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Biomedical subjects

H Ichikawa

Publications and source records attributed to H Ichikawa.

At least 217 records · Page 12Linked to original sources

[Isolated retrograde amnesia following viral encephalitis].

We describe a patient who presented with isolated retrograde amnesia of 2-year duration after recovery from viral encephalitis. The patient was a 29-year-old right-handed male dentist and was admitted to our hospital with a complaint of generalized convulsion. Cerebrospinal fluid (CSF) showed mononuclear pleocytosis. Neuroradiological examinations (X-ray CT, MRI and 123I-IMP SPECT) revealed no significant abnormality. Immunological method showed no specific increase of viral antibody titers. However, with a tentative diagnosis of viral encephalitis, administration of acyclovir was started. After 3 weeks he became comprehensive, and several kinds of neuropsychological tests were performed. His intelligence and immediate memory were normal, and his procedural memory of dentist was intact. On the other hand, he could not recall any information about events, both personal and public, occurred within 2 years before the onset of present illness. His autobiographical memory disorder was also demonstrated using a series of weekly comic. In isolated retrograde amnesia following viral encephalitis like this case, memory of relatively short time duration, acquired prior to the onset of present illness, tend to be disturbed.

Acyclovir↗

Reduction of substance P after chronic antidepressants treatment in the striatum, substantia nigra and amygdala of the rat.

We investigated the effects of chronic treatment with food containing one of five antidepressants on substance P (SP) content in the rat brain using radioimmunoassay and enzyme-immunoassay. The antidepressants used were imipramine, desipramine, clomipramine, amoxapine and mianserin. Following 40 days of treatment, all the antidepressants decreased SP concentrations in the striatum, substantia nigra and amygdala. Only imipramine and desipramine reduced the peptide content in the hippocampus, and only mianserin reduced it in the septum. We further examined the acute effects of antidepressants one hour after a single intraperitoneal administration. Acute imipramine and desipramine treatment reduced SP in the striatum, whereas acute mianserin decreased it in the striatum and substantia nigra. These results demonstrate that all antidepressants on chronic treatment had a common effect, a reduction of SP content in the striatum, substantia nigra and amygdala. This raises the possibility that such a decrease may contribute to the therapeutic action of antidepressants in affective disorders.

Amoxapine↗

Coexistence of calbindin D-28k and NADPH-diaphorase in vagal and glossopharyngeal sensory neurons of the rat.

The presence and coexistence of calbindin D-28k-immunoreactivity (ir) and nicotinamide adenosine dinucleotide phosphate (NADPH)-diaphorase activity (a marker of neurons that are presumed to convert L-arginine to L-citrulline and nitric oxide) were examined in the glossopharyngeal and vagal sensory ganglia (jugular, petrosal and nodose ganglia) of the rat. Calbindin D-28k-ir nerve cells were found in moderate and large numbers in the petrosal and nodose ganglia, respectively. Some calbindin D-28k-ir nerve cells were also observed in the jugular ganglion. NADPH-diaphorase positive nerve cells were localized to the jugular and nodose ganglia and were rare in the petrosal ganglion. A considerable portion (33-51%) of the NADPH-diaphorase positive neurons in these ganglia colocalized calbindin D-28k-ir. The presence and colocalization of calbindin D-28k-ir and NADPH-diaphorase activity in neurotransmitter-identified subpopulations of visceral sensory neurons were also studied. In all three ganglia, calcitonin gene-related peptide (CGRP)-ir was present in many NADPH-diaphorase positive neurons, a subset of which also contained calbindin D-28k-ir. In the nodose ganglion, many (42%) of tyrosine hydroxylase (TH)-ir neurons also contained NADPH diaphorase activity but did not contain calbindin D-28k-ir. These data are consistent with a potential co-operative role for calbindin D-28k and NADPH-diaphorase in the functions of a subpopulation of vagal and glossopharyngeal sensory neurons.

Animals↗

Bax protein-like immunoreactivity in primary sensory and hypothalamic neurons of adult rats.

Bax protein-like immunoreactivity (Bax-ir) was examined in the perfusion-fixed, cryosectioned rat nervous system. In the central nervous system, hypothalamic neurons were the only neurons that exhibited Bax-ir in the cell body. Their axons traveled toward the median eminence, suggesting that the Bax-like immunoreactive (Bax-ir) hypothalamic neurons included neurosecretory ones. Bax-ir axons were observed in the solitary tract nucleus, and spinal and medullary dorsal horns. They appear to have been derived from Bax-ir primary sensory neurons in the viscerosensory nodose ganglion and somatosensory dorsal root and trigeminal ganglia. In the somatosensory ganglia, smaller cells exhibited stronger Bax-ir. Accordingly, the ir axons in the dorsal horn were most concentrated in lamina II.

Animals↗

Leukocyte depletion attenuates reperfusion injury in patients with left ventricular hypertrophy.

BACKGROUND: Reperfusion injury can occur after a long period of aortic cross-clamping in patients with left ventricular hypertrophy during open-heart surgery, even with the most up-to-date techniques of myocardial protection. In the present study, we examined whether leukocyte depletion as an adjunct to terminal blood cardioplegia (LDTC) attenuates reperfusion injury in patients with left ventricular hypertrophy (LV mass, >300 g; left ventricular end-systolic volume index, >100 mL/m2) in a group of 30 patients undergoing aortic valve replacement. METHODS AND RESULTS: We used basic cold potassium crystalloid cardioplegic solution. Terminal blood cardioplegic solution (TC) or LDTC was accomplished by mixing a cold potassium crystalloid cardioplegic solution with warm arterial blood obtained through cardiopulmonary bypass and administered to the aortic root for the first 10 minutes of reperfusion. During delivery of LDTC, warm arterial blood was passed through a leukocyte-removal filter. Patients were randomized into one of three groups for reperfusion: whole blood (WB) (n=10), TC (n=10), and LDTC (n=10). Left ventricular biopsies were obtained before ischemia, at the end of ischemia, and 15 minutes after reperfusion. Semiquantitative scoring for ultrastructural alterations indicated that the LDTC group achieved significantly better recoveries of both scores at reperfusion for myocyte damage and for endothelial cell damage of capillaries than did the WB and TC groups. The LDTC group had significantly fewer neutrophils adhering to endothelial cells at reperfusion and a lower level of malondialdehyde derived from myocardium than did the WB and TC groups. Regarding the clinical data, the LDTC group had a lower maximum creatine kinase-MB, a higher percentage of spontaneous defibrillation, a lower pulmonary capillary wedge pressure, and a lower requirement for dopamine that did the WB group, whereas the TC group failed to do better than the WB group. CONCLUSIONS: These results demonstrate that leukocyte-depleted reperfusion is potentially beneficial as an adjunct to terminal cardioplegia during cardiac surgery to attenuate reperfusion injury in patients with left ventricular hypertrophy.

Adult↗

Two transcripts with different sizes derived from a rice homeobox gene, OSH1.

A rice homeobox gene, OSH1, contains two functionally independent promoters which generate a larger transcript and a smaller transcript. In Arabidopsis, each promoter can drive the expression of a reporter gene in a different manner, indicating that the expression of different sized transcripts is independently regulated by each promoter. Over-expression of the larger transcript in transformed plants caused altered morphologies (Matsuoka et al., Plant Cell, 1993, 5, 1039-1048); in contrast, over-expression of the smaller transcript did not cause any morphological changes. The results suggest that the product of the smaller transcript fails to alter the expression of its target gene(s) in the transformants, while that of the larger transcript is capable of altering the expression of its target gene(s).

Amino Acid Sequence↗

Calbindin-D28k-immunoreactivity in the trigeminal ganglion neurons and molar tooth pulp of the rat.

The cell body size and coexpression of carbonic anhydrase (CA), calretinin (CR) and calcitonin gene-related peptide (CGRP) of primary neurons with calbindin-D28k (CB) was examined in the trigeminal ganglion (TG) of the rat. CB-immunoreactive (-ir) cells were mostly large and preferentially distributed in the maxillary and mandibular divisions of the TG. 48% of CB-ir TG cells exhibited enzyme CA activity. 10% of CB-ir TG cells contained CR-ir. Most TG cells coexpressing CB- and CR-irs were localized to the maxillary and mandibular divisions and exhibited CA activity. 6.5% of CB-ir TG cells coexisted with CGRP-ir. 46% of TG cells coexpressing CB and CGRP exhibited CA activity. The innervation of the molar tooth pulp by CB-ir TG primary neurons was also examined. CB-ir thick and smooth nerve fibers projected from the root pulp to the pulp horn and the roof of the pulp chamber, where they became thinner and rarely entered the subodontoblastic layer. However, they could not be traced to the odontoblastic layer, predentin or dentine. The distribution pattern of CB-ir pulpal fibers was different from that of CR-ir ones. The trigeminal neurons cells retrogradely labeled with fast blue (FB) from the maxillary molar tooth pulp contained CB- and CR-irs. 23% and 1% of the labeled cells were immunoreactive for CB and CR, respectively. The coexpression of CB- and CR-immunoreactivities (-irs) in FB-labeled cells was negligible. An immunoelectron microscopic method revealed that 21% of pulpal nerve fibers were immunoreactive for CB, and that all CB-ir nerve fibers in the root pulp were myelinated. The present study indicated that the tooth pulp primary neurons contained CB-ir but did not coexpress CB- and CR-irs and that these neurons projected their myelinated axons to the pulp.

Animals↗

A 1.6-Mb P1-based physical map of the Down syndrome region on chromosome 21.

The Down syndrome (DS) region on chromosome 21, which is responsible for the main features of DS such as characteristic facial features, a congenital heart defect, and mental retardation, has been defined by molecular analysis of DS patients with partial trisomy 21. The 2. 5-Mb region around the marker D21S55 between D21S17 and ERG in 21q22 is thought to be important, although contributions of other regions cannot be excluded. In this region, we focused on a 1.6-Mb region between a NotI site, LA68 (D21S396, which is mapped distal to D21S17) and ERG, because analysis of a Japanese DS family with partial trisomy 21 revealed that the proximal border of its triplicated region was distal to LA68. We constructed P1 contigs with 46 P1 clones covering more than 95% of the 1.6-Mb region. A high-resolution restriction map using BamHI was also constructed for more detailed analysis. Our P1 contig map supplements other physical maps previously reported and provides useful materials for further analysis including gene isolation and sequencing of the DS region.

Base Sequence↗

Identification of a novel human gene containing the tetratricopeptide repeat domain from the Down syndrome region of chromosome 21.

The Down syndrome (DS) region on chromosome 21, which is responsible for the DS main features, has been defined by analysis of DS patients with partial trisomy 21. Within the DS region, we constructed a 1.6-Mb P1 contig map previously. To isolate gene fragments from the 1.6-Mb region, we performed direct cDNA library screening and exon trapping using the P1 clones and a human fetal brain cDNA library, and obtained 67 cDNA fragments and 52 possible exons. Among them, 23 cDNA fragments and 4 exons were interpreted to be derived from a single gene by localization on P1 clones and by Northern analysis. To obtain the full-length cDNA sequence, longer cDNA clones were further screened from another human cDNA library which was enriched with longer cDNA species. These clones were sequenced and assembled to a sequence of 9045 bp. This transcribed sequence encodes a novel 2025 amino-acid protein containing tetratricopeptide repeat (TPR) motifs and therefore the gene was designated as TPRD (a gene containing the TPR motifs on the Down syndrome region). The TPR domain has been found in a certain protein phosphatase and in other proteins involved in the regulation of RNA synthesis or mitosis. The TPRD gene, the novel gene which was proved to be in the 1.6-Mb region and to have the interesting features described above, is a candidate for genes responsible for the DS phenotypes.

Amino Acid Sequence↗

Rapid expulsion of the intestinal trematodes Echinostoma trivolvis and E. caproni from C3H/HeN mice after infection with Nippostrongylus brasiliensis.

The number of goblet cells in the small intestines of C3H/HeN mice increased rapidly following their infection with about 500 third-stage larvae (L3) of the intestinal nematode Nippostrongylus brasiliensis. The number of goblet cells reached its peak on day 9 postinfection (p.i.). Worm burdens in the hosts' small intestines were determined following a challenge infection with encysted metacercariae of the intestinal trematodes Echinostoma trivolvis or E. caproni on days 8 and 16 after primary infections with N. brasiliensis. All metacercariae of E. trivolvis or E. caproni used to challenge the hosts on day 8 p.i. were expelled. Considerable numbers of E. trivolvis (48.6%) and E. caproni (67.1%) remained in the intestines of hosts challenged with these echinostomes on day 16 p.i. All the controls used for E. trivolvis and E. caproni infections without primary infections with N. brasiliensis showed recovery rates greater than 70%. An enzyme-linked immunosorbent assay (ELISA) showed that the IgM titer rose remarkably and plateaued on day 11 p.i. No marked rise in the IgG or IgA titer occurred during the experiment. These results indicate that mucins increased by hyperplastic goblet cells associated with primary infections with N. brasiliensis are responsible for a rapid expulsion of the worms of the challenge infection with E. trivolvis or E. caproni from the mouse host.

Animals↗

Rapid expulsion of the intestinal trematodes Echinostoma trivolvis and E. caproni from C3H mice by trapping with increased goblet cell mucins.

Echinostoma trivolvis (Cort, 1914) adults were rejected from C3H mice by 15 days post-exposure, corresponding to the increase in the number of goblet cells. Homologous and heterologous infections with the allopatric species E. caproni (Richard, 1964) were used to confirm the effect of increased secretion of goblet cell mucins in rejecting metacercariae of challenge infections of E. trivolvis or E. caproni on days 10, 16 and 20 p.i. after primary infections of E. trivolvis metacercariae. Five-day-old juveniles of E. trivolvis and E. caproni, which were recovered from C3H mice or hamsters, were also used for challenge infections on day 10 p.i. The metacercariae and juveniles, which were challenged homologously and heterologously on day 10 p.i., were almost all expelled. The metacercariae of E. trivolvis, which were challenged homologously on day 16, were completely rejected, but only a few challenged metacercariae of E. caproni in heterologous infection were recovered. Considerable numbers of E. caproni were recovered when challenge infections with the metacercariae were done on day 20 p.i., while only a small number of E. trivolvis was recovered. All controls without primary infections showed a recovery rate of over 50% of the worms. These results indicate that increased secretion of mucins by hyperplastic goblet cells associated with primary infections of E. trivolvis may be responsible for the expulsion of worms challenged homologously with E. trivolvis and heterologously with E. caproni from the mouse host.

Animals↗

Gastric intramucosal pH and hepatic venous oximetry after cardiopulmonary bypass in valve replacement patients.

To determine splanchnic perfusion after cardiopulmonary bypass, gastric intramucosal pH (pH(i)) and hepatic venous oxygen saturation (SHVO2) were measured in 14 patients with cardiac valve replacement. Blood samples were analysed at 6, 12 and 24 h after admission to an intensive care unit. Gastric pH(i) increased significantly (P < 0.01) from 7.21 at 6 h to 7.31 at 12h and increased to 7.37 at 24 h while SHVO2 increased significantly (P < 0.05) from 48% at 6 h to 57% at 12 h and 24 h. Cardiac index was > 4 l/min per m2 and mixed venous oxygen saturation > 70%. Despite sufficient cardiac output, splanchnic perfusion decreased after cardiopulmonary bypass and recovered within 24 h after admission to the intensive care unit. It is concluded that gastric pH(i) and SHVO2 are useful parameters for monitoring postoperative splanchnic perfusion in patients with open-heart surgery.

Acid-Base Equilibrium↗

Parvalbumin-immunoreactive nerve endings in the periodontal ligaments of rat teeth.

Parvalbumin-immunoreactive nerve fibres were most abundant in the lingual periodontal ligaments of incisor teeth. In the part of the ligament adjacent to the alveolar bone, thick and smooth parvalbumin-immunoreactive nerve fibres left main nerve bundles and passed towards the part of the ligament adjacent to the tooth. In the ligament, halfway between the bone and tooth surfaces, these nerve fibres repeatedly branched and extended one to four twigs to produce bush-like endings. Parvalbumin-immunoreactive fibres and terminals were infrequent in the periodontal ligaments of the molar teeth. It is possible that parvalbumin-immunoreactive endings are periodontal mechanoreceptors, but at present it is difficult to account for the different representations around rat molar and incisor teeth.

Alveolar Process↗

Transient reperfusion with acidic solution affects postischemic functional recovery: studies in the isolated working rat heart.

This isolated working rat heart study was designed to investigate the effect of duration of reperfusion and degree of acidity of the reperfusate on myocardial protection. The experimental time course was as follows: 20 minutes of perfusion with the heart working, 3 minutes of infusion with the St. Thomas' Hospital cardioplegic solution followed by global ischemia for 33 minutes at 37 degrees C, and 20 minutes of Langendorff reperfusion followed by 20 minutes of working perfusion. During the initial 3 minutes of Langendorff reperfusion, the pH of the reperfusate was changed to 5.6, 6.8, and 7.5 by addition of sodium hydroxide into Krebs-Henseleit nonbicarbonate HEPES buffer. A respiratory acidic reperfusate was used for the initial 0.5, 1, 2, 3, 5, and 15 minutes during reperfusion. The results were as follows: (1) Reperfusion with a mildly acidic solution (i.e., pH 6.8) yielded better recovery than reperfusion with solutions having pH levels of 5.8 or 7.5. (2) Reperfusion for less than 3 minutes with a reperfusate having a pH level of 6.8 provided better recovery, although reperfusion for longer than 3 minutes exacerbated reperfusion injury. In conclusion, the effects of reperfusion with acidic solution were influenced by degree and duration with biphasic response characteristics.

Analysis of Variance↗

Increased Fas antigen on T cells in multiple sclerosis.

Programmed cell death of antigen specific T cells (apoptosis) may be an important process in the pathogenesis of autoimmune diseases such as multiple sclerosis (MS). Fas antigen was recognized as an apoptosis-related antigen. To investigate Fas antigen in multiple sclerosis (MS), we measured the expression rate of Fas antigen and activation markers on T cells in peripheral blood (PB) of 19 MS patients, 18 controls and in cerebrospinal fluid (CSF) of nine MS patients by flow cytometry. The positive rate of Fas antigen in MS patients was higher than that of healthy controls in PB. In patients with MS, the expression rates of Fas antigen and activation markers were higher in CSF than in PB. The above findings suggest that there is acceleration or impairment of apoptosis on activated T cells in MS.

Antigens, CD↗