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Summary A major concern in neuroscience is how cognitive ability in adulthood is affected and regulated by developmental mechanisms. The molecular bases of cognitive development are not well understood. We provide evidence for the involvement of the α2 isoform of Rac-specific guanosine triphosphatase (GTPase)-activating protein (RacGAP) α-chimaerin (chimerin) in this process. We generated and analyzed mice with global and conditional knockouts of α-chimaerin and its isoforms (α1-chimaerin and α2-chimaerin) and found that α-chimaerin plays a wide variety of roles in brain function and that the roles of α1-chimaerin and α2-chimaerin are distinct. Deletion of α2-chimaerin, but not α1-chimaerin, beginning during early development results in an increase in contextual fear learning in adult mice, whereas learning is not altered when α2-chimaerin is deleted only in adulthood. Our findings suggest that α2-chimaerin acts during development to establish normal cognitive ability in adulthood. [ABSTRACT FROM AUTHOR]

Highlights: [•] GTP cyclohydrolase I (GCH) is the enzyme for biosynthesis of tetrahydrobiopterin. [•] We examined the association of a functional rs841 with attentional function. [•] There was significant difference in scores of the CPT-IP test among the genotypes. [•] Our data suggest relation of the GCH expression to attentional function. [ABSTRACT FROM AUTHOR]

Abstract: Schizophrenia is a complex disorder with a high heritability. Relatives with schizophrenia have an increased risk not only for schizophrenia but also for schizophrenia spectrum disorders, such as schizotypal personality disorder. A single nucleotide polymorphism (SNP), rs1344706, in the Zinc Finger Protein 804A (ZNF804A) gene, has been implicated in susceptibility to schizophrenia by several genome-wide association studies, follow-up association studies and meta-analyses. This SNP has been shown to affect neuronal connectivities and cognitive abilities. We investigated an association between the ZNF804A genotype of rs1344706 and schizotypal personality traits using the Schizotypal Personality Questionnaire (SPQ) in 176 healthy subjects. We also looked for specific associations among ZNF804A polymorphisms and the three factors of schizotypy—cognitive/perceptual, interpersonal and disorganization—assessed by the SPQ. The total score for the SPQ in carriers of the risk T allele was significantly higher than that in individuals with the G/G genotype (p =0.042). For the three factors derived from the SPQ, carriers with the risk T allele showed a higher disorganization factor (p =0.011), but there were no differences in the cognitive/perceptual or interpersonal factors between genotype groups (p >0.30). These results suggest that the genetic variation in ZNF804A might increase susceptibility not only for schizophrenia but also for schizotypal personality traits in healthy subjects. [Copyright &y& Elsevier]

Sensory over-responsivity (SOR) causes social and daily distress in individuals with autism spectrum disorder (ASD). Compared to typically developed (TD) individuals, ASD individuals are at higher risk of adverse childhood experiences (ACEs), which induce abnormal neuronal development. However, whether or how ACEs are associated with abnormal neural development and SOR in ASD remains to be determined. Forty-five individuals with ASD and 43 TD individuals underwent T1-weighted and neurite orientation dispersion and density imaging; the axonal and dendritic densities were defined as the neurite density index (NDI). Voxel-based analyses were performed to explore the brain regions associated with SOR. The relationships between severity of ACEs and SOR, and NDI in the brain regions were examined. ASD individuals showed a significantly positive association between SOR severity and NDI in the right superior temporal gyrus (STG), which was not found in TD individuals. Severity of ACEs correlated significantly with that of SOR and NDI in the right STG in ASD; ASD individuals having severe SOR showed significantly higher NDI in the right STG than those with mild SOR and TD individuals. In individuals with ASD, NDI in the right STG, but not ACEs, could predict the severity of SOR, which was not shown in TD subjects. Our findings suggest that severe ACEs are involved in excessive neurite density in the right STG in ASD. ACE-associated excessive neurite density in the right STG is critical for SOR in ASD, which may be a therapeutic target in the future. [ABSTRACT FROM AUTHOR]

The current diagnostic tests for mood disorders, including major depressive disorder (MDD) and bipolar disorder (BD), have limitations. Inflammatory markers, growth factors, and oxidative stress markers are involved in the pathophysiology of mood disorders. A multi-assay biological diagnostic test combining these biomarkers might improve diagnostic efficiency. The plasma levels of soluble tumor necrosis factor receptor 2 (sTNFR2), epidermal growth factor (EGF), and myeloperoxidase were measured in 40 MDD patients, 40 BD patients and 40 controls in a Japanese population. We also investigated the plasma levels of these markers in 40 patients with schizophrenia to determine the utility of these markers in differential diagnosis. The plasma levels of sTNFR2 were significantly higher in BD and schizophrenia patients than in controls. The plasma levels of EGF and myeloperoxidase were significantly higher in patients with BD than in controls. The correct classification rate obtained from discriminant analysis with sTNFR2 and EGF between controls and mood disorders was 69.2%, with a sensitivity and specificity of 62.5% and 82.5%, respectively. The correct classification rate obtained from discriminant analysis with sTNFR2 and EGF between controls and BD was 85.0%, with a sensitivity and specificity of 77.6% and 92.5%, respectively. Our results suggest that sTNFR2 and EGF could be biological markers of BD. Further studies are needed to determine the utility of these markers in diagnostic tests for mood disorders. [ABSTRACT FROM AUTHOR]

• Aortic dissection is a rare and infrequently reported event before transplantation. • Transplant surgeons must consider whether the flow from the true lumen imposes adequate blood flow. • A vascular clamp close to the internal iliac artery can be used for aortic dissection. Aortoiliac lesions can influence the results of kidney transplantation and increase technical difficulties during surgery. Aortic dissection (AD) is a rare and infrequently reported event before transplantation, whereas immediate optimal perfusion is paramount for kidney transplantation. Thus, adequate blood flow imposed by the flow from the true lumen must be considered when choosing a target inflow vessel. A 67-year-old man on dialysis with end-stage renal disease caused by immunoglobulin A nephropathy was referred for kidney transplantation. He had successfully undergone conventional Stanford type A AD surgery 3 years ago. Pretransplant contrast-enhanced computed tomography angiography revealed termination of the distal intimal flaps within the common iliac arteries. Dilation of the descending aorta was also observed. Based on the meticulous vascular assessment, including consultation with the cardiovascular surgery department, the right internal iliac artery (IIA) was considered usable for anastomosis. He underwent living unrelated kidney transplantation from his 66-year-old wife. The patency and blood flow in the right IIA were also verified using intraoperative findings. Without any special procedure, we used a side-to-end arterial anastomosis between the donor renal artery and recipient IIA. After vascular clamp removal, the allograft was perfused homogeneously and immediately functioned. Patients receiving previous surgery for type A AD can successfully undergo kidney transplantation if the patency of the iliac arteries from the true lumen is confirmed by perioperative evaluation, and the artery can be carefully clamped to avoid possible further dissection. [ABSTRACT FROM AUTHOR]

• Autosomal dominant polycystic kidney disease is related to cardiovascular disorders. • Kidney transplantation performed after repair for aortic dissection is challenging. • A vascular clamp close to the internal iliac artery can be used for aortic dissection. Autosomal dominant polycystic kidney disease (ADPKD) is associated with several cardiovascular disorders, including aortic dissection, which preferentially occurs at the thoracic or abdominal level. Because there are few case reports describing surgical repair for aortic dissection followed by renal transplantation in patients with ADPKD, kidney transplantation performed after repair for aortic dissection remains challenging. A 34-year-old Japanese man with end-stage renal disease secondary to ADPKD underwent thoracic endovascular aortic repair for complicated acute type B aortic dissection 12 months earlier. A contrast computed tomography scan before transplantation revealed an aortic dissection involving the descending aorta proximal to the common iliac arteries and confirmed multiple large bilateral renal cysts. After simultaneous right native nephrectomy, the patient underwent preemptive living-donor kidney transplantation obtained from his mother. Intraoperatively, we noted that dissection of the external iliac vessels was difficult because of dense adhesions. Arterial clamping was performed immediately below the bifurcation of the internal iliac artery to prevent further aortic dissection of the external iliac artery. After end-to-end anastomosis to the internal iliac artery was completed and the vascular clamp was released, the kidney began to produce urine immediately. This case suggests that kidney transplantation in patients undergoing endovascular aortic repair for aortic dissection can be performed by adequately applying a vascular clamp proximal to the internal iliac artery during vascular anastomosis. [ABSTRACT FROM AUTHOR]

Abstract: Personality is considered to be an important aspect of schizophrenia, primarily because it may influence patients'' symptoms and social functioning. Specific personality traits are related to schizophrenia. The Temperament and Character Inventory (TCI) measures four traits of temperament – novelty seeking (NS), harm avoidance (HA), reward dependence (RD) and persistence (PS) – and three traits of character — self-directedness (SD), cooperativeness (CO) and self-transcendence (ST). We investigated associations between schizophrenia and personality traits using the TCI in a Japanese case–control sample (99 patients and 179 controls). Patients with schizophrenia scored higher on HA and ST and lower on NS, RD, SD and CO compared with controls in our case–control sample. We then performed a meta-analysis of samples from the published literature and our sample (384 patients and 656 controls). We found no evidence of heterogeneity among studies, except for NS in the overall population. Possible associations between personality traits (HA, RD, PS, SD, CO and ST) and schizophrenia were revealed. The effect sizes (Hedges'' g) of the temperament traits were 0.98 for HA, −0.43 for RD and −0.23 for PS, and those of the character traits were −0.96 for SD, −0.47 for CO and 0.61 for ST. These findings suggest that patients with schizophrenia have a unique temperament and character profile compared with the general population. [Copyright &y& Elsevier]

Abstract: Prepulse inhibition (PPI) of acoustic startle reflex (ASR) and personality, such as temperament and character, are considered candidate endophenotypes of schizophrenia. Gene polymorphism studies have provided evidence that both PPI and self-transcendence (ST) are polygenetic traits that involve several neurotransmitters, including the serotonin and dopamine signaling pathways. However, the relationship between PPI and temperament/character has not been properly addressed to date. Here, we investigated the link between PPI and temperament/character in 169 healthy Japanese subjects. A human startle response monitoring system was used to deliver acoustic startle stimuli and to record and score the electromyographic activity of the orbicularis oculi muscle. PPI was evaluated at signal-to-noise ratios (SnRs: intensity difference between background noise and prepulse) of +12, +16, and +20dB. The lead interval (from prepulse onset to pulse onset) was 120ms, and Temperament and Character Inventory was used in both groups. Significant correlations at SnR of +16 and +20dB to ST were identified. Our results suggest that impaired sensorimotor gating, evaluated as lower PPI of ASR, of healthy subjects is correlated with self transcendence, the character which is closely related with schizophrenia and schizotypy. [Copyright &y& Elsevier]

Abstract: Several studies have identified the possible involvement of sigma non-opioid intracellular receptor 1 (SIGMAR1) in the pathogenesis of schizophrenia. The Gln2Pro polymorphism in the SIGMAR1 gene has been extensively examined for an association with schizophrenia. However, findings across multiple studies have been inconsistent. We performed a meta-analysis of the association between the functional Gln2Pro polymorphism and schizophrenia using combined samples (1254 patients with schizophrenia and 1574 healthy controls) from previously published studies and our own additional samples (478 patients and 631 controls). We then used near-infrared spectroscopy to analyze the effects of the Gln2Pro genotype, a schizophrenia diagnosis and the interaction between genotype and diagnosis on activation of the prefrontal cortex (PFC) during a verbal fluency task (127 patients and 216 controls). The meta-analysis provided evidence of an association between Gln2Pro and schizophrenia without heterogeneity across studies (odds ratio=1.12, p =0.047). Consistent with previous studies, patients with schizophrenia showed lower bilateral activation of the PFC when compared to controls (p <0.05). We provide evidence that Pro carriers, who are more common among patients with schizophrenia, have significantly lower activation of the right PFC compared to subjects with the Gln/Gln genotype (p =0.013). These data suggest that the SIGMAR1 polymorphism is associated with an increased risk of schizophrenia and differential activation of the PFC. [Copyright &y& Elsevier]

Abstract: The Bcl2-interacting killer (BIK) gene interacts with cellular and viral survival-promoting proteins, such as Bcl-2, to enhance apoptosis. The BIK protein promotes cell death in a manner analogous to Bcl-2-related death-promoting proteins, Bax and Bak. There have been lower Bcl-2 levels and increased Bax/Bcl-2 ratio in the temporal cortex of patients with schizophrenia compared with those in controls. Because the death-promoting activity of BIK was suppressed in the presence of the cellular and viral survival-promoting proteins, the BIK protein is suggested as a likely target for antiapoptotic proteins. The purpose of this study is to investigate the association between genetic variants in the BIK gene and schizophrenia in a large Japanese population (1181 patients with schizophrenia and 1243 healthy controls). We found nominal evidence for association of alleles, rs926328 (χ 2 =4.44, p =0.035, odds ratio=1.13) and rs2235316 (χ 2 =4.41, p =0.036, odds ratio=1.13), with schizophrenia. However, these associations were no longer positive after correction for multiple testing (rs926328: corrected p =0.105, rs2235316: corrected p =0.108). We conclude that BIK might not play a major role in the susceptibility of schizophrenia in Japanese population. [Copyright &y& Elsevier]

Recent literature examining associations between cognitive function, clinical features, and violence in patients with schizophrenia has been growing; however, the results are inconsistent. Reports on social function and personality are limited. These studies are yet to be reflected in risk assessment tools and management plans. The aim of this study is to provide a resource for risk assessment and intervention studies by conducting multifaceted well-established assessments in a large population. Data from 355 patients with schizophrenia (112 patients with a history of violence; 243 patients without a history of violence) and 1265 healthy subjects were extracted from a large database of individuals with mental disorders in a general psychiatric population in Japan. The associations between violence in patients with schizophrenia and intellectual function, cognitive function (memory function, executive function, attentional function, verbal learning, processing speed, social cognition), clinical variables, personality traits, social function, and quality of life (QOL) were analyzed. Compared with healthy subjects, the schizophrenia group had broadly impaired cognitive function and social cognition, and their personality traits showed similar differences as those reported previously. Patients with schizophrenia with a history of violence showed significantly more impaired visual memory function (P = 1.9 × 10−5, Cohen's d = 0.34), longer hospitalization (P = 5.9 × 10−4, Cohen's d = 0.38), more severe excited factor on Positive and Negative Syndrome Scale (P = 1.6 × 10−4, Cohen's d = 0.47), higher self-transcendence personality construct on the Temperament and Character Inventory (P = 1.8 × 10−4, Cohen's d = 0.46), and shorter total working hours per week (P = 4.8 × 10−4, Cohen's d = 0.53) than those with schizophrenia without a history of violence. New findings, including impaired visual memory, a high self-transcendence personality trait, and shorter total working hours, could be focused on in future interventional research. • Schizophrenia with a history of violence involves prolonged hospitalization. • Schizophrenia with a history of violence involves excitation and fewer work hours. • Schizophrenia with a history of violence involves visual memory impairment. • Attentional function, executive function, or processing speed are not affected. • Schizophrenia with a history of violence is associated with self-transcendence. [ABSTRACT FROM AUTHOR]

This study aimed to analyze the incidence of subclinical rejection (SCR) in kidney transplantation patients and risk factors associated with SCR. We assessed 80 protocol biopsies taken within 2 years postoperatively in 41 adult patients who underwent living donor kidney transplantation between 2017 and 2020. All patients were on immunosuppressant therapy that included tacrolimus, mycophenolate mofetil, and steroids. The prevalence of Banff Borderline classification at 3, 6, and 12 months after transplantation was 4%, 5%, and 8 %, respectively, whereas none of the biopsies met the Banff criteria for acute T cell-mediated rejection throughout the study period. Active antibody-mediated rejection (ABMR) was only present in 8% of patients at 3 months after transplantation and chronic active ABMR at 6, 12, and 24 months after transplantation was detected in 10%, 13%, and 11% of the patients, respectively. Subgroup analysis revealed that 50% of the 6 patients with preformed anti-donor specific antibodies (DSAs) developed clinical or subclinical active ABMR within 3 months after transplantation, followed by chronic active ABMR according to serial histologic assessment. Conversely, only a small proportion of patients (3%) without preformed DSAs exhibited clinically active ABMR. SCR occurs too infrequently in patients with low immunologic risk and strong contemporary immunosuppression therapy to justify the diagnostic effort of serial protocol biopsies. However, protocol biopsies remain an indispensable tool in renal transplant monitoring and may be especially important in immunologically high-risk patients with pre-existing DSAs. [ABSTRACT FROM AUTHOR]

The Wechsler Adult Intelligence Scale (WAIS) has been widely used to assess intellectual functioning not only in healthy adults but also people with psychiatric disorders. The purpose of the study was to develop an optimal WAIS-3 short form (SF) to evaluate intellectual status in patients with schizophrenia. One hundred and fifty patients with schizophrenia and 221 healthy controls entered the study. To select subtests for SFs, following criteria were considered: 1) predictability for the full IQ (FIQ), 2) representativeness for the IQ structure, 3) consistency of subtests across versions, 4) sensitivity to functional outcome measures, 5) conciseness in administration time. First, exploratory factor analysis (EFA) and multiple regression analysis were conducted to select subtests satisfying the first and the second criteria. Then, candidate SFs were nominated based on the third criterion and the coverage of verbal IQ and performance IQ. Finally, the optimality of candidate SFs was evaluated in terms of the fourth and fifth criteria. The results suggest that the dyad of Similarities and Symbol Search was the most optimal satisfying the above criteria. [ABSTRACT FROM AUTHOR]

Background Clozapine-induced agranulocytosis (CIA)/clozapine-induced granulocytopenia (CIG) (CIAG) is a life-threatening event for schizophrenic subjects treated with clozapine. Methods To examine the genetic factor for CIAG, a genome-wide pharmacogenomic analysis was conducted using 50 subjects with CIAG and 2905 control subjects. Results We identified a significant association in the human leukocyte antigen (HLA) region (rs1800625, p = 3.46 × 10 −9 , odds ratio [OR] = 3.8); therefore, subsequent HLA typing was performed. We detected a significant association of HLA-B*59:01 with CIAG ( p = 3.81 × 10 −8 , OR = 10.7) and confirmed this association by comparing with an independent clozapine-tolerant control group ( n = 380, p = 2.97 × 10 −5 , OR = 6.3). As we observed that the OR of CIA (OR: 9.3~15.8) was approximately double that in CIG (OR: 4.4~7.4), we hypothesized that the CIG subjects were a mixed population of those who potentially would develop CIA and those who would not develop CIA (non-CIA). This hypothesis allowed the proportion of the CIG who were non-CIA to be calculated, enabling us to estimate the positive predictive value of the nonrisk allele on non-CIA in CIG subjects. Assuming this model, we estimated that 1) ~50% of CIG subjects would be non-CIA; and 2) ~60% of the CIG subjects without the risk allele would be non-CIA and therefore not expected to develop CIA. Conclusions Our results suggest that HLA-B*59:01 is a risk factor for CIAG in the Japanese population. Furthermore, if our model is true, the results suggest that rechallenging certain CIG subjects with clozapine may not be always contraindicated. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess postural instability in patients with schizophrenia using a pressure-sensitive platform and to examine the effects of anxiety, psychiatric symptoms, and the use of neuroleptic medications on postural sway. Participants were 23 patients with schizophrenia and 23 healthy controls. We found that the patients showed greater overall postural instability than the controls. Furthermore, they demonstrated greater instability when the test was performed with the eyes closed than with the eyes open. However, removal of visual input had less impact on the indices of postural instability in the patients than in the controls, suggesting that schizophrenia is associated with difficulties in integrating visual information and proprioceptive signals. Furthermore, in contrast to the controls, anxiety exacerbated postural instability in the patients. There were significant associations between postural stability and psychiatric symptoms in the patients without extrapyramidal symptoms, whereas medication dose did not significantly correlate with postural stability. [ABSTRACT FROM AUTHOR]

Hypofunction of the N-methyl- d -aspartate (NMDA) subtype of glutamate receptors may be involved in the pathophysiology of schizophrenia. Many studies have investigated peripheral NMDA receptor-related glutamatergic amino acid levels because of their potential as biological markers. Peripheral d -serine levels and the ratio of d -serine to total serine have been reported to be significantly lower in patients with schizophrenia than in controls. Peripheral d -serine levels and the d -/ l -serine ratio have also been reported to significantly increase in patients with schizophrenia as their clinical symptoms improve from the time of admission to the time of discharge. In this study, we examined whether peripheral NMDA receptor-related glutamatergic amino acids levels were altered in patients with treatment-resistant schizophrenia compared to controls and whether these peripheral amino acids levels were altered by clozapine treatment. Twenty-two patients with treatment-resistant schizophrenia and 22 age- and gender-matched healthy controls were enrolled. The plasma levels of d -serine, l -serine, glycine, glutamate, and glutamine were measured before and after clozapine treatment. We found that the plasma levels of d -serine and the d -/ l -serine ratio were significantly lower in the patients before clozapine treatment than in the controls. The d -/ l -serine ratio was significantly increased by clozapine treatment in patients, and no significant difference was observed in the plasma levels of d -serine and the d -/ l -serine ratio between the patients after clozapine treatment and the controls. We also found that plasma glycine levels and the glycine/ l -serine ratio were significantly increased following clozapine treatment in the patients, and the glycine/ l -serine ratio was significantly higher in the patients after clozapine treatment than in the controls. There was no significant difference in the plasma levels of glutamate and glutamine both between the controls and patients and between before and after clozapine treatment. This study firstly demonstrated changes of d -/ l -serine and glycine/ l -serine ratio between before and after clozapine treatment, suggesting that the plasma d -/ l -serine ratio and glycine/ l -serine ratio could be markers of therapeutic efficacy or clinical state in treatment-resistant schizophrenia. [ABSTRACT FROM AUTHOR]

Background Tyrosinase, the rate-limiting enzyme required for melanin production, has been targeted to develop active brightening/lightening materials for skin products. Unexpected depigmentation of the skin characterized with the diverse symptoms was reported in some subjects who used a tyrosinase-competitive inhibiting quasi-drug, rhododendrol. Objective To investigate the mechanism underlying the depigmentation caused by rhododendrol-containing cosmetics, this study was performed. Methods The mechanism above was examined using more than dozen of melanocytes derived from donors of different ethnic backgrounds. The RNAi technology was utilized to confirm the effect of tyrosinase to induce the cytotoxicity of rhododendrol and liquid chromatography-tandem mass spectrometry was introduced to detect rhododendrol and its metabolites in the presence of tyrosinase. Results Melanocyte damage was related to tyrosinase activity at a certain threshold. Treatment with a tyrosinase -specific siRNA was shown to dramatically rescue the rhododendrol-induced melanocyte impairment. Hydroxyl-rhododendrol was detected only in melanocytes with higher tyrosinase activity. When an equivalent amount of hydroxyl-rhododendrol was administered, cell viability was almost equally suppressed even in melanocytes with lower tyrosinase activity. Conclusion The generation of a tyrosinase-catalyzed hydroxyl-metabolite is one of the causes for the diminishment of the melanocyte viability by rhododendrol. [ABSTRACT FROM AUTHOR]

Highlights: [•] Expression levels of the genes identified in GWAS of schizophrenia were measured. [•] Two separate sample sets of postmortem brains of schizophrenia patients were used. [•] No difference was observed between the schizophrenia patients and controls. [•] No relationship between the associated SNPs and the gene expression was observed. [•] RPGRIP1L gene expression was significantly increased in the bipolar disorder. [Copyright &y& Elsevier]

Highlights: [•] Plasma levels of mature BDNF in schizophrenia were measured for the first time. [•] No significant difference was observed in mature BDNF levels in schizophrenia. [•] MMP-9 plasma levels were significantly increased in patients with schizophrenia. [•] Plasma mature BDNF levels were significantly correlated with plasma MMP-9 levels. [Copyright &y& Elsevier]

Abstract: The chitinase 3-like 1 (CHI3L1) gene, a cellular survival factor against several environmental and psychosocial stresses, has been sown to be more highly expressed in the hippocampus and prefrontal cortex of patients with schizophrenia than unaffected individuals. We recently reported a significant association between schizophrenia and SNP rs4950928, which is located in the promoter region of the CHI3L1 gene, in a Japanese population. The G-allele at this SNP in the gene has been associated with higher transcriptional activity in a luciferase reporter assay and with higher mRNA levels in the peripheral blood cells of patients with schizophrenia. We investigated the impact of the CHI3L1 polymorphism rs4950928 on serum YKL-40 levels, the protein product of CHI3L1. We found that individuals with the G-allele, who were more prevalent among patients with schizophrenia, had significantly higher serum YKL-40 levels (p =0.043). Personality traits are considered to be an important aspect of schizophrenia primarily because they may influence symptoms and social functioning. Personality trait analyses using the temperament and character inventory (TCI) indicated that schizophrenic patients have a unique personality profile that appears to be present across cultures. We hypothesized that higher serum YKL-40 levels are associated with personality trait in patients with schizophrenia. Thus, we next examined the impact of the risk CHI3L1 polymorphism on personality traits using the TCI. We found that individuals with the G-allele had significantly higher self-transcendence scores (p =0.0054). These findings suggest possible associations between the SNP in the CHI3L1 gene, the risk for schizophrenia, and higher serum YKL-40 levels and personality traits in a Japanese population. [Copyright &y& Elsevier]