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Headache persisting after aneurysmal subarachnoid hemorrhage: A narrative review of pathophysiology and therapeutic strategies.

This narrative review of the literature concerns persistent headache attributed to past non-traumatic subarachnoid hemorrhage (SAH), based off demographic and clinical features, what are pathophysiologic mechanisms by which these headaches occur, which medical and interventional treatments have the most evidence for pain alleviation, and what pre-clinical evidence is there for emerging treatments for these patients.

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The lipid transporter HDLBP promotes hepatocellular carcinoma metastasis through BRAF-dependent epithelial-mesenchymal transition.

Tumor metastasis is a major cause of cancer mortality. However, little is known regarding the regulation of abnormal cholesterol metabolism in hepatocellular carcinoma (HCC) metastasis. Here, we show that the expression of high-density lipoprotein binding protein (HDLBP), a lipid transporter, is clinically correlated with tumor metastasis in HCC patients. Moreover, HDLBP was required for cholesterol-induced HCC metastasis. We revealed that knockdown and overexpression of HDLBP significantly inhibited and enhanced, respectively, the metastasis, invasion and epithelial-mesenchymal transition (EMT) of HCC cells in vitro and in vivo. Mechanistically, coimmunoprecipitation and mass spectrometry screening uncovered BRAF as a protein target of HDLBP. HDLBP was found to promote EMT signaling in a BRAF-dependent manner. Furthermore, HDLBP interacts with BRAF and inhibits its ubiquitinated degradation by abrogating BRAF-ITCH interactions. Notably, further studies suggest that dabrafenib exhibited a greater metastasis-suppressive effect in HDLBP knockout HCC than isolated treatment. Overall, our findings imply that cholesterol-induced HDLBP contributes to the metastasis and invasion of HCC through BRAF-dependent EMT signaling and that HDLBP may be applied as a biomarker and therapeutic target for HCC.

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A non-oral gepant for acute treatment of migraine.

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What makes a home? Designing home personas to represent the homes of families caring for children with medical complexity.

Personas are widely recognized as valuable design tools for communicating dimensions of individuals, yet they often lack critical contextual factors. For those people managing chronic health conditions, the home is a critical context of their patient work system (PWS). We propose the development of 'home personas' to convey essential aspects of the home context to those tasked with designing technologies and interventions to fit it. We used an iterative, multi-stakeholder design process to design 'home personas' for a model population, families caring for children with medical complexity. Each of the four resultant home personas-Multi-level, Customized, Ranch, and Rental-has a unique home layout, pain points, and are described on three dimensions that emerged from the data. This study builds on a foundation of work in the emerging field of Patient Ergonomics, describing a mechanism for distilling rich descriptions of the PWS into brief yet informative design tools.

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Myelin Oligodendrocyte Glycoprotein (MOG) antibody-associated meningoencephalitis due to Mycoplasma pneumoniae infection.

Although myelin oligodendrocyte glycoprotein (MOG) antibody-associated disorders include a wide spectrum of syndromes, manifestations with meningoencephalitis symptoms due to infection were quite infrequent. We admitted an 8-years-old girl who presented with recurrent fever accompanied by headache and mild cough, her Cerebral spinal fluid polynucleated cells was elevated and progressively higher, her cranial MRI showed meningeal enhancement initially and multiple intracranial lesions later, serum M. pneumoniae-IgM and MOG-IgG were positive, she was diagnosed with MOG-IgG associated meningoencephalitis due to M. pneumoniae infection, the treatment consisted of intravenous immunoglobulin, glucocorticoid, and erythromycin, then she was completely recovered.

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Association Between Hypercholesterolemia and Neck Pain in a Cross-Sectional Population-Based Study.

Retrospective cross-sectional analysis.

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Neural signatures of auditory hypersensitivity following acoustic trauma.

Neurons in sensory cortex exhibit a remarkable capacity to maintain stable firing rates despite large fluctuations in afferent activity levels. However, sudden peripheral deafferentation in adulthood can trigger an excessive, non-homeostatic cortical compensatory response that may underlie perceptual disorders including sensory hypersensitivity, phantom limb pain, and tinnitus. Here, we show that mice with noise-induced damage of the high-frequency cochlear base were behaviorally hypersensitive to spared mid-frequency tones and to direct optogenetic stimulation of auditory thalamocortical neurons. Chronic 2-photon calcium imaging from ACtx pyramidal neurons (PyrNs) revealed an initial stage of spatially diffuse hyperactivity, hyper-correlation, and auditory hyperresponsivity that consolidated around deafferented map regions three or more days after acoustic trauma. Deafferented PyrN ensembles also displayed hypersensitive decoding of spared mid-frequency tones that mirrored behavioral hypersensitivity, suggesting that non-homeostatic regulation of cortical sound intensity coding following sensorineural loss may be an underlying source of auditory hypersensitivity. Excess cortical response gain after acoustic trauma was expressed heterogeneously among individual PyrNs, yet 40% of this variability could be accounted for by each cell's baseline response properties prior to acoustic trauma. PyrNs with initially high spontaneous activity and gradual monotonic intensity growth functions were more likely to exhibit non-homeostatic excess gain after acoustic trauma. This suggests that while cortical gain changes are triggered by reduced bottom-up afferent input, their subsequent stabilization is also shaped by their local circuit milieu, where indicators of reduced inhibition can presage pathological hyperactivity following sensorineural hearing loss.

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Impact of Potentially Inappropriate Medications on Kidney Function in Chronic Kidney Disease: Retrospective Cohort Study.

Chronic kidney disease (CKD) represents a major public health burden. Potential inappropriate medications (PIMs) are common in patients with CKD. However, its impact on kidney outcomes has not been adequately elucidated for middle-aged patients. This study aimed to clarify the prescription status of PIMs for middle-aged patients with CKD and its effect on kidney function decline.

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A phase IV clinical trial of gastrointestinal motility in adult patients with migraine before and after initiation of a calcitonin gene-related peptide ligand (galcanezumab) or receptor (erenumab) antagonist.

To compare effects of an initial dose of calcitonin gene-related peptide (CGRP) monoclonal antibody (mAb) antagonists on gastrointestinal (GI) motility in patients with migraine and to explore if the mechanistic difference contributes to GI adverse events (AEs).

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Techniques for Safe Removal of Spinal Cord Stimulation Paddle Leads.

Spinal cord stimulation (SCS) is a safe neuromodulatory treatment used to treat failed back surgery syndrome, chronic neuropathic pain, and complex regional pain syndrome. Despite its efficacy, some patients fail to achieve pain relief and elect to undergo removal of SCS paddle leads. The safety and best practices of these procedures have not been defined.

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