Bladder injury during infected tola hip arthroplasty prosthesis removal: Report of a case and review of the literature

The bladder is the most frequently injured organ during pelvic surgery. However, during hip surgery, this complication is extremely rare. We report a case of bladder injury during total hip arthroplasty prosthesis removal surgery. A 65-year-old male was admitted to our hospital with left hip pain and wound infection. On plain radiograms, acetabular protrusion was identified. We decided to remove protruzed acetabular cup and place spacer. During the operation, unexpectedly bladder injury occurred. The rupture was sutured intraoperatively. We left a catheter in the bladder after internal urethrotomy to drain the urine.Keywords: Arthroplasty, Bladder injury, Cystogram, Hip prosthesis removal, Infectio

Transit timing variation analysis of the low-mass brown dwarf KELT-1 b

We investigate whether there is a variation in the orbital period of the short-period brown dwarf-mass KELT-1 b, which is one of the best candidates to observe orbital decay. We obtain 19 high-precision transit light curves of the target using six different telescopes. We add all precise and complete transit light curves from open databases and the literature, as well as the available Transiting Exoplanet Survey Satellite (TESS) observations from sectors 17 and 57, to form a transit timing variation (TTV) diagram spanning more than 10 yr of observations. The analysis of the TTV diagram, however, is inconclusive in terms of a secular or periodic variation, hinting that the system might have synchronized. We update the transit ephemeris and determine an informative lower limit for the reduced tidal quality parameter of its host star of Q ′⋆>(8.5±3.9)×106 assuming that the stellar rotation is not yet synchronized. Using our new photometric observations, published light curves, the TESS data, archival radial velocities, and broadband magnitudes, we also update the measured parameters of the system. Our results are in good agreement with those found in previous analyses

Interruption of torus doubling bifurcation and genesis of strange nonchaotic attractors in a quasiperiodically forced map : Mechanisms and their characterizations

A simple quasiperiodically forced one-dimensional cubic map is shown to exhibit very many types of routes to chaos via strange nonchaotic attractors (SNAs) with reference to a two-parameter $(A-f)$ space. The routes include transitions to chaos via SNAs from both one frequency torus and period doubled torus. In the former case, we identify the fractalization and type I intermittency routes. In the latter case, we point out that atleast four distinct routes through which the truncation of torus doubling bifurcation and the birth of SNAs take place in this model. In particular, the formation of SNAs through Heagy-Hammel, fractalization and type--III intermittent mechanisms are described. In addition, it has been found that in this system there are some regions in the parameter space where a novel dynamics involving a sudden expansion of the attractor which tames the growth of period-doubling bifurcation takes place, giving birth to SNA. The SNAs created through different mechanisms are characterized by the behaviour of the Lyapunov exponents and their variance, by the estimation of phase sensitivity exponent as well as through the distribution of finite-time Lyapunov exponents.Comment: 27 pages, RevTeX 4, 16 EPS figures. Phys. Rev. E (2001) to appea

Mitochondrial carrier homolog 1 (Mtch1) antibodies in neuro-Behçet's disease

Cataloged from PDF version of article.Efforts for the identification of diagnostic autoantibodies for neuro-Behcet's disease (NBD) have failed. Screening of NBD patients' sera with protein macroarray identified mitochondrial carrier homolog 1 (Mtch1), an apoptosis-related protein, as a potential autoantigen. ELISA studies showed serum Mtch1 antibodies in 68 of 144 BD patients with or without neurological involvement and in 4 of 168 controls corresponding to a sensitivity of 47.2% and specificity of 97.6%. Mtch1 antibody positive NBD patients had more attacks, increased disability and lower serum nucleosome levels. Mtch1 antibody might be involved in pathogenic mechanisms of NBD rather than being a coincidental byproduct of autoinflammation. © 2013 Elsevier B.V

Gastrointestinal dysfunction in patients and mice expressing the autism-associated R451C mutation in neuroligin-3

Gastrointestinal (GI) problems constitute an important comorbidity in many patients with autism. Multiple mutations in the neuroligin family of synaptic adhesion molecules are implicated in autism, however whether they are expressed and impact GI function via changes in the enteric nervous system is unknown. We report the GI symptoms of two brothers with autism and an R451C mutation in Nlgn3 encoding the synaptic adhesion protein, neuroligin-3. We confirm the presence of an array of synaptic genes in the murine GI tract and investigate the impact of impaired synaptic protein expression in mice carrying the human neuroligin-3 R451C missense mutation (NL3R451C ). Assessing in vivo gut dysfunction, we report faster small intestinal transit in NL3R451C compared to wild-type mice. Using an ex vivo colonic motility assay, we show increased sensitivity to GABAA receptor modulation in NL3R451C mice, a well-established Central Nervous System (CNS) feature associated with this mutation. We further show increased numbers of small intestine myenteric neurons in NL3R451C mice. Although we observed altered sensitivity to GABAA receptor modulators in the colon, there was no change in colonic neuronal numbers including the number of GABA-immunoreactive myenteric neurons. We further identified altered fecal microbial communities in NL3R451C mice. These results suggest that the R451C mutation affects small intestinal and colonic function and alter neuronal numbers in the small intestine as well as impact fecal microbes. Our findings identify a novel GI phenotype associated with the R451C mutation and highlight NL3R451C mice as a useful preclinical model of GI dysfunction in autism. LAY SUMMARY: People with autism commonly experience gastrointestinal problems, however the cause is unknown. We report gut symptoms in patients with the autism-associated R451C mutation encoding the neuroligin-3 protein. We show that many of the genes implicated in autism are expressed in mouse gut. The neuroligin-3 R451C mutation alters the enteric nervous system, causes gastrointestinal dysfunction, and disrupts gut microbe populations in mice. Gut dysfunction in autism could be due to mutations that affect neuronal communication.This work was supported by an Idea Development Award from the United States Department of Defense’s Congressionally Directed Medical Research Programs (CDMRP) Autism Research Program (AR110134) to E.L.H.-Y. and J.C.B.; the Victorian Government through the Operational Infrastructure Scheme, National Health and Medical Research Council (NHMRC) project grants (APP566642 to J.C.B. and APP1047674 to E.L.H.-Y.) and the Royal Melbourne Hospital Neuroscience Foundation. E.L.H.-Y. also received an ARC Future Fellowship (FT160100126) and an RMIT Vice Chancellor’s Senior Research Fellowship which supported G.K.B. and S.H. T.S., P.U., and N.Y. were funded by grants RO1AI100914, P30-DK56338, and U01-AI24290 awards to Baylor College of Medicine funded from the National Institute of Allergy and Infectious Diseases and National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health (T.C.S.)

Novel VLDLR microdeletion identified in two Turkish siblings with pachygyria and pontocerebellar atrophy

Congenital ataxia with cerebellar hypoplasia is a heterogeneous group of disorders that presents with motor disability, hypotonia, incoordination, and impaired motor development. Among these, disequilibrium syndrome describes a constellation of findings including nonprogressive cerebellar ataxia, mental retardation, and cerebellar hypoplasia following an autosomal recessive pattern of inheritance and can be caused by mutations in the Very Low Density Lipoprotein Receptor (VLDLR). Interestingly, while the majority of patients with VLDLassociated cerebellar hypoplasia in the literature use bipedal gait, the previously reported patients of Turkish decent have demonstrated similar neurological sequelae, but rely on quadrupedal gait. We present a consanguinous Turkish family with two siblings with cerebellar atrophy, predominantly frontal pachygyria and ataxic bipedal gait, who were found to have a novel homozygous deletion in the VLDLR gene identified by using high-density single nucleotide polymorphism microarrays for homozygosity mapping and identification of CNVs within these regions. Discovery of disease causing homozygous deletions in the present Turkish family capable of maintaining bipedal movement exemplifies the phenotypic heterogeneity of VLDLRassociated cerebellar hypoplasia and ataxia. © Springer-Verlag 2010

Transition strengths in the neutron-rich 73,74,75Ni^73,74,75Ni isotopes

status: publishe