Suture-method versus Through-the-needle Catheters for Continuous Popliteal-sciatic Nerve Blocks: A Randomized Clinical Trial.

BACKGROUND:The basic perineural catheter design has changed minimally since inception, with the catheter introduced through or over a straight needle. The U.S. Food and Drug Administration recently cleared a novel perineural catheter design comprising a catheter attached to the back of a suture-shaped needle that is inserted, advanced along the arc of its curvature pulling the catheter past the target nerve, and then exited through the skin in a second location. The authors hypothesized that analgesia would be noninferior using the new versus traditional catheter design in the first two days after painful foot/ankle surgery with a primary outcome of average pain measured with the Numeric Rating Scale. METHODS:Subjects undergoing painful foot or ankle surgery with a continuous supraparaneural popliteal-sciatic nerve block 5 cm proximal to the bifurcation were randomized to either a suture-type or through-the-needle catheter and subsequent 3-day 0.2% ropivacaine infusion (basal 6 ml/h, bolus 4 ml, lockout 30 min). Subjects received daily follow-up for the first four days after surgery, including assessment for evidence of malfunction or dislodgement of the catheters. RESULTS:During the first two postoperative days the mean ± SD average pain scores were lower in subjects with the suture-catheter (n = 35) compared with the through-the-needle (n = 35) group (2.7 ± 2.4 vs. 3.4 ± 2.4) and found to be statistically noninferior (95% CI, -1.9 to 0.6; P < 0.001). No suture-style catheter was completely dislodged (0%), whereas the tips of three (9%) traditional catheters were found outside of the skin before purposeful removal on postoperative day 3 (P = 0.239). CONCLUSIONS:Suture-type perineural catheters provided noninferior analgesia compared with traditional catheters for continuous popliteal-sciatic blocks after painful foot and ankle surgery. The new catheter design appears to be a viable alternative to traditional designs used for the past seven decades

The Lantern Vol. 20, No. 1, Fall 1951

• The Interim • The Salami Festival • The Little Soldier • On the Practical and Esthetic Aspects of the Nose • A Study in White • Dorm 5-6: Notes • Dishwashing • Hoorah for Pooh-Bah! • To a Young Student • A Heavy Bomber Takes Off • When Dad Burns the Leaves • Fourteen Lines That Aren\u27t a Sonnet • Roderick, We All Pine For You! • A Young Girlhttps://digitalcommons.ursinus.edu/lantern/1055/thumbnail.jp

Copy Number Variants in Extended Autism Spectrum Disorder Families Reveal Candidates Potentially Involved in Autism Risk

Copy number variations (CNVs) are a major cause of genetic disruption in the human genome with far more nucleotides being altered by duplications and deletions than by single nucleotide polymorphisms (SNPs). In the multifaceted etiology of autism spectrum disorders (ASDs), CNVs appear to contribute significantly to our understanding of the pathogenesis of this complex disease. A unique resource of 42 extended ASD families was genotyped for over 1 million SNPs to detect CNVs that may contribute to ASD susceptibility. Each family has at least one avuncular or cousin pair with ASD. Families were then evaluated for co-segregation of CNVs in ASD patients. We identified a total of five deletions and seven duplications in eleven families that co-segregated with ASD. Two of the CNVs overlap with regions on 7p21.3 and 15q24.1 that have been previously reported in ASD individuals and two additional CNVs on 3p26.3 and 12q24.32 occur near regions associated with schizophrenia. These findings provide further evidence for the involvement of ICA1 and NXPH1 on 7p21.3 in ASD susceptibility and highlight novel ASD candidates, including CHL1, FGFBP3 and POUF41. These studies highlight the power of using extended families for gene discovery in traits with a complex etiology

Role of Inflammation in the Pathogenesis of Arterial Stiffness

Increased arterial stiffness is an independent predictor of cardiovascular disease independent from blood pressure. Recent studies have shed new light on the importance of inflammation on the pathogenesis of arterial stiffness. Arterial stiffness is associated with the increased activity of angiotensin II, which results in increased NADPH oxidase activity, reduced NO bioavailability and increased production of reactive oxygen species. Angiotensin II signaling activates matrix metalloproteinases (MMPs) which degrade TGFβ precursors to produce active TGFβ, which then results in increased arterial fibrosis. Angiotensin II signaling also activates cytokines, including monocyte chemoattractant protein-1, TNF-α, interleukin-1, interleukin-17 and interleukin-6. There is also ample clinical evidence that demonstrates the association of inflammation with increased arterial stiffness. Recent studies have shown that reductions in inflammation can reduce arterial stiffness. In patients with rheumatoid arthritis, increased aortic pulse wave velocity in patients was significantly reduced by anti tumor necrosis factor-α therapy. Among the major classes of anti hypertensive drugs, drugs that block the activation of the RAS system may be more effective in reducing the progression of arterial stiffness. Thus, there is rationale for targeting specific inflammatory pathways involved in arterial stiffness in the development of future drugs. Understanding the role of inflammation in the pathogenesis of arterial stiffness is important to understanding the complex puzzle that is the pathophysiology of arterial stiffening and may be important for future development of novel treatments

International Veterinary Epilepsy Task Force recommendations for a veterinary epilepsy-specific MRI protocol

Epilepsy is one of the most common chronic neurological diseases in veterinary practice. Magnetic resonance imaging (MRI) is regarded as an important diagnostic test to reach the diagnosis of idiopathic epilepsy. However, given that the diagnosis requires the exclusion of other differentials for seizures, the parameters for MRI examination should allow the detection of subtle lesions which may not be obvious with existing techniques. In addition, there are several differentials for idiopathic epilepsy in humans, for example some focal cortical dysplasias, which may only apparent with special sequences, imaging planes and/or particular techniques used in performing the MRI scan. As a result, there is a need to standardize MRI examination in veterinary patients with techniques that reliably diagnose subtle lesions, identify post-seizure changes, and which will allow for future identification of underlying causes of seizures not yet apparent in the veterinary literature. There is a need for a standardized veterinary epilepsy-specific MRI protocol which will facilitate more detailed examination of areas susceptible to generating and perpetuating seizures, is cost efficient, simple to perform and can be adapted for both low and high field scanners. Standardisation of imaging will improve clinical communication and uniformity of case definition between research studies. A 6–7 sequence epilepsy-specific MRI protocol for veterinary patients is proposed and further advanced MR and functional imaging is reviewed

Estimating the Accuracy of Anal Cytology in the Presence of an Imperfect Reference Standard

Background: The study aim is to estimate sensitivity and specificity of anal cytology for histologic HSIL in analyses adjusted for the imperfect biopsy reference standard. Methods and Principal Findings: Retrospective cohort study of an anal dysplasia screening program for HIV infected adults. We estimated the prevalence of histologic HSIL by concurrent cytology category and the associated cytology ROC area. Cytology operating characteristics for HSIL were estimated and adjusted for the imperfect reference standard by 3 methodologies. The study cohort included 261 patients with 3 available measures: (1) referral cytology; (2) HRA cytology; and (3) HRA directed biopsy. The prevalence of biopsy HSIL varied according to the concurrent HRA cytology result: 64.5

Controlled Experiments of Hillslope Coevolution at the Biosphere 2 Landscape Evolution Observatory: Toward Prediction of Coupled Hydrological, Biogeochemical, and Ecological Change

Understanding the process interactions and feedbacks among water, porous geological media, microbes, and vascular plants is crucial for improving predictions of the response of Earth’s critical zone to future climatic conditions. However, the integrated coevolution of landscapes under change is notoriously difficult to investigate. Laboratory studies are limited in spatial and temporal scale, while field studies lack observational density and control. To bridge the gap between controlled laboratory and uncontrollable field studies, the University of Arizona built a macrocosm experiment of unprecedented scale: the Landscape Evolution Observatory (LEO). LEO comprises three replicated, heavily instrumented, hillslope-scale model landscapes within the environmentally controlled Biosphere 2 facility. The model landscapes were designed to initially be simple and purely abiotic, enabling scientists to observe each step in the landscapes’ evolution as they undergo physical, chemical, and biological changes over many years. This chapter describes the model systems and associated research facilities and illustrates how LEO allows for tracking of multiscale matter and energy fluxes at a level of detail impossible in field experiments. Initial sensor, sampler, and soil coring data are already providing insights into the tight linkages between water flow, weathering, and microbial community development. These interacting processes are anticipated to drive the model systems to increasingly complex states and will be impacted by the introduction of vascular plants and changes in climatic regimes over the years to come. By intensively monitoring the evolutionary trajectory, integrating data with mathematical models, and fostering community-wide collaborations, we envision that emergent landscape structures and functions can be linked, and significant progress can be made toward predicting the coupled hydro-biogeochemical and ecological responses to global change

Clinical outcomes of ED patients with bandemia

BackgroundAlthough an elevated white blood cell count is a widely utilized measure for evidence of infection and an important criterion for evaluation of systemic inflammatory response syndrome, its component band count occupies a more contested position within clinical emergency medicine. Recent studies indicate that bandemia is highly predictive of a serious infection, suggesting that clinicians who do not appreciate the value of band counts may delay diagnosis or overlook severe infections.ObjectivesWhereas previous studies focused on determining the quantitative value of the band count (ie, determining sensitivity, threshold for bandemia, etc.), this study directs attention to patient-centered outcomes, hypothesizing that the degree of bandemia predisposes patients to subsequent negative clinical outcomes associated with underappreciated severe infections.MethodsThis retrospective study of electronic medical records includes patients who initially presented to the emergency department (ED) with bandemia and were subsequently discharged from the ED. These patients were screened for repeat ED visits within 7 days and death within 30 days.ResultsIn patients with severe bandemia who were discharged from the ED, there was a 20.9% revisit rate at 7 days and a 4.9% mortality rate at 30 days, placing severely bandemic patients at 5 times significantly greater mortality compared to nonbandemic patients (P = .032).ConclusionOur review of patient outcomes suggests that the degree of bandemia, especially in the setting of concurrent tachycardia or fever, is associated with greater likelihood of negative clinical outcomes

Genomic and Proteomic Analysis of the Impact of Mitotic Quiescence on the Engraftment of Human CD34+ Cells

It is well established that in adults, long-term repopulating hematopoietic stem cells (HSC) are mitotically quiescent cells that reside in specialized bone marrow (BM) niches that maintain the dormancy of HSC. Our laboratory demonstrated that the engraftment potential of human HSC (CD34+ cells) from BM and mobilized peripheral blood (MPB) is restricted to cells in the G0 phase of cell cycle but that in the case of umbilical cord blood (UCB) -derived CD34+ cells, cell cycle status is not a determining factor in the ability of these cells to engraft and sustain hematopoiesis. We used this distinct in vivo behavior of CD34+ cells from these tissues to identify genes associated with the engraftment potential of human HSC. CD34+ cells from BM, MPB, and UCB were fractionated into G0 and G1 phases of cell cycle and subjected in parallel to microarray and proteomic analyses. A total of 484 target genes were identified to be associated with engraftment potential of HSC. System biology modeling indicated that the top four signaling pathways associated with these genes are Integrin signaling, p53 signaling, cytotoxic T lymphocyte-mediated apoptosis, and Myc mediated apoptosis signaling. Our data suggest that a continuum of functions of hematopoietic cells directly associated with cell cycle progression may play a major role in governing the engraftment potential of stem cells. While proteomic analysis identified a total of 646 proteins in analyzed samples, a very limited overlap between genomic and proteomic data was observed. These data provide a new insight into the genetic control of engraftment of human HSC from distinct tissues and suggest that mitotic quiescence may not be the requisite characteristic of engrafting stem cells, but instead may be the physiologic status conducive to the expression of genetic elements favoring engraftment