Further deliberating the relationship between do-not-resuscitate and the increased risk of death.
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ABSTRACT:
SUBMITTER: Chen YY
PROVIDER: S-EPMC4796796 | biostudies-other | 2016 Mar
REPOSITORIES: biostudies-other
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Project description:Death of a spouse is associated with poorer physical and mental health. We followed all married individuals, born from 1902 to 1942, during the period from 1987 to 2002, and found that widows and widowers had higher risk for hip fracture, compared with still married women and men.IntroductionSpousal bereavement can lead to poorer physical and mental health. We aimed to determine whether married women and men had an elevated risk of hip fracture after death of a spouse.MethodsIn a retrospective cohort study, we followed all Swedish married individuals aged 60 to 100 years (n = 1,783,035), from 1987 to 2002. Data are presented as mean with 95% confidence interval (CI).ResultsDuring the follow-up period, 21,305 hip fractures among widows and 6538 hip fractures among widowers were noted. The hazard ratio (HR) for hip fracture in widows compared with married women was 1.34 (95% CI 1.31 to 1.37) and for widowers compared with married men 1.32 (95% CI 1.29 to 1.35). The HR for hip fracture in the first 6 months after death of a spouse was in widows compared with married women 1.62 (95% CI 1.53 to 1.71) and in widowers compared with married men 1.84 (95% CI 1.68 to 2.03). The elevated risk was especially prominent in young widowers in the age range 60-69 years. During the first 6 months they showed a HR of 2.76 (95% CI 1.66 to 4.58) for a hip fractvure compared with age matched married men. Widows aged 60-69 years showed a HR of 1.59 (95% CI 1.26 to 1.99) compared with age matched married women.ConclusionOur observation of a higher hip fracture risk in both genders in connection with the death of a spouse indicates a possible effect of bereavement on frailty.
| S-EPMC7075824 | biostudies-literature
Project description:ObjectiveTo estimate the contribution of health insurance status to the risk of death among hospitalized neonates.Data sourcesKids' Inpatient Databases (KID) for 2003, 2006, and 2009.Study designKID 2006 subpopulation of neonatal discharges was analyzed by weighted frequency distribution and multivariable logistic regression analyses for the outcome of death, adjusted for insurance status and other variables. Multivariable linear regression analyses were conducted for the outcomes mean adjusted length of stay and hospital charges. The death analysis was repeated with KID 2003 and 2009.Principal findingsOf 4,318,121 estimated discharges in 2006, 5.4 percent were uninsured. There were 17,892 deaths; 9.5 percent were uninsured. The largest risks of death were five clinical conditions with adjusted odds ratios (AOR) of 13.7-3.1. Lack of insurance had an AOR of 2.6 (95 percent CI: 2.4, 2.8), greater than many clinical conditions; AOR estimates in alternate models were 2.1-2.7. Compared with insureds, uninsureds were less likely to have been admitted in transfer, more likely to have died in rural hospitals and to have received fewer resources. Similar death outcome results were observed for 2003 and 2009.ConclusionsUninsured neonates had decreased care and increased risk of dying.
| S-EPMC3725523 | biostudies-literature
Project description:ObjectiveThis study aimed to assess the relationship between increased intracranial pressure (ICP) and mastoid effusions (ME).MethodsBetween January 2015 and October 2018, patients who underwent intracranial surgery and had ICP monitoring catheters placed were enrolled. ICP was recorded hourly for at least 3 days. ME was determined by the emergence of opacification in mastoid air cells on follow-up brain imaging. C-reactive protein (CRP) levels, presence of endotracheal tube (ETT) and nasogastric tube (NGT), duration of intensive care unit (ICU) stay, duration of mechanical ventilator application, diagnosis, surgical modalities, and presence of sinusitis were recorded. Each factor's effect on the occurrence of ME was analyzed by binary logistic regression analyses. To analyze the independent effects of ICP as a predictor of ME a multivariable logistic regression analysis was performed.ResultsTotal of 61 (53%) out of 115 patients had ME. Among the patients who had unilateral brain lesions, 94% of subject (43/50) revealed the ipsilateral development of ME. ME developed at a mean of 11.1±6.2 days. The variables including mean ICP, peak ICP, age, trauma, CRP, ICU stays, application of mechanical ventilators and presence of ETT and NGT showed statistically significant difference between ME groups and non-ME groups in univariate analysis. Sex and the occurrence of sinusitis did not differ between two groups. Adding the ICP variables significantly improved the prediction of ME in multivariable logistic regression analysis.ConclusionWhile multiple factors affect ME, this study demonstrates that ICP and ME are probably related. Further studies are needed to determine the mechanistic relationship between ICP and middle ear pressure.
| S-EPMC7477151 | biostudies-literature
Project description:Background: Liver steatosis is considered the onset of the non-alcoholic fatty liver disease (NAFLD), a major public health challenge. Nevertheless, NAFLD detection and diagnosis remain a difficult task. Fatty acid binding protein 4 (FABP4) has been proposed as potential biomarker for the ectopic fat accumulation in non-adipose tissues, although its role reflecting liver steatosis in metabolic patients is not fully explored. The aim of this study was to assess the relationship between FABP4 and the fatty liver index (FLI) in metabolic patients and to evaluate its potential role in the fatty liver disease. Methods: A cross-sectional study involving 389 participants at increased cardiometabolic risk was performed. FLI was calculated in order to assess liver fatty disease and a FLI ≥ 60 was considered to define liver steatosis. The serum FABP4 levels were assessed by using a sandwich enzyme-linked immunosorbent assay. Multivariable regression models were used to examine the associations of FABP4 with fatty liver after adjusting for demographic and clinical characteristics. Results: Both, FLI and serum FABP4 levels were upregulated in diabetic, obese, and metabolic syndrome patients. Serum FABP4 levels were higher in individuals with liver steatosis. Serum FABP4 were robustly associated with FLI in metabolic patients in both linear and logistic regression analyses. Conclusion: Our findings show that the serum FABP4 is associated to liver steatosis in metabolic patients.
| S-EPMC8711782 | biostudies-literature
Project description:Background & aimsIdentifying shared and disease-specific susceptibility loci for Crohn's disease (CD) and ulcerative colitis (UC) would help define the biologic relationship between the inflammatory bowel diseases. More than 30 CD susceptibility loci have been identified. These represent important candidate susceptibility loci for UC. Loci discovered by the index genome scans in CD have previously been tested for association with UC, but those identified in the recent meta-analysis await such investigation. Furthermore, the recently identified UC locus at ECM1 requires formal testing for association with CD.MethodsWe analyzed 45 single nucleotide polymorphisms, tagging 29 of the loci recently associated with CD in 2527 UC cases and 4070 population controls. We also genotyped the UC-associated ECM1 variant rs11205387 in 1560 CD patients and 3028 controls.ResultsNine regions showed association with UC at a threshold corrected for the 29 loci tested (P < .0017). The strongest association (P = 4.13 x 10(-8); odds ratio = 1.27) was identified with a 170-kilobase region on chromosome 1q32 that contains 3 genes. We also found association with JAK2 and replicated a recently reported association with STAT3, further implicating the role of this signaling pathway in inflammatory bowel disease. Additional novel UC susceptibility genes were LYRM4 and CDKAL1. Twenty of the loci were not associated with UC, and several appear to be specific to CD. ECM1 variation was not associated with CD.ConclusionsCollectively, these data help define the genetic relationship between CD and UC and characterize common, as well as disease-specific mechanisms of pathogenesis.
| S-EPMC2675137 | biostudies-literature
Project description:BackgroundMethamphetamine (MA) use has been linked anecdotally to rampant dental disease. The authors sought to determine the relative prevalence of dental comorbidities in MA users, verify whether MA users have more quantifiable dental disease and report having more dental problems than nonusers and establish the influence of mode of MA administration on oral health outcomes.MethodsParticipating physicians provided comprehensive medical and oral assessments for adults dependent on MA (n=301). Trained interviewers collected patients' self-reports regarding oral health and substance-use behaviors. The authors used propensity score matching to create a matched comparison group of nonusers from participants in the the Third National Health and Nutrition Examination Survey (NHANES III).ResultsDental or oral disease was one of the most prevalent (41.3 percent) medical cormorbidities in MA users who otherwise were generally healthy. On average, MA users had significantly more missing teeth than did matched NHANES III control participants (4.58 versus 1.96, P<.001) and were more likely to report having oral health problems (P<.001). Significant subsets of MA users expressed concerns with their dental appearance (28.6 percent), problems with broken or loose teeth (23.3 percent) and tooth grinding (bruxism) or erosion (22.3 percent). The intravenous use of MA was significantly more likely to be associated with missing teeth than was smoking MA (odds ratio=2.47; 95 percent confidence interval=1.3-4.8).ConclusionsOvert dental disease is one of the key distinguishing comorbidities in MA users. MA users have demonstrably higher rates of dental disease and report long-term unmet oral health needs. Contrary to common perception, users who smoke or inhale MA have lower rates of dental disease than do those who inject the drug. Many MA users are concerned with the cosmetic aspects of their dental disease, and these concerns could be used as behavioral triggers for targeted interventions.Clinical implicationsDental disease may provide a temporally stable MA-specific medical marker with discriminant utility in identifying MA users. Dentists can play a crucial role in the early detection of MA use and participate in the collaborative care of MA users.
| S-EPMC2947197 | biostudies-literature
Project description:BACKGROUND:The relationship between metabolic syndrome (MetS) and Barrett's esophagus (BE) is still a challenging issue, and inconsistent results have been reported in different studies. Therefore, this study was conducted to determine the relationship between MetS and BE. METHODS:In this study, we followed the MOOSE protocol and results were reported according to the PRISMA guidelines. All study steps were performed independently by two authors. If necessary, the dispute was resolved by consultation with a third author. The search strategy is designed to find published studies. Comprehensive search was done in the following databases until July 2019: Cochrane Library, PubMed/Medline, Web of Science, Science Direct, EMBASE, Scopus, CINAHL, EBSCO, and Google Scholar search engine. All analyses were performed using Comprehensive Meta-Analysis Software Ver.2, while p-value lower than 0.05 was considered significant. RESULTS:In 14 studies with a sample size of 108,416, MetS significantly increased the risk of BE (OR?=?1.354; 95% CI: 1.145-1.600; P?<?0.001; Heterogeneity: I2 =?81.95%; P?<?0.001). Sensitivity analysis by omitting one study showed that overall estimates are still robust. Subgroup analysis was significant for continent (P?<?0.001) and MetS diagnostic criteria (P?=?0.043), but was not significant for variables of study type (P?=?0.899), study setting (P?=?0.115), control groups (P?=?0.671) and quality of studies (P?=?0.603). The Begg (P?=?0.912) and Egger's (P?=?0.094) tests were not significant; therefore, the publication bias did not play a role in the results. CONCLUSION:MetS increases the risk of BE compared to control groups. The results of this study can help health practitioners by identifying a treatable risk factor for the most important risk factor for esophageal carcinoma (ie, BE). Future studies should examine whether treatment for MetS reduces the risk of BE.
| S-EPMC7412848 | biostudies-literature
Project description:BackgroundFucose is utilized for the modification of different molecules involved in blood group determination, immunological reactions, and signal transduction pathways. We have recently reported that enhanced activity of the fucosyltransferase 3 and/or 6 promoted TGF-ß-mediated epithelial mesenchymal transition and was associated with increased metastatic potential of colorectal cancer (CRC), suggesting that fucose is required by CRC cells. With this in mind, we examined requirement of L-fucose in CRC cells and developed fucose-bound nanoparticles as vehicles for delivery of anticancer drugs specific to CRC.MethodsIn this study, we first examined the expression of fucosylated proteins in 50 cases of CRC by immunochistochemical staining with biotinylated Aleuria aurantia lectin (AAL). Then we carried out an L-fucose uptake assay using three CRC cell lines. Finally, we developed fucose-bound nanoparticles as vehicles for the delivery of an anticancer drug, SN38, and examined tumor growth inhibition in mouse xenograft model (n = 6 mice per group). All statistical tests were two-sided.ResultsWe found a statistically significant relationship between vascular invasion, clinical stage, and intensity score of AAL staining (P≤ .02). L-fucose uptake assay revealed that L-fucose incorporation, as well as fucosylated protein release, was high in cells rich in fucosylated proteins. L-fucose-bound liposomes effectively delivered Cy5.5 into CRC cells. The excess of L-fucose decreased the efficiency of Cy5.5 uptake through L-fucose-bound liposomes, suggesting an L-fucose receptor dependency. Intravenously injected, L-fucose-bound liposomes carrying SN38 were successfully delivered to CRC cells, mediating efficient tumor growth inhibition (relative tumor growth ratio: no treatment group [NT], 8.29 ± 3.09; SN38-treated group [SN38], 3.53 ± 1.47; liposome-carrying, SN38-treated group [F0], 3.1 ± 1.39; L-fucose-bound, liposome-carrying, SN38-treated group [F50], 0.94 ± 0.89; F50 vs NT,P= .003; F50 vs SN38,P= .02, F50 vs F0,P= .04), as well as prolonging survival of mouse xenograft models (log-rank test,P< .001).ConclusionsThus, fucose-bound liposomes carrying anticancer drugs provide a new strategy for the treatment of CRC patients.
| S-EPMC5017955 | biostudies-literature
Project description:An increased risk of cardiovascular death in Cytomegalovirus (CMV)-infected individuals remains unexplained, although it might partly result from the fact that CMV infection is closely associated with the accumulation of CD28null T-cells, in particular CD28null CD4 T-cells. These cells can directly damage endothelium and precipitate cardiovascular events. However, the current paradigm holds that the accumulation of CD28null T-cells is a normal consequence of aging, whereas the link between these T-cell populations and CMV infection is explained by the increased prevalence of this infection in older people. Resolving whether CMV infection or aging triggers CD28null T-cell expansions is of critical importance because, unlike aging, CMV infection can be treated. Methods: We used multi-color flow-cytometry, antigen-specific activation assays, and HLA-typing to dissect the contributions of CMV infection and aging to the accumulation of CD28null CD4 and CD8 T-cells in CMV+ and CMV- individuals aged 19 to 94 years. Linear/logistic regression was used to test the effect of sex, age, CMV infection, and HLA-type on CD28null T-cell frequencies. Results: The median frequencies of CD28null CD4 T-cells and CD28null CD8 T-cells were >12-fold (p=0.000) but only approximately 2-fold higher (p=0.000), respectively, in CMV+ (n=136) compared with CMV- individuals (n=106). The effect of CMV infection on these T-cell subsets was confirmed by linear regression. Unexpectedly, aging contributed only marginally to an increase in CD28null T-cell frequencies, and only in CMV+ individuals. Interestingly, the presence of HLA-DRB1*0301 led to an approximately 9-fold reduction of the risk of having CD28null CD4 T-cell expansions (OR=0.108, p=0.003). Over 75% of CMV-reactive CD4 T-cells were CD28null. Conclusion: CMV infection and HLA type are major risk factors for CD28null CD4 T-cell-associated cardiovascular pathology. Increased numbers of CD28null CD8 T-cells are also associated with CMV infection, but to a lesser extent. Aging, however, makes only a negligible contribution to the expansion of these T-cell subsets, and only in the presence of CMV infection. Our results open up new avenues for risk assessment, prevention, and treatment.
| S-EPMC6134924 | biostudies-literature
Project description:Obesity, metabolic syndrome and type 2 diabetes are associated with cancer-related mortality. We assessed whether hyperinsulinemia is a risk factor for cancer death in nonobese people without diabetes. We conducted a prospective cohort study using data from the National Health and Nutrition Examination Survey 1999-2010 and followed up the participants until December 31, 2011. For the primary analysis of cancer mortality, we used Cox proportional hazard models to estimate hazard ratios (HRs) in the participants with hyperinsulinemia and those without. Hyperinsulinemia was defined as a fasting insulin level of ≥10 μU/mL. To identify causes of deaths, the International Classification of Diseases, Tenth Revision codes were used. This study included 9,778 participants aged 20 years or older without diabetes or a history of cancer: 6,718 nonobese participants (2,057 with hyperinsulinemia [30.6%]) and 3,060 obese participants (2,303 with hyperinsulinemia [75.3%]). A total of 99.9% completed follow-up. Among all study participants, cancer mortality was significantly higher in those with hyperinsulinemia than in those without hyperinsulinemia (adjusted HR 2.04, 95% CI 1.24-3.34, p = 0.005). Similarly, among nonobese participants, multivariable analysis showed that cancer mortality was significantly higher in those with hyperinsulinemia than in those without (adjusted HR 1.89, 95% CI 1.07-3.35, p = 0.02). Considering that nonobese people with hyperinsulinemia were at higher risk of cancer mortality than those without hyperinsulinemia, improvement of hyperinsulinemia may be an important approach for preventing cancer regardless of the presence or absence of obesity.
| S-EPMC5435954 | biostudies-literature