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Migraine is a highly prevalent disorder with an enormous burden on societies. Different types of medications are used for controlling both acute attacks and prevention. This article reviews some non-pharmacological recommendations aiming to manage migraine disorder better and prevent headache attacks. Different triggers of migraine headache attacks, including environmental factors, sleep pattern changes, diet, physical activity, stress and anxiety, some medications, and hormonal changes, are discussed. It is advised that they be identified and managed. Patients should learn the skills to cope with the trigger factors that are difficult to avoid. In addition, weight control, management of migraine comorbidities, lifestyle modification, behavioural treatment and biofeedback, patient education, using headache diaries, and improving patients' knowledge about the disease are recommended to be parts of migraine management. In addition, using neuromodulation techniques, dietary supplements such as riboflavin, coenzyme Q10 and magnesium, and acupuncture can be helpful. Non-pharmacological approaches should be considered in migraine management. Furthermore, the combination of pharmacological and non-pharmacological approaches is more effective than using each separately.

Paracoccidioidomycosis is a systemic infection caused by the fungus Paracoccidioides. It may present in two forms: an acute/subacute form, whose most frequent manifestations include weight loss, fever, anemia, and adenopathy, and a chronic condition with mainly respiratory symptoms. Digestive symptoms, although they may occur, are not frequently reported. Paracoccidioidomycosis usually affects adult male agricultural workers; thus, its presentation in children is rare.

The association between reporting adverse coronavirus disease 2019 (COVID-19) vaccination effects and those with a history of audiovestibular difficulties is unknown. The aim of this research is therefore to investigate adverse vaccination effects in adults with a history of Ménière's disease. Specifically, the incidence of adverse effects, the factors associated with those reporting adverse effects and the relationship between the reporting of audiovestibular and other adverse effects. A mixed-methods exploratory cross-sectional survey study design was used. Data were collected from 333 members of the Finnish Ménière Association. The survey was designed to obtain demographic information that may be associated with having adverse effects or not, vaccination-specific information and adverse vaccination effects. Both health and audiovestibular adverse events were identified. Data analysis included comparing those reporting and not reporting adverse vaccination effects. The mean age was 63 years with 81% being female. Of the 327 respondents who had one of the COVID-19 vaccinations (Comirnatry/ Pfizer, Astra Zeneca, or Moderna), 203 (62%) reported no adverse effects. The type of or number of vaccinations were not related to the reporting of adverse effects. The most frequently reported adverse effects were injection site tenderness (38%), arm pain (21%), fever (15%) and headaches (15%). Post-vaccination tinnitus and vertigo (both 7%) were the most frequently reported audiovestibular-related symptoms, followed by aural fullness (6%) and hearing loss (4%). Those reporting previous pre-vaccination vertigo were more likely to have post-vaccination vertigo. The presence of post-vaccination tinnitus, hearing loss, and aural fullness, predicted the presence of post-vaccination vertigo. A small proportion of patients with a history of Ménière's disease may experience adverse post-vaccination effects. Further research is required to explore whether adverse post-vaccination audiovestibular effects are more prevalent in those with a history of otological disorders compared with the general population.

Acute lung injury (ALI) is a severe clinical disorder characterized by dysregulated inflammatory responses, leading to high rates of morbidity and mortality. Cinobufagin, a primary component isolated from cinobufotalin, exerts strong anticancer effects. However, there are few reports on its role in ALI, and it is unclear whether cinobufagin affects lipopolysaccharide (LPS)-induced ALI. Therefore, the present study aimed to investigate the effect of cinobufagin on LPS-induced ALI and to assess its potential mechanism of action. The results showed that cinobufagin alleviated lung histopathological changes and protected the permeability of lung tissues in LPS-induced ALI. In addition, cinobufagin effectively suppressed inflammatory responses through the induction of autophagy in LPS-induced ALI cells and in a mouse model. Moreover, cinobufagin enhanced autophagy through the p53/mTOR pathway in LPS-induced ALI. Herein, it was reported for the first time that cinobufagin inhibited the inflammatory response of LPS-induced ALI, which laid the foundation for further understanding and development of cinobufagin as a potential new drug for ALI.

Spinal α-adrenoceptor induces analgesia by neuronal inhibition of primary afferent fibers. This family receptor coupled to G proteins can be subdivided into three functional subtypes: α, α and α-adrenoceptors, and current evidence on spinal analgesia supports the relevance of α and seems to exclude the role of α, but the functional contribution of α-adrenoceptors remains elusive. The present study was designed to pharmacologically dissect the contribution of spinal α-adrenoceptor subtypes modulating tonic or acute peripheral nociception. Using male Wistar rats, we analyzed the effect of spinal clonidine (a non-selective ααα-adrenoceptor agonist) and/or selective subtype α-adrenoceptor antagonists on: 1) tonic nociception induced by subcutaneous formalin (flinching behavior) or 2) acute nociception induced by peripheral electrical stimulus in extracellular recordings of spinal dorsal horn second-order wide dynamic range (WDR) neurons. Clonidine inhibited the nocifensive behavior induced by formalin, an effect blocked by BRL 44408 (α-adrenoceptor antagonist) but not by imiloxan (α-adrenoceptor antagonist) or JP 1302 (α-adrenoceptor antagonist). Similarly, spinal BRL 44408 reversed the clonidine-induced inhibition of nociceptive WDR activity. Interestingly, spinal JP 1302 produced behavioral antinociception (an effect blocked by bicuculline, a preferent GABA channel blocker), but no correlation was found with the electrophysiological experiments. These data imply that, at the spinal level, 1) presynaptic α-adrenoceptor activation produces antinociception during acute or tonic nociceptive stimuli; and 2) under tonic nociceptive (inflammatory) input, spinal α-adrenoceptors are pronociceptive, probably by the inactivation of GABAergic transmission. This result supports a differential role of α and α-adrenoceptors modulating nociception.

The incidence of thyroid diseases has tripled in the last three decades, and the prevalence is rising rapidly irrespective of gender and genetics. This study aimed to assess the Knowledge, awareness of risk factors, and perceptions of thyroid disease among the Saudi Community in Saudi Arabia.

[This retracts the article DOI: 10.1155/2021/7344102.].

The selection strategy of non-steroidal anti-inflammatory drugs (NSAIDs) for migraine is hard to judge whether it is effective, leading to unnecessary exposure to insufficient or lengthy treatment trials. The goal of the study was to investigate potential predictors of NSAIDs efficacy in migraine therapy and to explore their influence on efficacy. 610 migraine patients were recruited and assigned into responders and non-responders. Potential predictors among demographic and clinical characteristics for NSAIDs efficacy were extracted using multivariable logistic regression (LR) analysis, and were applied to construct prediction models machine learning (ML) algorithms. Finally, Cochran-Mantel-Haenszel tests were used to examine the impact of each predictor on drug efficacy. Multivariate LR analysis revealed migraine-related (disease duration, headache intensity and frequency) and psychiatric (anxiety, depression and sleep disorder) characteristics were predictive of NSAIDs efficacy. The accuracies of ML models using support vector machine, decision tree and multilayer perceptron were 0.712, 0.741, and 0.715, respectively. Cochran-Mantel-Haenszel test showed that, for variables with homogeneity of odds ratio, disease duration, frequency, anxiety, and depression and sleep disorder were associated with decreased likelihood of response to all NSAIDs. However, the variabilities in the efficacy of acetaminophen and celecoxib between patients with mild and severe headache intensity were not confirmed. Migraine-related and psychiatric parameters play a critical role in predicting the outcomes of acute migraine treatment. These models based on predictors could optimize drug selection and improve benefits from the start of treatment.

Chronic, abdominal pain remains a problem in a subset of patients after cholecystectomy. The cause is often obscure but central sensitization may be an important component and could theoretically be mediated by spinal PGE2, which is regulated by several cytokines. The aim of the study was to examine cerebrospinal fluid (CSF) of participants with post cholecystectomy syndrome and healthy volunteers for signs of PGE2 and cytokine mediated central sensitization.

Bone-marrow mesenchymal stem cells (BM-MSCs) have not yet proven any significant therapeutic efficacy in spinal cord injury (SCI) clinical trials, due to the hostile microenvironment of the injured spinal cord at the acute phase. This study aims to modulate the inflammatory milieu by lipopolysaccharide (LPS) and granulocyte colony-stimulating factor (G-CSF) to improve the BM-MSCs therapy. For this purpose, we determined the optimum injection time and sub-toxic dosage of LPS following a T10 contusion injury. Medium-dose LPS administration may result in a local anti-inflammatory beneficial role. This regulatory role is associated with an increase in NF-200-positive cells, significant tissue sparing, and improvement in functional recovery compared to the SCI control group. The second aim was to examine the potential ability of LPS and LPS + G-CSF combination therapy to modulate the lesion site before BM-MSC (1 × 105 cells) intra-spinal injection. Our results demonstrated combination therapy increased potency to enhance the anti-inflammatory response (IL-10 and Arg-1) and decrease inflammatory markers (TNF-α and CD86) and caspase-3 compared to BM-MSC monotherapy. Histological analysis revealed that combination groups displayed better structural remodeling than BM-MSC monotherapy. In addition, Basso-Beattie-Bresnahan (BBB) scores show an increase in motor recovery in all treatment groups. Moreover, drug therapy shows faster recovery than BM-MSC monotherapy. Our results suggest that a sub-toxic dose of LPS provides neuroprotection to SCI and can promote the beneficial effect of BM-MSC in SCI. These findings suggest that a combination of LPS or LPS + G-CSF prior BM-MSC transplantation is a promising approach for optimizing BM-MSC-based strategies to treat SCI. However, because of the lack of some methodological limitations to examine the survival rate and ultimate fate of transplanted BM-MSCs followed by LPS administration in this study, further research needs to be done in this area. The presence of only one-time point for evaluating the inflammatory response (1 week) after SCI can be considered as one of the limitations of this study. We believed that the inclusion of additional time points would provide more information about the effect of our combination therapy on the microglia/macrophage polarization dynamic at the injured spinal cord.