LGBTI Healthcare in Medical Education.

ABSTRACT: Our aim is to reveal the interaction of cultural and religious influences with professional equipment by determining the level of knowledge, sexual attitudes, and homophobia of medical students about LGBTI+ individuals. The study included 324 students from our faculty of medicine. The Hudson and Ricketts Homophobia scale, the Attitudes Towards Lesbians and Gay Men scale, and the Hendrick Sexual Attitudes scale were used with the sociodemograpic data form. Data were collected and analyzed using descriptive and inferential statistical tests. The mean score of the students from the Hudson and Ricketts Homophobia scale was 58.50. The findings of our study support that medical students consider that the education they receive in this regard is inadequate. One of the goals of undergraduate medical education is the provision of health services to all segments of society; therefore, it is recommended to make improvements in the curriculum in this regard.

The effect of Vortioxetine on the NLRP3 pathway and microglial activity in the prefrontal cortex in an experimental model of depression.

BACKGROUND: Increasing evidence suggests that early life stress (ELS) and neuroinflammation are associated with the pathophysiology of depression. The purpose of this study was to determine the effects of Vortioxetine (VOR), a novel antidepressant, on ELS-induced behavioral changes and neuroinflammation. METHOD: Wistar Albino 4-week-old male rats were divided into four groups: control; chronic unpredictable stress (CUMS), VOR, CUMS + VOR. Neurobehavioral assessment was performed on the first, 21st, and 42nd days. RT-PCR was used to detect the expression of P2X7, NLRP3, IL1ß, IL18 in the prefrontal cortex. To assess the microglial activities of the prefrontal cortex, immunohistochemically stained CD68, and leukocyte common antigen (LCA) preparations were scanned with Manual WSI software, Basler camera, and scored. RESULT AND DISCUSSION: Exposure to CUMS was associated with depression and anxiety-like behaviors, and administration of VOR led to improvement in these behaviors. NLRP3, IL-1ß, and IL-18 were shown to be upregulated in the prefrontal cortex of CUMS rats, while their high expression was inhibited by VOR treatment. CD68 and LCA expressions were significantly higher in the CUMS group compared to the other groups. CONCLUSION: According to these results, it may be considered that NLRP3 inflammasome-associated neuroinflammatory response and microglial activation may play a role in the etiopathogenesis of ELS.

Increased NLRP3 inflammasome expression in peripheral blood mononuclear cells of patients with schizophrenia: a case-control study.

OBJECTIVE: This study aimed to evaluate the gene expression of the P2X purinoceptor 7 (P2X7R)- nod-like receptor pyrin domain-containing protein 3 (NLRP3) signal pathway in peripheral blood mononuclear cells (PBMCs) between schizophrenia (SCZ) patients and healthy controls (HC) to reveal its relationship with clinical variables. METHODS: Thirty-two SCZ patients and 41 healthy controls were included in this study. The Scale for the Assessment of Positive Symptoms (SAPS) and the Scale for the Assessment of Negative Symptoms (SANS), The Global Assessment of Functioning (GAF) scale and the Functioning Assessment Short Test (FAST) scales were applied. P2X7R, NLRP3, IL-1ß and IL-18 gene expression levels were evaluated by real-time polymerase chain reaction in PBMCs. RESULTS: NLRP3, P2RX7, IL-1ß and IL-18 expression levels were significantly higher in PBMCs of SCZ patients than in HC subjects. Negative correlations were found between NLRP3 gene expression levels and GAF and FAST scales scores. There was a negative correlation between IL-18 expression levels and the GAF and FAST scales scores and a positive correlation with the SAPS scale scores. CONCLUSIONS: Systemic inflammation is implicated in SCZ pathogenesis, according to our findings, which suggest that the NLRP3 pathway may be involved. The NLRP3 inflammasome may serve as a biomarker for SCZ, and its pharmacological regulation may be a promising treatment approach.Key pointsWe hypothesised that the NLRP3 pathway may contribute to the etiopathogenesis of schizophrenia.NLRP3, IL-1ß and IL-18 mRNA levels were higher in patients with schizophrenia compared to healthy controls.Negative correlations were found between NLRP3 gene expression levels and GAF and FAST scales scores.There was a negative correlation between IL-18 expression levels and the GAF and FAST scales scores.The SAPS scale scores and IL-18 expression levels had a positive correlation.Given all these findings, it can be stated that NLRP3 inflammasome may play a role in the pathogenesis and symptoms of schizophrenia.

Agomelatine attenuates calcium signaling and apoptosis via the inhibition of TRPV1 channel in the hippocampal neurons of rats with chronic mild stress depression model.

Chronic stress plays a key role in inducing various clinical disorders through mechanistic pathways, including oxidative stress and apoptosis. Transient receptor potential vanilloid 1 (TRPV1) channels, which are permeable to cations, mainly Ca2+, are susceptible to oxidative stress. Agomelatine (AGOM) is an antidepressant drug analogous to the antioxidant melatonin hormone, although its action has not been fully clarified yet. We aimed to investigate the protective role of AGOM on TRPV1-induced Ca2+ signaling and apoptosis in rats with chronic mild stress (CMS). The rats were divided into six main groups: control, dimethyl sulfoxide (DMSO), AGOM, CMS, CMS+DMSO, and CMS+AGOM. Five weeks of CMS were applied to rats in the CMS groups. The induction of CMS was confirmed with the sucrose preference test. The AGOM treatments were administered in the last three weeks of the experiment. The depression-like behavior, TRPV1-mediated cytosolic Ca2+ influx, lipid peroxidation, apoptosis, caspase - 3, and - 9 levels increased in the hippocampal neurons of CMS groups, although cell viability level was diminished by the CMS exposure. However, AGOM treatment downregulated stress-related behaviors, hippocampal oxidant and apoptotic markers by modulating the TRPV1 activity. In conclusion, TRPV1-mediated Ca2+ signaling and apoptosis may play a role in the etiopathogenesis of experimental depression. By regulating these changes with AGOM treatment, a positive contribution may be made to depression treatment.

The occurrence and consequences of violence against healthcare workers in Turkey: before and during the COVID-19 pandemic.

BACKGROUND: Before and throughout the COVID-19 pandemic, healthcare workers (HCWs) were victims of workplace violence (WPV). There are no reliable statistics on the occurrence and consequences of WPV against HCWs in Turkey throughout the pandemic period. OBJECTIVE: We investigated the rates of WPV against HCWs in Turkey in the pre-pandemic and pandemic periods, variables associated with WPV, and the relationship between these variables and job satisfaction and burnout. METHODS: A structured online questionnaire was disseminated through social media channels to HCWs in various healthcare settings. All the respondents also completed the Maslach Burnout Inventory (MBI) and Job Satisfaction Scale. Based on the data obtained, we determined the frequency, causes, and consequences of WPV against HCWs before and during the pandemic. RESULTS: There were 701 completed questionnaires. 68.2% of participants were female, and 65.6% of them were doctors. The rate of WPV was 54.1% and 24.3% before and during the pandemic, respectively. Verbal abuse was the most common kind of WPV. Female HCWs were more likely to be physically assaulted than their male counterparts, especially those working in COVID-19 units. The majority of HCWs who were exposed to the violence at least once did not report WPV. HCWs exposed to WPV during the pandemic reported more emotional exhaustion and depersonalization and a lower perceived level of personal achievement. CONCLUSION: HCWs were exposed to significant levels of violence both before and during the pandemic. Preventing WPV against HCWs and removing barriers to reporting abuse is crucial.

Maternal prenatal stress and depression-like behavior associated with hippocampal and cortical neuroinflammation in the offspring: An experimental study.

Prenatal stress can negatively impact neonatal health, growth, and bonding with the mother. However, molecular basis of these modifications is not completely understood. The aim of this experimental study was to test the hypothesis that intrauterine stress exposure may contribute to subsequent depression-like comorbidities associated with neuroinflammation. Wistar Albino nulliparous female rats were divided into two groups (each, n = 6): controls and pregnancy stress (Days 1 through 21). Two live rat pups (one female and one male) from each term delivery were randomly selected, and depression-like behavior tests were performed on Postpartum Days 30-34, followed by euthanasia on Day 35. NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) pathway gene expressions in the hippocampus and immunohistochemical caspase 3 (cas-3), mammalian target of rapamycin (mTOR), and transient receptor potential melastatin (TRPM) staining in the temporal and prefrontal cortices were evaluated. Compared with controls, exposure to prenatal stress was associated with increased depression and anxiety-like behavior, hippocampal NLRP3 inflammasome activation (p = 0.022 and p = 0.035 for female and male pups, respectively), neuronal degeneration and increased cas-3, mTOR, and TRPM immunostaining in the prefrontal and temporal cortices of both female and male offspring (p < 0.05 for all comparisons except p < 0.01 for cas-3 in the male cortex and female temporal cortex). Exposure to antenatal stress can lead to depression-like behavior in the infant, mainly driven by hippocampal NLRP3 inflammasome activation, cortical neuroinflammation, and neurodegeneration. Future perspectives include NLRP3-targeted therapies with anti-inflammatory and anti-apoptotic effects against adverse prenatal effects of maternal stress.

Experimental model of unpredictable maternal stress and diabetes risk of offspring: An immunohistochemical study.

The effect of stress on the occurrence of diabetes mellitus (DM) is commonly reported in recent studies. Maternal stress may have a negative effect on the later life of offspring. However, most studies only investigated long-term intrauterine stress on behavioral, emotional, psychological, and immunological disorders of offspring. The relationship between maternal stress and DM occurrence in the later life period of offspring is not known. This rat model study aimed to evaluate the susceptibility of offspring to DM after exposure to intrauterine stress. The purpose of this study is to examine serum glucose levels of mothers and offspring exposed to maternal stress and to evaluate pancreatic tissues pathologically and immunohistochemically. Twelve, Wistar Albino female rats were equally divided into two groups: controls and maternal stress groups. Normal routine conditions were applied to the control group without any stress. The pregnant rats in the maternal stress group were exposed to chronic unpredictable stressors throughout the 21-day gestation. One female and one male offspring and mothers from each term delivery were randomly selected and euthanatized at the 35th day. During the necropsy, blood and pancreatic tissue samples were collected from both mothers and pups. High serum glucose levels from mothers and offspring in the maternal stress group and the control group were compared. Additionally, histopathological examinations assessed the increased cell degeneration in mother rats and offspring. Immunohistochemical examinations revealed decreased insulin, amylin, and insulin receptor expressions and slightly increased glucagon expression in Langerhans islet cells in the maternal stress group. These results indicated that maternal stress may be a predisposing factor for DM in both mothers and offspring in their later life periods.

Dexpanthenol may protect the brain against lipopolysaccharide induced neuroinflammation via anti-oxidant action and regulating CREB/BDNF signaling.

BACKGROUND: Neuroinflammation plays an important role in the pathogenesis of many psychiatric and neurodegenerative diseases. Dexpanthenol (Dex) is an alcoholic analogue of pantothenic acid with antioxidant, anti-inflammatory and anti-apoptotic properties. The purpose of this study was to determine the effect of dexpanthenol on lipopolysaccharide (LPS)-induced brain injury, specifically on the CREB/BDNF pathway. METHOD: Thirty-two rats were distributed into four groups: control, LPS, LPS + Dex and Dex groups. In this study, using real-time PCR, we evaluated changes in the gene expression of BDNF and CREB in the hippocampal brain tissue. Total antioxidant status (TAS), total oxidant status (TOS) were measured spectrophotometrically in the cortical tissue. Brain and cerebellum tissues were collected for histopathological examination and immunohistochemical assessment of tumor necrosis factor alpha (TNF-α) and caspase-3 (Cas-3). RESULT AND DISCUSSION: In the LPS + Dex group, TAS levels were significantly higher while TOS and OSI levels were significantly lower than the LPS group. In the LPS + Dex and Dex group, BDNF relative mRNA expressions were significantly higher than the LPS group. The levels of CREB relative mRNA expression in LPS and LPS + Dex group were significantly lower than the control group. An increased expression of Cas-3 and TNF-α in the LPS group and a decreased expression in the LPS + Dex group were observed in the immunohistochemical examination. CONCLUSION: According to these results, it may be considered that CREB-mediated BDNF synthesis may play a role in the etiopathogenesis of neuroinflammation. By regulating these changes with dexpanthenol treatment, a positive contribution may be made to neuroinflammation treatment.

Late-life Onset Mania After Varenicline Use: A Case Report.

Late-life onset manic attacks generally occur secondary to general medical conditions or drug use. Varenicline is an α4ß2 nicotinic acetylcholine receptor partial agonist, used for the cessation of smoking. In this case report, we present a 67-year-old male patient with a new-onset manic episode following varenicline treatment. The patient's manic symptoms started on the seventh day of varenicline treatment. His symptoms started on the 7th day of treatment. He was admitted to the psychiatric outpatient clinic since his symptoms did not improve despite discontinuing varenicline treatment. In the initial mental status examination, he scored 35/60 on the Young Mania Rating Scale (YMRS). On the twenty-fifth day of the hospitalization, the patient was discharged since his YMRS score improved (5/60). Varenicline may cause manic episodes in patients with bipolar disorder and in healthy individuals. An increasing number of serious psychiatric disorders are being reported due to varenicline treatment. Mental state examination before and during varenicline treatment seems necessary.