Pelvic and perineal complications of Crohn's disease: assessment using magnetic resonance imaging

This study evaluated the role of magnetic resonance imaging (MRI) in the demonstration of the pelvic and perianal complications of Crohn's disease. Twenty five patients with active Crohn's disease were studied (12 male; mean age 41.1 years). MRI examinations were performed using a 1.5 Tesla system, within 14 days after clinical assessment. T1 and T2 weighted fast spin echo sequences in two or three orthogonal planes were performed, with fat suppression in some cases. The MRI results were correlated with surgical and clinical findings. In 16 patients, cutaneous, deep perineal or enterovesical fistulas or abscesses were diagnosed at MRI which showed close correlation with findings at examination under anaesthetic. In eight patients no fistulas or abscesses were seen at MRI nor was there any evidence of complications on clinical examination and flexible sigmoidoscopy. There was one false negative examination in a patient who had a colovesical fistula. In conclusion, MRI can accurately show the pelvic and perineal complications of Crohn's disease and may render examination under anaesthetic unnecessary.     

Biphasic synovial sarcomas arising in the pleural cavity. A clinicopathologic study of five cases

Trichoderma reesei endoglucanase I (EGI) was used as a reporter enzyme for screening mutagenized yeast strains for increased ability to produce protein. Sixteen haploid Saccharomyces cerevisiae strains, transformed with a yeast multicopy vector pALK222, containing the EGI cDNA under the ADH1 promoter, produced EGI activity of 10(-5)-10(-4) g/l. On the average 93% of the total activity was secreted into the culture medium. Two strains with opposite mating types were mutagenized, and several mutants were isolated possessing up to 45-fold higher EGI activity. The best mutants were remutagenized and a second-generation mutant, strain 2804, with an additional twofold increase in EGI activity was selected. The mutant strain 2804 grew more slowly and reached a lower final cell density than the parental strain. In the selective minimal medium, the 2804 strain produced 40 mg/l immunoreactive EGI protein, but only 2% was active enzyme. In the rich medium the secreted EGI enzyme stayed active, but without selection pressure the EGI production ceased after 2 days of cultivation, when the strain 2804 had produced 10 mg/l of EGI. A sevenfold difference was found between the parental and the 2804 strain in their total EGI production relative to cell density. The difference in favour of the mutant strain was also detected on the mRNA level. The 2804 mutant was found to be more active than the parental strain also in the production of T. reesei cellulases, cellobiohydrolase I, and cellobiohydrolase II.     

Types of dissociation and dissociative types: A taxometric analysis of dissociative experiences.

This article examined evidence for dimensional and typological models of dissociation. The authors reviewed previous research with the Dissociative Experiences Scale (DES; E. B. Bernstein-Carlson & F. W. Putnam; see record 1987-14407-001) and note that this scale, like other dissociation questionnaires, was developed to measure that so called dissociative continuum. Next, recently developed taxometric methods for distinguishing typological from dimensional constructs are described and applied to DES item-response data from 228 adults with diagnosed multiple personality disorder and 228 normal controls. The taxometric findings empirically justify the distinction between two types of dissociative experiences. Nonpathological dissociative experiences are manifestations of a dissociative trait, whereas pathological dissociative experiences are manifestations of a latent class variable. The taxometric findings also indicate that there are two types of dissociators. Individuals in the pathological dissociative class (taxon) can be identified with a brief, 8-item questionnaire called the DES-T. Scores on the DES-T and DES are compared in 11 clinical and nonclinical samples. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Pathology of mitral valve stenosis and pure mitral regurgitation--Part I

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis are reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenital malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation will be discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendinae.     

Numerical analysis of hydrogen risk mitigation measures for support of ITER licensing

In the ITER wet bypass scenario, water leakage, air ingress and hot dust (Be, W, and C) in the vacuum vessel could generate combustible hydrogen-air-steam mixture. Hydrogen combustion may threaten the integrity of the ITER VV and lead to radioactivity release. To prevent hydrogen energetic combustion, nitrogen injection system in VV and hydrogen recombination system in the pressure suppression tank (ST) were proposed. The main objectives of this analysis are to study the distribution of hydrogen-air-steam mixtures in the ITER sub-volumes, to investigate the feasibility of the nitrogen injection system to fully inert the atmosphere in the VV and to evaluate the capability and efficiency of the hydrogen recombination system to remove hydrogen in the ST. 3D computational fluid dynamics (CFD) code GASFLOW was used to calculate the evolution of the mixtures and to evaluate the hydrogen combustion risks in the ITER sub-volumes. The results indicate that the proposed hydrogen risk mitigation systems will generally prevent the risks of hydrogen detonation and fast deflagration. However, the atmosphere in ITER sub-volumes cannot be completely inerted at the early stage of the scenario. Slow deflagrations could still generate quasi-static pressures above 1 bar in the VV. The structural impact of the thermal and pressure loads generated by hydrogen combustions will be investigated in future studies.     

Novel transmit protection scheme for ultrasound systems

The problem of protecting or isolating extremely sensitive receive circuitry from high-voltage transmit circuitry is commonly addressed through the use of diode bridges, transformers, or high-voltage switches, which prove to be prohibitively expensive, bulky, and power consuming for use in portable, low-cost, battery-powered systems. These approaches also compound the interconnect difficulties associated with two-dimensional (2-D) transducer arrays. In this paper we present a novel transmit protection scheme that allows compact MOSFET shunting devices to be brought on-chip within each receive channel implemented in a standard CMOS integrated circuit process. During transmit, the high voltage transmit pulse is driven onto the common connection of the transducer array and the on-chip MOSFET devices shunt the current to ground. During receive, these devices are turned off, the common connection of the transducer array is shunted to ground, and the received echo can be detected as usual. The transmit protection scheme was experimentally shown to shunt a 16 mA peak current resulting from the equivalent of a 100-V, 25-ns-risetime transmit pulse through a 4 pF transducer element. The scheme was also incorporated into a prototype 1024-channel, low-cost, ultrasound system successfully used to form pulse echo images.     

Creating three-dimensional lattice patterns using programmable Dammann gratings

We demonstrate the creation of a three dimensional (3D) lattice of focus spots using a 3D Dammann grating structure. Such a 3D lattice of focus spots can be used for probing 3D structures or for creating 3D photonic crystal structures in optically sensitive media. Experimental results are included where the patterns are encoded onto a programmable liquid crystal display. We demonstrate the generation of five planar arrays each having 6×6 points surrounding another set of four planar arrays each having 5×5 points with a single pattern.     

The Adipose Tissue-Derived Secretome (ADS) in Obesity Uniquely Induces L-Type Amino Acid Transporter 1 (LAT1) and mTOR Signaling in Estrogen-Receptor-Positive Breast Cancer Cells

Obesity increases the risk of postmenopausal breast cancer (BC). This risk is mediated by obesity-induced changes in the adipose-derived secretome (ADS). The pathogenesis of BC in obesity is stimulated by mTOR hyperactivity. In obesity, leucine might support mTOR hyperactivity. Leucine uptake by BC cells is through L-Type Amino Acid Transporter 1 (LAT1). Our objective was to link obesity-ADS induction of LAT1 to the induction of mTOR signaling. Lean- and obese-ADS were obtained from lean and obese mice, respectively. Breast ADS was obtained from BC patients. Estrogen-receptor-positive BC cells were stimulated with ADS. LAT1 activity was determined by uptake of ³H-leucine. The LAT1/CD98 complex, and mTOR signaling were assayed by Western blot. The LAT1 antagonists, BCH and JPH203, were used to inhibit LAT1. Cell migration and invasion were measured by Transwell assays. The results showed obese-ADS-induced LAT1 activity by increasing transporter affinity for leucine. Consistent with this mechanism, LAT1 and CD98 expression were unchanged. Induction of mTOR by obese-ADS was inhibited by LAT1 antagonists. Breast ADS from patients with BMIs > 30 stimulated BC cell migration and invasiveness. Collectively, our findings show that obese-ADS induction of LAT1 supports mTOR hyperactivity in luminal BC cells.     

Urinary metabolic profiles of inflammatory bowel disease in interleukin-10 gene-deficient mice

Inflammatory bowel disease (IBD) is a chronic debilitating disorder that is thought to have both genetic and environmental contributors. Commensal microflora have been shown to play a key part in the disease process. Metabolomics, the study of large numbers of small molecule metabolites, has demonstrated that disease and/or changes in gut microbial composition modulate mammalian urine metabolite fingerprints. The aim of this project was to associate the development of IBD with specific changes in a mouse urinary metabolic fingerprint. Interleukin-10 (IL-10) gene-deficient mice were raised alongside age-matched 129/SvEv controls in conventional housing. Urine samples (22 h) were collected at ages 4, 6, 8, 12, 16, and 20 weeks. Metabolite concentrations were derived from analysis of nuclear magnetic resonance spectra, and both multivariate and two-way analysis of variance (ANOVA) statistical techniques were applied to the resulting data. Principal component analysis and partial least-squares-discriminant analysis of urine derived from the control and IL-10 gene-deficient mice revealed that while both groups initially had similar metabolic profiles, they diverged substantially with the onset of IBD as assessed through external phenotypic changes. Several metabolites, including trimethylamine (TMA) and fucose, changed dramatically in the IL-10 gene-deficient mice following 8 weeks of age, concomitant with the known timeline for development of severe histological injury. This study illustrates that metabolomics is effective at distinguishing IBD using urinary metabolite profiles.