Comparison of quality-of-care measures in U.S. patients with end-stage renal disease secondary to lupus nephritis vs. other causes

BACKGROUND: Patients with end-stage renal disease (ESRD) due to lupus nephritis (LN-ESRD) may be followed by multiple providers (nephrologists and rheumatologists) and have greater opportunities to receive recommended ESRD-related care. We aimed to examine whether LN-ESRD patients have better quality of ESRD care compared to other ESRD patients. METHODS: Among incident patients (7/05–9/11) with ESRD due to LN (n = 6,594) vs. other causes (n = 617,758), identified using a national surveillance cohort (United States Renal Data System), we determined the association between attributed cause of ESRD and quality-of-care measures (pre-ESRD nephrology care, placement on the deceased donor kidney transplant waitlist, and placement of permanent vascular access). Multivariable logistic and Cox proportional hazards models were used to estimate adjusted odds ratios (ORs) and hazard ratios (HRs). RESULTS: LN-ESRD patients were more likely than other ESRD patients to receive pre-ESRD care (71% vs. 66%; OR = 1.68, 95% CI 1.57-1.78) and be placed on the transplant waitlist in the first year (206 vs. 86 per 1000 patient-years; HR = 1.42, 95% CI 1.34–1.52). However, only 24% had a permanent vascular access (fistula or graft) in place at dialysis start (vs. 36%; OR = 0.63, 95% CI 0.59–0.67). CONCLUSIONS: LN-ESRD patients are more likely to receive pre-ESRD care and have better access to transplant, but are less likely to have a permanent vascular access for dialysis, than other ESRD patients. Further studies are warranted to examine barriers to permanent vascular access placement, as well as morbidity and mortality associated with temporary access, in patients with LN-ESRD

The non-contact detection and identification of blood stained fingerprints using visible wavelength reflectance hyperspectral imaging: Part 1

© 2016 The Chartered Society of Forensic Sciences. Blood is one of the most commonly encountered types of biological evidence found at scenes of violent crime and one of the most commonly observed fingerprint contaminants. Current visualisation methods rely on presumptive tests or chemical enhancement methods. Although these can successfully visualise ridge detail, they are destructive, do not confirm the presence of blood and can have a negative impact on DNA sampling.A novel application of visible wavelength reflectance hyperspectral imaging (HSI) has been used for the detection and positive identification of blood stained fingerprints in a non-contact and non-destructive manner on white ceramic tiles. The identification of blood was based on the unique visible absorption spectrum of haemoglobin between 400 and 500 nm.HSI has been used to successfully visualise ridge detail in blood stained fingerprints to the ninth depletion. Ridge detail was still detectable with diluted blood to 20-fold dilutions. Latent blood stains were detectable to 15,000-fold dilutions. Ridge detail was detectable for fingerprints up to 6 months old. HSI was also able to conclusively distinguish blood stained fingerprints from fingerprints in six paints and eleven other red/brown media with zero false positives

A high ankle-brachial index is associated with increased cardiovascular disease morbidity and lower quality of life

ObjectivesThe purpose of this study is to determine if an ankle-brachial index (ABI) ≥1.40 is associated with reduced quality of life (QoL).BackgroundAnkle-brachial index values ≥1.40 have been associated with some cardiovascular disease (CVD) risk factors and increased mortality, but the relationship to other disease morbidity such as reduced QoL has not been previously evaluated.MethodsThe PARTNERS (PAD Awareness, Risk and Treatment: New Resources for Survival) program was a national cross-sectional study of 7,155 patients age >50 years recruited from 350 primary care sites. All sites performed the ABI using a Doppler device and a standardized technique.ResultsA total of 296 subjects had an ABI ≥1.40 in at least 1 leg, and 4,420 had an ABI between 0.90 and 1.40. Diabetes, male gender, and waist circumference were positively associated with a high ABI, and smoking and dyslipidemia were inversely associated with a high ABI. After adjustment for age, gender, and the traditional CVD risk factors, and accounting for multiple comparisons, the high ABI group had significantly higher odds for foot ulcers (p < 0.005) and borderline associations with heart failure, stroke, and neuropathy. After the same adjustments and adjusting for patients with other CVD, the high ABI group scored 2.0 points lower on the physical component scale on the Medical Outcomes Study Standard Form–36 and 5.5 points lower on the Walking Impairment Questionnaire walking distance domain (p < 0.05 for both).ConclusionIndividuals with a high ABI have higher odds for foot ulcers and neuropathy, as well as lower scores on some physical functioning QoL domains

IFNalpha activates dormant haematopoietic stem cells in vivo.

Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. After injury these cells are induced to proliferate to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNalpha), HSCs efficiently exit G(0) and enter an active cell cycle. HSCs respond to IFNalpha treatment by the increased phosphorylation of STAT1 and PKB/Akt (also known as AKT1), the expression of IFNalpha target genes, and the upregulation of stem cell antigen-1 (Sca-1, also known as LY6A). HSCs lacking the IFNalpha/beta receptor (IFNAR), STAT1 (ref. 3) or Sca-1 (ref. 4) are insensitive to IFNalpha stimulation, demonstrating that STAT1 and Sca-1 mediate IFNalpha-induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-fluoro-uracil, HSCs pre-treated (primed) with IFNalpha and thus induced to proliferate are efficiently eliminated by 5-fluoro-uracil exposure in vivo. Conversely, HSCs chronically activated by IFNalpha are functionally compromised and are rapidly out-competed by non-activatable Ifnar(-/-) cells in competitive repopulation assays. Whereas chronic activation of the IFNalpha pathway in HSCs impairs their function, acute IFNalpha treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNalpha on leukaemic cells, and raise the possibility for new applications of type I interferons to target cancer stem cells