Aim To investigate development of refeeding hypophosphatemia during the refeeding period and the extent of the decrease in the serum phosphorus level among anorexia nervosa patients with severe malnutrition. Objective The accurate prediction of the severity of refeeding hypophosphatemia in patients with anorexia nervosa during acute treatment is of great importance. Although some predictors were found in previous reports, these studies used binominal data—the presence or absence of hypophosphatemia—as an outcome indicator but not the extent of serum phosphorus level decrease. It is crucial in clinical settings to predict the extent of the serum phosphorus level decrease as well as development of refeeding hypophosphatemia, in particular, for patients with severe malnutrition, who has a higher risk of death. Methods We investigated 63 admissions from 37 patients with anorexia nervosa who had severe malnutrition (admission body mass index 11.5 ± 1.6) and carried out a linear discriminant regression analysis for the development of refeeding hypophosphatemia. The extent of the decrease in the serum phosphorus level were investigated using multiple linear regression analysis. Explanatory variables included data upon admission (age, sex, body mass index, blood urea nitrogen to creatinine ratio, albumin, initial serum phosphorus level, anorexia nervosa type, i.e., restrictive or binge-purge) as well as treatment-related indicators (calorie intake, amount of phosphate administered, and rate of weight gain). Results Development of refeeding hypophosphatemia and a change in serum phosphorus levels were predicted by body mass index and elevated blood urea nitrogen to creatinine ratio. Conclusions Our study found that refeeding hypophosphatemia among patients with severe malnutrition was predicted by a lower body mass index and elevated blood urea nitrogen to creatinine ratio.

Background: Glutathione is among the important antioxidants to prevent oxidative stress. However, the relationships between abnormality in the glutathione system and pathophysiology of schizophrenia remain uncertain due to inconsistent findings on glutathione levels and/or glutathione-related enzyme activities in patients with schizophrenia. Methods: A systematic literature search was conducted using Embase, Medline, PsycINFO, and PubMed. Original studies, in which three metabolite levels (glutathione, glutathione disulfide, and total glutathione (glutathione+glutathione disulfide)) and five enzyme activities (glutathione peroxidase, glutathione reductase, glutamate-cysteine ligase, glutathione synthetase, and glutathione S-transferase) were measured with any techniques in both patients with schizophrenia and healthy controls, were included. Standardized mean differences were calculated to determine the group differences in the glutathione levels with a random-effects model. Results: We identified 41, 9, 15, 38, and seven studies which examined glutathione, glutathione disulfide, total glutathione, glutathione peroxidase, and glutathione reductase, respectively. Patients with schizophrenia had lower levels of both glutathione and total glutathione and decreased activity of glutathione peroxidase compared to controls. Glutathione levels were lower in unmedicated patients with schizophrenia than those in controls while glutathione levels did not differ between patients with first-episode psychosis and controls. Conclusions: Our findings suggested that there may be glutathione deficits and abnormalities in the glutathione redox cycle in patients with schizophrenia. However, given the small number of studies examined the entire glutathione system, further studies are needed to elucidate a better understanding of disrupted glutathione function in schizophrenia, which may pave the way for the development of novel therapeutic strategies in this disorder.

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A BS TRACT: Background: We recently developed a positron emission tomography (PET) probe, [ 18 F]PM-PBB3, to detect tau lesions in diverse tauopathies, including mixed three-repeat and four-repeat (3R + 4R) tau fibrils in Alzheimer's disease (AD) and 4R tau aggregates in progressive supranuclear palsy (PSP). For wider availability of this technology for clinical settings, biasfree quantitative evaluation of tau images without a priori disease information is needed. Objective: We aimed to establish tau PET pathology indices to characterize PSP and AD using a machine learning approach and test their validity and tracer capabilities. Methods: Data were obtained from 50 healthy control subjects, 46 patients with PSP Richardson syndrome, and 37 patients on the AD continuum. Tau PET data from 114 regions of interest were subjected to Elastic Net cross-validation linear classification analysis with a oneversus-the-rest multiclass strategy to obtain a linear function that discriminates diseases by maximizing the area under the receiver operating characteristic curve.We defined PSP-and AD-tau scores for each participant as values of the functions optimized for differentiating PSP (4R) and AD (3R + 4R), respectively, from others. Results: The discriminatory ability of PSP-and AD-tau scores assessed as the area under the receiver operating characteristic curve was 0.98 and 1.00, respectively. PSPtau scores correlated with the PSP rating scale in patients with PSP, and AD-tau scores correlated with Mini-Mental State Examination scores in healthy control-AD continuum patients. The globus pallidus and amygdala were highlighted as regions with high weight coefficients for determining PSP-and AD-tau scores, respectively. Conclusions: These findings highlight our technology's unbiased capability to identify topologies of 3R + 4R versus 4R tau deposits.

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