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Serum PON1 concentrations and activities were higher in LL (comparison with LM and MM) and RR (comparison with QR and QQ) genotypes while we did not observe any significant differences in arylesterase levels among mentioned polymorphisms. CONCLUSION In the current study, we reported associations between PON1 polymorphisms (55, 192) and enzyme activities in Parkinson's disease as there was a significant reduction in PON1 levels in patients with Parkinson compared with healthy. Taken together, paraoxonase enzyme in subjects with different genotypes could be a potential biomarker for determining the severity and prognosis of Parkinson. However, more studies are needed to clarify its clinical values. Key words Parkinson's disease; paraoxonase1; Polymorphism.Abtract Objective The auditory brainstem response (ABR) has been reported as normal in patients with vitamin B12 deficiency, but there have also been reported cases of interference in amplitude responses. However, studies investigating the effects of vitamin B12 on auditory response are limited in patients with tinnitus. The aim of this study was to investigate the ABR findings in patients with tinnitus together with vitamin B12 deficiency. MATERIAL AND METHODS Twenty-eight patients with tinnitus-related vitamin B12 deficiency were included in the study. Their serum vitamin B12 levels were lower than 200 pg/ml. Patients were between 19 and 58 years with a mean age of 36.82 ± 11.19 (ratio male/female, 6/22). ABR was performed in all patients. Latencies ( I, II, III, IV, V), interpeak latencies (I-III, III-V, I-V) and amplitudes were evaluated. Neurologic and ear physical examinations were evaluated and brain magnetic resonance imaging (MRI) was also performed in all patients. Caspase Inhibitor VI RESULTS Neurologic,ear-auditory physical examinations and brain MRI findings were normal in all patients. Wave latencies and interpeak latencies were normal in all patients. Six patients (21.42 %) had low amplitude in their ABR. In one of them, the left-sided response showed a mild amplitude decrease in all waves compared to the right-side. Bilateral mild low amplitude was observed in 4 (66.6 %) patients in ABR findings. CONCLUSION These results support that ABR findings can be influenced in vitamin B12 deficiency patients having tinnitus. More detailed studies are needed in tinnitus associated with vitamin B12 deficient patients. Key words Auditory brainstem response, Tinnitus, Vitamin B12 deficiency, Neurophysiology, Low amplitude.Recent data has linked anxiety and its disorders in late life to increased morbidity and mortality, especially related to a higher cardiovascular burden and an increased cognitive decline. Clinically, anxiety symptoms may be more difficult to elicit in older adults who are less accurate in identifying anxiety symptoms and tend to minimize symptoms and to attribute symptoms to physical illness. Although SSRIs have proven more effective than psychotherapy in late-life anxiety, many elderly anxious subjects prefer psychotherapeutic interventions. These interventions appear to work best when tailored for the needs, expectations, and cultural background of older anxious subjects.Anxiety is prevalent in childhood and adolescence. Youth with maladaptive responses to common situations and stressors are at risk of having anxiety disorders. Persistent anxiety symptoms and anxiety disorders can be debilitating with long-term adverse outcomes in adulthood. Hence, decreasing the burden of anxiety disorders is an important public health priority. Development of anxiety disorders has a multifactorial etiology. There is a considerable complex interaction of genetics, temperament, parenting behavior, environmental triggers, and physiologic factors. Identification of these risk factors is key to early detection, prevention, and development of applicable management approaches. Despite several evidence-based treatments published, there are limited prevention strategies available. Effective implementation of prevention strategies is essential and can be achieved by either elimination or reduction of the negative risk factors or strengthening the protective factors on anxiety symptoms and anxiety disorders. This chapter reviews the common risk and protective factors and provides current literature on prevention strategies for pediatric and adolescent anxiety disorders.Exposure therapy, a key treatment for anxiety disorders, can be modelled in the laboratory using Pavlovian fear extinction. Understanding the hormonal and neurobiological mechanisms underlying fear extinction in females, who are twice more likely than males to present with anxiety disorders, may aid in optimising exposure therapy outcomes in this population. This chapter will begin by discussing the role of the sex hormones, estradiol and progesterone, in fear extinction in females. We will also propose potential mechanisms by which these hormones may modulate fear extinction. The second half of this chapter will discuss the long-term hormonal, neurological and behavioural changes that arise from pregnancy and motherhood and how these changes may alter the features of fear extinction in females. Finally, we will discuss implications of this research for the treatment of anxiety disorders in women with and without prior reproductive experience.Anxiety disorders (ADs) are common psychiatric disorders, with a lifetime prevalence estimated at 33.7% in epidemiological studies. ADs are associated with serious disability and severe impairment in quality of life. Although several treatments [e.g. selective serotonin reuptake inhibitors (SSRIs), serotonin-noradrenaline reuptake inhibitors (SNRIs), pregabalin, tricyclic antidepressants and benzodiazepines and/or cognitive-behaviour therapy (CBT)] are recommended, a large number of patients (i.e. from 30 to 70%) do not achieve complete remission. According to the novel paradigm of personalized medicine, the search of possible predictors of both disease vulnerability and treatment response might be the best way to prevent more accurately disease risk and to tailor the most effective treatment for each individual. Although a growing body of studies have proposed several endophenotypes/markers (i.e. neurochemical, neuroimaging, physiological, genetic and epigenetic endophenotypes/markers) as possible predictors of ADs susceptibility and/or treatment response, findings are not robust enough to be considered acceptable to incorporate in the clinical practice.
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