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Biomedical subjects

H Kanemitsu

Publications and source records attributed to H Kanemitsu.

At least 19 recordsLinked to original sources

[Aortic valve/root replacement using a stentless bioprosthesis (Medtronic Freestyle valve)].

BACKGROUND: The purpose of the study is to assess the clinical and hemodynamic performance of aortic valve replacement (AVR) with the Freestyle bioprosthesis. METHODS: Twenty-one patients received AVR with a Freestyle aortic root bio-prosthesis between May 1998 and October 1999. Eighteen patients underwent AVR with subcoronary method and three patients with aortic root (full root) method. Patients were evaluated postoperatively at discharge by clinical examination and color Doppler echocardiography. RESULTS: There was one death due to multi-organ failure. No patients experienced valve deterioration, paravalvular leak, unacceptable hemodynamic performance, nor thromboembolic event. Excellent function is demonstrated by very low gradient (mean gradient 7.2 +/- 4.7 mmHg) through aortic valve and no significant aortic regurgitation (none: 11, trivial/mild: 10). All patients had been in New York Heart Association Functional Class III and IV preoperatively, and after surgery, 17 patients were in Class I, and 3 were in Class II. CONCLUSION: The Freestyle bioprosthesis has good clinical and hemodynamic performance without Coumadin. Further follow-up is required to evaluated valve durability.

Adult↗

[Combined valve and coronary artery bypass surgery].

Between January 1997 and November 1999, 31 patients underwent combined valve and coronary artery bypass grafting (CABG) surgery in our institute. There was no hospital death and clinical symptom improved in all patients after surgery. Mean follow-up was 16.3 months. The actuarial survival rate was 96.8% at 1 year. There were 4 late deaths (CHF in 3, arrhythmia in 1). Tepid blood cardioplegia was effective for those operations. Operation of CABG combined with valve surgery or LV surgery could be safely performed. We therefore considered that complete correction of the lesion with not only CABG but also combined valve surgery or LV surgery was the procedures of choice in patients with complicated lesions.

Aged↗

Cerebral acetylcholine levels and long-term spatial cognitive impairment following middle cerebral artery occlusion in rats.

The behavioral and neurochemical changes in the chronic phase of permanent occlusion of the right middle cerebral artery (MCA) in rats were investigated. Nineteen MCA-occluded rats failed to solve the 8-arm radial maze task (cognitively impaired rats), while 11 MCA-occluded rats could complete it (cognitively unimpaired rats). When a delay of 60 min was imposed in the task, however, 5 cognitively unimpaired rats failed to complete the task. The rats that underwent behavioral testing were studied for any changes in ACh levels in various brain regions using HPLC with electrochemical detection. The ACh levels in the infarcted areas decreased considerably in all MCA-occluded rats, but no region of the infarcted areas correlated with the spatial cognitive deficit. The ACh levels tended to decrease in the frontal cortex of the cognitively impaired rats and greatly increased in both ipsilateral and contralateral parietal cortex of the cognitively unimpaired rats. A significant correlation was observed between the ACh levels and spatial cognitive deficit in the contralateral frontal cortex, and ipsilateral and contralateral parietal cortex. These results suggest that the cholinergic function of the frontal and parietal cortices might play a role in acquiring spatial cognition in MCA-occluded rats.

Acetylcholine↗

Enhanced protein synthesis in the ipsilateral substantia nigra following middle cerebral artery occlusion in the rat.

Following focal cerebral ischemia, neuronal cell death is detected in remote areas of the brain, including the ipsilateral thalamus and substantia nigra (SN), as well as in the ischemic core. We have investigated protein synthesis in the remote areas of rats exposed to focal ischemia using autoradiography. The proximal portion of the left middle cerebral artery (MCA) was permanently occluded, and at various periods (6 h, 2, 4 and 7 days and 2 and 4 weeks following ischemia) animals received a single dose of L-[2,3-3H]valine (6.7 mCi/kg). Brain sections containing the thalamus and SN were processed for autoradiography. In the ipsilateral cerebral cortex and striatum, marked impairment of protein synthesis was observed and was never completely recovered during the experiment. No changes in protein synthesis in the ipsilateral thalamus were detected during the experiment. However, a change in protein synthesis was demonstrated in the ipsilateral SN. At 2 days after MCA occlusion, incorporation of [3H]valine into the whole zona reticulata of the ipsilateral SN was slightly enhanced and the increase became evident at 4 days after ischemia. Increased incorporation of [3H]valine began to be localized in the lateral portion of the zona reticulata after 7 days and continued up to 4 weeks following ischemia. Enhanced protein synthesis during the early stage (2 and 4 days after ischemia) may be due to the activated function of the neurons in the zona reticulata and that during the late stage (7 days and 2 and 4 weeks) after ischemia to astroglial proliferation

Animals↗

Complement activation by diesel exhaust particles (DEP).

The effect of diesel exhaust particles (DEP) on the hemolytic activity of human serum complement was investigated. Previous treatment of human serum with DEP extracts at 37 degrees C decreased the hemolytic activity of human serum complement dose dependently, to 20% of its original value. This decrease in complement activity by DEP extracts was observed with previous incubation at 37 degrees C but not at 4 degrees C. A decrease in complement activity was observed after previous incubation at 37 degrees C in the presence of EGTA/Mg but not in the presence of EDTA, indicating that the alternative pathway of the complement system had been activated by DEP extracts. Activation of the complement system by DEP extracts was further demonstrated by observation of the cleavage of the third component of the complement (C3) in serum to C3b with immunoelectrophoresis using goat anti-human C3 antiserum. This cleavage of C3 was similarly observed in the presence of EGTA/Mg, indicating the activation of the alternative pathway of the complement system by DEP extracts. These results indicate that DEP can activate the alternative pathway of the complement system, resulting in a decrease in the hemolytic activity of complement and in the production of biologically active degradation products of complement proteins such as C3a. The biological significance of the activation of the complement by DEP in the alveolus is discussed in relation to the influx of neutrophiles.

Animals↗

[Changes in acetylcholine level and its related enzyme activities in rat brain following focal ischemia].

At 1 to 4 weeks following middle cerebral artery occlusion in Wistar rats, levels of acetylcholine, which is neuro-transmitter, were measured. In the hippocampus, which plays an important role in memory, levels of acetylcholine in the ischemic group could not be detected the significant difference compared with those in the sham-operated group. But in the anterior cortex and the caudate-putamen, levels of acetylcholine in the ischemic group were recognized the significant difference compared with those in the sham operated group. Moreover activities of choline acetyltransferase, which is the synthetic enzyme of acetylcholine, and activities of acetylcholinesterase, which is the degradative enzyme of acetylcholine, were measured in the anterior cortex which was recognized decrease of the acetylcholine level and the hippocampus which could not be detected the difference of the acetylcholine level. Activities of both enzymes in the hippocampus could not be recognized the significant difference between the ischemic group and the normal group. But in the anterior cortex activities of both enzymes in the ischemic group were significantly decreased compared with those in the normal group. These results suggest that these decreases in the ischemic group were due to damage of injection of cholinergic neuron from Meynert nucleus (basal nucleus of Meynert) to anterior cortex.

Acetylcholine↗

[Determinants of long-term outcome for operative survivors of acute aortic dissection].

Predictability of aorta-related complications and survival was examined in 79 operative survivors of acute aortic dissection. Follow-up was 94.9% complete and totaled 458 patient-years. Actuarial survival was 93 +/- 3% (+/- S.E.) (n = 43) at 5 years, and 74 +/- 8% (n = 13) at 10 years. Survival was significantly lower in patients having neurological complication. Freedom from aorta-related complications was 82 +/- 5% (n = 37) at 5 years, and 67 +/- 8% (n = 11) at 10 years. Multivariate Cox regression analysis identified residual entry and leak on anastomotic site as independent predictors of aorta-related complications. We conclude that in the treatment of acute aortic dissections, reducing the incidence of residual entry and leak on anastomotic site improves long-term outcome.

Acute Disease↗

Effect of L-arginine and NG-nitro-L-arginine on delayed neuronal death in the gerbil hippocampus.

To assess the role of nitric oxide (NO) in cerebral ischemia, we investigated the effect of L-arginine, a substrate of NO synthase (NOS), and NG-nitro-L-arginine (L-NNA), a NOS inhibitor, on neuronal death in the CA1 hippocampal region. Seventy-two Mongolian gerbils were used in the study. Both carotid arteries were occluded for 4 min to induce forebrain ischemia. Temporal muscle temperature was strictly maintained at 37.5 +/- 0.3 degrees C during the ischemia. L-arginine (10 and 100 mg kg-1) or L-NNA (1, 10 and 100 mg kg-1) was administered intraperitoneally 4 times: 30 min before, 3 h, 6 h and 24 h after induction of ischemia. Four days after ischemic insult, the animals were perfusion-fixed, and the neuronal densities in the medial, middle and lateral CA1 subfield were estimated. Average neuronal cell density of the control group was 2-3 mm in each subfield. L-arginine at doses of 10 and 100 mg kg-1 did not prevent neuronal death. L-NNA at doses of 1 and 10 mg kg-1 did not protect neuronal cells from ischemia either. However, in ischemia gerbils treated with 100 mg kg-1 L-NNA, the average neuronal cell density in the lateral CA1 subfield was 54.4 +/- 19.1, L-NNA (100 mg kg-1) significantly (p < 0.05) reduced the occurrence of neuronal death in the lateral CA1 subfield. The present results suggest that NO plays an important role in the development of neuronal injury after global ischemia.

Animals↗

Modulation of protein kinases and microtubule-associated proteins and changes in ultrastructure in female rat pituitary cells: effects of estrogen and bromocriptine.

This study focused on the intracellular signal transduction system and microtubule-associated proteins (MAPs), such as MAP-2 and Tau protein. The modulation of these proteins and their correlation with ultrastructural changes were investigated in rat pituitary prolactin (PRL) cells. Adult female Wistar rats were treated with estrogen and bromocriptine and their pituitary glands were removed for analysis of the expression of tubulin, MAP-2, Tau protein, protein kinase C (PKC), and calcium calmodulin (CaM) kinase. Western blot analysis showed that estrogen increased and bromocriptine decreased the expression of PKC alpha, beta 1, beta 2, CaM kinase alpha, beta, MAP-2, and Tau protein. MAP-2 and Tau protein, which are cytosolic proteins, being translated on free ribosomes, were associated with the membrane of whirling rough endoplasmic reticulum (RER) in estrogen-treated cells and dissociated with vesiculated RER induced by bromocriptine. These results suggested that the modulation of MAP-2 and Tau protein may reflect changes of PKC and CaM kinase, and that the quantitative changes and intracellular modulation of MAPs induced by estrogen and bromocriptine, i.e., estrogen-induced association and bromocriptine-induced dissociation of MAP-2 and Tau protein with membrane of RER, may reflect the dynamics of microtubules and are associated with structural changes in the RER and changes in the synthesis and intracellular transport of PRL.

Animals↗

[The case of left atrial myxoma originating from posterior leaflet of mitral valve].

We experienced the case of left atrial myxoma originating from posterior leaflet mitral valve. Mitral valve repair was performed in that case, because of the presence mitral leaflet defect due to removal of the myxoma. Transesophageal echocardiography was a useful tool for perioperative evaluation of the mitral valve and precise localization of the origin of the myxoma.

Adolescent↗

Up-regulation of c-myc gene expression following focal ischemia in the rat brain.

Changes in gene expression including that of c-fos occur following cerebral ischemia. Proto-oncogenes c-myc and s-myc and oncosuppressor gene p53 are known to induce apoptosis in some types of cells, whereas proto-oncogene bcl-2 inhibits apoptosis. Possible induction of mRNAs for c-myc, N-myc, s-myc, c-fos, p53 and bcl-2 was examined following focal ischemia in the rat anterior cortex, hippocampus, thalamus and cerebellum by Northern blot analysis. Animals were decapitated 1, 2, 6, 12, and 24 hours following the left middle cerebral artery (MCA) occlusion. In sham-operated control rats, the mRNAs for c-myc, N-myc, c-fos and p53 were present in the anterior cortex, hippocampus, thalamus on both sides, and in the cerebellum, whereas those for s-myc and bcl-2 were not. The c-myc gene expression was rapidly and markedly induced by the MCA occlusion in the ipsilateral anterior cortex, hippocampus and thalamus in a time-dependent manner. In these regions, the c-fos gene expression was also induced as early as 1 hour after the MCA occlusion. The p-53 mRNA was induced in the ipsilateral hippocampus at 24 hours after MCA occlusion. In contrast, mRNAs for N-myc, s-myc and bcl-2 were not induced following MCA occlusion. These results indicate a possibility that high-level expression of the c-myc gene may be involved in the ischemic cellular events including apoptosis.

Animals↗

[A case of contralateral pneumothorax after right pneumonectomy].

A 46-year old man, who had a history of right pneumonectomy for pulmonary tuberculosis 28 years ago, was referred to our hospital for surgical treatment of contralateral pneumothorax. The patient underwent multiple excisions of bullae and parietal pleurectomy through the median sternotomy in order to save pulmonary function. The postoperative course was satisfactory as he could maintain preoperative pulmonary function. He returned to his work soon. We consider that the median sternotomy would be the most useful approach to save pulmonary function of patients who plan to undergo surgical treatment of contralateral pneumothorax after pneumonectomy.

Humans↗

Key of induced tolerance to ischaemia in gerbil hippocampal CA1 is not at transcriptional level of hsp70 gene: in situ hybridization of hsp70 mRNA.

Hippocampal neurons, when pretreated with sublethal ischaemia, acquired tolerance to future treatments of normally lethal ischaemia. The level of transcription of the stress protein hsp70 was studied by in situ hybridization in control, ischaemic and tolerance-induced-ischaemic hippocampal neurons. Mongolian gerbils were subjected to single forebrain ischaemia for 2 min (2-min ischaemia group: sublethal) or 5 min (5-min ischaemia group: lethal). Other animals, were exposed to sublethal ischaemia for 2 min and were subjected subsequently to ischaemia for 5 min, 2 days later. Animals were sacrificed at 6, 12, 24 and 48 h following ischaemia and in situ hybridization was performed with thin cross sections including the hippocampus. Hybridization of the hsp70 probe in the control group (no ischaemia) was barely visible in the brain. In the 2-min ischaemia group, intense hybridization was seen in the CA1 sector from 6 through 24 h of recirculation but hybridization almost disappeared at 48 h of recirculation. In the 5-min and the double ischaemic groups, the intense induction in the CA1 sector occurred during the period from 6 through 48 h of recirculation. Our present study by in situ hybridization reveals high levels of transcription of hsp70 message following 5-min of ischaemia, however no protein was detectable based on our previous experiments employing immunocytochemistry. In tolerance-induced hippocampal neurons, both hsp70 message and protein are present. These results suggest that tolerance-induced neurons are modified such that the hsp70 gene is both transcribed and translated. These changes most likely give rise to the tolerance observed in the double ischaemia group.

Animals↗

The s-Myc protein having the ability to induce apoptosis is selectively expressed in rat embryo chondrocytes.

Gene transfection experiments demonstrated that over-expression of the s-myc gene under the control of a human metallothionein promoter induced apoptosis in cells such as rat and human glioma cells. In contrast to c-Myc-mediated apoptosis requiring withdrawal of serum growth factors, s-myc expression induced apoptosis in glioma cells in the presence of 10% fetal calf serum. Whereas, s-Myc-mediated apoptosis was suppressed in proportion to the increase of bcl-2 expression as seen in c-Myc mediated apoptosis. The s-myc gene was expressed in rat embryo cells being committed to differentiate to hypertrophic chondrocytes which undergo programmed cell death. CAT assay demonstrated that in the NH2-terminal region, the s-Myc protein contains a domain structure required for expression of transactivation activity that is approximately six times higher than that of c-Myc. Therefore, these findings strongly suggest that s-Myc may play an important role in transcription regulation of a set of genes whose expression induces programmed cell death in vitro and in vivo.

3T3 Cells↗