The association between serum vitamin B<Subscript>12</Subscript> deficiency and tension-type headache in Turkish children

This study aimed to determine the relationship between serum vitamin B₁₂ level and tension-type headache. The study groups consisted of 75 patients (40 females, 35 males) with headache and a control group of 49 healthy children (25 females, 24 males). Serum vitamin B₁₂ level <?200 pg/ml was defined as deficient, and <?160 pg/ml as severely deficient. The serum vitamin B₁₂ level was measured by the electrochemiluminescence (ECLIA) method. The serum vitamin B₁₂ levels in the headache and control groups were 273.01?±?76.77 and 316.22?±?74.53 pg/ml, with the difference determined as statistically significant (p?=?0.003). In the case group, 18/75 patients (24%) had a serum vitamin B12 level below the normal of 200 pg/ml, and in the control group 4/49 (8%) patients were also below the normal range (p?=?0.021). The serum vitamin B₁₂ level in the children with tension-type headache was significantly lower than that in the control group. From the results of the study, it was concluded that there may be an association between vitamin B₁₂ level and tension-type headache. However, further clinical studies are needed.     

Composition of the immunoglobulin classic antigen-binding site regulates allergic airway inflammation in a murine model of experimental asthma

Background When bound to mast cell FcɛRI, IgE serves as antigen receptor for allergic reactions, permitting specific identification of the allergen. Although the core of the classic antigen-binding site is heavy chain complementarity determining region 3 (CDR-H3), recent studies suggest that allergens might also bind IgE in a superantigen-like fashion outside the classic antigen-binding site.
Objective We sought to evaluate the contribution of the classic CDR-H3-centric antigen-binding site to the development of an allergic phenotype.
Methods Using a murine model of experimental asthma, we characterized a gene-targeted mouse strain expressing an altered range of CDR-H3s (ΔD-iD mice) in response to the hydrophobic allergen ovalbumin (OVA). Mutant and wild-type ( wt ) mice were sensitized intraperitoneally with OVA; non-sensitized mice served as controls.
Results We found the composition of the classic CDR-H3-centric antigen-binding site to be critical for the development of characteristic aspects of allergic asthma. (i) Compared with wt animals, ΔD-iD mice showed a significantly less pronounced OVA -induced rise in allergen-specific IgE levels and hence in total serum IgE levels. (ii) In addition, ΔD-iD mice demonstrated a significant reduction in eosinophilic airway inflammation, as well as in interleukin-4 (IL-4), IL-5 and IL-13 levels in BAL fluids.
Conclusion Allergic sensitization and airway inflammation depend on the composition of the predominant CDR-H3 repertoire, suggesting that the classic CDR-H3-centric antigen-binding site plays a crucial role in creating the immunological interface between allergen and IgE. Our results further emphasize a central role of IgE, not only in mediating but also in regulating the allergic immune response.     

De novo 8p23.1 deletion in a patient with absence epilepsy

The 8p23.1 deletion syndrome is a rare multisystem disorder with high penetrance and a variable phenotypic spectrum that includes congenital heart disease (CHD), intellectual disability, behavioural problems, microcephalia, and sometimes epilepsy. Genomic copy number variations (CNVs) constitute an important genetic risk factor for common genetic generalised epilepsy syndromes (GGEs) and absence seizures. These variations, resulting either from copy loss (microdeletion) or copy gain (duplications), disrupt genes associated with neuronal development. Herein, we report an epilepsy patient who was affected by developmental delay, microcephalia, behavioural problems, CHD, and childhood‐onset absence seizures. The patient had a 4‐Mb de novo microdeletion at 8p23.1. Some of the genes in this region, particularly XKR6 and MIR597, may be involved in the pathogenesis of absence seizures, suggesting that epilepsy may possibly be part of the phenotypic spectrum of the syndrome rather than a comorbid disorder. Thus, CNV screening for GGE plus patients may have important implications in clinical practice with regards to diagnostic classification, clinical management of the syndromic multisystem disorders, and, potentially, genetic counselling.     

The role of standing flexion-extension radiographs for spondylolisthesis following single level disk surgery

OBJECTIVES: Spondylolisthesis is the forward displacement of a lumbar vertebra relative to the adjacent vertebra, occurs as result degeneration or surgery and is a special type of lumbar instability. There is no consensus about which radiologic modality or findings truly reflect the lumbar instability and the exact incidence after single level disk surgery is unknown. METHODS: In this prospective study, we have included 90 patients who were operated by the same surgeon with single level disk herniation. We aimed at evaluating the post-operative lumbar spondylolisthesis, with flexion and extension lateral radiographs in addition to standard magnetic resonance imaging (MRI). RESULTS: We have seen spondylolisthesis in six of 90 cases with standing lateral flexion-extension radiographs, which were undefinable with MRI. Pain intensity and functional-economic rating scale (Prolo scale) were unremarkable. DISCUSSION: We have concluded that standing flexion-extension radiographs should be routinely combined in patients with failed back surgery syndrome and even if lumbar instability is clinically suspected, especially when conventional MR examination is normal. When the MR examination showed spondylolisthesis, standing flexion-extension radiographs could not give additional information.     

Pituitary volumes in hypochondriac patients

To date, no study has examined the pituitary volumes in patients with hypochondriasis. In the present study, we evaluated pituitary volumes in patients with hypochondriasis and healthy controls. Twenty individuals with hypochondriasis (ten males, ten females), aged 20 to 48 years, and healthy controls were included into the study. The pituitary volumes were obtained. Volumetric measurements were made with T1-weighted coronal MRI images, with 2.4-mm-thick slices, at 1.5 T, and were done blindly. Volumetric measurements did not demonstrate group differences in the brain measurements, i.e., whole brain volume, white, and gray matter volumes (P > 0.05). We found significantly smaller pituitary volumes of the whole group of hypochondriac patients compared to healthy controls (age and ICV as covariates). To conclude, the results from the current investigation suggest that hypochondriac patients had smaller pituitary volumes compared with healthy controls. This could be the keystone to a better understanding of the neurobiological basis of hypochondriasis.     

The role of BDNF and HPA axis in the neurobiology of burnout syndrome

Chronic stress is known to affect the HPA axis. The few clinical studies which have been conducted on HPA-axis function in burnout have produced inconsistent results. The etiological relationship between sBDNF and burnout has not yet been studied. The aim of the current study was to investigate the role of BDNF and HPA axis in the neurobiology of burnout. In the current study 37 clinically diagnosed burnout participants were compared with 35 healthy controls in terms of BDNF, HPA axis, burnout symptoms, depression, anxiety and psychosomatic complaints. Basal serum cortisol, sBDNF and cortisol level after 1 mg DST was sampled. We found no significant differences in terms of HPA-axis function (for basal serum cortisol, p=0.592; for cortisol level after 1 mg DST, p=0.921), but we did find lowered sBDNF levels in burnout group (88.66+/-18.15 pg/ml) as compared to healthy controls (102.18+/-20.92 pg/ml) and the difference was statistically significant (p=0.005). Logistic Regression Analysis revealed that emotional exhaustion (p=0.05), depersonalization (p=0.005) and depression (p=0.025) were significantly associated with burnout. sBDNF levels correlated negatively with emotional exhaustion (r=-,268, p=0.026), depersonalization (r=-,333, p=0.005) and correlated positively with competence (r=0.293, p=0.015) sub-scales of burnout inventory. However, there were no significant relationships between cortisol levels and sBDNF levels (r=0.80, p=0.51), depression, anxiety, psychosomatic complaints and burnout inventory. Our results suggest that low BDNF might contribute to the neurobiology of burnout syndrome and it seems to be associated with burnout symptoms including altered mood and cognitive functions.     

Inhibition of histone deacetylation protects wildtype but not gelsolin-deficient mice from ischemic brain injury

Acetylation/deactylation of histones is an important mechanism to regulate gene expression and chromatin remodeling. We have previously demonstrated that the HDAC inhibitor trichostatin A (TSA) protects cortical neurons from oxygen/glucose deprivation in vitro which is mediated--at least in part--via the up regulation of gelsolin expression. Here, we demonstrate that TSA treatment dose-dependently enhances histone acetylation in brains of wildtype mice as evidenced by immunoblots of total brain lysates and immunocytochemical staining. Along with increased histone acetylation dose-dependent up regulation of gelsolin protein was observed. Levels of filamentous actin were largely decreased by TSA pre-treatment in brain of wildtype but not gelsolin-deficient mice. When exposed to 1 h filamentous occlusion of the middle cerebral artery followed by reperfusion TSA pre-treated wildtype mice developed significantly smaller cerebral lesion volumes and tended to have improved neurological deficit scores compared to vehicle-treated mice. These protective effects could not be explained by apparent changes in physiological parameters. In contrast to wildtype mice, TSA pre-treatment did not protect gelsolin-deficient mice against MCAo/reperfusion suggesting that enhanced gelsolin expression is an important mechanism by which TSA protects against ischemic brain injury. Our results suggest that HDAC inhibitors such as TSA are a promising therapeutic strategy for reducing brain injury following cerebral ischemia.     

Relationship of olfactory function with olfactory bulbus volume,disease duration and Unified Parkinson’s disease rating scale scores in patients with early stage of idiopathic Parkinson’s disease

We aimed to investigate the relationship between olfactory function and olfactory bulbus (OB) volume, disease duration and Unified Parkinson’s disease rating scale (UPDRS) scores in early stage idiopathic Parkinson’s disease patients. The University of Pennsylvania Smell Identification Test (UPSIT) was used for the evaluation of olfactory function. UPSIT scores for patients with Parkinson’s disease were significantly lower than controls. There was no significant difference between stage 1 and stage 2 patients. OB volumes were higher in stage 1 and 2 patients than controls, but there was no statistical difference between the three groups. No significant correlation was found between UPSIT and UPDRS total scores, nor between UPSIT scores and disease duration in stage 1 and 2 patients. According to our results, we propose UPSIT be used as a screening test to diagnose presymptomatic patients, but not OB volumes.