Viral infections are increasingly recognized as triggers for depressive disorders, particularly following the SARS-CoV-2 pandemic and the rise of long COVID. Viruses such as Herpes Simplex Virus (HSV), Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) are linked to depression through complex neurobiological mechanisms. These include immune system dysregulation, chronic inflammation, and neurotransmitter imbalances that affect brain function and mood regulation. Viral activation of the immune system leads to the release of pro-inflammatory cytokines, resulting in neuroinflammation and associated depressive symptoms. Furthermore, specific viruses can disrupt neurotransmitter systems, including serotonin, dopamine, and glutamate, all of which are essential for mood stabilization. The unique interactions of different viruses with these systems underscore the need for virus-specific therapeutic approaches. Current broad-spectrum treatments often overlook the precise neurobiological pathways involved in post-viral depression, reducing their efficacy. This review emphasizes the need to understand these virus-specific interactions to create tailored interventions that directly address the neurobiological effects induced by each type of virus. These interventions may include immunomodulatory treatments that target persistent inflammation, antiviral therapies to reduce the viral load, or neuroprotective strategies that restore neurotransmitter balance. Precision medicine offers promising avenues for the effective management of virus-induced depression, providing patient-specific approaches that address the specific biological mechanisms involved. By focusing on the development of these targeted treatments, this review aims to pave the way for a new era in psychiatric care that fully addresses the root causes of depression induced by viral infections.

Viral infections are increasingly recognized as triggers for depressive disorders, particularly following the SARS-CoV-2 pandemic and the rise of long COVID. Viruses such as Herpes Simplex Virus (HSV), Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) are linked to depression through complex neurobiological mechanisms. These include immune system dysregulation, chronic inflammation, and neurotransmitter imbalances that affect brain function and mood regulation. Viral activation of the immune system leads to the release of pro-inflammatory cytokines, resulting in neuroinflammation and associated depressive symptoms. Furthermore, specific viruses can disrupt neurotransmitter systems, including serotonin, dopamine, and glutamate, all of which are essential for mood stabilization. The unique interactions of different viruses with these systems underscore the need for virus-specific therapeutic approaches. Current broad-spectrum treatments often overlook the precise neurobiological pathways involved in post-viral depression, reducing their efficacy. This review emphasizes the need to understand these virus-specific interactions to create tailored interventions that directly address the neurobiological effects induced by each type of virus. These interventions may include immunomodulatory treatments that target persistent inflammation, antiviral therapies to reduce the viral load, or neuroprotective strategies that restore neurotransmitter balance. Precision medicine offers promising avenues for the effective management of virus-induced depression, providing patient-specific approaches that address the specific biological mechanisms involved. By focusing on the development of these targeted treatments, this review aims to pave the way for a new era in psychiatric care that fully addresses the root causes of depression induced by viral infections.

Viral infections are increasingly recognized as triggers for depressive disorders, particularly following the SARS-CoV-2 pandemic and the rise of long COVID. Viruses such as Herpes Simplex Virus (HSV), Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) are linked to depression through complex neurobiological mechanisms. These include immune system dysregulation, chronic inflammation, and neurotransmitter imbalances that affect brain function and mood regulation. Viral activation of the immune system leads to the release of pro-inflammatory cytokines, resulting in neuroinflammation and associated depressive symptoms. Furthermore, specific viruses can disrupt neurotransmitter systems, including serotonin, dopamine, and glutamate, all of which are essential for mood stabilization. The unique interactions of different viruses with these systems underscore the need for virus-specific therapeutic approaches. Current broad-spectrum treatments often overlook the precise neurobiological pathways involved in post-viral depression, reducing their efficacy. This review emphasizes the need to understand these virus-specific interactions to create tailored interventions that directly address the neurobiological effects induced by each type of virus. These interventions may include immunomodulatory treatments that target persistent inflammation, antiviral therapies to reduce the viral load, or neuroprotective strategies that restore neurotransmitter balance. Precision medicine offers promising avenues for the effective management of virus-induced depression, providing patient-specific approaches that address the specific biological mechanisms involved. By focusing on the development of these targeted treatments, this review aims to pave the way for a new era in psychiatric care that fully addresses the root causes of depression induced by viral infections.

Despite the various medications used in clinics, the efforts to develop more effective treatments for depression continue to increase in the past decades mainly because of the treatment-resistant population, and the testing of several hypotheses- and target-based treatments. Undesirable side effects and unresponsiveness to current medications fuel the drive to solve this top global health problem. In this study, we focused on neuroinflammatory response-mediated depression which represents a cluster of depression etiology both in animal models and humans. Several meta-analyses reported that proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were increased in major depressive disorder patients. Inflammatory mediators implicated in depression include type-I interferon and inflammasome pathways. To elucidate the molecular mechanisms of neuroinflammatory cascades underlying the pathophysiology of depression, we introduced hycanthone, an antischistosomal drug, to check whether it can counteract depressive-like behaviors in vivo and normalize the inflammation-induced changes in vitro. Lipopolysaccharide (LPS) treatment increased proinflammatory cytokine expression in the murine microglial cells as well as the stimulation of type I interferon-related pathways that are directly or indirectly regulated by Janus kinase-signal transducer and activator of transcription (JAK-STAT) activation. Hycanthone treatment attenuated those changes possibly by inhibiting the JAK-STAT pathway and inflammasome activation. Hycanthone also ameliorated depressive-like behaviors by LPS. Taken together, we suggest that the inhibitory action of hycanthone against the interferon pathway leading to attenuation of depressive-like behaviors can be a novel therapeutic mechanism for treating depression.

Purpose: An adequate minimal surgical margin for partial nephrectomy (PN) has not yet been conclusively established. Therefore, we aimed to compare PN recurrence rates according to surgical margin status and to establish an adequate minimal surgical margin. Materials and Methods: We retrospectively studied patients with clinically localized renal cell carcinoma who underwent PN between 2005 and 2014. Surgical margin width (SMW) was assessed for all surgical tissues and divided into three groups: SMW <1 mm, SMW ≥1 mm, and positive surgical margin (PSM). The data were analyzed using the Kaplan-Meier method with log-rank tests and multivariate Cox regression models. Results: Of 748 patients (median age, 55 years; interquartile range, 46–64 years; 220 female), 704 (94.2%) and 44 (5.8%) patients had negative and PSMs, respectively. Recurrence-free survival was significantly lower in patients with PSMs (p<0.001) and was not significantly different between SMW ≥1 mm and <1 mm groups (p=0.604). PSM was a significant predictor of recurrence (hazard ratio: 8.03, 95% confidence interval: 2.74–23.56, p<0.001), in contrast to SMW <1 mm (p=0.680). Conclusion A PSM after PN significantly increases the risk of recurrence. We discovered that even a submillimeter safety surgical margin may be enough to prevent recurrence. To maximize normal renal parenchyma preservation and to avoid cancer recurrence in renal parenchymal tumor patients, PN may be a safe treatment, except for those with a PSM in the final pathology.

Asthma is a heterogeneous disease whose development is shaped by a variety of environmental and genetic factors. While several recent studies suggest that microbial dysbiosis in the gut may promote asthma, little is known about the relationship between the recently discovered lung microbiome and asthma. Innate lymphoid cells (ILCs) have also been shown recently to participate in asthma. To investigate the relationship between the lung microbiome, ILCs, and asthma, we recruited 23 healthy controls (HC), 42 patients with non-severe asthma, and 32 patients with severe asthma. Flow cytometry analysis showed severe asthma associated with fewer natural cytotoxicity receptor (NCR) + ILC3s in the lung.Similar changes in other ILC subsets, macrophages, and monocytes were not observed. The asthma patients did not differ from the HC in terms of the alpha and beta-diversity of the lung and gut microbiomes. However, lung function correlated positively with both NCR + ILC3 frequencies and microbial diversity in the lung. Sputum NCR + ILC3 frequencies correlated positively with lung microbiome diversity in the HC, but this relationship was inversed in severe asthma. Together, these data suggest that airway NCR + ILC3s may contribute to a healthy commensal diversity and normal lung function.

PURPOSE: This study aimed to compare the diagnostic performance of contrast-enhanced digital mammography (CEDM) and contrast-enhanced magnetic resonance imaging (CEMRI) in preoperative evaluations, and to evaluate the effect of each modality on the surgical management of women with breast cancer. METHODS: This single-center, prospective study was approved by the Institutional Review Board, and informed consent was obtained from all patients. From November 2016 to October 2017, 84 patients who were diagnosed with invasive carcinoma (69/84) and ductal carcinoma in situ (15/84), and underwent both CEDM and CEMRI, were enrolled. Imaging findings and surgical management were correlated with pathological results and compared. The diagnostic performance of both modalities in the detection of index and secondary cancers (multifocality and multicentricity), and occult cancer in the contralateral breast, was compared. The authors also evaluated whether CEDM or CEMRI resulted in changes in the surgical management of the affected breast due to imaging-detected findings. RESULTS: Eighty-four women were included in the analysis. Compared with CEMRI, CEDM demonstrated a similar sensitivity (92.9% [78/84] vs. 95.2% [80/84]) in detecting index cancer (p=0.563). For the detection of secondary cancers in the ipsilateral breast and occult cancer in the contralateral breast, no significant differences were found between CEDM and CEMRI (p=0.999 and p=0.999, respectively). Regarding changes in surgical management, CEDM resulted in similar changes compared with CEMRI (30.9% [26/84] vs. 29.7% [25/84], p=0.610). Regarding changes in surgical management due to false-positive findings, no significant differences were found between CEDM and CEMRI (34.6% [9/26] vs. 44.0% [11/25], p=0.782). CONCLUSION: CEDM demonstrated a diagnostic performance comparable with CEMRI in depicting index cancers, secondary cancers, and occult cancer in the contralateral breast. CEDM demonstrated similar changes in surgical management compared with CEMRI.
Breast Neoplasms* ; Breast* ; Carcinoma, Intraductal, Noninfiltrating ; Contrast Media ; Ethics Committees, Research ; Female ; Humans ; Informed Consent ; Magnetic Resonance Imaging* ; Mammography* ; Prospective Studies

BACKGROUND/AIMS: The aim of this study was to evaluate the effect of the synthetic S-allyl-l-cysteine (SAC) PMK-S005 on gastric acid secretion, inflammation, and antioxidant enzymes in aging rats. METHODS: The rats were divided into four groups at 31 weeks of age and were continuously fed a diet containing a vehicle control, PMK-S005 (5 or 10 mg/kg), or lansoprazole (5 mg/kg). Gastric acid secretion and connective tissue thickness of the lamina propria were evaluated at 74 weeks and 2 years of age. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and COX-2 levels were measured by using enzyme-linked immunosorbent assays (ELISAs) or Western blot assays. Levels of antioxidant enzymes, including heme oxyganase 1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO-1), were also measured. RESULTS: As the rats aged, gastric acid secretion significantly decreased, and the connective tissue of the lamina propria increased. However, 74-week-old rats in the PMK-S005 group exhibited greater levels of gastric acid secretion than those of the control and lansoprazole groups. The increase of TNF-α, IL-1β, and COX-2 expression in 74-week and 2-year-old control rats were inhibited by PMK-S005. In addition, the decrease in HO-1 and NQO-1 protein expression that occurred with aging was inhibited by PMK-S005 in the 74-week-old rats. CONCLUSIONS: These results suggest that PMK-S005 has therapeutic potential as an antiaging agent to ameliorate age-related gastric acid secretion, inflammation, and oxidative stress in the stomach.
Aging ; Animals ; Antioxidants ; Blotting, Western ; Child, Preschool ; Connective Tissue ; Diet ; Enzyme-Linked Immunosorbent Assay ; Gastric Acid* ; Heme ; Humans ; Inflammation* ; Interleukins ; Lansoprazole ; Mucous Membrane ; Oxidative Stress ; Rats* ; Stomach* ; Tumor Necrosis Factor-alpha

OBJECTIVES: The purpose of this study is to identify the level of psychosocial stress of residents near asbestos mines, and to investigate the relationship between psychosocial stress and asbestos exposure history as well as, asbestos exposure awareness. METHODS: The survey was conducted in 297 individuals, by one-on-one interviews with a standard questionnaire including demographic characteristics, health status, asbestos exposure history, and awareness of asbestos exposure. The levels of psychosocial stress were measured through the Psychosocial Wellbeing Index-Short Form(PWI-SF). Multivariate logistic regression was conducted using psychosocial stress as a dependent variable. Demographic characteristics, health status, asbestos exposure history, and asbestos exposure awareness were examined as independent variable. RESULTS: The average PWI-SF score was 17.5 +/- 8.0, with 40 people (13.5%) in the high-risk stress group (PWI-SF 27 points or more). The group having an asbestos-related occupational history had a 2.53 times higher proportion of psychosocial stress (95% CI: 1.03~6.21). The group recognizing asbestos exposure had an even higher proportion of high psychosocial stress group (4.84 times, 95% CI: 1.41~16.55). CONCLUSIONS: The incidence of psychosocial stress is significantly higher in residents near asbestos mines having an asbestos-related occupational history who recognize their frequent asbestos exposure. Therefore, mental health is affected by the awareness of environmental asbestos exposure as well as an occupational exposure to asbestos.
Asbestos ; Incidence ; Logistic Models ; Mental Health ; Occupational Exposure ; Questionnaires

A biloma is a rare abnormal accumulation of intrahepatic or extrahepatic bile caused by a traumatic or spontaneous rupture of the biliary tree. The reported incidence of postoperative biloma ranges from 4.8% to 7.6%. Biliary drainage is usually important and necessary for the treatment of biloma, but sometimes bile leakage fails to improve despite prolonged conservative drainage. We report a case of postoperative refractory biliary leakage managed with percutaneous ablation by N-butyl cyanoacrylate.
Bile ; Bile Ducts ; Biliary Tract ; Cyanoacrylates ; Drainage ; Incidence ; Rupture, Spontaneous