Objective:To explore the effects of aerobic exercise therapy and anaerobic exercise therapy on improving depressive symptoms, sleep quality, and cognitive function in patients with mild and moderate depression.Methods:A prospective study was conducted to collect clinical data from 148 inpatients with mild to moderate depression treated at the Second Affiliated Hospital of Xinxiang Medical College from February 2019 to May 2023 including 74 males and 74 females aged 18 to 60 (40.08±11.03) years. They were randomly assigned the conventional treatment group (group A, 49 cases), the conventional treatment+moderate-intensity aerobic exercise therapy intervention group (group B, 51 cases), and the conventional treatment+moderate intensity anaerobic exercise therapy intervention group (group C, 48 cases). Patients in each group were treated the corresponding intervention for 4 weeks. The 24-item Hamilton Depression Scale (HAMD 24), Pittsburgh Sleep Quality Index (PSQI), and the Montreal Cognitive Assessment (MOCA) were used to score depressive symptoms, sleep quality, and cognitive function, respectively, before and after intervention. Paired sample t-tests were used to compare the changes in scores before and after the intervention. One-way ANOVA was used to analyze and compare the score differences on each scale among the groups. Results:After the intervention, HAMD 24 and PSQI scores in all groups decreased compared with those before the intervention (Group A: HAMD 24 (15.08±4.15) vs (29.33±4.75), PSQI (12.76±2.52) vs (14.88±3.64); Group B: HAMD 24 (12.82±3.83) vs (28.61±5.08), PSQI (11.59±2.26) vs (14.55±4.14); Group C: HAMD 24 (14.44±3.60) vs (29.44±4.98), PSQI (11.40±2.30) vs (15.13±4.62)) (all P<0.001). After the intervention, the MOCA scores in all groups were higher than those before the intervention (Group A: (26.04±2.21) vs (25.92±2.34), t=-2.20, P=0.032; Group B: (26.22±1.59) vs (25.35±1.95), t=-4.45, P<0.001; Group C: (26.10±2.15) vs (25.21±2.13), t=-3.15, P=0.003). After the intervention, the HAMD 24 scores of Group B were lower than those of Group A and Group C ((12.82±3.83) vs (15.08±4.15) vs (14.44±3.60)) (all P<0.05), and the PSQI scores of groups B and C were lower than those of group A ((11.59±2.26) and (11.40±2.30) vs (12.76±2.52)) (all P<0.05). No statistically significant differences in MOCA scores among Group A, Group B, and Group C after the intervention ( P=0.906). Conclusion:Exercise therapy is helpful in improving depressive symptoms and sleep quality in patients with mild to moderate depression, but it does not have a significant advantages in improving cognitive function.

Objective:To explore the effects of aerobic exercise therapy and anaerobic exercise therapy on improving depressive symptoms, sleep quality, and cognitive function in patients with mild and moderate depression.Methods:A prospective study was conducted to collect clinical data from 148 inpatients with mild to moderate depression treated at the Second Affiliated Hospital of Xinxiang Medical College from February 2019 to May 2023 including 74 males and 74 females aged 18 to 60 (40.08±11.03) years. They were randomly assigned the conventional treatment group (group A, 49 cases), the conventional treatment+moderate-intensity aerobic exercise therapy intervention group (group B, 51 cases), and the conventional treatment+moderate intensity anaerobic exercise therapy intervention group (group C, 48 cases). Patients in each group were treated the corresponding intervention for 4 weeks. The 24-item Hamilton Depression Scale (HAMD 24), Pittsburgh Sleep Quality Index (PSQI), and the Montreal Cognitive Assessment (MOCA) were used to score depressive symptoms, sleep quality, and cognitive function, respectively, before and after intervention. Paired sample t-tests were used to compare the changes in scores before and after the intervention. One-way ANOVA was used to analyze and compare the score differences on each scale among the groups. Results:After the intervention, HAMD 24 and PSQI scores in all groups decreased compared with those before the intervention (Group A: HAMD 24 (15.08±4.15) vs (29.33±4.75), PSQI (12.76±2.52) vs (14.88±3.64); Group B: HAMD 24 (12.82±3.83) vs (28.61±5.08), PSQI (11.59±2.26) vs (14.55±4.14); Group C: HAMD 24 (14.44±3.60) vs (29.44±4.98), PSQI (11.40±2.30) vs (15.13±4.62)) (all P<0.001). After the intervention, the MOCA scores in all groups were higher than those before the intervention (Group A: (26.04±2.21) vs (25.92±2.34), t=-2.20, P=0.032; Group B: (26.22±1.59) vs (25.35±1.95), t=-4.45, P<0.001; Group C: (26.10±2.15) vs (25.21±2.13), t=-3.15, P=0.003). After the intervention, the HAMD 24 scores of Group B were lower than those of Group A and Group C ((12.82±3.83) vs (15.08±4.15) vs (14.44±3.60)) (all P<0.05), and the PSQI scores of groups B and C were lower than those of group A ((11.59±2.26) and (11.40±2.30) vs (12.76±2.52)) (all P<0.05). No statistically significant differences in MOCA scores among Group A, Group B, and Group C after the intervention ( P=0.906). Conclusion:Exercise therapy is helpful in improving depressive symptoms and sleep quality in patients with mild to moderate depression, but it does not have a significant advantages in improving cognitive function.

Objective:To investigate the role of mitogen-activated protein kinase phosphatase-1 (MKP-1) on depressive-like behaviors and hippocampal neuron apoptosis in chronic unpredictable mild stress (CUMS) rats.Methods:A total of 36 Sprague-Dawley male rats were randomly divided into 4 groups using a random number table, including the control group( n=8), CUMS group( n=8), virus control group( n=10), and MKP-1 down-regulated group( n=10), with 8 rats in each group. Except for the control group, rats in other groups were stressed by CUMS model of depression. Rats in the virus control group and MKP-1 down-regulated group received adeno-associated virus injections in the hippocampal CA1 and CA3 regions before CUMS modeling. Sucrose preference test, forced swimming test, and open field test were used to observe the behavioral changes of rats. Western blotting was used to detect the protein expression of MKP-1, B-cell lymphoma-2 gene (Bcl-2) and B-cell lymphoma-2 gene-related X protein (Bax), in the hippocampus. TUNEL staining was utilized to observe the morphology of apoptotic cells in the hippocampus CA1 area. Repeated measures variance was used to analyze body weight and behaviors, while an independent sample t-test was used to analyze protein levels. Results:Compared with the control group, the body weight of rats in the CUMS group decreased ( F=44.664); the sucrose preference rate decreased ( F=14.978); the forced swimming immobility time increased ( F=8.436); the number of defecation in the open field test increased ( F=9.572); the relative expression level of MKP-1 and Bax/Bcl-2 also significantly increased ( t=4.415,3.410), P<0.05 for all; Compared with the virus control group, rats in the MKP-1 down-regulation group showed a higher sucrose preference rate ( F=11.922) and a shorter forced swimming immobility time ( F=12.868), furthermore, the activity distance ratio in the central area increased ( F=6.291), the number of uprights in the open field test increased ( F=14.372), and the relative expression levels of MKP-1 and Bax/Bcl-2 ( t=3.775,6.193) decreased, P<0.05 for all. The number of DNA fragments in the nucleus of the hippocampal CA1 region of the CUMS group was significantly more than that of the control group. In comparison, the number of DNA fragments in the nucleus of the MKP-1 down-regulated group was substantially less than that of the virus control group. Conclusion:Down-regulation of MKP-1 gene alleviated depressive-like behavior and hippocampal neuron apoptosis in CUMS rats.

Objective:To investigate the role of mitogen-activated protein kinase phosphatase-1 (MKP-1) on depressive-like behaviors and hippocampal neuron apoptosis in chronic unpredictable mild stress (CUMS) rats.Methods:A total of 36 Sprague-Dawley male rats were randomly divided into 4 groups using a random number table, including the control group( n=8), CUMS group( n=8), virus control group( n=10), and MKP-1 down-regulated group( n=10), with 8 rats in each group. Except for the control group, rats in other groups were stressed by CUMS model of depression. Rats in the virus control group and MKP-1 down-regulated group received adeno-associated virus injections in the hippocampal CA1 and CA3 regions before CUMS modeling. Sucrose preference test, forced swimming test, and open field test were used to observe the behavioral changes of rats. Western blotting was used to detect the protein expression of MKP-1, B-cell lymphoma-2 gene (Bcl-2) and B-cell lymphoma-2 gene-related X protein (Bax), in the hippocampus. TUNEL staining was utilized to observe the morphology of apoptotic cells in the hippocampus CA1 area. Repeated measures variance was used to analyze body weight and behaviors, while an independent sample t-test was used to analyze protein levels. Results:Compared with the control group, the body weight of rats in the CUMS group decreased ( F=44.664); the sucrose preference rate decreased ( F=14.978); the forced swimming immobility time increased ( F=8.436); the number of defecation in the open field test increased ( F=9.572); the relative expression level of MKP-1 and Bax/Bcl-2 also significantly increased ( t=4.415,3.410), P<0.05 for all; Compared with the virus control group, rats in the MKP-1 down-regulation group showed a higher sucrose preference rate ( F=11.922) and a shorter forced swimming immobility time ( F=12.868), furthermore, the activity distance ratio in the central area increased ( F=6.291), the number of uprights in the open field test increased ( F=14.372), and the relative expression levels of MKP-1 and Bax/Bcl-2 ( t=3.775,6.193) decreased, P<0.05 for all. The number of DNA fragments in the nucleus of the hippocampal CA1 region of the CUMS group was significantly more than that of the control group. In comparison, the number of DNA fragments in the nucleus of the MKP-1 down-regulated group was substantially less than that of the virus control group. Conclusion:Down-regulation of MKP-1 gene alleviated depressive-like behavior and hippocampal neuron apoptosis in CUMS rats.

Depressive disorder is a common mental disorder.At present, the diagnosis of depressive disorder mainly relies on patients' self-reported symptoms and clinical interviews which are relatively subjective.As one of the new technologies assisting diagnosis and therapeutic effect evaluation of depressive disorder, near-infrared spectroscopy (NIRS) has received a lot of attention in recent years.This article reviewed studies of using NIRS in the diagnosis and therapeutic effect evaluation of depressive disorder in the past five years.The review showed that NIRS could reflect abnormal hemodynamic activities of the prefrontal cortex and temporal cortex of patients with depressive disorder, especially the dorsolateral prefrontal cortex and inferior frontal gyrus.Changes of concentration of oxygenated hemoglobin in these areas showed higher accuracy in assisting the diagnosis of depression disorder.Until now, only a few longitudinal studies utilized NIRS to compare changes of cerebral hemodynamic activities at different time points of treatment which preliminarily confirmed the potential of NIRS in the evaluation of therapeutic effects of depressive disorder.In future, more large-scale studies will be needed to further determine the specific application standards for NIRS in the diagnosis and therapeutic effect evaluation of depressive disorder.

The accurate position of the center of rotation (COR) is a key factor to ensure the quality of computed tomography (CT) reconstructed images. The classic cross-correlation matching algorithm can not satisfy the requirements of high-quality CT imaging when the projection angle is 0 and 180°, and thus needs to be improved and innovated. In this study, considering the symmetric characteristic of the 0° and flipped 180° projection data in sinogram, a novel COR correction algorithm based on the translation and match of the 0° and 180° projection data was proposed. The OTSU method was applied to reduce noise on the background, and the minimum offset of COR was quantified using the -norm, and then a precise COR was obtained for the image correction and reconstruction. The Sheep-Logan simulation model with random gradients and Gaussian noise and the real male SD rats samples which contained the heterogenous tooth image and the homogenous liver image, were adopted to verify the performance of the new algorithm and the cross-correlation matching algorithm. The results show that the proposed algorithm has better robustness and higher accuracy of the correction (when the sampled data is from 10% to 50% of the full projection data, the COR value can still be measured accurately using the proposed algorithm) with less computational burden compared with the cross-correlation matching algorithm, and it is able to significantly improve the quality of the reconstructed images.

Objective To investigate the effect of enriched environment (EE) on behavior and expression of mitogenactivated protein kinase phosphatase-1 (MKP-1) in hippocampus of depression rats induced by chronic unpredicted mild stress (CUS) and to provide clues for the molecular mechanism of treating depression.Methods Forty Sprague-Dawley rats were randomly divided into control group,CUS group,fluoxetine group and EE group,with 10 rats in each group.The rats in CUS group,fluoxetine group and EE group were given 8 weeks of CUS,and from the fifth week,the rats in EE group and fluoxetine group were given EE and fluoxetine for 4 weeks,respectively.The changes of behavioristic of the rats in the four groups were evaluated by body mass gain,open field test,and sucrose preference.The expression of MKP-1 in hippocampus was detected by Western blot.Results There was no significant difference in body mass,distance of horizontal movement,the number of upright,the times of passing through the grid and sucrose preference index among the four groups(P ＞ 0.05).After modeling,compared with the control group,the body mass gain,distance of horizontal movement,the number of up-right,the times of passing through the grid and sucrose preference index in the CUS group,fluoxetine group and EE group were decreased significantly(P ＜ 0.05);there was no significant difference in the body mass gain,distance of horizontal movement,the number of up-right,the times of passing through the grid and sucrose preference index among the CUS group,fluoxetine group and EE group(P ＞ 0.05).After intervening by fluoxetine and EE,the body mass gain,distance of horizontal movement,the number of up-right,the times of passing through the grid and sucrose preference index in the CUS group were lower than those in the control group(P ＜0.05);but there was no significant difference in the body mass gain,distance of horizontal movement,the number of up-right,the times of passing through the grid and sucrose preference index between the control group and the fluoxetine group and EE group(P ＞ 0.05).Compared with the CUS group,the body mass gain,distance of horizontal movement,the number of up-right,the times of passing through the grid and sucrose preference index in the fluoxetine group and EE group were higher(P ＜ 0.05);there was no significant difference in the body mass gain,distance of horizontal movement,the number of up-right,the times of passing through the grid and sucrose preference index between the fluoxetine group and EE group (P ＞ 0.05).The expression of MKP-1 in hippocampus of CUS group and EE group was higher than that in the control group (P ＜0.05).There was no significant difference in the expression of MKP-1 in hippocampus between the fluoxetine group and control group(P ＞ 0.05).Compared with the CUS group,the expression of MKP-1 in hippocampus in the fluoxetine group decreased (P ＜ 0.05).There was no significant difference in the expression of MKP-1 in hippocampus between the EE group and CUS group(P ＞0.05).Compared with the fluoxetine group,the expression of MKP-1 in hippocampus in the EE group was higher(P ＜ 0.05).Conclusion EE can significantly improve depressive symptoms in rats,but it has no significant effect on MKP-1 protein expression in hippocampus,and EE may not act on depression by affecting MKP-1.

Objective To investigate the effects of intervention with the fluoxetine and the enriched environment on chronic stress induced depression behavior of rats,and the changes of myelin basic protein in hippocampus and prefrontal regions.Methods 50 adult male SD rats were randomly divided into control group,fluoxetine group,model group,enriched environment (EE) group and EE plus fluoxetine group.Fluoxetine group,model group,EE group and EE plus fluoxetine group underwent chronic unpredictable stress stimulus in the first to third week,and fluoxetine group,EE group,EE plus fluoxetine group underwent the intervention with EE and (or) fluoxetine in the fourth to sixth week.The changes of behavior in rats were evaluated by sucrose water consumption,open field test and weight changes.The content of MBP in each subregion of hippocampus and prefrontal regions of rats was measured with immunocytochemical methods.Results At the third weekend,the assessed behaviors of stressed rats decreased significantly compared with control group (P＜0.05);and at the sixth weekend,the behaviors of stressed rats restored after treated with EE and (or) fluoxetine.The content of MBP in the rat hippocampus CA1,DG area and prefrontal area of model group declined clearly compared with control group (mean density of model group orderly:0.199±0.024,0.204±0.021,0.225±0.028;control group orderly:0.279±0.034,0.288±0.043,0.308±0.053,P＜0.05).The content of MBP in the rat of fluoxetine group,EE group and EE plus fluoxetine group increased obviously compared with model group (fluoxetine group orderly:0.259± 0.047,0.266± 0.052,0.284 ± 0.031;EE group orderly:0.257±0.038,0.258±0.042,0.286±0.037;EE plus fluoxetine group orderly:0.271± 0.046,0.279±0.040,0.289±0.041,P＜0.05).Conclusion The depression-like behavior of rats induced by chronic unpredictable stress is associated with the change of the content of MBP in hippocampal CA1,DG area and prefrontal area;and the depression-like behavior and the content of MBP decrease are reversed after the intervention with fluoxetine and EE.

Objective To review the neuron synaptic plasticity in hioppocampus in the pathogenesis of depression in present studies,and expected to provide reference and basis for study of depression in clinic and model.Methods The wordsdepression, antidepression, chronic unpredictable stimulate, hippocampus, synapse,plasticity were used as index words.Analysis the relationship of depression or antidepression and synaptic plasticity in hippocampus from the results of researches enrolled at home or abroad.Summarize the effect of neuron synaptic plasticity in hioppocampus in the pathogenesis of depression.Result Totally 37 articles enrolled.They show the onset of depression or antidepressant processes always combine with the damage or recover of neuron synaptic plasticity.Conclusion The reduction or damage in synaptic plasticity in hippocampus is likely to be the pathogenesis of depression,like the changes of function or expression of SYN-1,MAP-2,SYT-1,PSD-95 or any other synapse-associated proteins.Meanwhile,studies of using enrich environment to treat depression indicated that depression is likely related to the synaptic plasticity in hippocampus in another way.But who are the synapse-associated proteins related to synaptic plasticity in depression? How to design the enrich environment.? These still need further study.

Cisplatin is effective in the treatment of various solid tumors. However, its clinical application is limited because of the severe side-effects such as nephrotoxicity, hepatotoxicity, ototoxicity and so on. Drug combination is advocated in clinics for synergism and detoxication. In order to provide some referencs for the research of drug combination and clinical treatment regimen, the research advances in the synergism and detoxication of drug combination of cisplatin with chemicals/ traditional Chinese medicines in recent years are reviewed in the paper.