Hepatitis B surface antigen in urine of hemodialysis patients

Hepatitis B surface antigen in urine of hemodialysis patients. As part of an extensive epidemiological survey of chronic hemodialysis patients in Michigan, hepatitis B surface antigen (HBsAg) was identified in the sera of 79 of 701 (11%) patients. Of these patients, 59 were carriers of HBsAg for three or more months. Urine samples were collected from 36 of 39 HBsAg carriers having urinary output. Of these samples, 19 (52%) were positive for HBsAg by radioimmunoassay; this was confirmed by specific antibody neutralization. The HBsAg was not identified in the urine of seven hemodialysis patients who were lacking serum HBsAg or in urine samples from three HBsAg sero-carriers who had normal renal function. Patients undergoing maintenance hemodialysis appear to constitute a large reservoir of HBsAg chronic carriers. This study indicates that a minimum of 50% of persistent HBsAg carriers who are producing urine have detectable. HBsAg in single, randomly timed, unconcentrated urine specimen. These data suggest that urine may represent a potential vehicle for transmission in nonparenterally acquired hepatitis B.Antigène de surface de l'hépatite B dans l'urine de malades en hémodialyse. Dans le cadre d'une large enquête épidémiologique à propos des malades en hémodialyse chronique dans le Michigan, l'antigène de surface de l'hépatite B (HBsAg) a été identifié dans le sérum de 79 parmi 701 malades (11%). Parmi ces malades, 59 étaient des porteurs de HBsAg depuis 3 mois ou plus. L'urine de 36 des 39 porteurs de HBsAg, qui avaient une diurèse, a été recueillie. Parmi ces 36 urines, 19 (52%) sont positives pour HBsAg par radio-immunologie, ce qui est confirmé par la neutralisation au moyen d'anticorps spécifique. Le HBsAg n'apas été identifié dans l'urine de 7 malades en hémodialyse qui n'avaient pas le HBsAg sérique et dans l'urine de 3 porteurs de HBsAg dont les fonctions rénales étaient normales. Les malades soumis à l'hémodialyse itérative paraissent constituer un grand réservoir de porteurs chroniques de HBsAg. Cette étude indique qu'au minimum 50% des porteurs chroniques de HBsAg qui ont une diurèse, ont un HBsAg détectable dans un échantillon unique d'urine, prélevé au hasard, non concentré. Ces résultats suggèrent que l'urine peut être un véhicule de transmission de l'hépatite B acquise par voie non parentérale

Thromboembolism After Intramedullary Nailing for Metastatic Bone Lesions.

BACKGROUND: The risk of venous thromboembolism (VTE) in patients undergoing intramedullary nailing for skeletal metastatic disease is currently undefined. The purpose of our study was to determine the risk of thromboembolic events, to define the risk factors for VTE, and to define the rate of wound complications in this population. METHODS: A retrospective review of surgical databases at three National Cancer Institute (NCI)-designated cancer centers identified 287 patients with a total of 336 impending or pathologic long-bone fractures that were stabilized with intramedullary nailing between February 2001 and April 2013. Statistical analysis was performed utilizing multivariable logistic regression and Fisher exact tests. RESULTS: The overall rate of VTE was twenty-four (7.1%) of the 336; thirteen (3.9%) were pulmonary embolism (PE), and eleven (3.3%), deep venous thrombosis (DVT). In two patients, adequate anticoagulation data were not available. We found no significant relationship between the type of anticoagulant used and VTE. There was a significant positive correlation found between lung-cancer histology and the development of VTE (p \u3c 0.001) or PE (p \u3c 0.001). The absence of radiation therapy approached significance (p = 0.06) with respect to decreased overall VTE risk. Wound complications were documented for 11 (3.3%) of the operations. CONCLUSIONS: There is a high rate of VTE among those with skeletal metastatic disease who undergo intramedullary nailing, even while receiving postoperative thromboembolic prophylaxis. Current anticoagulation protocols may be inadequate. Wound-complication risk with anticoagulant use in this population is low and should not be a deterrent to adequate anticoagulant use for this population

Enhanced surgical site infection surveillance following hysterectomy, vascular, and colorectal surgery

Objective.To evaluate the use of inpatient pharmacy and administrative data to detect surgical site infections (SSIs) following hysterectomy and colorectal and vascular surgery.Design.Retrospective cohort study.Setting.Five hospitals affiliated with academic medical centers.Patients.Adults who underwent abdominal or vaginal hysterectomy, colorectal surgery, or vascular surgery procedures between July 1, 2003, and June 30, 2005.Methods.We reviewed the medical records of weighted, random samples drawn from 3,079 abdominal and vaginal hysterectomy, 4,748 colorectal surgery, and 3,332 vascular surgery procedures. We compared routine surveillance with screening of inpatient pharmacy data and diagnosis codes and then performed medical record review to confirm SSI status.Results.Medical records from 823 hysterectomy, 736 colorectal surgery, and 680 vascular surgery procedures were reviewed. SSI rates determined by antimicrobial- and/or diagnosis code-based screening followed by medical record review (enhanced surveillance) were substantially higher than rates determined by routine surveillance (4.3% [95% confidence interval, 3.6%—5.1%] vs 2.7% for hysterectomies, 7.1% [95% confidence interval, 6.7%–8.2%] vs 2.0% for colorectal procedures, and 2.3% [95% confidence interval, 1.9%–2.9%] vs 1.4% for vascular procedures). Enhanced surveillance had substantially higher sensitivity than did routine surveillance to detect SSI (92% vs 59% for hysterectomies, 88% vs 22% for colorectal procedures, and 72% vs 43% for vascular procedures). A review of medical records confirmed SSI for 31% of hysterectomies, 20% of colorectal procedures, and 31% of vascular procedures that met the enhanced screening criteria.Conclusion.Antimicrobial- and diagnosis code-based screening may be a useful method for enhancing and streamlining SSI surveillance for a variety of surgical procedures, including those procedures targeted by the Centers for Medicare and Medicaid Services.</jats:sec

Apicomplexan Parasites Co-Opt Host Calpains to Facilitate Their Escape from Infected Cells

Apicomplexan parasites, including Plasmodium falciparum and Toxoplasma gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for considerable morbidity and mortality worldwide. These pathogenic protozoa replicate within an intracellular vacuole inside of infected host cells, from which they must escape to initiate a new lytic cycle. By integrating cell biological, pharmacological, and genetic approaches, we provide evidence that both Plasmodium and Toxoplasma hijack host cell calpain proteases to facilitate parasite egress. Immunodepletion or inhibition of calpain-1 in hypotonically lysed and resealed erythrocytes prevented the escape of P. falciparum parasites, which was restored by adding purified calpain-1. Similarly, efficient egress of T. gondii from mammalian fibroblasts was blocked by either small interfering RNA– mediated suppression or genetic deletion of calpain activity and could be restored by genetic complementation

Specific human leukocyte antigen DQ influence on expression of antiislet autoantibodies and progression to type 1 diabetes

Human leukocyte antigen (HLA) DQ haplotypes have the strongest genetic association with type 1 diabetes (T1DM) risk. OBJECTIVE: The objective of the study was to analyze whether HLA DQ alleles influence the development of antiislet autoantibodies, the progression to T1DM among autoantibody-positive relatives, or both. DESIGN: The Diabetes Prevention Trial-1 screened more than 90,000 nondiabetic relatives of patients for cytoplasmic islet-cell autoantibody (ICA) expression between 1994 and 2002. SETTING: The study was conducted in the general community. PARTICIPANTS: The Diabetes Prevention Trial-1 found 2817 ICA-positive relatives who were tested for biochemical autoantibodies (GAD65, ICA512, and insulin) and HLA-DQ haplotypes, and 2796 of them were followed up for progression to diabetes for up to 8 yr (median, 3.6 yr). MAIN OUTCOME MEASURE: Progression to T1DM was measured. RESULTS: High-risk DQ haplotypes and genotypes were associated with a higher percentage of relatives expressing multiple biochemical autoantibodies and higher T1DM risk (e.g., respectively, 59 and 36% at 5 yr for carriers of the DQA1*0301-DQB1*0302/DQA1*0501-DQB1*0201 genotype). The number of autoantibodies expressed significantly increased T1DM risk and across different DQ genotypes, autoantibody positivity directly correlated with diabetes risk. However, multivariate analyses indicated that the influence of most genotypes on T1DM risk was not independent from autoantibody expression, with the possible exception of DQA1*0102-DQB1*0602. Specific genotypic combinations conferred 5-yr diabetes risks significantly lower (e.g. 7%-DQA1*0201-DQB1*0201/DQA1*0501-DQB1*0201 and 14%-DQA1*0301-DQB1*0301/DQA1*0501-DQB1*0201) than when those haplotypes were found in other combinations. CONCLUSION: HLA DQ alleles determine autoantibody expression, which is correlated with diabetes progression. Among autoantibody-positive relatives, most HLA DQ genotypes did not further influence T1DM risk

The Peculiar Debris Disk of HD 111520 as Resolved by the Gemini Planet Imager

Using the Gemini Planet Imager (GPI), we have resolved the circumstellar debris disk around HD 111520 at a projected range of ~30-100 AU in both total and polarized $H$-band intensity. The disk is seen edge-on at a position angle of ~165$^{\circ}$ along the spine of emission. A slight inclination or asymmetric warping are covariant and alters the interpretation of the observed disk emission. We employ 3 point spread function (PSF) subtraction methods to reduce the stellar glare and instrumental artifacts to confirm that there is a roughly 2:1 brightness asymmetry between the NW and SE extension. This specific feature makes HD 111520 the most extreme examples of asymmetric debris disks observed in scattered light among similar highly inclined systems, such as HD 15115 and HD 106906. We further identify a tentative localized brightness enhancement and scale height enhancement associated with the disk at ~40 AU away from the star on the SE extension. We also find that the fractional polarization rises from 10 to 40% from 0.5" to 0.8" from the star. The combination of large brightness asymmetry and symmetric polarization fraction leads us to believe that an azimuthal dust density variation is causing the observed asymmetry.Comment: 9 pages, 8 Figures, 1 table, Accepted to Ap

HLA-DRB1*15:01-DQA1*01:02-DQB1*06:02 Haplotype Protects Autoantibody-Positive Relatives From Type 1 Diabetes Throughout the Stages of Disease Progression

The HLA-DRB1*15:01-DQA1*01:02-DQB1*06:02 haplotype is linked to protection from the development of type 1 diabetes (T1D). However, it is not known at which stages in the natural history of T1D development this haplotype affords protection. We examined a cohort of 3,358 autoantibody-positive relatives of T1D patients in the Pathway to Prevention (PTP) Study of the Type 1 Diabetes TrialNet. The PTP study examines risk factors for T1D and disease progression in relatives. HLA typing revealed that 155 relatives carried this protective haplotype. A comparison with 60 autoantibody-negative relatives suggested protection from autoantibody development. Moreover, the relatives with DRB1*15:01-DQA1*01:02-DQB1*06:02 less frequently expressed autoantibodies associated with higher T1D risk, were less likely to have multiple autoantibodies at baseline, and rarely converted from single to multiple autoantibody positivity on follow-up. These relatives also had lower frequencies of metabolic abnormalities at baseline and exhibited no overall metabolic worsening on follow-up. Ultimately, they had a very low 5-year cumulative incidence of T1D. In conclusion, the protective influence of DRB1*15:01-DQA1*01:02-DQB1*06:02 spans from autoantibody development through all stages of progression, and relatives with this allele only rarely develop T1D

Characterizing 51 Eri b from 1-5 μ\mum: a partly-cloudy exoplanet

We present spectro-photometry spanning 1-5 $\mu$m of 51 Eridani b, a 2-10 M$_\text{Jup}$ planet discovered by the Gemini Planet Imager Exoplanet Survey. In this study, we present new $K1$ (1.90-2.19 $\mu$m) and $K2$ (2.10-2.40 $\mu$m) spectra taken with the Gemini Planet Imager as well as an updated $L_P$ (3.76 $\mu$m) and new $M_S$ (4.67 $\mu$m) photometry from the NIRC2 Narrow camera. The new data were combined with $J$ (1.13-1.35 $\mu$m) and $H$ (1.50-1.80 $\mu$m) spectra from the discovery epoch with the goal of better characterizing the planet properties. 51 Eri b photometry is redder than field brown dwarfs as well as known young T-dwarfs with similar spectral type (between T4-T8) and we propose that 51 Eri b might be in the process of undergoing the transition from L-type to T-type. We used two complementary atmosphere model grids including either deep iron/silicate clouds or sulfide/salt clouds in the photosphere, spanning a range of cloud properties, including fully cloudy, cloud free and patchy/intermediate opacity clouds. Model fits suggest that 51 Eri b has an effective temperature ranging between 605-737 K, a solar metallicity, a surface gravity of $\log$(g) = 3.5-4.0 dex, and the atmosphere requires a patchy cloud atmosphere to model the SED. From the model atmospheres, we infer a luminosity for the planet of -5.83 to -5.93 ($\log L/L_{\odot}$), leaving 51 Eri b in the unique position as being one of the only directly imaged planet consistent with having formed via cold-start scenario. Comparisons of the planet SED against warm-start models indicates that the planet luminosity is best reproduced by a planet formed via core accretion with a core mass between 15 and 127 M$_{\oplus}$.Comment: 27 pages, 19 figures, Accepted for publication in The Astronomical Journa

Fall in C-peptide during first 2 years from diagnosis: Evidence of at least two distinct phases from composite type 1 diabetes trialnet data.

Interpretation of clinical trials to alter the decline in β-cell function after diagnosis of type 1 diabetes depends on a robust understanding of the natural history of disease. Combining data from the Type 1 Diabetes TrialNet studies, we describe the natural history of β-cell function from shortly after diagnosis through 2 years post study randomization, assess the degree of variability between patients, and investigate factors that may be related to C-peptide preservation or loss. We found that 93% of individuals have detectable C-peptide 2 years from diagnosis. In 11% of subjects, there was no significant fall from baseline by 2 years. There was a biphasic decline in C-peptide; the C-peptide slope was −0.0245 pmol/mL/month (95% CI −0.0271 to −0.0215) through the first 12 months and −0.0079 (−0.0113 to −0.0050) from 12 to 24 months (P \u3c 0.001). This pattern of fall in C-peptide over time has implications for understanding trial results in which effects of therapy are most pronounced early and raises the possibility that there are time-dependent differences in pathophysiology. The robust data on the C-peptide obtained under clinical trial conditions should be used in planning and interpretation of clinical trials