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Numazu, Japan

Yamashita T.,Numazu City Hospital
Kyobu geka. The Japanese journal of thoracic surgery | Year: 2013

A 64-year-old woman with liver cirrhosis caused by hepatitis C was presented with aggravated dyspnea. She had refractory hepatic hydrothorax, requiring pleural puncture and drainage of approximately 3,000 ml per week. Four days after the last puncture, she consulted the emergency department and chest films revealed right tension pneumothorax. A drainage tube was inserted to her right pleural cavity, but middle and lower lobes were not expanded, and air leaks persisted. We thought that she was in high-risk of infections, like empyema, and needed surgical treatment to close the pulmonary fistula promptly. Considering her poor general condition, we performed local anesthetic thoracoscopic talc poudrage, and air leaks were controlled successfully. Perioperative period was uneventful. Source

Osmond D.A.,Georgia Regents University | Zhang S.,Georgia Regents University | Pollock J.S.,Georgia Regents University | Yamamoto T.,Numazu City Hospital | And 2 more authors.
American Journal of Physiology - Renal Physiology | Year: 2014

This study tested the hypothesis that P2Y12 receptor blockade with clopidogrel preserves renal autoregulatory ability during ANG II-induced hypertension. Clopidogrel was administered orally to male Sprague-Dawley rats chronically infused with ANG II. After 14 days of treatment, whole kidney autoregulation of renal blood flow was assessed in vivo in pentobarbital- anesthetized rats using an ultrasonic flow probe placed around the left renal artery. In ANG II-vehicle-treated rats, decreasing arterial pressure over a range from 160 to 100 mmHg resulted in a 25±5% decrease in renal blood flow, demonstrating a significant loss of autoregulation with an autoregulatory index of 0.66 ±0.15. However, clopidogrel treatment preserved autoregulatory behavior in ANG II-treated rats to levels indistinguishable from normotensive shamoperated (sham) rats (autoregulatory index: 0.04 ± 0.14). Compared with normotensive sham-vehicle-treated rats, ANG II infusion increased renal CD3-positive T cell infiltration by 66 ± 6%, induced significant thickening of the preglomerular vessels and glomerular basement membrane and increased glomerular collagen I deposition, tubulointerstitial fibrosis, damage to the proximal tubular brush border, and protein excretion. Clopidogrel significantly reduced renal infiltration of T cells by 39 ± 9% and prevented interstitial artery thickening, ANG II-induced damage to the glomerular basement membrane, deposition of collagen type I, and tubulointerstitial fibrosis, despite the maintenance of hypertension. These data demonstrate that systemic P2Y12 receptor blockade with clopidogrel protects against impairment of autoregulatory behavior and renal vascular injury in ANG II-induced hypertension, possibly by reducing renal T cell infiltration. © 2014 the American Physiological Society. Source

Kato F.,Numazu City Hospital
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society | Year: 2011

A 74-year-old man was referred to our hospital with complaint of dyspnea and left pleural effusion. The pleural effusion was exudative and lymphocytic with elevation of adenosine deaminase (ADA). Antitubercular agents were administered on a diagnosis of tuberculous pleuritis, but the pleural effusion did not improve. After he had been followed up with diuretic agents during about 2 years, he suffered cardiac tamponade and right pleural effusion. We diagnosed primary effusion lymphoma based on the cytology findings of the pleural effusion. The measurement of ADA activity in pleural effusions was useful for diagnosis of tuberculous pleuritis, but not only tuberuculous pleuritis but also lymphoma or other diseases can show elevation of ADA activity in pleural effusions. Source

Guan Z.,Health Science University | Giddens M.I.,Health Science University | Osmond D.A.,Health Science University | Cook A.K.,Health Science University | And 6 more authors.
American Journal of Physiology - Renal Physiology | Year: 2013

Autoregula-tion is critical for protecting the kidney against arterial pressure elevation and is compromised in some forms of hypertension. Evidence indicates that activated lymphocytes contribute importantly to cardiovascular injury in hypertension. We hypothesized that activated lymphocytes contribute to renal vascular dysfunction by impairing autoregulation and P2X1 receptor signaling in ANG II-infused hypertensive rats. Male Sprague-Dawley rats receiving ANG II infusion were treated with a lymphocyte proliferation inhibitor, mycophenolate mofetil (MMF) for 2 wk. Autoregulation was assessed in vitro and in vivo using the blood-perfused juxtamedullary nephron preparation and anesthetized rats, respectively. ANG II-treated rats exhibited impaired autoregulation. At the single vessel level, pressure-mediated afferent arteriolar vasoconstriction was significantly blunted (P < 0.05 vs. control rats). At the whole kidney level, renal blood flow passively decreased as renal perfusion pressure was reduced. MMF treatment did not alter the ANG II-induced hypertensive state; however, MMF did preserve autoregulation. The autoregulatory profiles in both in vitro or in vivo settings were similar to the responses from control rats despite persistent hypertension. Autoregulatory responses are linked to P2X1 receptor activation. Accordingly, afferent arteriolar responses to ATP and the P2X1 receptor agonist (3,7-methylene ATP were assessed. ATP- or β,γ-methylene ATP-induced vasoconstriction was significantly attenuated in ANG II-infused hypertensive rats but was normalized by MMF treatment. Moreover, MMF prevented elevation of plasma transforming growth factor-(31 concentration and lymphocyte and macrophage infiltration in ANG II-infused kidneys. These results suggest that anti-inflammatory treatment with MMF prevents lymphocyte infiltration and preserves autoregulation in ANG II-infused hypertensive rats, likely by normalizing P2X1 receptor activation. © 2013 the American Physiological Society. Source

Loria A.S.,University of Georgia | Yamamoto T.,Numazu City Hospital | Pollock D.M.,University of Georgia | Pollock J.S.,University of Georgia
American Journal of Physiology - Regulatory Integrative and Comparative Physiology | Year: 2013

Maternal separation (MatSep) is a model of behavioral stress during early life. We reported that MatSep exacerbates ANG II-induced hypertension in adult male rats. The aims of this study were to determine whether exposure to MatSep in female rats sensitizes blood pressure to ANG II infusion similar to male MatSep rats and to elucidate renal mechanisms involved in the response in MatSep rats. Wistar Kyoto (WKY) pups were exposed to MatSep 3 h/day from days 2 to 14, while control rats remained with their mothers. ANG II-induced mean arterial pressure (MAP; telemetry) was enhanced in female MatSep rats compared with control female rats but delayed compared with male MatSep rats. Creatinine clearance (Ccr) was reduced in male MatSep rats compared with control rats at baseline and after ANG II infusion. ANG II infusion significantly increased T cells in the renal cortex and greater histological damage in the interstitial arteries of male MatSep rats compared with control male rats. Plasma testosterone was greater and estradiol was lower in male MatSep rats compared with control rats with ANG II infusion. ANG II infusion failed to increase blood pressure in orchidectomized male MatSep and control rats. Female MatSep and control rats had similar Ccr, histological renal analysis, and sex hormones at baseline and after ANG II infusion. These data indicate that during ANG II-induced hypertension, MatSep sensitizes the renal phenotype in male but not female rats. © 2013 the American Physiological Society. Source

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