Corrigendum: The association between metabolic disturbance and cognitive impairments in early-stage schizophrenia.

[This corrects the article DOI: 10.3389/fnhum.2020.599720.].

Alterations in sorting and secretion of hepatic apoA5 induce hypertriglyceridemia due to short-term use of olanzapine.

Long-term use of olanzapine, an antipsychotic drug, induces hypertriglyceridemia, resulting in a higher risk of cardiovascular disease. However, the effects and underlying mechanisms of short-term use of olanzapine on circulating triglyceride levels remain poorly understood. Here, the role of apolipoprotein A5 (apoA5), a regulator of triglyceride metabolism, was investigated in olanzapine-induced hypertriglyceridemia. Our multi-center clinical study recruited 36 schizophrenia patients who received short-term (8 weeks) of olanzapine. Besides, female C57BL/6J mice were treated with olanzapine (3 mg/kg/day versus 6 mg/kg/day) for 6 weeks. We demonstrated that short-term use of olanzapine increased plasma triglyceride and decreased plasma apoA5 levels in the patients and mice, with a negative correlation between the two factors. However, no obesity was observed in the patients and mice. Interestingly, olanzapine increased hepatic apoA5 protein in the mice, without significant changes in hepatic Apoa5 mRNA. Consistently, in vitro studies indicated that olanzapine increased medium triglyceride levels and decreased medium apoA5 levels in a dose-dependent manner in human HepG2 cells and primary mouse hepatocytes. Whereas the olanzapine treatment increased hepatic apoA5 protein in vitro, without effects on hepatic APOA5 mRNA. Of note, olanzapine increased the co-localization between apoA5 protein and accumulated lipid droplets in hepatocytes, as opposed to at the hepatocellular plasma membrane, in mouse liver as demonstrated by fluorescence staining. Therefore, our study indicated that short-term use of olanzapine induced hypertriglyceridemia due to defects of sorting and secretion of hepatic apoA5.

Corrigendum: The association between cognitive deficits and clinical characteristic in first-episode drug naïve patients with schizophrenia.

[This corrects the article DOI: 10.3389/fpsyt.2021.638773.].

Corrigendum: The Association Between Cognitive Deficits and Clinical Characteristic in First-Episode Drug Naïve Patients With Schizophrenia.

[This corrects the article DOI: 10.3389/fpsyt.2021.638773.].

The Association Between Cognitive Deficits and Clinical Characteristic in First-Episode Drug Naïve Patients With Schizophrenia.

Background: Schizophrenia is a severe mental disease which characterized by positive symptom, negative symptom, general pathology syndrome and cognitive deficits. In recent years, many studies have investigated the relationship between cognitive deficits and clinical characteristics in schizophrenia, but relatively few studies have been performed on first-episode drug-naïve patients. Methods: Eighty seven first-episode drug-naïve schizophrenia patients were assessed for positive symptom, negative symptom, general pathology symptom and cognitive deficits from the Positive and Negative Symptom Scale and MATRICS Consensus Cognitive Battery. Psychotics depression were assessed using the Calgary depressing scale for schizophrenia. The relationship between clinical characteristics and cognitive deficits were assessed using correlation analysis and linear regression analysis. Results: The prevalence of cognitive deficits among the patients in our study was 85.1% (74/87) which was much higher than that in the general population. According to correlation analysis, negative symptom was negatively correlated with speed of processing and social cognition, and general pathology showed a negative correlation with attention/vigilance. In addition, a positive correlation was found between age and speed of processing. No correlation was found between cognitive deficits and positive symptom. Conclusions: This study confirmed that negative symptom is negatively related with some domains of cognitive function in first-episode drug naïve schizophrenia patients. Trail Registration: NCT03451734. Registered March 2, 2018 (retrospectively registered).

Increased Appetite Plays a Key Role in Olanzapine-Induced Weight Gain in First-Episode Schizophrenia Patients

Weight gain and metabolic disturbances, potentially influenced by increased appetite, are common effects of olanzapine treatment in patients with schizophrenia. In this study, we explored the association between olanzapine-induced weight gain and metabolic effects with increased appetite. Drug-naïve, first-episode schizophrenia patients were treated with olanzapine for 12 weeks. Assessments included time to increased appetite, body weight, body mass index, biochemical indicators of blood glucose and lipids, proportion of patients who gained more than 7% or 10% of their baseline weight upon treatment conclusion, patients who developed dyslipidemia, and Positive and Negative Syndrome Scale scores. In total, 33 patients with schizophrenia receiving olanzapine were enrolled and 31 completed the study. During the 12-week olanzapine treatment, 77.4% (24/31) patients had increased appetite with 58.1% (18/31) patients having increased appetite within the first 4 weeks. The mean time for increased appetite was 20.3 days. More patients in the increased appetite group increased their initial body weight by more than 7% after 12 weeks when compared to patients with unchanged appetite (22/24 [91.7%] vs. 3/7 [42.9%], p = 0.004). Earlier increased appetite led to more weight gain during the following month. Overall, 50% of patients in the increased appetite group had dyslipidemia after 12 weeks. Our results demonstrated that olanzapine induced significantly appetite increase in first-episode patients with schizophrenia and appetite increase played a key role in olanzapine-induced weight gain and dyslipidemia. Clinical Trial Registration: NCT03451734. Registered March 2, 2018 (retrospectively registered).

Corrigendum: Increased Appetite Plays a Key Role in Olanzapine-Induced Weight Gain in First-Episode Schizophrenia Patients.

[This corrects the article DOI: 10.3389/fphar.2020.00739.].

The Association Between Metabolic Disturbance and Cognitive Impairments in Early-Stage Schizophrenia.

Background: Cognitive impairment is one of the core symptoms of schizophrenia, which is considered to be significantly correlated to prognosis. In recent years, many studies have suggested that metabolic disorders could be related to a higher risk of cognitive defects in a general setting. However, there has been limited evidence on the association between metabolism and cognitive function in patients with early-stage schizophrenia. Methods: In this study, we recruited 172 patients with early-stage schizophrenia. Relevant metabolic parameters were examined and cognitive function was evaluated by using the MATRICS Consensus Cognitive Battery (MCCB) to investigate the relationship between metabolic disorder and cognitive impairment. Results: Generally, the prevalence of cognitive impairment among patients in our study was 84.7% (144/170), which was much higher than that in the general population. Compared with the general Chinese setting, the study population presented a higher proportion of metabolic disturbance. Patients who had metabolic disturbance showed no significant differences on cognitive function compared with the other patients. Correlation analysis showed that metabolic status was significantly correlated with cognitive function as assessed by the cognitive domain scores (p < 0.05), while such association was not found in further multiple regression analysis. Conclusions: Therefore, there may be no association between metabolic disorder and cognitive impairment in patients with early-stage schizophrenia. Trial Registration: Clinicaltrials.gov, NCT03451734. Registered March 2, 2018 (retrospectively registered).

catena-Poly[bis[1-chloromethyl-1,4-diazoniabicyclo[2.2.2]octane] [cadmium(II)-tri-µ-chlorido-[chloridocadmium(II)]-di-µ-chlorido-[chloridocadmium(II)]-tri-µ-chlorido] tetrahydrate].

The title compound, {(C(7)H(15)N(2)Cl)(2)[Cd(3)Cl(10)]·4H(2)O}(n), consists of 1-chloromethyl-1,4-diazoniabicyclo[2.2.2]octane dications, one-dimensional inorganic chains of {[Cd(3)Cl(10)](4-)}(infinity) anions and uncoordinated water molecules. Each of the two independent Cd(II) ions, one with site symmetry 2/m and the other with site symmetry m, is octahedrally coordinated by chloride ions (two with site symmetry m and one with site symmetry 2), giving rise to novel polymeric zigzag chains of corner-sharing Cd-centred octahedra parallel to the c axis. The organic cations, bisected by mirror planes that contain the two N atoms, three methylene C atoms and the Cl atom, are ordered. Hydrogen bonds (O-H...Cl and O-H...O) between the water molecules (both with O atoms in a mirror plane) and the chloride anions of neighbouring chloridocadmate chains form a three-dimensional supramolecular network.

1-(2-Bromo-ethyl)-1,4-diazo-niabicyclo-[2.2.2]octane bromide dihydrogen phosphate-phospho-ric acid (1/1).

In the crystal structure of the title compound, C(8)H(17)BrN(2) (2+)·Br(-)·H(2)PO(4) (-)·H(3)PO(4), the cations, anions and phospho-ric acid mol-ecules are linked by O-H⋯O, N-H⋯O and O-H⋯Br hydrogen bonds into layers parallel to (101).

1-(2-Bromo-ethyl)-1,4-diazo-niabicyclo-[2.2.2]octane bromide tetra-fluoro-borate.

In the crystal of the title compound, C(8)H(17)BrN(2) (2+)·Br(-)·BF(4) (-), a weak inter-molecular N-H⋯Br hydrogen bond is observed between the cation and the bromide anion. A two-part disorder model was applied to the BF(4) (-) anion with a refined major-minor occupancy ratio of 0.837 (14):0.163 (14).

Dimethyl-ammonium 4-nitro-phenolate-4-nitro-phenol (1/1).

The title compound, C(2)H(8)N(+)·C(6)H(4)NO(3) (-)·C(6)H(5)NO(3), was synthesized from dimethyl-amine and 4-nitro-phenol in an overall yield of 85%. The dihdral angles between the nphenyl rings and their attached nitro groups are 5.7 (6) and 2.5 (7)°. In the crystal, there are strong hydrogen bonds between the ammonium group and the nitro-phenol and nitro-phenolate O atoms, and between the nitro-phenol and nitro-phenolate O atoms, forming a chain along the b-axis direction.

1-Hydroxy-4-aza-1-azoniabicyclo[2.2.2]octane picrate.

In the crystal structure of the title compound, C(6)H(13)N(2)O(+)·C(6)H(2)N(3)O(7) (-), the anions and cations are linked by O-H⋯O, C-H⋯O and C-H⋯N hydrogen bonds into a three-dimensional network. The O atoms of a nitro group of the picrate anion are disordered over two positions of equal occupancy.

(S)-2-(1H-Imidazol-1-yl)succinic acid.

The title compound, C(7)H(8)N(2)O(4), is a zwitterion, [formal name = (S)-3-carb-oxy-2-(imidazol-3-ium-1-yl)propano-ate], in which the deproton-ated negatively charged carboxyl-ate end shows almost identical C-O bond distances [1.248 (4) and 1.251 (4) Å] due to resonance. The mol-ecules are involved in inter-molecular O-H⋯O and N-H⋯O hydrogen bonds, which define a tightly bound three-dimensional structure.