Biomedical subjects

M Fujishima

Publications and source records attributed to M Fujishima.

At least 919 records · Page 51Linked to original sources

PubMedDate not supplied

Structure and expression of a GroE-homologous operon of a macronucleus-specific symbiont Holospora obtusa of the ciliate Paramecium caudatum.

The reproductive form of a macronucleus-specific symbiont Holospora obtusa, when harbored by the macronucleus of the ciliate Paramecium caudatum, selectively synthesized a 63-kDa protein which is immunologically related to GroEL, or HSP60, of Escherichia coli. Heat shock treatment of isolated cells of the reproductive and infectious form of the bacterium also induced the synthesis of the GroEL homolog. Immunoblotting showed that the amount of this protein per cell, whether the reproductive or infectious form, is roughly constant. Cloning and sequencing of a gene coding for the GroEL homolog suggested that the protein is 55.2% identical to GroEL of E. coli at the amino acid sequence level, and that the gene is preceded by an open reading frame which encodes a protein 39.6% identical to GroES of E. coli. Northern blot hybridization showed that the groEL homologous gene is highly expressed in the reproductive form, but only in a trace amount in the intermediate and infectious form. Immunoelectron microscopy revealed that the GroEL homolog is localized in the cytoplasm of the reproductive and infectious form.

Amino Acid Sequence↗

PubMedDate not supplied

Purification of GVBD-inducing protein from the ciliate Tetrahymena thermophila.

Germinal-vesicle-breakdown (GVBD) was induced if a 132,000-g supernatant of Tetrahymena thermophila homogenates was injected into Xenopus oocytes. Using this induction of GVBD as a bioassay system, a GVBD-inducing substance was purified from the Tetrahymena by ultra-filtration, liquid chromatography, and electroelution from a band on native-PAGE gel. Proteins eluted from the single band on the native-PAGE gel induced GVBD in the absence of oocyte protein synthesis. This band resolved into two bands on SDS-PAGE: 60 and 112 kDa. The 60 kDa protein was the active fraction inducing GVBD. Immunoprecipitation of the 60 kDa protein prevented the GVBD-inducing activity, supporting the conclusion that the 60 kDa protein is the GVBD-inducing substance. An immunoblot with anti-60 kDa monoclonal antibody and PSTAIR antibody showed that p13suc1-beads could remove cdc2 homologues from T. thermophila supernatant but could not remove the GVBD-inducing activity. The 60-kDa protein appeared at the same time as micronuclear division and disappeared at the beginning of the macronuclear division during synchronous cell division. The cyclic appearance of the 60-kDa protein in the T. thermophila cell cycle suggests that this protein has a cell cycle function.

Animals↗

PubMedDate not supplied

Is vitamin E depleted in Crohn's disease at initial diagnosis?

We measured serum and red blood cell concentrations of vitamin E and serum lipid concentrations in 13 inpatients at the initial diagnosis of Crohn's disease and compared them with those of 12 healthy controls. Although the serum concentrations of vitamin E were significantly lower in the patients with Crohn's disease than in the controls, the red blood cell concentrations of this vitamin did not differ between the two groups. The serum concentrations of total lipids and total cholesterol were decreased in the patients with Crohn's disease. A significant correlation was found between the red blood cell concentration of vitamin E and the serum vitamin E/serum total lipids ratio in both the groups. There was no correlation between the Crohn's disease activity index and serum or red blood cell levels of vitamin E. These findings suggest that the lowered serum vitamin E levels in patients with Crohn's disease are a symptom of hypolipidemia, and that vitamin E deficiency may not actually become a serious problem in patients diagnosed with Crohn's disease.

Adolescent↗

PubMedDate not supplied

Influence of sex on cerebral ischemia following bilateral carotid occlusion in spontaneously hypertensive rats: a metabolic study.

Cerebral lactate, pyruvate and adenosine triphosphate (ATP), and acid-base balance were measured in male and female spontaneously hypertensive rats (SHR) before, and 1, 3 and 5 hours after bilateral carotid occlusion. In male SHR, cerebral lactate and the lactate/pyruvate (L/P) ratio progressively increased after occlusion, while cerebral ATP decreased. In female SHR, an increase in lactate and the L/P ratio was less marked than in male SHR. Cerebral ATP remained unchanged 5 hours after occlusion. These data suggest that bilateral carotid artery occlusion may cause more pronounced ischemic changes in the brain in male SHR than in female SHR, resulting in a greater increase in lactate with a concomitant decrease in ATP in male SHR. Results suggest that female SHR are more resistant to cerebral ischemia following bilateral carotid occlusion than male SHR. Blood pressure and gonads in the susceptibility to cerebral ischemia are discussed.

Adenosine Triphosphate↗

PubMedDate not supplied

Brain metabolism following bilateral carotid occlusion in 2 different models of experimental hypertensive rats.

Brain metabolites and arterial acid-base measurements were made one hr after bilateral carotid artery occlusion in 2 different models of hypertensive rats. Animals used included renovascular hypertensive rats (RHR) with an altered renin-angiotensin system and desoxycorticosterone hypertensive rats (DHR) with low plasma renin activity (PRA). The mean value for supratentorial lactate of 7.41 mM/kg in RHR was significantly higher than in DHR (3.90 MM/kg) or in control normotensive rats (3.10 - 2.56 mM/kg). Concomitantly, the lactate/pyruvate ratio tended to increase and ATP to decrease in RHR only. In these same rats (RHR) infratentorial lactate was also increased. The results suggest that bilateral carotid occlusion leads to anaerobic metabolism of the brain in RHR but not in DHR, suggesting that the renin-angiotensin system may play some role in the susceptibility to cerebral ischemia following carotid occlusion in the hypertensive rats.

Adenosine Triphosphate↗

PubMedDate not supplied

Experimental cerebral ischemia in spontaneously hypertensive rats (SHR): Importance of degree of hypertension.

To study the relationship between the degree of hypertension and experimentally-induced cerebral ischemia, brain metabolites, including lactate, pyruvate and adenosine triphosphate (ATP) were determined one hour after bilateral carotid occlusion in 119 spontaneously hypertensive rats (SHR) with a variety of mean arterial pressures (MAP). Of these, 36 SHR were given antihypertensive agents for 10 weeks to reduce blood pressure prior to the experiment. There was a significant linear correlation between MAP before and either supratentorial lactate (r = 0.482, p less than 0.001) or the lactate/pyruvate ratio (r = 0.388, p less than 0.001) in the brain after carotid occlusion. An inverse correlation was observed between supratentorial lactate and either ATP (r = -0.627, p less than 0.001) or arterial PCO2 (r = -0.477, p less than 0.001) after carotid occlusion. The changes suggest that the animals with a higher MAP had a greater increase in ischemic metabolites with a decrease in ATP and a more pronounced hypocapnia after carotid occlusion. This hypocapnia is believed to be due to hyperventilation induced by cerebral ischemia. It is concluded that hypertensive rats are more susceptible to cerebral ischemia and the susceptibility is related to the degree of hypertension. By long-term lowering of the blood pressure prior to carotid occlusion, the ischemic changes are lessened in this experimental model.

Adenosine Triphosphate↗

PubMedDate not supplied

Effects of arterial hypotension on brain metabolism in normotensive and spontaneously hypertensive rats.

The effects of graded systemic hypotension induced by the combination of bleeding and trimethaphan camsylate infusion on brain metabolism were studied in normotensive rats (NTR) and spontaneously hypertensive rats (SHR). Metabolites such as lactate, pyruvate and adenosine triphosphate (ATP) of the brain frozen in situ were measured at the end of 1 hour of hypotension. In SHR, either cerebral lactate or the lactate/pyruvate (L/P) ratio increased rapidly and progressively with a concomitant decrease in ATP, when mean arterial blood pressure (MAP) fell below about 50 mm Hg. In NTR, on the other hand, the metabolites changed little until MAP fell to about 40 mm Hg. Metabolic derangements of the brain during profound hypotension were more marked and severe in SHR than in NTR. These results suggest that the SHR is more vulnerable to severe hypotension than NTR, probably due to hemodynamic difference of the cerebral circulation between the 2 groups. The increased cerebral vascular resistance and upward shift of cerebral autoregulation in hypertension might be responsible for this vulnerability.

Adenosine Triphosphate↗

PubMedDate not supplied

Changes in local cerebral blood flow following bilateral carotid occlusion in spontaneously hypertensive and normotensive rats.

Local blood flow in the cortex and thalamus was measured by the hydrogen clearance method in spontaneously hypertensive rats (SHR) and normotensive rats (NTR) before and after bilateral carotid occlusion. There were no differences in the resting blood flow values between SHR and NTR. Following carotid occlusion cortical blood flow in SHR was markedly reduced to 17% of the resting level at 1 h and, further, to less than 10% at 3--5 h period, while in NTR it decreased only to 36--38% during 5 h occlusion. Thalamic blood flow in SHR was decreased to 39% at 1 hr and to below 20% at 3--5 h, while in NTR it remained approximately 40% of the resting level during 5 h occlusion. The blood flow reduction in either cortex or thalamus after carotid occlusion was much greater in SHR than in NTR. This difference was highly significant. The increased cerebral vascular resistance caused by persistent hypertension may play an important role in a greater reduction of blood flow in SHR after carotid occlusion. Relation of the blood flow reduction to the brain metabolism is discussed.

Animals↗

PubMedDate not supplied

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral blood flow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induce hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paCO2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p less than 0.05). When paCO2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypocapnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.

Adenosine Triphosphate↗

PubMedDate not supplied

Disruption of blood-brain barrier following bilateral carotid artery occlusion in spontaneously hypertensive rats. A quantitative study.

The present study was designed to clarify the relationship of cerebral blood flow (CBF) to blood-brain barrier (BBB) in the ischemic brains with or without recirculation, which were produced by clipping of both common carotid arteries in spontaneously hypertensive rats. CBF was measured by the hydrogen clearance method and BBB function was evaluated by the permeability of 131I-albumin and Evans blue dye. Cortical CBF was reduced from 48.8 +/- 9.5 to 4.0 +/- 1.2 ml/100 gm/min during 1 hr ischemia and further to 2.6 +/- 0.3 ml/100 gm/min during 3 hrs ischemia, while thalamic CBF was reduced much less from 50.0 +/- 3.6 to 17.9 +/- 6.5 ml/100 gm/min and to 17.5 +/- 11.0 ml/100 gm/min, respectively. There was no increase in permeability to protein tracers observed in such 1 hr or 3 hrs ischemic brain. Both cortical and thalamic CBF were markedly increased 2.5 to 6 fold of resting values at 5 min after recirculation in the 1 hr ischemic brain. In the 3 hrs ischemic brain, however, both CBF were only slightly increased but never restored to the resting level even at 30 min after recirculation. In such reperfused brains, exudation to Evans blue dye was observed in none of 16 animals with 1 hr ischemia, but in 18 of 23 with 3 hrs ischemia. Disruption of BBB was twice more frequent in the cortex (77.8%) than in either thalamus (33.3%) or hippocampus (33.3%). Permeability index of 131I-albumin (brain albumin/blood albumin) was significantly higher in the ischemic areas stained with blue dye (2.07 +/- 0.45%) than in non-ischemic control brain (0.10 +/- 0.01%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Upper limit of cerebral autoregulation during development of hypertension in spontaneously hypertensive rats--effect of sympathetic denervation.

The upper limit of cerebral autoregulation was studied in pre- or early established hypertension in spontaneously hypertensive rats (SHR). Cerebral blood flow (CBF) was measured with the hydrogen clearance method, and wall/lumen ratio of cerebral arteries was morphometrically measured with the freeze-substitution technique. To test autoregulation, phenylephrine was intravenously infused to cause stepwise increments of blood pressure. Unilateral superior cervical ganglionectomy was carried out to examine the effects of sympathetic denervation on CBF autoregulation and thickness of vascular wall. Resting blood pressure at 4 weeks, 3 months and 6 months of age were 89 +/- 3 mm Hg (mean +/- SEM), 140 +/- 6 and 165 +/- 6, respectively. Baseline CBF was slightly diminished with age; 50.6 +/- 9.2 ml/100 g/min at 4 weeks, 49.8 +/- 8.1 at 3 months and 44.1 +/- 5.6 at 6 months. The upper limit of autoregulation was markedly raised with age; 118 +/- 5 mm Hg at 4 weeks, 180 +/- 7 at 3 months and 208 +/- 10 at 6 months. Acute sympathetic denervation lowered the upper limits to 105 +/- 2, 162 +/- 4 and 185 +/- 7 mm Hg, respectively. On the other hand, in chronic denervation which was made at 4 weeks of age, the upper limit of autoregulation in the denervated hemisphere was slightly lower than that in innervated hemisphere at 2 months (165 +/- 5 and 178 +/- 6 mm Hg), and at 5 months (202 +/- 8 and 215 +/- 8 mm Hg) after ganglionectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMedDate not supplied

Effects of hematocrit on brain metabolism in experimentally induced cerebral ischemia in spontaneously hypertensive rats (SHR).

Brain tissue lactate, pyruvate, and adenosine triphosphate (ATP) were measured 60 min after bilateral carotid ligation in spontaneously hypertensive rats, of which hematocrit (HCT) was varied by exchanging with isovolemic homologous red cells, plasma or whole blood. Supratentorial lactate of the ischemic brain was increased more in high HCT (greater than or equal to 50%) and less in low HCT (30-39%) compared with normal HCT (40-49%). In very low HCT (less than 30%), however, lactate was increased to further extent compared with any other group of HCT (ANOVA p less than 0.0001). Lactate/pyruvate (L/P) ratio of the ischemic brain showed similar changes, namely U-shaped correlation to HCT. In contrast, supratentorial ATP was decreased more markedly in very low HCT, followed by high and normal HCT, and minimally decreased in low HCT, demonstrating an inverse U-shaped relationship to HCT. Mean arterial pressure and arterial acid-base parameters in ischemic animals did not differ among HCT groups. There were no HCT-related changes of brain metabolites in non-ischemic control rats. These findings indicate that cerebral ischemia following carotid ligation is more severe in high HCT but less in low HCT, probably due to hemodynamic effects of HCT changes. When HCT is reduced to below 30%, however, insufficient oxygen supply to the brain or anemic hypoxia may superimpose on ischemia, resulting in more markedly impairment of brain metabolism. The role of HCT as a cause of cerebral ischemia and its severity is discussed.

Acid-Base Equilibrium↗

PubMedDate not supplied

Cerebral blood flow and tissue metabolism in experimental cerebral ischemia of spontaneously hypertensive rats with hyper-, normo-, and hypoglycemia.

The present study was designed to clarify the effect of blood glucose level on cerebral blood flow and metabolism during and after acute cerebral ischemia induced by bilateral carotid ligation (BCL) in spontaneously hypertensive rats (SHR). Blood glucose levels were varied by intraperitoneal infusion of 50% of glucose (hyperglycemia), insulin with hypertonic saline (hypoglycemia) or hypertonic saline (normoglycemia). Cerebral blood flow (CBF) in the parietal cortex and thalamus was measured by hydrogen clearance technique, and the supratentorial metabolites of the brain frozen in situ were determined by the enzymatic method. In non-ischemic animals, blood glucose levels had no influence on the supratentorial lactate, pyruvate or adenosine triphosphate (ATP) concentrations. In ischemic animals, however, cortical CBF was reduced to less than 1% of the resting value at 3 hours after BCL. However, there were no substantial differences of CBF during and after ischemia among 3 glycemic groups. Cerebral lactate in the ischemic brain greatly increased in hyperglycemia (34.97 +/- 1.29 mmol/kg), moderately in normoglycemia (23.43 +/- 3.13 mmol/kg) and less in hypoglycemia (7.20 +/- 1.54 mmol/kg). In contrast, cerebral ATP decreased in hyperglycemia (0.93 +/- 0.19 mmol/kg) as much as it did in normoglycemia (1.04 +/- 0.25 mmol/kg), while ATP reduction was much greater in hypoglycemia (0.45 +/- 0.05 mmol/kg). At 1-hour recirculation after 3-hour ischemia, ATP tended to increase in all groups of animals, indicating the recovery of energy metabolism. Such metabolic recovery after recirculation was good in hypo- and normoglycemia, and was also evident in hyperglycemia. Our results suggest that hyperglycemia is not necessarily an unfavorable condition in acute incomplete cerebral ischemia.

Adenosine Triphosphate↗

PubMedDate not supplied

The effect of long-term antihypertensive treatment on medial hypertrophy of cerebral arteries in spontaneously hypertensive rats.

The effects of antihypertensive treatment on the structural changes of middle cerebral arteries (MCA) were studied quantitatively and morphometrically in young spontaneously hypertensive rats (SHR). Fifteen male SHR, 10 weeks of age, were divided into control and experimental groups. In the experimental group, the animals were administered hydralazine and guanethidine for the following 10 weeks. At the age of 20 weeks, mean arterial blood pressure of experimental animals was 177 +/- 9 mm Hg (mean +/- SD), being significantly lower than that of 195 +/- 12 mm Hg in control ones. Media thickness of large (external diameter greater than or equal to 200 micron) and medium sized MCA (150-200 micron) in treated SHR was 12.3 +/- 2.8 and 6.3 +/- 1.1 micron, respectively, being significantly smaller than that of 14.0 +/- 2.2 and 8.5 +/- 2.6 micron, respectively, in control SHR. The media cross-sectional area and the ratio of media thickness to external diameter were also significantly reduced by antihypertensive treatment. In the smaller vessels (75-150 micron), however, vascular morphometry revealed no difference between the two groups. Long-term antihypertensive treatment during the early phase of hypertension attenuates the development of medial hypertrophy in large cerebral arteries.

Animals↗

PubMedDate not supplied

Hematocrit as a risk factor of cerebral infarction: long-term prospective population survey in a Japanese rural community.

To elucidate the relation of hematocrit (Hct) to the incidence of cerebral infarction, a prospective follow-up study of 16 years (1965-81) was performed in a general population sample of 1220 Hisayama residents aged 44 and over, of both sexes. Most of the subjects who died during the follow-up period were autopsied, the rate being 89.0%. Hct decreased with advancing age in men, but not in women. The average value for Hct was significantly lower in women than in men. According to the mean value +/- 1 SD of Hct, the subjects were grouped into 3, in each sex as follows: low (less than 35%), normal (35-45%) and high (greater than or equal to 45%) for men, and, low (less than 30%), normal (30-40%) and high (greater than or equal to 40%) for women. During the follow-up period, cerebral infarction occurred in 117 patients. The cumulative incidence of cerebral infarction in the low Hct group for men was the lowest, even after adjustments for age and blood pressure. Conversely, the incidence in the low Hct group of women was significantly higher than that in the normal Hct group and was consistently increased with time during 2-5 years of the follow-up. After the 6th year or later, however, the incidence was gradually but significantly increased in the high Hct group, compared with the normal Hct group. Since Hct levels were related with other variables such as serum total cholesterol, serum total protein, Quetelet index and prevalence of hypertension in both sexes, heavy alcohol consumption in men, and glucose intolerance in women, such variables were taken into account using Cox's proportional hazards regression model.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Regional cerebral blood flow autoregulation in normotensive and spontaneously hypertensive rats--effects of sympathetic denervation.

The present study was designed to investigate the effect of acute sympathetic denervation on the regional cerebral blood flow (CBF) autoregulation during acute elevation of blood pressure in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). CBF to the parietal cortex and thalamus was measured by the hydrogen clearance method and, to test autoregulation, systemic arterial blood pressure was elevated by intravenous infusion of phenylephrine. Superior cervical ganglia were removed on both sides to interrupt sympathetic innervation in the deeper structures of the brain. Acute bilateral sympathetic denervation did not alter the resting blood pressure or CBF in either SHR or WKY. In innervated SHR, resting mean arterial pressure (MAP) was 165 +/- 5 mm Hg (mean +/- SEM) and the upper limit of autoregulation in the cortex was 210 +/- 3 mm Hg, which was significantly lower than that in the thalamus (229 +/- 3 mm Hg, p less than 0.02). In bilaterally denervated SHR, the upper limits were lowered to 193 +/- 4 mm Hg in the cortex (p less than 0.02 vs. innervated SHR) and to 207 +/- 5 mm Hg in the thalamus (p less than 0.02 vs. innervated). In WKY, resting MAP was approximately 55 mm Hg lower than that in SHR. Acute denervation reduced the upper limits from 142 +/- 3 mm Hg to 130 +/- 4 in the cortex (p less than 0.05) and from 158 +/- 4 to 145 +/- 4 in the thalamus (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Effects of long-term antihypertensive treatment on cerebral, thalamic and cerebellar blood flow in spontaneously hypertensive rats (SHR).

Cerebral blood flows (CBF) were measured in the parietal cortex, the thalamus and the cerebellum by the hydrogen clearance technique in anesthetized spontaneously hypertensive rats, of which hypertension was treated for 16 weeks (long-term) or 8 weeks (short-term) with antihypertensive agents of hydralazine and guanethidine. As compared to non-treated control animals, CBF in the three regions were significantly increased while the calculated cerebrovascular resistances (CVR) were decreased in hypertension-treated animals. Such CBF and CVR changes were greater in SHR with long-term than short-term therapy. Both an increase in CBF and a decrease in CVR were closely related to a fall in the blood pressure. From the present results, it was concluded that earlier and longer treatment of hypertension could lessen or even prevent the increased CVR due to the hypertensive vascular changes, and increase CBF as a result.

Animals↗

PubMedDate not supplied

Cerebral and cerebellar blood flow autoregulations in acutely induced cerebral ischemia in spontaneously hypertensive rats--transtentorial remote effect.

Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 +/- 6.2 and 58.9 +/- 4.6 ml/100 g/min (mean +/- SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 +/- 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74% and further to 58% of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 +/- 4.9 and CeBF to 53.9 +/- 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗