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Beersheba, Israel

Kamari Y.,Hypertension Unit | Kamari Y.,Bert rassburger Lipid Center | Kamari Y.,Tel Aviv University | Peleg E.,Hypertension Unit | And 4 more authors.
American Journal of Hypertension | Year: 2012

Background Premenopausal women have lower blood pressure (BP) levels than men of similar age. Adiponectin has been shown to play a role in the pathogenesis of hypertension. The aim of the present study was to compare the effect of various stress stimuli on BP and plasma adiponectin levels in male and female Sprague Dawley (SD) rats. Methods In three experimental models of hypertension, fructose-enriched diet, high salt diet, or L-NAME, were administered for up to 4 weeks. BP, metabolic parameters, and plasma adiponectin were measured at baseline and during the studies. The fructose diet protocol was repeated in female rats for 2 weeks with the addition of testosterone injections or vehicle. Results Females, in contrast to males, did not develop fructose-induced hypertension. Total plasma triglycerides (TGs) were half in females at baseline (P < 0.001) and a third at 4 weeks (P < 0.05). Plasma insulin levels were 23% lower in females than in males at baseline (P < 0.05) and 42% lower after 4 weeks of fructose-enriched diet (P = 0.001). Plasma adiponectin levels were 65% higher in females than in males at baseline (P = 0.001) and 45% higher after 4 weeks of fructose-enriched diet (P < 0.05). Furthermore, female rats showed blunted BP response and elevated plasma adiponectin in the salt-induced and L-NAME-induced hypertension models. Testosterone injection to female rats reduced plasma adiponectin and reversed the blunted BP response. Conclusions Elevated plasma adiponectin levels, perhaps due to lack of suppression by testosterone, are associated with a blunting of BP response in female compared to male SD rats. © 2012 American Journal of Hypertension, Ltd.

Hollander K.S.,Minerva Center for Cholesterol | Konikoff F.M.,Minerva Center for Cholesterol | Fainaru M.,Tel Aviv University | Leikin-Frenkel A.,Minerva Center for Cholesterol | And 2 more authors.
Archives of Physiology and Biochemistry | Year: 2014

Objective: Our objective was to test the contribution of dietary enrichment in essential or saturated fatty acids, in normocaloric diets, on the lipid accumulation and insulin resistance in the adult offspring in a C57Bl6/J mice model. Methods: Pregnant mothers were fed normocaloric diets containing 6% fat enriched in essential fatty acids (EFA): alpha-linolenic (ALA-18:3, n-3), linoleic (LA-18:2, n-6), or saturated fatty acids (SFA). After a washing-out period with regular diet, the offspring received a high-fat diet before euthanization. Results: Adult mice fed maternal ALA showed lower body weight gain and lower liver fat accumulation, lower HOMA index and lower stearoyl-CoA desaturase (SCD1) activity than those fed maternal SFA. Conclusion: The results observed using this novel model suggest that ALA in maternal diet may have the potential to inhibit insulin resistance in adult offspring. © 2014 Informa UK Ltd.

Bitzur R.,Bert rassburger Lipid Center
Diabetes Care | Year: 2016

The issue of statin-associated cognitive impairment has been a hot topic among both patients and health care providers, especially since the U.S. Food and Drug Administration (FDA) issued a statement regarding rare postmarketing reports of ill-defined cognitive impairment associated with statin use. This statement was based on case reports, and no objectivemeasures of cognitive functionwere used. Nevertheless,many patients at high risk of cardiovascular disease have expressed concerns about possible cognitive decline and may have opted to forgo statin therapy. In this overview, the evidence leading to the statement by the FDA is reviewed. Potential mechanisms of the effect of LDL cholesterol reduction and statin therapy on cognition are discussed. Evidence from observational and prospective randomized trials is summarized, leading to the conclusion that as for now, there is no good evidence that statins cause cognitive impairment to a significant degree. Reported cases seem to be rare, and a causal relationship has not been established.

Sharir R.,Heart Institute | Sharir R.,Hebrew University of Jerusalem | Sharir R.,Tel Aviv Sourasky Medical Center | Sharir R.,Tel Aviv University | And 12 more authors.
Cardiovascular Research | Year: 2014

Aims Ischaemic damage is associated with up-regulation of pro-inflammatory cytokines, as well as invasion of leucocytes and lymphocytes to the injured muscle. Regulatory T cells (Tregs) exert suppressive effects on several immune and nonimmunecellular elements.We hypothesized that adoptive Treg cell transfer and depletion will influence re-establishment of flow in the hindlimb ischaemia model, and that this effect would be mediated by the cytokine interleukin (IL)-10. Methods and results To study the functional role of Tregs in hindlimb ischaemia, we either adoptively transferred Tregs or functionally blocked Tregs by antibodies to CD25. Initially, we showed that the number and function of Tregs is altered after the induction of ischaemia. Treg ablation resulted in reduced blood flow by laser Doppler at Day 7 that became more robust at Day 14. Adoptive Treg transfer led to a significant improvement of flow in the ligated limb. Treg-mediated improvement in flow was abolished by employing blocking anti-IL-10 antibodies. Conclusions These results show thatTregs play an important role in processes that control flowre-establishment after inducible hindlimb ischaemia, and that IL-10 plays a requisite role mediating these effects. © The Author 2014.

Ben-David U.,Hebrew University of Jerusalem | Gan Q.-F.,Hoffmann-La Roche | Golan-Lev T.,Hebrew University of Jerusalem | Arora P.,Hoffmann-La Roche | And 9 more authors.
Cell Stem Cell | Year: 2013

The use of human pluripotent stem cells (hPSCs) in cell therapy is hindered by the tumorigenic risk from residual undifferentiated cells. Here we performed a high-throughput screen of over 52,000 small molecules and identified 15 pluripotent cell-specific inhibitors (PluriSIns), nine of which share a common structural moiety. The PluriSIns selectively eliminated hPSCs while sparing a large array of progenitor and differentiated cells. Cellular and molecular analyses demonstrated that the most selective compound, PluriSIn #1, induces ER stress, protein synthesis attenuation, and apoptosis in hPSCs. Close examination identified this molecule as an inhibitor of stearoyl-coA desaturase (SCD1), the key enzyme in oleic acid biosynthesis, revealing a unique role for lipid metabolism in hPSCs. PluriSIn #1 was also cytotoxic to mouse blastocysts, indicating that the dependence on oleate is inherent to the pluripotent state. Finally, application of PluriSIn #1 prevented teratoma formation from tumorigenic undifferentiated cells. These findings should increase the safety of hPSC-based treatments. © 2013 Elsevier Inc.

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