Estimation of energy requirements for mechanically ventilated, critically ill patients using nutritional status

BACKGROUND: There is very little information on what is considered an adequate energy intake for mechanically ventilated, critically ill patients. The purpose of the present study was to determine this energy requirement by making use of patients' nutritional status. METHODS: The study was conducted in a multidisciplinary intensive care unit of Taichung Veterans General Hospital, Taiwan. Patients were hemodynamically stable and not comatose, and were requiring at least 7 days of mechanical ventilation. Fifty-four patients successfully completed this study. The resting energy expenditure was measured using indirect calorimetry. The total energy requirement was considered 120% of the measured energy expenditure. The daily nutrient intake was recorded. Nutritional status was assessed using single and multiple parameters, nitrogen balance, and medical records, and was performed within 24 hours of admission and after 7 days in the intensive care unit. RESULTS: Fifteen patients were being underfed (<90% of total energy requirement), 20 patients were in the appropriate feeding (AF) group (within ± 10% of total energy requirement), and 19 patients received overfeeding (>110% of total energy requirement). Patients in the underfeeding group received only 68.3% of their energy requirement, while the overfeeding group patients received up to 136.5% of their required calories. Only patients in the AF group had a positive nitrogen balance (0.04 ± 5.1) on day 7. AF group patients had a significantly higher Nutritional Risk Index value at day 7 than at day 1. CONCLUSION: AF patients had more improvement in nutritional status than patients in the other feeding groups. To provide at least 120% of the resting energy expenditure seemed adequate to meet the caloric energy needs of hemodynamically stable, mechanically ventilated, critically ill patients

Nicastrin Functions as a γ-Secretase-Substrate Receptor

Summaryγ-secretase catalyzes the intramembrane cleavage of amyloid precursor protein (APP) and Notch after their extracellular domains are shed by site-specific proteolysis. Nicastrin is an essential glycoprotein component of the γ-secretase complex but has no known function. We now show that the ectodomain of nicastrin binds the new amino terminus that is generated upon proteolysis of the extracellular APP and Notch domains, thereby recruiting the APP and Notch substrates into the γ-secretase complex. Chemical- or antibody-mediated blocking of the free amino terminus, addition of purified nicastrin ectodomain, or mutations in the ectodomain markedly reduce the binding and cleavage of substrate by γ-secretase. These results indicate that nicastrin is a receptor for the amino-terminal stubs that are generated by ectodomain shedding of type I transmembrane proteins. Our data are consistent with a model where nicastrin presents these substrates to γ-secretase and thereby facilitates their cleavage via intramembrane proteolysis

Activation of myosin-I by members of the Ste20p protein kinase family

NRC publication: Ye

Morphological Characters of Bird Species in Taiwan

We documented body measurements of birds captured during 1987-1995 banding research in Taiwan by Wild Bird Society Taiwan. A total of 223 bird species with measurements of body mass, length of body, head, tail, bill and tarsus, and maximum wing span were compiled for the database. Body mass, length of bill, and length of tarsus of 85 species that had sample sizes > 20 were reported. In addition, we also compared our data with that from Dunning (1993). Among the ten species eligible for further analyses, we found that eight species showed significant differences in body mass between our data and that of Dunning (1993). Our results together with our recent studies (Lee et al, 2004; Ding et al., 2005) showed that compiling banding research data contribute to predict ecological parameters of bird studies in community, ecosystem and landscape levels

Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations

Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disorder. Mutations in presenilins 1 and 2 (PS1 and PS2) account for approximately 40% of familial AD (FAD) cases. FAD mutations and genetic deletions of presenilins have been associated with calcium (Ca(2+)) signaling abnormalities. We demonstrate that wild-type presenilins, but not PS1-M146V and PS2-N141I FAD mutants, can form low-conductance divalent-cation-permeable ion channels in planar lipid bilayers. In experiments with PS1/2 double knockout (DKO) mouse embryonic fibroblasts (MEFs), we find that presenilins account for approximately 80% of passive Ca(2+) leak from the endoplasmic reticulum. Deficient Ca(2+) signaling in DKO MEFs can be rescued by expression of wild-type PS1 or PS2 but not by expression of PS1-M146V or PS2-N141I mutants. The ER Ca(2+) leak function of presenilins is independent of their gamma-secretase activity. Our data suggest a Ca(2+) signaling function for presenilins and provide support for the "Ca(2+) hypothesis of AD."status: publishe