Functional near-infrared spectroscopy-based diagnosis support system for distinguishing between mild and severe depression using machine learning approaches.

Significance: Early diagnosis of depression is crucial for effective treatment. Our study utilizes functional near-infrared spectroscopy (fNIRS) and machine learning to accurately classify mild and severe depression, providing an objective auxiliary diagnostic tool for mental health workers. Aim: Develop prediction models to distinguish between severe and mild depression using fNIRS data. Approach: We collected the fNIRS data from 140 subjects and applied a complete ensemble empirical mode decomposition with an adaptive noise-wavelet threshold combined denoising method (CEEMDAN-WPT) to remove noise during the verbal fluency task. The temporal features (TF) and correlation features (CF) from 18 prefrontal lobe channels of subjects were extracted as predictors. Using recursive feature elimination with cross-validation, we identified optimal TF or CF and examined their role in distinguishing between severe and mild depression. Machine learning algorithms were used for classification. Results: The combination of TF and CF as inputs for the prediction model yielded higher classification accuracy than using either TF or CF alone. Among the prediction models, the SVM-based model demonstrates excellent performance in nested cross-validation, achieving an accuracy rate of 92.8%. Conclusions: The proposed model can effectively distinguish mild depression from severe depression.

Abnormal prefrontal cortical activation during the GO/NOGO and verbal fluency tasks in adult patients with comorbid generalized anxiety disorder and attention-deficit/hyperactivity disorder: An fNIRS study.

Generalized anxiety disorder (GAD) and adult attention-deficit/hyperactivity disorder (ADHD) are commonly reported comorbidities. Adult GAD patients with comorbid ADHD are often underdiagnosed and undertreated. To explore the clinical value of functional near-infrared spectroscopy (fNIRS) data for assisting in the accurate diagnosis of ADHD in individuals with GAD, haemoglobin (HbO) concentration changes in the prefrontal cortex (PFC) were detected via fNIRS in 49 patients with both GAD and ADHD, 46 patients with GAD, and 34 healthy controls (HCs) during a verbal fluency task (VFT) and a GO/NOGO task. The correlations between PFC fNIRS data and the severity of inattention and hyperactivity symptoms assessed using the adult ADHD Self-Report Scale (ASRS) were analyzed. Our results showed that, during the GO/NOGO task, channels in the left dorsolateral PFC (channels 28 and 29) were hyperactivated, while channels in the medial PFC (channels 36, 37, and 47) were hypoactivated in participants with ADHD and GAD compared with those with GAD alone. During the VFT, compared with the HC group, both the ADHD + GAD group and the GAD group exhibited significantly decreased HbO activation in the medial PFC (channels 37, 38, and 48) and in the left ventrolateral PFC (channel 39); moreover, no difference was found between the ADHD + GAD group and the GAD group. Activation in the left dorsolateral PFC (channels 28 and 29) during the GO/NOGO task showed a significant positive correlation with ASRS-inattention scores. Our results indicated that fNIRS data collected during the GO/NOGO task may help to distinguish patients with comorbid GAD and ADHD from those with GAD alone.

Tumor cell-secreted exosomal miR-22-3p inhibits transgelin and induces vascular abnormalization to promote tumor budding.

Tumor budding (TB) is considered a histomorphological marker of poor prognosis in patients with breast cancer (BC). Tumor vasculature is disordered and unstable in BC, which causes restricted drug delivery, hypoxia, and tumor metastasis. Traditional anti-angiogenic treatments cause extreme hypoxia, increased invasion, metastasis, and drug resistance due to blood vessel rarefaction or regression. Therefore, the application of anti-angiogenic strategies for vascular normalization in tumors is crucial to improve therapeutic efficacy in BC. In the present study, we found that transgelin (TAGLN) promoted the normalization of tumor vessels by regulating the structure and function of endothelial cells, and knockout of TAGLN in tumor-bearing mice resulted in tumor vessel abnormalization, an increase in epithelial-mesenchymal transition characteristics of tumor cells, and promotion of TB. Moreover, BC cells secrete exosomal miR-22-3p that mediates tumor vessel abnormalization by inhibiting TAGLN. We demonstrated for the first time that TAGLN plays an essential role in tumor vessel normalization, and thus it impairs TB and metastasis. Additionally, the findings of this study indicate that exosomal miR-22-3p is a potential therapeutic target for BC.

Interaction between laminin-5γ2 and integrin ß1 promotes the tumor budding of colorectal cancer via the activation of Yes-associated proteins.

Colorectal cancer (CRC) is a common cancer type and a threat to human health. Tumor budding (TB) is the presence of a single cancer cell or clusters of up to five cancer cells prior to the invasive front of an aggressive carcinoma and is an independent prognosis factor for CRC. The molecular mechanism of TB is still unclear, and drugs that inhibit this process are still in the blank stage. This study found that TBs exhibit characteristics of partial EMT with a decreased expression of E-cadherin and no substantial differences in the expression of N-cadherin and vimentin. We also observed the interaction of integrin with extracellular matrix components, laminin-5γ2 (LN-5γ2), play essential roles in the TB of CRC. We then verified that the interaction between LN-5γ2 and integrin ß1 promotes the TB of CRC via the activation of FAK and Yes-associated proteins (YAP). A natural drug monomer, cucurbitacin B, was screened using virtual screening methods for the interaction interface of proteins. We found that this monomer could block the interaction interface between LN-5γ2 and integrin ß1 and substantially inhibit the TB of CRC cells via inactivation of YAP. This study provides new insights into the mechanism of TB mechanism and the development of drugs targeting the TB of CRC.

Correction: Interaction between laminin-5γ2 and integrin ß1 promotes the tumor budding of colorectal cancer via the activation of Yes-associated proteins.

The original version of this Article contained an error in the author affiliations. Affiliation number 4 incorrectly read "Department of Gastroenterology and Hepatology, Tianjin Institute of Digestive Disease, Tianjin Institute of Digestive Disease". It should be "Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300052, China".