Influencing Factors of Physical Activity in Patients with Lung Cancer Surgery and Its Correlation with Exercise Self-Efficacy and Perceived Social Support.

Purpose: The aim of the study is to understand the current status of physical activity in patients with lung cancer surgery, explore its influencing factors, and analyze the correlation between physical activity and exercise self-efficacy and perception of social support. Methods: The General Information Questionnaire was designed for 145 patients, Chinese version of EPIC-PAQ physical activity scale for lung cancer patients. The Exercise Self-Efficacy Scale (SEE) is used to evaluate the ability of people to organize and execute motor behaviors in various difficult situations. The Perceived Social Support Scale (PSSS) was used to emphasize individual self-understanding and self-feeling. Results: The median and quartile of total physical activity scores in lung cancer surgery patients were 73.0 (34.8, 129.7) points; univariate analysis showed that there were statistically significant differences in physical activity levels among lung cancer surgery patients with different ages, work status before hospitalization, and perceived disease severity. The results of multivariate analysis showed that age, perceived disease severity, exercise self-efficacy, and total score of perceived social support affected the physical activity level of patients (P < 0.05). Efficacy were positively correlated with perceived social support (P < 0.01). Conclusion: The level of physical activity of patients undergoing lung cancer surgery needs to be further improved. Physical activity is affected by patient age, perceived disease severity, exercise self-efficacy, and perceived social support and is positively correlated with exercise self-efficacy and perceived social support. Medical staff should provide targeted activity guidance according to the age and other characteristics of patients undergoing lung cancer surgery, enhance patients' exercise self-efficacy and comprehend social support, and improve their physical activity level, thereby promoting patients' early recovery.

The right thalamic glutamate level correlates with functional connectivity with right dorsal anterior cingulate cortex/middle occipital gyrus in unmedicated obsessive-compulsive disorder: A combined fMRI and 1H-MRS study.

OBJECTIVE: The imbalance in neurotransmitter and neuronal metabolite concentration within cortico-striato-thalamo-cortical (CSTC) circuit contributes to obsessive-compulsive disorder's (OCD) onset. Previous studies showed that glutamate mediated upregulation of resting-state activity in healthy people. However, there have been few studies investigating the correlational features between functional and neurochemical alterations in OCD. METHODS: We utilize a combined resting-state functional magnetic resonance imaging (rs-fMRI) and proton magnetic resonance spectroscopy (1H-MRS) approach to investigate the altered functional connectivity (FC) in association with glutamatergic dysfunction in OCD pathophysiology. Three regions of interest are investigated, i.e., medial prefrontal cortex and bilateral thalamus, for seed-based whole-brain FC analysis as well as MRS data acquisition. There are 23 unmedicated adult OCD patients and 23 healthy controls recruited for brain FC analysis. Among them, 12 OCD and 8 controls are performed MRS data acquisition. RESULTS: Besides abnormal FC within CSTC circuit, we also find altered FCs in large-scale networks outside CSTC circuit, including occipital area and limbic and motor systems. The decreased FC between right thalamus and right middle occipital gyrus (MOG) is correlated with glutamatergic signal within right thalamus in OCD patients. Moreover, the FC between right thalamus and right dorsal anterior cingulate cortex (dACC) is associated with glutamate level in right thalamus, specifically in patient's group. Finally, the FC between right thalamus and right MOG is correlated with patient's Yale-Brown Obsessive Compulsive Scale (YBOCS) compulsion and total scores, while the right thalamic glutamatergic signal is associated with YBOCS-compulsion score. CONCLUSION: Our findings showed that the coupled intrinsic functional-biochemical alterations existed both within CSTC circuit and from CSTC to occipital lobe in OCD pathophysiology.

Anterior thalamic radiation structural and metabolic changes in obsessive-compulsive disorder: A combined DTI-MRS study.

Numerous studies indicate the cortico-striato-thalamo-cortical (CSTC) circuit plays an important role in the pathophysiology of obsessive-compulsive disorder (OCD). The anterior thalamic radiation (ATR), as a major fiber in the fronto-thalamic circuitry, contributes to symptomology of OCD. However, the underlying biochemical mechanism in relation with its structural alteration remains not understood. This study investigated the structural abnormality of ATR and its correlation with thalamic metabolic alteration in OCD, using diffusion tensor image (DTI) and proton magnetic resonance spectroscopy (1H-MRS). Twenty-six unmedicated adult OCD patients and twenty-six matched healthy controls participated in DTI study. Thirteen OCD patients and thirteen healthy controls, a subset of DTI participants, took part in MRS study. The results showed that mean fiber length of right ATR negatively correlated with ipsilateral thalamic choline (Cho) level in OCD patients. Additionally, significantly higher Cho concentration was detected in right thalamus of OCD patients compared to healthy controls. Moreover, the mean fractional anisotropy (FA) value of right ATR positively correlated with patients Yale-Brown Obsessive Compulsive Scale (YBOCS) total score, as well as YBOCS compulsion score. These results suggested the coupling of structural and metabolic changes in right ATR, which might serve as a multi-modal biomarker contributing to the pathogenesis of OCD.

Decreased thalamic glutamate level in unmedicated adult obsessive-compulsive disorder patients detected by proton magnetic resonance spectroscopy.

BACKGROUND: Previous neuroimaging studies implied that the dysfunction of cortico-striato-thalamo-cortical (CSTC) circuit served as the neural basis for the pathophysiology of obsessive-compulsive disorder (OCD). The imbalances in neuronal metabolite and neurotransmitter within CSTC circuit have been shown as the leading reasons of the OCD onset. The aim of this study is to investigate the metabolic alterations, especially the glutamatergic signal dysfunction within CSTC circuit, and the relationships between neural metabolites and the symptom severity of OCD patients. METHODS: Single voxel magnetic resonance spectroscopy (MRS) was conducted in medial prefrontal cortex (mPFC) and bilateral thalamus areas for thirteen unmedicated adult OCD patients with age-, gender-, and education-matched healthy controls. Quantification and multivariate analysis were performed to identify vital metabolic biomarkers for patients and healthy controls group differentiation. Moreover, we performed Spearman׳s rank correlation analysis for OCD patients to examine the relationship between the metabolite concentration level and OCD symptomatology. RESULTS: Patients with OCD showed significantly decreased glutamate level in mPFC (p=0.021) and right thalamus (p=0.039), and significantly increased choline compounds in left thalamus (p=0.044).The glutamate in right thalamus was shown as the most important metabolite for group separation from multivariate analysis (Q(2)=0.134) and was significantly correlated with the patients׳ compulsion scores (Spearman r=-0.674, p=0.016). LIMITATIONS: Limited sample size, the use of creatine and phosphocreatine (Cr) ratios rather than absolute concentrations and unresolved glutamine (Gln) are limitations of the present study. CONCLUSION: Our study results consolidated the hypothesis about glutamatergic signaling dysfunction in OCD. To our knowledge, it is the first finding about a reduced thalamic glutamate level in adult unmedicated OCD patients. The dysregulation of glutamate serves as a potential target for the OCD pharmacotherapy and the detailed mechanisms underlying the glutamate alterations within CSTC circuits merit further investigations.