Pancreaticogastrostomy: Effect of Partial Gastrectomy on the Pancreatic Stump in Rabbits

To assess the influence of digestive juice on the pancreatic stump when pancreaticogastrostomy was performed after pancreatoduodenectomy, the pancreatic stump was anastomosed to the intact stomach (group I), the stomach after partial gastrectomy (group II), or the jejunum (group III) in rabbits, and the nature of the digestive juice at the anastomotic site as well as the histologic changes of the pancreatic tissue were investigated. The digestive juice was highly acidic in group I, slightly acidic in group II, and almost neutral in group III. Histological examination of the pancreatic stump revealed extensive coagulative necrosis and delayed replacement with granulation tissue in group I, while there was less prominent liquefactive necrosis and early replacement with granulation tissue in groups II and III. Intraperitoneal abscess formation around the anastomotic site and atrophic fibrosis of the pancreas (similar to the changes after pancreatic duct ligation) occurred in 27.8% and 46.2% of group I rabbits, respectively, but no such changes were detected in groups II and III (both P &#60; 0.05). These results indicate that the highly acidic gastric juice had a widespread corrosive effect on the anastomosed pancreatic tissue, and that partial gastrectomy may be necessary to prevent anastomotic leakage and pancreatic duct obstruction after pancreaticogastrostomy.</p

Layer-specific longitudinal strain predicts left ventricular maximum wall thickness in patients with hypertrophic cardiomyopathy.

peer reviewedAIMS: The aim of this study was (a) to clarify the detailed mechanisms of structural and functional abnormalities of myocardial tissue in hypertrophic cardiomyopathy (HCM) using layer-specific strain (LSS) and compare it with healthy subjects (b) to investigate the diagnostic accuracy of LSS for HCM. METHODS AND RESULTS: Forty-one patients with HCM and preserved left ventricular ejection fraction (LVEF; 66% male, 52 ± 18 years, LVEF 62.9% ± 3.7%) and 41 controls matched for age and sex (66% male, 52 ± 20 years, LVEF 63.5% ± 8.2%) underwent 2D-speckle tracking echocardiography. Absolute values of LSS were globally lower and the ratio of endocardial/epicardial layer (End/Epi ratio) was higher in HCM. LSS gradually increased from the epicardial toward the endocardial layer at all chamber views and at all levels of the LV. LSS and End/Epi ratio at the apex were higher than those at the middle or basal level of the LV. End/Epi ratio was correlated with LV maximal wall thickness both controls (r = .35, P = .03) and HCM (r = .81, P < .001). End/Epi ratio was an independent factor associated with LV maximal wall thickness (β = 0.96, P < .001). A higher End/Epi ratio (≥1.31) was associated with diagnostic criteria for HCM (sensitivity 98%, specificity 95%, area under the curve 0.99, P < .001). CONCLUSION: LSS has the potential for unraveling the mechanism of impaired LV wall motion in HCM and to accurately detect HCM

Very delayed sinus arrest during complete remission of diffuse large B-cell lymphoma invading right atrium.

peer reviewedDiffuse large B-cell lymphoma (DLBCL)-associated arrhythmias may be due to cardiac involvement or may be chemotherapy-induced. There have been no reports of significant arrhythmias with normal cardiac function occurring during the complete remission of DLBCL. A 57-year-old female, who had had no history of abnormal electrocardiograms (ECGs) in annual medical checkups, was admitted to our hospital because of low-grade fever, night sweats, and weight loss. On admission, ECG revealed a variable rhythm consisting of sinus beats and occasional escape beats. Computed tomography and 18F-fluorodeoxyglucose positron emission tomography and computed tomography (FDG-PET/CT) revealed two masses in the right atrium (RA) and the uterus. Total hysterectomy was performed, and pathological findings were consistent with diffuse large B-cell lymphoma (DLBCL). Chemotherapy (R-CHOP) was initiated. After two chemotherapy cycles, RA tumors disappeared, and bradyarrhythmia simultaneously converted to sinus rhythm without antiarrhythmic drug therapy. Six months after completion of chemotherapy, FDG-PET/CT revealed negative uptake in the RA and the uterus. The patient attained complete remission of DLBCL, but ECG showed bradycardia because of sinus arrest. Our case suggests that DLBCL-induced arrhythmia can occur even after its remission and should be monitored

İdiyopatik pulmoner fibrozun akut alevlenmesine bağlı olarak hipoksinin seyrindeki çeşitli ekokardiyografik değişiklikler.

peer reviewedIdiopathic pulmonary fibrosis (IPF) is a progressive parenchymal disease. Pulmonary hypertension (PH) is a potentially lethal complication in the course of IPF. In almost all cases of IPF-PH there is gradual deterioration, but patients can also decline suddenly due to hypoxia. This case report describes the different echocardiographic changes observed in 2 episodes of hypoxic attack in a 73-year-old man. On admission, the tricuspid regurgitation peak gradient (TRPG) was 21 mmHg and the oxygen saturation rate was 94% (O2: 4 L/min). Five days after admission, the TRPG and oxygen saturation rate deteriorated [TRPG: 85 mmHg, oxygen saturation: 72% (O2; 4 L/min)]. He was diagnosed with IPF-PH due to hypoxic pulmonary vasoconstriction. Oxygen therapy and methylprednisolone pulse therapy (MPT) were administered. Five days after the MPT treatment, the hypoxia and PH improved [TRPG: 21 mmHg, oxygen saturation: 95% (O2: 4 L/min)]. Acute exacerbation of IPF (IPF-AE) occurred 20 days after the MPT, and a second dose of MPT was administered. The TRPG and oxygen saturation rate did not decline [TRPG: 27 mmHg, oxygen saturation: 94% (O2: 4 L/min)]. The patient died 10 days after the second dose of MPT. Divergent echocardiographic findings were observed during the deterioration of IPF-AE in the presence of IPF-PH

The biology of a prostate cancer metastasis suppressor protein: Raf kinase inhibitor protein

Raf kinase inhibitor protein (RKIP) was originally identified as a protein that bound membrane phospholipids and was named phosphatidylethanolamine binding protein-2 (PEBP-2). RKIP was than identified as a protein that bound Raf and blocked its ability to phosphorylate MEK, thus earning its new name of RKIP. Subsequent to identification of its role in the Raf:MEK pathway, RKIP has been demonstrated to regulate several other signaling pathways including G-protein signaling and NF-ΚB signaling. Its involvement in several signaling pathways has engendered RKIP to contribute to several physiological processes including membrane biosynthesis, spermatogenesis, neural development, and apoptosis. RKIP is expressed in many tissues including brain, lung, and liver and thus, dysregulation of RKIP expression or function has potential to contribute to pathophysiology in these tissues. Loss of RKIP expression in prostate cancer cells confers a metastatic phenotype on them. Additionally, restoration of RKIP expression in a metastatic prostate cancer cell line does not effect primary tumor growth, but it does inhibit prostate cancer metastasis. These parameters identify RKIP as a metastasis suppressor gene. In this review, the biology and pathophysiology of RKIP is described. © 2004 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34907/1/20169_ftp.pd

Imprinted CDKN1C Is a Tumor Suppressor in Rhabdoid Tumor and Activated by Restoration of SMARCB1 and Histone Deacetylase Inhibitors

SMARCB1 is deleted in rhabdoid tumor, an aggressive paediatric malignancy affecting the kidney and CNS. We hypothesized that the oncogenic pathway in rhabdoid tumors involved epigenetic silencing of key cell cycle regulators as a consequence of altered chromatin-remodelling, attributable to loss of SMARCB1, and that this hypothesis if proven could provide a biological rationale for testing epigenetic therapies in this disease. We used an inducible expression system to show that the imprinted cell cycle inhibitor CDKN1C is a downstream target for SMARCB1 and is transcriptionally activated by increased histone H3 and H4 acetylation at the promoter. We also show that CDKN1C expression induces cell cycle arrest, CDKN1C knockdown with siRNA is associated with increased proliferation, and is able to compete against the anti-proliferative effect of restored SMARCB1 expression. The histone deacetylase inhibitor (HDACi), Romidepsin, specifically restored CDKN1C expression in rhabdoid tumor cells through promoter histone H3 and H4 acetylation, recapitulating the effect of SMARCB1 on CDKNIC allelic expression, and induced cell cycle arrest in G401 and STM91-01 rhabdoid tumor cell lines. CDKN1C expression was also shown to be generally absent in clinical specimens of rhabdoid tumor, however CDKN1A and CDKN1B expression persisted. Our observations suggest that maintenance of CDKN1C expression plays a critical role in preventing rhabdoid tumor growth. Significantly, we report for the first time, parallels between the molecular pathways of SMARCB1 restoration and Romidepsin treatment, and demonstrate a biological basis for the further exploration of histone deacetylase inhibitors as relevant therapeutic reagents in the treatment of rhabdoid tumor