Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Medical imaging technology plays a crucial role in clinical diagnosis and treatment. Image compression technology provides robust technical support for the storage and transmission of massive medical imaging data, serving as an effective safeguard for hospital data backup and telemedicine. The technology holds broad application prospects in the medical field, enabling the processing of various imaging modalities, multidimensional imaging, and medical video imaging. This study elaborates on general image and video compression algorithms, the application of compression algorithms in the medical field, and the performance metrics of medical image compression, thereby providing critical technical support for enhancing clinical diagnostic efficiency and data management security.

This case report presents a 16-year-old male patient with deficiency of adenosine deaminase 2(DADA2). The patient had a history of Raynaud′s phenomenon with digital ulcers since childhood. As the disease progressed, the patient developed retinal vasculitis, intracranial hemorrhage, skin necrosis, severe malnutrition, refractory hypertension, and gastrointestinal bleeding. Genetic testing revealed compound heterozygous mutations in the ADA2 gene (paternal c.1072G > A pathogenic mutation + maternal c.1065C > A variant of unknown clinical significance). ADA2 enzyme activity was significantly reduced (0.1 U/L). A multidisciplinary treatment team developed an individualized plan to address key issues, including nutritional support, blood pressure control, rehabilitation, pain management, and balancing anticoagulation/bleeding risks. After systematic intervention, the patient′s condition showed partial improvement. This case reveals clinical challenges such as anticoagulation decisions and nutritional support of DADA2. It also emphasizes the importance of early molecular diagnosis, tumor necrosis factor-α inhibitor targeted therapy, and multidisciplinary collaboration in management, underlining the core value of precision medicine in rare disease management.

BACKGROUND: T cell dysfunction, which includes exhaustion, anergy, and senescence, is a distinct T cell differentiation state that occurs after antigen exposure. Although T cell dysfunction has been a cornerstone of cancer immunotherapy, its potential in transplant research, while not yet as extensively explored, is attracting growing interest. Interferon regulatory factor 4 (IRF4) has been shown to play a pivotal role in inducing T cell dysfunction. METHODS: A novel ultra-low-dose combination of Trametinib and Rapamycin, targeting IRF4 inhibition, was employed to investigate T cell proliferation, apoptosis, cytokine secretion, expression of T-cell dysfunction-associated molecules, effects of mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) signaling pathways, and allograft survival in both in vitro and BALB/c to C57BL/6 mouse cardiac transplantation models. RESULTS: In vitro , blockade of IRF4 in T cells effectively inhibited T cell proliferation, increased apoptosis, and significantly upregulated the expression of programmed cell death protein 1 (PD-1), Helios, CD160, and cytotoxic T lymphocyte-associated antigen (CTLA-4), markers of T cell dysfunction. Furthermore, it suppressed the secretion of pro-inflammatory cytokines interferon (IFN)-γ and interleukin (IL)-17. Combining ultra-low-dose Trametinib (0.1 mg·kg -1 ·day -1 ) and Rapamycin (0.1 mg·kg -1 ·day -1 ) demonstrably extended graft survival, with 4 out of 5 mice exceeding 100 days post-transplantation. Moreover, analysis of grafts at day 7 confirmed sustained IFN regulatory factor 4 (IRF4) inhibition, enhanced PD-1 expression, and suppressed IFN-γ secretion, reinforcing the in vivo efficacy of this IRF4-targeting approach. The combination of Trametinib and Rapamycin synergistically inhibited the MAPK and mTOR signaling network, leading to a more pronounced suppression of IRF4 expression. CONCLUSIONS Targeting IRF4, a key regulator of T cell dysfunction, presents a promising avenue for inducing transplant immune tolerance. In this study, we demonstrate that a novel ultra-low-dose combination of Trametinib and Rapamycin synergistically suppresses the MAPK and mTOR signaling network, leading to profound IRF4 inhibition, promoting allograft acceptance, and offering a potential new therapeutic strategy for improved transplant outcomes. However, further research is necessary to elucidate the underlying pharmacological mechanisms and facilitate translation to clinical practice.
Animals ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Interferon Regulatory Factors/metabolism* ; Heart Transplantation/methods* ; T-Lymphocytes/immunology* ; Sirolimus/therapeutic use* ; Pyridones/therapeutic use* ; Graft Survival/drug effects* ; Pyrimidinones/therapeutic use* ; Cell Proliferation/drug effects* ; Apoptosis/drug effects* ; Male ; Signal Transduction/drug effects*

Compounds isolated from Epimedium include the total flavonoids of Epimedium , icariin, and its metabolites (icaritin, icariside I, and icariside II), which have similar molecular structures. Modern pharmacological research and clinical practice have proved that Epimedium and its active components have a wide range of pharmacological effects, especially in improving sexual function, hormone regulation, anti-osteoporosis, immune function regulation, anti-oxidation, and anti-tumor activity. To date, we still need a comprehensive source of knowledge about the pharmacological effects of Epimedium and its bioactive compounds on the male reproductive system. However, their actions in other tissues have been reviewed in recent years. This review critically focuses on the Epimedium , its bioactive compounds, and the biochemical and molecular mechanisms that modulate vital pathways associated with the male reproductive system. Such intrinsic knowledge will significantly further studies on the Epimedium and its bioactive compounds that protect the male reproductive system and provide some guidances for clinical treatment of related male reproductive disorders.
Male ; Epimedium/chemistry* ; Humans ; Genitalia, Male/drug effects* ; Flavonoids/therapeutic use* ; Animals

Despite that sleep disturbance and poor neurocognitive performance are common complaints among coronavirus disease 2019 (COVID-19) survivors, few studies have focused on the effect of post-COVID-19 sleep disturbance (PCSD) on cognitive function. This study aimed to identify the impact of PCSD on neurocognitive function and explore the associated risk factors for the worsening of this condition. This cross-sectional study was conducted via the web-based assessment in Chinese mainland. Neurocognitive function was evaluated by the modified online Integrated Cognitive Assessment (ICA) and the Number Ordering Test (NOT). Propensity score matching (PSM) was utilized to match the confounding factors between individuals with and without PCSD. Univariate analyses were performed to evaluate the effect of PCSD on neurocognitive function. The risk factors associated with worsened neurocognitive performance in PCSD individuals were explored using binary logistic regression. A total of 8692 individuals with COVID-19 diagnosis were selected for this study. Nearly half (48.80%) of the COVID-19 survivors reported sleep disturbance. After matching by PSM, a total of 3977 pairs (7954 individuals in total) were obtained. Univariate analyses revealed that PCSD was related to worse ICA and NOT performance (P<0.05). Underlying disease, upper respiratory infection, loss of smell or taste, severe pneumonia, and self-reported cognitive complaints were associated with worsened neurocognitive performance among PCSD individuals (P<0.05). Furthermore, aging, ethnicity (minority), and lower education level were found to be independent risk factors for worsened neurocognitive performance in PCSD individuals (P<0.05). PCSD was related to impaired neurocognitive performance. Therefore, appropriate prevention and intervention measures should be taken to minimize or prevent PCSD and eliminate its potential adverse effect on neurocognitive function.
Humans ; COVID-19/epidemiology* ; Male ; Female ; Sleep Wake Disorders/epidemiology* ; Propensity Score ; Middle Aged ; Cross-Sectional Studies ; Adult ; SARS-CoV-2 ; Aged ; Risk Factors ; China/epidemiology* ; Cognition ; Cognitive Dysfunction/etiology* ; Neuropsychological Tests