Gonzales Jakobsen (areabrick24)
INTRODUCTION The B-cell chemoattractant CXCL13 has been suggested as a cerebrospinal fluid (CSF) biomarker for Lyme neuroborreliosis (LNB). Our aim was to substantiate the value of CXCL13 in a large unselected cohort and determine a practical cut-off value to diagnose LNB. METHODS We retrospectively studied clinical and CSF data of consecutive patients who underwent CSF CXCL13 testing over a period of three years (February 2015 to January 2018) at our academic teaching hospital. Patients were classified into 12 groups according to their final diagnosis. To diagnose LNB (definite or probable/possible), definitions of the respective guideline of the German Neurological Society were applied. RESULTS Of 1410 patients, 29 were diagnosed with definite LNB and 9 with probable/possible LNB. Median CXCL13 levels were highly elevated in both LNB groups (554 pg/mL and 649 pg/mL, respectively) and the group with bacterial/fungal CNS infections (410 pg/mL; n = 6), while all other groups had markedly lower median CXCL13 levels (p less then .001). For definite LNB, the best CXCL13 test cut-off was 55.5 pg/mL with a sensitivity of 96.6% (95% confidence interval, CI, 80.4%-99.8%) and a specificity of 94.9% (95% CI 93.5%-95.9%). All patients with LNB showed clinical improvement after antibiotic treatment. CONCLUSION In this large monocentric cohort, CSF CXCL13 was found to be a highly sensitive and useful marker for LNB. In conditions with low index of suspicion for LNB, CXCL13 testing may be unwarranted. A review of the literature on the sensitivity and specificity of CSF CXCL13 in the differential of LNB is provided. Overt stroke in adults with sickle cell anemia (SCA) continues to be a major cause of morbidity and mortality, while no evidence-based strategy for prevention has been reached so far. Although transcranial Doppler ultrasonography represents the most important tool for identifying young patients with SCA at risk of primary stroke, strategies for stroke prediction in adulthood remain challenging. Emerging data suggest that oxidative stress may exert a pivotal role in the pathogenesis of ischemic brain injury. Combining these pieces of evidences with the well-known genetic contribution to the development of stroke in SCA, we hypothesized that genetic variants related to the biology of oxidative stress could be used to identify adult patients at higher risk of stroke. Overall, 499 unrelated patients with SCA aged >18 years were genotyped for SOD2 Val16Ala (rs4880), GPX3 T-568C (rs8177404), GPX3 T-518C (rs8177406), GPX3 T-65C (rs8177412), and CAT01 C-262 T (rs1001179) polymorphisms, along with α-thalassemia status and β-globin gene haplotypes. Of these, only the SOD2 Val16Ala polymorphism was associated with stroke. SOD2 Val16Ala polymorphism was independently associated with risk of stroke (odds ratio 1.98; 95% confidence interval [CI] 1.18-3.32; P = .009) and with the long-term cumulative incidence of stroke (hazard ratio 2.24, 95% CI 1.3-3.9; P = .004). In summary, we provide evidence that oxidative stress-related genetic variants, in particular, the SOD2 Val16Ala polymorphism, may represent a simple and inexpensive alternative for identifying patients at risk of stroke. MLN2480 Macrophage autophagy has been shown to exert a protective role in atherosclerosis. Beclin 1 is an essential autophagic protein, and the Beclin-1-interacting complex promotes the formation of autophagosomes. However, the localization of Beclin 1 in human atherosclerotic lesions has not been clarified to date. We hence investigated the immunolocalization of Beclin 1 in atherosclerotic lesions of human carotid and major intracranial arteries. Furthermore, we investigated the colocalization of Beclin 1 with the 14-3-3 eta isoform and high mobility group box 1 (HMGB1). Beclin 1 was observed in the cytoplasm of many foamy macrophages located near to or in the periphery of lipid-rich ne