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Bondesen Hermansen posted an update 6 months, 1 week ago
23 (95% CI = 1.06, 1.40), 26 or older 1.27 (95% CI = 1.06, 1.52), Ptrend = .010). The use of oral contraceptives appeared to be protective with an OR of 0.69 (95% CI = 0.57, 0.83). Stronger for adenocarcinoma than squamous cell carcinoma, these relationships were not clearly modified by smoking status, probably because of lower prevalence of smoking. This is a first and largest pooling study of lung cancer among Asian women and the results suggested potential roles of hormone-related pathways in the etiology of this disease.
We investigated the branching pattern and topographic anatomy of the nerves to the teres minor (Tm) and the long head of the triceps brachii (LHT) in relation to reference lines extending between surface landmarks, to identify the innervation patterns of, and the optimal needle placement points within, the Tm and the LHT.
The anatomical courses of the nerves to the Tm and the LHT were investigated in 37 upper limbs of fresh-frozen cadavers. Distances from the acromion to nerve penetration points, and crossing points of reference lines with the Tm and LHT were measured in 27 cadaveric upper limbs.
The Tm was innervated by the axillary nerve in all specimens in three patterns, and the LHT was innervated exclusively by the radial nerve. Our dissection and measurements indicate that the midpoint of the reference line from the acromion to the inferior angle of the scapula is the optimal needle insertion point for the Tm. The target point for the LHT appears to be the one-third point of the reference line from the acromion to the medial epicondyle, or the two-thirds point of the reference line from the acromion to the axillary fold.
We investigated the branching pattern of the nerves to the Tm and the LHT and propose optimal needle placement points for electromyography of the Tm and LHT.
We investigated the branching pattern of the nerves to the Tm and the LHT and propose optimal needle placement points for electromyography of the Tm and LHT.In non-small cell lung cancer (NSCLC), activating mutations in the epidermal growth factor receptor (EGFR) induce sensitivity to EGFR tyrosine kinase inhibitors. Despite impressive clinical responses, patients ultimately relapse as a reservoir of drug-tolerant cells persist, which ultimately leads to acquired resistance mechanisms. We performed an unbiased high-throughput siRNA screen to identify proteins that abrogate the response of EGFR-mutant NSCLC to EGFR-targeted therapy. The deubiquitinase USP13 was a top hit resulting from this screen. Targeting USP13 increases the sensitivity to EGFR inhibition with small molecules in vitro and in vivo. Nutlin-3 mw USP13 selectively stabilizes mutant EGFR in a peptidase-independent manner by counteracting the action of members of the Cbl family of E3 ubiquitin ligases. We conclude that USP13 is a strong mutant EGFR-specific cotarget that could improve the treatment efficacy of EGFR-targeted therapies.
Many injured workers are reinjured, but reinjury risk is challenging to quantify. Because many injured workers face delayed return-to-work, or return to part-time or intermittent jobs, a calendar timescale may overestimate actual work-time at risk, yielding underestimated reinjury rates. Objectives included determining (1) reinjury risk by degree of permanent impairment and other factors, and (2) how choice of timescale affects reinjury estimates.
This retrospective cohort study included Washington State workers’ compensation (WC) claims for 43,114 injured workers, linked to state wage files (2003-2018). Three timescales were used to define at-risk denominators (1) calendar quarters; (2) quarters with any wages; and (3) full-time equivalent (FTE) quarters, defined as cumulative work hours ÷ 520. Associations between reinjury outcomes and worker, injury, job, and WC vocational rehabilitation program participation characteristics were assessed using Cox proportional hazards regression.
Overall reinjury ratimates.The aetiology of childhood leukaemia is poorly understood. Knowledge about differences in risk by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register-based case-control study to evaluate socioeconomic differences in the risk of childhood leukaemia in Denmark and to access whether associations varied by different measures of SES, time point of assessment, leukaemia type and age at diagnosis. We identified all cases of leukaemia in children aged 0 to 19 years, born and diagnosed between 1980 and 2013 from the Danish Cancer Registry (N = 1336) and sampled four individually matched controls per case (N = 5330). We used conditional logistic regression models for analysis. Medium and high level of parental education was associated with a higher risk of acute myeloid leukaemia (AML) in the offspring, mainly driven by children diagnosed at ages 0 to 4 years . We also observed a modestly increased risk for lymphoid leukaemia (LL) in association with higher level of parental education, but only in children diagnosed at ages 5 to 19 years. Higher parental income was associated with an increased risk of LL but not AML among children aged 5 to 19 years at diagnosis (OR for high maternal income = 2.78; 95% CI 1.32-5.89). Results for neighbourhood SES measures indicated null associations. Bias or under-ascertainment of cases among families with low income or basic education are unlikely to explain the observed socioeconomic differences. Future research addressing explicitly the underlying mechanisms of our results may help to enhance etiologic insights of the disease.Maintenance of the mature blood cells requires controlled cell fate decisions by hematopoietic stem and progenitor cells (HSPCs). While our knowledge of the gene expression changes that facilitate differentiation has made a leap forward, less is known about the cellular triggers that induce them. Biedzinski et al (2020) now uncover a new intracellular mechanism that drives myeloid differentiation Microtubule bundles squeeze the nucleus of HSPCs and form large invaginations, thus causing changes in chromatin organization. These microtubule-induced nuclear shape changes result in gene expression profiles that favor myeloid differentiation.
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