Tar pollution event (2021) at the Southeastern Levantine oligotrophic basin, short-term impacts and operational oceanography perspectives.

The Levantine basin (LB) in the Southeastern Mediterranean Sea is a high-risk oil pollution hot spot owing to its dense maritime traffic and intense oil and gas exploration and exploitation activities. In February 2021 the Israeli LB shorelines were impacted by an exceptional tar pollution event (~550 tons; average distribution: ~3 kg tar m-1 front beach) of an unknown oil spill source. Here we report on the immediate numerical modelling assessment of the oil spill propagation and tar distribution; operational use of underwater gliders for tracking water column anomalies of dissolved polycyclic aromatic hydrocarbons (PAHs) and turbidity signals; the beached tar composition and amounts and the short-term response of the microbial population along the ~180 km shoreline. This pollution event emphasizes the need for improving the early warning systems for oil spills and implementing continuous operational monitoring at high-risk, ecologically sensitive and valuable resource areas like the Israeli LB waters.

Downwind gas condensate volatiles affect phytoplankton communities.

We investigated the effects of volatile organic carbons (VOCs) evaporated from gas condensate on the cyanobacteria Synechococcus sp. WH8103, the diatom Asterionellopsis glacialis, and the dinoflagellate Alexandrium minutum. We used custom algal incubation chambers enabling only the gas condensate-derived VOCs to interact with the cell cultures via an atmospheric bridge, without direct contact with the hydrocarbon oil. The exposure to gas condensate VOCs reduced the abundance, growth rate, and photosynthetic efficiency of Synechococcus sp. WH8103. Thiobarbituric acid reactive substances (TBARS) assays hint at oxidative damage to the chloroplasts and/or the thylakoid membranes in this organism. A.glacialis abundance, physiological state and growth rates remained unchanged, whereas A.minutum abundance and photosynthetic efficiency increased relative to their respective controls. Our results demonstrate that the effects of a gas condensate formed due to an oil spill will not be restricted to the polluted area, but may be prominent in downwind locations through atmospheric transport.

GM-CSF induces STAT5 binding at epigenetic regulatory sites within the Csf2 promoter of non-obese diabetic (NOD) mouse myeloid cells.

Myeloid cells from non-obese diabetic (NOD) mouse and human type 1 diabetic (T1D) patients overexpress granulocyte-macrophage colony stimulation factor (GM-CSF). This overproduction prolongs the activation of signal transduction and activator of transcription 5 (STAT5) proteins, involved in GM-CSF-induced control of myeloid cell gene expression. We found that GM-CSF can regulate the binding of STAT5 on the promoter of its own gene, Csf2, within regions previously identified as sites of chromatin epigenetic modification important to the regulation of GM-CSF during myeloid differentiation and inflammation. We found multiple sequence polymorphisms within NOD mouse chromosome 11 Idd4.3 diabetes susceptibility region that alter STAT5 GAS binding sequences within the Csf2 promoter. STAT5 binding at these sites in vivo is increased significantly in GM-CSF-stimulated-bone marrow cells and in unactivated, high GM-CSF-producing macrophages from NOD mice as compared to non-autoimmune C57BL/6 mouse myeloid cells. Thus, GM-CSF overproduction by NOD myeloid cells may be perpetuating a positive epigenetic regulatory feedback on its own gene expression through its induction of STAT5 binding to its promoter. These findings suggest that aberrant STAT5 binding at epigenetic regulatory sites may contribute directly to immunopathology through cytokine-induced gene expression dysregulation that can derail myeloid differentiation and increase inflammatory responsiveness.

M-CSF and GM-CSF regulation of STAT5 activation and DNA binding in myeloid cell differentiation is disrupted in nonobese diabetic mice.

Defects in macrophage colony-stimulating factor (M-CSF) signaling disrupt myeloid cell differentiation in nonobese diabetic (NOD) mice, blocking myeloid maturation into tolerogenic antigen-presenting cells (APCs). In the absence of M-CSF signaling, NOD myeloid cells have abnormally high granulocyte macrophage colony-stimulating factor (GM-CSF) expression, and as a result, persistent activation of signal transducer/activator of transcription 5 (STAT5). Persistent STAT5 phosphorylation found in NOD macrophages is not affected by inhibiting GM-CSF. However, STAT5 phosphorylation in NOD bone marrow cells is diminished if GM-CSF signaling is blocked. Moreover, if M-CSF signaling is inhibited, GM-CSF stimulation in vitro can promote STAT5 phosphorylation in nonautoimmune C57BL/6 mouse bone marrow cultures to levels seen in the NOD. These findings suggest that excessive GM-CSF production in the NOD bone marrow may interfere with the temporal sequence of GM-CSF and M-CSF signaling needed to mediate normal STAT5 function in myeloid cell differentiation gene regulation.

Signal transduction activator of transcription 5 (STAT5) dysfunction in autoimmune monocytes and macrophages.

Autocrine granulocyte macrophage-colony stimulating factor (GM-CSF) sequentially activates intracellular components in monocyte/macrophage production of the pro-inflammatory and immunoregulatory prostanoid, prostaglandin E2 (PGE2). GM-CSF first induces STAT5 signaling protein phosphorylation, then prostaglandin synthase 2 (COX2/PGS2) gene expression, and finally IL-10 production, to downregulate the cascade. Without activation, monocytes of at-risk, type 1 diabetic (T1D), and autoimmune thyroid disease (AITD) humans, and macrophages of nonobese diabetic (NOD) mice have aberrantly high GM-CSF, PGS2, and PGE2 expression, but normal levels of IL-10. After GM-CSF stimulation, repressor STAT5A and B isoforms (80-77kDa) in autoimmune human and NOD monocytes and activator STAT5A (96-94kDa) and B (94-92kDa) isoforms in NOD macrophages stay persistently tyrosine phosphorylated. This STAT5 phosphorylation persisted despite treatment in vitro with IL-10, anti-GM-CSF antibody, or the JAK2/3 inhibitor, AG490. Phosphorylated STAT5 repressor isoforms in autoimmune monocytes had diminished DNA binding capacity on GAS sequences found in the PGS2 gene enhancer. In contrast, STAT5 activator isoforms in NOD macrophages retained their DNA binding capacity on these sites much longer than in healthy control strain macrophages. These findings suggest that STAT5 dysfunction may contribute to dysregulation of GM-CSF signaling and gene activation, including PGS2, in autoimmune monocytes and macrophages.

Home laundering of soiled surgical scrubs: surgical site infections and the home environment.

An increasing number of hospitals have implemented programs that permit their operating room (OR) personnel to launder their soiled "scrubs" at home. Not only have they not experienced an increase in the incidence of surgical site infections (SSIs), but they have also found the policy to be financially rewarding. Whereas the Association of periOperative Registered Nurses (AORN) opposes the practice, the Centers for Disease Control and Prevention (CDC) describes it as an unresolved issue. The variances in the positions taken by these two organizations obviously accounts for the differences in positions taken by the infection control community. In the absence of any evidence in the literature, the only alternative is to draw from knowledge and experience to determine whether the practice can be considered clinically effective and does not have a harmful effect on the home environment. On the basis of the results of that examination, it is concluded that the need for having soiled scrubs laundered by a facility-approved laundry is indefensible and simply predicated on the "that's the way we've always done it" syndrome.

Testing surgical gowns for the "anticipated level of exposure".

Although the use of the surgeon's gown dates back to the turn of the century, the need for it to be made of a liquid-repellent material was disclosed only in 1952. Because of the relatively poor performance of the products that were introduced early on, the entire textile industry--makers of nonwoven disposable and woven reusable materials alike--was challenged to develop a test method to demonstrate a fabric's capability "under usual conditions of use." A cooperative attempt to do that was abandoned in 1983. With the emergence of HIV, the need to protect the wearer became the gown's priority. However, because there was no standard test method, the manufacturers used any of an array of tests to promote a product's suitability for use under what the Occupational Safety and Health Administration describes as the "level of exposure anticipated." Now, a standard test method has been adopted that describes the results on a pass/fail basis. However, the literature indicates that gowns made of materials that have passed this test have failed "under usual conditions of use." Nevertheless, the Food and Drug Administration is permitting manufacturers to mislead the surgical community by describing products as being "impervious" or "liquid proof."