Videolaryngoscopes versus direct laryngoscopes in children: Ranking systematic review with network meta-analyses of randomized clinical trials.

BACKGROUND: Videolaryngoscopes improve tracheal intubation in adult patients, but we currently do not know whether they are similarly beneficial for children. We designed this ranking systematic review to compare individual video and direct laryngoscopes for efficacy and safety of orotracheal intubation in children. METHODS: We searched PubMed and five other databases on January 27, 2021. We included randomized clinical trials with patients aged ≤18 years, comparing different laryngoscopes for the outcomes: failed first intubation attempt; failed intubation within two attempts; failed intubation; glottic view; time for intubation; complications. In addition, we assessed the quality of evidence according to GRADE recommendations. RESULTS: We included 46 studies in the meta-analyses. Videolaryngoscopy reduced the risk of failed first intubation attempt (RR = 0.43; 95% CI: 0.31-0.61; p = .001) and failed intubation within two attempts (RR = 0.33; 95% CI: 0.33-0.33; p < .001) in children aged <1 year. Videolaryngoscopy also reduced the risk of major complications in both children aged <1 year (RR = 0.33; 95% CI: 0.12-0.96; p = .046) and children aged 0-18 years (RR = 0.40; 95% CI: 0.25-0.65; p = .002). We did not find significant difference between videolaryngoscopy and direct laryngoscopy for time to intubation in children aged <1 year (MD = -0.95 s; 95% CI: -5.45 to 3.57 s; p = .681), and children aged 0-18 years (MD = 1.65 s; 95% CI: -1.00 to 4.30 s; p = .222). Different videolaryngoscopes were associated with different performance metrics within this meta-analysis. The overall quality of the evidence ranged from low to very low. CONCLUSION: Videolaryngoscopes reduce the risk of failed first intubation attempts and major complications in children compared to direct laryngoscopes. However, not all videolaryngoscopes have the same performance metrics, and more data is needed to clarify which device may be better in different clinical scenarios. Additionally, care must be taken while interpreting our results and rankings due to the available evidence's low or very low quality.

Nutritional impact of bariatric surgery: a comparative study of Roux-en-Y Gastric Bypass and Sleeve gastrectomy between patients from the public and private health systems. / Impacto nutricional da cirurgia bariátrica: estudo comparativo do Bypass gástrico em Y de Roux e do Sleeve entre pacientes dos sistemas público e privado de saúde.

PURPOSE: To compare the nutritional status follow up of patients who underwent Roux-en-Y gastric bypass (BGYR) and Sleeve gastrectomy (SG) in hospitals of the private and public health systems, in Pernambuco. METHODS: This study included patients who underwent bariatric surgery in the public and private health systems, in Pernambuco, from 2008 to 2016. Anthropometric and biochemical (hemoglobin, B12, iron and ferritin) data were evaluated in the preoperative period and at 3, 6 and 12 months after the operation. RESULTS: There were no significant difference between patients seen at the two health systems regarding the levels of hemoglobin, iron, anemia and vitamin B12. Patients who underwent the RYGB, presented with iron deficiency which was significantly lower for those in the private system, but only at the 3 month evaluation. Low levels of ferritin were observed at the 6 month evaluation, and patients in the private health system presented with the highest ferritin deficiency. The rate of surgical success was significantly higher in those patients undergoing the RYGB at the private system. CONCLUSIONS: After a 12-month bariatric surgery follow-up, there was no statistically significant difference regarding micronutrient deficiency between patients followed up at the private and public health systems.

OBJETIVOS: Comparar a evolução do perfil nutricional de pacientes submetidos ao bypass gástrico em Y de Roux (BGYR) e ao Sleeve, em hospitais dos setores público e privado da Saúde de Pernambuco. MÉTODO: O estudo incluiu pacientes submetidos à cirurgia bariátrica nos setores público e privado de saúde de Pernambuco no período de 2008 a 2016. Foram avaliados dados antropométricos e bioquímicos (Hemoglobina, Vitamina B12, Ferro e Ferritina) no período pré-operatório e com 3, 6 e 12 meses de pós-operatório. RESULTADOS: Não foram registradas diferenças significativas entre os pacientes internados nos dois setores da Saúde no tocante às variáveis: níveis hemoglobina, anemia por deficiência de ferro e vitamina B12 em nenhuma das avaliações e conforme o tipo de cirurgia. Entre os pacientes submetidos ao BGYR, os níveis de ferro sérico foram significativamente menores nos pacientes do setor privado da Saúde apenas na primeira avaliação. Baixos níveis de ferritina sérica foram observados na segunda avaliação, sendo os pacientes do setor privado os que apresentaram menores valores. O sucesso cirúrgico foi significativamente maior no grupo que realizou o BGYR na rede privada. CONCLUSÕES: Com um seguimento de 12 meses pós-cirurgia bariátrica, não foi observada diferença estatisticamente significante no que diz respeito às deficiências de micronutrientes entre pacientes usuários dos setores público e privado de Saúde.

Impacto nutricional da cirurgia bariátrica: estudo comparativo do Bypass gástrico em Y de Roux e do Sleeve entre pacientes dos sistemas público e privado de saúde / Nutritional impact of bariatric surgery: a comparative study of Roux-en-Y Gastric Bypass and Sleeve gastrectomy between patients from the public and private health systems

RESUMO Objetivos: Comparar a evolução do perfil nutricional de pacientes submetidos ao bypass gástrico em Y de Roux (BGYR) e ao Sleeve, em hospitais dos setores público e privado da Saúde de Pernambuco. Método: O estudo incluiu pacientes submetidos à cirurgia bariátrica nos setores público e privado de saúde de Pernambuco no período de 2008 a 2016. Foram avaliados dados antropométricos e bioquímicos (Hemoglobina, Vitamina B12, Ferro e Ferritina) no período pré-operatório e com 3, 6 e 12 meses de pós-operatório. Resultados: Não foram registradas diferenças significativas entre os pacientes internados nos dois setores da Saúde no tocante às variáveis: níveis hemoglobina, anemia por deficiência de ferro e vitamina B12 em nenhuma das avaliações e conforme o tipo de cirurgia. Entre os pacientes submetidos ao BGYR, os níveis de ferro sérico foram significativamente menores nos pacientes do setor privado da Saúde apenas na primeira avaliação. Baixos níveis de ferritina sérica foram observados na segunda avaliação, sendo os pacientes do setor privado os que apresentaram menores valores. O sucesso cirúrgico foi significativamente maior no grupo que realizou o BGYR na rede privada. Conclusões: Com um seguimento de 12 meses pós-cirurgia bariátrica, não foi observada diferença estatisticamente significante no que diz respeito às deficiências de micronutrientes entre pacientes usuários dos setores público e privado de Saúde.

ABSTRACT Purpose: To compare the nutritional status follow up of patients who underwent Roux-en-Y gastric bypass (BGYR) and Sleeve gastrectomy (SG) in hospitals of the private and public health systems, in Pernambuco. Methods: This study included patients who underwent bariatric surgery in the public and private health systems, in Pernambuco, from 2008 to 2016. Anthropometric and biochemical (hemoglobin, B12, iron and ferritin) data were evaluated in the preoperative period and at 3, 6 and 12 months after the operation. Results: There were no significant difference between patients seen at the two health systems regarding the levels of hemoglobin, iron, anemia and vitamin B12. Patients who underwent the RYGB, presented with iron deficiency which was significantly lower for those in the private system, but only at the 3 month evaluation. Low levels of ferritin were observed at the 6 month evaluation, and patients in the private health system presented with the highest ferritin deficiency. The rate of surgical success was significantly higher in those patients undergoing the RYGB at the private system. Conclusions: After a 12-month bariatric surgery follow-up, there was no statistically significant difference regarding micronutrient deficiency between patients followed up at the private and public health systems.

An alternative explanation for the occurrence of short circuit current increases in the small intestine following challenge by bacterial enterotoxins.

Secretory diarrhoeal disease due to enterotoxins is thought to arise from the enhancement to pathologically high rates of normally occurring chloride ion and therefore fluid secretion from enterocytes. In support of this concept, many enterotoxins increase intestinal short-circuit current, regarded now as faithfully reflecting the increased chloride ion secretion. Contradicting this assumption, STa reduces absorption but does not cause secretion in vivo although short-circuit current is increased in vitro. There is therefore a mismatch between an assumed enterocyte mediated secretory event that should but does not cause net fluid secretion and an undoubtedly increased short-circuit current. It is proposed here that short-circuit current increases are not themselves secretory events but result from interrupted fluid absorption. A noteworthy feature of compounds that inhibit the increase in short-circuit current is that the majority are vasoactive, neuroactive or both. In general, vasodilator substances increase current. An alternative hypothesis for the origin of short-circuit current increases is that these result from reflex induction of electrogenic fluid absorption. This reflex enhances a compensatory response that is also present at a cellular level. An intestinal reflex is therefore proposed by which decreases in interstitial and intravascular volume or pressure within the intestine initiate an electrogenic fluid absorption mechanism that compensates for the loss of electrically neutral fluid absorption. This hypothesis would explain the apparently complex pharmacology of short-circuit current increases since many depressor substances have receptors in common with enterocytes and enteric nerves. The proposed alternative view of the origin of short-circuit current increases assumes that these do not represent chloride secretion from the enterocytes. This view may therefore aid the successful development of anti-diarrhoeal drugs to overcome a major cause of infant mortality worldwide, if short-circuit current data are being persistently misinterpreted. The putative but testable link between interstitial volume or pressure and fluid absorption also provides support for the alternative view of secretion; namely, that enhanced capillary and epithelial cell tight junctional permeability together with increased intracapillary pressure may cause secretion and not chloride exit from the enterocytes.

Lack of Restoration in Vivo by K-Channel Modulators of Jejunal Fluid Absorption after Heat Stable Escherichia coli Enterotoxin (STa) Challenge.

Enhanced potassium ion permeability at the enterocyte basolateral membrane is assumed to facilitate sustained chloride ion and fluid secretion into the intestinal lumen during episodes of secretory diarrhoeal disease. To examine this concept in vivo, two potassium ion channel blockers and a channel opener were coperfused with E. coli heat stable STa enterotoxin to determine whether such compounds improved or worsened the inhibited fluid absorption. In the STa (80 ng/mL) challenged jejunal loop, the fluid absorption rate of 28.6 ± 5.8 (14) µL/cm/hr was significantly below (P < .001) the normal rate of 98.8 ± 6.2 (17) µL/cm/hr. Intraluminal (300 uM) glibenclamide added to STa perfused loops failed to improve the inhibited fluid absorption rate, which was 7.4 ± 3.2 (6) µL/cm/hr on coperfusion with STa. Similarly, on coperfusion with 30 uM clotrimazole, the fluid absorption rate with STa present remained inhibited at 11.4 ± 7.0 (4) µL/cm/hr. On coperfusion with intraluminal 1 uM cromakalim, STa reduced fluid absorption significantly (P < .02) to 24.7 ± 8.0 (10) µL/cm/hr, no different from STa challenge in the absence of cromakalim. Infusion i.v. with these agents also failed to restore fluid absorption after STa challenge. These observations do not support the proposed potassium ion permeability event as a necessary corollary of enterotoxin-mediated secretion. This makes it unlikely that modulators of such permeability prevent enterocyte secretion in diarrhoeal disease.

Enterocyte chloride and water secretion into the small intestine after enterotoxin challenge: unifying hypothesis or intellectual dead end?

Many forms of diarrhoeal disease, particularly so called "secretory" diarrhoeal disease are thought to arise by the active secretion of chloride ion from the enterocytes, creating an osmotic gradient for fluid movement into the small intestinal lumen. This model implies that normally occurring intestinal secretion is catastrophically enhanced by bacterial enterotoxins. This review advocates that neither normal nor abnormal intestinal secretion from the enterocytes occurs and that no competent proof for chloride secretion exists. Prior to 1970, the physiological evidence failed to support the concept of the formation of intestinal juice as a normal intestinal event. The concept was later revived to explain the high rate of fluid entry into the lumen after exposure to cholera toxin. Much evidence has been advanced for the chloride secretion hypothesis, the dominant secretory paradigm after 1974, but is the evidence sufficiently compelling for it to be regarded as proving the chloride secretory model? The evidence falls into four categories and a fifth conjectural argument that proposes that an abnormal chloride ion channel in cystic fibrotic sufferers confers a natural selective advantage by preventing diarrhoeal disease. Secretion is putatively demonstrated by 1) showing that mass transfer of fluid is into the lumen (secretion) and not merely a failure to transport out of the lumen (failed absorption). Support is offered by 2) chloride ion flux measurements in vitro in Ussing chambers and by 3) short-circuit current measurements that are consistent with and purport to show chloride ion movement into the lumen. In addition, 4) pharmacological agents are identified that affect short-circuit current and these are assumed to be anti-secretory, consistent with the biochemical mechanism for secretion, confirmed wherever possible by mouse knock-out models. Finally, the proxy methods used to study water movement such as elevated short-circuit current measurements show these to be absent in cystic fibrotic patients. The enterocyte secretion hypothesis is challenged here on the basis of an examination of the methods used to show secretion, particularly after exposing the small intestine to heat stable enterotoxin (STa) from E. coli. STa is thought to be secretory because fluid entry into the lumen is claimed, enhanced isotopic flux of chloride ion towards the lumen occurs, an increase in short-circuit current is found, preventable by various drugs that are deemed likely to be anti-secretory and also because the short-circuit current changes after STa are not seen in cystic fibrotic patients. Using volume recovery in vivo, STa is found not to be secretory but only anti-absorptive. Hence, other techniques used to show secretion are not fit for that purpose. If STa is identified as secretory and yet no secretion occurs, how reliable is the evidence for other toxins being secretory when these methods are used? This review concludes that chloride ion secretion is unproven. A review of the literature indicates that secretion occurs not because epithelial cells actively pump water but by interdiction of fluid absorption, increased conductivity through tight junctions and an increased hydrostatic driving force through elevated capillary pressure. The exclusive focus on chloride secretion may explain the failure to develop antisecretory drugs over the last three decades.

Enterocyte chloride and water secretion into the small intestine after enterotoxin challenge: Unifying hypothesis or intellectual dead end?

Many forms of diarrhoeal disease, particularly so called "secretory" diarrhoealdisease are thought to arise by the active secretion of chloride ion from the enterocytes,creating an osmotic gradient for fluid movement into the small intestinallumen. This model implies that normally occurring intestinal secretion is catastrophicallyenhanced by bacterial enterotoxins. This review advocates that neither normalnor abnormal intestinal secretion from the enterocytes occurs and that no competentproof for chloride secretion exists. Prior to 1970, the physiological evidence failed tosupport the concept of the formation of intestinal juice as a normal intestinal event.The concept was later revived to explain the high rate of fluid entry into the lumenafter exposure to cholera toxin. Much evidence has been advanced for the chloridesecretion hypothesis, the dominant secretory paradigm after 1974, but is the evidencesufficiently compelling for it to be regarded as proving the chloride secretory model?. The evidence falls into four categories and a fifth conjectural argument that proposes that an abnormal chloride ion channel in cystic fibrotic sufferers confers a natural selective advantage by preventing diarrhoeal disease. Secretion is putatively demonstrated by 1) showing that mass transfer of fluid is into the lumen (secretion) and not merely a failure to transport out of the lumen (failed absorption). Support is offered by 2) chloride ion flux measurements in vitro in Ussing chambers and by 3) shortcircuit current measurements that are consistent with and purport to show chloride ion movement into the lumen. In addition, 4) pharmacological agents are identified that affect short-circuit current and these are assumed to be anti-secretory, consistent with the biochemical mechanism for secretion, confirmed wherever possible by mouse knock-out models. Finally, the proxy methods used to study water movement such as elevated short-circuit current measurements show these to be absent in cystic fibrotic patients. The enterocyte secretion hypothesis is challenged here on the basis of an examination of the methods used to show secretion, particularly after exposing the small intestine to heat stable enterotoxin (STa) from E.coli. STa is thought to be secretory because fluid entry into the lumen is claimed, enhanced isotopic flux of chloride ion towards the lumen occurs, an increase in short-circuit current is found, preventable by various drugs that are deemed likely to be anti-secretory and also because the short-circuit current changes after STa are not seen in cystic fibrotic patients. Using volume recovery in vivo, STa is found not to be secretory but only anti-absorptive. Hence, other techniques used to show secretion are not fit for that purpose. If STa is identified as secretory and yet no secretion occurs, how reliable is the evidence for other toxins being secretory when these methods are used? This review concludes that chloride ion secretion is unproven. A review of the literature indicates that secretion occurs not because epithelial cells actively pump water but by interdiction of fluid absorption, increased conductivity through tight junctions and an increased hydrostatic driving force through elevated capillary pressure.The exclusive focus on chloride secretion may explain the failure to develop antisecretory drugs over the last three decades (AU)

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Lack of evidence in vivo for a remote effect of Escherichia coli heat stable enterotoxin on jejunal fluid absorption.

On contact with the mucosa, heat stable (STa) enterotoxin from Escherichia coli reduces fluid absorption in vivo in the perfused jejunum of the anaesthetized rat. The question of whether it also has a vagally mediated remote action on jejunal absorption, when instilled into the ileum, was re-examined, given contradictory findings in the literature. A standard perfused loop preparation was used to measure luminal uptake of fluid in vivo by means of volume recovery. STa in the ileum was found to have no effect on jejunal absorption, regardless of cervical or sub-diaphragmatic vagotomy and also regardless of the nature of the perfusate anion. The batches of toxin were shown in parallel experiments to reduce fluid absorption directly in the jejunum and also in the ileum. Similarly, vagal nerves prior to section had demonstrable in vivo physiological function. There was therefore no evidence for an indirect, vagally mediated ileal effect of STa on proximal fluid absorption.

Lack of evidence in vivo for nitrergic inhibition by Escherichia coli (STa) enterotoxin of fluid absorption from rat proximal jejunum.

Fluid absorption from the proximal jejunum of the anaesthetised rat was measured in vivo by fluid recovery. As expected, heat stable (STa) enterotoxin from E. coli reduced fluid absorption. Neither intraperitoneal L-NAME, thought to inhibit a putative neurally mediated action of STa, nor similar doses of D-NAME, ameliorated the inhibitory effect on jejunal fluid absorption of STa. Luminally perfused 10 mM sodium nitroprusside (SNP) had no effect on fluid absorption when expressed per gram dry weight per hour but reduced fluid absorption when expressed per cm length per hour. Similarly, 80 but not 40 mg/Kg of L-NAME reduced fluid absorption when expressed per cm length per hour, while the same dose of D-NAME did not. L-NAME and SNP significantly increased the wet weight to dry weight and the length to dry weight ratio of perfused loops. We conjecture that smooth muscle relaxation caused by these compounds increases interstitial fluid volumes that can be misconstrued as changes in absorption when this is expressed per cm length or per tissue wet weight. When fluid absorption is expressed per gram dry weight of tissue, there is no evidence for a role of nitric oxide in normal or STa inhibited fluid absorption.

Amendments to the theory underlying Ussing chamber data of chloride ion secretion after bacterial enterotoxin exposure.

Bacterial enterotoxins may cause life-threatening diarrhoeal fluid loss in part because they stimulate enterocytes to secrete fluid into the small intestine as well as preventing normal fluid uptake. Abnormal chloride ion secretion is believed to provide the osmotic driving force for the inappropriate fluid movement. Evidence for enhanced chloride secretion consists of isotopic flux measurements in Ussing chambers, the standard apparatus for permeation studies. Flux from the lumen of the intestine is assumed to be determined solely by absorptive processes and flux towards the lumen solely by secretory processes. Bacterial enterotoxin increased flux towards the lumen is taken as an evidence of enhanced secretion. Examination of the flux equation solutions shows that the existing theoretical treatment of the Ussing chamber consists of the super-imposition of two contradictory unidirectional models. In contrast, the present analysis shows that a measured 'unidirectional' flux contains information both about absorptive and secretory processes, regardless of which flux is measured. Reciprocity is predicted for the fluxes, as decreases in the absorptive processes will cause increases in apparent secretory flux. Data from the literature show that mucosal-to-serosal chloride ion flux in rabbit ileum after exposure to secretagogues correlates inversely and highly significantly (r=0.74, n=17, p<0.001) with increases in serosal-to-mucosal chloride ion flux. As a category of evidence, flux data do not provide conclusive evidence of enhanced chloride secretion after exposure to enterotoxins, since an apparently enhanced serosal-to-mucosal flux would also be noted after inhibition of the mucosal-to-serosal flux. As interruption of absorptive processes can be misinterpreted as enhanced secretion in the Ussing chamber, this is a serious deficiency in the evidence for direct enterotoxin enhancement of the intestinal chloride ion channel as a basis for diarrhoeal disease.

Escherichia coli heat stable (STa) enterotoxin and the upper small intestine: lack of evidence in vivo for net fluid secretion.

Heat stable (STa) enterotoxin from E. coli reduced fluid absorption in vivo in the perfused jejunum of the anaesthetized rat in Krebs-phosphate buffer containing lactate and glucose (nutrient buffer), in glucose saline and in glucose free saline. Bicarbonate ion enhanced fluid absorption of 98 +/- 7 (6) microl/cm/h was very significantly (P < 0.0001) reduced by STa to 19 +/- 4 (6) microl/cm/h, but net secretion was not found. When impermeant MES substituted for bicarbonate ion, net fluid absorption of 29 +/- 3 (6) microl/cm/h was less (P < 0.01) than the values for phosphate buffer and bicarbonate buffer. With STa in MES buffer, fluid absorption of 3 +/- 2 (6) microl/cm/h was less than (P < 0.001) that in the absence of STa and not significantly different from zero net fluid absorption. E. coli STa did not cause net fluid secretion in vivo under any of the above circumstances. Neither bumetanide nor NPPB when co-perfused with STa restored the rate of fluid absorption. In experiments with zero sodium ion-containing perfusates, STa further reduced fluid absorption modestly by 20 microl/cm/h. Perfusion of ethyl-isopropyl-amiloride (EIPA) with STa in zero sodium ion buffers prevented the small increment in fluid entry into the lumen caused by STa, indicating that the STa effect was attributable to residual sodium ion and fluid uptake that zero sodium-ion perfusates did not eradicate. These experiments, using a technique that directly measures mass transport of fluid into and out of the in vivo proximal jejunum, do not support the concept that E. coli STa acts by stimulating a secretory response.

Absorption of biologically active peptide hormones from the small intestine of rat.

Absorption of the 4, 10 and 34 amino acid forms of gastrin from the small intestine has been investigated in anaesthetized rats. The method of assessment of successful absorption of the hormone into the systemic circulation was when the amount of acid secreted by the stomach over consecutive 15-min periods was increased. When the natural hormones were infused into the ileum in a relatively high dose, there was no increase in gastric acid secretion, indicating that they had not been absorbed. Each of the forms of gastrin was conjugated at the free amino terminus to the carboxyl group of cholic acid. Subsequent infusion of the conjugated form of gastrin into the ileum, this time in relatively low doses, resulted in substantial and prolonged increases in gastric acid secretion, indicating that these hormones had been successfully absorbed. In addition, conjugation of the 10 and 34 amino acid forms of gastrin with cholic acid was shown to increase markedly the potency in evoking an increase in gastric acid secretion in response to intravenous injection of the hormone. Absorption of the gastrin conjugates was specific to the ileum thus indicating that they had been absorbed through the bile salt transporters.

Beneficial effect of alpha-tocopherol in renal ischemia-reperfusion in rats.

We evaluated the effects of alpha-tocopherol (vitamin E) on the products of lipid peroxidation and serum creatinine levels in a rat model of renal ischemia-reperfusion. The animals were submitted to sham operation or renal ischemia-reperfusion, and they were pretreated with alpha-tocopherol or the vehicle saline. In four groups, we analyzed the lipid peroxidation products by measuring malondialdehyde and chemiluminescence levels. In the other three groups, we studied the serum creatinine levels after the procedures. In our study, the pretreatment with alpha-tocopherol reduced significantly the lipid peroxidation of renal cells and renal dysfunction induced by renal ischemia-reperfusion in rats.

Dissociation between intentional and incidental sequence learning in Huntington's disease.

The ability to acquire and act upon serial order information is fundamental to almost all forms of adaptive behaviour. There is growing evidence that such knowledge may be acquired through a number of different means, each perhaps with its own neuronal substrate. One major distinction is between serial order information acquired intentionally and leading to explicit conscious knowledge of the sequence structure, and information acquired incidentally through experience. While this latter form of knowledge influences behaviour, it may do so without the participant being aware of the sequential information, i.e. it is acquired implicitly. Evidence from physiological and lesion studies in animals and imaging studies in humans suggests that these two forms of learning may have dissociable neuronal substrates. Specifically, the striato-thalamo-cortical circuit centred on the caudate nucleus is proposed to be involved in intentional sequence learning and that based on the putamen on incidental learning. The present study tested one part of this proposed dissociation by assessing patients with Huntington's disease on tasks of the two forms of learning. On the test of trial-and-error intentional learning there were marked deficits, which were closely related to disease progression and to measures of executive cognitive dysfunction. This finding was in contrast to the finding from the incidental learning task. Performance of the Huntington's disease group was essentially normal and unrelated to measures of disease progression and cognitive status. The results, although supportive of the proposed dual-system hypothesis, offer only partial confirmation. Further direct study is required using similar tasks in patients with putamenal disorder or lesions within the skeletomotor striato-thalamo-cortical circuit.

Effects of L-arginine on the kidney levels of malondialdehyde in rats submitted to renal ischaemia-reperfusion.

OBJECTIVE: To evaluate the effects of L-arginine, a nitric oxide donor, on kidney levels of malondialdehyde (MDA, a product of cellular lipid peroxidation), serum creatinine levels, and urinary volume in rats undergoing unilateral renal ischaemia-reperfusion. MATERIALS AND METHODS: Wistar rats (117) were randomly distributed into three experimental groups (of four subgroups each) in which were assessed renal cell-lipid peroxidation (kidney levels of MDA), serum creatinine levels and urinary volume. The rats underwent unilateral nephrectomy followed by contralateral renal ischaemia-reperfusion with or with no pretreatment with L-arginine (200 mg/kg) given intraperitoneally. RESULTS: Pretreatment with L-arginine caused significantly higher kidney levels of MDA than in the untreated group (P < 0.05). Furthermore, L-arginine given before surgery attenuated the increase in serum creatinine and significantly increased urinary volume in rats subjected to renal ischaemia-reperfusion (P < 0.05). CONCLUSION: L-arginine tended to be of benefit for renal function during renal ischaemia-reperfusion in rats. Pretreatment with L-arginine (200 mg/kg intraperitoneally) seems to increase the renal damage by increasing kidney levels of MDA.

In vivo electroporation using an exponentially enhanced pulse: a new waveform.

In vivo electroporation is currently accomplished by one of two types of common waveforms: exponential decay or square-wave pulses. The purpose of this report is to present a new electroporation waveform, the exponentially enhanced pulse (EEP). Pulsing protocols including the EEP resulted in high levels of luciferase expression in muscle and skin, equal to or greater than expression resulting from low-voltage, millisecond square-wave pulses. This high level of expression requires fewer pulses when using an EEP protocol. Therefore, similar or greater plasmid DNA expression levels are obtained using fewer pulses with the EEP protocol than with current protocols. This is the first report of this new waveform and shows the success of using protocols employing the EEP to deliver plasmid DNA to various tissue types.