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Biomedical subjects

Y Hashimoto

Publications and source records attributed to Y Hashimoto.

At least 307 records · Page 17Linked to original sources
PubMed1999

Embolectomy for acute embolic occlusion of the internal carotid artery bifurcation.

BACKGROUND: Acute occlusion of the distal intracranial segment of the internal carotid artery (ICA) causes sudden severe hemispheric ischemia. A low rate of recanalization and a high mortality rate for this condition have been noted, even with endovascular treatment. METHODS: We report the results of emergency embolectomy in six patients with acute embolic occlusion of the internal carotid artery (ICA) bifurcation. All six patients were admitted to our institute within 2 h of the onset of symptoms. Computed tomography (CT) scans on admission revealed no low-density or high-density regions in any patients. The time between onset of symptoms and completion of angiography ranged from 2 to 4 h (2.8 +/- 0.7 h). RESULTS: Emergency embolectomy was performed for each patient. Recanalization was confirmed angiographically in four of the patients. In the remaining two patients, massive infarction in the territory of the ICA was detected on the CT scans obtained the day of the operation, and postoperative angiography was not performed in these two cases. These two patients died of uncal herniation 6 days after onset. Two of the six patients were able to walk with a cane 2 months after surgery. The remaining two patients were unable to walk or attend to their own bodily needs without assistance. The time elapsed between onset of symptoms to reopening of the occluded vessel was within 6 h in the four surviving patients. The recanalization rate was 66.7% (4/6) for the embolectomy procedure, significantly higher than that (12.5%) of the thrombolytic therapy reported in a previous study. CONCLUSIONS: In summary, open embolectomy can be performed when the time after onset of symptoms is less than 6 h.

Acute Disease↗
PubMed1999

Effects of ALCAR on the fast axoplasmic transport in cultured sensory neurons of streptozotocin-induced diabetic rats.

The effects of acetyl-L-carnitine (ALCAR) on fast axoplasmic transport were studied in cultured dorsal root ganglion (DRG) neurons of diabetic rats. Three-month-old male rats were used 7 days after streptozotocin injection. Neurons obtained from ganglia were cultured with a high concentration of glucose. The amount and the mean velocity of retrogradely transported particles, reduced in the diabetic animal, were transiently recovered by 1 mM ALCAR. The number of particles moving at 0.8-1.2 microm/s, considered to be lysosomes, increased in the velocity distribution. ALCAR did not modify the amount and mean velocity of anterograde particles which were unaffected by diabetes, or of bidirectional particles in neurons of control rats. This study suggests that diabetic neuropathy may be relieved by ALCAR via recovering retrograde axoplasmic transport.

Acetylcarnitine↗
PubMed1999

Microtubule-associated protein-2 in the hypothalamo-neurohypophysial system: low-molecular-weight microtubule-associated protein-2 in pituitary astrocytes.

Microtubule-associated protein-2 is the most abundant microtubule-associated protein in the brain and is responsible for morphogenesis and maintenance of the nervous system. In the present experiments, we have examined the localization of microtubule-associated protein-2 in the hypothalamo-neurohypophysial system of the rat using western blots and immunohistochemistry. Two monoclonal antibodies against microtubule-associated protein-2, antibody C and AP20, were used: antibody C recognizes both the high- and low-molecular-weight isoforms of microtubule-associated protein-2; antibody AP20 specifically detects high-molecular-weight microtubule-associated protein-2 only. Western blot analysis revealed expression of high-molecular-weight microtubule-associated protein-2 in the whole brain, hippocampus and whole hypothalamus. While the supraoptic nucleus expressed only high-molecular-weight microtubule-associated protein-2, the adult posterior pituitary predominantly expressed low-molecular-weight microtubule-associated protein-2, which was also seen in the embryonic whole brain. Light microscopic immunohistochemistry revealed that both antibody C and AP20 intensely stained dendrites of the dendritic and somatic zones in the supraoptic nucleus. Double labeling with antibodies against microtubule-associated protein-2 and oxytocin (or vasopressin) demonstrated that microtubule-associated protein-2 was localized in dendrites of magnocellular neurons in the supraoptic nucleus. In the posterior pituitary, however, antibody C stained fine processes and cell bodies of astrocytes, which were identified by an antibody against glial fibrillary acidic protein. Antibody AP20 also stained fine processes of some astrocytes in the posterior pituitary, but the intensity of immunoreactivity with antibody AP20 was weaker than that with antibody C. This result suggests that microtubule-associated protein-2 in astrocytes of the posterior pituitary is predominantly of the low-molecular-weight type. Moreover, western blots revealed low-molecular-weight microtubule-associated protein-2 of the posterior pituitary at a molecular weight slightly higher than embryonically expressed low-molecular-weight microtubule-associated protein-2, indicating that low-molecular-weight microtubule-associated protein-2 in the posterior pituitary is possibly the isoform microtubule-associated protein-2d. The present results demonstrate that astrocytes in the posterior pituitary of adult rats still retain the ability to express the immature variant of microtubule-associated protein-2, low-molecular-weight microtubule-associated protein-2, and its expression is probably linked to structural plasticity.

Animals↗
PubMed1999

Sudden recurrent laryngeal nerve paralysis due to apoplexy of parathyroid adenoma.

Neoplastic lesions of the parathyroid are rare, and most of these are adenomas. Even rarer is a secondary involvement of the recurrent laryngeal nerve. A case is presented of sudden onset hoarseness in a 64-year-old man caused by acute vocal cord paralysis due to bleeding within an adenoma of the lower right parathyroid gland. Acute onset of vocal cord paralysis is rarely associated with benign processes; the current case is only the second report associated with parathyroid adenoma.

Adenoma↗
PubMed1999

Deformation of the acetabular polyethylene liner and the backside gap.

Polyethylene wear of acetabular components may cause osteolysis and aseptic loosening in total hip arthroplasty. Case reports of wear between the polyethylene liner and acetabular metal backing (backside wear) have promoted speculation on the clinical importance of debris generation at this site and the potential importance of insert conformity. We examined 90 retrieved nonconforming acetabular components from a single manufacturer. Twenty-four liners (27%) showed polyethylene deformation corresponding to screw holes on the backside surface. The location of screw-hole deformations corresponded to the direction of polyethylene deformation (wear) on the articular surface in all cases. The polyethylene liners with backside deformations were significantly thinner than the liners without deformation (P = .02). The presence of acetabular osteolysis did not significantly correlate with backside deformation, but there was a significant association between osteolysis and wear of the articular surface (P = .0004). In this implant design, backside deformation (wear) may not be due to micromotion at the interface but to the viscoelastic nature of ultra-high-molecular weight polyethylene.

Acetabulum↗
PubMed1999

Pericardial fluid as an alternative specimen to blood for postmortem toxicological analyses.

In actual forensic cases, we occasionally encounter victims with their blood being completely lost. In this study, pericardial fluid has been proposed as a specimen for toxicological analysis, and its utility has been evaluated. Fifteen autopsy cases with little putrefaction were selected. Fairly good correlations were observed between blood and pericardial fluid for all drugs, neutral and basic drugs and acidic drugs with regression equations of y=1.09x - 0.086 (r=0.989, n=21), y=0.969x - 0.072 (r=0.993, n=16) and y=1.01x + 0.355 (r=0.970, n=5), respectively. The correlations of drug concentrations between blood and cerebrospinal fluid/femoral muscle were not as good as those between blood and pericardial fluid. No correlations were observed between blood and urine/bile. The ratios of pesticide concentrations in each specimen to those in blood showed a large variation. Although our study was limited to a small number of cases, we have concluded that pericardial fluid is a good sample for quantitative confirmation of analyses performed on blood samples or a quantitative alternative to blood in exsanguinated victims. Cerebrospinal fluid, urine, bile and the skeletal muscle were found to be suitable only for qualitative analyses.

Journal Article↗
PubMed1999

Concentrations of morphine and codeine in urine of heroin abusers.

We have measured concentrations of morphine, codeine and 6-monoacetylmorphine in urine of people admitted to the Los Angeles County + University of Southern California Medical Center. Of 60 patients positive for morphine and/or codeine, 10 were judged to be heroin abusers based on positive results for 6-monoacetylmorphine, a specific metabolite of heroin. In nine of these ten patients, 0.028-39.4 microg/ml free codeine and 0.070-307 microg/ml total codeine were detected along with 1.74-218 microg/ml of free morphine and 11.2-2870 microg/ml of total morphine; the morphine-to-codeine ratios were 3.65-228 and 2.27-207 for the free forms and total amounts of these opiates, respectively. In the one patient who was negative for codeine, the concentrations of free and total morphine were 0.114 and 2.22 microg/ml, respectively. Based on our data and literature data available, the following criteria are proposed for judging heroin use from the results of urinalysis, especially when no 6-monoacetylmorphine is detected: (1) a detectable amount of free morphine exists and the concentration of total morphine is higher than 10 microg/ml; (2) a detectable amount of codeine exists; and (3) the morphine-to-codeine ratio is higher than 2 for both the free forms and total amounts of these opiates.

Journal Article↗
PubMed1999

Vitrectomy for macular edema combined with retinal vein occlusion.

This study was performed in order to evaluate the effect of vitrectomy in eyes with retinal vein occlusion associated with macular edema. Twenty-nine years eyes (27 patients) with branch retinal vein occlusion (BRVO), and 14 eyes (13 patients) with central retinal vein occlusion (CRVO) both associated with macular edema underwent phacoemulsification, intraocular lens implantation, pars plana vitrectomy and peeling of the posterior hyaloid membrane. Follow-up ranged from 12 to 32 months. Macular edema was reduced, and visual improvement was observed (p < 0.0001 in BRVO, p = 0.0257 in CRVO, paired t-test). Visual outcome was better in eyes with better visual acuity before surgery. Early vitrectomy may be recommended for retinal vein occlusion associated with macular edema.

Aged↗
PubMed1999

Cystotomy for diabetic cystoid macular edema.

The purpose of this study was to evaluate the role of vitrectomy with cystotomy in the treatment of diabetic cystoid macular edema (CME). Among 22 eyes of 21 patients with diabetic CME underwent phacoemulsification, intraocular lens implantation, pars plana vitrectomy, induction of posterior vitreous detachment, and cystotomy or cystectomy. Follow-up ranged from 3 to 29 months. Under biomicroscopic examination, Cystoid macular edema was eliminated in 16 of 22 eyes during the follow-up period. Ring-shaped residual edema was observed in one eye. Corrected visual acuity improved in 7 of 22 eyes by more than one Snellen line (P = 0.0391, paired t-test), remained the same in 13 eyes, and decreased by more than one line in 2 eyes. This pilot study shows that cystotomy may have a role in the treatment of cystoid macular edema in diabetic patients.

Aged↗
PubMed1999

Distribution characteristics of levofloxacin and grepafloxacin in rat kidney.

PURPOSE: To elucidate the renal distribution of quinolones, we examined the uptake of levofloxacin and grepafloxacin in vivo and in rat renal cortical slices. METHODS: The plasma and various tissue concentrations of levofloxacin and grepafloxacin were measured after a bolus injection in rats, and tissue uptake clearance was calculated. Transport characteristics of quinolones in rat renal cortical slices were evaluated. RESULTS: The tissue distribution of levofloxacin and grepafloxacin in the kidney was greater than in any other tissue, and the tissue uptake clearances of levofloxacin and grepafloxacin in the kidney cortex were 1.2 and 4.6 ml/min/g tissue, respectively. The uptake of levofloxacin and grepafloxacin in rat renal cortical slices was concentrative, as indicated by slice/medium ratios of 2.3 and 9.6 at 60 min, respectively. The uptake of levofloxacin and grepafloxacin in rat renal cortical slices showed saturation, and was significantly inhibited in the presence of quinidine (p<.05), but not of tetraethylammonium or p-aminohippurate. CONCLUSIONS: Renal distribution of levofloxacin and grepafloxacin may be mediated by a specific transport system for quinolones, distinct from the organic cation and organic anion transport systems in the kidney.

Animals↗
PubMed1999

Effects of glibenclamide on glycylsarcosine transport by the rat peptide transporters PEPT1 and PEPT2.

1 Glibenclamide is a widely used sulphonylurea for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). This agent has been reported to inhibit the activities of various ion channels and transporters. In the present study, we examined the effects of glibenclamide on the function of the H+/peptide cotransporters PEPT1 and PEPT2 by using stable transfectants. 2 Uptake of [14C]-glycylsarcosine, a typical substrate for peptide transporters, by PEPT1- or PEPT2-expressing transfectant was inhibited by glibenclamide as well as other sulphonylureas including tolbutamide. 3 Kinetic analysis revealed that the inhibition by glibenclamide was noncompetitive. Dixon plot analyses showed that the Ki values of this agent were 25 and 7.8 microM for PEPT1 and PEPT2, respectively. 4 Glibenclamide did not inhibit Na+-coupled alanine and alpha-methyl-D-glucoside transport, suggesting that the inhibitory effects of glibenclamide on peptide transporters were not due to nonspecific interactions. 5 There was little uptake of [3H]-glibenclamide by PEPT-expressing transfectants as compared to mock-transfected cells, suggesting that glibenclamide was not a substrate for these peptide transporters. 6 In summary, glibenclamide inhibited the [14C]-glycylsarcosine transport by PEPT1 and PEPT2 in a noncompetitive fashion, although glibenclamide per se was not transported through these transporters. These findings would provide important information for clinical, physiological and biochemical aspects of peptide transporters.

Alanine↗
PubMed1999

The role of Ets family transcription factor PU.1 in hematopoietic cell differentiation, proliferation and apoptosis.

The PU.1 gene encodes an Ets family transcription factor which controls expression of many B cell- and macrophage-specific genes. Expression of the gene is critical for development of lymphoid and myeloid cell lineages, since PU.1-deficient mice exhibit defects in the development of these cell lineages. The PU.1 gene is identical to the Spi-1 gene isolated from common proviral integration sites in Friend virus-induced murine erythroleukemia (MEL), and deregulated expression of the gene is believed to be an essential step of the disease. We recently demonstrated that overexpression of PU.1 inhibits erythroid differentiation of MEL cells induced with the differentiating agent DMSO. We also noticed unexpectedly that overexpression of PU.1 together with DMSO induces marked growth arrest and apoptosis in MEL cells, supporting the notion that some oncogenes induce growth inhibition and apoptosis rather than cell proliferation and transformation under specific circumstances as shown with the c-myc gene. In this review, the role of PU.1 in hematopoietic cell differentiation, proliferation and apoptosis is described and the possible molecular mechanisms of PU.1-induced effects in MEL cells are discussed.

Animals↗
PubMed1999

Programmed cell death in normal epidermis and loricrin keratoderma. Multiple functions of profilaggrin in keratinization.

The terminal differentiation of epidermal keratinocytes has been regarded as an example of programmed cell death. Among the proteins specifically expressed in this process is profilaggrin, which consists offilaggrin repeats and N- and C-terminal domains. Profilaggrin is proteolytically processed into individual domains during the terminal differentiation. Filaggrin released from profilaggrin aggregates keratin filaments to form compacted cornified cells with a keratin pattern. A recent transfection experiment has indicated initiation of cell death by filaggrin expression constructs. The transitional cells between the granular and cornified cells show morphologic characteristics of apoptotic cells, and their nuclei contain fragmented DNA and profilaggrin N-terminal domains. This suggests that the N-terminus of profilaggrin may participate in nuclear events accompanying programmed cell death. Among inherited skin disorders with abnormal keratinization, progressive symmetric erythrokeratoderma is caused by loricrin mutation (loricrin keratoderma). In this disease, profilaggrin N-terminal domains are aggregated with mutant loricrin within condensed nuclei. These nuclei persist in the cornified layer as parakeratosis. Loricrin keratoderma could therefore be regarded as a representative form of disrupted cell death.

Animals↗
PubMed1999

Analysis of the immunoglobulin heavy chain gene variable region of 101 cases with peripheral B cell neoplasms and B cell chronic lymphocytic leukemia in the japanese population.

We have analyzed the immunoglobulin heavy chain (VH) gene variable regions (CDR2 and FW3) of 101 Japanese cases with peripheral B cell neoplasms. When all except one case with a deletion were graphed by frequency of replacement mutation, the 100 cases could be separated into two groups: 24 cases with zero, one and two mutations (germline or low frequency of somatic mutation); and 76 cases with three or more mutations (medium to high frequency of somatic mutation). While most mantle cell lymphoma cases (11/13) showed germline or low frequency of somatic mutation, all cases of mucosa-associated lymphoid tissue (MALT) lymphoma (11/11), follicular lymphoma (three of three cases), plasma cell myeloma (seven of seven cases) and most cases of diffuse large B cell lymphoma (DLBCL; 42/47) belonged to the latter group. These 76 cases, therefore, may be considered to show somatic hypermutation. More than half of chronic lymphocytic leukemia/small lymphocytic lymphoma cases (CLL/SLL; eight of 13) showed a hypermutated VH gene and the ratio of replacement mutation: silent mutation in CDR2 of CLL/SLL was considerably higher compared with DLBCL and MALT lymphoma, showing somatic hypermutation. When comparing VH gene type of B cell-CLL (B-CLL) among our series and those in the literature, more cases of CD5+ B-CLL in the Western literature have the VH5 and VH6 family types, while more cases in Japan are reported to have VH4 family. The occurrence of VH families in B-CLL between Japanese and Western people seems to be comparable.

Aged↗
PubMed1999

Tumor cell growth suppression by tannic acid.

Tannic acid was cultured together with tumor cells that had originated from human malignant tumors (HCT-15 & AGS). Significant suppression of tumor growth was observed. The 50% suppression was observed at the concentration between 50 micrograms/ml and 12.5 micrograms/ml. When tannic acid was injected into HCT-15 cells by electroporation at 1180 mu p and 200 ohm, the suppression rate was 34.3% at the concentration of 50 micrograms/ml in HBS solution. The suppression rate of cells only in contact with tannic acid solution for one hour under the same conditions as used for electroporation, was 26.1%. Histographic findings suggested that tannic acid almost completely blocked the S phase of the cell cycle.

Adenocarcinoma↗
PubMed1999

Tannic acid raises survival rate of mice bearing syngeneic tumors.

Tannic acid which was found earlier to have growth suppressive activity against cultured tumor cells, was given to Balb/c mice p.o. The mice had been inoculated with syngeneic tumor cells (Meth/A) i.p. When tannic acid was suspended in drinking water and given daily at doses of approximately 875 mg/kg/day and 1750 mg/kg/day, the respective survival rates were 59% and 48%, with that of the control mice being 29%. To study the cytotoxicity of tannic acid, we administered the tannic acid to mice at 875 and 1750 mg/kg/day for 35 days. The weight gain for each dose was lower than that of the control, although the difference was not significant. When tannic acid was given at 8750 mg/kg/day, the weight gain was significantly lower than the control. A histologic study did not show any pathological findings in the kidney, liver, or lungs in the mice given tannic acid at the above doses.

Administration, Oral↗
PubMed1999

Effect of gold on tumor-associated antigens.

A gold compound, which is an anti-rheumatoid agent, was clinically applied to patients showing a high level of tumor-associated antigens. Two patients showed no clear evidence of recurrence except for a high level of tumor-associated antigens. The gold compound was injected i.m. every week at the dose of 25 mg/body for 10 times to a patient showing a high CEA level that had arisen eight years after cervical dissection for a tongue carcinoma. It was also administered every other week for 30 times at the dose of 25 mg/body to a patient showing high CA19-9 and SLX levels five years after palliative left pulmonary resection followed by radiation therapy for left pulmonary carcinoma. The CEA level dropped to the normal limit after 10 injection and remained at that level after cessation of the gold treatment. SLX and CA19-9 levels of the second patient showed lower than initial values, although SLX did not fall to the normal range after the 30 injections. No side effects such as lowering of white blood cell count, BUN elevation, or kidney dysfunction were seen.

Aged↗