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Ang bulag at ang pag-ibig: Isang pag-aaral tungkol sa interpersonal attraction ng mga bulag
No full textAng pag-aaral na ito ay tungkol sa interpersonal attraction ng mga bulag. Ang layunin ng papel na ito ay alamin kung ano: (1) ang proseso ng interpersonal na attraction ang dinadaanan ng mga bulag at (2) ang basehan ng interpersonal attraction para sa mga bulag. Gumamit ng disenyong descriptive ang pag-aaral na ito. Sa pagkalap ng datos ay ginamit ang di-tuwirang malalimang pakikipanayam. Kinalap ang datos mula sa anim na mag-asawang bulag na: (1) nabulag bago sila tumuntong sa gulang na 6 at pataas: (2) nasa edad na 25 at pataas at (3) may limang taon nang kasal. Ang mga datos na nakalap ay sinuri sa pamamagitan ng content analysis at cross-case analysis. Sa pagsusuring nagawa, nabatid na ang basehan ng interpersonal attraction para sa mga bulag ay ang boses at ugali. Ang huli ay nakabuo ng konseptual na balangkas ng proseso ng interpersonal attraction ng mga bulag
Angiotensin II induces soluble fms-Like tyrosine kinase-1 release via calcineurin signaling pathway in pregnancy
Get PDFMaternal endothelial dysfunction in preeclampsia is associated with increased soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating antagonist of vascular endothelial growth factor and placental growth factor. Angiotensin II (Ang II) is a potent vasoconstrictor that increases concomitant with sFlt-1 during pregnancy. Therefore, we speculated that Ang II may promote the expression of sFlt-1 in pregnancy. Here we report that infusion of Ang II significantly increases circulating levels of sFlt-1 in pregnant mice, thereby demonstrating that Ang II is a regulator of sFlt-1 secretion in vivo. Furthermore, Ang II stimulated sFlt-1 production in a dose- and time-dependent manner from human villous explants and cultured trophoblasts but not from endothelial cells, suggesting that trophoblasts are the primary source of sFlt-1 during pregnancy. As expected, Ang II-induced sFlt-1 secretion resulted in the inhibition of endothelial cell migration and in vitro tube formation. In vitro and in vivo studies with losartan, small interfering RNA specific for calcineurin and FK506 demonstrated that Ang II-mediated sFlt-1 release was via Ang II type 1 receptor activation and calcineurin signaling, respectively. These findings reveal a previously unrecognized regulatory role for Ang II on sFlt-1 expression in murine and human pregnancy and suggest that elevated sFlt-1 levels in preeclampsia may be caused by a dysregulation of the local renin/angiotensin system
Ang-2 over-expression impairs islet function but protects from cytokine treatment in isolated islets.
No full textIsolated islets from RIP-rtTA;tet-O-Ang-2 (Ang2-rtTA) and RIP-rtTA control (rtTA) mice were cultured for 3 days in presence of 10 μg/ml doxycycline to achieve Ang-2 overexpression. Mouse or human islets were cultured in 11.1 (mouse) or 5.5 mM glucose (human) or treated with diabetic conditions of 22.2 mM glucose + 0.5mM palmitic acid or mixture of cytokines: 2 ng/mL IL-1β, 1000 U/ml IFN-ɣ and TNF-α (cyto). (A) Western blot from treated mouse islets shows Ang-2 overexpression in islets by myc-Ang-2. (B) GSIS is shown by the stimulatory index assessed by 16.7/2.8 mM glucose stimulation and normalized to control. (C,D) Treated mouse islets fixed post-GSIS and apoptotic cells detected by double staining for TUNEL and insulin. Representative images from different treatments. (E,F) qPCR analysis for CD31 (E) and ICAM (F) from mouse islets overexpressing Ang-2. (G,H) Representative western blots (upper panel) and densitometric analyses of proteins (lower panels) showing myc-Ang-2, ICAM-1, cleaved caspase 3 and actin/tubulin as housekeeping control, in human islets overexpressing Ang-2 by Ad-Ang-2 or control Ad-GFP (G; MOI = 50) or treated with 100 nM Tie-2 inhibitor for 72h (H). Data are means +/-SE from 3–5 independent experiments from 3–5 different organ donors (human islets) or 3–5 independent mouse islet isolations. *p<0.05, treated vs. 11.1 mM glucose control, #p<0.05, Ang2-rtTA vs. rtTA.</p
c-Src inhibition improves cardiovascular function but not remodeling or fibrosis in Ang II-induced hypertension
Get PDFc-Src plays an important role in angiotensin II (Ang II) signaling. Whether this member of the Src family kinases is involved in the development of Ang II–induced hypertension and associated cardiovascular damage in vivo remains unknown. Here, we studied Ang II–infused (400 ng/kg/min) mice in which c-Src was partially deleted (c-Src+/−) and in wild-type (WT, c-Src+/+) mice treated with a c-Src inhibitor (CGP077675; 25 mg/kg/d). Ang II increased blood pressure and induced endothelial dysfunction in WT mice, responses that were ameliorated in c-Src+/− and CGP077675-treated mice. Vascular wall thickness and cross-sectional area were similarly increased by Ang II in WT and c-Src+/− mice. CGP077675 further increased cross-sectional area in hypertensive mice. Cardiac dysfunction (ejection fraction and fractional shortening) in Ang II–infused WT mice was normalized in c-Src+/− mice. Increased oxidative stress (plasma thiobarbituric acid–reactive substances, hydrogen peroxide, and vascular superoxide generation) in Ang II–infused WT mice was attenuated in c-Src–deficient and CGP077675-treated mice. Hyperactivation of vascular c-Src, ERK1/2 (extracellular signal–regulated kinase 1/2), and JNK (c-Jun N-terminal kinase) in hypertensive mice was normalized in CGP077675-treated and c-Src+/− mice. Vascular fibronectin was increased by Ang II in all groups and further augmented by CGP077675. Cardiac fibrosis and inflammation induced by Ang II were amplified in c-Src+/− and CGP-treated mice. Our data indicate that although c-Src downregulation attenuates development of hypertension, improves endothelial and cardiac function, reduces oxidative stress, and normalizes vascular signaling, it has little beneficial effect on fibrosis. These findings suggest a divergent role for c-Src in Ang II–dependent hypertension, where c-Src may be more important in regulating redox-sensitive cardiac and vascular function than fibrosis and remodeling
Ang-II stimulates proliferation in melanoma cells.
No full text(A) Real-Time PCR analysis for expression of ACE in melan-a and TM-5 cells. (B) ACE activity measured by cleavage of Abz-FRK(Dnp)P-OH in melan-a and TM-5 cells. For A and B, mean ± S.E.M, n = 6 (**p<0.01). (C-D) BrDU uptake assay 24 hours after stimulation with Ang-II (1μM) in the presence of lisinopril (1μM), showing inhibition of cell proliferation in TM-5 cells (D) but not in melan-a cells (C). Mean ± S.E.M., n = 6. (*p<0.05).</p
C-97G Stratofreighter painting
No full textThe C-97G Stratofreighter was a starategic airlifter transport flown by the DE ANG from 1962-197
C-45 Expeditor painting
No full textThe Beehcraft C-45 Expeditor was used as a light transport and liaison airraft in the later 1050's by the DE ANG. Signed Acrylic Painting
C-97G Stratofreighter painting
No full textThe C-97G Stratofreighter was a starategic airlifter transport flown by the DE ANG from 1962-197
Role of protein kinase C in renal vasoconstriction caused by angiotensin II
Get PDFIn this study we have examined the subcellar pathways along which angiotensin II (ANG II) causes renal vasoconstriction. Using the isolated perfused rat kidney model, we found that renal vasoconstriction produced by ANG II (100 pM) was not altered by the calmodulin antagonists calmidazolium (1 microM) and N-(6-aminohexyl)-5-chloro-1-naphthalensulfonamide (W-7, 10 microM) but was blunted by staurosporine (100 nM) and 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H-7, 50 microM), two structurally distinct putative protein kinase C inhibitors. The phorbol ester 4 alpha-phorbol 12,13-didecanoate (1-100 nM) did not alter renal vascular resistance, whereas phorbol 12-myristate 13-acetate (PMA, 1-100 nM) caused potent and dose-dependent vasoconstriction that was prevented by staurosporine (100 nM) and H-7 (50 microM). The vasoconstrictory effects of ANG II and PMA were attenuated by the calcium channel blockers verapamil (5 microM) and nifedipine (5 microM) and were reversibly inhibited when cobaltous chloride (2 mM) was added to the perfusate. Taken together, our findings support the concept that the renal vasoconstrictory effect of ANG II is essentially mediated by protein kinase C activation, which either requires or enhances the entrance of extracellular calcium
C-45 Expeditor painting
No full textThe Beehcraft C-45 Expeditor was used as a light transport and liaison airraft in the later 1050's by the DE ANG. Signed Acrylic Painting
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