[Prevalence and associated factors of hospital malnutrition in a general hospital; Perú, 2012]. / Prevalencia y factores asociados a desnutrición hospitalaria en un hospital general; Perú, 2012.

INTRODUCTION: Hospital malnutrition is a prevalent problem that cause higher morbidity and mortality, poorer response to treatment and higher hospital stay and cost. OBJECTIVES: To determine the prevalence and factors associated with hospital malnutrition in a peruvian General Hospital. METHODS: Cross-sectional study including 211 hospitalized patients in Medicine and Surgery wards. Demographic, clinical and anthropometrical indicators' data was collected. Multivariate analysis was binary logistic regression. All tests had a significance level of 5% (p < 0.05). RESULTS: Prevalence of hospital malnutrition was 46.9%. Prevalences of caloric and protein malnutrition were 21.3% and 37.5%, respectively. Bivariate analysis found that hospitalization in Surgery wards was associated with a major risk of caloric (OR = 4.41, IC 95% [1.65-11.78]) and protein malnutrition (OR = 2.52, IC 95% [1.297-4.89]). During the analysis of quantitative variables, significant associations between number of comorbidities and caloric malnutrition (p = 0.031) was found, and also between the beginning of food intake changes and the presence of protein malnutrition (p = 0.031). Multivariate analysis showed significant association between diagnosis of neoplasm and presence of caloric malnutrition (OR = 5.22, IC [1.43-19.13]). CONCLUSIONS: Prevalence of hospital malnutrition was near 50%, as in similar studies. Protein-caloric malnutrition prevalences obtained, differ from the ones in a previous study in this hospital, which is explained by the different diagnostic criteria and particular characteristics of groups of patients, such as procedence ward and comorbidities. An association between protein-caloric and hospitalization in a Surgery ward was found; the reasons should be investigated in further studies.

Introducción: La desnutrición hospitalaria es un problema prevalente que genera mayor morbi-mortalidad, peor respuesta al tratamiento, mayor estancia y costo hospitalario. Objetivos: Determinar la prevalencia y factores asociados a desnutrición hospitalaria en un hospital general peruano. Métodos: Estudio analítico transversal de 211 pacientes en servicios de Medicina y Cirugía. Se analizó variables demográficas, clínicas e indicadores antropométricos. El análisis multivariado fue de regresión logística binaria. El nivel de significancia fue 5% (p < 0,05). Resultados: La prevalencia de desnutrición hospitalaria fue 46.9% y las de desnutrición calórica y proteica fueron 21,3% y 37,5% respectivamente. En el análisis bivariado, estar hospitalizado en el servicio de Cirugía se asoció a un mayor riesgo de desnutrición calórica (OR = 4,41, IC 95% [1,65-11,78]) y proteica (OR = 2,52, IC 95% [1,30-4,90]). Hubo asociación significativa entre el número de comorbilidades del paciente y desnutrición calórica (p = 0,031), y el tiempo de cambio de ingesta alimentaria y presencia de desnutrición proteica (p = 0,031). El análisis multivariado mostró asociación significativa entre el diagnóstico de neoplasia y la presencia de desnutrición calórica (OR = 5,22, IC 95% [1,43-19,13]). Conclusiones: La prevalencia de desnutrición hospitalaria fue cerca del 50%, coincidiendo con estudios similares. Las prevalencias de desnutrición calórica/proteica halladas difieren de las de un estudio anterior en este hospital, explicándose por parámetros de diagnóstico diferentes y características particulares de las poblaciones, como el servicio de procedencia y comorbilidades. Se encontró asociación entre desnutrición proteica/calórica y estar hospitalizado en el servicio de Cirugía; las razones deben investigarse en estudios posteriores.

Bimodal effects of platelet-derived growth factor on rat mesangial cell proliferation and death, and the role of lysophosphatidic acid in cell survival.

Although mesangial cell death has been shown to be correlated with mesangial cell mitosis in vivo, little is known about how these two apparently opposite events are regulated. We show that the addition of platelet-derived growth factor (PDGF; 10-50 ng/ml) to primary cultured rat mesangial cells for 24 h caused continuous proliferation along with simultaneous cell death. This process was accompanied by the fragmentation of DNA into nucleosomal oligomers, the development of apoptotic morphological changes in the nucleus, and increased expression of p53. Accumulation of lactate dehydrogenase (LDH) was also observed in the culture medium, suggesting that both apoptosis and necrosis are involved in the cell death mechanisms observed. We also observed that addition of 30 microM lysophosphatidic acid (LPA) to the culture medium greatly suppressed PDGF-induced cell death, leading to synergistically enhanced mesangial cell proliferation. DNA fragmentation, p53 expression and LDH release were all suppressed by LPA. We suggest that PDGF is a bifunctional molecule in mesangial cells that evokes both cell proliferation and cell death simultaneously, whereas LPA is a survival factor. We speculate that PDGF and LPA may play important roles in the progression or exacerbation of proliferative glomerulonephritis.

[ERPs changes during neuroleptic treatment in schizophrenia--a vulnerability marker in schizophrenia].

P300 amplitude reduction and P300 latency prolongation are consistent findings in schizophrenia, but it is unclear if these abnormalities were the effect of current or past neuroleptic treatment or were present at the onset of illness. We previously recorded ERPs in drug free schizophrenic patients (45 neuroleptic-naive and 56 previously treated with neuroleptics). In that study, P300 amplitude reduction was observed in both the neuroleptic-naive and the previously treated patients. However, both N200 and P300 latencies were prolonged only in the previously treated schizophrenic patients. In this study, we investigated ERPs in 60 drug free schizophrenic patients before and after neuroleptic treatment was begun. According to DSM-IV, schizophrenia subtype classification, 26 cases were paranoid type, 14 were disorganized, 2 catatonic and 18 undifferentiated. Twenty six of the patients were neuroleptic-naive and 34 had been previously treated. Sixty gender- and age-matched healthy controls were also investigated. ERPs were recorded during an auditory oddball task. The scalp EEGs were recorded from AgAgCl electrodes at 16 sites according to the international 10-20 system. Clinical symptoms were assessed using the Brief Psychiatric Rating Scale (BPRS). Before treatment, all schizophrenic patients displayed larger N200 amplitudes than the controls; however, increases in N200 amplitudes were not observed after neuroleptic treatment was begun. Both N200 and P300 latencies in the patients before treatment were prolonged only in those previously treated. Neuroleptic-naive patients demonstrated prolongation of both N200 and P300 latencies only after treatment. P300 amplitudes in patients were increased by neuroleptic treatment; but patients had smaller P300 amplitudes than the controls even after treatment. The change in P300 amplitudes (Pz) and the change in total BPRS scores by neuroleptic treatment were positively correlated in the patients whose duration of illness was six months or less (mean: 2.4 months). However, no correlation was observed for patients whose duration of illness was over six months (mean: 49.7 months). There were no significant differences in ERPs changes among subtypes. These results suggested that the P300 amplitude should be considered a vulnerability marker in schizophrenia and that both N200 and P300 latencies might be markers for neuroleptic exposure.

Abnormalities of auditory event-related potentials in schizophrenia prior to treatment.

BACKGROUND: P300 amplitude reduction is a consistent finding in schizophrenic patients, but it is unclear if this abnormality predates neuroleptic treatment or is present at onset of illness. METHODS: Auditory event-related potentials (ERPs), during a standard oddball paradigm, were recorded from 45 neuroleptic-naive schizophrenics, 56 drug-free, previously treated schizophrenics, and 73 healthy normal controls. Forty-seven of the schizophrenic subjects had their first episode within the past year. RESULTS: N200 amplitude did not differ among groups. P300 amplitude was significantly smaller in both neuroleptic-naive and previously treated schizophrenic groups compared to the control groups. There were no significant differences between the two schizophrenic groups in P300 amplitude. N200 and P300 latency were prolonged in previously treated schizophrenics compared to neuroleptic-naive schizophrenics and normal controls. CONCLUSIONS: The present study suggests that ERP abnormalities, especially P300 amplitude reduction, are already present prior to the administration of neuroleptic medication in the earliest stage of schizophrenia.

Activation studies of the multiple forms of prochymosin (prorennin).

Activation of the four separate components of prochymosin (prorennin) at pH 5.0 demonstrated that each zymogen was the precursor to an electrophoretically distinct chymosin (rennin). When the increase in milk-clotting activity with time was analysed, the mechanism of activation of unfractionated prochymosin, individual prochymosin components, and a mixture of the prochymosin fractions at pH 5.0 was shown to follow essentially autocatalytic kinetics. The activation of prochymosin C was completed in 70 h, whereas the other three fractions each required more than 110 h for complete activation under the same conditions. Intact prochymosin, the mixture of four components and prochymosin C were activated at similar rates. Interaction of the individual fractions during activation is suggested to explain the increased rate of the activation for the mixture. Comparison of autocatalytic activation of unfractionated prochymosin purified chromatographically at pH 6.7 and 5.7 demonstrated an increased rate of reaction of the zymogen prepared at the lower pH value. The possibility that prochymosin became susceptible to activation during preparation at pH values slightly below 6.0, as a result of changes in the proportion of the components or a conformational change and exposure of the active site, is discussed.

Binding of 63Ni (II) to ultrafiltrable constituents of rabbit serum in vivo and in vitro.

Binding of 63Ni(ll) to ultrafiltrable constituents of rabbit serum was studied (a) after in vitro incubation (2 h, 37 degrees C) of rabbit serum with 63NiCl2 (10-100 mumol/liter), and (b) at intervals (0.25-2 h) after in vivo administration of 63NiCl2(40-160 mumol/kg body wt,i.v.). Serum ultrafiltrates were fractionated by thin-layer chromatography, and the separated compounds made visible by autoradiography and by ninhydrin staining. Severel (congruent to 5) ultrafilitrable 63Ni-complexes were demonstrable as distinct radiodense 63Ni-bands with chromatographic mobilities corresponding to those of ninhydrin-positive bands. Unbound 63Ni(ll) was not detected in serum ultraviltrates in either the in vitro or in vivo experiments. In sera (n equals 10) incubated in vitro with 63Ni(ll) (10 mumol/liter), the mean percentage of ultrafiltrable 63Ni was 36% (range equals 33-38) of total serum 63Ni. In contrast, in sera (n equals 10) obtained 2 h after i.v. injection of 63Ni(ii) (40 mumol/kg), the mean concentration of total serum 63Ni was 10.8 mumol/kg), the mean concentration of total serum 63Ni was 10.8 mumol/liter (ranger equals 6-14), and the mean percentage of ultrafiltrable 63Ni was 15% (range equals 9-21) of total serum 63Ni. The disparity between the percentages of ultrafiltrable 63Ni obtained in vitro and in vivo was obviated when the in vivo experiments were performed in rabbits bilaterally nephrectomized, with ligated common bile ducts. This investigation confirms the existence of several nickel receptors in serum ultrafilitrates and substantiates the role of ultrafiltrable complexes in the excretion of nickel.

Fractionation and isolation of the multiple forms of prorennin (prochymosin).

The heterogeneity of prorennin was studied by chromatography on DEAE-cellulose and microgranular DEAE-cellulose columns, as well as by polyacrylamide-gel electrophoresis. Prorennin prepared by alum treatment, salting-out and chromatography was resolved into three components by a compound gradient of sodium phosphate on microgranular DEAE-cellulose. Polyacrylamide-gel electrophoresis confirmed the chromatographic results, but crystalline rennin was shown to consist of four bands. When prorennin was isolated directly by chromatography, four zymogen components were resolved on microgranular DEAE-cellulose with a modified compound gradient of sodium phosphate. Polyacrylamide-gel electrophoresis confirmed the existence of four multiple forms of prorennin as well as homogeneity of the chromatographic fractions.