417 research outputs found

    Dynamic response of a quantum wire structure

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    Dynamic response of a double barrier system : the effect of contacts

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    Author name used in this publication: W. K. ChowVersion of RecordPublishe

    Can you trust clinical practice guidelines for laparoscopic surgery? A systematic review of clinical practice guidelines for laparoscopic surgery

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    BACKGROUND: Clinical practice guidelines aim to support clinicians in providing clinical care and should be supported by evidence. There is currently no information on whether clinical practice guidelines in laparoscopic surgery are supported by evidence. METHODS: We performed a systematic review and identified clinical practice guidelines of laparoscopic surgery published in PubMed and Embase between March 2016 and February 2019. We performed an independent assessment of the strength of recommendation based on the evidence provided by the guideline authors. We used the 'Appraisal of Guidelines for Research & Evaluation II' (AGREE-II) Tool's 'rigour of development', 'clarity of presentation', and 'editorial independence' domains to assess the quality of the guidelines. We performed a mixed-effects generalised linear regression modelling. RESULTS: We retrieved 63 guidelines containing 1905 guideline statements. The median proportion of 'difference in rating' of strength of recommendation between the guideline authors and independent assessment was 33.3% (quartiles: 18.3%, 55.8%). The 'rigour of development' domain score (odds ratio 0.06; 95% confidence intervals 0.01-0.48 per unit increase in rigour score; P value = 0.0071) and whether the strength of recommendation was 'strong' by independent evaluation (odds ratio 0.09 (95% confidence intervals 0.06-0.13; P value < 0.001) were the only determinants of difference in rating between the guideline authors and independent evaluation. CONCLUSION: A considerable proportion of guideline statements in clinical practice guidelines in laparoscopic surgery are not supported by evidence. Guideline authors systematically overrated the strength of the recommendation (i.e., even when the evidence points to weak recommendation, guideline authors made strong recommendations)

    Are Preoperative Kattan and Stephenson Nomograms Predicting Biochemical Recurrence after Radical Prostatectomy Applicable in the Chinese Population?

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    Purpose. Kattan and Stephenson nomograms are based on the outcomes of patients with prostate cancer recruited in the USA, but their applicability to Chinese patients is yet to be validated. We aim at studying the predictive accuracy of these nomograms in the Chinese population. Patients and Methods. A total of 408 patients who underwent laparoscopic or open radical resection of prostate from 1995 to 2009 were recruited. The preoperative clinical parameters of these patients were collected, and they were followed up regularly with PSA monitored. Biochemical recurrence was defined as two or more consecutive PSA levels >0.4 ng/mL after radical resection of prostate or secondary cancer treatment. Results. The overall observed 5-year and 10-year biochemical recurrence-free survival rates were 68.3% and 59.8%, which was similar to the predicted values by the Kattan and Stephenson nomograms, respectively. The results of our study achieved a good concordance with both nomograms (Kattan: 5-years, 0.64; Stephenson: 5-years, 0.62, 10-years, 0.71). Conclusions. The incidence of prostate cancer in Hong Kong is increasing together with the patients’ awareness of this disease. Despite the fact that Kattan nomograms were derived from the western population, it has been validated in our study to be useful in Chinese patients as well

    On the Low Rank Solutions for Linear Matrix Inequalities

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    Distinct but overlapping roles of LRRTM1 and LRRTM2 in developing and mature hippocampal circuits

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    LRRTMs are postsynaptic cell adhesion proteins that have region-restricted expression in the brain. To determine their role in the molecular organization of synapses in vivo, we studied synapse development and plasticity in hippocampal neuronal circuits in mice lacking both Lrrtm1 and Lrrtm2. We found that LRRTM1 and LRRTM2 regulate the density and morphological integrity of excitatory synapses on CA1 pyramidal neurons in the developing brain but are not essential for these roles in the mature circuit. Further, they are required for long-term-potentiation in the CA3-CA1 pathway and the dentate gyrus, and for enduring fear memory in both the developing and mature brain. Our data show that LRRTM1 and LRRTM2 regulate synapse development and function in a cell-type and developmental-stage-specific manner, and thereby contribute to the fine-tuning of hippocampal circuit connectivity and plasticity

    Cag rnas induce dna damage and apoptosis by silencing nudt16 expression in polyglutamine degeneration

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    DNA damage plays a central role in the cellular pathogenesis of polyglutamine (polyQ) diseases, including Huntington's disease (HD). In this study, we showed that the expression of untranslatable expanded CAG RNA per se induced the cellular DNA damage response pathway. By means of RNA sequencing (RNA-seq), we found that expression of the Nudix hydrolase 16 (NUDT16) gene was down-regulated in mutant CAG RNA-expressing cells. The loss of NUDT16 function results in a misincorporation of damaging nucleotides into DNAs and leads to DNA damage. We showed that small CAG (sCAG) RNAs, species generated from expanded CAG transcripts, hybridize with CUG-containing NUDT16 mRNA and form a CAG-CUG RNA heteroduplex, resulting in gene silencing of NUDT16 and leading to the DNA damage and cellular apoptosis. These results were further validated using expanded CAG RNAexpressing mouse primary neurons and in vivo R6/2 HD transgenic mice. Moreover, we identified a bisamidinium compound, DB213, that interacts specifically with the major groove of the CAG RNA homoduplex and disfavors the CAG-CUG heteroduplex formation. This action subsequently mitigated RNA-induced silencing complex (RISC)-dependent NUDT16 silencing in both in vitro cell and in vivo mouse disease models. After DB213 treatment, DNA damage, apoptosis, and locomotor defects were rescued in HD mice. This work establishes NUDT16 deficiency by CAG repeat RNAs as a pathogenic mechanism of polyQ diseases and as a potential therapeutic direction for HD and other polyQ diseases

    Mayer and virial series at low temperature

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    We analyze the Mayer pressure-activity and virial pressure-density series for a classical system of particles in continuous configuration space at low temperature. Particles interact via a finite range potential with an attractive tail. We propose physical interpretations of the Mayer and virial series' radius of convergence, valid independently of the question of phase transition: the Mayer radius corresponds to a fast increase from very small to finite density, and the virial radius corresponds to a cross-over from monatomic to polyatomic gas. Our results have consequences for the search of a low density, low temperature solid-gas phase transition, consistent with the Lee-Yang theorem for lattice gases and with the continuum Widom-Rowlinson model.Comment: 36 pages, 1 figur

    Alcohol consumption and lifetime change in cognitive ability:a gene × environment interaction study

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    Studies of the effect of alcohol consumption on cognitive ability are often confounded. One approach to avoid confounding is the Mendelian randomization design. Here, we used such a design to test the hypothesis that a genetic score for alcohol processing capacity moderates the association between alcohol consumption and lifetime change in cognitive ability. Members of the Lothian Birth Cohort 1936 completed the same test of intelligence at age 11 and 70 years. They were assessed for recent alcohol consumption in later life and genotyped for a set of four single-nucleotide polymorphisms in three alcohol dehydrogenase genes. These variants were unrelated to late-life cognition or to socioeconomic status. We found a significant gene × alcohol consumption interaction on lifetime cognitive change (p = 0.007). Individuals with higher genetic ability to process alcohol showed relative improvements in cognitive ability with more consumption, whereas those with low processing capacity showed a negative relationship between cognitive change and alcohol consumption with more consumption. The effect of alcohol consumption on cognitive change may thus depend on genetic differences in the ability to metabolize alcohol
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