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A patient with severe mitral regurgitation and chronic systolic heart failure taking inotropic support at home presents for transcatheter edge-to-edge mitral valve repair, complicated by torrential mitral regurgitation from damaged mitral leaflets requiring escalating mechanical circulatory support and ultimately expedited orthotopic heart transplantation. (Level of Difficulty: Intermediate.)

Although remote sensing of lake surface water temperature has been ongoing for decades and has led to important discoveries regarding the warming of lake surface temperature in some regions, the ability to access and use remote sensing data is still primarily limited to remote sensing experts. Effective use of remote sensing data involves technical skills in coding (often in multiple programming languages), application of appropriate atmospheric corrections, and integrating spatially heterogeneous remote sensing data with in situ data obtained at specific geographic locations. To improve access to remote sensing data and broaden the understanding of changes in lake surface water temperature over the past four decades, we created lakeCoSTR (lake Collection 2 Surface Temperature Retrieval), a user‐friendly, cloud‐based script that gives ecologists lacking specialized training in remote sensing the ability to access the Landsat Collection 2 temperature estimates for lakes with a surface area of at least 0.4 ha. Additionally, if in situ data are provided, a paired dataset can be created within the tool. To demonstrate lakeCoSTR, we retrieved surface water temperature data for a lake with a long monitoring history, Lake Sunapee, NH, USA, and compared long‐term surface temperature trends between data obtained via lakeCoSTR and in situ measurements. When compared with Landsat Collection 1 temperature estimates derived from a single‐channel algorithm, the Landsat Collection 2 data from lakeCoSTR required no calibration to in situ data. This suggests that lakeCoSTR can be used to document temporal trends in lakes and to reprocess analyses that relied on Collection 1 data. From 1983 until 2020, remotely sensed surface water temperature estimates at Lake Sunapee increased by 0.07–0.09°C year−1 during July and August, a trend that agreed with long‐term in situ record. As climate change continues to impact freshwater systems, a better understanding of long‐term temperature data will be vital. Remotely sensed data, like those acquired using lakeCoSTR, may provide a window into temperature trends for lakes. [ABSTRACT FROM AUTHOR]

In humans and sheep, endotoxin (LPS) administration results in increased growth hormone (GH) concentrations. To determine the role of cytokines in the effect of LPS on GH, sheep were challenged with IL-1[beta] or TNF-[alpha]. GH data were compared with results with LH, where the major effects of LPS are known to act via the hypothalamus. Intracerebroventricular (icv) administration of IL-1[beta] or TNF-[alpha] did not alter plasma concentrations of GH. Endotoxin was then administered intravenously (iv) in combination with icv injection of IL-1 receptor antagonist (IL-1RA), TNF antagonist (sTNF-R1), or saline. Administration of LPS increased GH (P < 0.0001), although coadministration of IL-1ra or sTNF-R1 icv did not alter GH response to LPS. In contrast, plasma concentrations of LH were profoundly inhibited by icv administration of either cytokine (P < 0.03), but the LH response to LPS was not altered by cytokine antagonists. Intravenous administration GH (P < 0.0001). Administration of IL-1RA and sTNF-R1 iv prevented of either IL-1[beta] or TNF-[alpha] increased plasma concentrations of LPS-induced increases in GH. Although LH was suppressed by high iv doses of IL-1[beta] (P = 0.0063), the antagonists did not alter the LH response to LPS. To determine whether LPS might directly activate GH release, confocal microscopy revealed colocalization of CD14, the LPS receptor, with GH and, to a lesser extent, LH and some prolactin (PRL)-containing cells, but not ACTH or TSH. These data are consistent with the effects of LPS on GH secretion originating through peripheral cytokine presentation to the pituitary, as well as a potential to act directly on selective populations of pituitary cells via CD14. luteinizing hormone; cytokines; sheep; CD14; lipopolysaccharide

Four studies were designed to determine whether 1) tumor necrosis factor-[alpha] (TNF) and the Lipopolysaccharide (LPS) binding ligand, CD14, are produced by sheep adipose tissue; 2) nutritional reserves and/or short-term fasting affect circulating concentrations of TNF; 3) there is a relationship between TNF and metabolic factors in sheep; and 4) inflammation alters circulating concentrations of leptin. In Exp. 1 and 2, ewes were assigned, based on ultrasonic assessments of last-rib subcutaneous fat measurements to fat (fat thickness >1 cm; mean = 1.52 [+ or -] 0.03 cm) or thin (fat thickness 0.39). In Exp. 4, wethers were injected with LPS. Blood samples were collected every 15 min for 8 h following injection. Plasma concentration of leptin was not altered by LPS (P > 0.20). These results provide evidence: 1) of TNF-like immunoreactivity within fat tissue; 2) that elements within fatty tissues have CD14 that may allow adipocyte function to be directly affected by LPS; 3) that plasma concentrations of leptin are not altered by LPS treatment; and 4) that circulating concentrations of TNF are elevated with obesity in sheep. Key Words: Fat, Leptin, Lipopolysaccharides, Receptors, Sheep, Tumor necrosis factor.

Estradiol plus progesterone (EP) implants have been shown to favorably alter the time course or decrease the severity of many of the clinical manifestations associated with coccidiosis and endotoxemia in calves. This study evaluated the effect of EP treatment on plasma tumor necrosis factor-[alpha] (TNF), thromboxane (TXB), prostacyclin (PRC), nitrite and nitrate (N[O.sub.[x]]), and cortisol. Holstein steer calves were divided into four groups: control, EP, endotoxin (LPS), and EP+LPS (n = five/group). Estradiol/progesterone pellets (Synovex-S) were implanted subcutaneously when calves reached 20 wk of age. One week after implantation, calves were injected IV with endotoxin (i.e., lipopolysaccharide; LPS, 0.6 [micro]g/kg of BW) or nonpyrogenic saline placebo. Body temperature was measured and blood was collected before injection and at 1, 2, 3, 4, 6, and 8 h thereafter. Plasma concentrations of TNF, cortisol, TXB, PRC, N[O.sub.[x]], were measured. Body temperature increased in both LPS and LPS-EP calves, but had returned to normal by 6 h in the LPS-EP group (P < 0.05). Plasma TNF and cortisol increased after LPS (P < 0.01), but were not differentially affected by EP treatment. Likewise, EP did not affect the magnitude of increase in LPS-induced PRC, but EP decreased the magnitude of increase in TXB (P < 0.05). Plasma N[O.sub.[x]]] levels were increased (P < 0.01) in calves after LPS; treatment with EP attenuated the LPS-associated increase in plasma N[O.sub.[x]] levels. These results suggest that EP exerts specific effects on different components of the proinflammatory cytokine cascade. Although the initiation of responses mediated by TNF, cortisol, and PRC do not seem to be differentially affected by EP, components of the nitric oxide- and TXB-axis responses to LPS are decreased in calves pretreated with EP. Key Words: Cattle, Cortisol, Endotoxins, Growth Promoters, Prostacyclin, Tumor Necrosis Factor