Very little research has examined how career constructs are related to career plateaus. Given the dysfunctional consequences of plateauing, it is important to understand how career constructs, such as career adaptability, influence plateauing. Drawing on career construction theory and the theory of work adjustment, we propose that fit perceptions will mediate the career adaptability and plateauing relationship. Using data collected from 294 banking employees from the Punjab Province of Pakistan, we used the PROCESS macro to test for mediation. Results indicate that career adaptability reduces the likelihood of experiencing job content and hierarchical plateaus. Perceptions of fit related negatively to perceptions of plateauing, with one exception—demands–ability fit perceptions were unrelated to hierarchical plateaus. Mediation analysis indicated that needs–supply fit perceptions mediate the influence of career adaptability on both job content and hierarchical plateaus, whereas demands–ability fit perceptions mediate the influence of career adaptability on job content plateau but not hierarchical plateau. Implications of results for theory and practice are discussed.

Purpose In spite of the recent meta-analysis by Martin et al. (2016), we have very little insight about the theoretical mechanism explaining the leader–member exchange–counterproductive work behavior (LMX–CWB) relationship. Drawing on social cognitive theory, the purpose of this paper is to test if occupational self-efficacy functions as a mediating mechanism to explain the relationship between LMX quality and counterproductive performance directed toward the supervisor. In addition, based on the conservation of resources theory, the paper investigates if supervisor–subordinate relationship tenure acted as a second-stage moderator of this mediated relationship. Design/methodology/approach The authors used two-wave time-lagged data from a sample of 189 high-tech professionals to test the hypotheses, controlling for age, sex, and trust. Findings The results of this paper showed that occupational self-efficacy carried the effect of LMX quality on counterproductive performance, but only for workers who have longer supervisor–subordinate relationship tenure. Originality/value This paper is unique in proposing and testing a social cognitive mechanism to explain the relationship between LMX quality and counterproductive performance. As Johns (2017) advocated, the authors incorporated length of time, a contextual variable into this study by investigating supervisor–subordinate relationship tenure as moderating the proposed mediated relationship.

We used the polymerase chain reaction (PCR) to demonstrate cytomegalovirus (CMV) DNA in the CSF of a patient with the CMV radiculomyelopathy syndrome. To investigate the significance of this finding, we also performed PCR for CMV on CSF samples from 30 patients with human immunodeficiency virus (HIV) infection and neurologic disease, four patients with solid organ transplants including three with active CMV infection, and 10 patients with no clinical suspicion of HIV or CMV infection. There was CMV DNA only in patients with HIV, and it was present more often in patients with evidence of spinal cord dysfunction. Our results suggest that PCR may be useful in the rapid diagnosis of CMV infection of the CNS in patients with HIV and that the radiculomyelopathy syndrome may represent only part of a spectrum of CMV-induced spinal cord dysfunction in these patients.

The human immunodeficiency virus type 1 (HIV-1) capsid (CA) protein forms a conical lattice around the viral ribonucleoprotein complex (vRNP) consisting of a dimeric viral genome and associated proteins, together constituting the viral core. Upon entry into target cells, the viral core undergoes a process termed uncoating, during which CA molecules are shed from the lattice. Although the timing and degree of uncoating are important for reverse transcription and integration, the molecular basis of this phenomenon remains unclear. Using complementary approaches, we assessed the impact of core destabilization on the intrinsic stability of the CA lattice in vitro and fates of viral core components in infected cells. We found that substitutions in CA can impact the intrinsic stability of the CA lattice in vitro in the absence of vRNPs, which mirrored findings from assessment of CA stability in virions. Altering CA stability tended to increase the propensity to form morphologically aberrant particles, in which the vRNPs were mislocalized between the CA lattice and the viral lipid envelope. Importantly, destabilization of the CA lattice led to premature dissociation of CA from vRNPs in target cells, which was accompanied by proteasomal-independent losses of the viral genome and integrase enzyme. Overall, our studies show that the CA lattice protects the vRNP from untimely degradation in target cells and provide the mechanistic basis of how CA stability influences reverse transcription. IMPORTANCE The human immunodeficiency virus type 1 (HIV-1) capsid (CA) protein forms a conical lattice around the viral RNA genome and the associated viral enzymes and proteins, together constituting the viral core. Upon infection of a new cell, viral cores are released into the cytoplasm where they undergo a process termed “uncoating”, i.e. shedding of CA molecules from the conical lattice. Although proper and timely uncoating has been shown to be important for reverse transcription, the molecular mechanisms that link these two events remain poorly understood. In this study, we show that destabilization of the CA lattice leads to premature dissociation of CA from viral cores, which exposes the viral genome and the integrase enzyme for degradation in target cells. Thus, our studies demonstrate that the CA lattice protects the viral ribonucleoprotein complexes from untimely degradation in target cells and provide the first causal link between how CA stability affects reverse transcription.

Two PIEZO mechanosensitive cation channels, PIEZO1 and PIEZO2, have been identified in mammals, where they are involved in numerous sensory processes. While structurally similar, PIEZO channels are expressed in distinct tissues and exhibit unique properties. How different PIEZOs transduce force, how their transduction mechanism varies, and how their unique properties match the functional needs of the tissues they are expressed in remain all-important unanswered questions. The nematode Caenorhabditis elegans has a single PIEZO ortholog (pezo-1) predicted to have twelve isoforms. These isoforms share many transmembrane domains but differ in those that distinguish PIEZO1 and PIEZO2 in mammals. We used transcriptional and translational reporters to show that putative promoter sequences immediately upstream of the start codon of long pezo-1 isoforms predominantly drive GFP expression in mesodermally derived tissues (such as muscle and glands). In contrast, sequences upstream of shorter pezo-1 isoforms resulted in GFP expression primarily in neurons. Putative promoters upstream of different isoforms drove GFP expression in different cells of the same organs of the digestive system. The observed unique pattern of complementary expression suggests that different isoforms could possess distinct functions within these organs. We used mutant analysis to show that pharyngeal muscles and glands require long pezo-1 isoforms to respond appropriately to the presence of food. The number of pezo-1 isoforms in C. elegans, their putative differential pattern of expression, and roles in experimentally tractable processes make this an attractive system to investigate the molecular basis for functional differences between members of the PIEZO family of mechanoreceptors.