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BackgroundAn overlap of clinical symptoms between major depressive disorder (MDD) and social anxiety disorder (SAD) suggests that the two disorders exhibit similar brain mechanisms. However, few studies have directly compared the brain structures of the two disorders. The aim of this study was to assess the gray matter volume (GMV) and cortical thickness alterations between non-comorbid medication-naive MDD patients and SAD patients.MethodsHigh-resolution T1-weighted images were acquired from 37 non-comorbid MDD patients, 24 non-comorbid SAD patients and 41 healthy controls (HCs). Voxel-based morphometry analysis of the GMV (corrected with a false discovery rate of p < 0.001) and vertex-based analysis of cortical thickness (corrected with a clusterwise probability of p < 0.001) were performed, and group differences were compared by ANOVA followed by post hoc tests.OutcomesRelative to the HCs, both the MDD patients and SAD patients showed the following results: GMV reductions in the bilateral orbital frontal cortex (OFC), putamen, and thalamus; cortical thickening in the bilateral medial prefrontal cortex, posterior dorsolateral prefrontal cortex, insular cortex, left temporal pole, and right superior parietal cortex; and cortical thinning in the left lateral OFC and bilateral rostral middle frontal cortex. In addition, MDD patients specifically showed a greater thickness in the left fusiform gyrus and right lateral occipital cortex and a thinner thickness in the bilateral lingual and left cuneus. SAD patients specifically showed a thinner cortical thickness in the right precentral cortex.InterpretationOur results indicate that MDD and SAD share common patterns of gray matter abnormalities in the orbitofrontal-striatal-thalamic circuit, salience network and dorsal attention network. These consistent structural differences in the two patient groups may contribute to the broad spectrum of emotional, cognitive and behavioral disturbances observed in MDD patients and SAD patients. In addition, we found disorder-specific involvement of the visual processing regions in MDD and the precentral cortex in SAD. These findings provide new evidence regarding the shared and specific neuropathological mechanisms that underlie MDD and SAD.

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miR-17-5p is abnormally expressed in various tumor types. The aim of this study was to investigate the expression level of miR-17-5p in serum of patients with lung cancer and to determine whether serum miR-17-5p expression is related to the prognosis of patients with lung cancer. RT-qPCR was used to examine expression of miRNA-17-5p in 20 pairs of lung cancer and adjacent normal tissues, and sera from 221 patients with lung cancer and 54 matched controls. The correlation of serum miR-17-5p with clinicopathological factors or prognosis of patients with lung cancer was analyzed. The expression level of miR-17-5p obviously increased in lung cancer tissues (P = 0.004). Furthermore, serum miR-17-5p expression also significantly increased in patients with lung cancer compared with healthy individuals (P = 0.03). The survival analysis showed that serum miR-17-5p expression was closely related to the survival of patients with lung cancer. Patients with high miR-17-5p expression had shorter survival times [hazard ratio (HR) = 1.767, 95 %CI 1.039-3.005, P = 0.035]. A lower expression level of serum miR-17-5p helps extend the survival of patients with lung cancer. Thus, miR-17-5p may be potential biomarker for prediction the prognosis in patients with lung cancer.

These findings of focal spontaneous hyper- and hypofunction, together with altered brain connectivity in the large-scale resting-state networks, which correlates with executive dysfunction, point to a connectivity-based pathophysiologic process in ADHD.

Gray matter (GM) anomalies may represent a critical pathology underlying obstructive sleep apnea (OSA). However, the evidence regarding their clinical relevance is inconsistent. We conducted a meta-analysis of voxel-based morphometry (VBM) studies of patients with OSA to identify their brain abnormalities. A systematic search was conducted based on PRISMA guidelines, and a meta-analysis was performed using the anisotropic effect-size-based algorithms (ASE-SDM) to quantitatively estimate regional GM changes in patients with OSA. Fifteen studies with 16 datasets comprising 353 untreated patients with OSA and 444 healthy controls were included. Our results revealed GM reductions in the bilateral anterior cingulate/paracingulate gyri (ACG/ApCG), left cerebellum (lobules IV/V and VIII), bilateral superior frontal gyrus (SFG, medial rostral part), right middle temporal gyrus (MTG), and right premotor cortex. Moreover, GM reductions in the bilateral ACG/ApCG were positively associated with body mass index (BMI) and age among patients with OSA, and GM reductions in the SFG (medial rostral part) were negatively associated with Epworth sleepiness scale (ESS) scores and sex (male). These abnormalities may represent structural brain underpinnings of neurocognitive abnormalities and respiratory-related abnormalities in OSA. In particular, this study adds to Psychoradiology, which is a promising subspecialty of clinical radiology mainly for psychiatric disorders.

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