Alopecia areata (AA) is an autoimmune-mediated disorder in which the proximal hair follicle (HF) attack results in non-scarring partial to total scalp or body hair loss. Despite the growing knowledge ...about AA, its exact cause still needs to be understood. However, immunity and genetic factors are affirmed to be critical in AA development. While the genome-wide association studies proved the innate and acquired immunity involvement, AA mouse models implicated the IFN-γ- and cytotoxic CD8+ T-cell-mediated immune response as the main drivers of disease pathogenesis. The AA hair loss is caused by T-cell-mediated inflammation in the HF area, disturbing its function and disrupting the hair growth cycle without destroying the follicle. Thus, the loss of HF immune privilege, autoimmune HF destruction mediated by cytotoxic mechanisms, and the upregulation of inflammatory pathways play a crucial role. AA is associated with concurrent systemic and autoimmune disorders such as atopic dermatitis, vitiligo, psoriasis, and thyroiditis. Likewise, the patient’s quality of life (QoL) is significantly impaired by morphologic disfigurement caused by the illness. The patients experience a negative impact on psychological well-being and self-esteem and may be more likely to suffer from psychiatric comorbidities. This manuscript aims to present the latest knowledge on the pathogenesis of AA, which involves genetic, epigenetic, immunological, and environmental factors, with a particular emphasis on immunopathogenesis.
Low-grade chronic inflammation is associated with obesity and related cardiometabolic disorders, such as cardiovascular diseases, type 2 diabetes, and some types of cancer. A growing body of evidence ...suggests that a variety of dietary factors can modulate obesity-induced chronic low-grade inflammation and thus the course of obesity-related chronic non-communicable diseases. We are aiming to evaluate the effect of an energy-restricted anti-inflammatory diet on weight loss, body composition, cardiometabolic risk factors, and immune system response among younger adults with obesity.
A two-arm, parallel design randomized controlled trial will be conducted in Croatia among 220 adults with obesity aged 18–50 years. Following baseline assessments, participants will be randomized into the intervention or control group in a 1:1 ratio. A nutritional intervention based on an energy-restricted anti-inflammatory diet (low-glycemic, low in omega-6, rich in omega-3 fatty acids, spices, herbs) will be compared with an isocaloric standard diet (55–60 % carbohydrates, 25–30 % fat, 15–20 % protein). The inflammatory potential of the diet will be assessed with the Dietary Inflammatory Index®. The change in body weight from baseline to the week 24 will be the main outcome measure. Secondary outcomes will include changes in body composition, cardiometabolic parameters, and the impact of the anti-inflammatory diet on immune system response and thyroid function.
If the energy-restricted anti-inflammatory diet is found to be effective in the management of obesity, it has the potential to be implemented into management for reducing obesity and related chronic non-communicable disease in younger adults.
Sleep-related hypermotor epilepsy (SHE) is a rare epileptic syndrome characterized by epileptic seizures which occur during the non-rapid eye movement (NREM) stage of sleep. It manifests with ...hypermotor semiology resembling violent limb movements and an asymmetric tonic-dystonic posture. The genes which are responsible for the autosomal dominant form of SHE (ADSHE) and whose function is to code the sub-unit of the neuronal acetylcholine receptor are well known. Considering that ADSHE is a prototype of SHE, it is thought that the dysfunction of the cortico-subcortical cholinergic network, which regulates the cycle of sleep, has a key role in the epileptogenesis of this syndrome. Namely, studies to date, have shown that the hypercholinergic activity is sufficient for the development of epileptic seizures, even though the exact mechanism remains to be elucidated. NREM parasomnias are sleep disorders that are the most difficult to differentiate from SHE due to a similar clinical presentation. Considering the clinical similarities, NREM occurrence and probable genetic connection, it is considered that fundamentally, both of these conditions share a common pathophysiological mechanism i.e. cholinergic dysfunction. The main difference between SHE and NREM parasomnias are the genuine epileptic seizures that are responsible for the semiology in SHE. These genuine seizures are not present in NREM parasomnias. Why this is so, remains to be elucidated. Considering that animal studies have shown that dynamic changes and the decreased levels of microRNA-211 contribute to epileptic seizures and to changes in cholinergic pathways, our hypothesis is that epileptic seizures and the development of epileptogenesis in SHE are a consequence of cholinergic dysfunction and decreased levels of microRNA-211 as opposed to NREM parasomnias where there is a stable level of microRNA-211, preventing epileptogenesis despite the cholinergic system dysfunction.
