Search PubMed⌕ Search

Biomedical subjects

H Imai

Publications and source records attributed to H Imai.

At least 217 records · Page 12Linked to original sources
PubMed1997

Mosaic pattern of ornithine transcarbamylase expression in spfash mouse liver.

Mosaicism of ornithine transcarbamylase expression was immunohistochemically examined in hepatocytes of spfash heterozygous female mouse livers. An immunohistochemical method using polyclonal antibodies against ornithine transcarbamylase visualized the mosaicism in serial paraffin sections. Very complicated mosaic patterns consisting of positive and negative hepatocytes were obtained in a section of adult liver, but a computer-aided three-dimensional analysis of serial sections demonstrated that patches with complicated shapes and various sizes, which are contiguous groups of positive or negative hepatocytes and are isolated in sections, connected very well with one another. No definite orientation such as portal-central was observed in the three-dimensional images of each patch. In balanced regions of the mosaicism, most individual plates along their straight portal-central lengths did not appear to be composed of only marker-positive or marker-negative hepatocytes. By contrast, in unbalanced regions of the mosaicism, individual plates along their total portal-central lengths often consisted entirely of a major type of hepatocytes. A patch appeared to be present in more than two lobules, but each patch did not constitute a complete lobule. Complicated mosaic patterns of patches were also seen in neonatal and postnatal livers. These results suggest that, although hepatocytes proliferate and migrate extensively during development, they might allocate their daughter cells contiguously and the orientation of their allocation might be random, leading to the formation of three-dimensionally large contiguous quasiclones of hepatocytes, the shapes of which are very complicated.

Animals↗
PubMed1997

[CREST syndrome].

Explore the source record for details and available documents.

Acute Kidney Injury↗
PubMed1997

[A 76-year-old man with loss of vision and dementia].

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa

Aged↗
PubMed1997

[Neurological CPC.57. An 80-year-old woman with four years history of muscle atrophy involving lower extremities predominantly on the right side].

We report an 80-year-old woman with progressive muscular atrophy predominantly involving her right lower extremity. She was well until 1992 (75 years of age) when she noted an onset of weakness in her right leg which had got progressively worse. She was admitted to our service in July 1994. On admission, general physical examination was unremarkable. She was alert and well oriented without dementia. Higher cerebral functions were normal. Cranial nerves also appeared intact. She dragged her right leg in walking. Mild to moderate weakness (2/5 to 4/5) was noted in muscles in her right lower extremity more in the distal part. Deep tendon reflexes were within normal limits, and the plantar response was flexor bilaterally. Sensation was intact. Laboratory examinations were also unremarkable except for slight increase in CK which was 470 IU/l. CSF was also normal. EMG revealed neurogenic changes in the lower extremities. She was admitted to Aoki Hospital on October 21, 1994, by that time, her weakness in the right lower extremity had gotten worse in that the muscle strength of the right extensor hallucis longus was 0 and tibialis anterior 2; muscle atrophy was also prominent in her right leg; the right ankle jerk could not be elicited. In the subsequent course, weakness and atrophy appeared in her left lower extremity, however, upper extremities and cranial nerves had never been affected. Babinski sign was always negative. In February 1996, she developed delusional ideation of self persecution, and showed difficulty in communication with medical staffs. She developed fever of 38.7 degrees C on June 13, 1996 expired on the next day. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a form of spinal muscular atrophy. Opinions were divided between ALS and spinal muscular atrophy. Post-mortem examination revealed marked loss of anterior horn neurons in the lumbar area with astrogliosis. Bunina bodies were seen in some of the remaining neurons. No myelin pallor was noted in the pyramidal tracts, however, atrophy and loss of Betz cells were noted in the motor cortex. Other cortical areas were unremarkable. The neuropathologist arrived at the conclusion that the patient had ALS. This patient was unique in that she had asymmetric atrophy and weakness limited to the lower extremities. This is quite unusual as ALS of four years duration. In addition, the patient developed some mental change which was thought to represent dementia by some participants. But no clear morphologic changes were seen to account for her mental change.

Aged↗
PubMed1997

[A case of papillary adenocarcinoma of the stomach with liver metastases and carcinomatous peritonitis treated effectively by methotrexate/5-fluorouracil sequential chemotherapy].

A 54-year-old male was admitted to receive treatment by anticancer drug for advanced gastric cancer with liver metastases and carcinomatous peritonitis. Upper gastrointestinal series showed a Borrmann type 4 gastric cancer occupying the body and antrum, and a pathological diagnosis of papillary adenocarcinoma was made by endoscopic biopsy. Two cycles of neoadjuvant chemotherapy consisting of 5-FU and low-dose CDDP (FP therapy) were given. No effect was observed, so that the next chemotherapy schedule of sequential MTX/5-FU therapy was performed. We adopted the intermediate (MTX: 100 mg/m2 and 5-FU 600 mg/m2 weekly) dose regimen. When six courses of this regimen were completed, the primary lesion of the stomach was decreased to 60% and the metastatic liver tumor to 72%, basel on criteria for the evaluation of clinical effects of solid cancer chemotherapy. However, pylorous stenosis remained, and we performed gastrojejunostomy and biopsy of the regional lymph node to determine the response to the chemotherapy. A pathological examination of lymph node revealed metastatic papillary adenocarcinoma with xanthogranulomatous change, and was judged as an effect showing grade 2. He was discharged and had the outpatient hospital treatment. He died of exacerbation of carcinomatous peritonitis 10 months after his initial admission. The response duration for sequential MTX/5-FU therapy was 4 months. This therapy was usually effective in patients with poorly differentiated adenocarcinoma of the stomach. Our result indicates that this therapy can be effective for not only poorly differentiated adenocarcinoma but also papillary adenocarcinoma of the stomach in an advanced stage.

Adenocarcinoma, Papillary↗
PubMed1997

Enumerating suboptimal alignments of multiple biological sequences efficiently.

The multiple sequence alignment problem is very applicable and important in various fields in molecular biology. Because the optimal alignment that maximizes the score is not always biologically most significant, providing many suboptimal alignments as alternatives for the optimal one is very useful. As for the alignment of two sequences, this suboptimal problem is well-studied, but for the alignment of multiple sequences, it has been considered impossible to investigate such suboptimal alignments because of the enormous size of the problem. The optimal multiple alignment can be obtained with A* algorithm, and an efficient algorithm for the k shortest paths problem on general graphs is discovered recently. We extend these algorithms for computation of set of all aligned groups of residues in optimal and suboptimal alignments, and for enumeration of suboptimal alignments. The suboptimal alignments are numerous. Thus we discuss what kind of suboptimal alignment is unnecessary to enumerate, and propose an efficient technique to enumerate only necessary alignments. The practicality of these algorithms are demonstrated through experiments. Moreover, the property of suboptimal alignments of multiple sequences are also examined through experiments.

Algorithms↗
PubMed1996

Microsatellite instability in latent prostate cancers.

Forty-seven latent prostate cancers obtained from 46 Japanese men were examined for microsatellite instability (MSI). This study with examination at 23 microsatellite loci revealed replication error (RER) in II of the 47 cases (23%), 4 of them showing RER with 2 loci that was defined as MSI. Histological grade was significantly associated with RER; 9 of the 11 RER positive cases were of infiltrative type, and the 4 of them exhibiting MSI were all poorly differentiated. While the frequency of MSI in latent prostate cancer was lower than in clinical cases, it was found in the more aggressive lesions thought most likely to develop into clinical cancers.

Aged↗
PubMed1996

Import into mitochondria of phospholipid hydroperoxide glutathione peroxidase requires a leader sequence.

An in vitro import system was used to characterize the mechanism of import of phospholipid hydroperoxide glutathione peroxidase (PHGPx) into mitochondria. Mitochondria were isolated from rat liver and incubated at 25 degrees C with [35S]methionine-labeled products of the in vitro translation of mRNA that encoded 23-kDa and 20-kDa PHGPx. 23-kDa PHGPx was imported into mitochondria in a time-dependent manner and was processed to yield the 20-kDa form of PHGPx. The 20-kDa form of PHGPx, without a leader sequence, associated weakly with mitochondria but was not imported. An analysis with an uncoupler of oxidative phosphorylation showed that a membrane potential in the mitochondria was also required for the import of PHGPx. It appears, therefore, that the leader sequence in the precursor to PHGPx is the signal for import into the mitochondria. This is the first report to indicate that the precursor to PHGPx is imported into the mitochondria via the action of a leader sequence.

Animals↗
PubMed1996

Molecular cloning of rat phosphatidylinositol synthase cDNA by functional complementation of the yeast Saccharomyces cerevisiae pis mutation.

Phosphatidylinositol synthase (CDP-1,2-diacyl-sn-glycerol: 3-phosphatidyltransferase, EC 2.7.8.11) catalyzes the formation of phosphatidylinositol and CMP from CDP-diacylglycerol and myo-inositol. We have cloned a phosphatidylinositol synthase cDNA from rat brain by functional complementation of the yeast pis mutation, which is defective in phosphatidylinositol synthase. The deduced protein comprised 213 amino acids with a calculated molecular mass of 23,613 Da. The predicted protein sequence is highly homologous to the previously determined yeast phosphatidylinositol synthase sequence. The cDNA hybridized to a 1.7-kb mRNA that was abundantly expressed in rat brain and kidney.

Amino Acid Sequence↗
PubMed1996

Contribution of early-emigrating midbrain crest cells to the dental mesenchyme of mandibular molar teeth in rat embryos.

Teeth are formed by reciprocal interactions between the epithelium and mesenchyme in the first pharyngeal arch. Although the contribution of midbrain and hindbrain crest cells to the first pharyngeal arch has been previously examined in rodent embryos, no direct evidence exists that these cells are actually involved in the dental mesenchyme. In order to elucidate the contribution of the cranial neural crest cells in tooth formation, we first identified the emigration sites and stages providing the crest cells that migrate to the presumed tooth-forming region of the mandibular prominence. Focal labeling with DiI was performed at the midbrain and anterior hindbrain crests in rat embryos, and the labeled embryos were cultured for 30 or 60 hr. The resultant migration patterns indicated that posterior midbrain crest cells emigrating by the end of the 4-somite stage predominantly migrated to the region where tooth buds normally develop. Second, we established a new type of long-term culture system in which whole embryo culture is followed by a mandibular organ culture. Using this system, rat embryos were maintained from the early-somite stage and the molars in the explants were able to reach the bud stage within 8 days. Finally, to ascertain if posterior midbrain crest cells emigrating by the end of the 4-somite stage were involved in the dental mesenchyme, these cells were labeled with DiI and processed for the long-term culture. Labeled crest cells were clearly detectable in the dental mesenchyme. These findings indicate that the early-emigrating posterior midbrain crest cells contribute to mandibular molar tooth development in rat embryos.

Animals↗
PubMed1996

An immuno-histochemical study of ferritin in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced hemiparkinsonian monkeys.

Iron is increased in the substantia nigra of patients with Parkinson's disease, but the mechanism of its accumulation is unknown. We report the distribution of ferritin in the basal ganglia of hemiparkinsonian monkeys made by MPTP. We stereotactically injected MPTP unilaterally into the caudate nucleus of four monkeys, and the substantia nigra and the basal ganglia regions were stained for L-ferritin by an immunohistochemical method. The ferritin immuno-staining was most intense in the pallidum and the pars reticulata of the substantia nigra on both injected and non-injected sides. No significant difference was noted in the immunostaining for ferritin in the pars compacta of the substantia nigra between the injected and the non-injected side. Iron was increased in the pars compacta of the substantia nigra of this hemiparkinsonian monkeys in our previous study. Normal ferritin immunostaining on the injected side would indicate that iron accumulation is not related to altered metabolism of L-ferritin in this model.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1996

Overexpression of phospholipid hydroperoxide glutathione peroxidase suppressed cell death due to oxidative damage in rat basophile leukemia cells (RBL-2H3).

The role of phospholipid hydroperoxide glutathione peroxidase (PHGPx) in the cellular defense against oxidative stress was investigated in a novel cell model. We isolated stable transfectants of RBL-2H3 cells that overexpressed PHGPx. The activity of PHGPx in RBL2H3 cells that had been transfected with the 761bp cDNA for rat PHGPx (RPHGPx2) that we had cloned previously was 3.8 times higher than that in parent cells and in cells that had been mock-transfected with the vector without a cDNA insert. Cells that overexpressed PHGPx were three times more resistant than parent cells and mock-transfected cells to the cytotoxic effects of an radical initiator (AAPH) that induced the oxidative stress. This resistance to damage by AAPH of cells that overexpressed PHGPx was not observed after pretreatment with buthionine sulfoximine (BSO), an inhibitor of the synthesis of glutathione. Overexpression of PHGPx could suppress the peroxidation of membrane lipids and, in particular, the production of phosphatidylcholine hydroperoxide by AAPH in RBL2H3 cells. PHGPx was also able to prevent cell death in response to extracellular attack by a lipid peroxide. This is the first report to indicate directly that PHGPx can scavenge phosphatidylcholine hydroperoxide, which induces oxidative damage at the cellular level.

Amidines↗
PubMed1996

Successful implantation of in vitro cultured rabbit embryos after uterine transfer: a role for mucin.

The functional role of the mucin layer for development of rabbit embryos was examined by uterine transfer of embryos with different thicknesses of mucin. Embryos collected at various intervals after human chorionic gonadotropin (hCG) injection were cultured until 90 hr post-coitum (p.c.) and transferred to the uterus of synchronized recipients. When embryos collected at 20 or 25 hr p.c. were used for transfer, no implantation occurred. By contrast, embryos collected at 35 or 40 hr p.c. developed to term at high rates (53 and 80%, respectively). The thickness of the mucin layer on the embryos was different between these two groups. Embryos collected before 25 hr p.c. have less than 11.2 +/- 0.2 microns of thickness of mucin and embryos collected after 35 hr p.c. have more than 34.3 +/- 5.5 microns. To examine whether mucin deposition is required for in vitro cultured rabbit blastocysts to continue development after uterine transfer, embryos were collected at 20 hr p.c., cultured for 60 or 70 hr in vitro, and then temporarily transferred to the oviducts of recipient does to add mucin. These embryos were recovered from the oviducts at 24 hr after transfer, classified according to the thickness of mucin deposition, and transferred again to the uterus of synchronized recipients. Twenty live young were obtained from 67 embryos with a 20-40 microns thick mucin layer. No live young were obtained from 57 embryos with less than a 20 microns thick mucin. The thickness of the mucin layer appears to be an important factor for successful implantation of rabbit embryos.

Animals↗