Pathomechanisms of ulnar ligament lesions of the wrist in a cadaveric distal radius fracture model

Background and purpose: Mechanisms of injury to ulnar sided ligaments, stabilizing the distal radioulnar joint and the ulna to the carpus, associated with dorsally displaced distal radius fractures are poorly described. We investigated the injury patterns in a human cadaver fracture model. Methods: Fresh frozen human cadaver arms were used. A dorsal open wedge osteotomy was made in the distal radius. In 8 specimens pressure was applied to the palm with the wrist in dorsiflexion and ulnar sided stabilizing structures subsequently severed. Dorsal angulation was measured on digitized radiographs. In 8 more specimens the triangular fibrocartilage complex was forced into rupture by axially loading the forearm with the wrist in dorsiflexion. The ulnar side was dissected and injuries were recorded. Results: Intact ulnar soft tissues limited the dorsal angulation of the distal radius fragment to a median of 32o (16-34o). A combination of bending and shearing of the distal radius fragment was needed to create TFCC injuries. Both palmar and dorsal injuries were observed simultaneously in 6/8 specimens. Interpretation: A TFCC injury can be expected when dorsal angulation of a distal radius fracture exceeds 32o. The extensor carpi ulnaris subsheath may be a functionally integral part of the TFCC. Both dorsal and palmar structures can tear simultaneously. These findings may have implications for reconstruction of ulnar sided soft tissue injuries

Using surveillance data to monitor entry into care of newly diagnosed HIV-infected persons: San Francisco, 2006–2007

<p>Abstract</p> <p>Background</p> <p>Linkage to care after HIV diagnosis is associated with both clinical and public health benefits. However, ensuring and monitoring linkage to care by public health departments has proved to be a difficult task. Here, we report the usefulness of routine monitoring of CD4 T cell counts and plasma HIV viral load as measures of entry into care after HIV diagnosis.</p> <p>Methods</p> <p>Since July 1, 2006, the San Francisco Department of Public Health (SFDPH) incorporated monitoring initial primary care visit into standard HIV public health investigation for newly diagnosed HIV-infected patients in select clinics. Entry into care was defined as having at least one visit to a primary HIV care provider after the initial diagnosis of HIV infection. Investigators collected reports from patients, medical providers, laboratories and reviewed medical records to determine the date of the initial health care visit after HIV diagnosis. We identified factors associated with increased likelihood of entering care after HIV diagnosis.</p> <p>Results</p> <p>One -hundred and sixty new HIV-infected cases were diagnosed between July 1, 2006 and June 30, 2007. Routine surveillance methods found that 101 of those cases entered HIV medical care and monitoring of CD4 T cell counts and plasma HIV viral load confirmed entry to care of 25 more cases, representing a 25% increase over routine data collection methods. We found that being interviewed by a public health investigator was associated with higher odds of entry into care after HIV diagnosis (OR 18.86 [1.83–194.80], p = .001) compared to cases not interviewed. Also, HIV diagnosis at the San Francisco county hospital versus diagnosis at the county municipal STD clinic was associated with higher odds of entry into care (OR 101.71 [5.29–1952.05], p < .001).</p> <p>Conclusion</p> <p>The time from HIV diagnosis to initial CD4 T cell count, CD4 T cell value and HIV viral load testing may be appropriate surveillance measures for evaluating entry into care, as well as performance outcomes for local public health departments' HIV testing programs. Case investigation performed by the public health department or case management by clinic staff was associated with increased and shorter time to entry into HIV medical care.</p

Surface and Temporal Biosignatures

Recent discoveries of potentially habitable exoplanets have ignited the prospect of spectroscopic investigations of exoplanet surfaces and atmospheres for signs of life. This chapter provides an overview of potential surface and temporal exoplanet biosignatures, reviewing Earth analogues and proposed applications based on observations and models. The vegetation red-edge (VRE) remains the most well-studied surface biosignature. Extensions of the VRE, spectral "edges" produced in part by photosynthetic or nonphotosynthetic pigments, may likewise present potential evidence of life. Polarization signatures have the capacity to discriminate between biotic and abiotic "edge" features in the face of false positives from band-gap generating material. Temporal biosignatures -- modulations in measurable quantities such as gas abundances (e.g., CO2), surface features, or emission of light (e.g., fluorescence, bioluminescence) that can be directly linked to the actions of a biosphere -- are in general less well studied than surface or gaseous biosignatures. However, remote observations of Earth's biosphere nonetheless provide proofs of concept for these techniques and are reviewed here. Surface and temporal biosignatures provide complementary information to gaseous biosignatures, and while likely more challenging to observe, would contribute information inaccessible from study of the time-averaged atmospheric composition alone.Comment: 26 pages, 9 figures, review to appear in Handbook of Exoplanets. Fixed figure conversion error

Absorption Enhancement in Peridinin–Chlorophyll–Protein Light-Harvesting Complexes Coupled to Semicontinuous Silver Film

We report on experimental and theoretical studies of plasmon-induced effects in a hybrid nanostructure composed of light-harvesting complexes and metallic nanoparticles in the form of semicontinuous silver film. The results of continuous-wave and time-resolved spectroscopy indicate that absorption of the light-harvesting complexes is strongly enhanced upon coupling with the metallic film spaced by 25 nm of a dielectric silica layer. This conclusion is corroborated by modeling, which confirms the morphology of the silver island film

Within-trial economic evaluation of diabetes-specific cognitive behaviour therapy in patients with type 2 diabetes and subthreshold depression

<p>Abstract</p> <p>Background</p> <p>Despite the high prevalence of subthreshold depression in patients with type 2 diabetes, evidence on cost-effectiveness of different therapy options for these patients is currently lacking.</p> <p>Methods/Design</p> <p>Within-trial economic evaluation of the diabetes-specific cognitive behaviour therapy for subthreshold depression. Patients with diabetes and subthreshold depression are randomly assigned to either 2 weeks of diabetes-specific cognitive behaviour group therapy (n = 104) or to standard diabetes education programme only (n = 104). Patients are followed for 12 months. During this period data on total health sector costs, patient costs and societal productivity costs are collected in addition to clinical data. Health related quality of life (the SF-36 and the EQ-5D) is measured at baseline, immediately after the intervention, at 6 and at 12 months after the intervention. Quality adjusted life years (QALYs), and cumulative costs will be estimated for each arm of the trial. Cost-effectiveness of the diabetes-specific cognitive behaviour group therapy will be analysed from the perspective of the German statutory health insurance and from the societal perspective. To this end, incremental cost-effectiveness ratio (ICER) in terms of cost per QALY gained will be calculated.</p> <p>Discussion</p> <p>Some methodological issues of the described economic evaluation are discussed.</p> <p>Trial registration</p> <p>The trial has been registered at the Clinical Trials Register (NCT01009138).</p

Genome-wide association analysis of self-reported daytime sleepiness identifies 42 loci that suggest biological subtypes

This is the final version. Available from the publisher via the DOI in this record.UK Biobank Sleep Traits GWAS summary statistics are available at the Sleep Disorder Knowledge Portal (SDKP) website (http://www.sleepdisordergenetics.org). All other data are contained within the article and its supplementary information or available upon request.Excessive daytime sleepiness (EDS) affects 10–20% of the population and is associated with substantial functional deficits. Here, we identify 42 loci for self-reported daytime sleepiness in GWAS of 452,071 individuals from the UK Biobank, with enrichment for genes expressed in brain tissues and in neuronal transmission pathways. We confirm the aggregate effect of a genetic risk score of 42 SNPs on daytime sleepiness in independent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and sleep traits (duration, chronotype, accelerometer-derived sleep efficiency and daytime naps or inactivity). However, individual daytime sleepiness signals vary in their associations with objective short vs long sleep, and with markers of sleep continuity. The 42 sleepiness variants primarily cluster into two predominant composite biological subtypes - sleep propensity and sleep fragmentation. Shared genetic links are also seen with obesity, coronary heart disease, psychiatric diseases, cognitive traits and reproductive ageing.Medical Research Council (MRC

Mammalian Neurogenesis Requires Treacle-Plk1 for Precise Control of Spindle Orientation, Mitotic Progression, and Maintenance of Neural Progenitor Cells

The cerebral cortex is a specialized region of the brain that processes cognitive, motor, somatosensory, auditory, and visual functions. Its characteristic architecture and size is dependent upon the number of neurons generated during embryogenesis and has been postulated to be governed by symmetric versus asymmetric cell divisions, which mediate the balance between progenitor cell maintenance and neuron differentiation, respectively. The mechanistic importance of spindle orientation remains controversial, hence there is considerable interest in understanding how neural progenitor cell mitosis is controlled during neurogenesis. We discovered that Treacle, which is encoded by the Tcof1 gene, is a novel centrosome- and kinetochore-associated protein that is critical for spindle fidelity and mitotic progression. Tcof1/Treacle loss-of-function disrupts spindle orientation and cell cycle progression, which perturbs the maintenance, proliferation, and localization of neural progenitors during cortical neurogenesis. Consistent with this, Tcof1+/− mice exhibit reduced brain size as a consequence of defects in neural progenitor maintenance. We determined that Treacle elicits its effect via a direct interaction with Polo-like kinase1 (Plk1), and furthermore we discovered novel in vivo roles for Plk1 in governing mitotic progression and spindle orientation in the developing mammalian cortex. Increased asymmetric cell division, however, did not promote increased neuronal differentiation. Collectively our research has therefore identified Treacle and Plk1 as novel in vivo regulators of spindle fidelity, mitotic progression, and proliferation in the maintenance and localization of neural progenitor cells. Together, Treacle and Plk1 are critically required for proper cortical neurogenesis, which has important implications in the regulation of mammalian brain size and the pathogenesis of congenital neurodevelopmental disorders such as microcephaly

Effect of extended morning fasting upon ad libitum lunch intake and associated metabolic and hormonal responses in obese adults

Background/Objectives: Breakfast omission is positively associated with obesity and increased risk of disease. However, little is known about the acute effects of extended morning fasting upon subsequent energy intake and associated metabolic/regulatory factors in obese adults. Subjects/Methods: In a randomised cross-over design, 24 obese men (n=8) and women (n=16) extended their overnight fast by omitting breakfast consumption or ingesting a typical carbohydrate-rich breakfast of 2183±393 kJ (521±94 kcal), before an ad libitum pasta lunch 3 h later. Blood samples were obtained throughout the day until 3 h post lunch and analysed for hormones implicated in appetite regulation, along with metabolic outcomes and subjective appetite measures. Results: Lunch intake was unaffected by extended morning fasting (difference=218 kJ, 95% confidence interval −54 kJ, 490 kJ; P=0.1) resulting in lower total intake in the fasting trial (difference=−1964 kJ, 95% confidence interval −1645 kJ, −2281 kJ; P<0.01). Systemic concentrations of peptide tyrosine–tyrosine and leptin were lower during the afternoon following morning fasting (Pless than or equal to0.06). Plasma-acylated ghrelin concentrations were also lower following the ad libitum lunch in the fasting trial (P<0.05) but this effect was not apparent for total ghrelin (Pgreater than or equal to0.1). Serum insulin concentrations were greater throughout the afternoon in the fasting trial (P=0.05), with plasma glucose also greater 1 h after lunch (P<0.01). Extended morning fasting did not result in greater appetite ratings after lunch, with some tendency for lower appetite 3 h post lunch (P=0.09). Conclusions: We demonstrate for the first time that, in obese adults, extended morning fasting does not cause compensatory intake during an ad libitum lunch nor does it increase appetite during the afternoon. Morning fasting reduced satiety hormone responses to a subsequent lunch meal but counterintuitively also reduced concentrations of the appetite-stimulating hormone-acylated ghrelin during the afternoon relative to lunch consumed after breakfast