Comparison of conventional anterior surgery and laparoscopic surgery for inguinal-hernia repair

BACKGROUND: Inguinal hernias can be repaired by laparoscopic techniques, which have had better results than open surgery in several small studies. METHODS: We performed a randomized, multicenter trial in which 487 patients with inguinal hernias were treated by extraperitoneal laparoscopic repair and 507 patients were treated by conventional anterior repair. We recorded information about postoperative recovery and complications and examined the patients for recurrences one and six weeks, six months, and one and two years after surgery. RESULTS: Six patients in the open-surgery group but none in the laparoscopic-surgery group had wound abscesses (P=0.03), and the patients in the laparoscopic-surgery group had a more rapid recovery (median time to the resumption of normal daily activity, 6 vs. 10 days; time to the return to work, 14 vs. 21 days; and time to the resumption of athletic activities, 24 vs. 36 days; P<0.001 for all comparisons). With a median follow-up of 607 days, 31 patients (6 percent) in the open-surgery group had recurrences, as compared with 17 patients (3 percent) in the laparoscopic-surgery group (P=0.05). All but three of the recurrences in the latter group were within one year after surgery and were caused by surgeon-related errors. In the open-surgery group, 15 patients had recurrences during the first year, and 16 during the second year. Follow-up was complete for 97 percent of the patients. CONCLUSIONS: Patients with inguinal hernias who undergo laparoscopic repair recover more rapidly and have fewer recurrences than those who undergo open surgical repair.     

Evidence for an inhibitory effect of physiological levels of insulin on the growth hormone (GH) response to GH-releasing hormone in healthy subjects

It has been previously reported that in healthy subjects, the acute reduction of free fatty acids (FFA) levels by acipimox enhances the GH response to GHRH. In the present study, the GH response to GHRH was evaluated during acute blockade of lipolysis obtained either by acipimox or by insulin at different infusion rates. Six healthy subjects (four men and two women, 25.8 +/- 1.9 yrs old, mean +/- SE) underwent three GHRH tests (50 micrograms iv, at 1300 h) during: 1) iv 0.9% NaCl infusion (1200-1500 h) after oral acipimox administration (250 mg) at 0700 h and at 1100 h; 2) 0.1 mU.kg-1.min-1 euglycemic insulin clamp (1200-1500 h) after oral acipimox administration (250 mg at 0700 h and at 1100 h); 3) 0.4 mU.kg-1.min-1 euglycemic insulin clamp (1200-1500 h) after oral placebo administration (at 0700 and 1100 h). Serum insulin (immunoreactive insulin) levels were significantly different in the three tests (12 +/- 2, 100 +/- 10, 194 +/- 19 pmol/L, P < 0.06), plasma FFA were low and similar (0.04 +/- 0.003, 0.02 +/- 0.005, 0.02 +/- 0.003, not significant), and the GH response to GHRH was progressively lower (4871 +/- 1286, 2414 +/- 626, 1076 +/- 207 micrograms/L 120 min), although only test 3 was significantly different from test 1 (P < 0.05). Pooling the three tests together, a significant negative regression was observed between mean serum immunoreactive insulin levels and the GH response to GHRH (r = -0.629, P < 0.01). Our results indicate that in healthy subjects, acipimox and hyperinsulinemia produce a similar decrease in FFA levels and that at similar low FFA, the GH response to GHRH is lower during insulin infusion than after acipimox. These data suggest that insulin exerts a negative effect on GH release. Because the insulin levels able to reduce the GH response to GHRH are commonly observed during the day, for instance during the postprandial period, we conclude that the insulin negative effect on GH release may have physiological relevance.     

Detection and some properties of membrane-bound and soluble polyphosphatases in mitochondria of the yeast Saccharomyces cerevisiae

Saccharomyces cerevisiae mitochondria possess polyphosphatases that are tightly bound to the membranes and differ from soluble polyphosphatase of these organelles in a number of properties. Molecular weights of the membrane-bound polyphosphatases are 120 and 76 kD, and the molecular weight of the soluble polyphosphatase is about 36 kD. All three enzymes are evidently monomers, since antibodies against purified cell-envelope polyphosphatase of S. cerevisiae reacted with 115, 78, and 37 kD polypeptides in immunoblotting. The activities of membrane-bound and soluble polyphosphatase are maximal at neutral pH. The soluble polyphosphatase activity is stimulated by divalent cations, unlike the membrane-bound enzymes which are inhibited by the same cations including Mg2+. Monovalent cations do not affect the activity of the soluble enzyme but stimulate polyphosphatases in the membrane preparation. The specific activities for hydrolysis of polyphosphates with average chain lengths of 9 to 188 phosphate residues are enhanced by increasing the degree of substrate polymerization in the case of the membrane preparation and are unchanged in case of the soluble enzyme. Affinity of the soluble enzyme to polyphosphates is 5-10 times higher than that of the membrane-bound polyphosphatases. In the soluble fraction of mitochondria, high tripolyphosphatase activity is detected which is approximately 80% of that in isolated mitochondria.     

Plasticity of the visual system and learning]

Seckel syndrome is a clinical picture which associates four main features: intrauterine growth retardation, microcephaly often due to craniosynostosis, orofacial dysmorphology with bird headed appearance and variable mental retardation which is present after several months. Malformations of the central nervous system, limbs, and hair, may also be observed. On the basis of 78 cases reported in the literature, the authors discuss the validity of the morphological features of the syndrome. It is likely that the variability in the expressivity of each symptom explains its heterogeneity. According to the radiological abnormalities, three different forms of the syndrome have been described. Seckel syndrome is a genetic disorder with autosomal recessive inheritance. Its ethiopatogeny remains unclear. Hopefully linkage studies will allow to map the gene in order to determine the underlying abnormal protein.     

What five regulatory trends mean to nursing practice

Officials from the National Council of State Boards of Nursing report how developments in key areas will affect nursing practice.     

Correlates of performance-based measures of muscle function in the elderly: the Cardiovascular Health Study

BACKGROUND: It is unknown how much age-related changes in muscle performance represent normal aging versus the effects of chronic disease and life style. We examined the correlates of four performance measures-gait speed, timed chair stands (TCS), grip strength, and maximal inspiratory pressure (MIP)-using baseline data from the Cardiovascular Health Study (CHS), a population-based study of risk factors for heart disease and stroke in persons > or = age 65. METHODS: We analyzed data from the 5,201 CHS participants. Variables were arranged into nine categories: Personal Characteristics, Anthropometry, Physical Condition, Reported Functional Status, Subjective Health, Psychological Factors, Symptoms, Cognitive Status, Habits and Lifestyle, and Prevalent Disease. Independent correlates were identified using stepwise linear regression. RESULTS: The regression models explained 17.7-25.4% of the observed variability. Although age significantly correlated with each measure, it explained little of the variability (< or = 5.7%). Anthropometric features plus physical condition explained 14.0-17.4% of the variability for grip strength and MIP, but 2.8-12.9% of the variability for gait speed and the log of TCS. Subjective health and psychological factors explained 1.8-9.4% of the variability in gait speed and the log of TCS, but < or = 1.2% of the variability in grip strength and MIP. Variables for prevalent disease explained < or = 1.3% of the variability in each measure. CONCLUSIONS: After age 64, age explained little of the variability in muscle performance in a large sample of mostly functionally intact, community-dwelling older persons. Complex measures such as gait speed were more associated with subjective factors than were direct measures of strength. Prevalent disease contributed surprisingly little to muscle performance.     

Excitotoxicity and oxidative stress during inhibition of energy metabolism

Glutamate receptor involvement and oxidative stress have both been implicated in damage to neurons due to impairment of energy metabolism. Using two different neuronal in vitro model systems, an ex vivo chick retinal preparation and dopamine neurons in mesencephalic culture, the involvement and interaction of these events as early occurring contributors to irreversible neuronal damage have been examined. Consistent with previous reports, the early acute changes in the retinal preparation, as well as irreversible loss of dopamine neurons due to inhibition of metabolism, can be prevented by blocking NMDA receptors during the time of energy inhibition. Oxidative stress was suggested to be a downstream consequence and contributor to neuronal cell loss due to either glutamate receptor overstimulation or metabolic inhibition since trapping of free radicals with the cyclic nitrone spin-trapping agent MDL 102,832 (1 mM) attenuated acute excitotoxicity in the retinal preparation or loss of mesencephalic dopamine neurons due to either metabolic inhibition by the succinate dehydrogenase inhibitor, malonate, or exposure to excitotoxins. In mesencephalic culture, malonate caused an enhanced efflux of both oxidized and reduced glutathione into the medium, a significant reduction in total reduced glutathione and a significant increase in total oxidized glutathione at time points that preceded those necessary to cause toxicity. These findings provide direct evidence for early oxidative events occurring following malonate exposure and suggest that the glutathione system is important for protecting neurons during inhibition of energy metabolism. Consistent with this, lowering of glutathione by buthionine sulfoxamine (BSO) pretreatment greatly potentiated malonate toxicity in the mesencephalic dopamine population. In contrast, BSO pretreatment did not potentiate glutamate toxicity. This latter finding indicates dissimilarities in the type of oxidative stress that is generated by the two insults and suggests that the oxidative challenge during energy inhibition is not solely a downstream consequence of glutamate receptor overstimulation.