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Migrant Domestic Workers (MDWs) face adverse living and working conditions that place them at a heightened risk of poor mental health outcomes. While prior research has examined MDWs' coping strategies and resilience, little is known about how they understand and engage in self-compassion, an intrapersonal process strongly linked to mental well-being. This study aimed to examine how MDWs conceptualize self-compassion and the sociocultural factors that influence their capacity to practice it. Semi-structured interviews were conducted with ten female Filipino and Indonesian MDWs living in Singapore recruited through purposive and snowball sampling. Data were analyzed using reflexive thematic analysis. Three interrelated themes were generated: (1) grounding self-compassion in self-worth and identity, (2) contextual conditions shaping self-compassion, and (3) enacting self-compassion in everyday life. These themes illustrate the complex interplay between participants' internalized self-perceptions, cultural narratives, and structural conditions that shape their engagement with self-compassion. The findings contribute to a more nuanced understanding of self-compassion in marginalized caregiving populations. They advocate for the need to address structural determinants of MDWs' well-being and to develop culturally sensitive psychoeducation and interventions.

Immune checkpoint inhibitor (ICI) therapies carry the risk of major immune-related adverse events (irAEs). Among the most severe irAEs is epidermal necrosis that may clinically mimic Stevens-Johnson syndrome (SJS) and toxic epidermal necrosis (TEN). The aim of this study was to provide a summary of the clinical and histological features of ICI-associated epidermal necrosis, with a special focus on factors associated with fatal outcomes in cases of extensive disease. A total of 98 cases, 2 new cases and 96 reported on PubMed and in the literature, of ICI-associated epidermal necrosis were assessed. Development of epidermal necrosis occurred between 1 day and 3 years after starting ICI therapy, with an average onset of 13.8 weeks for patients with limited (< 30% BSA) and 11.3 weeks for those with extensive (≥ 30% BSA) involvement, and a median onset of 5.8 weeks and 4 weeks respectively. A preceding rash was seen in 52 cases and was more common in extensive cases. Mucosal involvement was only reported in 65% of extensive cases but was significantly associated with fatal reactions. Co-administration of cytotoxic chemotherapy was associated with more extensive disease. Recovery was observed in 96% and 65% of those with limited and extensive involvement respectively and no specific therapy was associated with improved survival. Young age was significantly associated with poor outcomes in extensive disease, the average age of surviving patients was 64.5 years old versus 55.1 years old for deceased patients, p  < 0.01. Both superficial perivascular and interface/lichenoid inflammatory infiltrates were commonly seen. These findings suggest that ICI-associated epidermal necrosis should be considered a distinct clinical entity from drug-induced SJS/TEN.

Chondroitin sulphate proteoglycans (CSPGs) upregulated in the glial scar inhibit axon regeneration via their sulphated glycosaminoglycans (GAGs). Chondroitin 6-sulphotransferase-1 (C6ST-1) is upregulated after injury leading to an increase in 6-sulphated GAG. In this study, we ask if this increase in 6-sulphated GAG is responsible for the increased inhibition within the glial scar, or whether it represents a partial reversion to the permissive embryonic state dominated by 6-sulphated glycosaminoglycans (GAGs). Using C6ST-1 knockout mice (KO), we studied post-injury changes in chondroitin sulphotransferase (CSST) expression and the effect of chondroitin 6-sulphates on both central and peripheral axon regeneration. After CNS injury, wild-type animals (WT) showed an increase in mRNA for C6ST-1, C6ST-2 and C4ST-1, but KO did not upregulate any CSSTs. After PNS injury, while WT upregulated C6ST-1, KO showed an upregulation of C6ST-2. We examined regeneration of nigrostriatal axons, which demonstrate mild spontaneous axon regeneration in the WT. KO showed many fewer regenerating axons and more axonal retraction than WT. However, in the PNS, repair of the median and ulnar nerves led to similar and normal levels of axon regeneration in both WT and KO. Functional tests on plasticity after the repair also showed no evidence of enhanced plasticity in the KO. Our results suggest that the upregulation of 6-sulphated GAG after injury makes the extracellular matrix more permissive for axon regeneration, and that the balance of different CSs in the microenvironment around the lesion site is an important factor in determining the outcome of nervous system injury.

ABSTRACT Purpose To understand the relationship between the risk of opioid-related gastrointestinal adverse effects (AEs) and exposure to tapentadol and oxycodone as well as its active metabolite, oxymorphone, using pharmacokinetic/pharmacodynamic models. Methods The analysis was based on a study in patients with moderate-to-severe pain following bunionectomy. Population PK modeling was conducted to estimate population PK parameters for tapentadol, oxycodone, and oxymorphone. Time to AEs was analyzed using Cox proportional-hazards models. Results Risk of nausea, vomiting, and constipation significantly increased with exposure to tapentadol or oxycodone/oxymorphone. However, elevated risk per drug exposure of AEs for tapentadol was ~3–4 times lower than that of oxycodone, while elevated AE risk per drug exposure of oxycodone was ~60 times lower than that for oxymorphone, consistent with reported in vitro receptor binding affinities for these compounds. Simulations show that AE incidence following administration of tapentadol IR is lower than that following oxycodone IR intake within the investigated range of analgesic noninferiority dose ratios. Conclusions This PK/PD analysis supports the clinical findings of reduced nausea, vomiting and constipation reported by patients treated with tapentadol, compared to patients treated with oxycodone.

Skin diseases affect millions of Americans, imposing a large financial burden on the U.S. healthcare system annually. Inpatient dermatology is a subspecialty focused on treating complicated skin diseases in hospitalized patients. Utilization of these services enhances diagnostic accuracy, shorten hospital stays, lower readmission rates, and improve patient outcomes. However, studies have indicated an overall decline in inpatient dermatology consultations and dermatology as primary admitting services. Currently, only two academic hospitals in the United States grant dermatologists admitting privileges, indicating decreased exposure to inpatient dermatology in residency despite the need for more hospital-based dermatologists. Therefore, this narrative review aims to characterize the financial impact and utilization of inpatient dermatology services. Historical and recent data consistently highlight the financial benefit of dermatologic hospitalizations and poor utilization of inpatient dermatology consultations. Teledermatology consultations also improve diagnostic accuracy and expedite interventions to improve patient outcomes. However, challenges like reduced reimbursement, lack of protocols, and limited resident training in inpatient dermatology have discouraged dermatologists from providing inpatient consultations. Policy changes are needed to promote these services that benefit patients as well as health systems.

Abstract CRC is the third leading cause of cancer-related deaths among older adults in the US. CRC screening can prevent disease by early identification, yet there are disparities in CRC screening. This study aimed to determine the impact of race, social determinants, and geographic location at zip-codes level on CRC screening.We conducted a retrospective cross-sectional study of CRC screening among different races, evaluating the relationship with the social deprivation index (SDI) and annual income as health determinant factors using the public available data of 2016-2019 CDC 500 cities project and PLACES project 2020 database combined with 2019 American Community Survey for zip code-based analysis. We conducted a multivariate analysis and a confirmatory factor analysis among race, income, lack of health insurance, access to check-up visits and SDI.Increasing SDI tertile increased the likelihood of being Black and Hispanic and having lower median household income (p< 0.01). Lack of health insurance and lower regular checkup visits were less common in the third tertile of SDI (p< 0.01). The multivariate analysis showed that being black, Hispanic, having a lower income, not having health insurance, not having regular check-ups and SDI were related to decreased screening. In the confirmatory factor analysis, the variables most associated with decreased screening are SDI and access to health insurance.Race, SDI, insurance status, socioeconomic status, all impact CRC screenings, but the two most important factors are SDI and access to healthcare. These data may help implement interventions that specifically target these barriers to promote CRC screenings within disadvantaged communities.

Increasing evidence supports a role for abnormal immune activation and inflammatory responses in Huntington disease (HD). In this study, we evaluated the therapeutic potential of laquinimod (1 and 10 mg/kg), a novel immunomodulatory agent shown to be protective in a number of neuroinflammatory conditions, in the YAC128 mouse model of HD. Treatment with laquinimod for 6 months rescued atrophy in the striatum, in certain cortical regions, and in the corpus callosum of YAC128 HD mice. Diffusion tensor imaging showed that white matter microstructural abnormalities in the posterior corpus callosum were improved following treatment with low dose (1 mg/kg) laquinimod, and were paralleled by reduced levels of interleukin-6 in the periphery of YAC128 HD mice. Functionally, treatment with laquinimod (1 and 10 mg/kg) led to modest improvements in motor function and in depressive-like behaviour. Taken together, these results suggest that laquinimod may improve some features of pathology in HD, and provides support for the role of immune activation in the pathogenesis of HD.