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Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are two highly prevalent and commonly co-occurring neurodevelopmental disorders. The neural mechanisms underpinning the comorbidity of ASD and ADHD (ASD + ADHD) remain unclear. We focused on the topological organization and functional connectivity of brain networks in ASD + ADHD patients versus ASD patients without ADHD (ASD-only). Resting-state functional magnetic resonance imaging (rs-fMRI) data from 114 ASD and 161 typically developing (TD) individuals were obtained from the Autism Brain Imaging Data Exchange II. The ASD patients comprised 40 ASD + ADHD and 74 ASD-only individuals. We constructed functional brain networks for each group and performed graph-theory and network-based statistic (NBS) analyses. Group differences between ASD + ADHD and ASD-only were analyzed at three levels: nodal, global, and connectivity. At the nodal level, ASD + ADHD exhibited topological disorganization in the temporal and occipital regions, compared with ASD-only. At the global level, ASD + ADHD and ASD-only displayed no significant differences. At the connectivity level, the NBS analysis revealed that ASD + ADHD showed enhanced functional connectivity between the prefrontal and frontoparietal regions, as well as between the orbitofrontal and occipital regions, compared with ASD-only. The hippocampus was the shared region in aberrant functional connectivity patterns in ASD + ADHD and ASD-only compared with TD. These findings suggests that ASD + ADHD displays altered topology and functional connectivity in the brain regions that undertake social cognition, language processing, and sensory processing. [ABSTRACT FROM AUTHOR]

Objective. This study aims to determine the curative effect of Fuyuan Xingshen Decoction combined with butylphthalide sodium chloride injection in acute cerebral infarction (ACI) treatment and its effect on hemodynamics. Methods. In our hospital, a total of 84 ACI patients from May 2020 to February 2022 were randomly divided into two groups: observation and control (n = 42 each). Fuyuan Xingshen Decoction in combination with butylphthalide sodium chloride injection was provided to the observation group, while the control group received butylphthalide sodium chloride injection alone. Both groups' clinical efficacy was observed. Before and after treatment, the neurological function of the two groups was evaluated using the National Institutes of Health Stroke Scale (NIHSS), while the daily living ability of both groups was determined using the Barthel index rating scale. Both groups were investigated for their cognitive function, before and after treatment, by using the Mini-Cog scale and Montreal Cognitive Assessment (MoCA) scale. The pulsatility index (PI), peak velocity (Vp), and mean velocity (Vm) of intracranial arteries were measured by transcranial Doppler ultrasonography before and after treatment. The levels of ubiquitin carboxy-terminal hydrolase-1 (UCH-L1), Fibulin-5, and visinin-like protein-1 (VILIP-1) in serum and the expression levels of miR-34c, miR-25, and miR-182 in peripheral blood of the two groups were compared. Both groups were observed for the incidence of adverse reactions. Results. Compared with the control (71.43%), the observation group exhibited a significantly higher effective rate of around 90.48%. In the observation group, the improvement in NIHSS, Barthel index, Mini-cog, and MoCA scores; hemodynamic indexes including Vp, PI, and Vm; serum UCH-L1, Fibulin-5, and VILIP-1 levels; and the miR-34c, miR-25, and miR-182 expression levels in peripheral blood was better than the control group, with significant difference (all P < 0.05). The incidence of adverse reactions between the groups demonstrated no significant differences (P > 0.05). Conclusions. Fuyuan Xingshen Decoction combined with butylphthalide sodium chloride injection can effectively improve patients' daily living ability, neurological function, cognitive function, and cerebral hemodynamics in the treatment of ACI, with good effect and safety. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is an inflammation-related disease. Tumor necrosis factor alpha (TNF-α) is an important inflammatory factor and it has been confirmed to promote tumor growth and poor prognosis of HCC. Hepatic progenitor cells (HPCs) are thought to play an important role in liver injury and repair, as well as tumorigenesis. Chronic inflammation influences HPCs activation as well as differentiation. However, the mechanism is still unclear. In our study, the rat liver cancer model was constructed by DEN treatment, TNFR2-Fc fusion protein variant (TNFR2-FcV) and TNF-α-/- rats were used to detect the role of TNF-α in liver injury and tumorigenesis. And the effect of TNF-α on HPCs activation and proliferation was investigated, and the specific molecular mechanism was explored. We found that TNF-α inhibition and deletion could reduce tumor incidence but shorten survival time by increasing apoptosis and decreasing proliferation of hepatocytes. Further analysis indicated that TNF-α knochdown cloud inhibit HPCs activation and proliferation through TNFR2/STAT3 signaling pathway. And clinically TNF-α expression was correlated to HPCs activation and HCC recurrences. Our work suggested that TNF-α played a key role in liver injury and tumorigenesis. [ABSTRACT FROM AUTHOR]

Background: Fear of cancer recurrence (FCR), anxiety, and depression are common psychological disturbances that frequently occur together among cancer patients. This study investigated network connectivity between FCR, anxiety, and depressive symptoms in a large representative sample of breast cancer patients.Methods: This was a multicenter, cross-sectional study of 803 women with breast cancer. All participants completed the 4-item FCR scale, Generalized Anxiety Disorder Scale (GAD-7), and Patient Health Questionnaire (PHQ-9). Network analysis was conducted to investigate the network structure, central symptoms, bridge symptoms, and network stability of these disturbances.Results: The generated network model indicated that anxiety and depression symptom communities were well-connected with each other, while FCR emerged as a distinct cluster with only a few weak links to anxiety and depression communities. Depressive and anxiety symptoms were more central than FCR symptoms were in the model. 'Having trouble relaxing' (#GAD4, strength = 1.147) was the most central node within the whole network, and 'strong feelings about recurrence' (#FCR4, strength = 0.531) was the least central node. Several anxiety symptoms (e.g., 'feeling afraid', 'uncontrollable worry', and 'restlessness') acted as important bridging symptoms connecting FCR, depression and anxiety communities. 'Uncontrollable worry' (#GAD2) had the highest node-specific predictive betweenness value. The network stability of this model was high.Conclusion: Depression and anxiety symptoms are highly interactive with each other among women with breast cancer. Conversely, FCR may have attenuated relations with anxiety and depression communities and emerged as a relatively independent, unique experience. Anxiety symptoms, particularly 'uncontrollable worry', acted as important trans-diagnostic symptoms that connected different communities. Findings suggested interventions to alleviate excessive worries and enhance feelings of personal control might be helpful in preventing or reducing related symptoms of FCR, anxiety and depression. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) usually occurs at the late stage of chronic liver injury. Oncostatin M (OSM) is a tumor-associated cytokine highly expressed in cirrhosis and HCC patients; however, its role in hepatocarcinogenesis has not been clearly elucidated. In this study, we investigated the effect of OSM on HCC occurrence in a rat model of N-diethylnitrosamine-induced HCC. OSM overexpression significantly increased the number of tumor nodules and shortened the overall survival of the rats. Notably, OSM promoted HPC activation in vivo but did not directly regulate the proliferation of the HPC cell line in vitro. Further, OSM induced tumor necrosis factor-α (TNF-α) secretion and CD68+ macrophage accumulation, which were positively correlated with HPC activation. Additionally, TNF-α or macrophage depletion inhibited the promoting effect of OSM on hepatocarcinogenesis and HPC activation. Furthermore, OSM expression in the peritumoral tissues of HCC was positively correlated with poor overall survival of patients. In conclusion, OSM plays an important role in hepatocarcinogenesis by regulating the liver inflammation environment. Hence, OSM could be used as a potential target for HCC prevention and therapy or as an indicator of HCC prognosis. [ABSTRACT FROM AUTHOR]