Rejected

Klippel-Trenaunay syndrome (KTS) is a congenital mixed mesenchymal malformation syndrome that includes varicose veins, capillary and venous malformations, lymphatic abnormalities and hypertrophy of various connective tissue elements. The purpose of this study was to describe clinical characteristics and outcomes in a subset of patients with KTS in whom venous interventions, including iliofemoral venous stenting, were performed after the failure of conservative therapy.

We aimed to evaluate the efficacy and tolerance of A1 pulley release using the needle technique, under ultrasound guidance, in patients with symptomatic trigger finger.

Migraine is a complex neurological disorder with a high disability rate. Although the precipitating factors of migraine remain unclear, previous studies suggest that when there is excess nitrogen dioxide (NO) pollution in the atmosphere, the medical demand due to migraine attacks increases sharply. However, the main role of NO as a trigger for migraine is not yet well understood. The purpose of this study was to explore the relationship between NO exposure and the occurrence of migraine as well as the possible underlying mechanisms. We first investigated whether repeated short-term NO exposure could induce behavioural and biological migraine phenotypes in rats. Next, capsazepine (CZP) was used to block transient receptor potential cation channel subfamily V member 1 (TRPV1) in vivo, and CZP and vitamin E (VE) were used to verify the role of reactive oxygen species (ROS)-TRPV1 signalling in NO-induced migraine in primary trigeminal neurones in vitro. We demonstrated that short-term repeated NO exposure can significantly induce migraine in rats, and its key molecular mechanism may be related to ROS burst and its downstream TRPV1 channel activation. The findings of this study will enhance the understanding of the neurotoxic mechanism of NO, provide new clues for identifying the aetiology of migraine, and lay a new experimental basis for implementing migraine-related preventive and therapeutic control measures.

Neurological disorders are the leading cause of disability and the second leading cause of death worldwide. The increasing social and economic burdens of neurological disorders are driven by global population growth and aging. Depression is a common psychiatric symptom in numerous neurological disorders. It is also a risk factor for Alzheimer's disease (AD) and other dementias, Parkinson's disease (PD), and stroke. The rapid-acting and sustained antidepressant actions of (R,S)-ketamine for severe depression was accidentally discovered. Interestingly, (R)-ketamine has greater potency and longer-lasting antidepressant-like effects than (S)-ketamine in rodents. Importantly, its side effects in rodents and humans are lower than those of (R,S)-ketamine and (S)-ketamine. Furthermore, (R)-ketamine could elicit beneficial actions in various rodent models of neurological disorders, including PD, multiple sclerosis (MS), and stroke. In this article, we review the potential of (R)-ketamine as a prophylactic or therapeutic drug for neurological disorders including AD and other dementias, PD, MS, and stroke.

Enhanced recovery protocols (ERPs) have been shown to decrease in-hospital opioid use following thoracic surgery. However, the impact on opioid use after discharge has not been reported. We hypothesized that prolonged opioid use would decrease following implementation of a comprehensive ERP.

The first proposed emergency care alternative payment model seeks to reduce avoidable admissions from the emergency department (ED), but this initiative may increase risk of adverse events after discharge. Our study objective was to describe variation in ED discharge rates and determine whether higher discharge rates were associated with more ED revisits.

Enhanced recovery after surgery (ERAS) has been associated with improved perioperative outcomes after thoracic surgery, however the impact on long-term opioid use remains unknown. The aim of our study was to evaluate the effects of ERAS on long-term opioid use.

This study assessed the effects of botulinum toxin type A (BoNT-A) in mandibular range of motion and muscle tenderness to palpation in persistent myofascial pain (MFP) patients (ReBEC RBR-2d4vvv). Eighty consecutive female subjects with persistent MFP, were randomly divided into four groups ( = 20): three BoNT-A groups with different doses and a saline solution group (placebo control group). Treatments were injected bilaterally in the masseter and anterior temporalis muscle in a single session. Clinical measurements of mandibular movements included: pain-free opening, maximum unassisted and assisted opening, and right and left lateral excursions. Palpation tests were performed bilaterally in the masseter and temporalis muscle. Follow-up occurred 28 and 180 days after treatment. For the statistical analysis the Mann-Whitney U-test with Bonferroni correction was used for groups comparisons. Regardless of dose, all parameters of mandibular range of motion significantly improved after 180 days in all BoNT-A groups, compared with the control group. Palpation pain over the masseter and temporalis muscles were significantly reduced in all BoNT-A groups regardless of dose, compared with the control group, after 28 and 180 days of treatment. Independent of doses, BoNT-A improved mandibular range of motion and muscle tenderness to palpation in persistent MFP patients.

There are known differences in vaccine reactogenicity and immunogenicity by sex. Females have been shown to report greater reactogenicity and generate higher humoral and cellular immune responses than males following vaccination with several different vaccines. Whether this is also the case for COVID-19 vaccines is currently unknown, as COVID-19 vaccine study data disaggregated by sex are not routinely reported. Therefore, we have assessed the influence of sex on reactogenicity, immunogenicity and efficacy of COVID-19 vaccine ChAdOx1 nCoV-19.

To examine the associations of changes in serum urate (SU) with health-related quality of life (HRQOL) in gout.