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Ultrasound is a routine investigation for the assessment of scrotal masses. Many of the detected lesions involve the paratesticular structures. The most common paratesticular masses in clinical practice are epididymal cysts and spermatoceles, but there are a large number of other pathologies that can be encountered and may result in diagnostic uncertainty. This review covers a wide range of the common and the rare, but important, causes of paratesticular masses. The ultrasound findings (both typical and atypical) of these lesions are clarified, and emphasis is given to the features that help to differentiate between them. [Copyright &y& Elsevier]

Reviews the health consequences of human-induced climate change on sustainable development, focusing on the potential impact of such change on food supply, natural disasters, infectious diseases, ecosystems, and sea level rise. Reason for concept; Model discussed; Examination conducted in study.

Extremely mild hypothermia to 36.0 °C is not thought to appreciably differ clinically from 37.0 °C. However, it is possible that 36.0 °C stimulates highly sensitive hypothermic signaling mechanism(s) and alters biochemistry. To the best of our knowledge, no such ultra-sensitive pathway/mechanisms have been described. Here we show that cold stress protein RNA binding motif 3 (RBM3) increases in neuron and astrocyte cultures maintained at 33 °C or 36 °C for 24 or 48 h, compared to 37 °C controls. Neurons cultured at 36 °C also had increased global protein synthesis (GPS). Finally, we found that melatonin or fibroblast growth factor 21 (FGF21) augmented RBM3 upregulation in young neurons cooled to 36 °C. Our results show that a 1 °C reduction in temperature can induce pleiotropic biochemical changes by upregulating GPS in neurons which may be mediated by RBM3 and that this process can be pharmacologically mimicked and enhanced with melatonin or FGF21. [ABSTRACT FROM AUTHOR]

Abstract: A recent epidemiological study suggested that higher caffeine intake over decades reduces the risk of Alzheimer’s disease (AD). The present study sought to determine any long-term protective effects of dietary caffeine intake in a controlled longitudinal study involving AD transgenic mice. Caffeine (an adenosine receptor antagonist) was added to the drinking water of amyloid precursor protein, Swedish mutation (APPsw) transgenic (Tg) mice between 4 and 9 months of age, with behavioral testing done during the final 6 weeks of treatment. The average daily intake of caffeine per mouse (1.5 mg) was the human equivalent of 500 mg caffeine, the amount typically found in five cups of coffee per day. Across multiple cognitive tasks of spatial learning/reference memory, working memory, and recognition/identification, Tg mice given caffeine performed significantly better than Tg control mice and similar to non-transgenic controls. In both behaviorally-tested and aged Tg mice, long-term caffeine administration resulted in lower hippocampal β-amyloid (Aβ) levels. Expression of both Presenilin 1 (PS1) and β-secretase (BACE) was reduced in caffeine-treated Tg mice, indicating decreased Aβ production as a likely mechanism of caffeine’s cognitive protection. The ability of caffeine to reduce Aβ production was confirmed in SweAPP N2a neuronal cultures, wherein concentration-dependent decreases in both Aβ1–40 and Aβ1–42 were observed. Although adenosine A1 or A2A receptor densities in cortex or hippocampus were not affected by caffeine treatment, brain adenosine levels in Tg mice were restored back to normal by dietary caffeine and could be involved in the cognitive protection provided by caffeine. Our data demonstrate that moderate daily intake of caffeine may delay or reduce the risk of AD. [Copyright &y& Elsevier]

CD39 and CD73 are key enzymes in the adenosine (ADO) pathway. ADO modulates pathophysiological responses of immune cells, including B cells. It has recently emerged that a subpopulation of ADO-producing CD39+CD73+B cells has regulatory properties. Here, we define the CD39highsubset of these cells as the major contributor to the regulatory network operated by human B lymphocytes. Peripheral blood B cells were sorted into CD39neg, CD39interand CD39highsubsets. The phenotype, proliferation and IL-10 secretion by these B cells were studied by flow cytometry. 5′-AMP and ADO levels were measured by mass spectrometry. Agonists or antagonists of A1R, A2AR and A3R were used to study ADO-receptor signaling in B cells. Inhibition of effector T-cell (Teff) activation/proliferation by B cells was assessed in co-cultures. Cytokine production was measured by Luminex. Uponin vitroactivation and culture of B cells, the subset of CD39highB cells increased in frequency (p< 0.001). CD39highB cells upregulated CD73 expression, proliferated (approximately 40% of CD39highB cells were Ki-67+and secreted fold-2 higher IL-10 and ADO levels than CD39negor CD39interB cells. CD39highB cells co-cultured with autologous Teff suppressed T-cell activation/proliferation and secreted elevated levels of IL-6 and IL-10. The A1R and A2AR agonists promoted expansion and functions of CD39highB cells. CD39 ectonucleotidase is upregulated in a subset ofin vitro-activated B cells which utilize ADO and IL-10 to suppress Teff functions. Proliferation and functions of these CD39highB cells are regulated by A1R- and A2AR-mediated autocrine signaling. [ABSTRACT FROM AUTHOR]

An abstract of the article "Chronic adenosine receptor blockade with BG9928 attenuates cardiac and renal histopathology and improves diabetes in animals with the metabolic syndrome," by S. Tofovic and colleagues is presented.