Biomedical subjects

M Yamaguchi

Publications and source records attributed to M Yamaguchi.

At least 1,207 records · Page 67Linked to original sources

PubMed1991

A new risk grouping for IgD myeloma based on analysis of 165 Japanese patients.

The common staging systems for myeloma do not include IgD myeloma because its rarity makes analysis difficult. We studied a series of 165 Japanese patients with IgD myeloma retrospectively to assess which of the easily assessable parameters present at the time of diagnosis were of prognostic significance. The important individual variables detected in a previous univariate analysis were placed in a multiple regression model to identify the major prognostic factors for survival. This analysis showed that light-chain subtype and white blood cell (WBC) count had a strong predictive relationship for the length of survival. These two factors were used to construct a model containing four categories of patients at increased risk for shortened survival. These categories divided the patients into three groups with respective 5-year survival rates of 66% (low risk), 23% (moderate risk), and 0% (high risk). This new risk grouping showed prognostic validity for IgD myeloma.

Analysis of Variance↗

PubMed1991

Repression of the Drosophila proliferating-cell nuclear antigen gene promoter by zerknüllt protein.

A 631-bp fragment containing the 5'-flanking region of the Drosophila melanogaster proliferating-cell nuclear antigen (PCNA) gene was placed upstream of the chloramphenicol acetyltransferase (CAT) gene of a CAT vector. A transient expression assay of CAT activity in Drosophila Kc cells transfected with this plasmid and a set of 5'-deletion derivatives revealed that the promoter function resided within a 192-bp region (-168 to +24 with respect to the transcription initiation site). Cotransfection with a zerknüllt (zen)-expressing plasmid specifically repressed CAT expression. However, cotransfection with expression plasmids for a nonfunctional zen mutation, even-skipped, or bicoid showed no significant effect on CAT expression. RNase protection analysis revealed that the repression by zen was at the transcription step. The target sequence of zen was mapped within the 34-bp region (-119 to -86) of the PCNA gene promoter, even though it lacked zen protein-binding sites. Transgenic flies carrying the PCNA gene regulatory region (-607 to +137 or -168 to +137) fused with lacZ were established. When these flies were crossed with the zen mutant, ectopic expression of lacZ was observed in the dorsal region of gastrulating embryos carrying the transgene with either construct. These results indicate that zen indirectly represses PCNA gene expression, probably by regulating the expression of some transcription factor(s) that binds to the PCNA gene promoter.

Amino Acid Sequence↗

PubMed1991

Membranous lipodystrophy: MR imaging appearance of the brain.

Five patients with membranous lipodystrophy (lipomembranous polycystic osteodysplasia with progressive dementia) underwent magnetic resonance (MR) imaging of the brain. T2-weighted MR images showed atrophied cerebral white matter with dilated ventricles; increased signal intensity of the white matter; and decreased signal intensity of the thalamus, putamen, caudate nucleus, and cerebral cortex. Although each single finding is not specific, the combination of the above MR findings when coupled with skeletal lesions strongly suggests this rare disease.

Adult↗

PubMed1991

Chronic recording of electrophysiological manifestation of the hypothalamic gonadotropin-releasing hormone pulse generator activity in the goat.

A characteristic increase in multiple-unit activity (MUA volley) synchronized with the pulsatile secretion of luteinizing hormone (LH) by the pituitary gland was recorded from electrodes chronically implanted in the medial basal hypothalamus of ovariectomized goats. The MUA volley always preceded the LH pulse, and the temporal correlation was consistent even when the pulse frequency was altered with an anesthetic or exogenous steroids. The electrophysiological manifestation of the hypothalamic 'pulse generator' governing the secretion of gonadotropin-releasing hormone was thus demonstrated in the ruminant.

Animals↗

PubMed1991

Glucose affects the release of thyrotropin-releasing hormone from the rat hypothalamus.

We have attempted to elucidate the effect of glucose concentrations on the release of thyrotropin-releasing hormone (TRH), a brain neuropeptide possessing glucoregulatory function, from rat hypothalamic slices in vitro. Rat hypothalamic slices were preincubated for 60 min at 37 degrees C in Krebs-Ringer bicarbonate (KRB) buffer (pH 7.4) containing varying concentrations of glucose (10, 5, 2.5 and 1 mM), and then tissues were incubated in KRB buffer, followed by stimulation with 60 mM K+ or 1 mM ouabain. In addition, after inducing hypoglycemia by insulin administration in the rat, hypothalamic tissues were dissected out and preincubated in KRB buffer (10 mM glucose) and then incubated in fresh KRB buffer containing 1 mM ouabain. A decrease in the glucose concentration of incubation medium caused a dose-dependent decrease in both K(+)- and ouabain-stimulated TRH release from rat hypothalamic slices. Furthermore, the ouabain-stimulated TRH release from the hypothalamus of rats with insulin-induced hypoglycemia was significantly reduced (45% of control values; p less than 0.01). The present results indicate that in vitro and in vivo hypoglycemia resulted in a significant decrease in the release of TRH from the hypothalamus, suggesting that circulating glucose levels affect TRH release which, in turn, might be responsible for peripheral glucoregulation.

Animals↗

PubMed1991

Temporary portal vein arterialization as an attractive option in canine orthotopic partial liver transplantation.

We performed 22 canine orthotopic partial liver transplantations (PLTs) with three different revascularization methods; portal vein arterialization (PVA group, n = 11), hepatic arterial shunt (HAS group, n = 5), and conventional portal vein reperfusion (control group, n = 6). Our purpose was to evaluate the feasibility of PVA as a revascularization technique in PLT assessing the changes in arterial ketone body ratio (KBR) as an index of hepatic energy status. After the first anastomosis (left hepatic vein), the ischemic partial liver graft was revascularized with arterial blood flow shunted from the external iliac artery to the hepatic side of the portal vein (PVA group) or the proper hepatic artery (HAS group). Both anhepatic period and ischemia time were significantly shortened in groups PVA and HAS as compared with those in control. In the PVA group, 10 out of 11 recipients survived for at least 5 days (14.2 +/- 3.8 days, mean +/- SEM), while 3 out of 5 (5.2 +/- 1.0) survived in the HAS group and 4 out of 6 (6.2 +/- 1.3) in the controls. Although portal blood flow during PVA was only about 25% of the total hepatic blood flow at preclamping, the KBR was rapidly restored after PVA and showed almost the same values at preclamping. The KBR values during the arterialization time and initial velocity of KBR recovery in the PVA group were significantly higher than those in the HAS and control groups. These results suggest that PVA presents an attractive option in PLT.

Animals↗

PubMed1991

Stimulatory effect of beta-alanyl-L-histidinato zinc on bone formation in tissue culture.

The present investigation was undertaken to clarify the in vitro effect of beta-alanyl-L-histidinato zinc (AHZ) on bone metabolism in tissue culture. Calvaria were removed from weanling rats (3-week-old male) and cultured for periods up to 96 h in Dulbecco's modified Eagle medium (high glucose, 4.5%) supplemented with antibiotics and bovine serum albumin. The experimental cultures contained 10(-8) to 10(-4) mol/l AHZ. The bone cellular zinc content was significantly increased in cultures with concentrations of AHZ greater than 10(-6) mol/l. With 10(-5) mol/l zinc sulfate, the bone cellular zinc content was significantly elevated. Bone calcium content was significantly increased by the presence of 10(-7) to 10(-4) mol/l AHZ. This increase was blocked by the presence of 10(-7) mol/l cycloheximide. Bone alkaline phosphatase activity was elevated in the presence of AHZ (10(-7) to 10(-4) mol/l), whereas it did not significantly alter acid phosphatase activity Bone collagen and DNA contents were significantly increased by 10(-7) to 10(-5) mol/l AHZ, while they were not significantly elevated by zinc sulfate (10(-7) and 10(-6) mol/l). The AHZ (10(-5) mol/l)-induced increase in bone alkaline phosphatase activity and DNA content were prevented by 10(-4) mol/l dipicolinate, a chelator of zinc. Furthermore, the AHZ (10(-5) mol/l)-induced increase in bone alkaline phosphatase activity, collagen and DNA contents were blocked by 10(-7) mol/l cycloheximide. These findings indicate that AHZ had a direct stimulatory effect on bone mineralization in vitro, and that bone protein synthesis was a necessary component of this response. The AHZ effect was more intensive than that of zinc sulfate.

Alkaline Phosphatase↗

PubMed1991

Effect of beta-alanyl-L-histidinato zinc on osteoblastic MC3T3-E1 cells: increases in alkaline phosphatase and proliferation.

The effect of beta-alanyl-L-histidinato zinc (AHZ) on bone metabolism was investigated in osteoblastic MC3T3-E1 cells. Cells were cultured for 3 days at 37 degrees C in a CO2 incubator in plastic dishes containing alpha-modified minimum essential medium supplemented with 10% fetal bovine serum. After the cultures, the medium was exchanged for that containing 0.1% bovine serum albumin plus various concentrations of AHZ or zinc sulfate, and the cells were cultured further for appropriate periods of time. The presence of AHZ (10(-6)-10(-4) mol/l) stimulated proliferation of cells. AHZ increased alkaline phosphatase activity in a dose-related manner up to 10(-5) mol/l; the increase was about 2-fold over the control value. Studies on the effect of actinomycin D or cycloheximide treatment indicated that AHZ may enhance de novo synthesis of the enzyme. AHZ also increased deoxyribonucleic acid (DNA) content dose dependently (10(-6)-10(-4) mol/l). This increase was completely blocked by treatment with cycloheximide. The AHZ (10(-5) mol/l)-induced increases in alkaline phosphatase activity and DNA content were entirely abolished by the presence of dipicolinate (10(-4) mol/l), a chelator of zinc, indicating that the effect of AHZ needs zinc. However, AHZ had a potent effect, more than that of zinc sulfate, on alkaline phosphatase activity and DNA content. The present results indicate that AHZ has a direct specific anabolic effect on osteoblastic cells in vitro and that this effect is related to protein synthesis.

Alkaline Phosphatase↗

PubMed1991

Effects of the methylprednisolone pulse therapy on renal function.

The effect of the methylprednisolone (MP) pulse therapy on renal function was examined in 15 patients with renal or collagen disease. Three nephrotic patients who had reduced renal function and active renal disease with progressive deterioration of renal function prior to the use of MP developed transient renal failure following an MP pulse therapy. The renal failure in each case was reversed by discontinuation of MP and/or by forced diuresis using albumin and furosemide. We examined the correlations between the individual changes in serum creatinine (Scr), body weight (BW) and urine volume (UV) before and after the pulse therapy and other laboratory data such as Scr, total serum protein and albumin. There were significant correlations between a change in Scr on the one hand and changes in BW and UV, Scr and serum albumin on the other. These findings mean that the effect of the MP pulse therapy on renal function depends on the clinical state of the patient and that renal deterioration after the pulse therapy may be more marked in patients who are more nephrotic and more impaired in renal function and suggest that increasing sodium and water retention during an MP therapy and the associated renal interstitial edema, proposed as one of the mechanisms of acute renal failure occurring in patients with minimal-change nephrotic syndrome, may be responsible for the MP-induced transient renal failure.

Acute Kidney Injury↗

PubMed1991

Interleukin-6 stimulates gonadotropin-releasing hormone secretion from rat hypothalamic cells.

There are reports that both interleukin-1 beta and interleukin-6 (IL-6) stimulate the release of adrenocorticotropin through stimulation of hypothalamic corticotropin-releasing factor. We established a primary culture system for hypothalamic neurons producing gonadotropin-releasing hormone (GnRH) and examined whether IL-6 stimulated their GnRH secretion. We demonstrated immunohistochemically that some of these neurons contained GnRH-like immunoreactivity. In primary cultures of these GnRH neurons, we found that the calcium ionophore A23187 stimulated GnRH secretion in a dose- and time-dependent manner. These hypothalamic cells secreted IL-6 spontaneously, producing about 10 ng/l in 24 h, and their IL-6 secretion was significantly stimulated by E2 at 10(-9)-10(-8) mol/l. This stimulatory effect was observed within 3 h. IL-6 also stimulated the release of GnRH in a dose- and time-dependent manner, and these effects of IL-6 were significantly blocked by anti-IL-6 antiserum. These results suggest that the central action of IL-6 on the GnRH neurons may be an important physiological event in the hypothalamus.

Animals↗

PubMed1991

Effect of prolactin on the secretion of hypothalamic GnRH and pituitary gonadotropins.

In order to clarify the mechanism by which excess PRL inhibits gonadotropin release, in vivo and in vitro studies were performed with adult female rats. First, we examined the effect of hyperprolactinemia, produced by implantation of anterior pituitary glands under the kidney capsule, on catecholamine turnover in the medial basal hypothalamus (MBH) and on GnRH concentrations in MBH and hypophyseal portal blood. Rats bearing pituitary transplants exhibited increased turnovers of dopamine (DA) in the MBH, decreased concentrations of GnRH in the MBH and in plasma of hypophyseal portal blood and impaired gonadotropin release from the pituitary gland. Second, we examined the effects of PRL on DA release and of DA on GnRH release from rat hypothalamic cells. We observed that PRL stimulated [3H] DA release, and DA inhibited ionophore-induced GnRH release from dispersed hypothalamic cells. Third, we examined the effect of PRL on estrogen-induced LH release using the in vitro perfusion system. We found that administration of PRL suppressed estrogen-induced LH release by suppressing GnRH release from the hypothalamus. These findings suggest that chronic hyperprolactinemia may increase dopaminergic tone in the MBH that may inhibit GnRH secretion from the MBH and LH release from the pituitary and that these processes may be responsible for disturbances of cyclic hypothalamic pituitary-ovarian activity.

Animals↗

PubMed1991

Tumor necrosis factor-alpha stimulates prolactin release from anterior pituitary cells: a possible involvement of intracellular calcium mobilization.

We investigated the effects of tumor necrosis factor-alpha (TNF alpha), a cytokine produced as one aspect of inflammatory reactions, on the intracellular free calcium concentration in single pituitary cells using a calcium-sensitive fluorescent dye, indo-1, and a digital imaging fluorescence microscopic system. TNF alpha induced an increase in intracellular free calcium immediately after administration, reaching a peak after 30 sec and then returning to nearly the basal level after 120 sec in the pituitary cells. The cells responding to TNF alpha constitute about 15% of the pituitary cell population, and these cells never responded to the hypothalamic releasing hormones TRH, GnRH, GH-releasing hormone, or CRH. To define the role of calcium in TNF alpha-induced PRL release, dispersed pituitary cells were exposed to agents that modify TNF alpha-induced calcium mobilization. Such calcium channel blockers as cobalt and verapamil decreased basal and TNF alpha-induced PRL release. A low calcium medium also decreased TNF alpha-induced PRL release. These data suggest that intracellular calcium mobilization may be involved in the process of TNF alpha-induced PRL release.

Animals↗

PubMed1991

Tumor necrosis factor-alpha increases release of arachidonate and prolactin from rat anterior pituitary cells.

We investigated the effect of tumor necrosis factor-alpha (TNF alpha), a product of activated macrophages, on the release of arachidonate from dispersed anterior pituitary cells. Primary cultures of anterior pituitary cells from rats were preincubated with [3H]arachidonate to label their phospholipid-containing components. The cells were then washed and incubated with vehicle or test agents, and PRL release into the medium and [3H]arachidonate cleaved from phospholipid were measured. TNF alpha significantly increased the release of both PRL and [3H] arachidonate release in a time- and dose-dependent manner. Other cytokines, such as interleukin-1 alpha, interleukin-1 beta, and gamma-interferon, had no effect on [3H]arachidonate release. To define the role of calcium in TNF alpha-induced arachidonate release, dispersed pituitary cells were incubated with low calcium medium, which decreased arachidonate release in response to TNF alpha. TNF alpha potentiated the release of [3H]arachidonate and PRL promoted by phospholipase-A2 and melittin, and markedly shifted the dose-response curve to the left. Inhibitors of phospholipase-A2, such as p-bromophenacyl bromide and quinacrine, had no effect on TNF alpha-induced [3H]arachidonate and PRL release. BW755C, an inhibitor of the conversion of arachidonate to its metabolites, decreased TNF alpha-induced PRL release, while indomethacin, a prostaglandin synthesis inhibitor, had no effect on TNF alpha-induced PRL release. These data indicate that arachidonate metabolites may be involved in the process of TNF alpha-induced PRL release.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

PubMed1991

Immunoreactive inhibin concentrations in adult men: presence of a circadian rhythm.

The circadian and chronological changes in inhibin secretion were studied in normal adult men. To determine the diurnal release of inhibin, blood samples were collected every hour for 24 h from five healthy young adult men, and serum inhibin was measured by RIA. During the evening and the night, serum inhibin concentrations were relatively low; the lowest value was observed at 2200 h. At 0700 h, inhibin started to increase, reached a peak at 0900 h, and then gradually decreased. These results suggest that inhibin secretion is circadian. Testosterone and cortisol also showed circadian rhythms. In some of the five volunteers, the serum concentrations of inhibin, testosterone, and cortisol were superimposable, but no significant relationship was observed between the serum inhibin and FSH concentrations. With regard to the age-related changes in basal inhibin levels, the highest values were observed in the twenties, and lower values were found with aging. This relationship suggests that increased FSH in elderly men might be due to the reduced amount of peripheral inhibin.

Adult↗

PubMed1991

Distribution of PCNA in Drosophila embryo during nuclear division cycles.

An immunocytochemical method using a specific antibody was employed to detect the proliferating cell nuclear antigen (PCNA) in Drosophila embryos during the first 13 nuclear division cycles. Strong nuclear staining with the anti-PCNA antibody was observed at interphase throughout 13 cycles. Metaphase chromosomes were not stained throughout these cycles. The chromosomal (nuclear) staining reappeared at anaphase until cycle 10 and at telophase in cycle 11. During cycles 12 and 13, nuclear staining was detected exclusively at interphase. Relatively uniform staining of syncytial cytoplasm was observed throughout mitotic phases until cycle 9. In the following cycles, strong staining in both the central yolk mass and the cortical layer of cytoplasm was detected at metaphase and telophase. During interphase of cycles later than the 9th, staining in the central yolk mass got much fainter and that in the cortical cytoplasm completely disappeared. These results suggest that the PCNA dissociates from chromosomes at metaphase; then in later mitotic phases, it is transported from the syncytial cytoplasm into nuclei to participate in formation of the active DNA-replication enzyme complexes.

Anaphase↗

PubMed1991

Immunohistochemical demonstration of calcium-binding protein regucalcin in the tissues of rats: the protein localizes in liver and brain.

A calcium-binding protein, regucalcin, was isolated from rat liver cytosol. Rabbit-anti-regucalcin antiserum, which was raised against regucalcin conjugated by glutaraldehyde to bovine serum albumin, was applied to glutaraldehyde-fixed whole mounts and subsequently visualized using the peroxidase-antiperoxidase methods. Rat hepatic regucalcin immunoreactivity was most pronounced in the liver and brain of rats, while it was not seen in the duodenum, testicle, spleen, lung and smooth muscle (bladder), and appeared only slightly in the kidney and heart. Control experiments using non-immune sera or adsorbed anti-rat liver regucalcin antiserum showed no staining. The present finding suggests that regucalcin localizes in the liver and brain of rats.

Animals↗

PubMed1991

Calcium-binding protein regucalcin stimulates the uptake of Ca2+ by rat liver mitochondria.

The effect of the calcium-binding protein regucalcin on the Ca2+ transport system in rat liver mitochondria was investigated. Ca2+ transport was assayed by the method of Millipore filtration to estimate mitochondrial 45Ca2+ accumulation. 45Ca2+ uptake was stimulated by the presence of regucalcin (1.0 and 2.0 microM). This stimulation was remarkable during 1.0 min after 45Ca2+ addition, while appreciable stimulation was no longer seen at 3 min. Regucalcin (2.0 microM)-induced stimulation of 45Ca2+ uptake was prevented by the presence of ruthenium red (1.0 microM) and lanthanum chloride (0.1 mM). Regucalcin (2.0 microM) did not increase the mitochondrial adenosine triphosphatase (ATPase) activity during 3.0 min after Ca2+ addition. Meanwhile, 45Ca2+, which accumulated in the mitochondria during 5.0 min after 45Ca2+ addition, was not released by the addition of regucalcin. Regucalcin may stimulate Ca2+ uptake in rat liver mitochondria independently of the energy.

Animals↗

PubMed1991

Oral administration of calcium hydroxide stimulates bone metabolism in the femoral diaphysis of rats with skeletal unloading.

The preventive effect of calcium hydroxide on the disorder of bone metabolism caused by skeletal unloading was investigated. Skeletal unloading was designed using the model of hindlimb hang in rats. Skeletal unloading for 7 d caused a significant decrease of inorganic phosphorus concentration in the serum and of alkaline phosphatase activity and deoxyribonucleic acid (DNA) content in the femoral diaphysis of rats. Oral administration of calcium hydroxide (16 and 24 mg Ca/kg) caused a significant increase in serum inorganic phosphorus concentration and femoral-diaphyseal calcium content and alkaline phosphatase activity of rats with skeletal unloading. Bone DNA content was significantly increased by the dose of 24 mg Ca/kg. These results clearly indicate that skeletal unloading-induced disorder of bone metabolism is partly prevented by oral administration of calcium hydroxide. Calcium ingestion may be useful as a therapeutic tool in the disorder of bone metabolism caused by skeletal unloading.

Animals↗