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- BDNF (2)
- acute coronary syndrome (2)
- coronary heart disease (2)
- depression (2)
- heart failure (2)
- somatic comorbidity (2)
- Familiengeschichte (1)
- Frühe Neuzeit (1)
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- Jewish Studies (1)
The Jewish family has been the subject of much admiration and analysis, criticism and myth-making, not just but especially in modern times. As a field of inquiry, its place is at the intersection – or in the shadow – of the great topics in Jewish Studies and its contributing disciplines. Among them are the modernization and privatization of Judaism and Jewish life; integration and distinctiveness of Jews as individuals and as a group; gender roles and education. These and related questions have been the focus of modern Jewish family research, which took shape as a discipline in the 1910s.
This issue of PaRDeS traces the origins of academic Jewish family research and takes stock of its development over a century, with its ruptures that have added to the importance of familial roots and continuities. A special section retrieves the founder of the field, Arthur Czellitzer (1871–1943), his biography and work from oblivion and places him in the context of early 20th-century science and Jewish life.
The articles on current questions of Jewish family history reflect the topic’s potential for shedding new light on key questions in Jewish Studies past and present. Their thematic range – from 13th-century Yiddish Arthurian romances via family-based business practices in 19th-century Hungary and Germany, to concepts of Jewish parenthood in Imperial Russia – illustrates the broad interest in Jewish family research as a paradigm for early modern and modern Jewish Studies.
Objective:
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.
Objective:
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.