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Flourishing, a construct encompassing optimal human functioning, is an indicator of well-being. The purpose of this study was to examine the direct and indirect effects of employees’ achievement goal orientation (mastery-approach, mastery-avoidance, performance-approach and performance-avoidance goal orientation) on flourishing, through the appraisal of quantitative (concerns about continued existence of the job) and qualitative (concerns about continued existence of important job features) job insecurity. Data were collected from 275 employees in an organization on the brink of a substantive downsizing. The results of structural equation modelling showed that mastery approach and—avoidance goal orientation positively predicted flourishing. Furthermore, flourishing was negatively predicted by qualitative job insecurity but not by quantitative job insecurity. Qualitative job insecurity mediated the effects of mastery- and performance-approach goal orientation on flourishing but the effects were not significant. Hence, in an environment with a substantial threat of job loss, a mastery goal orientation contributed directly to flourishing. Our results plead for more attention for the effects of achievement goal orientation and qualitative job insecurity on flourishing under uncertainty.

The aim of this study was to propose a tentative model of employment counseling based on 31 critical incident interviews with supervisors, employment counselors, and unemployed job seekers. The incidents (N= 599) mentioned in the interviews were inductively used to develop a category framework describing behaviors of employment counselors. On the basis of the interviews, categories, and incidents within these categories, the authors proposed a 4‐phase preliminary model of the employment counseling process. Findings suggest that employment counseling is a complex and dynamic process involving several distinct and consecutive steps focused on clients, governmental funding agencies, colleagues, and employers.

Allogeneic hematopoietic stem cell transplantation (HSCT) is a curative treatment for various hematological, immunological and metabolic diseases, replacing the patient’s hematopoietic system with donor-derived healthy hematopoietic stem cells. HSCT can be complicated by early and late events related to impaired immunological recovery such as prolonged hypogammaglobulinemia post-HSCT. We present a 16-year-old female patient with sickle-cell disease who underwent HSCT with stem cells from a human leukocyte antigen (HLA) class-II mismatched family donor. While cellular recovery was good post-HSCT, the patient developed mixed chimerism and suffered from cervical lymphadenopathy, recurrent airway infections and cutaneous SLE. She presented with hypogammaglobulinemia and was started on immunoglobulin substitution therapy and antibiotic prophylaxis. B-cell phenotyping showed that she had increased transitional and naïve mature B cells, reduced memory B cells, and diminished marginal zone/natural effector cells. In-depth immunophenotyping and B-cell receptor repertoire sequencing ruled out an intrinsic B-cell defect by expression of activation-induced cytidine deaminase (AID), presence of somatic hypermutations and differentiation into IgG- and IgA-producing plasma cells in vitro. Immunohistochemistry and flow cytometry of lymph node tissue showed a clear block in terminal B-cell differentiation. Chimerism analysis of sorted lymph node populations showed that exclusively patient-derived B cells populated germinal centers, while only a minor fraction of follicular helper T cells was patient-derived. Given this discrepancy, we deduced that the HLA class-II disparity between patient and donor likely hinders terminal B-cell differentiation in the lymph node. This case highlights that studying disturbed cognate T-B interactions in the secondary lymphoid organs can provide unique insights when deciphering prolonged hypogammaglobulinemia post-HSCT.

Spectral imaging has many applications, from methane detection using satellites to disease detection on crops. However, spectral cameras remain a costly solution ranging from 10 thousand to 100 thousand euros for the hardware alone. Here, we present a low-cost multispectral camera (LC-MSC) with 64 LEDs in eight different colors and a monochrome camera with a hardware cost of 340 euros. Our prototype reproduces spectra accurately when compared to a reference spectrometer to within the spectral width of the LEDs used and the ±1σ variation over the surface of ceramic reference tiles. The mean absolute difference in reflectance is an overestimate of 0.03 for the LC-MSC as compared to a spectrometer, due to the spectral shape of the tiles. In environmental light levels of 0.5 W m−2 (bright artificial indoor lighting) our approach shows an increase in noise, but still faithfully reproduces discrete reflectance spectra over 400 nm–1000 nm. Our approach is limited in its application by LED bandwidth and availability of specific LED wavelengths. However, unlike with conventional spectral cameras, the pixel pitch of the camera itself is not limited, providing higher image resolution than typical high-end multi- and hyperspectral cameras. For sample conditions where LED illumination bands provide suitable spectral information, our LC-MSC is an interesting low-cost alternative approach to spectral imaging.

Pediatric patients with unexplained bone marrow failure (BMF) are often categorized as aplastic anemia (AA). Based on the accepted hypothesis of an auto-immune mechanism underlying AA, immune suppressive therapy (IST) might be effective. However, due to the lack of diagnostic tools to identify immune AA and prognostic markers to predict IST response together with the unequaled curative potential of hematopoietic stem cell transplantation (HSCT), most pediatric severe AA patients are momentarily treated by HSCT if available. Although several studies indicate oligoclonal T-cells with cytotoxic activities towards the hematopoietic stem cells, increasing evidence points towards defective inhibitory mechanisms failing to inhibit auto-reactive T-cells. We aimed to investigate the role of NK- and B-cells in seven pediatric AA patients through a comprehensive analysis of paired bone marrow and peripheral blood samples with spectral flow cytometry in comparison to healthy age-matched bone marrow donors. We observed a reduced absolute number of NK-cells in peripheral blood of AA patients with a skewed distribution towards CD56 NK-cells in a subgroup of patients. The enriched CD56 NK-cells had a lower expression of CD45RA and TIGIT and a higher expression of CD16, compared to healthy donors. Functional analysis revealed no differences in degranulation. However, IFN-γ production and perforin expression of NK-cells were reduced in the CD56 -enriched patient group. The diminished NK-cell function in this subgroup might underly the auto-immunity. Importantly, NK-function of AA patients with reduced CD56 NK-cells was comparable to healthy donors. Also, B-cell counts were lower in AA patients. Subset analysis revealed a trend towards reduction of transitional B-cells in both absolute and relative numbers compared to healthy controls. As these cells were previously hypothesized as regulatory cells in AA, decreased numbers might be involved in defective inhibition of auto-reactive T-cells. Interestingly, even in patients with normal distribution of precursor B-cells, the transitional compartment was reduced, indicating partial differentiation failure from immature to transitional B-cells or a selective loss. Our findings provide a base for future studies to unravel the role of transitional B-cells and CD56 NK-cells in larger cohorts of pediatric AA patients as diagnostic markers for immune AA and targets for therapeutic interventions.

Human lymphoid tissues harbor, in addition to CD56 and CD56 natural killer (NK) cells, a third NK cell population: CD69 CXCR6 lymphoid tissue (lt)NK cells. The function and development of ltNK cells remain poorly understood. In this study, we performed RNA sequencing on the three NK cell populations derived from bone marrow (BM) and blood. In ltNK cells, 1,353 genes were differentially expressed compared to circulating NK cells. Several molecules involved in migration were downregulated in ltNK cells: and . By flow cytometry we confirmed that the expression profile of adhesion molecules (CD49e , CD29 , CD81 , CD62L , CD11c ) and transcription factors (Eomes , Tbet ) of ltNK cells differed from their circulating counterparts. LtNK cells were characterized by enhanced expression of inhibitory receptors TIGIT and CD96 and low expression of DNAM1 and cytolytic molecules ( ). Their proliferative capacity was reduced compared to the circulating NK cells. By performing gene set enrichment analysis, we identified DUSP6 and EGR2 as potential regulators of the ltNK cell transcriptome. Remarkably, comparison of the ltNK cell transcriptome to the published human spleen-resident memory CD8 T (Trm) cell transcriptome revealed an overlapping gene signature. Moreover, the phenotypic profile of ltNK cells resembled that of CD8 Trm cells in BM. Together, we provide transcriptional and phenotypic data that clearly distinguish ltNK cells from both the CD56 and CD56 NK cells and substantiate the view that ltNK cells are tissue-resident cells, which are functionally restrained in killing and have low proliferative activity.