700 research outputs found
Toward a Human-Centered AI-assisted Colonoscopy System
AI-assisted colonoscopy has received lots of attention in the last decade.
Several randomised clinical trials in the previous two years showed exciting
results of the improving detection rate of polyps. However, current commercial
AI-assisted colonoscopy systems focus on providing visual assistance for
detecting polyps during colonoscopy. There is a lack of understanding of the
needs of gastroenterologists and the usability issues of these systems. This
paper aims to introduce the recent development and deployment of commercial
AI-assisted colonoscopy systems to the HCI community, identify gaps between the
expectation of the clinicians and the capabilities of the commercial systems,
and highlight some unique challenges in Australia.Comment: 9 page
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Exposure to Secondhand Smoke and Risk of Tuberculosis: Prospective Cohort Study
Background: Prospective evidence on the association between secondhand-smoke exposure and tuberculosis is limited. Methods: We included 23,827 never smokers from two rounds (2001 and 2005) of Taiwan National Health Interview Survey. Information on exposure to secondhand smoke at home as well as other sociodemographic and behavioral factors was collected through in-person interview. The participants were prospectively followed for incidence of tuberculosis through cross-matching the survey database to the national tuberculosis registry of Taiwan. Results: A total of 85 cases of active tuberculosis were identified after a median follow-up of 7.0 years. The prevalence of exposure to secondhand smoke at home was 41.8% in the study population. In the multivariable Cox proportional hazards analysis, secondhand smoke was not associated with active tuberculosis (adjusted hazard ratio [HR], 1.03; 95% CI, 0.64 to 1.64). In the subgroup analysis, the association between secondhand smoke and tuberculosis decreased with increasing age; the adjusted HR for those = 18 and = 40 and = 60 years old was 8.48 (0.77 to 93.56), 2.29 (0.75 to 7.01), 1.33 (0.58 to 3.01), and 0.66 (0.35 to 1.23) respectively. Results from extensive sensitivity analyses suggested that potential misclassification of secondhand-smoke exposure would not substantially affect the observed associations. Conclusions: The results from this prospective cohort study did not support an overall association between secondhand smoke and tuberculosis. However, the finding that adolescents might be particularly susceptible to secondhand smoke's effect warrants further investigation
Genetic ablation of ryanodine receptor 2 phosphorylation at Serâ2808 aggravates Ca 2+ âdependent cardiomyopathy by exacerbating diastolic Ca 2+ release
Phosphorylation of the cardiac ryanodine receptor (RyR2) by protein kinase A (PKA) at Serâ2808 is suggested to mediate the physiological âfight or flightâ response and contribute to heart failure by rendering the sarcoplasmic reticulum (SR) leaky for Ca 2+ . In the present study, we examined the potential role of RyR2 phosphorylation at Serâ2808 in the progression of Ca 2+ âdependent cardiomyopathy (CCM) by using mice genetically modified to feature elevated SR Ca 2+ leak while expressing RyR2s that cannot be phosphorylated at this site (S2808A). Surprisingly, rather than alleviating the disease phenotype, constitutive dephosphorylation of Serâ2808 aggravated CCM as manifested by shortened survival, deteriorated in vivo cardiac function, exacerbated SR Ca 2+ leak and mitochondrial injury. Notably, the deteriorations of cardiac function, myocyte Ca 2+ handling, and mitochondria integrity were consistently worse in mice with heterozygous ablation of Serâ2808 than in mice with complete ablation. Wildâtype (WT) and CCM myocytes expressing unmutated RyR2s exhibited a high level of baseline phosphorylation at Serâ2808. Exposure of these CCM cells to protein phosphatase 1 caused a transitory increase in Ca 2+ leak attributable to partial dephosphorylation of RyR2 tetramers at Serâ2808 from more fully phosphorylated state. Thus, exacerbated Ca 2+ leak through partially dephosphorylated RyR2s accounts for the prevalence of the disease phenotype in the heterozygous S2808A CCM mice. These results do not support the importance of RyR2 hyperphosphorylation in Ca 2+ âdependent heart disease, and rather suggest roles for the opposite process, the RyR2 dephosphorylation at this residue in physiological and pathophysiological Ca 2+ signalling.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106986/1/tjp6067.pd
Mutagenesis identifies the critical amino acid residues of human endonuclease G involved in catalysis, magnesium coordination, and substrate specificity
Gene Transfer of Engineered Calmodulin Alleviates Ventricular Arrhythmias in a Calsequestrin-Associated Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a familial arrhythmogenic syndrome characterized by sudden death. There are several genetic forms of CPVT associated with mutations in genes encoding the cardiac ryanodine receptor (RyR2) and its auxiliary proteins including calsequestrin (CASQ2) and calmodulin (CaM). It has been suggested that impairment of the ability of RyR2 to stay closed (ie, refractory) during diastole may be a common mechanism for these diseases. Here, we explore the possibility of engineering CaM variants that normalize abbreviated RyR2 refractoriness for subsequent viral-mediated delivery to alleviate arrhythmias in non-CaM-related CPVT
Genetic and Functional Analysis of the DLG4 Gene Encoding the Post-Synaptic Density Protein 95 in Schizophrenia
Hypofunction of N-methyl-D-aspartate (NMDA) receptor-mediated signal transduction has been implicated in the pathophysiology of schizophrenia. Post-synaptic density protein 95 (PSD95) plays a critical role in regulating the trafficking and activity of the NMDA receptor and altered expression of the PSD95 has been detected in the post-mortem brain of patients with schizophrenia. The study aimed to examine whether the DLG4 gene that encodes the PSD95 may confer genetic susceptibility to schizophrenia. We re-sequenced the core promoter, all the exons, and 3Ⲡuntranslated regions (UTR) of the DLG4 gene in 588 Taiwanese schizophrenic patients and conducted an association study with 539 non-psychotic subjects. We did not detect any rare mutations at the protein-coding sequences of the DLG4 gene associated with schizophrenia. Nevertheless, we identified four polymorphic markers at the core promoter and 5ⲠUTR and one single nucleotide polymorphism (SNP) at the 3â˛UTR of the DLG4 gene in this sample. Genetic analysis showed an association of a haplotype (CâD) derived from 2 polymorphic markers at the core promoter (odds ratioâ=â1.26, 95% confidence intervalâ=â1.06â1.51, pâ=â0.01), and a borderline association of the T allele of the rs13331 at 3â˛UTR with schizophrenia (odds ratioâ=â1.19, 95% confidence intervalâ=â0.99â1.43, pâ=â0.06). Further reporter gene assay showed that the C-D-C-C and the T allele of the rs13331 had significant lower activity than their counter parts. Our data indicate that the expression of the DLG4 gene is subject to regulation by the polymorphic markers at the core promoter region, 5Ⲡand 3â˛UTR of the gene, and is associated with the susceptibility of schizophrenia
The Different Clinical Features Between Autoimmune and Infectious Status Epilepticus
Objective: The prognosis of status epilepticus (SE) is highly related to the underlying etiology. Inflammation of the central nervous system (CNS), including infection and autoimmune encephalitis, is one of the treatable conditions causing SE. The initial presentation of infectious and autoimmune CNS disorders can be quite similar, which may be difficult to differentiate at the beginning. However, treatment for these entities can be quite different. In this study, we aim to identify the differences in clinical features among patients with infectious and autoimmune SE, which could help the clinicians to select initial investigation and ensuing therapies that may improve overall outcomes.Methods: This was a retrospective study that included 501 patients with SE within a period of 10.5-years. Patients with inflammatory etiology were collected and separated into infectious and autoimmune SE. The symptoms at onset, SE semiology, status epilepticus severity score, and END-IT score at admission, treatment for SE, and outcome (modified Rankin Scale) on discharge and last follow-up were recorded. Data on the first cerebrospinal fluid, electroencephalography, and magnetic resonance imaging were also collected.Results: Forty-six (9.2%) of the 501 patients had SE with inflammatory etiology. Twenty-five (5%) patients were autoimmune SE and 21 (4.2%) were infectious SE. Patients with autoimmune SE have younger age and female predominance. As for clinical presentations, psychosis, non-convulsive SE, and super refractory SE were more common in patients with autoimmune SE. Nevertheless, the prognosis showed no difference between the two groups.Conclusion: The different initial clinical presentations and patient characteristics may provide some clues about the underlying etiology of SE. When inflammatory etiology is suspected in patients with SE, younger age, female sex, psychosis, non-convulsive SE, and super refractory SE are clinical features that suggest an autoimmune etiology
Trypsin-induced proteome alteration during cell subculture in mammalian cells
<p>Abstract</p> <p>Background</p> <p>It is essential to subculture the cells once cultured cells reach confluence. For this, trypsin is frequently applied to dissociate adhesive cells from the substratum. However, due to the proteolytic activity of trypsin, cell surface proteins are often cleaved, which leads to dysregulation of the cell functions.</p> <p>Methods</p> <p>In this study, a triplicate 2D-DIGE strategy has been performed to monitor trypsin-induced proteome alterations. The differentially expressed spots were identified by MALDI-TOF MS and validated by immunoblotting.</p> <p>Results</p> <p>36 proteins are found to be differentially expressed in cells treated with trypsin, and proteins that are known to regulate cell metabolism, growth regulation, mitochondrial electron transportation and cell adhesion are down-regulated and proteins that regulate cell apoptosis are up-regulated after trypsin treatment. Further study shows that bcl-2 is down-regulated, p53 and p21 are both up-regulated after trypsinization.</p> <p>Conclusions</p> <p>In summary, this is the first report that uses the proteomic approach to thoroughly study trypsin-induced cell physiological changes and provides researchers in carrying out their experimental design.</p
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