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V.Androgens in asthmatic men may be linked to asthma severity, acting via nongenomic and genomic effects. This ailment affects boys more than girls during infancy, and this proportion reverses in puberty. Plasmatic androgen concentration in young men increases at this age and might be related to lower asthma symptoms. Nongenomic actions occur in a brief period and are independent of the androgen receptor (AR), while genomic effects depend on AR, take hours-days and are modified by transcription or protein synthesis inhibitors. Guinea pig tracheas chronic incubation with testosterone (TES, 40 nM, 48 h) potentiates salbutamol-induced relaxation, an effect that was reversed by flutamide, not observed when tissues were pre-incubated with TES-bovine serum albumin (TES-BSA) nor when tissues were preincubated with TES for 15-60 min. In tracheal myocytes, TES chronic incubation increases salbutamol-induced K+ currents (IK+), an effect that was also reversed by flutamide, actinomycin D and cycloheximide and not seen with TES-BSA. The increment in IK+ was blocked by 4-aminopyridine and iberiotoxin, indicating that delayed rectifier K+ and high-conductance Ca2+ activated K+ channels were involved in the TES potentiation effect. Immunofluorescence studies showed that chronic TES augmented the β2 adrenergic receptor (β2-AR) expression in ASM and this finding was corroborated by q-PCR and Western blot assays. β2-AR affinity for salbutamol after TES incubation was increased. In conclusion, chronic exposure to physiological TES concentration of the guinea pig ASM promotes β2-AR upregulation favoring β2 adrenergic responses and probably limiting the severity of the asthmatic exacerbations in teenage boys and men. INTRODUCTION Ablating the slow pathway (SP) is the superior treatment for atrioventricular nodal reentrant tachycardia (AVNRT) with a low complication rate. However, the ablation of the SP could result in either complete elimination or modification of the SP. We aimed to investigate whether the duration of AH jump pre-ablation associated with the outcome of elimination of SP. METHODS We included 56 patients with typical AVNRT (slow-fast), 20 males and 36 females, aged 44.2 ± 15.1 years. Slow pathway ablation was performed using classical approach. Univariate and multivariate analysis was performed for potential predictors of SP elimination. RESULTS Typical AVNRT was inducible in all patients. Post-ablation, non-inducibility of AVNRT was obtained in all 56 (100%) patients, with SP elimination in 33 (61%) patients and SP modification in 23 (39%) patients. learn more Patients with SP elimination had significantly longer AH jump than patients with SP modification. Cox regression analysis showed that AH jump duration was the independent predictor of SP elimination, in which every 20 ms increase in AH jump duration was associated with 1.30 higher rate of SP elimination. Furthermore, ROC curve analysis indicated that the AH jump duration of ≥100 ms had 6.14 times higher probability for complete elimination of the SP with a sensitivity of 79%, specificity of 70%, PPV of 79% and NPV of 70%. CONCLUSIONS AH jump duration pre-ablation is associated with complete elimination of slow pathway during AVNRT ablation. BACKGROUND Prior research suggests that the proportion of a shockable initial rhythm (SIR) in out-of-hospital cardiac arrest (OHCA) declined during the last decades. This study aims to investigate if this decline is still ongoing and explore the relationship between location of OHCA and proportion of a SIR as initial rhythm. METHODS We calculated the proportion of patients with a SIR between 2006-2015 using pooled data from the COSTA-group (Copenhagen, Oslo, Stockholm, Amsterdam). Analyses were stratified according to location of OHCA (residential vs. public). RESULTS A total of 19,054 OHCA cases were included. Overall, the total proportion of cases with a SIR decreased from 42% to 37% (P  less then  0.01) from 2006 to 2015. When stratified according to location, the proportion of cases with a SIR decreased for OHCAs at a residential location (34% to 27%; P = 0.03), while the proportion of a SIR was stable among OHCAs in public locations (59% to 57%; P = 0.2). During the last years of the study period (2011-2015), the overall proportion of a SIR remained stable (38% to 37%; P = 0.45); this was observed for both residential and public OHCA. CONCLUSION We found a decline in the proportion of patients with a SIR in OHCAs at a residential location; this decline levelled off during the second half of the study period (2011-2015). In public locations, we observed no decline in SIR over time. V.Previous studies have shown an association between coiled-coil domain-containing (CCDC) genes and different cancers. Our previous studies revealed that CCDC43 is highly expressed in colorectal cancer, but the expression and molecular mechanisms of CCDC43 in gastric cancer (GC) are yet to be determined. Here, we show that CCDC43 is overexpressed in gastric tissues. CCDC43 expression is closely related to tumor differentiation, lymph-node-metastasis, and prognosis of gastric cancer. Overexpression of CCDC43 promotes the proliferation, invasion, and metastasis of GC cells. CCDC43 may upregulate and stabilize ADRM1, resulting in the construction of the ubiquitin-mediated proteasome. In contrast, inhibition of ADRM1 could reverse the function of CCDC43 in GC both in vitro and in vivo. Our data demonstrate that transcription factor YY1 directly binds to CCDC43 and ADRM1 gene promoters, leading to over-expression of CCDC43 and ADRM1. Furthermore, in vitro experiments demonstrate that knock down of CCDC43 or ADRM1 attenuates the YY1-mediated malignant phenotypes. Finally, the association among YY1, CCDC43 and ADRM1 is validated in clinical samples. Our findings suggest that the CCDC43-ADRM1 axis regulated by YY1, promotes proliferation and metastasis of GC, and the axis may be a potential therapeutic target for GC. V.Lymphatic vessels, as a means to metastasize, are frequently recruited by tumor tissues during their progression. However, reliable in vitro models to dissect the intricate crosstalk between lymphatic vessels and tumors are still in urgent demand. Here, we describe a tissue-engineering method based on sacrificial bioprinting, to develop an enabling model of the human breast tumor with encapsulated multiscale lymphatic vessels, which is compatible with existing microscopy to examine the processes of lymphatic vessel sprouting and breast tumor cell migration in a physiologically relevant volumetric microenvironment. This platform will potentially help shed light on the complex biology of the tumor microenvironment, tumor lymphangiogenesis, lymphatic metastasis, as well as tumor anti-lymphangiogenic therapy in the future. We further anticipate wide adoption of the method to the production of various tissues and their models with incorporation of lymphatics vessels towards relevant applications.