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Biomedical subjects

T Matsusaka

Publications and source records attributed to T Matsusaka.

At least 19 recordsLinked to original sources

EXAFS measurements for liquid Ge-Si alloys.

EXAFS measurements around the Ge-K edge have been carried out for liquid Ge-Si alloys for the first time to investigate the local structure around a Ge atom. To perform the EXAFS measurements for the liquid alloys with high melting temperatures, a new sapphire cell have been developed. The measurements were carried out for the liquid alloys from 10% to 60% of Si and the crystalline ones from 10% to 70% of Si as a reference. EXAFS oscillations, x(k), are observed even at 1480 degrees C for liquid Ge(0.4)Si(0.6). The position of the first peak in the radial distribution function obtained from Fourier transform of x(k) is shifted towards smaller distance for liquid and crystalline alloys with increasing Si concentration. The results of a curve-fit analysis in a harmonic approximation show that Ge-Ge and Ge-Si bonds in the liquid alloys become long with increasing Si concentration while those become slightly short in the crystaline ones.

Journal Article↗

Direct hypogastric artery reconstruction for threatened lower limb ischemia: report of a case.

The hypogastric artery is one of the major collateral arteries in aortoiliac occlusive disease. This report describes a case of limb-threatening ischemia caused by acute arterial thrombosis of the right hypogastric artery. The external iliac and distal arteries were obstructed and the hypogastric artery was a major collateral artery. A diagnostic arteriogram taken after intra-arterial thrombolytic therapy revealed a stenotic lesion in the orifice of the hypogastric artery. Open thromboendarterectomy of the hypogastric artery and patch angioplasty, using an expanded polytetrafluoroethylene graft, were performed to salvage the limb. The hypogastric artery was successfully revascularized and ischemic rest pain was relieved.

Aged↗

Scc1/Rad21/Mcd1 is required for sister chromatid cohesion and kinetochore function in vertebrate cells.

Proteolytic cleavage of the cohesin subunit Scc1 is a consistent feature of anaphase onset, although temporal differences exist between eukaryotes in cohesin loss from chromosome arms, as distinct from centromeres. We describe the effects of genetic deletion of Scc1 in chicken DT40 cells. Scc1 loss caused premature sister chromatid separation but did not disrupt chromosome condensation. Scc1 mutants showed defective repair of spontaneous and induced DNA damage. Scc1-deficient cells frequently failed to complete metaphase chromosome alignment and showed chromosome segregation defects, suggesting aberrant kinetochore function. Notably, the chromosome passenger INCENP did not localize normally to centromeres, while the constitutive kinetochore proteins CENP-C and CENP-H behaved normally. These results suggest a role for Scc1 in mitotic regulation, along with cohesion.

Animals↗

Bir1/Cut17 moving from chromosome to spindle upon the loss of cohesion is required for condensation, spindle elongation and repair.

BACKGROUND: In mammals, proteins containing BIR domains (IAPs and survivin) are implicated in inhibiting apoptosis and sister chromatid separation. In the nematode, Bir1 is required for a proper localization of aurora kinase, which moves from the mitotic chromosome in metaphase to the spindle midzone in anaphase as a passenger. Fission yeast Bir1/Pbh1 is essential for normal mitosis. RESULTS: A temperature sensitive mutant cut17-275 exhibits the defect in condensation and spindle elongation at 36 degrees C, while securin is degraded. Gene cloning shows that the cut17+ gene is identical to bir1+/pbh1+. At 26 degrees C, cut17-275 is UV sensitive as the repair of DNA damage is severely compromised. Bir1/Cut17 is a nuclear protein in interphase, which is then required for recruiting condensin to the mitotic nucleus, and concentrates to form a discrete number of dots from prometaphase to metaphase. Once the chromatids are separated, Bir1/Cut17 no longer binds to kinetochores and instead moves to the middle of spindle. Chromatin immunoprecipitation suggested that Bir1/Cut17 associates with the outer repetitious centromere region in metaphase. Following the initiation of anaphase the protein switches from being a chromosomal protein to a spindle protein. This transit is stringently regulated by the state of sister chromatid cohesion proteins Mis4 and Rad21. Ark1, is an aurora kinase homologue whose mitotic distribution is identical to, and under the control of Bir1/Cut17. CONCLUSIONS: Bir1/Cut17 and Ark1 act as "passengers" but they may play a main role as a recruitment factor, essential for condensation, spindle elongation and DNA repair. Bir1/Cut17 should have roles both in mitotic and in interphase chromosome. The proper location of Ark1 requires Bir1/Cut17, and the mitotic localization of Bir1/Cut17 requires sister cohesion.

Amino Acid Sequence↗

In situ demonstration of angiotensin-dependent and independent pathways for hyperaldosteronism during chronic extracellular fluid volume depletion.

In wild-type mice, 2-wk administration of losartan, an angiotensin (Ang) II type 1 (AT1) receptor antagonist, along with dietary sodium restriction, resulted in an elevation of plasma aldosterone greater than that seen with sodium restriction alone (2.75 +/- 0.35 vs. 1.38 +/- 0.16 ng/ml, P < 0.01). Plasma potassium increased in sodium-restricted, losartan-treated mice (6.0 +/- 0.2 mEq/liter), while potassium remained unchanged in mice with sodium restriction alone. To study the effect of Ang II on glomerulosa cells that may operate independently of plasma potassium in situ, we used chimeric mice made of cells with or without the intact AT1A gene (Agtr1a). When animals were fed a normal diet or chronically infused with Ang II, the aldosterone synthase mRNA was detectable only in Agtr1a+/+ but not Agtr1a-/- zona glomerulosa cells. After 2 wk of sodium restriction, plasma aldosterone increased (1.51 +/- 0.27 ng/ml) and potassium remained on average at 4.5 +/- 0.2 mEq/liter, with aldosterone synthase mRNA expressed intensively in Agtr1a+/+, but not detectable in Agtr1a-/- cells. Simultaneous sodium restriction and losartan treatment caused increases in plasma potassium (5.5 +/- 0.1 mEq/liter) and aldosterone (1.84 +/- 0.38 ng/ml), with both Agtr1a-/- and Agtr1a+/+ cells intensively expressing aldosterone synthase mRNA. Thus, aldosterone production is regulated by Ang II in the adrenal gland during chronic alterations in extracellular fluid volume when plasma potassium is maintained within the normal range. In the light of a previous observation that dietary potassium restriction superimposed on sodium restriction abolished secondary hyperaldosteronism in angiotensinogen null-mutant mice, the present findings demonstrate that when the renin-Ang system is compromised, plasma potassium acts as an effective alternative mechanism for the volume homeostasis through its capacity to induce hyperaldosteronism.

Adrenal Glands↗

[Treatment outcomes with vinorelbine for metastatic breast cancer patients previously treated with both doxorubicin and docetaxel].

The purpose of this study was to evaluate the efficacy and toxicity of weekly vinorelbine (VNB) in patients with metastatic breast cancer previously treated with both adriamycin (ADM) and docetaxel (TXT). VNB was administered weekly at the dose 20 mg/m2 by i.v. infusion over 20 minutes followed by flushing the vein with 100 ml of normal saline. From June 1999 to August 2000, ten patients were enrolled in this study. Patient characteristics were that the cumulative doses (median) of previous ADM and TXT were 300 mg (range, 120-880 mg), 560 mg (range, 120-960 mg) respectively. The median number of metastatic sites was four, with poor performance status (ECOG 1-2: 40%, 3-4: 60%). The median cycles of weekly VNB were seven (range: 2-12). Two of 10 assessable patients obtained partial response, with an overall response rate of 20%. The main toxicity (NCI grade 4) was leukopenia in 10% of 10 patients. Phlebitis (grade 2) was observed in 4 of 10 patients (40%). VNB is an active agent against metastatic breast cancer pretreated with both ADM and TXT, possessing no severe toxicities.

Adult↗

Dual renin gene targeting by Cre-mediated interchromosomal recombination.

This study describes a new approach to targeting clustered genes. Our study began with the establishment of two lines of mice carrying different mutations in either Ren1 or Ren2. These two genes, both encoding renin, span over 40 kb in tandem on chromosome 1. Each gene was mutated by gene targeting to contain loxP sites. These two mutants and Cre transgenic mice were mated to produce offspring carrying the mutant Ren1 and Ren2 genes, as well as the Cre transgene concurrently. Initially, two mutant Ren genes were located on separate chromosomes. Southern analysis of mice from the second generation revealed that the mutant Ren1 and Ren2 were interchromosomally recombined at the loxP sites to produce a new dually mutated allele on the chromosome at the rate of 9.6% (7/73). Thus, interchromosomal recombination can be efficiently programmed by mating as designed using the Cre-loxP system.

Animals↗

Effect of inhaled nitric oxide on cardiovascular response to catecholamine in heart failure.

We examined the dose responses to continuous infusion of isoproterenol (ISO) and norepinephrine (NE) in normal (control) and procainamide-induced heart failure dogs with or without inhalation of 70 ppm nitric oxide (NO). Inhaled NO affected neither left ventricular (LV) function nor hemodynamics at baseline in both control and heart failure dogs. There were no significant differences in the responses to ISO and NE with or without inhaled NO in the control. The responses of LV dP/dt to ISO and NE were significantly enhanced in heart failure; however, they were not affected by inhaled NO. In contrast, LV pressure and dimension at end diastole were significantly increased, and pulmonary vascular resistance (PVR) was significantly decreased by inhaled NO during infusion of both ISO and NE in heart failure. In conclusion, the positive inotropic response to cathecholamine is not affected by inhaled NO even in heart failure. Inhaled NO decreases PVR, but potentially increases LV preload in the presence of additional stress of cathecholamine in heart failure.

Administration, Inhalation↗

Salutary role for angiotensin in partial urinary tract obstruction.

BACKGROUND: In the neonatal period, angiotensin II (Ang II) is up-regulated and induces a timely development of the renal pelvis and ureteral peristalsis, thereby protecting the kidney from hydronephrosis. We tested the possibility that in adulthood, Ang II may act salutarily on the kidney structure during partial urinary tract obstruction by inducing adaptive changes in the peristaltic machinery. METHODS: Adult male Sprague-Dawley rats were subjected to partial unilateral ureteral obstruction (UUO) and divided into two groups, that is, those treated with (group L, N = 21) and those without (group C, N = 21) an angiotensin type 1 (AT1) receptor antagonist (losartan). Control animals were sham operated (N = 10). Rats were sacrificed either at day 7 or day 14. RESULTS: The degree of hydronephrosis determined morphometrically was significantly more severe in group L than group C at both day 7 and day 14, indicating that Ang II inhibition accentuated hydronephrosis. The measurement of upstream pressure within the partially ligated ureter in vivo revealed that losartan significantly attenuates the frequency of ureteral peristaltic activities. In in vitro studies using ureteral strips harvested from normal adult Sprague-Dawley rats (N = 10), Ang II (10(-8) mol/L) was shown to augment contraction, which was completely inhibited by losartan (10(-6) mol/L). CONCLUSIONS: Ang II has a salutary effect of protecting kidneys from hydronephrosis during partial ureteral obstruction through its ability to augment ureteral peristalsis.

Angiotensin II↗

[Efficacy of UFT in the treatment of para-aortic lymph node metastasis following gastric cancer surgery: case report].

The patient was a 68-year-old man who underwent pyloric gastrectomy for advanced stomach cancer on December 6, 1996. The histopathological diagnosis was poorly differentiated adenocarcinoma, ss, ly3, v1, n2 (+), and stage IIIa. Postoperative adjuvant chemotherapy consisted of short-term intravenous infusion of 5-FU, 320 mg/m2/day (= 480 mg/body) for 5 days beginning on postoperative day (POD) 1, and oral 5-FU, 200 mg/day, for 1 year beginning on POD 14. The preoperative CEA value was 316.2 ng, but it fluctuated below 10 ng postoperatively. About one year after the operation, the patient began to complain of epigastric pain, loss of appetite, and general malaise. CT of the upper abdomen revealed a 1.5-cm para-aortic lymph node, and the CEA value of 319.0 ng was abnormally high. 5-FU was stopped, oral UFT at 300 mg/day was started, and the patient's course was followed. Three months after the start of UFT, the lymph node had shrunk on CT (shrinkage rate: 66.7%), and the CEA value had decreased to 14.3 ng. As though corresponding to these changes there was a gradual decrease in the epigastric pain, general malaise, etc., and the patient's appetite also returned. There were no subsequent elevations in the CEA values or increases in the size of the para-aortic lymph nodes, and the patient's general condition was favorably maintained. UFT appeared to be effective against the lymph node metastasis around the aorta in this case.

Adenocarcinoma↗

Superior mesenteric vein thrombosis due to diverticulitis and spontaneous thrombolysis after ilio-cecal resection. A case report.

Inflammation or infection is one of the major causes of superior mesenteric vein thrombosis. A case of secondary superior mesenteric vein thrombosis is presented, which was identified with enhanced CT. The mesenteric venous thrombosis was due to diverticulitis of the ileum, and ilio-cecal resection was performed. Because no findings of intestinal ischemia were present, thrombectomy was not attempted. After surgery, the patient was followed up by repeated CT scan, and spontaneous thrombolysis without thrombectomy or thrombolytic therapy was exhibited. The present case indicated abdominal inflammation or infection strongly related to the development and regression of mesenteric venous thrombosis.

Digestive System Surgical Procedures↗

Communication between myocytes and fibroblasts in cardiac remodeling in angiotensin chimeric mice.

To characterize the mode of action of angiotensin II (Ang II) in cardiac remodeling, we generated chimeric mice that are made of both homozygous Ang II receptor type 1A gene (Agtr1a) null mutant cells and Agtr1a intact cells expressing the lacZ gene (ROSA26). Both Agtr1a null and intact myocytes and interstitial cells independently form areas that are randomly distributed throughout the heart. The distribution of ROSA26 cardiomyocytes overlaps completely with that of Ang II binding, indicating that the majority of Ang II receptors reside on cardiomyocytes. When Ang II (1 ng/g body weight/min) was infused for 2 weeks, mice developed mild to moderate hypertension. The proliferating cardiac fibroblasts identified by bromodeoxyuridine staining were present predominantly in the areas surrounded by Agtr1a intact cardiomyocytes. When control chimeric mice made of wild-type cells and ROSA26 cells (i.e., both carrying intact Agtr1a) were infused with Ang II, fibroblast proliferation was found equally in these cardiomyocyte types. When compared with Agtr1a null mutant chimeras, the control chimeras had more extensive cardiac fibrosis, most prominently in perivascular regions. Therefore, in response to Ang II, cardiac fibroblasts proliferate through both the local and systemic action of Ang II. Importantly, the former is determined by the Ang II receptor of neighboring cardiomyocytes, indicating that a communication between myocytes and fibroblasts plays an important role during Ang II-dependent cardiac remodeling.

Angiotensin II↗

Malignant Adenomyoepithelioma of the Breast:A Case with Distant Metastases.

Adenomyoepithelioma is thought to be a low-grade malignancy, and cases showing malignant behavior are rare. A massive breast tumor with skin invasion in a 60-year-old woman was diagnosed as malignant adenomyoepithelioma. Despite the tumor size and skin invasion, noaxillary lymph node metastases were detected. Light microscopy showed proliferation of tubular structures composed of atypical epithelial and myoepithelial cells and occasional anaplastic cells with mitotic figures extending to the epidermis of the skin. Twenty-four months after the surgery the patient complained of dull pain in the right thigh, and was found to have bone, lung and mediastinal lymph node metastases. There was neither local recurrence nor axillary lymph node metastasis. Subsequent femur fracture was treated by osteotomy. Despite additional chemoradiotherapy, the patient died 43 months after the first operation. Our case and literature review indicated that this tumor tends to show hematogenous metastasis.

Journal Article↗

Laparoscopic splenectomy using a wall-lifting procedure.

A laparoscopic splenectomy using a hanger wall-lifting procedure is herein described. The patient is placed in the right lateral position. The left lower chest and left abdominal wall are then lifted by three wires in two directions, left laterally and vertical to the abdominal wall. The view of the operative field thus obtained is excellent. The lifting wires and bars do not hinder the movement of the forceps, since the angles of the instruments to approach the spleen are different from those of the wires. A laparoscopic splenectomy using this wall-lifting procedure avoids the usual complications associated with pneumoperitoneum while still being technically comparable to a procedure with pneumoperitoneum.

Humans↗

Mechanism of cardiac fibrosis by angiotensin. New insight revealed by genetic engineering.

Accumulating data show that excess of angiotensin II (Ang II) is involved in cardiac fibrosis. Many experimental studies suggested that Ang II induces cardiac fibrosis not by its blood pressure-raising action, but rather by a direct action on the heart. However, it has been difficult to distinguish the local and systemic actions in vivo. Recent genetic technology sheds new light on this problem. This review focuses on the recent advances and newly arising issues regarding the mechanism of Ang II-induced cardiac fibrosis.

Angiotensin II↗

Potent antihypertrophic effect of the bradykinin B2 receptor system on the renal vasculature.

BACKGROUND: Angiotensin type 1 (AT1) receptor-deficient mice (Agtr1-/-), which selectively lack both AT1A and AT1B receptor genes, are characterized by marked intrarenal vascular thickening. In the present study, we explored the possible involvement of the kinin-kallikrein system in the development of this renal vascular hypertrophy. METHODS: Wild-type and Agtr1-/- mice were examined for the developmental regulation pattern of the kinin-kallikrein system and treated with aprotinin (a kallikrein inhibitor), AcLys [D-b Nal7, Ile8] des-Arg9-bradykinin (a bradykinin B1 receptor antagonist), or Hoe-140 (a bradykinin B2 receptor antagonist) from 3 to 14 days of age. RESULTS: The normal postnatal up-regulation of kininase II was organ-specifically suppressed in Agtr1-/- kidneys at 2 and 3 weeks of age. Immunohistochemical staining in Agtr1-/- mice revealed tissue kallikrein staining along the nephron from connecting tubules to cortical collecting tubules in proximity to the hypertrophic vasculature, whereas tissue kallikrein staining was confined to connecting tubules in wild-type mice. Aprotinin and Hoe-140 accelerated the vascular hypertrophy significantly as determined by wall thickness ratio, whereas B1 receptor antagonism had no effect. CONCLUSION: The kinin-kallikrein system in the Agtr1-/- mouse kidney is functionally activated by local suppression of kininase II and extensive redistribution of kallikrein to perivascular areas. This activation, specific to the kidney, serves to dampen a development of the marked vascular hypertrophy. These results demonstrate, to our knowledge for the first time, the antihypertrophic effect of the bradykinin B2 receptor system on the renal vasculature in vivo.

Animals↗