Solitary right ventricle metastasis by renal cell carcinoma.

A 57-year-old man with a history of renal cell carcinoma presented with presyncope. He underwent nephrectomy years earlier followed by HLA-matched allogeneic peripheral-blood stem-cell transplantation. Echocardiographic investigation revealed a solitary right ventricle mass without contiguous vena caval or right atrial involvement. The mass was pathologically confirmed to be metastatic carcinoma in the right ventricular cavity. This case highlights the need to consider an underlying neoplastic syndrome in patients presenting isolated right ventricle mass by echocardiography.     

DNA microarray analysis of white adipose tissue from obese (fa/fa) Zucker rats treated with a beta3-adrenoceptor agonist, KTO-7924.

We aimed to examine the effects of KTO-7924 (beta3-adrenoceptor agonist) on lipid metabolism and mRNA expressions in retroperitoneal white adipose tissue (RP WAT) in obese (fa/fa) Zucker rats using DNA microarray. Oral KTO-7924 for 28 days significantly decreased RP WAT weight, plasma triglyceride, free fatty acid, and insulin, and improved insulin resistance in oral glucose tolerance tests. In RP WAT of KTO-7924-treated rats, DNA microarray analysis revealed specifically enhanced mRNA expressions of uncoupling protein 1 (UCP1) and cytochrome c oxidase subunit VIII-H (COX8H), which are reportedly highly expressed in brown adipose tissue (BAT). Since these mRNA expression levels in RP WAT were significantly lower in obese (fa/fa) Zucker rats than in lean Zucker rats, these genes may be important in lipid metabolism. Our results imply that in obese (fa/fa) Zucker rats, continuous stimulation of beta3-adrenoceptors by KTO-7924 causes BAT-like adipocytes to appear in RP WAT, and improves lipid metabolism.     

Oxygen Hyperbaric Pressure Therapy (OHPT) for Decubitus Ulcers

Aim:  This study aims to establish a pressure ulcers model that visualizes the microcirculation, and to examine the participation of ischemia‐reperfusion injury in the pathophysiology of pressure ulcers.
Methods:  An original system composed of a new skinfold chamber and compression device allowed loading quantitative vertical stress to the skin. An intravital microscopic technique enabled direct visualization of the microcirculation in the physiological condition and in response to pressure application. To estimate the effect of ischemia‐reperfusion injury, animals were divided into two groups: the compression‐release group in which the animals received four cycles of compression‐release which consisted of 2 hours of compression followed by 1 hour of pressure release; and the compression alone group in which the animals underwent continuous compression for 8 hours. Functional capillary density was quantified before the compression procedure and on day1 (35 hours) after the first evaluation.
Results and Conclusions:  The cyclic compression‐release procedure significantly decreased functional capillary density as compared to continuous compression, indicating that in our experimental setting repetition of ischemia‐reperfusion cycle more severely damaged the microcirculation than single prolonged ischemic insult. The finding supports the significant contribution of ischemia‐reperfusion injury to the pathophysiology of pressure ulcers at the level of dynamic in vivo microcirculation.     

Severely calcified constrictive pericarditis simulating a mediastinal tumor and obstructing the right ventricular inflow tract.

We report a rare case of constrictive pericarditis that stimulated a large mediastinal tumor obstructing the right ventricular inflow tract. A 58-year-old woman was referred to our hospital because of a recent increase of dyspnea and facial edema. Computed tomography revealed severely thickened calcification, including a low-density area, presenting as a mediastinal tumor, compressing the right ventricular inflow tract. A complete resection was performed, and her symptoms dramatically improved. Idiopathic constrictive pericarditis was diagnosed pathologically.     

Methylmercury causes diffuse damage to the somatosensory cortex: how to diagnose Minamata disease]

The first acute case of methylmercury (MeHg) poisoning by the consumption of fish arose in Minamata, Japan, in 1953. It was officially recognized and called Minamata disease (MD) in 1956. There are still arguments about the definition of MD in terms of its associated clinical symptoms and lesions even 50 years after the initial recognition of MD. Studies on this MD epidemic are reviewed along with its historical background. Since MeHg dispersed from Minamata to the Shiranui Sea, residents living around the sea had been exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). These chronic MeHg poisoning patients complained of paresthesia at the distal parts of their extremities and around the lips even 30 years after the cessation of exposure to MeHg of anthropogenic origin. The persisting somatosensory disorders after the discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex, but not by damage to the peripheral nervous system, as previously believed. Based on these findings, symptoms and lesions in MeHg poisoning are reappraised.     

Nationwide investigations of intestinal obstruction in Japan

Two nationwide questionnaire surveys of intestinal obstruction in Japan were undertaken, covering two two-year periods, from January, 1975 to December, 1976 and from January, 1985 to December, 1986, respectively. The findings of a comparative review of these two surveys indicated that although the overall mortality of intestinal obstruction had not changed between 1975/76 and 1985/86, being 6.8 per cent and 6.5 per cent, respectively, simple adhesive obstruction had decreased from 3.2 per cent in 1975/76 to 2.0 per cent in 1985/86. The main cause of adhesion was laparotomy and in cases of both simple adhesive obstruction and strangulated adhesive obstruction, the rate of adhesion secondary to laparotomy of the upper gastrointestinal tract and colon and rectum had increased between 1975/76 and 1985/86. Obstructions caused by neoplasms had increased from 8.2 per cent in 1975/76 to 10.0 per cent in 1985/86, while those caused by adhesions had incresed further still, from 42.5 per cent in 1975/76 to 60.8 per cent in 1985/86. Among the latter group, nonoperatively treated cases had increased, which may be accounted for by the fact that facilities which adopt non-operative treatment using intestinal decompression as the first choice for simple adhesive obstruction cases have increased. In both surveys, the mortality of cases receiving nonoperative treatment was lower than that of operative cases.     

Immunobead and Density Gradient Purification of Paget Cells: In vitro Studies of Proliferation

Previous studies using primary monolayer cultures of epithelial cells from the involved epidermis of patients with mammary and extramammary Paget's disease investigated whether Paget cells proliferate as other malignant cells do. Although epithelial monolayers from the involved skin were maintained for approximately 45 days, no permanent cell lines were established. The proportion of carcinoembryonic antigen (CEA)-positive cells did not increase in the long-term cultures. Herein, we report studies of whether there is a real reduction of Paget cell numbers or if this is merely a decrease in the expression of CEA by the cells. Furthermore, we investigated whether Paget cells survive longer when cultured free from any potential inhibitory keratinocytes or other epidermal cells. Skin samples were obtained from one patient with mammary Paget's disease and three with extramammary Paget's disease; epidermal cells were cultured in vitro. An enrichment of Paget cells was carried out from the cultured epidermal cells by combining an anti-epithelial membrane antigen monoclonal antibody, binding to immunobeads, and density gradient centrifugation in Nycodenz. The separated cells were re-cultured in Keratinocyte-SFM serum-free media. The proportion of CEA-positive cells did not increase in the cultures, and the purified cells did not show any increase in survival times compared to the non-purified cultured cells. These results suggest that the decrease of CEA-positive cells noted during culture results from a decline in expression of CEA in the Paget cells. Paget cells in the involved epidermis do not proliferate significantly and thus differ from many other malignant cells.     

Scaling Lichenoid Eruptions and Sjögren-like Syndrome: Manifestations of Nonfatal Postoperative Transfusion-Associated Graft-versus-Host Disease?

We report a case of an 81-year-old woman in whom lichenoid eruptions and Sjögren-like sicca syndrome developed 45 days after cholecystectomy. During surgery, one unit (130 ml) of unirradiated packed red blood cells from a male donor was transfused. The lichenoid eruptions cleared up with exfoliation; however, sicca symptoms remained during the follow-up period of four years. Histological examinations of both skin and lip biopsy specimens were in agreement with those of graft-versus-host disease (GVHD). A Y-chromosomal body was identified in the lymphocytes in the skin lesion by staining with quinacrine dihydrochloride and in the lip lesion by a method with in situ hybridization. The findings suggest that this case demonstrated the manifestations of non-fatal transfusion-associated GVHD.