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This study aims to understand and examine the relationship between socio-demographic factors and the attitudes toward women managers in the context of the United Arab Emirates (UAE). This research paper is an exploratory research and we have taken into consideration a basic framework to understand the relationship that exists among different factors responsible for different perceptions and attitudes toward women managers. The literature review has focused on the various overarching perspectives of women managers and the attitudes formed by different societal actors. The paper draws mainly from the Social Learning Theory of Albert Bandura (1977). A sample of 213 employees was drawn to understand the relationship. The respondents were administered the well-established (Women as Managers Survey) WAMS questionnaire to get responses on various dimensions. Multivariate Regression Analysis using SPSS 26.0 version was applied to analyze the data. The findings of the study are parallel to previous works such that age, work experience, and educational level found support to the hypothesized relationship whereas gender and marital status did not. Limitations and future direction along with practical implications and recommendations are also given to draw suitable inferences. Keywords: Women Manager, Employee Attitude, Gender, Workplace and, UAE, 1. Introduction In the last 30 years, countries have made significant progress in bridging the gap between genders. From multinational companies to local companies, all have tried their best to [...]

Coronary reactive hyperemia (CRH) protects the heart against ischemia. Adenosine A2AAR-deficient (A2AAR-/-) mice have increased expression of soluble epoxide hydrolase (sEH); the enzyme responsible for breaking down the cardioprotective epoxyeicosatrienoic acids (EETs) to dihydroxyeicosatrienoic acids (DHETs). sEH-inhibition enhances CRH, increases EETs, and modulates oxylipin profiles. We investigated the changes of oxylipins and their impact on CRH in A2AAR-/- and wild type (WT) mice. We hypothesized that the attenuated CRH in A2AAR-/- mice is mediated by changes in oxylipin profiles, and that it can be reversed by either sEH- or ω-hydroxylases-inhibition. Compared to WT mice, A2AAR-/- mice had attenuated CRH and changed oxylipin profiles, which were consistent between plasma and heart perfusate samples, including decreased EET/DHET ratios, and increased hydroxyeicosatetraenoic acids (HETEs). Plasma oxylipns in A2AAR-/- mice indicated an increased proinflammatory state including increased ω-terminal HETEs, decreased epoxyoctadecaenoic/dihydroxyoctadecaenoic acids (EpOMEs/DiHOMEs) ratios, increased 9-hydroxyoctadecadienoic acid, and increased prostanoids. Inhibition of either sEH or ω-hydroxylases reversed the reduced CRH in A2AAR-/- mice. In WT and sEH-/- mice, blocking A2AAR decreased CRH. These data demonstrate that A2AAR-deletion was associated with changes in oxylipin profiles, which may contribute to the attenuated CRH. Also, inhibition of sEH and ω-hydroxylases reversed the reduction in CRH.

Arachidonic acid is metabolized to epoxyeicosatrienoic acids (EETs) by cytochrome (CYP) P450 epoxygenases, and to ω-terminal hydroxyeicosatetraenoic acids (HETEs) by ω-hydroxylases. EETs and HETEs often have opposite biologic effects; EETs are vasodilatory and protect against ischemia/reperfusion injury, while ω-terminal HETEs are vasoconstrictive and cause vascular dysfunction. Other oxylipins, such as epoxyoctadecaenoic acids (EpOMEs), hydroxyoctadecadienoic acids (HODEs), and prostanoids also have varied vascular effects. Post-ischemic vasodilation in the heart, known as coronary reactive hyperemia (CRH), protects against potential damage to the heart muscle caused by ischemia. The relationship among CRH response to ischemia, in mice with altered levels of CYP2J epoxygenases has not yet been investigated. Therefore, we evaluated the effect of endothelial overexpression of the human cytochrome P450 epoxygenase CYP2J2 in mice (Tie2-CYP2J2 Tr) on oxylipin profiles and CRH. Additionally, we evaluated the effect of pharmacologic inhibition of CYP-epoxygenases and inhibition of ω-hydroxylases on CRH. We hypothesized that CRH would be enhanced in isolated mouse hearts with vascular endothelial overexpression of human CYP2J2 through modulation of oxylipin profiles. Similarly, we expected that inhibition of CYP-epoxygenases would reduce CRH, whereas inhibition of ω-hydroxylases would enhance CRH. Compared to WT mice, Tie2-CYP2J2 Tr mice had enhanced CRH, including repayment volume, repayment duration, and repayment/debt ratio (P < 0.05). Similarly, inhibition of ω-hydroxylases increased repayment volume and repayment duration, in Tie2-CYP2J2 Tr compared to WT mice (P < 0.05). Endothelial overexpression of CYP2J2 significantly changed oxylipin profiles, including increased EETs (P < 0.05), increased EpOMEs (P < 0.05), and decreased 8-iso-PGF2α (P < 0.05). Inhibition of CYP epoxygenases with MS-PPOH attenuated CRH (P < 0.05). Ischemia caused a decrease in mid-chain HETEs (5-, 11-, 12-, 15-HETEs P < 0.05) and HODEs (P < 0.05). These data demonstrate that vascular endothelial overexpression of CYP2J2, through changing the oxylipin profiles, enhances CRH. Inhibition of CYP epoxygenases decreases CRH, whereas inhibition of ω-hydroxylases enhances CRH.

Coronary reactive hyperemia (CRH) is a physiological response to ischemic insult that prevents the potential harm associated with an interruption of blood supply. The relationship between the pharmacologic inhibition of soluble epoxide hydrolase (sEH) and CRH response to a brief ischemia is not known. sEH is involved in the main catabolic pathway of epoxyeicosatrienoic acids (EETs), which are converted into dihydroxyeicosatrienoic acids (DHETs). EETs protect against ischemia/reperfusion injury and have numerous beneficial physiological effects. We hypothesized that inhibition of sEH by t-AUCB enhances CRH in isolated mouse hearts through changing the oxylipin profiles, including an increase in EETs/DHETs ratio. Compared to controls, t-AUCB-treated mice had increased CRH, including repayment volume (RV), repayment duration, and repayment/debt ratio (p < 0.05). Treatment with t-AUCB significantly changed oxylipin profiles, including an increase in EET/DHET ratio, increase in EpOME/DiHOME ratio, increase in the levels of HODEs, decrease in the levels of mid-chain HETEs, and decrease in prostanoids (p < 0.05). Treatment with MS-PPOH (CYP epoxygenase inhibitor) reduced CRH, including RV (p < 0.05). Involvement of PPARγ in the modulation of CRH was demonstrated using a PPARγ-antagonist (T0070907) and a PPARγ-agonist (rosiglitazone). T0070907 reduced CRH (p < 0.05), whereas rosiglitazone enhanced CRH (p < 0.05) in isolated mouse hearts compared to the non-treated. These data demonstrate that sEH inhibition enhances, whereas CYP epoxygenases-inhibition attenuates CRH, PPARγ mediate CRH downstream of the CYP epoxygenases-EET pathway, and the changes in oxylipin profiles associated with sEH-inhibition collectively contributed to the enhanced CRH.

High-salt intake can change the effect of adenosine on arterial tone in mice. The aim of this study was to clarify the mechanism by which this occurs. Using aortas from mice fed a 4% NaCl (HS) or 0.45% NaCl (NS) diet for 4-5 wks, concentration-response curves for ACh, 5'-N-ethylcarboxamidoadenosine (NECA; adenosine analog) and 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride hydrate [CGS-21680; [A.sub.2A] adenosine receptor ([A.sub.2A] AR) agonist] were obtained with [N.sup.w]-nitro-L-arginine methyl ester (L-NAME; nitric oxide inhibitor, [10.sup.-4] M), methylsulfonyl-propargyloxyphenylhexanamide [MS-PPOH; a CYP (cytochrome P-450) epoxygenase blocker, [10.sup.-5] M including CYP2J2], 12-(3-adamantan-l-yl-ureido)dodecanoic acid [AUDA; soluble epoxide hydrolase (sEH) blocker, [10.sup.-5] M], dibromo-dodecenylmethylsulfimide [DDMS; CYP [omega]-hydroxylase (CYP4A blocker), [10.sup.-5] M], glibenclamide ([K.sub.ATP] channel blocker; [10.sup.-5] M) and 5-hydroxydecanoate (5-HD; mitochondrial-[K.sub.ATP] channel blocker, [10.sup.-4] M). HS dose response to ACh ([10.sup.-7] - [10.sup.-5] M) was not different from NS (P > 0.05). Relaxation to [10.sup.-6] M NECA was greater in the HS group (28.4 [+ or -] 3.9%) than in the NS group (4.1 [+ or -] 2.3%). Relaxation to [10.sup.-6] M CGS-21680 was also greater in HS (27.9 [+ or -] 4.5%) than in NS (4.9 [+ or -] 2.2%). L-NAME was able to block the dose response of ACh ([10.sup.-7] [10.sup.-5] M) equally in both HS and NS (P > 0.05), whereas L-NAME did not block CGS-21680-induced response in HS. In HS the CGS-21680 response was greatly reduced by MS-PPOH (to 4.7 [+ or -] 2.0%) and 5-HD (to 8.9 [+ or -] 2.2%), and also abolished by glibenclamide (-1.0 [+ or -] 5.9%). In NS, the CGS-21680 response was increased by AUDA (to 26.3 [+ or -] 3.4%) and DDMS (to 27.2 [+ or -] 3.0%). Compared with NS, HS vessels showed increased CYP2J2 and [A.sub.2A] AR expression (46 and 74% higher, respectively) but decreased sEH, CYP4A, and [A.sub.l] AR expression (75, 30, and 55% lower, respectively). These data suggest that in mice fed NS-containing diet, upregulation of arterial [A.sub.1] receptor causes vasoconstriction via increased sEH and CYP4A proteins. However, in mice fed HS-containing diet, upregulation of [A.sub.2A] receptor protein triggers vascular relaxation through ATP-sensitive ([K.sup.+]) channels via upregulation of CYP2J2 enzyme. [K.sub.ATP] channels; relaxation; contraction; adenosine doi: 10.1152/ajpregu.00823.2009.

Platelet-derived endothelial cell growth factor (PDECGF) is a potent angiogenic peptide with anti-apoptotic activity expressed widely in tumours. However, its expression in myocardial infarction (MI) is not yet established. This study aimed to assess the myocardial expression of PDECGF in rats after MI. Extracellular matrix (ECM) remodeling plays an important role in angiogenesis; hence, changes in the ECM components were investigated in the myocardium after MI, which was induced in rats by coronary artery ligation (CAL) and verified using biochemical markers and histopathology. Immunohistochemistry, RT-PCR, and activity assays identified the expression pattern of PDECGF on days 1, 2, 4, 8, 16, and 32 after CAL. The levels of TNF-α, MMP-2, collagen, and glycosaminoglyeans in the ECM were assessed. Studies on immunohistochemistry, RT-PCR. and PDECGF activity demonstrated elevated levels of PDECGF expression from day 2 after CAL. Macrophages, endothelial cells, fibroblasts, and cardiomyocytes, especially at the border region of the lesion, showed an enhanced expression for PDECGF. Remodeling of the ECM was depicted by changes in the levels of TNF-α. MMP-2. collagen, and GAG. Hence, this study clearly indicated PDECGF as an important angiogenic molecule expressed during Ml and the alterations in ECM components facilitated the process of angiogenesis. Key words: PDECGF, myocardial infarction, coronary artery ligation, angiogenesis. collagen. Le PDECGF (<< platelet-derived endothelial cell growth factor >>) est un puissant peptide angiogene possedant une activite anti-apoptotique, exprime largement dans les tumeurs. Son expression lors de Tinfarctus du myocarde (IM) reste encore a demontrer. Cette elude avail pour but d'evaluer l'expression du PDECGF dans le myocarde de rat apres un IM. Le remodelage de la malrice extra-cellulaire (MEC) joue un role important dans L'angiogenese el ce faisani, des ehangements dans la composition de la MEC ont ete etudies dans le myocarde apres un IM. L'IM a ete induit chez le rat par une ligature de l'artere coronaire (LAC) et confirme a Faide de marqueurs biochimiques et par histopathologic. L'immunohistochimie, la RT-PCR et des essais d'activite ont ete realises pour identifier le patron d'expression du PDECFG aux jours 1, 2, 4, 8, 16 et 32 apres la LAC. Les niveaux de TNF-α. de MMP-2, de collagene et de glycosaminoglycanes de la MEC ont ete evalues. Les etudes en immunohistochimie. par RT-PCR et par mesure de l'activite du PDECGF ont mis en evidence des niveaux eleves d'expression de PDECGF a partir du jour 2 apres la LAC. Les macrophages, les cellules endotheliales, les fibroblastes et les cardiomyocytes retrouves specialement a la bordure de la region lesee, exprimaient davantage de PDECGF. Le remodelage de la MEC etait caracterise par des changements dans les niveaux de TNF-α, de MMP-2, de collagene et de GAG. Ainsi, cette etude a clairement demontre que le PDECGF est une importante molecule angiogene exprimee lors de l'IM el que les modifications de la composition de la MEC ont facilite le processus d'angiogenese. Mots-cles : PDECGF, infarctus du myocarde, ligature de l'artere coronaire. angiogenese. collagene. [Traduit par la Redaction], Introduction Angiogenesis is a complex multistep process controlled by a number of factors such as platelet-derived endothelial cell growth factor (PDECGF), also known as thymidine phosphorylasc or gliostatin. PDECGF has [...]

We hypothesize that [A.sub.2A] adenosine receptors ([A.sub.2A] AR) promote aortic relaxation in mice through cytochrome P450 (CYP)-epoxygenases and help to avoid salt sensitivity. Aortas from male mice maintained on a high-salt (HS; 7% NaCl) or normal-salt (NS; 0.45% NaCL) diet for 4-5 wks were used. Concentration-response curves ([10.sup.-11]-[10.sup.-5] M) for 5'-N-ethylcarboxamidoadenosine (NECA; a nonselective adenosine analog) and CGS 21680 ([A.sub.2A] AR agonist) were obtained with different antagonists including ZM 241385 ([A.sub.2A] AR antagonist; [10.sup.-6] M), SCH 58261 ([A.sub.2A] AR antagonist; [10.sup.-6] M), [N.sup.[omega]]-nitro-L-arginine methyl ester (L-NAME; endothelial nitric oxide synthase inhibitor; [10.sup.-4] M) and inhibitors including methylsulfonyl-propargyloxyphenylhexanamide (MS-PPOH; CYP epoxygenases inhibitor; [10.sup.-5]M), 14,15-epoxyeicosa-5(z)-enoic acid (14,15-EEZE; EET antagonist; [10.sup.-5]M), dibromo-dodecenyl-methylsulfimide (DDMS; CYP4A inhibitor; [10.sup.-5]M), and HET0016 (20-HETE inhibitor; [10.sup.-5]M). At [10.sup.-7] M of NECA, significant relaxation in HS (+22.58 [+ or -] 3.12%) was observed compared with contraction in NS (-10.62 [+ or -] 6.27%, P < 0.05). ZM 241385 changed the NECA response to contraction (P < 0.05) in HS. At [10.sup.-7] M of CGS 21680, significant relaxation in HS (+32.04 [+ or -] 3.08%) was observed compared with NS (+ 10.45 [+ or -] 1.34%, P < 0.05). SCH 58261, L-NAME, MS-PPOH, and 14,15-EEZE changed the CGS 21680-induced relaxation to contraction (P < 0.05) in HS. Interestingly, DDMS and HET0016 changed CGS 21680 response to relaxation (P < 0.05) in NS; however, there was no significant difference found between DDMS, HET0016-treated HS and NS vs. nontreated HS group (P > 0.05). CYP2C29 protein was 55% and 74% upregulated in HS vs. NS (P < 0.05) mice aorta and kidney, respectively. CYP4A protein was 30.30% and 35.70% upregulated in NS vs. HS (P < 0.05) mice aorta and kidneys, respectively. [A.sub.1] AR was downregulated, whereas [A.sub.2A] AR was upregulated in HS compared with NS. These data suggest that HS may activate CYP2C29 via [A.sub.2A] AR, causing relaxation, whereas NS may contribute to the upregulation of CYP4A causing contraction. vasodilation; vasoconstriction

We hypothesized that [A.sub.2A]adenosine receptor ([A.sub.2A]AR) activation causes vasorelaxation through cytochrome P-450 (CYP) epoxygenases and endothelium-derived hyperpolarizing factors, whereas lack of [A.sub.2A]AR activation promotes vasoconstriction through Cyp4a in the mouse aorta. Adenosine 5'-N-ethylcarboxamide (NECA; [10.sup.-6] M), an adenosine analog, caused relaxation in wild-type [A.sub.2A]AR ([A.sub.2A][AR.sup.+/+]; +33.99 [+ or -] 4.70%, P < 0.05) versus contraction in [A.sub.2A]AR knockout ([A.sub.2A][AR.sup.-/-]; -27.52 [+ or -] 4.11%) mouse aortae. An [A.sub.2A]AR-specific antagonist (SCH-58261; 1 [micro]M) changed the NECA ([10.sup.-6] M) relaxation response to contraction (-35.82 [+ or-] 4.69%, P < 0.05) in [A.sub.2A][AR.sup.+/+] aortae, whereas no effect was noted in [A.sub.2A][AR.sup.-/-] aortae. Significant contraction was seen in the absence of the endothelium in [A.sub.2A][AR.sup.+/+] (-2.58 [+ or -] 2.25%) aortae compared with endothelium-intact aortae. An endothelial nitric oxide synthase inhibitor (N-nitro-L-arginine methyl ester; 100 [micro]M) and a cyclooxygenase inhibitor (indomethacin; 10 [micro]M) failed to block NECA-induced relaxation in [A.sub.2A][AR.sup.+/+] aortae. A selective inhibitor of CYP epoxygenases (methylsulfonyl-propargyloxyphenylhexanamide; 10 [micro]M) changed NECA-mediated relaxation (-22.74 [+ or -] 4- 5.11% at [10.sup.-6] M) and CGS-21680-mediated relaxation (-18.54 [+ or -] 6.06% at [10.sup.-6] M) to contraction in [A.sub.2A][AR.sup.+/+] aortae, whereas no response was noted in [A.sub.2A][AR.sup.-/-] aortae. Furthermore, an epoxyeicosatrienoic acid (EET) antagonist [14,15-epoxyeicosa-5(Z)-enoic acid; 10 [micro]M] was able to block NECA-induced relaxation in [A.sub.2A][AR.sup.+/+] aortae, whereas to [omega]-hydroxylase inhibitors (10 [micro]M dibromo-dodecenyl-methylsulfimide and 10 [micro]M HET0016) changed contraction into relaxation in [A.sub.2A][AR.sup.-/-] aorta. Cyp2c29 protein was upregulated in [A.sub.2A][AR.sup.+/+] aortae, whereas Cyp4a was upregulated in [A.sub.2A][AR.sup.-/-] aortae. Higher levels of dihydroxyeicosatrienoic acids (DHETs; 14,15-DHET, 11,12-DHET, and 8,9-DHET, P < 0.05) were found in [A.sub.2A][AR.sup.+/+] versus [A.sub.2A][AR.sup.-/-] aortae. EET levels were not significantly different between [A.sub.2A][AR.sup.+/+] and [A.sub.2A][AR.sup.-/-] aortae. It is concluded that CYP epoxygenases play an important role in [A.sub.2A]AR-mediated relaxation, and the deletion of the [A.sub.2A]AR leads to contraction through Cyp4a. epoxyeicosatrienoic acids; dihydroxyeicosatrienoic acids; vasodilation; vasoconstriction; adenosine; cytochrome P-450s