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New particle formation in the upper free troposphere is a major global source of cloud condensation nuclei (CCN)1,2,3,4. However, the precursor vapours that drive the process are not well understood. With experiments performed under upper tropospheric conditions in the CERN CLOUD chamber, we show that nitric acid, sulfuric acid and ammonia form particles synergistically, at rates that are orders of magnitude faster than those from any two of the three components. The importance of this mechanism depends on the availability of ammonia, which was previously thought to be efficiently scavenged by cloud droplets during convection. However, surprisingly high concentrations of ammonia and ammonium nitrate have recently been observed in the upper troposphere over the Asian monsoon region5,6. Once particles have formed, co-condensation of ammonia and abundant nitric acid alone is sufficient to drive rapid growth to CCN sizes with only trace sulfate. Moreover, our measurements show that these CCN are also highly efficient ice nucleating particles—comparable to desert dust. Our model simulations confirm that ammonia is efficiently convected aloft during the Asian monsoon, driving rapid, multi-acid HNO3–H2SO4–NH3 nucleation in the upper troposphere and producing ice nucleating particles that spread across the mid-latitude Northern Hemisphere.
Despite the increasing interest in leaders’ health-promoting behavior, the employees’ role in the effectiveness of such behavior and the mechanisms underlying how such leadership behavior affects their well-being have largely been ignored. Drawing on implicit leadership theories, we advance the health-oriented leadership literature by examining employees’ ideals, that is, their expectations regarding such leader behavior, as a moderating factor. We propose that higher expectations increase the association between actual health-oriented leader behavior and employee-rated leader-member relationships (LMX) and health-oriented behaviors by employees, which, in turn, positively relate to their well-being (here: exhaustion and work engagement). We tested our theoretical model in three studies, using a cross-sectional design (Study 1, N = 307), a two-wave time-lagged design (Study 2, N = 144) and an experimental design (Study 3, N = 173). We found that the effect of actual health-oriented leader behavior on LMX is contingent on employees’ ideal health-oriented leader behavior. Yet, for employees’ self-care behavior, the proposed moderation was only significant in Study 1. High expectations strengthened the relationship between actual health-oriented leader behavior with LMX and self-care behavior, which, in turn, were associated with less exhaustion and more work engagement (only LMX), supporting most of our mediation hypotheses. Our results highlight the pivotal role of employees’ expectations regarding leaders’ health support and help in building practical interventions with regard to leaders’ health promotion.
Congenital lower urinary-tract obstruction (LUTO) is caused by anatomical blockage of the bladder outflow tract or by functional impairment of urinary voiding. About three out of 10,000 pregnancies are affected. Although several monogenic causes of functional obstruction have been defined, it is unknown whether congenital LUTO caused by anatomical blockage has a monogenic cause. Exome sequencing in a family with four affected individuals with anatomical blockage of the urethra identified a rare nonsense variant (c.2557C>T [p.Arg853∗]) in BNC2, encoding basonuclin 2, tracking with LUTO over three generations. Re-sequencing BNC2 in 697 individuals with LUTO revealed three further independent missense variants in three unrelated families. In human and mouse embryogenesis, basonuclin 2 was detected in lower urinary-tract rudiments. In zebrafish embryos, bnc2 was expressed in the pronephric duct and cloaca, analogs of the mammalian lower urinary tract. Experimental knockdown of Bnc2 in zebrafish caused pronephric-outlet obstruction and cloacal dilatation, phenocopying human congenital LUTO. Collectively, these results support the conclusion that variants in BNC2 are strongly implicated in LUTO etiology as a result of anatomical blockage.