Sexual racism is a specific form of racial prejudice enacted in the context of sex or romance. Online, people use sex and dating profiles to describe racialized attraction through language such as ...“Not attracted to Asians.” Among gay and bisexual men, sexual racism is a highly contentious issue. Although some characterize discrimination among partners on the basis of race as a form of racism, others present it as a matter of preference. In May 2011, 2177 gay and bisexual men in Australia participated in an online survey that assessed how acceptably they viewed online sexual racism. Although the men sampled displayed diverse attitudes, many were remarkably tolerant of sexual racism. We conducted two multiple linear regression analyses to compare factors related to men’s attitudes toward sexual racism online and their racist attitudes more broadly. Almost every identified factor associated with men’s racist attitudes was also related to their attitudes toward sexual racism. The only differences were between men who identified as Asian or Indian. Sexual racism, therefore, is closely associated with generic racist attitudes, which challenges the idea of racial attraction as solely a matter of personal preference.
Mobile health in the aging surgical patient Rubio-Chavez, Atziri; Cauley, Christy E.
Surgery,
April 2024, 2024-Apr, 2024-04-00, 20240401, Letnik:
175, Številka:
4
Journal Article
Recenzirano
Mobile health includes the use of mobile devices, patient monitoring devices, and digital assistants to improve the delivery of healthcare. Aging surgical patients (ie, 65 years and older) represent ...a unique patient population that demands increased resources to prepare for surgery and optimize recovery. Mobile health has the potential to improve surgical patient outcomes by increasing the accessibility of personalized care and reducing costs. However, there are some challenges to consider when using mobile health in older surgical patients, such as technological literacy, visual and hearing impairment, and cognitive changes before or after anesthesia. Despite the rapid uptake of mobile health in medical specialties, its application in the surgical field is gradual. The complexity of aging surgical patients requires surgical care teams, surgical leaders, and healthcare policymakers to consider unique solutions, such as mobile health, to address this growing population’s needs before and after surgery. This article will discuss the potential benefits and challenges of mobile health among aging surgical patients, as well as opportunities to support these patients and families with customizable tools to meet their preferences and needs.
Previous studies suggest that urgent colectomy and primary anastomosis with diversion is safe for perforated diverticulitis. Current guidelines support this approach.
The purpose of this study was to ...describe the use of urgent or emergent primary anastomosis with diversion in diverticulitis before the 2014 American Society of Colon and Rectal Surgeons guidelines and compare national outcomes of primary anastomosis with diversion to the Hartmann procedure.
This was a national retrospective cohort study.
The study was conducted with a national all-payer US sample from 1998 to 2011.
Patients included those admitted and treated with urgent or emergent colectomy for diverticulitis. Exclusion criteria were age <18 years, concurrent diagnosis of colorectal cancer or IBD, no fecal diversion performed, and operations >24 hours after admission.
In-hospital mortality was measured.
A total of 124,198 patients underwent emergent or urgent colectomy for acute diverticulitis; 67,721 underwent concurrent fecal diversion, including 65,084 (96.1%) who underwent end colostomy and 2637 (3.9%) who underwent anastomosis with ileostomy. The rate of primary anastomosis with diverting ileostomy increased from 30 to 60 diverting ileostomy cases per 1000 operative diverticulitis cases in 1998 versus 2011 (incidence rate ratio = 2.04 (95% CI, 1.70-2.50). However, overall use remained low, with >90% of patients undergoing end colostomy. Complication rates were higher (32.1% vs 23.3%; p < 0.001) and in-hospital mortality rates were higher (16.0% vs 6.4%; p < 0.001) for primary anastomosis with diversion patients compared with end colostomy. These findings were consistent on multivariable logistic regression. Other factors that contributed to in-hospital mortality included increasing age, increasing comorbid disease burden, and socioeconomic status.
Billing data can be inaccurate or biased because of nonmedically trained professional data entry. Selection bias could have affected the results of this retrospective study.
The use of primary anastomosis with proximal diversion for urgent colectomy in diverticulitis increased over our study period; however, overall use remained low. Poor national outcomes after primary anastomosis with proximal diversion might affect compliance with new guidelines. See Video Abstract at http://links.lww.com/DCR/A600.
Primary sclerosing cholangitis (PSC) is a chronic, idiopathic, fibroinflammatory cholangiopathy. The role of the microbiota in PSC etiopathogenesis may be fundamentally important, yet remains ...obscure. We tested the hypothesis that germ‐free (GF) mutltidrug resistance 2 knockout (mdr2−/−) mice develop a distinct PSC phenotype, compared to conventionally housed (CV) mdr2−/− mice. Mdr2−/− mice (n = 12) were rederived as GF by embryo transfer, maintained in isolators, and sacrificed at 60 days in parallel with age‐matched CV mdr2−/− mice. Serum biochemistries, gallbladder bile acids, and liver sections were examined. Histological findings were validated morphometrically, biochemically, and by immunofluorescence microscopy (IFM). Cholangiocyte senescence was assessed by p16INK4a in situ hybridization in liver tissue and by senescence‐associated β‐galactosidase staining in a culture‐based model of insult‐induced senescence. Serum biochemistries, including alkaline phosphatase, aspartate aminotransferase, and bilirubin, were significantly higher in GF mdr2−/− (P < 0.01). Primary bile acids were similar, whereas secondary bile acids were absent, in GF mdr2−/− mice. Fibrosis, ductular reaction, and ductopenia were significantly more severe histopathologically in GF mdr2−/− mice (P < 0.01) and were confirmed by hepatic morphometry, hydroxyproline assay, and IFM. Cholangiocyte senescence was significantly increased in GF mdr2−/− mice and abrogated in vitro by ursodeoxycholic acid (UDCA) treatment. Conclusions: GF mdr2−/− mice exhibit exacerbated biochemical and histological features of PSC and increased cholangiocyte senescence, a characteristic and potential mediator of progressive biliary disease. UDCA, a commensal microbial metabolite, abrogates senescence in vitro. These findings demonstrate the importance of the commensal microbiota and its metabolites in protecting against biliary injury and suggest avenues for future studies of biomarkers and therapeutic interventions in PSC. (Hepatology 2016;63:185–196)
Ageing of the immune system, or immunosenescence, contributes to the morbidity and mortality of the elderly
. To define the contribution of immune system ageing to organism ageing, here we ...selectively deleted Ercc1, which encodes a crucial DNA repair protein
, in mouse haematopoietic cells to increase the burden of endogenous DNA damage and thereby senescence
in the immune system only. We show that Vav-iCre
;Ercc1
mice were healthy into adulthood, then displayed premature onset of immunosenescence characterized by attrition and senescence of specific immune cell populations and impaired immune function, similar to changes that occur during ageing in wild-type mice
. Notably, non-lymphoid organs also showed increased senescence and damage, which suggests that senescent, aged immune cells can promote systemic ageing. The transplantation of splenocytes from Vav-iCre
;Ercc1
or aged wild-type mice into young mice induced senescence in trans, whereas the transplantation of young immune cells attenuated senescence. The treatment of Vav-iCre
;Ercc1
mice with rapamycin reduced markers of senescence in immune cells and improved immune function
. These data demonstrate that an aged, senescent immune system has a causal role in driving systemic ageing and therefore represents a key therapeutic target to extend healthy ageing.
Primary sclerosing cholangitis (PSC) is an incurable cholangiopathy of unknown etiopathogenesis. Here we tested the hypothesis that cholangiocyte senescence is a pathophysiologically important ...phenotype in PSC. We assessed markers of cellular senescence and senescence‐associated secretory phenotype (SASP) in livers of patients with PSC, primary biliary cirrhosis, hepatitis C, and in normals by fluorescent in situ hybridization (FISH) and immunofluorescence microscopy (IFM). We tested whether endogenous and exogenous biliary constituents affect senescence and SASP in cultured human cholangiocytes. We determined in coculture whether senescent cholangiocytes induce senescence in bystander cholangiocytes. Finally, we explored signaling mechanisms involved in cholangiocyte senescence and SASP. In vivo, PSC cholangiocytes expressed significantly more senescence‐associated p16INK4a and γH2A.x compared to the other three conditions; expression of profibroinflammatory SASP components (i.e., IL‐6, IL‐8, CCL2, PAI‐1) was also highest in PSC cholangiocytes. In vitro, several biologically relevant endogenous (e.g., cholestane 3,5,6 oxysterol) and exogenous (e.g., lipopolysaccharide) molecules normally present in bile induced cholangiocyte senescence and SASP. Furthermore, experimentally induced senescent human cholangiocytes caused senescence in bystander cholangiocytes. N‐Ras, a known inducer of senescence, was increased in PSC cholangiocytes and in experimentally induced senescent cultured cholangiocytes; inhibition of Ras abrogated experimentally induced senescence and SASP. Conclusion: Cholangiocyte senescence induced by biliary constituents by way of N‐Ras activation is an important pathogenic mechanism in PSC. Pharmacologic inhibition of N‐Ras with a resultant reduction in cholangiocyte senescence and SASP is a new therapeutic approach for PSC. (Hepatology 2014;59:2263–2275)
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•Peribiliary macrophages are increased in PSC and animal models of PSC.•Both M1-like and M2-like peribiliary macrophages are increased.•Genetic and pharmacologic CCR2 inhibition ...restrains monocyte recruitment.•CCR2 inhibition reduces fibrosis and cholestasis in animal models of PSC.•These studies support the use of CCR2 inhibitors in human PSC.
Macrophages contribute to liver disease, but their role in cholestatic liver injury, including primary sclerosing cholangitis (PSC), is unclear. We tested the hypothesis that macrophages contribute to the pathogenesis of, and are therapeutic targets for, PSC.
Immune cell profile, hepatic macrophage number, localization and polarization, fibrosis, and serum markers of liver injury and cholestasis were measured in an acute (intrabiliary injection of the inhibitor of apoptosis antagonist BV6) and chronic (Mdr2−/− mice) mouse model of sclerosing cholangitis (SC). Selected observations were confirmed in liver specimens from patients with PSC. Because of the known role of the CCR2/CCL2 axis in monocyte/macrophage chemotaxis, therapeutic effects of the CCR2/5 antagonist cenicriviroc (CVC), or genetic deletion of CCR2 (Ccr2−/− mice) were determined in BV6-injected mice.
We found increased peribiliary pro-inflammatory (M1-like) and alternatively-activated (M2-like) monocyte-derived macrophages in PSC compared to normal livers. In both SC models, genetic profiling of liver immune cells identified a predominance of monocytes/macrophages; immunohistochemistry confirmed peribiliary monocyte-derived macrophage recruitment (M1>M2-polarized), which paralleled injury onset and was reversed upon resolution in acute SC mice. PSC, senescent and BV6-treated human cholangiocytes released monocyte chemoattractants (CCL2, IL-8) and macrophage-activating factors in vitro. Pharmacological inhibition of monocyte recruitment by CVC treatment or CCR2 genetic deletion attenuated macrophage accumulation, liver injury and fibrosis in acute SC.
Peribiliary recruited macrophages are a feature of both PSC and acute and chronic murine SC models. Pharmacologic and genetic inhibition of peribiliary macrophage recruitment decreases liver injury and fibrosis in mouse SC. These observations suggest monocyte-derived macrophages contribute to the development of SC in mice and in PSC pathogenesis, and support their potential as a therapeutic target.
Primary sclerosing cholangitis (PSC) is an inflammatory liver disease which often progresses to liver failure. The cause of the disease is unclear and therapeutic options are limited. Therefore, we explored the role of white blood cells termed macrophages in PSC given their frequent contribution to other human inflammatory diseases. Our results implicate macrophages in PSC and PSC-like diseases in mice. More importantly, we found that pharmacologic inhibition of macrophage recruitment to the liver reduces PSC-like liver injury in the mouse. These exciting observations highlight potential new strategies to treat PSC.
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