Ms. hebr. oct. 63 - Derashot

Vorbesitzer: Abraham Merzbacher

Ms. hebr. oct. 76 - Ḥidushe masekhet Ḳidushin u-Ketubot

Vorbesitzer: Eljāqīm Carmoly; Abraham Merzbacher

Ms. hebr. oct. 93 - Midrash Tehilim

Vorbesitzer: Eljāqīm Carmoly; Abraham Merzbacher

Ms. hebr. oct. 94 - Derashot u-minhagim

Vorbesitzer: Abraham Merzbacher

Ms. hebr. oct. 95 - [Sefer] Musar

Vorbesitzer: Eljāqīm Carmoly; Abraham Merzbacher

Ms. hebr. oct. 111 - Seliḥot u-piyuṭim

Vorbesitzer: Abraham Merzbacher

Ms. hebr. oct. 113 - Perush ha-Ran

Vorbesitzer: Abraham Merzbacher

Ms. Barth. 58 - Deutsche Passion. Deutsche Tischlesungen für Weihnachten

Vorbesitzer: Bartholomaeusstift Frankfurt am Main

Ms. Barth. 84 - Postilla litteralis super Canticum canticorum, Isaiam, Ieremiam, Librum Threnorum, Ezechielem

Vorbesitzer: Johannes Oppeler de Butzbach; Bartholomaeusstift Frankfurt am Main

Ms. Praed. 57 - Sermones dominicales de epistolis et evangeliis (Pars hiemalis)

Vorbesitzer: Dominikanerkloster Frankfurt am Main

Clinical manifestation of Fuchs uveitis syndrome in childhood

PURPOSE The aim of this study was to describe clinical signs and complications of Fuchs uveitis syndrome (FUS) with onset in childhood. METHODS Ophthalmologic findings and complications in patients with FUS becoming manifest before the age of 16 years were analyzed in a retrospective study at a tertiary referral uveitis center. Inclusion criteria were the presence of pathognomonic FUS findings at any time point and exclusion of any systemic immune-mediated or infectious disease. RESULTS A total of 23 patients (male = 16, female = 7) with juvenile FUS (unilateral n = 20, bilateral n = 3 patients) were included in the study. Mean ages at uveitis and FUS diagnosis were 12.0 ± 4.2 and 22.7 ± 10.7 years, respectively. In six patients, inflammation was noted at age ≤ 7 years. The following inflammatory signs were observed in a total of 26 eyes: ≤ 1+ anterior chamber cell grade (n = 26), vitreous cells (n = 24), fine keratic precipitates (KPs; n = 23), stellate KPs (n = 11), mutton-fat KPs (n = 23), diffuse (n = 24) or inferior (n = 8) distribution of KPs, Koeppe nodules (n = 10), and iris heterochromia (n = 14). A representative subgroup of patients (n = 5) is shown who presented with non-specific clinical signs in the beginning and in whom typical FUS signs became manifest only at a later stage. Secondary complications such as cataract (n = 19), ocular hypertension (n = 3), or glaucomatous disc damage (n = 2) were found after a mean uveitis duration of 11.6, 19.5, and 20.3 years, respectively. CONCLUSION FUS may begin in early childhood, and the characteristic findings may not be present at onset of disease. The diagnosis is often delayed for years, occasionally with the consequence of overtreatment with anti-inflammatory drugs.

Ms. Barth. 101 - Theologische Sammelhandschrift

Vorbesitzer: Bartholomaeusstift Frankfurt am Main

Ms. Barth. 94 - Antiphonarium (Sommerteil) für St. Bartholomaeus

Vorbesitzer: Bartholomaeusstift Frankfurt am Main

Ms. Praed. 62 - Collectarius super librum Psalmorum

Vorbesitzer: Dominikanerkloster Frankfurt am Main

Diabetes, use of antidiabetic drugs, and the risk of glioma

BACKGROUND Prior epidemiologic studies suggest inverse relations between diabetes and glioma risk, but the underlying mechanisms, including use of antidiabetic drugs, are unknown. METHODS We therefore performed a matched case-control analysis using the Clinical Practice Research Datalink (CPRD). We identified incident glioma cases diagnosed between 1995 and 2012 and matched each case with 10 controls on age, gender, calendar time, general practice, and years of active history in the CPRD. We performed conditional logistic regression to estimate odds ratios (ORs) with 95% CIs, adjusted for body mass index and smoking. RESULTS We identified 2005 cases and 20 050 controls. Diabetes was associated with decreased risk of glioma (OR = 0.74; 95% CI = 0.60-0.93), particularly glioblastoma (OR = 0.69; 95% CI = 0.51-0.94). Glioblastoma risk reduction was markedly pronounced among diabetic men (OR = 0.60; 95% CI = 0.40-0.90), most apparently for those with diabetes of long-term duration (OR for >5 vs 0 y = 0.46; 95% CI = 0.26-0.82) or poor glycemic control (OR for HbA1c ≥8 vs <6.5% = 0.20; 95% CI = 0.06-0.70). In contrast, the effect of diabetes on glioblastoma risk was absent among women (OR = 0.85; 95% CI = 0.53-1.36). No significant associations with glioma were found for use of metformin (OR for ≥30 vs 0 prescriptions = 0.72; 95% CI = 0.38-1.39), sulfonylureas (OR = 0.71; 95% CI = 0.39-1.30), or insulin (OR = 0.79; 95% CI = 0.37-1.69). CONCLUSIONS Antidiabetic treatment appears to be unrelated to glioma, but long-term diabetes duration and increased HbA1c both show decreased glioma risk. Stronger findings in men than women suggest low androgen levels concurrent with diabetes as a biologic mechanism.