Nuclear morphometry of the myocardial cells as a diagnostic tool in cases of sudden death due to coronary thrombosis

One general signalling mechanism used to transfer the information delivered by agonists into appropriate intracellular compartments involves the rapid redistribution of ionised calcium throughout the cell, which results in transient elevations of the cytosolic free Ca2+ concentration. Various physiological stimuli increase [Ca2+]i transiently and, thereby, induce cellular responses. However, under pathological conditions, changes of [Ca2+]i are generally more pronounced and sustained. Marked elevations of [Ca2+]i activate hydrolytic enzymes, lead to exaggerated energy expenditure, impair energy production, initiate cytoskeletal degradation, and ultimately result in cell death. Such Ca(2+)-induced cytotoxicity may play a major role in several diseases, including neuropathological conditions such as chronic neurodegenerative diseases and acute neuronal losses (e.g. in stroke).     

Esophagogastrostomy with the EEA stapler

Esophagogastric anastomosis was performed with the EEA stapler in 31 patients who underwent esophageal resections. Anastomoses were accomplished at all levels of the thoracic and cervical esophagus by a variety of approaches. Routine barium cine-esophagograms obtained at seven days after operation failed to demonstrate an anastomotic leak in any patient. The operative mortality rate was 3% (1 of 31 patients). Technical problems occurred during the operation in three patients; in two of these an incomplete anastomosis may have resulted from the surgeon's error. All patients were able to swallow normally at the time of discharge. Late anastomotic stricture occurred in five patients, and responded to dilatation in all but one patient who had local tumor recurrence. We conclude that the EEA stapler allows rapid and reliable esophagogastric anastomosis. Successful use of the instrument requires strict attention to technical detail and awareness of possible pitfalls.     

Hypomagnesaemia in postoperative patients: an important contributing factor in postoperative mortality

Nine patients with sickle cell disease (SCD) were operated upon at our hospital for acute appendicitis, comprising only 0.43% of the total appendicectomies performed at our institution. Three appendices were acutely inflamed and six (66.7%) were perforated. Histologic evaluation of the six perforated specimens revealed congestion and haemorrhage by sickled erythrocytes (RBCs) in addition to acute transmural inflammatory cell infiltrates. The mucosa was extensively ulcerated, with haemorrhage both within the lumen and in the appendiceal wall. The blood vessels were dilated and packed with sickled RBCs. Two of the three acutely inflamed appendices showed features of acute transmural appendicitis, with marked congestion and haemorrhage by sickled RBCs. The third did not show any acute inflammatory cell infiltrate, however, the mucosa was partly ulcerated with both mucosal and intraluminal haemorrhage. These findings suggest that acute appendicitis is different in patients with SCD: while it is not common, when it does develop it has a rapid course with a high incidence of perforation due to blockage of appendiceal vessels by sickled RBCs, leading to transmural necrosis.     

Toxicology reviews: immunoassay in detecting drugs of abuse

Approximately half the women with the polycystic ovary syndrome (PCOS) are obese or overweight. Obesity and body fat distribution have independent roles in the development of hyperandrogenism in PCOS. Most obese and normal weight PCOS are insulin resistant and hyperinsulinemic. Moreover, a significant positive correlation exists between the degree of hyperandrogenism and that of hyperinsulinism. The pathogenetic role of obesity may involve different mechanisms, the major one being the hyperinsulemic state, since insulin is capable of stimulating ovarian androgen secretion and controlling androgen metabolism and transport in peripheral tissues. Abdominal body fat distribution in obese women with PCOS amplifies the degree of hyperandrogenism and related clinical symptoms and signs. Both loss of body weight and/or the reduction of the degree of hyperinsuliemia, induced by diet or insulin-sensitizing drugs, have important effects, since they reduce blood androgen levels and can improve ovulation and clinical signs of hyperandrogenism.