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Kenji Hayashi,1 Reiji Yoshimura,1 Shingo Kakeda,2 Taro Kishi,3 Osamu Abe,4 Wakako Umene-Nakano,1 Asuka Katsuki,1 Hikaru Hori,1 Atsuko Ikenouchi-Sugita,1 Keita Watanabe,2 Satoru Ide,2 Issei Ueda,2 Junji Moriya,2 Nakao Iwata,3 Yukunori Korogi,2 Marek Kubicki,5 Jun Nakamura1 1Department of Psychiatry, 2Department of Radiology, University of Occupational and Environmental Health, Kitakyushu, Japan; 3Department of Psychiatry, Fujita Health University, Toyoake, Japan; 4Department of Radiology, Nihon University School of Medicine, Tokyo, Japan; 5Psychiatry Neuroimaging Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Abstract: We investigated the association between the Val158Met polymorphism of the catechol-O-methyltransferase (COMT) gene, the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene, and white matter changes in patients with major depressive disorder (MDD) and healthy subjects using diffusion tensor imaging (DTI). We studied 30 patients with MDD (17 males and 13 females, with mean age ± standard deviation [SD] =44±12 years) and 30 sex- and age-matched healthy controls (17 males and 13 females, aged 44±13 years). Using DTI analysis with a tract-based spatial statistics (TBSS) approach, we investigated the differences in fractional anisotropy, radial diffusivity, and axial diffusivity distribution among the three groups (patients with the COMT gene Val158Met, those with the BDNF gene Val66Met, and the healthy subjects). In a voxel-wise-based group comparison, we found significant decreases in fractional anisotropy and axial diffusivity within the temporal lobe white matter in the Met-carriers with MDD compared with the controls (P

Naoki Goto1, Reiji Yoshimura1, Shingo Kakeda2, Joji Nishimura2, Junji Moriya2, Kenji Hayashi1, Asuka Katsuki1, Hikaru Hori1, Wakako Umene-Nakano1, Atsuko Ikenouchi-Sugita1, Yukunori Korogi2, Jun Nakamura11Department of Psychiatry, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, Japan; 2Department of Radiology, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, JapanObjective: To study the effects of treatment with atypical antipsychotic drugs on brain levels of glutamate plus glutamine in early-stage first-episode schizophrenia.Participants: Sixteen patients (eight males, eight females; aged 30 ± 11 years) completed the study.Methods: We used administered 6 months of atypical antipsychotic drugs and used proton magnetic resonance spectroscopy to evaluate the results.Results: We found that the administration of atypical antipsychotic drugs for 6 months decreased the glutamate plus glutamine/creatine ratio in the frontal lobe. These results suggest that the administration of atypical antipsychotic drugs for at least 6 months decreased glutamatergic neurotransmissions in the frontal lobe in early-stage first-episode schizophrenia, but there was no difference in frontal-lobe levels between patients and control subjects before administration.Conclusion: Taking these findings into account, the glutamatergic and GABAergic neurons are implicated in early-stage first-episode schizophrenia, but in complex ways.Keywords: Proton magnetic resonance spectroscopy, creatine, frontal lobe, parieto-occipital node, left basal ganglia

We compared the signal intensity of motor and sensory cortices on T2-weighted and FLAIR images obtained at 3T and 1.5T. MR images of 101 consecutive neurologically normal patients who underwent both 1.5T and 3T MRI were retrospectively evaluated. The signal intensities of motor and sensory cortices were analyzed both visually and quantitatively in comparison with superior frontal cortex. On T2-weighted images, decreased signal intensity of the motor cortex was seen in 6 (32%) of 19 patients aged 61-70 years and 14 (48%) of 29 at 71 years and older at 3T, compared with only 1 (5%) and 2 (7%) at 1.5T, respectively. On FLAIR images, the decreased signal intensity in the motor cortex was also more frequently seen at 3T than at 1.5T. The mean CNRs of motor and sensory cortices were significantly higher at 3T than at 1.5T on both T2-weighted and FLAIR images. The decreased signal intensity in the motor cortex was frequently seen at 3T compared with 1.5T. Knowledge of the finding at 3T can help the recognition of abnormalities of the motor cortex caused by various pathologic conditions. [ABSTRACT FROM AUTHOR]

Abstract Fibroblast growth factor (FGF) 23, a circulating 26-kDa peptide produced by osteogenic cells, is a novel phosphaturic factor. In our previous study, binge-eating/purging type anorexia nervosa (AN-BP) patients had elevated plasma intact FGF23 (iFGF23) levels, while restricting type (AN-R) patients had plasma iFGF23 levels similar to healthy controls. Although bulimia nervosa (BN) patients as well as some patients with AN-BP regularly engage in binge eating, there have been no studies regarding plasma iFGF23 levels in BN patients. Therefore, this study was performed to determine plasma iFGF23 concentrations in BN patients and healthy controls. The study population consisted of 13 female BN patients and 11 healthy female controls. Blood samples were collected from all subjects after overnight fasting. Plasma iFGF23 was measured using an ELISA kit in a cross-sectional manner. The two-tailed Mann-Whitney U-test was used to assess differences between BN patients and healthy controls. In addition, BN patients were divided into two groups based on questionnaire-reported binge eating frequency immediately prior to participation in this study: high frequency of binge eating (once a week or more; HF group; n = 8) and low frequency of binge eating (less than once a week; LF group; n = 5). Two-tailed Mann-Whitney U-test with Bonferroni's correction was performed after the Kruskal-Wallis test to assess differences between HF group, LF group, and healthy controls. Median (quartiles) plasma iFGF23 levels were greater in BN patients (35.5 [14.8-65.0] pg/ml) than in controls (3.8 [not detected-5.3] pg/ml; p = 0.002). In addition, median (quartiles) plasma iFGF23 levels were greater in the HF group (62.3 [44.4-73.4] pg/ml) than in controls (p < 0.001) and in the LF group (12.9 [not detected-30.3] pg/ml; p = 0.011), while there were no differences between the LF group and controls (p = 0.441). This is the first study to show that BN patients have elevated plasma iFGF23 levels. Moreover, this study showed that BN patients with a high frequency of binge eating have elevated plasma iFGF23 levels, while iFGF23 levels are similar to healthy controls in those with a low frequency of binge eating. Plasma iFGF23 level may be a suitable indicator of binge eating in BN patients.

Abstract Background Fibroblast growth factor (FGF)23 is a novel phosphaturic factor associated with inorganic phosphate homeostasis. Previous human studies have shown that serum FGF23 levels increase in response to a high phosphate diet. For anorexia nervosa (AN) patients, inorganic phosphate homeostasis is important in the clinical course, such as in refeeding syndrome. The purpose of this study was to determine plasma levels of intact FGF23 (iFGF23) in restricting-type AN (AN-R) patients, binge-eating/purging-type AN (AN-BP) patients, and healthy controls. Methods The subjects consisted of 6 female AN-R patients, 6 female AN-BP patients, and 11 healthy female controls; both inpatients and outpatients were included. Plasma iFGF23, 1,25-dihydroxyvitamin D (1,25-(OH)2D), and 25-hydroxyvitamin D (25-OHD) levels were measured. Data are presented as the median and the range. A two-tailed Mann-Whitney U-test with Bonferroni correction was used to assess differences among the three groups, and a value of p < 0.017 was considered statistically significant. Results There were no differences between AN-R patients and controls in the iFGF23 and 1,25-(OH)2D levels. In AN-BP patients, the iFGF23 level (41.3 pg/ml; range, 6.1–155.5 pg/ml) was significantly higher than in controls (3.8 pg/ml; range, not detected-21.3 pg/ml; p = 0.001), and the 1,25-(OH)2D was significantly lower in AN-BP patients (7.0 pg/ml; range, 4.2–33.7 pg/ml) than in controls (39.7 pg/ml; range, 6.3–58.5 pg/ml; p = 0.015). No differences in plasma 25-OHD levels were observed among the groups. Conclusion This preliminary study is the first to show that plasma iFGF23 levels are increased in AN-BP patients, and that these elevated plasma FGF23 levels might be related to the decrease in plasma 1,25-(OH)2D levels.

The restricted mean survival time provides a straightforward clinical measure that dispenses with the need for proportional hazards assumptions. We focus on two strategies to directly model the survival time and adjust covariates. Firstly, pseudo-survival time is calculated for each subject using a leave-one-out approach, followed by a model analysis that adjusts for covariates using all pseudo-values. This method is used to reflect information of censored subjects in the model analysis. The second approach adjusts for covariates for those subjects with observed time-to-event while incorporating censored subjects using inverse probability of censoring weighting (IPCW). This paper evaluates these methods' power to detect group differences through computer simulations. We find the interpretation of pseudo-values challenging with the pseudo-survival time method and confirm that pseudo-survival times deviate from actual data in a primary biliary cholangitis clinical trial, mainly due to extensive censoring. Simulations reveal that the IPCW method is more robust, unaffected by the balance of censors, whereas pseudo-survival time is influenced by this balance. The IPCW method retains a nominal significance level for the type-1 error rate, even amidst group differences concerning censor incidence rates and covariates. Our study concludes that IPCW and pseudo-survival time methods differ significantly in handling censored data, impacting parameter estimations. Our findings suggest that the IPCW method provides more robust results than pseudo-survival time and is recommended, even when censor probabilities vary between treatment groups. However, pseudo-survival time remains a suitable choice when censoring probabilities are balanced., Competing Interests: Declaration of competing interest Keisuke Hanada does not have a conflict of interest. Junji Moriya does not have a conflict of interest. Masahiro Kojima does not have a conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)