A literature review of the COVID-19 pandemic’s effect on sustainable HRM

The ramifications of the COVID-19 pandemic continue to emerge across all facets of the world of work, including the field of human resource management (HRM). Sustainable HRM, drawing on the triple bottom line elements of the economic, environmental and social pillars of sustainability, provides an ideal basis from which to understand the intersection of the COVID-19 pandemic and HRM. In this systematic literature review, we analyze peer reviewed articles published in the nexus of the pandemic and sustainable HRM, identifying the dimensions and extent of research in this topical area of study. Our CEDEL model—complicator–exposer–disruptor–enabler– legitimizer—conceptualizes our understanding of the role of COVID-19 in sustainable HRM. This paper provides a framework from which future studies can benefit when investigating the impacts of COVID-19, and a comprehensive identification of future research avenues. © 2022 by the authors. Licensee MDPI, Basel, Switzerland

Prevalence of intestinal parasites and related risk factors in rural localities from Pampa del Indio, Chaco, Argentina

Intestinal parasites are a significant cause of morbidity in endemic areas in many low- and middle-income countries (LMIC). Infections with intestinal parasites have been reported in multiple locations throughout Argentina, but infection prevalence is still unknown in many areas. The aim of this study was to determine the prevalence of intestinal parasites in rural areas surrounding Pampa del Indio, Chaco, Argentina, and to identify risk factors for human infections. In the current study, a survey of three rural neighborhoods surrounding the town of Pampa del Indio was conducted in July 2018. A total of 24 households were surveyed. A questionnaire to assess socio-economic and household variables was administered and fecal samples were collected. Of the 62 stool samples analyzed, an intestinal parasite prevalence of 46.8% (29 cases) was found. The most common parasite identified was Endolimax nana (22.6%), followed by Giardia intestinalis (17.7%), and Entamoeba coli (16.1%). Most of the intestinal parasites found were protozoa, but three cases of helminths (4.8%) were also identified. Participants were polyparasitized at a rate of 19.4%. This study did not identify any statistically significant risk factors for infection but revealed a high overall rate of parasitism in the selected communities.Fil: Richards, Lindsay Renee. University of Florida; Estados UnidosFil: Delgado, Cintia. Fundación Mundo Sano; ArgentinaFil: Goy, Marcia. Hospital Dante Tardelli; ArgentinaFil: Liang, Song. Fundación Mundo Sano; ArgentinaFil: Periago, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación Mundo Sano; Argentin

Distribution of raphespinal fibers in the mouse spinal cord

Background: Serotonergic raphespinal neurons and their fibers have been mapped in large mammals, but the non- serotonergic ones have not been studied, especially in the mouse. The present study aimed to investigate the termination pattern of fibers arising from the hindbrain raphe and reticular nuclei which also have serotonergic neurons by injecting the anterograde tracer BDA into them. Results: We found that raphespinal fibers terminate in both the dorsal and ventral horns in addition to lamina 10. There is a shift of the fibers in the ventral horn towards the dorsal and lateral part of the gray matter. Considerable variation in the termination pattern also exists between raphe nuclei with raphe magnus having more fibers terminating in the dorsal horn. Fibers from the adjacent gigantocellular reticular nucleus show similar termination pattern as those from the raphe nuclei with slight difference. Immunofluorescence staining showed that raphespinal fibers were heterogeneous and serotoninergic fibers were present in all laminae but mainly in laminae 1, 2, medial lamina 8, laminae 9 and 10. Surprisingly, immunofluorescence staining on clarified spinal cord tissue revealed that serotoninergic fibers formed bundles regularly in a short distance along the rostrocaudal axis in the medial part of the ventral horn and they extended towards the lateral motor neuron column area. Conclusion: Serotonergic and non-serotonergic fibers arising from the hindbrain raphe and reticular nuclei had similar termination pattern in the mouse spinal cord with subtle difference. The present study provides anatomical foundation for the multiple roles raphe and adjacent reticular nuclei play

Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer

Cholesterol accumulates in prostate lesions and has been linked to prostate cancer (PCa) incidence and progression. However, how accumulated cholesterol contributes to PCa development and progression is not completely understood. Cholesterol sulfate (CS), the primary sulfonation product of cholesterol sulfotransferase (SULT2B1b), accumulates in human prostate adenocarcinoma and precancerous prostatic intraepithelial neoplasia (PIN) lesions compared to normal regions of the same tissue sample. Given the enhanced accumulation of CS in these lesions, it was hypothesized that SULT2B1b-mediated production of CS provides a growth advantage to these cells. To address this, PCa cells with RNAi-mediated knockdown (KD) of SULT2B1b were used to assess the impact on cell growth and survival. SULT2B1b is expressed and functional in a variety of prostate cells and the data demonstrate that SULT2B1b KD, in LNCaP and other androgen-responsive (VCaP and C4-2) cells, results in decreased cell growth/viability and induces cell death. SULT2B1b KD also decreases androgen receptor (AR) activity and expression at mRNA and protein levels. While AR overexpression has no impact on SULT2B1b KD-mediated cell death, addition of exogenous androgen is able to partially rescue the growth inhibition induced by SULT2B1b KD in LNCaP cells. These results suggest that SULT2B1b positively regulates the AR either through alterations in ligand availability or by interaction with critical co-regulators that influence AR activity

Tree growth and aboveground biomass in a tropical mountain forest thirty years after selective logging in Sarawak, Borneo

Tropical mountain forests are vital components of global floristic diversity as well as the hydrological cycle but have been extensively exploited. However, the impacts of human disturbances on changes in biomass and regional forest variation are not well documented in tropical mountainous regions. This study was conducted on the Payeh Maga Highland, Sarawak, Malaysia thirty years after logging at three elevational zones namely upper dipterocarp forest (UDF), lower-montane oak-laurel forest (LOF), and upper montane forest (UMF). Stand and growth dynamics were assessed for 12 months to estimate the tree growth rate and the aboveground biomass (AGB) of logged and unlogged forests at various elevations. Significant differences between logged-over and primary plots were observed in diameter at breast height (dbh) and basal area growth in the UMF. AGB recovery in the LOF plots was significantly slower that in other plot types. After three decades, the UDF and the UMF plots had AGB values similar to those of their primary plots. This study indicated that selective logging practices need to be improved to enhance the sustainability of timber production. Long-term monitoring, along with the establishment of more plots and the measurement of additional tree-competition parameters, is needed to clarify outstanding uncertainties

Differentiation of Chronic Lymphocytic Leukemia B Cells into Immunoglobulin Secreting Cells Decreases LEF-1 Expression

Lymphocyte enhancer binding factor 1 (LEF-1) plays a crucial role in B lineage development and is only expressed in B cell precursors as B cell differentiation into mature B and plasma cells silences its expression. Chronic lymphocytic leukemia (CLL) cells aberrantly express LEF-1 and its expression is required for cellular survival. We hypothesized that modification of the differentiation status of CLL cells would result in loss of LEF-1 expression and eliminate the survival advantage provided by its aberrant expression. In this study, we first established a methodology that induces CLL cells to differentiate into immunoglobulin (Ig) secreting cells (ISC) using the TLR9 agonist, CpG, together with cytokines (CpG/c). CpG/c stimulation resulted in dramatic CLL cell phenotypic and morphologic changes, expression of cytoplasmic Ig, and secretion of light chain restricted Ig. CpG/c stimulation also resulted in decreased CLL cell LEF-1 expression and increased Blimp-1 expression, which is crucial for plasma cell differentiation. Further, Wnt pathway activation and cellular survival were impaired in differentiated CLL cells compared to undifferentiated CLL cells. These data support the notion that CLL can differentiate into ISC and that this triggers decreased leukemic cell survival secondary to the down regulation of LEF-1 and decreased Wnt pathway activation

A Novel and Critical Role for Oct4 as a Regulator of the Maternal-Embryonic Transition

Compared to the emerging embryonic stem cell (ESC) gene network, little is known about the dynamic gene network that directs reprogramming in the early embryo. We hypothesized that Oct4, an ESC pluripotency regulator that is also highly expressed at the 1- to 2-cell stages in embryos, may be a critical regulator of the earliest gene network in the embryo.Using antisense morpholino oligonucleotide (MO)-mediated gene knockdown, we show that Oct4 is required for development prior to the blastocyst stage. Specifically, Oct4 has a novel and critical role in regulating genes that encode transcriptional and post-transcriptional regulators as early as the 2-cell stage. Our data suggest that the key function of Oct4 may be to switch the developmental program from one that is predominantly regulated by post-transcriptional control to one that depends on the transcriptional network. Further, we propose to rank candidate genes quantitatively based on the inter-embryo variation in their differential expression in response to Oct4 knockdown. Of over 30 genes analyzed according to this proposed paradigm, Rest and Mta2, both of which have established pluripotency functions in ESCs, were found to be the most tightly regulated by Oct4 at the 2-cell stage.We show that the Oct4-regulated gene set at the 1- to 2-cell stages of early embryo development is large and distinct from its established network in ESCs. Further, our experimental approach can be applied to dissect the gene regulatory network of Oct4 and other pluripotency regulators to deconstruct the dynamic developmental program in the early embryo

Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis

A reduction in functional β-cell mass leads to both major forms of diabetes; pro-inflammatory cytokines, such as interleukin-1beta (IL-1β) and gamma-interferon (γ-IFN), activate signaling pathways that direct pancreatic β-cell death and dysfunction. However, the molecular mechanism of β-cell death in this context is not well understood. In this report, we tested the hypothesis that individual cellular death pathways display characteristic phenotypes that allow them to be distinguished by the precise biochemical and metabolic responses that occur during stimulus-specific initiation. Using 832/13 and INS-1E rat insulinoma cells and isolated rat islets, we provide evidence that apoptosis is unlikely to be the primary pathway underlying β-cell death in response to IL-1β+γ-IFN. This conclusion was reached via the experimental results of several different interdisciplinary strategies, which included: 1) tandem mass spectrometry to delineate the metabolic differences between IL-1β+γ-IFN exposure versus apoptotic induction by camptothecin and 2) pharmacological and molecular interference with either NF-κB activity or apoptosome formation. These approaches provided clear distinctions in cell death pathways initiated by pro-inflammatory cytokines and bona fide inducers of apoptosis. Collectively, the results reported herein demonstrate that pancreatic β-cells undergo apoptosis in response to camptothecin or staurosporine, but not pro-inflammatory cytokines