Health Literacy in Surgery.

BACKGROUND: Low health literacy is associated with poor health outcomes in many chronic diseases and may have an important role in determining surgical outcomes. This study aims to comprehensively review the current state of science on adult health literacy in surgery and to identify knowledge gaps for future research. METHODS: Using the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, a systematic search was conducted to identify all studies from January 2002 through May 2018 that used validated instruments to assess health literacy among adult patients undergoing surgery. Studies were assessed for quality using the Newcastle-Ottawa scale and evaluated on findings by their focus on identifying health literacy levels, understanding associations with surgical outcomes, and/or developing interventions to address low health literacy. KEY RESULTS: There were 51 studies on health literacy with data from 22,139 patients included in this review. Low health literacy was present in more than one-third of surgical patients (34%, interquartile range 16%-50%). The most commonly used validated instrument for assessment of health literacy in the surgical population was the Newest Vital Sign. Most studies were focused on identifying the prevalence of low health literacy within a surgery population (84%, n = 43). Few studies focused on understanding the association of health literacy to surgical outcomes (12%, n = 6) and even fewer studies developed interventions to address health literacy (4%, n = 2). DISCUSSION: Low health literacy is common among surgical patients. Important opportunities exist to better understand the role of health literacy in determining surgical outcomes and to develop more health literacy-sensitive models of surgical care. [HLRP: Health Literacy Research and Practice. 2020;4(1):e45-e65.] PLAIN LANGUAGE SUMMARY: Health literacy has not been well-studied in surgery but likely plays an important role. In this article, we reviewed all current research on health literacy in surgery to help us understand where we are at and where we need to go. We found that low health literacy is common and we need more ways to address it in surgery.

Ultraviolet Radiation-Induced Downregulation of SERCA2 Mediates Activation of NLRP3 Inflammasome in Basal Cell Carcinoma.

Basal cell carcinomas (BCCs) account for majority of skin malignancies in the United States. The incidence of BCCs is strongly associated with exposure of ultraviolet (UV) radiation. Nucleotide-binding domain, leucine-rich-repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasome plays an important role in innate immune responses. Different stimuli such as toxins, microorganisms and particles released from injured cells activate the NLRP3 inflammasome. Activated NLRP3 results in activation of caspase-1, which cleaves pro-IL-1ß to active IL-1ß. In this study, we have shown that NLRP3 is expressed in human basal cell carcinomas. The proximal steps in activation of NLRP3 inflammasome are not well understood. Here, we have attempted to elucidate a critical role for Ca2+ mobilization in activation of the NLRP3 inflammasome by UVB exposure using HaCaT keratinocytes. We have demonstrated that UVB exposure blocks Ca2+ mobilization by downregulating the expression of sarco/endoplasmic reticulum Ca2+ -ATPase (SERCA2), a component of store-operated Ca2+ entry that leads to activation of the NLRP3 inflammasome.

Baicalin Protects Keratinocytes from Toll-like Receptor-4 Mediated DNA Damage and Inflammation Following Ultraviolet Irradiation.

UVB radiation contributes to both direct and indirect damage to the skin including the generation of free radicals and reactive oxygen species (ROS), inflammatory responses, immunosuppression and gene mutations, which can ultimately lead to photocarcinogenesis. A plant-derived flavonoid, baicalin, has been shown to have antioxidant, anti-inflammatory and free radical scavenging activities. Previous studies from our laboratory have shown that in murine skin, Toll-like receptor-4 (TLR4) enhanced both UVB-induced DNA damage and inflammation. The aim of this study was to investigate the efficacy of baicalin against TLR4-mediated processes in the murine keratinocyte PAM 212 cell line. Our results demonstrate that treating keratinocytes with baicalin both before and after UV radiation (100 mJ cm(-2) ) significantly inhibited the level of intracellular ROS and decreased cyclobutane pyrimidine dimers and 8-Oxo-2'-deoxyguanosine (8-oxo-dG)-markers of DNA damage. Furthermore, cells treated with baicalin demonstrated an inhibition of TLR4 and its downstream signaling molecules, MyD88, TRIF, TRAF6 and IRAK4. TLR4 pathway inhibition resulted in NF-κB inactivation and down-regulation of iNOS and COX-2 protein expression. Taken together, baicalin treatment effectively protected keratinocytes from UVB-induced inflammatory damage through TLR pathway modulation.

Thymoquinone suppresses metastasis of melanoma cells by inhibition of NLRP3 inflammasome.

The inflammasome is a multi-protein complex which when activated regulates caspase-1 activation and IL-1ß and IL-18 secretion. The NLRP3 (NACHT, LRR, and pyrin domain-containing protein 3) inflammasome is constitutively assembled and activated in human melanoma cells. We have examined the inhibitory effect of thymoquinone (2-isopropyl-5-methylbenzo-1,4-quinone), a major ingredient of black seed obtained from the plant Nigella sativa on metastatic human (A375) and mouse (B16F10) melanoma cell lines. We have assessed whether thymoquinone inhibits metastasis of melanoma cells by targeting NLRP3 subunit of inflammasomes. Using an in vitro cell migration assay, we found that thymoquinone inhibited the migration of both human and mouse melanoma cells. The inhibitory effect of thymoquinone on metastasis was also observed in vivo in B16F10 mouse melanoma model. The inhibition of migration of melanoma cells by thymoquinone was accompanied by a decrease in expression of NLRP3 inflammasome resulting in decrease in proteolytic cleavage of caspase-1. Inactivation of caspase-1 by thymoquinone resulted in inhibition of IL-1ß and IL-18. Treatment of mouse melanoma cells with thymoquinone also inhibited NF-κB activity. Furthermore, inhibition of reactive oxygen species (ROS) by thymoquinone resulted in partial inactivation of NLRP3 inflammasome. Thus, thymoquinone exerts its inhibitory effect on migration of human and mouse melanoma cells by inhibition of NLRP3 inflammasome. Thus, our results indicate that thymoquinone can be a potential immunotherapeutic agent not only as an adjuvant therapy for melanoma, but also, in the control and prevention of metastatic melanoma.