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Biomedical subjects

T Murase

Publications and source records attributed to T Murase.

At least 109 records · Page 6Linked to original sources
PubMed1999

[A case of metastatic tumor of spermatic cord with hydrocele from gastric cancer].

A 70-year-old man, who had undergone total gastrectomy for Borrmann III gastric cancer one year previously, was referred to us with a complaint of left scrotal swelling. Physical examination showed left scrotal hydrocele and a hard nodule in the ipsilateral inguinal area. Excretory pyelography and abdominal computed tomography showed mild left hydronephrosis and no stone. A left orchiectomy was performed. The mass in the spermatic cord was 2.5 x 1.0 x 1.0 cm in size, and the pathological diagnosis was tubular adenocarcinoma, identical to that of the previous gastric cancer. Five months after orchiectomy, the patient underwent percutaneous nephrostomy to manage postrenal renal failure caused by massive metastasis of retroperitoneal lymph nodes. He died one month later. We found a total of 84 cases of metastatic tumors of the spermatic cord reported in Japan, approximately half of which were metastases from gastric cancer. In 10 cases, including ours, the tumor was accompanied by hydrocele of the scrotum or spermatic cord. Although this association is rare, cancerous lesions should be considered in the management of hydrocele.

Adenocarcinoma↗
PubMed1999

Acute myeloid leukemia in the elderly:--159 Nagoya case studies--Nagoya Cooperative Study Group for Elderly Leukemia.

To obtain background information on elderly acute myeloid leukemia (AML), unselected data covering 159 patients aged 60 years or over with AML from 14 hospitals in Nagoya, Japan was analyzed retrospectively. Among these patients, 119 had de novo acute AML, 32 had AML which evolved from myelodysplastic syndrome (MDS-AML), and 8 had other types of leukemia. The survey showed that MDS-AML tended to be more prevalent in patients aged 70 years and older and that MDS-AML showed a significantly more severe degree of leukopenia and anemia than de novo AML. MDS-AML also showed a significantly lower complete remission (CR) rate than that of de novo AML [6.9% (2/29) vs 58.3% (67/11), P < 0.01] and significantly shorter survival times than those of de novo AML [median: 3.6 months vs 9.6 months, P < 0.01 (generalized Wilcoxon test; GW]. In de novo AML, the proportion of patients treated with conventional therapy (CT group) decreased significantly, and that of those with attenuated therapy (AT group) increased significantly as age elevated (P < 0.01). The CT group showed a significantly higher CR rate (65.4% vs 41.2%, P < 0.05) and a significantly longer survival period than those of the AT group [median: 11.6 months vs 4.8 months, P < 0.05 (GW)]. Overall survival rates of the older age groups became significantly shorter with aging [P < 0.01 (GW)].

Acute Disease↗
PubMed1998

Expression of lectin-like oxidized low density lipoprotein receptor-1 in human and murine macrophages: upregulated expression by TNF-alpha.

Uptake of oxidized low density lipoprotein (Ox-LDL) and subsequent foam cell transformation have been implicated in early atherogenesis. Although multiple molecules, including class A and B scavenger receptors, have been identified as Ox-LDL receptors, additional receptors may also be involved in this process. Here, we provide evidence that lectin-like Ox-LDL receptor-1 (LOX-1), a novel Ox-LDL receptor initially identified in vascular endothelial cells, is also expressed in macrophages in humans and mice. Expression of LOX-1 can be induced after macrophage-like differentiation in vitro in human peripheral blood monocytes and the related cell line THP-1 cells. Furthermore, LOX-1 expression can also be detected in resident peritoneal macrophages, and can be upregulated by an inflammatory cytokine TNF-alpha. These results suggest that LOX-1 in macrophages may play an important role in Ox-LDL uptake and subsequent foam cell formation in this cell type.

Animals↗
PubMed1998

Inducible expression of lectin-like oxidized LDL receptor-1 in vascular endothelial cells.

Endothelial dysfunction, or activation, elicited by oxidized LDL (Ox-LDL) or its lipid constituent, has been implicated in the initiation and progression of atherosclerosis. We have recently identified a C-type lectin-like molecule, designated lectin-like Ox-LDL receptor-1 (LOX-1), which acts as a cell-surface receptor for Ox-LDL in cultured vascular endothelial cells. In this study, we provide evidence that LOX-1 expression can be upregulated by tumor necrosis factor-alpha (TNF-alpha) and phorbol 12-myristate 13-acetate (PMA) in cultured bovine aortic endothelial cells. TNF-alpha and PMA upregulated LOX-1 protein and mRNA in a time- and dose-dependent manner. Nuclear runoff assay revealed that TNF-alpha stimulates transcription of the LOX-1 gene. Chinese hamster ovary K1 cells stably expressing LOX-1 internalized 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI)-labeled Ox-LDL but did not significantly internalize acetylated LDL (Ac-LDL), which was effectively suppressed by excess amounts of unlabeled Ox-LDL but not by Ac-LDL. Upregulated expression of LOX-1 by TNF-alpha and PMA was associated with increased uptake of DiI-Ox-LDL that cannot be blocked by excess amounts of unlabeled Ac-LDL. Taken together, LOX-1 is a receptor specific for Ox-LDL, and enhanced uptake of Ox-LDL via this novel receptor on vascular endothelial cells may play an important role in endothelial activation in atherogenesis.

Animals↗
PubMed1998

Fluid shear stress transcriptionally induces lectin-like oxidized LDL receptor-1 in vascular endothelial cells.

Fluid shear stress has been shown to modulate various endothelial functions, including gene expression. In this study, we examined the effect of fluid shear stress on the expression of lectin-like oxidized LDL receptor-1 (LOX-1), a novel receptor for atherogenic oxidized LDL in cultured bovine aortic endothelial cells (BAECs). Exposure of BAECs to the physiological range of shear stress (1 to 15 dyne/cm2) upregulated LOX-1 protein and mRNA in a time-dependent fashion. LOX-1 mRNA levels peaked at 4 hours, and LOX-1 protein levels peaked at 8 hours. Inhibition of de novo RNA synthesis by actinomycin D totally abolished shear stress-induced LOX-1 mRNA expression. Furthermore, nuclear runoff assay showed that shear stress directly stimulates transcription of the LOX-1 gene. Chelation of intracellular Ca2+ with quin 2-AM completely reduced shear stress-induced LOX-1 mRNA expression; furthermore, the treatment of BAECs with ionomycin upregulated LOX-1 mRNA levels in a dose-dependent manner. Taken together, physiological levels of fluid shear stress can regulate LOX-1 expression by a mechanism dependent on intracellular Ca2+ mobilization. Inducible expression of LOX-1 by fluid mechanics may play a role in localized expression of LOX-1 and atherosclerotic lesion formation in vivo.

Animals↗
PubMed1998

Microsatellite instability and somatic mutations in endometrial carcinomas.

Recently, microsatellite instability (MI) has been demonstrated in some types of human cancers. In this study, we attempted to determine the frequency of MI in endometrial cancers and evaluate whether replication error (RER)-positive phenotype is correlated with known genetic mutations or the aberrations of other pathways in endometrial cancers. Seventy-two primary endometrial cancers were examined for microsatellite instability. Eleven tumors (15%) had RERs at two or more microsatellite loci, suggesting that generalized MI may be a molecular manifestation of endometrial cancers. We next examined whether the MI was associated with changes in the K-ras protooncogene, p53 tumor suppressor gene, and 18q LOH, which were frequently detected in endometrial cancers. The MI did not confer the potential to produce point mutations in the K-ras gene or 18q LOH, whereas the data were insufficient to identify the correlation between MI and p53 mutations in the cancers. These results suggest the presence of multiple mutation subsets that act in a complementary fashion in endometrial cancer development.

Chromosomes, Human, Pair 18↗
PubMed1998

Studies of renal aquaporin-2 expression during renal escape from vasopressin-induced antidiuresis.

In animal models of the syndrome of inappropriate antidiuresis (SIADH), sustained administration of vasopressin and water results in free-water retention and progressive hyponatremia for several days, which is then followed by escape from the vasopressin-induced antidiuresis. With the onset of vasopressin escape, water excretion increases despite sustained administration of vasopressin, allowing water balance to be re-established and the serum sodium to be stabilized at a steady, albeit decreased, level. Studies from our laboratories have investigated whether this escape phenomenon can be attributed to altered regulation of aquaporin water channels. After four-day pre-treatment with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) by osmotic minipump, rats were divided into control (continued dDAVP) and water-loaded (continued dDAVP plus a daily oral water load) groups. A significant increase in urine volume in the water-loaded rats was observed by the second day of water loading, indicating escape from antidiuresis. The onset of escape coincided temporally with a marked decrease in renal aquaporin-2 protein (measured by semi-quantitative immunoblotting), which began at day 2 and fell to 17% of control levels by day 3. In contrast, there was no decrease in the renal expression of aquaporins 1, 3, or 4. The marked suppression of whole kidney aquaporin-2 protein was accompanied by a concomitant suppression of whole kidney aquaporin-2 mRNA levels. Immunocytochemical localization and differential centrifugation studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact during vasopressin escape. Additional studies have indicated that the observed down-regulation of aquaporin-2 expression also occurs in the renal cortex as well as the inner and outer medullas, and can be reversed simply by water restriction despite maintenance of hyponatremia. Our results therefore suggest that escape from vasopressin-induced antidiuresis is attributable, at least in part, to a vasopressin-independent and osmolality-independent decrease in aquaporin-2 water channel expression in the renal collecting duct. Similar mechanisms likely contribute to the phenomenon of escape from antidiuresis seen clinically in patients with SIADH as well.

Animals↗
PubMed1998

A novel point mutation in an acceptor splice site of intron 32 (IVS32 A-12-->G) but no exon 3 mutations in the glycogen debranching enzyme gene in a homozygous patient with glycogen storage disease type IIIb.

Genetic deficiency of the glycogen-debranching enzyme (debrancher) causes glycogen storage disease type III (GSD III), which is divided into two subtypes: IIIa and IIIb. In GSD IIIb, glycogen accumulates only in the liver, whereas both liver and muscles are involved in GSD IIIa. The molecular basis for the differences between the two subtypes has not been fully elucidated. Recently, mutations in exon 3 of the debrancher gene were reported to be specifically associated with GSD IIIb. However, we describe a homozygous GSD IIIb patient without mutations in exon 3. Analysis of the patient's debrancher cDNA revealed an 11-bp insertion in the normal sequence. An A to G transition at position -12 upstream of the 3' splice site of intron 32 (IVS 32 A-12-->G) was identified in the patient's debrancher gene. No mutations were found in exon 3. Mutational analysis of the family showed the patient to be homozygous for this novel mutation as well as three polymorphic markers. Furthermore, the mother was heterozygous and the parents were first cousins. The acceptor splice site mutation created a new 3' splice site and resulted in insertion of an 11-bp intron sequence between exon 32 and exon 33 in the patient's debrancher mRNA. The predicted mutant enzyme was truncated by 112 amino acids as a result of premature termination. These findings suggested that a novel IVS 32 A-12-->G mutation caused GSD IIIb in this patient.

Adolescent↗
PubMed1998

Age-associated decrease in response of rat aquaporin-2 gene expression to dehydration.

It is well known that urine-concentrating ability decreases with aging and that this decreasing ability results from a reduced sensitivity of the renal collecting duct to arginine vasopressin (AVP). AVP regulates the water channel (aquaporin-2:AQP2) through V2 receptors and increases the water permeability of the collecting duct. To elucidate the mechanism of change with aging in urine-concentrating ability, we investigated the change of V2 receptor and AQP2 mRNA expression in young (8-week-old) and older (7-month-old) rats after dehydration for 2 days. After dehydration, plasma AVP levels in older rats were higher than young rats, and urinary osmolality in older rats was lower than young rats. By Northern blot analysis, there was no significant difference between young and older rats in both V2 receptor and AQP2 mRNA expression before dehydration. After dehydration, V2 receptor mRNA expression in young and older rats decreased in the same degree, suggesting the downregulation of V2 receptors may occur in the mRNA level. Northern blot analysis and in situ hybridization histochemistry showed that AQP2 mRNA expression increased and the increased expression in older rats was less than in young rats. The present study suggests the reduced response of AQP2 mRNA expression to dehydration, observed in 7-month-old rats, might be partially responsible for the decreasing urine-concentrating ability with aging.

Aging↗
PubMed1998

Antiserum against neuropeptide FF augments vasopressin release in conscious rats.

We previously reported that centrally administered neuropeptide FF (NPFF) inhibited arginine vasopressin (AVP) release. In this study, immunoneutralization of central NPFF was performed to evaluate the role of endogenous NPFF in the regulation of AVP release. Intracerebroventricular (ICV) injection of antiserum against NPFF (Anti-NPFF) significantly augmented the plasma AVP increase induced by hyperosmolality [intraperitoneal injection of hypertonic saline (600 mOsm/kg, 2% BW)] at 60 min after ICV injection compared with normal rabbit serum (NRS) (NRS: 4.20+/-0.30 pg/ml, Anti-NPFF: 5.83+/-0.46 pg/ml, p < 0.01). Anti-NPFF did not cause significant change in plasma osmolality, plasma volume or arterial blood pressure. This evidence indicates that endogenous NPFF might be physiologically involved in osmoregulation of the plasma AVP level through its inhibitory action.

Amino Acid Sequence↗
PubMed1998

Anorectic effect of pituitary adenylate cyclase activating polypeptide (PACAP) in rats: lack of evidence for involvement of hypothalamic neuropeptide gene expression.

We investigated the effect of centrally administered pituitary adenylate cyclase activating polypeptide (PACAP) on feeding in rats, and the involvement of hypothalamic neuropeptide gene expression using in situ hybridization. Intracerebroventricular injection of PACAP (1000 pmol/rat) significantly decreased food intake in a dose-dependent manner. In PACAP-treated rats, neuropeptide Y (NPY) mRNA levels in the arcuate nucleus and galanin mRNA levels in the paraventricular nucleus increased, and corticotropin-releasing hormone (CRH) mRNA levels in the paraventricular nucleus decreased. In rats fasted for 72 h, NPY mRNA levels increased, and CRH mRNA levels decreased, but galanin mRNA levels were unchanged. These results indicate that the anorectic function of PACAP is not mediated by NPY or CRH, and that PACAP increases galanin synthesis.

Animals↗
PubMed1998

Regulation of vasopressin synthesis and release by area postrema in rats.

There is evidence indicating that the area postrema (AP), the most caudal circumventricular organ located on the dorsal surface of the medulla, is involved in several physiological regulations. In this study, we investigated the role of AP in the regulation of arginine vasopressin (AVP) synthesis and release, using rats of which the AP was lesioned 6 weeks previously. The level of plasma AVP in the AP lesioned (APX) group was significantly lower than in the sham operated (Sham) group in the basal state. AVP release induced by either hyperosmolality or hypovolemia was significantly attenuated by APX. To clarify the role of AP in AVP synthesis in the hypothalamus, we examined the AVP gene expression using in situ hybridization. AVP messenger RNA levels in paraventricular (PVN) and supraoptic nuclei (SON) in the APX group were significantly lower than in the Sham group in the basal state. Moreover, the AVP messenger RNA levels in PVN and SON in the APX group were also significantly lower than in the Sham group after water deprivation for 3 days. These results suggest that AVP synthesis and release are tonically stimulated by AP in the basal state and that AVP synthesis and release in stimulated states are also regulated, at least partially, by AP.

Animals↗
PubMed1998

[Migration of surgical sponge retained at transvaginal hysterectomy into the bladder: a case report].

Urge incontinence and frequency, persisting despite oral anticholinergics and antibiotics for four months, brought a 72-year-old woman to our hospital. Plain abdominal X-ray followed by cystoscopy demonstrated a large stone (43 x 37 mm) in the bladder, and the patient underwent suprapubic cystotomy to remove the stone. The stone contained a surgical sponge, which was apparently left in situ at transvaginal hysterectomy two years previously. The sponge had most likely eroded the bladder wall and migrated into the cavity. We found a total of 17 cases reported in Japan of a surgical sponge migrating into the bladder. In particular, our case was associated with transvaginal surgery, while the other 16 cases involved transabdominal surgery.

Aged↗
PubMed1998

Effects of prefixation and fixation times on apoptosis detection by in situ end-labeling of fragmented DNA.

OBJECTIVE: Apoptosis is considered to play an important role in the pathogenesis and progression of neoplasia. An in situ 3'-end DNA labeling (TUNEL) method was recently developed and has been widely used to identify apoptotic cells in tissue sections. However, sometimes the TUNEL method labels many more cells than expected. We investigated the effects of prefixation time and fixation time on the apoptotic index detected by this method. MATERIALS AND METHODS: Using the spleen and thymus of rats, the effects of prefixation time (0, 1, 2, 4, 6, 12, 24, 48, and 72 hours) at 4 degrees C and fixation time (6, 12, 24, 48, 72, and 96 hours; 1, 2, and 3 weeks) on the apoptotic index were examined by the TUNEL method. Agarose gel electrophoresis of extracted DNA from the specimens of each prefixation time was also performed. RESULTS: In comparison with control tissue (no prefixation time), which showed scattered positive cells with distinct staining restricted to the nucleus, the splenic tissue unfixed for 2 hours or more and the thymic tissue unfixed for 4 hours or more showed cytoplasmic staining in the positive cells. Moreover, as the prefixation time was prolonged, the number of positive cells gradually increased. Agarose gel analysis of DNA extracted from tissue sections left unfixed longer than 24 hours showed a ladder pattern consisting of multiples of about 200 base pairs. CONCLUSIONS: Two hours was the limit of prefixation time for the precise identification of apoptosis by the TUNEL method. The false-positive cells in tissue sections left unfixed for longer time intervals may have been due to internucleosomal DNA cleavage following necrosis. In contrast, the length of fixation time in buffered formalin seemed to have no effect on the results obtained by this method.

Animals↗