Asociación entre obesidad y mortalidad en pacientes adultos que reciben ventilación mecánica invasiva: una revisión sistemática y metaanálisis / Association between obesity and mortality in adult patients receiving invasive mechanical ventilation: A systematic review and meta-analysis

Objetivo: Evaluar si existe asociación entre obesidad y mortalidad en la Unidad de Cuidados Intensivos (UCI) en pacientes adultos que reciben ventilación mecánica invasiva. Diseño: Revisión sistemática con metaanálisis. Ámbito: UCI. Fuente de datos: Se realizó una búsqueda en las bases de datos MEDLINE, Cochrane Library, CINAHL y Global Health sin restricción de lenguaje, hasta el 21 de febrero del año 2017. Selección de estudios: Se incluyeron estudios que informaron mortalidad en UCI en pacientes obesos versus no obesos que recibieron VMI. Variables principal: Mortalidad en UCI. Resultados: Se hallaron 2.163 artículos, de los cuales se incluyeron 14 estudios. No se encontraron diferencias estadísticamente significativas entre los pacientes obesos y no obesos respecto a la variable mortalidad en UCI (odds ratio: 0,94; intervalo de confianza del 95%: 0,81-1,10; p=0,45). Conclusión: No se halló relación entre el subgrupo de pacientes adultos obesos que reciben VMI y la variable mortalidad en UCI

Objective: To evaluate if there is an association between obesity and mortality in the Intensive Care Unit (ICU) in adult patients receiving invasive mechanical ventilation. Design: Systematic review with meta-analysis. Scope: ICU. Data source: A search was made in MEDLINE, Cochrane Library, CINAHL and Global Health databases without language restriction, until February 21, 2017. Selection of studies: Studies that reported mortality in the ICU in obese versus non-obese patients who received IMV were included. Main variables: Mortality in the ICU. Results: 2163 articles were found, of which 14 studies were included. No statistically significant differences were found between obese and non-obese patients with respect to the variable mortality in the ICU (OR: 0.94, 95% CI: 0.81-1.10, P=.45). Conclusion: No relationship was found between the subgroup of obese adult patients receiving IMV and the mortality variable in the ICU

Association between obesity and mortality in adult patients receiving invasive mechanical ventilation: A systematic review and meta-analysis. / Asociación entre obesidad y mortalidad en pacientes adultos que reciben ventilación mecánica invasiva: una revisión sistemática y metaanálisis.

OBJECTIVE: To evaluate if there is an association between obesity and mortality in the Intensive Care Unit (ICU) in adult patients receiving invasive mechanical ventilation. DESIGN: Systematic review with meta-analysis. SCOPE: ICU. DATA SOURCE: A search was made in MEDLINE, Cochrane Library, CINAHL and Global Health databases without language restriction, until February 21, 2017. SELECTION OF STUDIES: Studies that reported mortality in the ICU in obese versus non-obese patients who received IMV were included. MAIN VARIABLES: Mortality in the ICU. RESULTS: 2163 articles were found, of which 14 studies were included. No statistically significant differences were found between obese and non-obese patients with respect to the variable mortality in the ICU (OR: 0.94, 95% CI: 0.81-1.10, P=.45). CONCLUSION: No relationship was found between the subgroup of obese adult patients receiving IMV and the mortality variable in the ICU.

Interfaces Cerebro-Computadora: Conceptualización, Retos de Rediseño e Impacto Social / Brain Computer-Interfaces: Conceptualization, Redesign Challenges and Social Impact

Resumen Las Interfaces Cerebro-Computadora (ICCs) son sistemas que miden la actividad del Sistema Nervioso Central y la convierten en salidas que reemplazan, restauran, aumentan, suplementan o mejoran las salidas naturales de dicho sistema y, por lo tanto, cambian las interacciones en curso entre el ser humano y su ambiente interno o externo. Sin embargo, a más de medio siglo de ser investigadas en condiciones de laboratorio, las ICC no han podido ser trasladadas al mundo real. En el presente artículo de revisión se busca: (1) comprender a fondo la estructura de una ICC y los tipos de sistema, (2) analizar el reto que tiene la comunidad científica para mejorar la interacción entre usuario y sistema desde la perspectiva de la ingeniería de factores humanos y (3) describir la aplicación de este tipo de tecnología de asistencia en desarrollo en la sociedad mexicana. El futuro de estas ICC y la eficiencia con que logren el objetivo para el que fueron diseñadas parece depender, más que nunca, de factores relacionados a la percepción subjetiva del usuario, su adaptación al manejo de las ICC y el proceso de internalizarlas como propias en su espacio personal y su psique.

Abstract Brain-Computer Interfaces (BCIs) record the neural activity of the Central Nervous System, and then, produce outputs that replace, restore, increase, supplement or improve the natural outputs of such system. Therefore, the interaction between the human beings and their internal or external environment is transformed. However, over a century being investigated under laboratory conditions, BCIs have not been able to be transferred to the real world. This review aims to: (1) thoroughly understand the structure of a BCI and the system types, (2) analyze the challenge that the scientific community is facing to improve the interaction between user and system from the perspective of the engineering of human factors; and (3) describe the application of this type of assistive technology under development in the Mexican Society. The future of this technology and its effectiveness seem to depend more than ever on factors related to the user subjective perception, and the user adaptation to the system.

[Plasma malondialdehyde in patients with type 2 diabetes mellitus and in patients with coronary disease]. / Malondialdehído plasmático en pacientes con diabetes mellitus tipo 2 y en pacientes con enfermedad coronaria.

UNLABELLED: After intracoronary platelet aggregation, malondialdehyde (MDA), a lipid peroxide product is released. MDA renders some lipoproteins more atherogenic. OBJECTIVE: The objective of this study was to determine the sanguineous concentration of MDA in patients with type 2 diabetes mellitus (DM2) and patients with coronary disease. We measured methods and material MDA in plasma of 131 consecutive normal subjects, 44 hyperlipidemic, hyperglycemic patients with type 2-diabetes mellitus (DM2), 60 normolipidemic patients with angina, and 62 normolipidemic patients with acute myocardial infarction with and without DM2. STATISTICAL ANALYSIS: The concentration of MDA was lowest in normal subjects (42.5 +/- 7.2 micrograms per deciliter), intermediate in those with DM2 (62.7 +/- 10.1 micrograms per deciliter, p < 0.002), and highest in those with myocardial infarction (101.6 +/- 31.7 micrograms per deciliter, p < 0.001). The mean MDA concentration of patients with infarction was similar to that of patients with angina (121.8 +/- 51.9 micrograms per deciliter, p < 0.07). Stepwise logistic regression analysis showed that MDA was a possible predictor of myocardial infarction. CONCLUSIONS: The increase of plasma MDA might be a biochemical marker of coronary artery disease. We suggest that MDA levels greater than 62.7 micrograms per deciliter could indicate a high risk for myocardial infarction.

[Risk factors for asthenopia among computer terminal operators]. / Factores de riesgo para la astenopía en operadores de terminales de computadoras.

OBJECTIVE: To study the incidence of asthenopia among computer terminal operators as compared to unexposed administrative workers and to identify the risk factors associated with this condition. MATERIAL AND METHODS: A sample of 35 computer terminal operators and 70 unexposed administrative workers from eight computing centers at an educational institution were included in the study. The risk factors studied were: lighting, contrast, type of lighting, screen type, electrostatic field, eye to monitor distance, time and number of hours worked, age, use of corrective lenses, seniority and overtime. Asthenopia was clinically identified as the presence of at least one sign and symptom present in a given workday. RESULTS: Asthenopia was found in 68.5% of the exposed group and in 47.7% of the unexposed group (p < 0.05). Among the risk factors studied, working for more than four hours at the video display terminal was shown to have a significant association with asthenopia (p < 0.05). CONCLUSIONS: A recommendation is made to take breaks during the workday at computer terminals in order to avoid visual fatigue. Also, more extensive studies should be carried out in our population to establish safety criteria and to standardize work activities using computer terminals.

Total intravenous anesthesia with propofol vs. propofol/midazolam in oncology patients.

The goal of this study was to determine dose requirements of propofol vs. propofol/midazolam in oncology patients during total intravenous anesthesia. The design of the study was a controlled clinical trial. The setting was the Oncology Hospital, National Medical Center, IMSS, located in Mexico City. Sixty patients were allocated randomly into two groups, patients in control group received propofol and fentanyl to induced and to maintain the anesthesia. Twenty nine patients in the experimental group received propofol and midazolam to induce anesthesia and to maintain propofol and fentanyl. The combination of propofol and midazolam to induce general anesthesia in oncology patients reduced the requirements in propofol and fentanyl in total intravenous anesthesia.

Prevention of CCl4-induced liver necrosis by the calcium chelator arsenazo III.

Arsenazo III (AIII) (100 mg/kg ip in saline) administration to Sprague-Dawley male rats 30 min before or 6 or 10 hr after CCl4 [1 ml/kg ip as a 20% (v/v) solution in olive oil] significantly prevented liver necrosis but not fatty liver caused by the hepatotoxin at 24 hr as demonstrated either by histology or by determination of isocitric acid dehydrogenase in plasma. AIII did not modify the CCl4 concentrations reaching the liver, the intensity of the covalent binding of CCl4-reactive metabolites to hepatic microsomal lipids, or the CCl4-promoted lipid peroxidation process at either 1 or 3 hr of poisoning. AIII administration enhanced glutathione (GSH) levels in liver and significantly prevented the CCl4-induced minor decreases in GSH content and the CCl4-induced increases in calcium content at 24 hr of intoxication. AIII treatment further enhanced the CCl4-induced decreases in body temperature of the poisoned rats. Results suggest that AIII's preventive effects might be related to its very well-known calcium-chelating properties, but that additional factors related to AIII's ability to increase GSH content in liver or to decrease body temperature of CCl4-intoxicated animals may also play a role.

Prevention of carbon tetrachloride-induced liver necrosis by the chelator alizarin sodium sulfonate.

The administration of the calcium chelator alizarin sodium sulfonate (ASR) (100 mg/kg ip in saline) 30 min before or 6 or 10 hr after CCl4 (1 ml/kg ip as a 20% v/v solution in olive oil) partially prevents the necrogenic effect of the hepatotoxin at 24 hr, but prevention of CCl4 fat accumulation was not observed. Protective action cannot be attributed to potential decreasing effects of ASR on CCl4 levels reaching the liver, on the covalent binding of CCl4-reactive metabolites to cellular components, or on CCl4-induced lipid peroxidation because ASR does not modify these parameters significantly. ASR administration increases GSH levels in livers of both control and CCl4-poisoned animals and decreases the calcium content of intoxicated animals at 24 hr of poisoning. ASR significantly lowers the body temperature of CCl4-treated animals at different times of the intoxication process. Present and previous results from our laboratory on the preventive effects of another very specific calcium chelator, calcion, and several anticalmodulins suggest that the beneficial effects of ASR might be associated with its calcium chelating ability. Other protective effects of ASR, such as lowering body temperature or increasing GSH content in liver, cannot be excluded.

Modulation of the course of CCl4-induced liver injury by the anti-calmodulin drug thioridazine.

Thioridazine (TDZ) administration to rats (50 mg/kg i.p.) 6 or 10 h after CCl4 treatment (1 ml/kg in olive oil i.p.) partially prevented necrogenic effects of this compound at 24 h but not at 72 h. TDZ did not have inhibitory effects on CCl4 activation, covalent binding (CB) of reactive metabolites to cellular constituents or CCl4-induced lipid peroxidation (LP). Moreover, TDZ had enhancing effects on both LP and CB. TDZ was able to increase protein and phospholipid synthesis and slightly but significantly enhanced protein but not phospholipid degradation in livers from control rats. TDZ administration decreased calcium liver content in CCl4-poisoned animals but did not change the intensity of CCl4-induced fatty liver. TDZ lowered body temperature in CCl4-treated animals during the 24 h observation period. These results and previous studies from our laboratory suggest calcium and calmodulin (CaM) participation in the CCl4 necrogenic effects on the liver but not in the hepatotoxin-induced fatty liver. TDZ-lowering effects on body temperature might also be a determinant in the delaying effects of this drug on the onset of CCl4-induced necrosis. Present experiments did allow discrimination between these two or other possible mechanisms for TDZ modulation effects.

Further studies on the mechanism of the late protective effects of phenylmethylsulfonyl fluoride on carbon tetrachloride-induced liver necrosis.

We previously reported that phenylmethylsulfonyl fluoride (PMSF) administration to rats (100 mg/kg, ip in olive oil) as late as 6 or 10 hr after CCl4 (1 ml/kg, ip as a 20% v/v solution in olive oil) can partially prevent the necrogenic response to the hepatotoxin at 24 hr. Here we confirm that observation by electron microscopy and provide further evidence that only in these circumstances were nuclear clumping of chromatin, slight dilatation of the endoplasmic reticulum, myelin figures and lipid droplets in the cytoplasm, large numbers of lysosomes and peroxisomes, glycogen, and slightly swollen mitochondria observable in the protected animals. A very minor part of the late protective effects of PMSF might be due to the effects of this drug on decreasing the intensity of covalent binding of CCl4-reactive metabolites or the intensity of CCl4-induced lipid peroxidation still occurring 6 or 10 hr after CCl4. PMSF administration did not prevent CCl4-induced decreases in cytochrome P450 content or glucose-6-phosphatase activity but partially prevented CCl4-induced calcium accumulation in liver. PMSF treatment increased glutathione and glycogen content in CCl4-poisoned animals, but did not markedly modify protein/phospholipid synthesis or degradation processes. Results suggest that the late protective effects of PMSF administration in CCl4-induced liver necrosis might be due to a favorable modulation of the calcium-calmodulin system similar to that previously described for other drugs.

Carbon tetrachloride-induced liver cell injury in the Mongolian gerbil (Meriones unguiculatus).

1. Male Mongolian gerbils (Meriones unguiculatus) liver activates CCl4 to free radicals that bind covalently to cellular components (CB) and stimulate a lipid peroxidation (LP) process to a larger extent than the rat liver. 2. CCl4 administration results in a less intense necrogenic effect in gerbils than in rats and does not cause fatty liver. 3. CCl4 causes less intense effects on liver ultrastructure or calcium metabolism but more marked depression of glucose 6 phosphatase activity (G6P-ase) in gerbils than in rats. 4. Results suggest that a better ability of gerbil liver to keep calcium homeostasis than rat liver might be the cause of their relative resistance to necrosis. Higher intensity of CB and LP in gerbils than in rats might explain more intense effects on G6P-ase.

Late preventive effects against carbon tetrachloride-induced liver necrosis of the calcium chelating agent Calcion.

In agreement with the hypothesis that changes in calcium homeostasis might be significant in late stages of chemically-induced liver cell injury, a calcium chelating agent, Calcion, was able to partially prevent CCl4-induced liver necrosis observed at 24 h, when treatment was given as late as 6 or 10 h after the hepatotoxin. Calcion had minor or no effects on covalent binding of reactive metabolites to cellular components, or on lipid peroxidation or on CCl4 levels reaching the liver. Calcion treatment of CCl4-poisoned animals decreased CCl4-induced calcium increases in liver and increased glutathione levels decreased by hepatotoxin at 24 h. Calcion treatment was not able to prevent CCl4-induced fatty liver. Calcion protective effects were body temperature dependent but they were cancelled when Calcion-treated poisoned animals were kept normothermic. Results suggest that Calcion protective effects might be linked to calcium chelation or alternatively that they might derive from decreases in body temperature.

Further studies on the late preventive effects of the anticalmodulin trifluoperazine on carbon tetrachloride-induced liver necrosis.

Trifluoperazine (TFP) (50 mg/kg ip) administration to rats 6 or 10 hr after CCl4 (1 ml/kg ip in olive oil) significantly prevented liver necrosis but not fatty liver caused by the hepatotoxin at 24 hr as evidenced by either histology or electron microscopy. TFP given 6 hr after CCl4 significantly decreased the CCl4-induced increases in liver calcium content. TFP raised four to five times the liver glycogen content in control rats but was unable to modify decreased glycogen content of CCl4 poisoned animals. TFP administration increased phospholipid and protein synthesis as evidenced by studies on 32P incorporation into microsomal phospholipid and by experiments on [14C]leucine incorporation in microsomal protein fractions from control rat livers. No significant changes were observed in microsomal phospholipid degradation as studied by decay of label from 32P-prelabeled microsomal lipids or in increased protein degradation as evidenced by decay of label from [14C-guanidino]arginine-prelabeled microsomal proteins found in livers of control rats after TFP treatment. Electron microscopy observations of liver from control animals treated with TFP evidenced accumulation of glycogen in areas close to smooth endoplasmic reticulum (SER); large Golgi areas with an abundant number of lysosomes, and minor dilatation effects on the rough endoplasmic reticulum (RER) and nuclear membrane. Results suggest that TFP preventive effects might be due to the anticalmodulin actions of this drug.

Glutathione (GSH) content in livers from control and carbon tetrachloride poisoned rats treated with the calmodulin inhibitors thioridazine, imipramine or chlorpromazine.

Administration to rats of the calmodulin (CaM) inhibitors Thioridazine (TDZ) or Imipramine (IMP) (50 mg/kg ip) or Chlorpromazine (CPZ) at a dose of 25 mg/kg, ip 6 hr after olive oil or CCl4 (1 ml/kg, ip as a 20% olive oil solution) significantly increased the GSH content in liver of CCl4 poisoned animals but not in controls. The analysis of present observations and past results with Trifluoperazine, suggest that increases in GSH content in CCl4 poisoned animals treated with protective anticalmodulins are a consequence of prevention and not the cause of their preventive effects.

Early biochemical alterations in liver mitochondria from carbon tetrachloride poisoned rats.

Covalent binding of reactive metabolites of 14CCl4 were found 1 or 3 h after treatment with the solvent in the lipid and protein fractions of highly purified liver mitochondrial of rats. Most of the label was found in the phospholipid (PL) fraction, much less in cholesterol esters (ChE), and only minor quantities in other lipids. The reactive metabolites of 14CCl4 activated by isolated mitochondria interact mostly with ChE and far less with PL and other fractions. Both in vivo and in vitro covalent binding to PL is decreasing in the following order: phosphatidylethanolamine greater than diphosphatidylglycerol greater than phosphatidylcholine greater than sphingomyelin greater than lysophosphatidyl choline. No evidence of lipid peroxidation was found in liver mitochondrial lipids in the first 6 h and only a slight tendency of decrease in arachidonic acid concentration at 24 h. The incorporation of [14C] leucine in mitochondrial, microsomal or cytosolic proteins decreased as early as 1 h after treatment. These results, in agreement with previous reports suggest the existence of multiple sites in liver cells for the activation of CCl4. The transport of altered phospholipids and proteins and the inhibition of protein synthesis might contribute to the propagation of damage from the endoplasmic reticulum to other organelles.

Imipramine prevention of carbon tetrachloride-induced liver necrosis at late states of the intoxication process.

Imipramine administration (50 mg kg-1, i.p.) to Sprague-Dawley male rats (240-290 g) 6 or 10 h after CCl4 (1 ml kg-1, i.p.) partially prevents liver necrosis induced by the hepatotoxin. When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression. Imipramine administration prior to CCl4 does not modify levels of the hepatotoxin reaching the liver or the body temperature of CCl4 treated animals. Early preventive effects of imipramine on cytochrome P-450, might be attributed to inhibition of covalent interactions of reactive metabolites. The hypothesis that imipramine exerted late preventive effects by interfering with calcium deleterious effects or by modulation of protein and phospholipid synthesis or degradation is analyzed.

Late preventive effects of trifluoperazine on carbon tetrachloride-induced hepatic necrosis.

As a very preliminary test for a possible role of calmodulin in CCl4-induced hepatic injury, we studied the effects of the anticalmodulin drug trifluoperazine (TFP) on several deleterious actions of CCl4 on the liver. TFP administrated 30 min before or 6 or 10 hr after CCl4 significantly prevented hepatic necrosis induced by the hepatotoxin at 24 hr but not at 72 hr. TFP did not modify the CCl4 concentrations reaching the liver, or the intensity of the covalent binding of CCl4-reactive metabolites to hepatic microsomal proteins or lipids or the CCl4-induced cytochrome P-450 and glucose 6 phosphatase destruction. TFP administration decreased body temperature between 0 and 1 degree C in controls and between 1.2 and 3.5 degrees C in CCl4-treated animals during the 24-hr observation period. When TFP-treated CCl4-poisoned animals were kept normothermic, protective effects were eliminated. One possibility is that the protective effect of TFP might be due to a nonspecific action related to decreased body temperature. Alternatively, prevention might result from TFP inhibition of a late-occurring process critical for CCl4-induced cell necrosis requiring calmodulin participation. If this alternative were in operation, protective consequences of this inhibitory effect of TFP should be either canceled or counteracted in the normothermic TFP + CCl4-treated animal.

Effect of chlorpromazine on protein, phospholipid and RNA synthesis or degradation in rat liver.

Chlorpromazine (CPZ) administration to rats (25 mg/kg ip) significantly stimulated (14C)-leucine incorporation to liver microsomal proteins, (14C)-orotic acid incorporation to liver RNA and (32P) incorporation to liver microsomal lipids. CPZ administration did not modify the decay of radioactivity of liver microsomal lipids prelabeled with (32P) or that of microsomal proteins prelabeled with [(14C)-guanidino]-arginine. Results suggest that CPZ administration stimulates protein, phospholipids and RNA synthesis but does not affect their degradation. The relation of these findings with CPZ preventive effects on CCl4-induced liver injury is discussed.

Carbon tetrachloride activation by highly purified liver mitochondrial preparations.

Highly purified rat liver mitochondrial preparations were found to be able to activate CCl4 to reactive metabolites that bind covalently to lipids. Part of the process is of an enzymatic nature, but most of it is non-enzymatic. The enzymatic mitochondrial CCl4 activation operates more efficiently under anaerobic conditions; it requires NADPH, is CO sensitive, is inducible by phenobarbital pretreatment and is only weakly inhibited by high concentrations of cyanide or azide. The non-enzymatic mitochondrial CCl4 activation is not inhibited by CO and proceeds equally well under air or nitrogen.

Carbon tetrachloride-induced early biochemical alterations but not necrosis in pigeon's liver.

In contrast to what is well known to occur in rats, pigeons receiving CCl4 (1 ml/kg i.p.) were not susceptible to necrogenic effects of the hepatotoxin at 24 h. There were, however, other early biochemical alterations observable, such as depression of glucose 6 phosphatase activity, decrease in the cytochrome P-450 content and in aminopyrine-N-demethylase activity in pigeon liver microsomes at 3 and 6 h after CCl4 administration. Pigeon liver was able to activate CCl4 to reactive metabolites that bind covalently to lipids, but no CCl4-induced lipid peroxidation was proved by the diene hyperconjugation technique in pigeon liver microsomes at 1, 3 or 6 h after administration. Results suggest that covalent binding of CCl4-reactive metabolites are more relevant to early biochemical alterations induced by CCl4 than is lipid peroxidation. Absence of CCl4-induced necrosis in pigeon liver could be attributable to a smaller intensity of covalent binding interactions observed, when compared to susceptible species, and to absence of lipid peroxidation.