A Comparison of Quality of Care in Critical Access Hospitals and Other Rural Hospitals

Purpose: The United States has about 2100 rural hospitals. Approximately 1300 are Critical Access Hospitals (CAHs) with 25 beds or less. CAHs receive cost-based reimbursement through the federal Flex program with the goal to improve quality and access to health care. Reports on quality of care (QOC) and factors that influence quality in CAHs are mixed. This study compared QOC and factors that influence QOC in CAHs and other rural hospitals. Sample: 385 staff nurses in 6 CAHs and 9 other rural hospitals in North Carolina and Virginia. Method: Descriptive cross-sectional design using nurse surveys aggregated to the hospital level, data from provider of services file, and the United States Department of Agriculture, Economic Research files. Variables on community, hospital, and nursing unit characteristics, the nurse work environment, nurse rated QOC and community perception of hospital quality were compared using t-test or chi-square. Findings: There were no differences in the majority of factors influencing QOC. A culture of safety, the nurse work environment, and QOC were rated high in all hospitals. Compared to other rural hospitals CAHs tend to be located in communities with better economic status and their nurses had more years of nursing experience. More nurses in CAHs felt their community recognized their hospital as a good place for minor health issues and would recommend the hospital to family and friends. Conclusions: The high ratings of QOC were accompanied with the presence of safety cultures and work environments rated as highly as in Magnet hospitals. The lower poverty levels in communities with CAHs suggest possible community financial benefits from CAHs. More studies are warranted to explore these relationships. Further reporting to public quality indicator databases by all CAHs should be encouraged and QOC measures relevant for small rural hospitals should be developed

Hepcidin and sports anemia

Iron is an important mineral element used by the body in a variety of metabolic and physiologic processes. These processes are highly active when the body is undergoing physical exercises. Prevalence of exercise-induced iron deficiency anemia (also known as sports anemia) is notably high in athletic populations, particularly those with heavy training loads. The pathogenesis of sports anemia is closely related to disorders of iron metabolism, and a more comprehensive understanding of the mechanism of iron metabolism in the course of physical exercises could expand ways of treatment and prevention of sports anemia. In recent years, there have been remarkable research advances regarding the molecular mechanisms underlying changes of iron metabolism in response to physical exercises. This review has covered these advances, including effects of exercise on duodenum iron absorption, serum iron status, iron distribution in organs, erythropoiesis, and hepcidin’s function and its regulation. New methods for the treatment of exercise-induced iron deficiency are also discussed

Mitochondrial ferritin attenuates cerebral ischaemia/reperfusion injury by inhibiting ferroptosis

Ischaemic stroke is becoming the most common cerebral disease in aging populations, but the underlying molecular mechanism of the disease has not yet been fully elucidated. Increasing evidence has indicated that an excess of iron contributes to brain damage in cerebral ischaemia/reperfusion (I/R) injury. Although mitochondrial ferritin (FtMt) plays a critical role in iron homeostasis, the molecular function of FtMt in I/R remains unknown. We herein report that FtMt levels are upregulated in the ischaemic brains of mice. Mice lacking FtMt experience more severe brain damage and neurological deficits, accompanied by typical molecular features of ferroptosis, including increased lipid peroxidation and disturbed glutathione (GSH) after cerebral I/R. Conversely, FtMt overexpression reverses these changes. Further investigation shows that Ftmt ablation promotes I/R-induced inflammation and hepcidin-mediated decreases in ferroportin1, thus markedly increasing total and chelatable iron. The elevated iron consequently facilitates ferroptosis in the brain of I/R. In brief, our results provide evidence that FtMt plays a critical role in protecting against cerebral I/R-induced ferroptosis and subsequent brain damage, thus providing a new potential target for the treatment/prevention of ischaemic stroke

Mitochondrial Ferritin Deletion Exacerbates β

Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates β-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on β-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV) with Aβ25–35 to establish an Alzheimer’s disease model. Knockout of Ftmt significantly exacerbated Aβ25–35-induced learning and memory impairment. The Bcl-2/Bax ratio in mouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased in Ftmt knockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. Increased MDA levels were also detected in Ftmt knockout mice treated with Aβ25–35. In conclusion, this study demonstrated that the neurological impairment induced by Aβ25–35 was exacerbated in Ftmt knockout mice and that this may relate to increased levels of oxidative stress

Plasma Lipidomics Profiling Reveals Biomarkers for Papillary Thyroid Cancer Diagnosis

The objective of this study was to identify potential biomarkers and possible metabolic pathways of malignant and benign thyroid nodules through lipidomics study. A total of 47 papillary thyroid carcinomas (PTC) and 33 control check (CK) were enrolled. Plasma samples were collected for UPLC-Q-TOF MS system detection, and then OPLS-DA model was used to identify differential metabolites. Based on classical statistical methods and machine learning, potential biomarkers were characterized and related metabolic pathways were identified. According to the metabolic spectrum, 13 metabolites were identified between PTC group and CK group, and a total of five metabolites were obtained after further screening. Its metabolic pathways were involved in glycerophospholipid metabolism, linoleic acid metabolism, alpha-linolenic acid metabolism, glycosylphosphatidylinositol (GPI)—anchor biosynthesis, Phosphatidylinositol signaling system and the metabolism of arachidonic acid metabolism. The metabolomics method based on PROTON nuclear magnetic resonance (NMR) had great potential for distinguishing normal subjects from PTC. GlcCer(d14:1/24:1), PE-NME (18:1/18:1), SM(d16:1/24:1), SM(d18:1/15:0), and SM(d18:1/16:1) can be used as potential serum markers for the diagnosis of PTC

Direct and indirect costs associated with stereotactic radiosurgery or open surgery for medial temporal lobe epilepsy: Results from the ROSE trial

Objective To determine whether a less-invasive approach to surgery for medically refractory temporal lobe epilepsy is associated with lower health care costs and costs of lost productivity over time, compared to open surgery. Methods We compared direct medical costs and indirect productivity costs associated with treatment with stereotactic radiosurgery (SRS) or anterior temporal lobectomy (ATL) in the ROSE (Radiosurgery or Open Surgery for Epilepsy) trial. Health care use was abstracted from hospital bills, the study database, and diaries in which participants recorded health care use and time lost from work while seeking care. Costs of use were calculated using a Medicare costing approach used in a prior study of the costs of ATL. The power of many analyses was limited by the sample size and data skewing. Results Combined treatment and follow-up costs (in thousands of US dollars) did not differ between SRS (n = 20, mean = $76.6, 95$79.0, 95% CI = 60.09-103.8). Indirect costs also did not differ. More ATL than SRS participants were free of consciousness-impairing seizures in each year of follow-up (all P < 0.05). Costs declined following ATL (P = 0.005). Costs tended to increase over the first 18 months following SRS (P = 0.17) and declined thereafter (P = 0.06). This mostly reflected hospitalizations for SRS-related adverse events in the second year of follow-up. Significance Lower initial costs of SRS for medial temporal lobe epilepsy were largely offset by hospitalization costs related to adverse events later in the course of follow-up. Future studies of less-invasive alternatives to ATL will need to assess adverse events and major costs systematically and prospectively to understand the economic implications of adopting these technologies

Iron Metabolism, Redox Balance and Neurological Diseases

Iron is essential for life, and the dysregulation of iron homeostasis can lead to severe pathological changes in the neurological system [...

Younger black patients have a higher risk of infection mortality that is mostly non-dialysis related: A national study of cause-specific mortality among U.S. maintenance dialysis patients.

IntroductionWhile it has been well documented that in the U.S., black and Hispanic dialysis patients have overall lower risks of death than white dialysis patients, little is known whether their lower risks are observed in cause-specific deaths. Additionally, recent research reported that younger black patients have a higher risk of death, but the source is unclear. Therefore, this study examined cause-specific deaths among US dialysis patients by race/ethnicity and age.MethodsThis national study included 1,255,640 incident dialysis patients between 1995 and 2010 in the United States Renal Data System. Five cause-specific mortality rates, including cardiovascular (CVD), infection, malignancy, other known causes (miscellaneous), and unknown, were compared across blacks, Hispanics, and whites overall and stratified by age groups.FindingsAfter multiple adjustments, Hispanic patients had the lowest risk of mortality for every major cause in almost all ages. Compared with whites, blacks had a lower risk of death from CVD, malignancy and miscellaneous causes in most age groups, but not from infection. In fact, blacks had a higher risk of infection death than whites in ages 18-30 years (HR [95% CI] 1.94 [1.69-2.23]; P &lt; 0.001), 31-40 years (HR 1.51 [1.40-1.63]; P &lt; 0.001) and 41-50 years (HR 1.07 [1.02-1.12]; P = 0.009), which were partially attributed to their higher prevalence of AIDS nephropathy. For each race/ethnicity, more than two-thirds of infection deaths were due to non-dialysis related infections.DiscussionHispanics had the lowest risk for each major cause of death. Blacks were less likely to die than whites from most causes, except infection. The previously reported higher overall mortality rate for younger blacks is attributed to their two-fold higher infection mortality, which is mostly non-dialysis related, suggesting a new direction to improve their overall health status. Research is greatly needed to determine social and biological factors that account for the survival gap in dialysis among different racial/ethnic groups