Sustainable Low-Carbon Expansion for the Power Sector of an Emerging Economy: The Case of Kenya.

Fast growing and emerging economies face the dual challenge of sustainably expanding and improving their energy supply and reliability while at the same time reducing poverty. Critical to such transformation is to provide affordable and sustainable access to electricity. We use the capacity expansion model SWITCH to explore low carbon development pathways for the Kenyan power sector under a set of plausible scenarios for fast growing economies that include uncertainty in load projections, capital costs, operational performance, and technology and environmental policies. In addition to an aggressive and needed expansion of overall supply, the Kenyan power system presents a unique transition from one basal renewable resource-hydropower-to another based on geothermal and wind power for ∼90% of total capacity. We find geothermal resource adoption is more sensitive to operational degradation than high capital costs, which suggests an emphasis on ongoing maintenance subsidies rather than upfront capital cost subsidies. We also find that a cost-effective and viable suite of solutions includes availability of storage, diesel engines, and transmission expansion to provide flexibility to enable up to 50% of wind power penetration. In an already low-carbon system, typical externality pricing for CO2 has little to no effect on technology choice. Consequently, a "zero carbon emissions" by 2030 scenario is possible with only moderate levelized cost increases of between $3 and $7/MWh with a number of social and reliability benefits. Our results suggest that fast growing and emerging economies could benefit by incentivizing anticipated strategic transmission expansion. Existing and new diesel and natural gas capacity can play an important role to provide flexibility and meet peak demand in specific hours without a significant increase in carbon emissions, although more research is required for other pollutant's impacts.

Rethinking osteoporosis: balancing risk and benefit in diagnosis, prevention, and treatment.

The standard of care for osteoporosis is changing amid questions about the long-term safety and efficacy of curren drugs for preventing and treating osteoporosis. This article provides a guide for evidence-based treatment, but not over-treatment, as well as the selection and duration of available drug therapies.

Treatment of ovariectomized rats with 17ß-estradiol increases hepatic delta-6 desaturase enzyme expression and docosahexaenoic acid levels in hepatic and plasma phospholipids.

Higher docosahexaenoic acid (DHA) in females compared with males suggests ovarian hormones increase DHA production. Eight-week old rats were ovariectomized or sham operated (SHAM), and ovariectomized rats were treated with implanted pellets providing 17ß-estradiol (OVX+E), progesterone (OVX+P), both (OVX+PE) or neither (OVX) for 14 days. Immunoblot and fatty acid analysis were performed on all samples, and microarray analysis was performed on OVX and SHAM groups. Increased Δ6-desaturase in OVX relative to SHAM was observed by microarray (12% higher) and immunoblot (31% higher). OVX+E and OVX+PE rats had 39% and 42% higher Δ6-desaturase content, respectively, compared with OVX. OVX+E and OVX+PE also increased phospholipid DHA concentrations in liver (increase of 34% and 40%, respectively) and plasma (increase of 70% and 74%, respectively) relative to OVX. Progesterone exerted no effect on Δ6-desaturase or DHA. These results indicate that 17ß-estradiol increases DHA through increased Δ6-desaturase, possibly explaining sex differences in DHA.

Stearoyl-CoA desaturase 1, elongase 6 and their fatty acid products and precursors are altered in ovariectomized rats with 17ß-estradiol and progesterone treatment.

Sex differences in monounsaturated fatty acid (MUFA) levels suggest ovarian hormones may affect MUFA biosynthesis. Sprague-Dawley rats (8 weeks of age) were ovariectomized or sham operated with ovariectomized rats implanted with a constant-release hormone pellet providing 17ß-estradiol, progesterone, both or neither at 10 weeks of age. After 14 days, rats were fasted overnight and sacrificed to collect plasma and livers for analysis. Hepatic stearoyl-CoA desaturase (SCD1) expression was unchanged between ovariectomized and sham controls, as determined by microarray and immunoblotting. However, SCD1 protein was increased in rats treated with estradiol plus progesterone. Elongase 6 protein levels were increased with 17ß-estradiol treatment compared with sham. Rats treated with 17ß-estradiol and 17ß-estradiol plus progesterone had increased 16:0, 18:0, 16:1n-7 and 18:1n-7 in hepatic and plasma phospholipids. Ovarian hormones appear to be involved with MUFA biosynthesis, but the relationship appears complex and involves elongase 6 and SCD1.

Individual saturated and monounsaturated fatty acids trigger distinct transcriptional networks in differentiated 3T3-L1 preadipocytes.

BACKGROUND/AIMS: Saturated fatty acids (SFA) are widely thought to induce inflammation in adipose tissue (AT), while monounsaturated fatty acids (MUFA) are purported to have the opposite effect; however, it is unclear if individual SFA and MUFA behave similarly. Our goal was to examine adipocyte transcriptional networks regulated by individual SFA (palmitic acid, PA; stearic acid, SA) and MUFA (palmitoleic acid, PMA; oleic acid, OA). METHODS: Differentiated preadipocytes were treated with either 250 µM PA, SA, PMA, or OA for 48 h. Gene expression was analyzed using microarrays and real-time RT-PCR. Data were compared with those of a previous study reporting AT gene expression in humans following the consumption of SFA- or MUFA-enriched diets. RESULTS: Individual fatty acid treatments had significant effects on adipocyte gene expression. Functional analyses revealed that PA induced the TLR signalling pathway, while PMA had the opposite effect. SA and OA had similar effects, with increases in key metabolic pathways including mTOR and PPAR signalling and a reduction in TLR signalling. Ccl5 was validated as a candidate gene that may mediate the differential inflammatory effects of SFA and MUFA in AT. CONCLUSIONS: Individual SFA and MUFA trigger distinct transcriptional responses in differentiated preadipocytes, with inflammatory and metabolic pathways particularly sensitive to these fatty acids.