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Previous work in mouse models shows that urinary TNF-α levels become elevated when dietary salt (NaCl) intake increases. To examine if this relationship exists in humans, we conducted a secondary analysis of the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial to determine levels of urinary TNF-α in 367 subjects categorized by race, sex, and blood pressure. The DASH-Sodium trial is a multicenter feeding trial in which subjects were randomly assigned to either the DASH or control diet, and high, medium, and low sodium in random order. Multivariable linear regression was used to model baseline TNF-α and a mixed model was used to model TNF-α as a function of dietary intervention. At baseline, with all subjects on a “typical American diet”, urinary TNF-α levels were lowest in Black, p = 0.002 and male subjects, p < 0.001. After randomization to either the DASH or control diet, with increasing levels of sodium, urinary TNF-α levels increased only in subjects on the control diet, p < 0.05. As in the baseline analysis, TNF-α levels were highest in White females, then White males, Black females and lowest in Black males. The results indicate that urinary TNF-α levels in DASH-Sodium subjects are regulated by NaCl intake, modulated by the DASH diet, and influenced by both race and sex. The inherent differences between subgroups support studies in mice showing that increases in renal TNF-α minimize the extent salt-dependent activation of NKCC2.Baseline conditions- Blacks/Males ingesting a “Typical American Diet” exhibited lower urinary tumor necrosis factor-α (TNF-α) levels than Whites/Females, likely contributing to higher Na+ - K+ -2Cl- cotransporter type 2 (NKCC2) activity as previously suggested for Black vs White individuals. Higher urinary TNF-α in Females may be required to suppress inherently higher NKCC2 activity to maintain homeostasis. After randomization- Urinary TNF-α increased only for those on the high sodium & control diet, an effect which appeared to be attenuated for those on the Dietary Approaches to Stop Hypertension (DASH) diet.

The combined use of field data on anchovy (Engraulis encrasicolus, Linnaeus, 1758) egg distribution in the Central Mediterranean Sea on both sides of the Strait of Sicily (Sicilian–Maltese and Tunisian waters) and Lagrangian simulations were used to assess the pattern of connectivity between these two sub-areas as a result of spawning activity. The field data were collected during ichthyoplankton surveys carried out in summer 2008 and 2010. The simulation runs showed considerable (up to 20%) rates of particle exchange in both directions (from Tunisian to Sicilian–Maltese waters and vice versa). However, considering the typical high mortality rates of anchovy early stages, the actual larval exchange rates across the Sicily Strait are supposed to be significantly lower (<1%), supporting the hypothesis that the anchovy population sub-units in the Strait of Sicily can be considered as separate fish stocks for the evaluation of their optimum exploitation rates.

The Strait of Sicily plays a crucial role in determining the water-mass exchanges and related properties between the western and eastern Mediterranean. Hydrographic measurements carried out from 1998 to 2013 allowed the identification of the main water masses present in the Strait of Sicily: a surface layer composed of Atlantic water (AW) flowing eastward, intermediate and deep layers mainly composed of Levantine intermediate water (LIW), and transitional eastern Mediterranean deep water (tEMDW) flowing in the opposite direction. Furthermore, for the first time, the signature of intermittent presence of western intermediate water (WIW) is also highlighted in the northwestern part of the study area (12.235° E, 37.705° N). The excellent area coverage allowed to highlight the high horizontal and vertical inter-annual variability affecting the study area and also to recognize the permanent character of the main mesoscale phenomena present in the surface water layer. Moreover, strong temperature-salinity correlations in the intermediate layer, for specific time intervals, seem to be linked to the reversal of surface circulation in the central Ionian Sea. The analysis of CTD data in deeper water layer indicates the presence of a large volume of tEMDW in the Strait of Sicily during the summers of 2006 and 2009.

Most of the studies carried out in the past on economically important fish species rely on single species approach. Ecosystem dynamics are characterized by complex interaction among species, sharing common habitat needs and thus forming characteristic assemblages. The analysis of spatio-temporal variability of fish community, coupled to the analysis of spatial indices, provides a synthetic view of the fish community status evidencing, if any, the way a community changes. Such considerations drive also to the development of ecosystem-based fishery management paradigm. In the present study changes in pelagic fish community structure in an upwelling ecosystem of the central Mediterranean Sea during the last 10 years was analysed, by focusing the attention on the five most abundant small pelagic species: Engraulis encrasicolus, Sardina pilchardus, Sardinella aurita, Trachurus trachurus and Boops boops. Our results evidenced a quite stable community structure, characterized by spatial occupation strongly driven by ecosystem characteristics and modulated according to specie-specific behaviour. Obtained results lead us to hypothesize that the observed stability of community could be linked to the presence of different environments leading to efficient space partitioning and resources utilization among species.

An analysis of the influence of environmental conditions on the pelagic fish community structure and species distribution in two areas of the Central Mediterranean sea, the Sicilian–Maltese and the Libyan continental shelves, is presented. The Libyan waters suffer from the lack of historical information on these species, and a thorough characterisation of the pelagic fish community is missing for the entire study area. In summer 2008, two multidisciplinary surveys permitted for the first time the collection of acoustic, biological, and hydrological data in the Libyan, Maltese, and Italian waters of the Central Mediterranean. Satellite and in situ measurements were used here to describe the environmental conditions characterising the two ecosystems, and to analyse the relationships between environmental factors and pelagic community structure, and pelagic fish biomass. The datasets support the hypothesis of a more favourable feeding ground for pelagic fishes in the southwestern part of the study area, close to the Gulf of Gabes, characterised by a larger continental shelf and a higher productivity than the northern and the eastern sides. Environmental gradients, such as the ones related to temperature and salinity, may influence in different ways the pelagic fish community structure in the two areas. The Libyan waters, where environmental gradients develop longitudinally in about 700 nmi, likely produce a better spatially structured fish community. In the Sicilian–Maltese area, characterised by stronger environmental gradients and shorter longitudinal extension (150 nmi), such spatial structure is less evident. In this latter area a higher spatial overlap among pelagic species is mainly linked to the limited continental shelf and the spatially compressed environmental gradients.

Sertoli–Leydig cell tumor belongs to the group of sex cord–stromal tumors of the ovary. These neoplasms account for less than 0.5% of all ovarian tumors and are more often encountered in young women between the ages of 20 and 30 years who usually become virilized. We described an unusual case of Sertoli–Leydig cell tumor in a postmenopausal women who presented with a solid right pelvic mass, a large amount of ascites, and laboratory tests revealing an elevated CA125, all suggesting a pelvic malignancy. Although five similar cases of postmenopausal women with Sertoli–Leydig cell tumor of ovary have been reported in the literature, we believe that this is an useful addition to the literature.

Our initial studies on renal cyclooxygenase (COX)-2 expression and activity addressed the critical role of angiotensin II (Ang II) in increasing tumor necrosis factor alpha (TNF) that eventuated in expression of COX-2 in the medullary thick ascending limb (mTAL) of the nephron. COX-2 supplanted the dominant oxygenase, the cytochrome P450 (CYP) enzyme, w- hydroxylase, that synthesized 20-hydroxyeicosatetraenoic acid (20-HETE). These findings served as the basis for additional studies on: 1) the role of glucocorticoids in regulating COX-2 expression and activity in the mTAL; and 2) the utilization of the same signaling pathways in response to stimulation of the mTAL calcium receptor (CaR). These studies of mTAL COX-2 expression which are addressed in the first part of this chapter are followed by explorations of the expression of COX-2 in preglomerular microvessels (PGMV) and the relationship of COX-2 to 20- HETE, the principal eicosanoid of PGMV. The third and last component of this chapter explores the signaling events, focusing on COX-2, which are set in motion by diabetes.

The aim of this study was to investigate the role of COX in modulating vsmc proliferation. Serum and tumor necrosis factor-α (TNF) are known to increase COX expression and activity in vsmc. TNF [1nM]-mediated, COX-2-dependent, PGI2 and TXA2 production increased approximately 4.5-fold and 2-fold, respectively. Addition of serum (0-5%) increased vsmc proliferation in a dose-dependent manner; addition of 5% serum for 48hr increased cell number by 3-fold. TNF potentiated the response to 5% serum by ∼34%, an effect that also was confirmed by evaluating the changes in S and G2/M phases of the cell cycle using laser scanning cytometry. Exposure of vsmc to 5% serum for 20hr increased the percentage of cells in S and G2/M phases by 55%; TNF increased this response by an additional 50%. Treatment with NS-398 [1μM], a selective COX-2 inhibitor, prevented progression of the cell cycle induced by 5% serum and TNF+5% serum. The role of COX-2 was further investigated by increasing its expression and activity using NO-donors. Papanonoate (PN; 500μM), an NO donor, unlike TNF, preferentially increased PGI2 but not TXA2 synthesis (control: 86± 17, PN: 428± 54 pg 6-ketoPGF1α/μg protein; p<0.01, n=3). Sodium nitroprusside (SNP; 50μM), another NO-donor, increased PGI2 synthesis, which was blocked by NS-398 (1μM)(control: 16.69±1.08; SNP 50 μM: 53.81±8.90, SNP±NS-398: 18.75±4.17 pg/μg protein; p<0.01, n=3). SNP as well as Detanonoate (DN; 1mM) increased COX-2 protein expression, without affecting COX-1 protein expression. However, treatment with these NO-donors decreased cell number, an effect prevented by NS-398. The data indicate that NO donors preferentially stimulate PGI2 production by vsmc. TNF, on the other hand, stimulates both PGI2 and TXA2 synthesis. Thus, increased COX-2 activity can lead to an increased proliferative response of vsmc in the presence of co-mitogens; whereas in the absence of a mitogen, NO inhibits vsmc proliferation in a COX-2-dependent manner.

Primary cultures of rat mTAL cells express the G-protein coupled CaR, sensing changes in extracellular Ca2+ concentration that are transduced into several intracellular signals. Activation of this receptor increases expression and activity of cyclooxygenase-2 in a TNF-dependent manner, an interaction that regulates ion transport mechanisms in the TAL. TNF production has been linked to a calcineurin-dependent signaling pathway; however, activation of this pathway via CaR has not been described. Exposure of mTAL cells to Ca2+o (1.2mM) for 6 hr increased TNF production (control: 0.49±0.02; Ca2+: 2.26±0.06 pg TNF/μg protein). The CaR-selective agonist neomycin (100 μM) also increased TNF production. Transient transfection of mTAL cells with a dominant negative CaR (R796W) abolished Ca2+o- and neomycin-mediated TNF production in a concentration-dependent manner. These data indicate that the effects of extracellular Ca2+ and neomycin were dependent on signaling pathways initiated after stimulation of CaR. Additional evidence of TNF production via CaR-dependent signaling was provided, by demonstrating that inhibition of phospholipase C with U73122 (0.5 μM) or calmodulin kinase II with KN-62 (150 μM) abolished TNF production. Subsequently, CaR-mediated TNF production was inhibited by the calcineurin inhibitor cyclosporin A (CsA; 0.1 ng/ml) (control: 0.94±0.27; Ca2+: 2.25±0.21; CsA: 0.77±0.2; Ca2++CsA: 0.83±0.28 pg TNF/μg protein; p<0.001, n=4), implicating a role of downstream effectors of calcineurin in TNF gene transcription. Indeed, a peptide inhibitor (20 μM) of nuclear factor of activated T-cells (NF-AT) activation prevented CaR-mediated TNF production. Collectively, these data are the first to suggest that CaR-mediated TNF gene transcription in the mTAL is initiated via a Gq/11a signaling pathway that is calcineurin- and NF-AT-dependent. Characterization of the signaling pathways for CaR-dependent TNF production is crucial for understanding natriuretic/diuretic responses and metabolic disorders linked to CaR dysfunction.