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.     

Endotoxin preconditioning protects against the cytotoxic effects of TNFalpha after stroke: a novel role for TNFalpha in LPS-ischemic tolerance.

Lipopolysaccharide (LPS) preconditioning provides neuroprotection against subsequent cerebral ischemic injury. Tumor necrosis factor-alpha (TNFalpha) is protective in LPS-induced preconditioning yet exacerbates neuronal injury in ischemia. Here, we define dual roles of TNFalpha in LPS-induced ischemic tolerance in a murine model of stroke and in primary neuronal cultures in vitro, and show that the cytotoxic effects of TNFalpha are attenuated by LPS preconditioning. We show that LPS preconditioning significantly increases circulating levels of TNFalpha before middle cerebral artery occlusion in mice and show that TNFalpha is required to establish subsequent neuroprotection against ischemia, as mice lacking TNFalpha are not protected from ischemic injury by LPS preconditioning. After stroke, LPS preconditioned mice have a significant reduction in the levels of TNFalpha (approximately threefold) and the proximal TNFalpha signaling molecules, neuronal TNF-receptor 1 (TNFR1), and TNFR-associated death domain (TRADD). Soluble TNFR1 (s-TNFR1) levels were significantly increased after stroke in LPS-preconditioned mice (approximately 2.5-fold), which may neutralize the effect of TNFalpha and reduce TNFalpha-mediated injury in ischemia. Importantly, LPS-preconditioned mice show marked resistance to brain injury caused by intracerebral administration of exogenous TNFalpha after stroke. We establish an in vitro model of LPS preconditioning in primary cortical neuronal cultures and show that LPS preconditioning causes significant protection against injurious TNFalpha in the setting of ischemia. Our studies suggest that TNFalpha is a twin-edged sword in the setting of stroke: TNFalpha upregulation is needed to establish LPS-induced tolerance before ischemia, whereas suppression of TNFalpha signaling during ischemia confers neuroprotection after LPS preconditioning.     

The effect of adjuvant therapy with or without tamoxifen on the endocrine function of patients with breast cancer

The ovarian and pituitary functions of 64 operable breast cancer patients undergoing adjuvant therapy with cytotoxic chemotherapy and/or tamoxifen were investigated. The post menopausal patients, divided into 3 treatment groups, one with tamoxifen alone, one with tamoxifen and chemotherapy and the other with chemotherapy alone had serum estradiol 17-β (E2) and progesterone levels lower than the evaluable limits. Although there was no significant difference in the level of estrone sulfate (E1-S) between these three groups, the level of lutainizing hormone (LH) and follicle stimulating hormone (FSH) in the patients treated with tamoxifen alone and tamoxifen and chemotherapy were significantly lower than those treated with chemotherapy alone. The decrease in gonadotropin levels induced by tamoxifen treatment was reversible as it appeared after the initiation of tamoxifen and recovered after its cessation. In the premenopausal patients, a group treated with tamoxifen and chemotherapy had significantly higher E1-S, E2 and progesterone levels and significantly lower gonadotropin levels than a group treated with chemotherapy alone or one treated with a cyclophosphamide regimen. These increases in the levels of estrogen and progesterone were also reversible, and induced by tamoxifen. Thus, adjuvant endocrinochemotherapy causes profound alteration in the hypothalamo-pituitary-ovarian axis and therefore, monitoring a variety of hormonal levels is thought to be necessary for assessing the consequences of adjuvant therapy in breast cancer patients, especially in premenopausal patients using tamoxifen.     

Histologic Classification of Endoscopically Removed Flat Colorectal Polyps: A Multicentric Study

A total of 594 flat colorectal polyps, removed at endoscopy, were histologically classified into non-neoplastic (n=49) and neoplastic (n=545) polyps. Non-neoplastic polyps were subdivided into metaplastic (n=45) and hyperplastic (n=4), whereas neoplastic polyps were subdivided into adenomas (n=481), intramucosal carcinomas (n=28) and invasive adenocarcinomas (n=36). Several adenoma phenotypes were discerned: tubular (n=375), serrated (n=59), villous (n=39), mixed (n=7) and fenestrated (n=1). Intramucosal carcinomas were subdivided into tubular (n=26) and serrated (n=2), and invasive adenocarcinomas into tubular (n=32), serrated (n=3) and fenestrated (n=1). The microscopic characteristics of each histologic phenotype described in this communication are defined and illustrated.     

AUGMENTED ENDOGENOUS NITRIC OXIDE PRODUCTION IN PARTIAL PORTAL VEIN-LIGATED RATS

1. Endothelium-derived nitric oxide (NO) is a potent vasodilator. Because the body oxidizes it to nitrate ions, NO₃-, measurement of the serum concentration and the urinary excretion of NO₃- may be an index for endogenous NO. We investigated the role of NO on hyperdynamic circulation in cirrhotic and partial portal vein-ligated rats by measuring NO₃. 2. Liver cirrhosis was induced by administration of thioacetamide. Systemic and splanchnic haemodynamics and splenic-systemic shunting were determined by tracer microspheres. The concentration of NO₃- was measured by using high-performance liquid chromatography with an anion-column. 3. We found that systemic and splanchnic hyperdynamic circulation existed to almost the same extent in cirrhotic and in portal vein-ligated rats as compared to the controls and sham-operated rats, respectively. Splenic-systemic shunting was markedly greater in portal vein-ligated rats than in cirrhotic rats. 4. Serum NO₃- levels and urinary excretion of NO₃- in cirrhotic rats tended to increase as compared to the controls. On the other hand, the levels in portal vein-ligated rats were significantly increased as compared to those of the sham-operated rats, and were significantly and negatively correlated to the splanchnic arterial resistance and total vascular resistance. The amount of urinary excretion of NO₃- significantly correlated to splenic-systemic shunting (r = 0.61, P<0.05) only in portal vein-ligated rats. 5. We suggest that these high levels of NO₃- in portal vein-ligated rats relate to the extensive formation of porto-collateral vasculature or acute changes in systemic and splanchnic haemodynamics due to portal vein-ligation.     

A Case of Herpes Zoster Associated with Colitis

A 58-year-old Japanese woman who had herpes zoster in association with colitis was successfully treated with intravenously administrated acyclovir. Vesicular lesions with red haloes ranged from the left side of her buttock to the left extremity, corresponding to the L4 to S2 dermatomes. Her colitis was considered to have been induced by varicella-zoster virus, based on the facts that the clinical courses were correlated and that the innervation of the affected site of the colon corresponded to an infected dermatome (S2).     

Flat adenoma and flat mucosal carcinoma (IIb type)— A new precursor of colorectal carcinoma?

Two flat adenomas and a flat mucosal carcinoma of the colon were reported in patients with synchronous and metachronous colonic carcinomas. These lesions were almost flat and were not detected by preoperative endoscopic examinations. Colonoscopists should be aware of the presence of flat adenomas, which can be easily missed, and recognize them as lesions that play an important role in the "adenoma-carcinoma sequence."     

Microspectrophotometric analysis of DNA content in duct epithelial proliferation and invasive carcinoma of the pancreas]

Nuclear DNA content of 131 pancreatic duct epithelial lesions, including 10 normal ducts, 30 intraductal proliferations with mild atypia (groups I-II), 30 with moderate atypia (group III), 24 with severe atypia (group IV), 14 of carcinoma in situ (group V), and 23 invasive carcinomas, was analyzed using microspectrophotometry. DNA histograms were classified into diploid, polyploid and aneuploid patterns. All of normal duct epithelia showed diploidy. Polyploid patterns were observed in 3 (10%) lesions of groups I-II, 17 (56.7%) of group III, 14 (58.4%) of group IV, 7 (50%) of group V, and 6 (26.1%) of invasive carcinomas, and aneuploid patterns were observed in 0%, 10%, 33.3%, 50% and 73.9%, respectively. This distribution of ploidy patterns revealed a gradual shift to the main ploidy from diploid to polyploid followed by aneuploid in proportion to the increase of the degree of epithelial atypia. The frequencies of polyploid cells in each lesion were determined. Their averages were 0.2% in groups I-II, 1.9% in group III, 3.4% in group IV, 4.4% in group V, and 6.7% in invasive carcinoma. The S+G2M phase fractions were significantly higher in proliferative epithelia than in normal. The results of this study suggest that duct epithelial proliferations of the pancreas have "genetic instability" leading to a serial clonal evolution and play a significant role in the progression of pancreatic duct cell carcinoma.