment failed to affect the positive inotropic effect of histamine. 4. The transient negative inotropic effect was reduced by neither atropine, diphenhydramine, pyrilamine nor cimetidine, and potentiated by pyrilamine. 5. These results suggest that the positive inotropic effect of histamine observed in the ventricular muscle of carp heart is mediated by a direct stimulation of both H1-receptors and beta-adrenoceptors. The negative inotropic effect is unrelated to either cholinergic or histaminergic receptor stimulation.

Animals↗

Enhancement and inhibition of mutation by o-vanillin in Escherichia coli.

2-Hydroxy-3-methoxybenzaldehyde (omicron-vanillin), the antimutagenic effect of which has been reported on mutagenesis induced by 4-nitroquinoline 1-oxide (4NQO) in Escherichia coli WP2s, enhanced N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced mutagenesis in the same strain. A remarkable enhancement of mutagenesis provoked by N-methyl-N-nitrosourea (MNU) was also observed by the addition of omicron-vanillin. No enhancing effect was observed on mutagenesis induced by other mutagens such as methyl methanesulfonate (MMS), dimethylsulfate, N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG), N-ethyl-N-nitrosourea (ENU), ethyl methanesulfonate, diethylsulfate, 4NQO and furylfuramide (AF-2). On the contrary, omicron-vanillin greatly suppressed AF-2- and 4NQO-induced mutagenesis and showed a slight suppressing effect against mutagenesis induced by MMS, ENNG and ENU. One possible explanation for the enhancing effect of omicron-vanillin on the mutagenesis induced by MNNG or MNU in E. coli WP2s may be inhibition of an inducible adaptive response. Among 7 derivatives of omicron-vanillin, 2-hydroxy-3-ethoxy-benzaldehyde, omicron-hydroxybenzaldehyde and m-methoxybenzaldehyde showed an enhancing effect on MNNG-induced mutagenesis.

Benzaldehydes↗

The mutational load of a multigene family with uniform members.

The mutational load of a multigene family with uniform members was studied by computer simulations. Two models of selection, truncation and exponential fitness, were examined, by using a simple model of gene conversion. It was found that the load is much smaller than the Haldane-Muller prediction under the truncation selection, and that it becomes approximately equal to the value calculated by the formula, nv(1-q)/(m-nq), where n is the copy number, v is the rate of detrimental mutation per gene copy, m is the truncation point in terms of the number of detrimental genes eliminated, and q is the equilibrium frequency of detrimental mutation. However the equilibrium frequency cannot be analytically obtained. For the exponential fitness model, the load is close to the Haldane-Muller value. When there is no gene conversion, the load becomes larger than the cases with conversion both for the truncation and the exponential fitness models. Thus, gene conversion or other mechanisms that are responsible for contraction-expansion of mutants on chromosomes helps eliminating deleterious mutations occurring in multigene families.

Computer Simulation↗

Time for spreading of compensatory mutations under gene duplication.

Evolution by compensatory mutations is accelerated by gene duplication because selective constraint is relaxed by gene redundancy. A mutation is called compensatory if it corrects the effect of an earlier deleterious mutation. Without duplication, Kimura has shown that the time for spreading of compensatory mutations is much reduced by tight linkage between the two chromosomal sites of mutations. In this report, the time for spreading with gene duplication was studied by using the diffusion equation method of Kimura, together with computer simulations. It was shown that, when 2Nv- is much less than unity, the time for spreading is greatly shortened by gene duplication as compared with the case of complete linkage between the two sites of mutations, where 2N is the effective population size (haploid) and v- is the rate of compensatory mutations. However, if 2Nv- greater than 1, gene duplication is not effective for accelerating the evolution by such mutations.

Biological Evolution↗

Crystallization of and preliminary crystallographic data for allosteric L-lactate dehydrogenase from Bifidobacterium longum.

L-Lactate dehydrogenase from Bifidobacterium longum aM101-2 was overexpressed in Escherichia coli and then purified. The enzyme was crystallized from a polyethylene glycol 6000 solution by the hanging drop vapor diffusion method. Crystals grown in the presence of NADH (type II), both NADH and oxamate (type III), and NADH, oxamate, and FBP (type IV) were analyzed. All three crystal forms belong to the orthorhombic system, space group P2(1)2(1)2. The cell dimensions of the type II crystals were a = 106.2 A, b = 131.6 A, and c = 63.8 A. Those of the type III and type IV crystals were a = 106.4 A, b = 131.4 A, and c = 63.8 A. The type III crystals diffract X-rays to beyond 2.5 A spacing. The type II and type III crystals were stable as to X-ray irradiation.

Allosteric Site↗

A treatment trial of delayed sleep phase syndrome with triazolam.

Triazolam causes a phase-shift of the circadian rhythm of locomotor activity in golden hamsters. We attempted to treat two patients with delayed sleep phase syndrome (DSPS) with triazolam. In one male patient we administered triazolam when the sleep phase began to delay after chronotherapy. Triazolam combined with chronotherapy enabled him to normalize and stabilize his sleep-wake cycle. But in the other female patient despite normalization of her sleep-wake cycle, she became depressive and did not continue taking the drug. In some cases triazolam is useful for the treatment of DSPS, but in others, triazolam induces a depressive state.

Adult↗

Nucleotide sequence of the rodA gene, responsible for the rod shape of Escherichia coli: rodA and the pbpA gene, encoding penicillin-binding protein 2, constitute the rodA operon.

The rodA gene, which is responsible for the rod shape of Escherichia coli, was located 5 nucleotides downstream of another rod-shape-determining gene, pbpA, encoding penicillin-binding protein 2. The coding region for the RodA protein was 1,110 base pairs in length. Two plasmids, carrying a rodA-lacZ gene fusion with and without the pbpA promoter upstream of the gene fusion, were constructed. On the basis of the difference between the expression levels of the beta-galactosidase activity dependent on and independent of the pbpA promoter, we concluded that the pbpA and rodA genes constitute a single transcriptional unit called the rodA operon.

Amino Acid Sequence↗

Molecular structure and immunity specificity of colicin E6, an evolutionary intermediate between E-group colicins and cloacin DF13.

The primary structure of a 3.1-kilobase E6 or E3 segment carrying colicin and related genes was determined. Plasmid ColE6-CT14 showed striking homology to ColE3-CA38 throughout this segment, including homology to the secondary immunity gene, immE8, downstream of the E6 or E3 immunity gene. The ColE3-CA38 and ColE6-CT14 sequences, however, contained an exceptional hot spot region encoding both the colicin-active domain (RNase region) and the immunity protein, reflecting their different immunity specificities. On the other hand, some chimeric plasmids were constructed through homologous recombination between colicin E3 and cloacin DF13 operons. The resulting plasmids were deduced to produce chimeric colicins with a colicin E3-type N-terminal part, a cloacin DF13-type C-terminal-active domain, and the DF13 immunity protein. The killing spectra of the chimeric colicins and the immunities of the plasmids were identical to those of colicin E6 and ColE6-CT14, respectively, showing that the colicin E6 immunity specificity is completely equivalent to that of cloacin DF13. Nevertheless, colicin E6 has been found to show a sequence diversity from cloacin DF13 almost to the same extent as that from colicin E3 in their RNase and immunity regions, indicating that only a small number of amino acids defines the immunity specificity for discrimination between colicins E3 and E6 (or cloacin DF13).

Amino Acid Sequence↗

Role of gene duplication in evolution.

It is now known that many multigene and supergene families exist in eukaryote genomes: multigene families with uniform copy members like genes for ribosomal RNA, those with variable members like immunoglobulin genes, and supergene families such as those for various growth factor and hormone receptors. Many such examples indicate that gene duplication and subsequent differentiation are extremely important for organismal evolution. In particular, gene duplication could well have been the primary mechanism for the evolution of complexity in higher organisms. Population genetic models for the origin of gene families with diverse functions are presented, in which natural selection favors those genomes with more useful mutants in duplicated genes. Since any gene has a certain probability of degenerating by mutation, success versus failure in acquiring a new gene by duplication may be expressed as the ratio of probabilities of spreading of useful versus detrimental mutations in redundant gene copies. Also examined are the effects of gene duplication on evolution by compensatory advantageous mutations. Results of the analyses show that both natural selection and random drift are important for the origin of gene families. In addition, interaction between molecular mechanisms such as unequal crossing-over and gene conversion, and selection or drift is found to have a large effect on evolution by gene duplication.

Animals↗

Ca-induced Ca release in malignant hyperthermia-susceptible pig skeletal muscle.

To provide information regarding the cause of the muscle rigidity in malignant hyperthermia-susceptible (MHS) pigs, the Ca-induced Ca-release mechanism of the sarcoplasmic reticulum (SR), the Ca uptake by the SR, and the Ca-activated tension production of the contractile system were examined in skinned skeletal muscle fibers from MHS and normal pigs. In muscles of MHS pigs, the rate of Ca-induced Ca release was significantly higher than in normal muscle. The potentiation effect on Ca-induced Ca release by halothane and caffeine did not differ appreciably between MHS and normal fibers. The rate of Ca uptake by the SR and the Ca sensitivity of the contractile system of MHS fibers were not different from those of normal fibers, and halothane in an anesthetic concentration exerted no effect on them. Dantrolene inhibited the Ca-induced Ca release at 38 degrees C. These results suggest that the principal cause of malignant hyperthermia (MH) in MHS pigs is due to the enhancement of the Ca-induced Ca-release mechanism of the SR of the skeletal muscle.

Adenosine Triphosphate↗