New Results on the Existence of Periodic Solutions for Rayleigh Equation with State-Dependent Delay

We give certain sufficient conditions for the existence of periodic solutions to a Rayleigh-type equation with state-dependent delay. With this work we extend and improve some known results in the literature

Mast cells, vasoactive intestinal peptide (VIP), and the hemorrhagic shock: a possible relationship?

The key mechanisms associated with irreversible hemorrhagic shock have no so far been elucidated. The involvement of mast cells in this phenomenon, however, has already been studied. On the other hand, β-endorphin and various opiates, or any stressful stimuli mediated by endogenous opiates, cause mast cell degranulation and histamine release, as the study of the related literature shows. Hemorrhagic shock is one such stressful stimulus that leads to an increase in the plasma levels of endogenous opioids, especially β-endorphin. During hemorrhagic shock, therefore, mast cells can be activated by an elevation of the β-endorphin level; and the degranulated products of mast cells, histamine in particular, may contribute to the progress of hemorrhagic shock to the irreversible state. The investigation of the effect of hemorrhage on mast cell degranulation has shown that there is a positive correlation between the two phenomena. In addition, it has been established that the administration of vasoactive intestinal peptide (VIP) prevents such degranulation. Depending on these results, the effects of VIP have been studied in the treatment of severe experimental hemorrhagic shock in combination with other therapeutic means used in this type of shock, such as naloxone, hypertonic saline infusion and/or blood reperfusion. A combination of VIP and naloxone has yielded the best results on survival when it is used either alone or in conjunction with volume replacement after a severe hemorrhage. The important prospect of a combination of VIP and naloxone is that it has apparently the most potent inhibitory effect on mast cell degranulation. In the light of the related experiments, we may conclude that the inhibition of mast cell degranulation has a beneficial effect on severe hemorrhagic shock; mast cell degranulation may thus be accepted as a physiopathological mechanisms contributing to the progression of hemorrhagic shock state.Biomedical Reviews 1993; 2: 37-46

Hyers-Ulam-Rassias Stability for a First Order Functional Differential Equation

In this paper, by using the fixed point method, we prove two new results on the Hyers-Ulam-Rassias and the Hyers-Ulam stability for the first order delay differential equation of the formy"²(t) = F(t, y(t), y(t −τ )).Our results improve some related results in the literature.

Protein pieces of adipose tissue secretory puzzle

Over the past decade, the paradigm shift of adipose tissue as being far beyond its pivotal role in lipid and energy homeostasis has been increasingly recognized. Arguably, adipocytes as well as other adipose cells are at present considered bona fide secretory cell types, using pleiocrine pathways for delivery of multiple signaling proteins designated adipokines. Transcriptomic and proteomic studies `upregulate` more than hundred adipokines that are synthesized, stored, and released by adipose tissue cells. However, the functional description of adipose-secreted proteins look like an incomplete puzzle. Here we describe only adipsin, adiponectin, leptin, resistin, visfatin, tumor necrosis factor-alpha, interleukin-6, plasminogen activator inhibitor type 1, nerve growth factor, brain-derived neurotrophic factor, and metallothioneins, and focus on their implications for the pathogenesis of various diseases besides obesity and related disorders. Accordingly, a horizon of the adipopharmacology of disease is outlined.Biomedical Reviews 2007; 18: 27-43

Cold exposure and adipose nitric oxide and mast cells: influence on aorta contractility

Both nitric oxide (NO) and mast cells play important roles in adipose and vascular tissue biology. Chronic cold stress decreases the sensitivity of vascular smooth muscle to various contractile agents including norepinephrine (NE). In our previous cold exposure study we found that the contractile response of isolated rat aortas to NE was significantly reduced, and the number of rat aortic adventitial mast cells decreased. Histologically and functionally, white and brown adipose tissue (WAT and BAT) can be distinguished. Beyond its significance in energy store/release and heat production, adipose tissue secretes multiple signaling molecules that have endocrine and paracrine role in the regulation of vascular functions. The aims of the present study were to examine chronic cold exposure-induced alterations in (i) the concentration of NO released from selected regions of WAT and BAT in female and male rats, (ii) the histochemistry of white and brown adipose mast cells, and (iii) whether adipose-derived NO affects the contraction of isolated rat aorta to NE. Twelve females and 12 males Spraque-Dawley rats (150-200 g body weight) were used. The rats were exposed to a cold/freely moving stress for 2 hours each day for 5 consecutive days. At the end of cold exposure, the rats were sacrificed, and samples of thoracic aorta with associated periadventitial adipose tissue (tunica adiposa) were obtained. WAT and BAT were isolated from subcutaneous abdominal and interscapular areas, respectively. The concentration of NO was measured by capillary electrophoresis and mast cells were evaluated histochemically. The response of aorta smooth muscles to NE was recorded in the isolated organ bath. To determine whether adipose-derived NO affects aorta contraction to NE, cumulative dose response curves to NE (10-8-10-3 M) were obtained with or without isolated WAT/BAT suspended in the organ bath medium. In control animals, a gender-related significant difference in NO production in both WAT and BAT was found, NO levels being significantly higher in female than male rats. Data from the contractile response of isolated aorta to NE suggest that receptor affinity to NE is significantly different between female and male controls. Presence of BAT and WAT (isolated from cold-exposure animals) in the bath changed the response of aorta smooth muscle to NE. Displaying a gender dimorphism, BAT/WAT-derived NO, or other vasorelaxing factors, seem to reduce receptor density and/or affinity to NE. Adipose mast cell histochemistry also showed diversity in respect to subtype, gender, and cold exposure. Altogether, we found (i) a gender difference in adipose-released NO and in adipose mast cell histochemistry to cold exposure, and (ii) peripheral adipose tissues affect aortic contractile responses to NE likely by a NO-mediated pathway during cold exposure, suggesting that adipose tissue may limit cold-induced excessive vasoconstriction. Our ongoing study aims at the evaluation of whether aortic tunica adiposa itself could also contribute to this phenomenon.Adipobiology 2009; 1: 67-75

The mast cell: Another master in adipoimmunology

Recently, a large number of studies focus on (i) adipose tissue endocrine and paracrine function, and (ii) adipose-immune interactions herein referred to as adipoimmunology. In effect, a wide range of signaling proteins, dubbed adipokines, was identified as endocrine and paracrine secretory products of adipocytes and associated stromal vascular cells, including macrophages, lymphocytes and mast cells, the latter being less evaluated as compare to the formers. During obesity immune cells migrate into adipose tissue and inflame it by the secretion of a large amount of adipokines and thus trigger the development of so-called low grade inflammation-related diseases. Based on Steve Galli`s concept of mast cell as master cells in many biological and pathological processes (New Engl J Meet 1993; 328:257-265), here we highlight recent studies on the significance of adipose mast cells in the pathogenesis and therapy of cardiometabolic diseases (atherosclerosis, obesity, type 2 diabetes mellitus, metabolic syndrome) and breast cancer. Knowledge of the master work of these cells may provide a background for mast cell-targeted pharmacology for low grade inflammation-related diseases.Adipobiology 2015; 7: 15-19Key words: adipose tissue, adipokines, atherosclerosis, breast cancer, inflammation, mast cells, obesit

PVAT and Atherogenesis: a Crossroad of White and Brown Adipobiology

In 1999, the prevailing response-to-injury hypothesis of Russell Ross stated that atherosclerosis is an inflammatory disease, leading - through an inside-out road - to endothelial and smooth muscle dysfunction resulting in the formation of atherosclerotic plaques. Accordingly, intima-media thickness became an accepted measure of structural vascular remodeling and a strong predictor of atherosclerosis. However, it is unlikely that such a road may solely travel the whole multiplex network like that of atherogenesis. Recently things changed dramatically and the attention was moved from inside-out to outside-in road emphasizing the role for adventitial and adipose dysfunction in the processes of atherogenesis

State-of-the-artery: periadventitial adipose tissue (tunica adiposa)

Traditional view considers that the arterial wall is composed of three concentric tissue coats (tunicae): intima, media, and adventitia. However, large- and medium-sized arteries, where usually atherosclerosis develops, are consistently surrounded by periadventitial adipose tissue (PAAT). Here we update growing information about PAAT, and  conceptualize it as the fourth coat of arterial wall, that is, tunica adiposa (in brief, adiposa, like intima, media, adventitia). Recent evidence has revealed that adipose tissue expresses not only metabolic, but also secretory (endo- and paracrine) phenotype, producing/releasing a large number of signaling proteins collectively termed adipokines. Through paracrine ("vasocrine") way, adiposa-derived mediators may contribute to various arterial functions such as contraction-relaxation, smooth muscle cell growth, inflammation, hemostasis, and innervation, hence to "outside-in" signaling pathway of atherogenesis.Biomedical Reviews 2009; 20: 41-44

In the heart of adipobiology: cardiometabolic disease

Published on 1 December 1994 issue of Nature, the Jeffrey Friedman's discovery "gave leptin in the beginning" of the endocrine saga of adipose tissue. Onwards, studies on this tissue have enjoyed an explosive growth that conceptualized a novel field of research, adipobiology. Arguably, in the heart of adipobiology and adipopharmacology are studies focusing on the pathogenesis, prevention and therapy of cardiometabolic diseases (CMD) including atherosclerosis, hypertension, obesity, type 2 diabetes, metabolic syndrome (global cardiometabolic risk), and lipodystrophies.Biomedical Reviews 2009; 20: 1-5

SOS for Homo sapiens obesus

Published on 1 December 1994 issue of Nature, the Jeffrey Friedman's discovery "gave leptin in the beginning" of the endocrine saga of adipose tissue. Onwards, studies on this tissue have enjoyed an explosive growth that conceptualized a novel field of research, adipobiology. Arguably, in the heart of adipobiology and adipopharmacology are studies focusing on the pathogenesis, prevention and therapy of cardiometabolic diseases (CMD) including atherosclerosis, hypertension, obesity, type 2 diabetes, metabolic syndrome (global cardiometabolic risk), and lipodystrophies.Adipobiology 2010; 2: 5-8