Hepatocellular carcinoma(HCC)expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming.Aldolase A(ALDOA)plays a prominent role in glycolysis;however,little is known about its role in HCC development.In the present study,we aim to explore how ALDOA is involved in HCC proliferation.HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout,which is consistent with ALDOA overexpression encouraging HCC prolifera-tion.Mechanistically,ALDOA knockout partially limits the glycolytic flux in HCC cells.Meanwhile,ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase;ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function.A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun,and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells.In HCC patients,the expression level of ALDOA was correlated with the phosphorylation level of c-Jun(Thr93)and poor prognosis.Remarkably,hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models,and the knockdown of Aldoa strikingly decreased HCC development in vivo.Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription,opening additional avenues for anti-cancer therapies.

Objective:To analyze trends in urticaria incidence among children aged 0 - 14 years in China from 1990 to 2021, to explore its changing patterns in different age, period, and cohort groups, and to investigate the impact of age and air pollutants on the incidence trends.Methods:Data were obtained from the Global Burden of Disease Database (GBD2021) , including the number of urticaria cases, crude incidence rates, and age-standardized incidence rates among children aged 0 - 14 years of different genders in China from 1990 to 2021. The Joinpoint regression model was used to calculate the annual percentage change (APC) and average annual percentage change (AAPC) to assess temporal trends in incidence rates. An age-period-cohort model was applied to assess the effects of age, period, and cohort on urticaria incidence. Data on the annual emissions of 4 air pollutants (SO 2, CO, PM 2.5, and PM 10) in China from 1990 to 2021 were obtained from the Emissions Database for Global Atmospheric Research (EDGAR) , and a multivariable meta-regression model was used to explore the relationship between air pollutants and urticaria incidence. Results:From 1990 to 2021, the age-standardized incidence rate of urticaria among children aged 0 - 14 years in China demonstrated a slight overall downward trend (AAPC = -0.03%, P < 0.01) . The incidence rate was generally higher in female children than in male children, and the decline in incidence rates was greater in female children than in male children (female AAPC = -0.02%, male AAPC = -0.01%, both P < 0.01) . The age-period-cohort model indicated that the risk of urticaria decreased with advancing age: with the age group of 0 - 4 years as the reference ( RR = 1.000) , the risk of urticaria significantly decreased in the age group of 5 - 9 years ( RR = 0.790, 95% CI: 0.789 - 0.791) and further declined in the age group of 10 - 14 years ( RR = 0.711, 95% CI: 0.710 - 0.711) ; the period effect analysis showed that the risk of urticaria gradually decreased after the baseline period of 1992 - 1996 ( RR = 1.000) , and dropped to 0.995 (95% CI: 0.994 - 0.997) in the period of 2017 - 2021; in the cohort effect analysis of the overall population aged 0 - 14 years, with the 1988 - 1992 birth cohort as the base cohort, an earlier birth cohort 1978 - 1982 exhibited the highest risk of urticaria ( RR = 1.006, 95% CI: 1.004 - 1.009) , while the 2013 - 2017 cohort showed the lowest risk ( RR = 0.996, 95% CI: 0.994 - 0.997) . The multivariable meta-regression analysis indicated a significant association between PM 2.5 exposure and urticaria incidence ( β = 0.319, 95% CI: 0.022 - 0.616, P = 0.033) , although this association was not statistically significant in different age groups. Conclusions:From 1990 to 2021, children aged 0 - 4 years in China were the highest-risk group for urticaria; the decline in the incidence rate of urticaria was more pronounced in female children than in male children, and earlier birth cohorts exhibited higher risks of urticaria. Exposure to PM 2.5 appeared to be associated with the incidence of urticaria.

Objective:To analyze trends in urticaria incidence among children aged 0 - 14 years in China from 1990 to 2021, to explore its changing patterns in different age, period, and cohort groups, and to investigate the impact of age and air pollutants on the incidence trends.Methods:Data were obtained from the Global Burden of Disease Database (GBD2021) , including the number of urticaria cases, crude incidence rates, and age-standardized incidence rates among children aged 0 - 14 years of different genders in China from 1990 to 2021. The Joinpoint regression model was used to calculate the annual percentage change (APC) and average annual percentage change (AAPC) to assess temporal trends in incidence rates. An age-period-cohort model was applied to assess the effects of age, period, and cohort on urticaria incidence. Data on the annual emissions of 4 air pollutants (SO 2, CO, PM 2.5, and PM 10) in China from 1990 to 2021 were obtained from the Emissions Database for Global Atmospheric Research (EDGAR) , and a multivariable meta-regression model was used to explore the relationship between air pollutants and urticaria incidence. Results:From 1990 to 2021, the age-standardized incidence rate of urticaria among children aged 0 - 14 years in China demonstrated a slight overall downward trend (AAPC = -0.03%, P < 0.01) . The incidence rate was generally higher in female children than in male children, and the decline in incidence rates was greater in female children than in male children (female AAPC = -0.02%, male AAPC = -0.01%, both P < 0.01) . The age-period-cohort model indicated that the risk of urticaria decreased with advancing age: with the age group of 0 - 4 years as the reference ( RR = 1.000) , the risk of urticaria significantly decreased in the age group of 5 - 9 years ( RR = 0.790, 95% CI: 0.789 - 0.791) and further declined in the age group of 10 - 14 years ( RR = 0.711, 95% CI: 0.710 - 0.711) ; the period effect analysis showed that the risk of urticaria gradually decreased after the baseline period of 1992 - 1996 ( RR = 1.000) , and dropped to 0.995 (95% CI: 0.994 - 0.997) in the period of 2017 - 2021; in the cohort effect analysis of the overall population aged 0 - 14 years, with the 1988 - 1992 birth cohort as the base cohort, an earlier birth cohort 1978 - 1982 exhibited the highest risk of urticaria ( RR = 1.006, 95% CI: 1.004 - 1.009) , while the 2013 - 2017 cohort showed the lowest risk ( RR = 0.996, 95% CI: 0.994 - 0.997) . The multivariable meta-regression analysis indicated a significant association between PM 2.5 exposure and urticaria incidence ( β = 0.319, 95% CI: 0.022 - 0.616, P = 0.033) , although this association was not statistically significant in different age groups. Conclusions:From 1990 to 2021, children aged 0 - 4 years in China were the highest-risk group for urticaria; the decline in the incidence rate of urticaria was more pronounced in female children than in male children, and earlier birth cohorts exhibited higher risks of urticaria. Exposure to PM 2.5 appeared to be associated with the incidence of urticaria.

Hepatocellular carcinoma (HCC) expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming. Aldolase A (ALDOA) plays a prominent role in glycolysis; however, little is known about its role in HCC development. In the present study, we aim to explore how ALDOA is involved in HCC proliferation. HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout, which is consistent with ALDOA overexpression encouraging HCC proliferation. Mechanistically, ALDOA knockout partially limits the glycolytic flux in HCC cells. Meanwhile, ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase; ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function. A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun, and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells. In HCC patients, the expression level of ALDOA was correlated with the phosphorylation level of c-Jun (Thr93) and poor prognosis. Remarkably, hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models, and the knockdown of A ldoa strikingly decreased HCC development in vivo. Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription, opening additional avenues for anti-cancer therapies.

Objective: Sex differences have been observed in many aspects of schizophrenia, including cognitive deficits. Despite extensive research into the relationship between metabolic factors and cognitive deficits in schizophrenia, few studies have explored the potential sex difference in their association. Methods: We recruited 358 schizophrenia patients and 231 healthy controls. The participants underwent measurements of body mass index (BMI), waist circumference, blood pressure, triglycerides, high-density lipoprotein cholesterol, and fasting blood glucose. Metabolic risk factors included abdominal obesity, hypertension, hyperglycemia, and dyslipidemia. A collection of these metabolic risk factors has been defined as metabolic syndrome. These diagnoses were based on the criteria of the National Cholesterol Education Program’s Adult Treatment Panel III. Cognitive performance was measured using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). A descriptive analysis, difference analysis, and linear regression model were used to identify the metabolic risk factors for cognitive function in schizophrenia. Results: Our findings revealed sex differences in the rate of abdominal obesity and hypertension in schizophrenic patients. Additionally, we observed sex differences in the association between metabolic risk factors and cognitive impairment in schizophrenia. Specifically, hyperglycemia was associated with the immediate memory index score of RBANS in male patients, while dyslipidemia was associated with language, attention, delayed memory index scores, and RBANS total score in female patients. Conclusion Our results suggest that sex should be considered when evaluating the impact of metabolic disorders on the cognitive function of schizophrenic patients. Moreover, our study identifies hyperglycemia and dyslipidemia as potential targets for precise treatment by sex stratification, which could benefit the improvement of cognitive impairment in schizophrenic patients.

ObjectiveTo investigate the biological function and molecular mechanism of long non-coding RNA Linc‑pint in colorectal cancer. MethodsQuantitative real‑time quantitative （qRT‑PCR） was performed to detect the expression level of Linc‑pint in 31 pairs of colorectal cancer tumor and adjacent normal tissues； correlation between the expression level of Linc‑pint and the clinicopathological characteristics was analyzed by the chi‑square test. Kaplan-Meier survival analysis was used to assess the relationship between Linc‑pint expression level and the prognosis of patients. Cox regression model was used to analyze the relationship between clinicopathological characteristics and the prognosis of patients. Expression level of Linc‑pint were detected by qRT‑PCR in 5 common colorectal cancer cell lines. Effect of Linc‑pint on cell proliferation， invasion and migration was measured by cell counting kit‑8 assay， Transwell assay and harvested xenografts from nude mice. qRT‑PCR was performed to detect the expression level of Linc‑pint's target gene micro RNA（miR）‑21 in 31 pairs of colorectal cancer tumor tissues and adjacent normal tissues. Pearson correlation coefficient was used to assess the correlation between Linc‑pint and miR‑21. qRT‑PCR was used to detect the expression of overexpression of Linc‑pint on miR‑21 in colorectal cancer cells. ResultsExpression level of Linc‑pint in normal tissues （3.95±1.16） was significantly higher than that in colorectal cancer tissues （2.74±0.95） （t=6.17， P<0.05）. Overall survival rate of patients with high expression of Linc‑pint was 62.5%， which was significantly higher than that of patients with low expression of Linc‑pint （34.3%， P<0.05）. The proliferation， invasion and migration of CRC cells were inhibited after overexpression of Linc‑pint. In colorectal cancer tumor and adjacent normal tissues， Linc‑pint and miR‑21 showed opposite expression in tumor tissues and were negatively correlated （r=-0.288 and -0.908， both P<0.05）. ConclusionLinc‑pint acts as a tumor suppressor by down‑regulating the expression level of miR‑21 to inhibit the proliferation， invasion and migration of colorectal cancer.

Objective:To explore the electro-clinical characteristics of sleep-related hypermotor epilepsy (SHE) in rapid eye movement (REM) stage.Methods:Five patients of SHE in REM stage were studied and followed up in the Electroencephalogram Monitoring Center, Department of Neurology, Xijing Hospital, the Air Force Military Medical University, from January 2016 to August 2021.Results:Among the 5 patients, there are 3 male patients, aged 21 to 46 years. A total of 23 seizures were monitored in 5 patients, of which 22 occurred in REM sleep and 1 occurred in non-REM Ⅲ sleep. Each attack lasted from 30 seconds to 1 minute, and was manifested as "hyperkinetic attack" during sleep, with or without disturbance of consciousness. There were no obvious abnormalities in electroencephalography during 13 attacks, with the focal sharp slow waves or slow waves during 9 attacks, and the focal slow waves occurrence at the end of the 10 attacks.Conclusion:Most of the hypermotor epileptic seizures in REM stage started from awakening reaction, and the interictal discharges occured in waking and non-REM sleep stage, which is necessary to distinguish from the REM sleep behavior disorder.

Objective:To describe the electroclinical features of the coexistence of epilepsy and narcolepsy.Methods:The electroencephalography database was searched using the terms “epilepsy” and “narcolepsy” over a four-year period from January 2016 to December 2019 in the Xijing Hospital. The clinical and electrophysiological characteristics of patients with coexistence of epilepsy and narcolepsy were studied.Results:Five patients with comorbidity for epilepsy and narcolepsy were found, of which three patients were female, two patients were male. The age at epilepsy onset and narcolepsy onset was 2-12 years and 8-17 years, respectively. There were two patients with juvenile myoclonic epilepsy, one with sleep-related hypermoter epilepsy, one with epilepsy with retardation of brain development, one with symptomatic epilepsy with cognitive decline. All the patients had narcolepsy with cataplexy, which followed the onset of epilepsy by three months to eight years. All the patients accepted 24 h video electroencephalography monitoring and multiple sleep latency test. Interictal epileptic discharges were found, mean sleep latency was<8 min, and two or more sleep onset rapid eye movement periods were recorded. Duloxetine hydrochloride can effectively improve the drowsiness and catalepsy symptoms of narcolepsy, and seizures did not worsen in patients using duloxetine hydrochloride.Conclusions:Both generalized and focal epilepsy can occur in narcolepsy with cataplexy. Duloxetine hydrochloride may be safe and effective in treating narcolepsy in patients with epilepsy.

Major depressive disorder (MDD), also referred to as depression, is one of the most common psychiatric disorders with a high economic burden. The etiology of depression is still not clear, but it is generally believed that MDD is a multifactorial disease caused by the interaction of social, psychological, and biological aspects. Therefore, there is no exact pathological theory that can independently explain its pathogenesis, involving genetics, neurobiology, and neuroimaging. At present, there are many treatment measures for patients with depression, including drug therapy, psychotherapy, and neuromodulation technology. In recent years, great progress has been made in the development of new antidepressants, some of which have been applied in the clinic. This article mainly reviews the research progress, pathogenesis, and treatment of MDD.

A correction to this paper has been published: https://doi.org/10.1007/s12264-021-00694-9.