| مشخصات مقاله | |
| ترجمه عنوان مقاله | ارتباط عفونت های شدید دوران کودکی با افسردگی و خودآزاری عمدی در نوجوانان و جوانان |
| عنوان انگلیسی مقاله | Association of severe childhood infections with depression and intentional self-harm in adolescents and young adults |
| انتشار | مقاله سال ۲۰۲۲ |
| تعداد صفحات مقاله انگلیسی | ۹ صفحه |
| هزینه | دانلود مقاله انگلیسی رایگان میباشد. |
| پایگاه داده | نشریه الزویر |
| نوع نگارش مقاله |
مقاله پژوهشی (Research Article) |
| مقاله بیس | این مقاله بیس نمیباشد |
| نمایه (index) | Scopus – Master Journals List – JCR – Medline |
| نوع مقاله | ISI |
| فرمت مقاله انگلیسی | |
| ایمپکت فاکتور(IF) |
۷٫۲۱۷ در سال ۲۰۲۰ |
| شاخص H_index | ۱۵۳ در سال ۲۰۲۰ |
| شاخص SJR | ۲٫۵۵۷ در سال ۲۰۲۰ |
| شناسه ISSN | ۰۸۸۹-۱۵۹۱ |
| شاخص Quartile (چارک) | Q1 در سال ۲۰۲۰ |
| فرضیه | ندارد |
| مدل مفهومی | ندارد |
| پرسشنامه | ندارد |
| متغیر | ندارد |
| رفرنس | دارد |
| رشته های مرتبط | روانشناسی، پزشکی |
| گرایش های مرتبط | روانشناسی بالینی، مغز و اعصاب |
| نوع ارائه مقاله |
ژورنال |
| مجله | رفتار مغز و ایمنی – Brain Behavior and Immunity |
| دانشگاه | Janssen Pharmaceutical Companies of Johnson and Johnson, Solna, Sweden |
| کلمات کلیدی | عفونت های دوران کودکی، افسردگی، رفتار آسیب رسان به خود، خودکشی کردن، عوامل خطر خانوادگی، مقایسه خواهر و برادر |
| کلمات کلیدی انگلیسی | Childhood infections – Depression – Self-injurious behavior – Suicide – Familial risk factors – Sibling comparison |
| شناسه دیجیتال – doi |
https://doi.org/10.1016/j.bbi.2021.10.004 |
| کد محصول | E15820 |
| وضعیت ترجمه مقاله | ترجمه آماده این مقاله موجود نمیباشد. میتوانید از طریق دکمه پایین سفارش دهید. |
| دانلود رایگان مقاله | دانلود رایگان مقاله انگلیسی |
| سفارش ترجمه این مقاله | سفارش ترجمه این مقاله |
| فهرست مطالب مقاله: |
| Abstract Keywords Introduction Methods Results Discussion Conclusions Role of the funding source Data availability Declaration of Competing Interest Appendix A. Supplementary data References |
| بخشی از متن مقاله: |
| ABSTRACT Early-life infections have been linked with subsequent depression and self-harm. Examination of specific groups of infections and the role of familial factors may elucidate this observed relationship. We addressed these considerations in our investigations of the association of severe childhood infections with the risks of depression and self-harm in adolescence and early-adulthood. This population-based cohort study included all individuals born in Sweden between 1982 and 1996, with follow-up through 2013 (N = 1,506,070). Severe childhood infections were identified using inpatient and outpatient diagnoses from birth through age 12. Any infection as well as specific groups of infections were investigated. We examined diagnoses of depression and self-harm within inpatient and outpatient care and death by self-harm between ages 13 and 31. Cox proportional hazards regression models were used to estimate absolute risks, hazard ratios (HRs), and 95% CIs. When adjusting for sex and birth year, individuals exposed to any childhood infection demonstrated increased absolute risk differences for both outcomes (2.42% [95% CI, 0.41–۴٫۴۳%] of being diagnosed with depression up until age 31, and 0.73% [− ۲٫۰۵% to 3.51%] of self-harm up until age 31) and increased relative risks (HR, 1.22 [1.20–۱٫۲۴] for depression and HR, 1.29 [1.25–۱٫۳۲] for self-harm). When controlling for unmeasured factors shared between family members by comparing discordant siblings, no strong association persisted. Our findings show that childhood infections may not be involved in the etiology of later depression and self-harm, and highlight the importance of identifying these genetic and environmental familial risk factors, which may serve as targets for interventions. 1. Introduction Accumulating evidence suggests that infections, inflammatory response, and the immune system are associated with increased risks of depression (Benros et al., 2013; Kohler ¨ et al., 2017; Miller and Raison, 2016) and suicide (Lund-Sørensen et al., 2016; Brundin et al., 2017; Brundin et al., 2015; Hansen et al., 2019). While certain infectious agents reach the central nervous system directly (Okusaga et al., 2011; Yagmur et al., 2010; Zhang et al., 2012; Arling et al., 2009), others may affect the brain by altering the microbiome (Cryan and Dinan, 2012) or through innate immune system activation and inflammatory mediators (Setiawan et al., 2015; Dando et al., 2014). |