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T Nishimura

Publications and source records attributed to T Nishimura.

At least 181 records · Page 10Linked to original sources
PubMed2000

Synthesis of a molt-inhibiting hormone of the American crayfish, Procambarus clarkii, and determination of the location of its disulfide linkages.

A molt-inhibiting hormone (Prc-MIH) of the American crayfish, Procambarus clarkii, a member of the type II CHH family, was chemically synthesized and the location of its three disulfide linkages was determined. Prc-MIH consists of 75 amino acid residues and was synthesized by a thioester method. Two peptide segments, Boc-[Cys(Acm)(7,24,27), Lys(Boc)(19)]-Prc-MIH(1-39)-SCH(2)CH(2)CO-Nle-NH(2) and H-[Cys(Acm)(40,44,53), Lys(Boc)(42,51,67)]-Prc-MIH(40-75)-NH(2), were prepared using peptides obtained via the Boc solid-phase method. Condensation of the building blocks in the presence of silver chloride, 3,4-dihydro-3-hydroxy-4-oxo-1,2,3-benzotriazine, and N, N-diisopropylethylamine, followed by removal of the protecting groups, gave the reduced form of Prc-MIH(1-75)-NH(2). This product was converted to the native form of Prc-MIH (synthetic Prc-MIH) in a buffer which contained cysteine and cystine. The synthetic Prc-MIH showed the same behavior by RP-HPLC and biological activity assays as the natural Prc-MIH. The disulfide bond between Cys7 and Cys44 was determined by isolation of a fragment from an enzymatic digest of the synthetic Prc-MIH by RP-HPLC, followed by mass analysis. The disulfide bonds between Cys24 and Cys40 and between Cys27 and Cys53 were determined by comparing the elution position of an enzymatic digest of the synthetic Prc-MIH with authentic chemically synthesized samples, which contained three types of possible disulfide linkages.

Animals↗
PubMed2000

Fluorine-18 FDG myocardial positron emission tomographic findings before and after pituitary adenoma resection in a patient with acromegalic cardiomyopathy.

Because of persistently elevated growth hormone levels, acromegaly gives rise to various changes in organs mediated by insulin-like growth factor-I. In the heart, it causes myocardial hypertrophy, and, with time, heart failure. The authors performed pituitary adenomectomy in a patient with acromegalic cardiomyopathy who had heart failure; after operation, the blood growth hormone levels decreased to within the normal range and there was a marked improvement in left ventricular function by gated blood pool scintigraphy. Pre- and postoperative fluorine-18 fluorodeoxyglucose (FDG) myocardial positron emission tomography showed increased accumulation of FDG in the myocardium before surgery, but accumulation within the normal range after operation. Myocardial glucose metabolism changed when the long-term effects of growth hormone and insulin-like growth factor-I were eliminated, and this appears to be accurately reflected by FDG positron emission tomography.

Acromegaly↗
PubMed2000

Impact of burn injury on hepatic TGF-beta1 expression and plasma TGF-beta1 levels.

BACKGROUND: The liver plays a critical regulatory role in the acute inflammatory response to injury, although the mechanisms of this regulation are not well understood. transforming growth factor-beta1 (TGF-beta1) is induced after burn injury and may contribute to an inhibitory or fatal effect on hepatocytes. We investigated the association over time between plasma concentration of TGF-beta1, expression of TGF-beta1 m-RNA in liver tissue, and histologic analysis of liver apoptosis after burn injury. METHODS: Male BALB/c mice were anesthetized and randomized to receive 0% (sham), moderate (approximately 25%) (M), or large (approximately 50%) (L) body surface area full-thickness contact burn, followed by resuscitation and analgesia. Animals were killed over a time course from 15 minutes to 24 hours after burn injury, and liver tissue and peripheral blood were collected. Plasma levels of TGF-beta1 (nanograms per milliliter) were measured by enzyme-linked immunosorbent assay. TGF-beta1 m-RNA was extracted from liver and measured by reverse transcription-polymerase chain reaction. Histology of liver apoptosis was examined after fixation and staining with TdT-mediated dUTP nick-end labeling (TUNEL) method. RESULTS: The plasma concentration of TGF-beta in burn group L was significantly increased at 4 hours after burn when compared with sham and M burn groups. This rise in plasma TGF-beta1 was preceded by an increase in hepatic TGF-beta1 m-RNA expression at 30 minutes, 1, 2, and 4 hours after burn in the L group. Histologic analysis found greater hepatocyte death in the L group than in the M group at 8 hours after burn. CONCLUSION: The levels of induced TGF-beta1 and TGF-beta1 m-RNA after L burn injury are higher and peak earlier than after M burn injury. Elevated TGF-beta1 may be associated with cell death in hepatocytes. The TGF-beta1 rise may be associated with hepatocyte injury and systemic response to massive burn.

Acute Disease↗
PubMed2000

Microvascular angiogenesis and apoptosis in the survival of free fat grafts.

OBJECTIVES/HYPOTHESIS: Autologous fat is an ideal material for augmentation in plastic surgery because of its minimal tissue reaction and easy availability, but its long-term graft survival is somewhat unpredictable. This study was conducted to determine how fat grafts get their vascular supply from the recipient bed and why they keep reducing in volume and weight. STUDY DESIGN: Experimental study using animal models. METHODS: The expression of vascular endothelial growth factor (VEGF) in grafted fat tissue was examined by using immunohistochemical staining, and apoptotic cell death in the grafted fat was studied by using terminal deoxynucleotidyl transferase (TdT)-mediated deoxy-uridine triphosphate (dUTP)-biotin nick end-labeling method. Twenty-five Wistar rats were used as models of free fat grafts. Fat tissue taken from inguinal fat pads was grafted to the back skin with an 18-gauge needle injection. RESULTS: The weight of the injected fat was significantly reduced on the 180th day compared with the original weight (32% +/- 10%). VEGF+ cells were observed in fibrous connective tissue of the grafts on days 7 and 30 but not after day 90. Apoptotic cells were also observed on days 7 and 30. CONCLUSIONS: Angiogenic factors including VEGF started to revascularize the graft around day 7, and the extent of the vasculature was not reduced after the revascularization. In addition to necrosis in the graft's early stages, apoptosis induced by many factors in the graft's environment is also, at least in part, a cause of long-term volume reduction of the fat graft. Thus clinical application of angiogenic factors such as VEGF to fat grafts and control of apoptosis may contribute to improvements in fat-grafting techniques.

Adipose Tissue↗
PubMed2000

Effect of E5510, a novel antiplatelet agent, on platelet deposition in atherothrombotic lesions: evaluation by 111In platelet scintigraphy.

We evaluated the short-term effects of a novel antiplatelet agent, 4-cyano-5,5-bis(methoxyphenyl)-4-pentenoic acid (E5510), using 111In platelet scintigraphy (PSG) and B-mode ultrasonography (US). Fifteen patients with platelet deposition at either the carotid bifurcation or abdominal aorta on PSG were randomized into two groups: seven were followed without anti-thrombotic medication (Group A) and eight received E5510 (4 mg x day(-1)) (Group B). After 8 weeks, PSG and US were repeated in all patients. Platelet deposition was assessed visually and semi-quantitatively using a platelet accumulation index. Visual analysis showed that seven out of eight patients became negative for platelet deposition after treatment in Group B, while none changed in Group A. The platelet accumulation index of vessels with platelet deposition was significantly reduced after treatment in Group B (12.4+/-3.9% vs 6.0+/-7.1%, p <0.01), while there was no significant change in the vessels without platelet deposition (2.9+/-3.0% vs 2.9+/-4.1%). In Group A, none of the vessels showed any change (8.1+/-6.4% vs 8.9+/-7.3%). However, there was no significant reduction of carotid plaque size in either group. Short-term E5510 therapy inhibited platelet deposition in active atherothrombotic lesions, and the combination of PSG and US was useful for evaluating the effectiveness of anti-thrombotic drugs in vivo.

Aged↗
PubMed2000

Mammary glands of Aly mice: developmental changes and lactation-related expression of specific proteins, alpha-casein, GLyCAM-1 and MAdCAM-1.

PROBLEM: (1) Aly mouse is an autosomal recessive mutant mouse that lacks lymph nodes and Peyer's patches. Defects of mammary glands might explain why these mice fail to nurture their pups. (2) Expressions of glycosylation-dependent cell adhesion molecule 1 (GlyCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in mammary glands of lactating mice have been suggested, but only scant information is available. METHODS: The thickness and weight of mammary glands were measured directly. The expression of specific proteins, alpha-casein, GlyCAM-1, and MAdCAM-1 in mammary glands was detected by reverse transcription-polymerase chain reaction (RT-PCR). MAdCAM-1 expression was also confirmed by immunohistochemistry (IHC). RESULTS: Fat pads of mammary glands of homozygous (aly/aly) mice were small and weighed less than those of heterozygous (aly/+ ) mice. An increase in end-bud development was evident in aly/aly mice. During pregnancy, growth of the mammary gland and alveolar formation were noted in both groups. The expression of alpha-casein, GlyCAM-1 and MAdCAM-1 was detected in both groups of mice by RT-PCR from late-pregnancy. Immunohistochemically, MAdCAM-1 was noted in small vessels around the mammary globules. CONCLUSIONS: Our results demonstrated marked changes in the structure of the mammary glands of aly/aly mice. The expression of lactation-related proteins was detected during development, pregnancy, and lactation in both aly/aly and aly/+ mice.

Animals↗
PubMed2000

Kupffer cell-derived prostaglandin E(2) is involved in alcohol-induced fat accumulation in rat liver.

Destruction of Kupffer cells with gadolinium chloride (GdCl(3)) and intestinal sterilization with antibiotics diminished ethanol-induced steatosis in the enteral ethanol feeding model. However, mechanisms of ethanol-induced fatty liver remain unclear. Accordingly, the role of Kupffer cells in ethanol-induced fat accumulation was studied. Rats were given ethanol (5 g/kg body wt) intragastrically, and tissue triglycerides were measured enzymatically. Kupffer cells were isolated 0-24 h after ethanol, and PGE(2) production was measured by ELISA, whereas inducible cyclooxygenase (COX-2) mRNA was detected by RT-PCR. As expected, ethanol increased liver triglycerides about threefold. This increase was blunted by antibiotics, GdCl(3), the dihydropyridine-type Ca(2+) channel blocker nimodipine, and the COX inhibitor indomethacin. Ethanol also increased PGE(2) production by Kupffer cells about threefold. This increase was also blunted significantly by antibiotics, nimodipine, and indomethacin. Furthermore, tissue triglycerides were increased about threefold by PGE(2) treatment in vivo as well as by a PGE(2) EP(2)/EP(4) receptor agonist, whereas an EP(1)/EP(3) agonist had no effect. Moreover, permeable cAMP analogs also increased triglyceride content in the liver significantly. We conclude that PGE(2) derived from Kupffer cells, which are activated by ethanol, interacts with prostanoid receptors on hepatocytes to increase cAMP, which causes triglyceride accumulation in the liver. This mechanism is one of many involved in fatty liver caused by ethanol.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

Triptolide attenuates pulmonary arterial hypertension and neointimal formation in rats.

This paper reports the effect of triptolide (a diterpenoid triepoxide) on the development of monocrotaline (MCT)-induced pulmonary hypertension in pneumonectomized rats. Male Sprague- Dawley rats were injected with MCT (60 mg/kg) on Day 7 after left pneumonectomy. Rats received therapy from Day 5 to 35 with triptolide (0.25 mg/kg intraperitoneally, every other day, n = 10), or vehicle (0.1 ml of ethanol/cremophor intraperitoneally, every other day, n = 10). By Day 35, triptolide-treated rats demonstrated lower mean pulmonary arterial pressure (mPAP) than vehicle-treated rats (mPAP 21 +/- 3 versus 42 +/- 5 mm Hg, p < 0.001). Triptolide-treated rats also had significantly less right ventricular hypertrophy (RVH) and pulmonary arterial neointimal formation. In a rescue experiment, rats initiated therapy on Day 21. At Day 35, vehicle-treated rats (n = 4) had higher mPAP (40 +/- 9 mm Hg), greater RVH, and more severe pulmonary arterial neointimal formation than rats that received triptolide (0.25 mg/kg every other day, n = 7, mPAP 30 +/- 4 mm Hg) and rats that received triptolide (0.2 mg/kg daily, n = 7, mPAP 25 +/- 5 mm Hg, p < 0.01). In pneumonectomized rats that receive MCT, triptolide attenuates the development of pulmonary hypertension and RVH, and promotes regression of pulmonary arterial neointimal formation.

Analysis of Variance↗
PubMed2000

Deep venous thrombosis and pulmonary thromboembolism associated with a huge uterine myoma--a case report.

A 51-year-old woman with a large uterine myoma suffered from acute pulmonary thromboembolism. Venography revealed thrombosis in the right common iliac vein and almost complete obstruction of the left common iliac vein. The ascending lumbar vein showed collateral drainage. Treatment was initiated with continuous intravenous heparin sodium, and a Greenfield filter was inserted to prevent the extension of the pulmonary embolism during and after hysterectomy. After a total hysterectomy, venography revealed restoration of patency in the bilateral common iliac veins, and no flow was seen in the ascending lumbar vein. Thorough clinical examinations failed to identify any other prothrombotic conditions. These results suggest that a large uterine myoma compressed veins in the pelvis, and the resulting impaired blood flow caused deep venous thrombosis and pulmonary thromboembolism.

Female↗
PubMed2000

Immunocytochemical localization of bovine serum albumin (BSA) in the liver and testis of rats injected with testosterone-BSA, hydrocortisone-BSA or corticosterone-BSA.

Through observations of colloidal gold with silver enhancement, we have demonstrated that 2-nm colloidal gold labeled-testosterone-bovine serum albumin (BSA) conjugate or hydrocortisone-BSA conjugate injected intravenously enters the hormone-target cell nuclei of rats (Nishimura and Ichihara, 1997; Nishimura and Nakano, 1997, 1999). To confirm immunocytochemically whether the nature of BSA in the steroid hormone-BSA conjugates (steroid-BSAs) remains intact in the hormone-target cell nuclei, testosterone-BSA, hydrocortisone-BSA or corticosterone-BSA was injected into the vascular system of rats, then the liver and testes of rats killed 2 h postinjection were reacted with FITC-conjugated anti-BSA antibody, and examined under fluorescence microscopy and confocal laser scanning microscopy. In the liver of rat injected with testosterone-BSA, the fluorescence was observed in the nuclei of endothelial cells, but not in the nuclei of hepatocytes, hepatic stellate cells and Kupffer cells. In the liver of rat injected with hydrocortisone-BSA, intense fluorescence was seen in the nuclei of hepatic stellate cells, but did not seem to be present in the nuclei of the other three kinds of cells. In the liver of rat injected with corticosterone-BSA, the fluorescence seemed to be in a few nuclei of hepatic stellate cells, and appeared as speckles in a few nuclei of the hepatocytes and Kupffer cells. In some seminiferous tubules of rat injected with testosterone-BSA, fluorescence was observed in the nuclei of spermatocytes and spermatids. These results suggest that BSA conjugated with steroid hormone can enter the hormone-target cell nuclei with its antigenicity kept intact, and that the fate of steroid-BSAs is decided at the cell membrane level.

Animals↗
PubMed2000

Stable prostaglandin I1 analog SM-10906 modulates productions of tumor necrosis factor-alpha, interleukin-1 and interleukin-6 in mouse macrophages.

The present study investigated the effects of stable agonist for prostaglandin (PG) I2 receptor with PGI1 skeleton, SM-10906, on pro-inflammatory cytokine production by mouse peritoneal macrophages (PEMs) in comparison with PGE1 and PGI2. In mouse PEMs, SM-10906 and PGE1 slightly enhanced interleukin (IL)-6 secretion, but had no effects on tumor necrosis factor-alpha (TNF-alpha) or IL-1 production. SM-10906 concentration-dependently inhibited TNF-alpha, IL-1 and IL-6 releases from lipopolysaccharide-activated mouse PEMs, as with PGE1, PGI2 and cAMP analog. Additionally, SM-10906, PGE1 and PGI2 caused concentration-dependent accumulation of cAMP contents in mouse PEMs. It is concluded that PGI1 analog SM-10906 exerts anti-inflammatory effects on stimulated mouse PEMs by increasing in cAMP levels, as with E-series of PG.

Alprostadil↗
PubMed2000

Perianal mucinous carcinoma successfully treated with a combination of external beam radiotherapy and high dose rate interstitial brachytherapy.

The case of an 84-year-old man with perianal mucinous carcinoma is presented. The tumour was 6 cm in diameter and extended into the surrounding tissues. Taking the patient's advanced age and disease into account, rectosigmoidectomy and colostomy were carried out without resection of most of the tumour. Radiotherapy consisted of pre-operative external beam radiotherapy (EBRT) of 40 Gy in 20 fractions, post-operative EBRT of 24 Gy in 12 fractions, and high dose rate interstitial brachytherapy of 12 Gy in a single fraction. The patient tolerated the entire course of radiotherapy well. The patient is doing well without regrowth or complications 7 years after radiotherapy. To our knowledge, there have been no reports on the successful outcome of radiotherapy for perianal mucinous carcinoma. This case suggests that a combination of EBRT plus interstitial brachytherapy boost may play a role in the definitive treatment of perianal mucinous carcinoma.

Adenocarcinoma, Mucinous↗
PubMed2000

The aetiology of non-tumorous enhancement in the hepatic hilum shown on CT hepatic arteriography.

The causes of non-tumorous abnormalities in the hepatic hilum seen on CT hepatic arteriography were investigated. 13 patients with non-tumorous defects of portal perfusion in the hepatic hilum on CT arterial portography underwent both CT hepatic arteriography from the common hepatic artery and CT obtained during proper hepatic arteriography. The findings of non-tumorous portal defects on these two angiographic studies using helical CT were compared. In the 13 patients, 14 non-tumorous defects of portal perfusion in the hepatic hilum on CT arterial portography were detected as enhanced areas in 10 regions (dorsum of segment IV, 7/10; dorsum of the lateral segment, 3/4) on CT hepatic arteriography via the common hepatic artery, but none were enhanced on CT obtained during proper hepatic arteriography. In conclusion, the main cause of non-tumorous enhancement in the hepatic hilum seen on CT hepatic arteriography is non-portal direct inflow via the parabiliary venous system.

Aged↗
PubMed2000

Increased hepatic arterial blood flow after decreased portal supply to the liver parenchyma owing to intrahepatic portosystemic venous shunt: angiographic demonstration using helical CT.

This study was conducted to investigate the haemodynamics of the liver parenchyma in the presence of intrahepatic portosystemic venous shunt. 3 patients with intrahepatic portosystemic venous shunts and 24 patients with normal intrahepatic haemodynamics underwent both CT arterial portography and CT during hepatic arteriography. Angiographic findings with helical CT were compared, and CT attenuated values were measured in both groups. The liver parenchyma on CT arterial portography had lower attenuation than on CT during hepatic arteriography in all patients with intrahepatic portosystemic venous shunts. Overall average CT attenuation was 92.2 +/- 7.7 Hounsfield units (HU) on CT arterial portography and 149.9 +/- 8.5 HU after CT during hepatic arteriography, with the opposite findings in all patients without intrahepatic portosystemic venous shunt: CT attenuation 142.0 +/- 25.7 HU on CT arterial portography and 100.7 +/- 16.4 HU after CT during hepatic arteriography. In conclusion, the portal venous supply to the liver parenchyma decreased due to intrahepatic portosystemic venous shunts, with a compensatory increase in hepatic arterial blood supply.

Adult↗
PubMed2000

Non-tumorous enhancement caused by cholecystic venous inflow shown on biphasic CT hepatic arteriography: comparison with hepatocellular carcinoma.

The haemodynamics in non-tumorous abnormalities on CT arterial portography (CTAP) owing to cholecystic venous direct inflow to the liver were compared with the haemodynamics in hepatocellular carcinoma. 53 patients who simultaneously underwent CTAP and CT during hepatic arteriography (CTHA) to detect hepatocellular carcinoma had the late phase added to CTHA. Changes in size, shape and pattern of 47 non-tumorous enhancement abnormalities on the liver around the gall bladder or in the dorsum of segment IV between the early and late phases on biphasic CTHA as well as of 60 tumorous lesions were determined. Enhancement on biphasic CTHA was seen in all 47 lesions with a non-tumorous portal defect (early phase alone, n=8; late phase alone, n = 3; both, n = 36). In these 47 lesions, the size and the shape of enhancement changed in 63.8% and 51.1%, respectively, between the early and late phases on CTHA; the pattern of enhancement did not change in 72.3%. On the other hand, the size of enhancement on biphasic CTHA changed in only 16.7% of 60 tumours, and the shape in only 5%, although the enhancement pattern changed in a large proportion (80%). In conclusion, owing to the difference in haemodynamics, non-tumorous abnormalities caused by cholecystic venous inflow and tumours are clearly delineated on biphasic CTHA. Thus, adding the late phase to previous single phase CTHA (i.e. performing biphasic CTHA) is useful in differentiating the two entities.

Aged↗
PubMed2000

Effects of valproic acid on fertility and reproductive organs in male rats.

Crj:CD(SD)IGS rats were orally administered valproic acid at doses of 250, 500 or 1000 mg/kg/day for 4, 7 or 10 weeks. At each dose, one group of male rats was euthanized after 4-week dosage (4-week dose group) and the other two were mated with untreated females after 4 (7-week dose group) or 7 (10-week dose group) weeks of treatment with valproic acid and their fertility was evaluated. Females were euthanized on day 14-17 of gestation, and numbers of corpora lutea, implantations and live and dead fetuses were recorded. After 4, 7 or 10 weeks of treatment, males were euthanized, genital organs were weighed, the number of sperm in the cauda epididymis was counted, sperm motion analyzed, and histopathological examination of testes performed. The male rats of the 1000 mg/kg dose group died or were moribund 3 or 4 days after the start of treatment. No effects on fertility of male rats were observed up to the 500 mg/kg 10-week dose group. Treatment for 4 weeks at 500 mg/kg/day decreased epididymis weight. After 7 weeks at 500 mg/kg/day, the weights of epididymis, seminal vesicles and prostate were decreased, and the number of sperm heads per cauda epididymis and percentage of motile sperm were reduced. In the 500 mg/kg 10-week dose group, the weight of testis was decreased. On histopathological examination of the testis, degeneration of seminiferous tubules and loss or exfoliation of spermatids were observed, and the ratio of retention of step 19 spermatids in stage IX-XI was increased in the 500 mg/kg 4-, 7- and 10-week dose groups. These results suggest that analysis of sperm motion and histopathological evaluation of testes are sensitive methods for assessing toxicity of valproic acid on male reproductive organs.

Animals↗
PubMed2000

Collaborative work to evaluate toxicity on male reproductive organs by repeated dose studies in rats 9). Testicular toxicity in male rats given adriamycin for two or four weeks.

The present study was performed to determine whether testicular toxicity can be detected of the administration of adriamycin (ADR), an anticancer drug, for 2 weeks. ADR was intravenously administered to Slc:SD male rats at 1 mg/kg once a week for 4 or 2 weeks, and 2 mg/kg once a week for 2 weeks. Suppression of body weight gain was observed in the 1 mg/kg/week (4 w) and 2 mg/kg/week (2 w) groups. The testes weights in these groups were also lower than those of the control group. On histological examination, a decrease in spermatogonia was observed in the 1 mg/kg/week (4 w) and 2 mg/kg/week (2 w) groups. No abnormalities were detected in the control and 1 mg/kg/week (2 w) groups. Stage analysis of seminiferous tubules was performed for control and 1 mg/kg/week (2 w) groups. In the 1 mg/kg/week (2 w) group, the numbers of spermatogonia in stages II-III, V and XII-XIII were significantly decreased. The numbers of preleptotene spermatocytes in stage VII and zygotene spermatocytes in XII-XIII were also significantly reduced in the same group. These findings suggest that the testicular toxicity of ADR can be detected after 2 weeks administration at a sufficient high dosage, if simplified morphometrical analysis is used.

Animals↗