Changes in hook design and bait type were investigated as measures to reduce the bycatch of sea turtles on pelagic longlines in the western North Atlantic Ocean. Specifically, the effectiveness of 18/0 circle hooks and mackerel (Scomber scombrus) bait was evaluated with respect to reducing sea turtle interactions and maintaining swordfish (Xiphias gladius) and tuna (Thunnus spp.) catch rates. Individually, circle hooks and mackerel bait significantly reduced both loggerhead (Caretta caretta) and leatherback (Dermochelys coriacea) sea turtle bycatch. Circle hooks also significantly reduced the rate of hook ingestion by the loggerheads, potentially reducing postrelease mortality. The combination of circle hooks and mackerel bait was even more effective for loggerhead turtles and had no negative effect on swordfish catch. These modifications in fishing methods, in conjunction with tools developed to remove hooks and line from the turtles, significantly reduced the capture rate of sea turtles and potentially the post-hooking mortality of those that were caught and did not negatively impact the primary target species catch rate. In addition, these mitigation measures have the potential to reduce mortality of sea turtles and other bycatch species worldwide.

Summary. More precise analysis of causes of death is needed to focus research efforts and improve morbidity and mortality in sickle cell disease. In this study, the morphological evidence of the cause of death was studied in 306 autopsies of sickle cell disease, which were accrued between 1929 and 1996. The most common cause of death for all sickle variants and for all age groups was infection (33-48%). The terminal infection was heralded by upper respiratory tract syndromes in 72AE6% and by gastroenteritis in 13AE7%. The most frequent portal of entry in children was the respiratory tract but, in adults, a site of severe chronic organ injury. Other causes of death included stroke 9AE8%, therapy complications 7AE0%, splenic sequestration 6AE6%, pulmonary emboli/thrombi 4AE9%, renal failure 4AE1%, pulmonary hypertension 2AE9%, hepatic failure 0AE8%, massive haemolysis/red cell aplasia 0AE4% and left ventricular failure 0AE4%. Death was frequently sudden and unexpected (40AE8%) or occurred within 24 h after presentation (28AE4%), and was usually associated with acute events (63AE3%). This study shows that the first 24 h after presentation for medical care is an especially perilous time for patients with sickle cell disease and an acute event. Close monitoring and prompt aggressive treatment are warranted.

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This study demonstrated that aging men with obesity and the metabolic syndrome have a significant decrease in total serum testosterone levels compared to aging, metabolically healthy men. These data suggest that the well established association between erectile dysfunction and pre-diabetes/diabetes (particularly in obese pre-diabetic/diabetic patients) may involve a hormonal component.

FOR THE SCANDINAVIAN SIMVASTATIN SURVIVAL STUDY GROUPOBJECTIVE -To assess the effect of simvastatin treatment on the risk of cardiovascular events in nondiabetic patients with coronary heart disease (CHD) with and without the metabolic syndrome, as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP-III).RESEARCH DESIGN AND METHODS -Subgroup analyses were performed on data from 3,933 nondiabetic patients with clinically established CHD, serum total cholesterol level 5.5-8.0 mmol/l, and serum triglyceride level Յ2.5 mmol/l who were participating in the Scandinavian Simvastatin Survival Study (4S), a randomized, placebo-controlled trial. End points were total mortality, coronary mortality, major CHD event, myocardial revascularization, any CHD event, stroke, and any atherosclerotic event.RESULTS -Over the 5.4-year median follow-up period, simvastatin produced similar changes in serum lipid levels in 893 patients with the metabolic syndrome and in 3,040 patients without the metabolic syndrome. The relative risks of main end points in simvastatin-treated patients compared with placebo-treated patients with the metabolic syndrome were as follows: total mortality 0.54 (95% CI 0.36 -0.82), coronary mortality 0.39 (0.23-0.65), major CHD event 0.59 (0.45-0.77), and any atherosclerotic event 0.69 (0.56 -0.84). The corresponding RRs in patients without the metabolic syndrome were 0.72 (0.56 -0.91), 0.62 (0.45-0.84), 0.71 (0.61-0.82), and 0.76 (0.68 -0.85).CONCLUSIONS -Nondiabetic CHD patients with or without the metabolic syndrome realize from simvastatin treatment a similar, substantial relative reduction in the risk of cardiovascular events. The absolute benefit may be greater in patients with the metabolic syndrome because they are at a higher absolute risk.

Abstract. Irreversibly sickled cells (ISCs) remainsickled even under conditions where they are well oxygenated and hemoglobin is depolymerized. In our studies we demonstrate that triton extracted ISC core skeletons containing only spectrin, protein 4.1, and actin also retain their sickled shape; while reversibly sickled cell (RSC) skeletons remodel to a round or biconcave shape. We also demonstrate that these triton extracted ISC core skeletons dissociate more slowly upon incubation at 37°C than do RSC or control (AA) core skeletons. This observation may supply the basis for the inability of the ISC core skeleton to remodel its shape. Using an in vitro ternary complex dissociation assay, we demonstrate that a modification in /3-actin is the major determinant of the slow dissociation of the spectrin-protein 4.1-actin complex isolated from the ISC core skeleton. We demonstrate that the difference between ISC and control/3-actin is the inaccessibility of two cysteine residues in ISC ~/-actin to labeling by thiol reactive reagents; due to the formation of a disulfide bridge between cysteine TM and cysteine 373 in ISC/~-actin, or alternatively another modification of cysteine TM and cysteine 373 which is reversible with DTT and adds less than 100 D to the molecular weight of ~-actin.

The relationship between free radicals and scavenger enzymes, and the disorders called the neuronal ceroid-lipofuscinoses, has long been an argumentative one. Recent evidence would seem to support the fact that such a relationship might exist but that it is indirect. The relationship does not seem due to an inborn error of free radical scavenger enzyme metabolism. Anticonvulsants play a role, as they influence free radical generating systems. At this juncture, no one has studied the relationship of anticonvulsant therapy, neuronal ceroid-lipofuscinosis, and the free radical-scavenging enzyme system, and their interplay. We have studied a large number of patients with epilepsy who are on either monotherapeutic or polytherapeutic regimens of most of the common anticonvulsants. We have found excessive free radical production in many of these patients, ranging from minor effects in the simpler anticonvulsants when used monotherapeutically, to more complex changes in polytherapeutic combinations. Likewise, we have found subtle and inconsistent findings in the free radical-scavenging enzyme system in a variety of examples of neuronal ceroid-lipofuscinosis. When refractory seizure disorders stimulate the vigorous use of polytherapy with a variety of free radical-facilitating anticonvulsants, free radical production becomes deleterious. Likewise, in certain types of neuronal ceroid-lipofuscinosis, polypharmacy with anticonvulsants, by enhancing the production of free radicals or suppressing scavenging enzymes, tends to be deleterious and induces a worsening in the disease process.

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