Isolated cardiophrenic angle node metastasis from ovarian primary. report of two cases

Ovarian cancer is the most lethal gynaecologic malignancy. It usually spreads out of the abdomen involving thoraco-abdominal organs and serosal surface. This disease is poorly curable and surgery, at early stage, is supposed to achieve the best survival outcome. In systemic dissemination, chemiotherapy is indicated, sometimes with neoadjuvant aim. The most common clinical expressions of advanced ovarian carcinoma are multiple adenopathy, neoplastic pleuritis, peritoneal seeding and distant metastasis, mainly hepatic and pulmonary. Isolated adenopathy of the mediastinum is rare and isolated bilateral have never been described before. We report two cases of isolated bilateral cardiophrenic angle lymphnode metastasis from ovarian carcinoma, without peritoneal and pleural involvement. Both patients were successfully resected through minimally invasive thoracic surgery. About the role of surgery, few data are available but survival seems to be longer after resection thus, more investigation is required to make the indication to surgery more appropriate in advanced cases.     

Syringocystadenoma Papilliferum Arising on the Scrotum

Abstract: An 8‐year‐old boy presented to the pediatric dermatology service with an elevated, moist and vegetated pinkish mass, measuring 4 × 5 × 2 cm in diameter, located in the scrotum. The lesion has been gradually increasing in size showing a recent accelerated growth. Excisional biopsy demonstrated the histological picture of syringocystadenoma papilliferum (SCAP). The interest of this report lies in the rarity of syringocystadenoma papilliferum, its unusual presentation in the scrotum not yet reported in pediatric literature, and the importance of differential diagnoses in this location.     

Relaxin induces mast cell inhibition and reduces ventricular arrhythmias in a swine model of acute myocardial infarction.

Resident cardiac mast cells, located mainly around coronary vessels and in the right atrium close to the sinoatrial node, are the main repository of cardiac histamine. Inflammatory activation of cardiac mast cells, as occurs upon acute myocardial infarction, causes the release of histamine and prostanoids. These substances lead to severe tachyarrhythmias, cardiodepressive effects and coronary spasm, thus contributing to myocardial damage and early, lethal outcome. Relaxin, known to inhibit mast cell activation, has been recently validated as a cardiotropic hormone, being produced by the heart and acting on specific heart receptors. In this study, we report on a swine model of heart ischemia/reperfusion, currently used to test cardiotropic drugs, in which human recombinant relaxin (2.5 and 5 microg/kg b.w.), given at reperfusion upon a 30-min ischemia, markedly reduced cardiac injury as compared with the vehicle-treated animals. Evidence is provided that relaxin, at both the assayed doses, causes a clear-cut, significant reduction of plasma histamine, increase in cardiac histamine content and decrease in cardiac mast cell degranulation. This is accompanied by a reduction of oxidative cardiac tissue injury (assessed as tissue malondialdehyde) and of the occurrence of severe ventricular arrhythmias. In conclusion, this study provides further insight into the cardioprotective effects of relaxin, which also involve mast cell inhibition, and confirms the relevance of histamine in the pathophysiology of ischemia-reperfusion-induced cardiac injury and dysfunction. It also offers additional evidence for the potential therapeutic effects of relaxin in animal models of disease involving mast cell activation.     

Modeling and biological evaluation of 3,3'-(1,2-ethanediyl)bis[2-(4-methoxyphenyl)-thiazolidin-4-one], a new synthetic cyclooxygenase-2 inhibitor

Within the series of chiral 3,3'-(1,2-ethanediyl)bis[2-arylthiazolidin-4-ones], the 3,4-dimethoxyphenyl substituted derivative was found in the primary anti-inflammatory screening to be endowed with superior in vivo properties and good safety profile. Such a lead compound was modified by eliminating 3-methoxy group while retaining 4-methoxy group on the aryl rings at 2 and 2' stereogenic carbons. The 2R,2'S-meso isomer (VIG3b) of the resulting bisthiazolidinone has been widely investigated. The inhibitory effects on cyclo-oxygenase-1 and cyclo-oxygenase-2 isoenzymes were measured in a human whole blood assay. VIG3b was almost 50 times more selective on the inducible isoform. The cyclo-oxygenase-2 preferential selectivity has been confirmed by modeling VIG3b into the cyclo-oxygenase-1 and cyclo-oxygenase-2 active sites. Furthermore, VIG3b was assayed in the experimental model of carrageenan-induced lung injury by evaluating its ability to inhibit: (1) fluid accumulation in the pleural cavity, (2) neutrophil infiltration, (3) prostaglandin E(2) production and (4) lung injury. VIG3b exhibited interesting activity in all these tests.     

Schizophrenia and genetics: new insights

There is consistent evidence that the principal etiology of schizophrenia involves predisposing genetic factors. Recent years have seen several new insights in the genetics of schizophrenia. Several chromosomal regions show significant evidence that they contain schizophrenia susceptibility genes. A clinically relevant genetic subtype of schizophrenia (22q deletion syndrome) has been identified. There is new evidence that spontaneous mutations may play a role. There are new recommendations for genetic counseling. The progress to date suggests that understanding of a neurodevelopmental pathway from genetic susceptibility to schizophrenia will soon be fundamentally altered by molecular genetic advances in this complex disease.     

Mutational analysis of nicotinic acetylcholine receptor beta2 subunit gene (CHRNB2) in a representative cohort of Italian probands affected by autosomal dominant nocturnal frontal lobe epilepsy

Twenty-four autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) probands were analyzed for the presence of V287L and V287M mutations in the CHRNB2 gene, which have been recently associated with the disease. In all patients, the involvement of the two additional loci reported as being associated with ADNFLE (CHRNA4 gene and chromosome 15q24 region) had been previously excluded. Mutational screening was performed by sequencing a polymerase chain reaction-amplified CHRNB2 DNA fragment, spanning the whole exon 5, which contains the V287L and V287M mutations and codes for approximately 65% of the mature protein. In none of the patients were mutations in the analyzed region of CHRNB2 found. These data, obtained in the largest ADNFLE cohort so far analyzed, demonstrate the rarity of the identified CHRNB2 mutations in ADNFLE patients.