Determinants of genetically modified (GM) maize adoption and the intensity of adoption in OR Tambo District Municipality, Eastern Cape Province, South Africa.

The objective of the study was to establish the factors that have significant correlation with the increase in adoption and intensity of adoption of genetically modified (GM) maize varieties. The study utilized a cross-sectional, descriptive and quantitative survey of smallholder dry maize producers. Multiple purposive sampling was utilized in the selection of 704 respondents and semi-structured interviews and pre-coded questionnaires were adopted as data collection instruments. The study sites were Mqanduli, Port St Johns and Flagstaff in King Sabatha Dalindyebo, Port St Johns and Ingquza Hill Local Municipalities in OR Tambo District Municipality. Through a Cragg's double hurdle model, the study revealed that level of education (1% level), membership to a farmer group (5% level), access to extension services and farm size (5% level) had significant positive influence on the decision to adopt GM maize. Intensity of use of GM maize was positively influenced by membership to a farmers group (5% level), access to extension services (5% level) and farm size (1% level). The study concluded that being part of a farmer organization, education, access to extension services and farm size were the most significant determinants in the dual decision to adopt GM maize and the intensity of utilization of GM maize. The study recommends awareness in line with the implemented policies and GM information dissemination toward farmer groups be promoted. The study also recommends that a balance be struck between optimization of land size devoted to GM maize and its subsequent adoption and extensive use thereof.

Effect of radiation and repeated sub-culturing on the transforming growth factor-ß1 signaling pathway in FRTL-5 cells.

BACKGROUND/AIM: Fisher rat thyroid cells (FRTL-5) display increased proliferation, reduced follicularization and decreased thyroxin release with repeated sub-culturing. These changes occur earlier and more rapidly following exposure to ionizing radiation. We hypothesized that altered transforming growth factor-ß1 (TGF-ß1) signaling contributes to these differences. MATERIALS AND METHODS: Assessments included FRTL-5 cell growth rate and quantification of TGF-ß1 ligand and receptors. The levels and activity of Smads2, 3 and 4 were measured by western blotting and the ability of TGF-ß1 to regulate cyclin A and plasminogen activator inhibitor type 1 (PAI-1) activity was assessed using transfection assays. RESULTS: TGF-ß1 production increased after radiation but returned to control levels after repeated sub-culturing. There was no difference in TGF-ß1 levels between un-irradiated cells at low versus high-passage number. TGF-ß1 receptors and basal levels of Smads2, 3 and 4 remained unchanged. However, there were significant changes in cell proliferation, TGF-ß1-mediated Smads2 and 3 activation and in TGF-ß1's ability to regulate cyclin A and PAI-1 transcription in irradiated and repeatedly sub-cultured cells (p<0.05). CONCLUSION: Collectively, these results support the conclusion that alterations in the TGF-ß1 pathway contribute to phenotypic changes in FRTL-5 cells as a function of passage number and radiation.

Higher estrogen levels during pregnancy in Andean than European residents of high altitude suggest differences in aromatase activity.

CONTEXT: Uteroplacental hypoxia has been reported to lower estrogen levels in preeclampsia as the result of reduced aromatase activity. OBJECTIVE: We asked whether the chronic hypoxia of residence at high altitude in the absence of preeclampsia lowered estrogen, whether such effects differed in Andean vs European high-altitude residents, and whether such effects were related to uterine artery diameter or blood flow. DESIGN, SETTING, AND PARTICIPANTS: Studies at weeks 20 and 36 of pregnancy were conducted in 108 healthy Bolivian low- (400 m, n = 53) or high-altitude (3600 m, n = 55) residents of European (n = 28 low and 26 high altitude) or Andean (n = 25 low and 29 high altitude) ancestry. All groups were similar in age, nonpregnant body mass index, and pregnancy weight gain. RESULTS: High-altitude residence increased circulating progesterone, cortisol, estrone, 17ß-estradiol, and estriol levels (all P < .01). High-altitude Andeans vs Europeans at week 36 had higher progesterone, estrone, 17ß-estradiol, and estriol levels as well as product to substrate ratios for the reactions catalyzed by aromatase, whereas week 36 cortisol levels were greater in the European than Andean women (all P < .05). Lower cortisol, higher estriol (both P < .01), and trends for higher progesterone and 17ß-estradiol levels were associated with greater uterine artery diameters and blood flow at high altitude. CONCLUSIONS: Chronic hypoxia does not lower but rather raises estrogen levels in multigenerational Andeans vs shorter-term Europeans, possibly as the result of greater aromatase activity. Because hypoxia alone does not lower estrogen, other attributes of the disease may be responsible for the lower estrogen levels seen previously in preeclamptic women.

Pregnancy increases myometrial artery myogenic tone via NOS- or COX-independent mechanisms.

Myogenic tone (MT) is a primary modulator of blood flow in the resistance vasculature of the brain, kidney, skeletal muscle, and perhaps in other high-flow organs such as the pregnant uterus. MT is known to be regulated by endothelium-derived factors, including products of the nitric oxide synthase (NOS) and/or the cyclooxygenase (COX) pathways. We asked whether pregnancy influenced MT in myometrial arteries (MA), and if so, whether such an effect could be attributed to alterations in NOS and/or COX. MA (200-300 µm internal diameter, 2-3 mm length) were isolated from 10 nonpregnant and 12 pregnant women undergoing elective hysterectomy or cesarean section, respectively. In the absence of NOS and/or COX inhibition, pregnancy was associated with increased MT in endothelium-intact MA compared with MA from nonpregnant women (P < 0.01). The increase in MT was not due to increased Ca(2+) entry via voltage-dependent channels since both groups of MA exhibited similar levels of constriction when exposed to 50 mM KCl. NOS inhibition (N(ω)-nitro-L-arginine methyl ester, L-NAME) or combined NOS/COX inhibition (L-NAME/indomethacin) increased MT in MA from pregnant women (P = 0.001 and P = 0.042, respectively) but was without effect in arteries from nonpregnant women. Indomethacin alone was without effect on MT in MA from either nonpregnant or pregnant women. We concluded that MT increases in MA during human pregnancy and that this effect was partially opposed by enhanced NOS activity.

Capsaicin pre-treatment provides neurovascular protection against neonatal hypoxic-ischemic brain injury in rats.

Capsaicin, a transient receptor potential vanilloid 1 (TRPV1) agonist, has recently been shown to provide neuroprotection against brain injury in experimental adult models of cerebral ischemia. Accordingly, in this study, we investigated the way in which capsaicin-mediated TRPV1 modulation could attenuate damage in an experimental hypoxic-ischemic (HI) neonatal brain injury model. The Rice-Vannucci method was used in 10-day-old rat pups by performing unilateral carotid artery ligation followed by 2 h of hypoxia (8% O2 at 37°C). Capsaicin was administered intraperitoneally (0.2 mg/kg or 2.0 mg/kg) at 3 h pre-HI or 1 h post-HI. Post assessment included measurement of infarction volume at 24 and 72 h in addition to an assessment of the vascular dynamics of the middle cerebral artery (MCA) at 6 h post-HI. The results indicated that pre-treatment with capsaicin reduced infarction volume significantly with either low-dose or high-dose treatment. Pre-treatment also improved myogenic tone and decreased apoptotic changes in the distal MCA. We concluded that capsaicin pre-treatment may provide neurovascular protection against neonatal HI.

Humans at high altitude: hypoxia and fetal growth.

High-altitude studies offer insight into the evolutionary processes and physiological mechanisms affecting the early phases of the human lifespan. Chronic hypoxia slows fetal growth and reduces the pregnancy-associated rise in uterine artery (UA) blood flow. Multigenerational vs. shorter-term high-altitude residents are protected from the altitude-associated reductions in UA flow and fetal growth. Presently unknown is whether this fetal-growth protection is due to the greater delivery or metabolism of oxygen, glucose or other substrates or to other considerations such as mechanical factors protecting fragile fetal villi, the creation of a reserve protecting against ischemia/reperfusion injury, or improved placental O(2) transfer as the result of narrowing the A-V O(2) difference and raising uterine P(v)O2. Placental growth and development appear to be normal or modified at high altitude in ways likely to benefit diffusion. Much remains to be learned concerning the effects of chronic hypoxia on embryonic development. Further research is required for identifying the fetoplacental and maternal mechanisms responsible for transforming the maternal vasculature and regulating UA blood flow and fetal growth. Genomic as well as epigenetic studies are opening new avenues of investigation that can yield insights into the basic pathways and evolutionary processes involved.

Diabetes and adverse mental health among African Americans.

This article reviews the connection between diabetes and adverse mental health among African Americans. Concern about safe insulin prescribing and administration is raised, and the importance of integrated physical and mental health care in the prevention and control of diabetes is highlighted.

Roles of cytosolic Ca2+ concentration and myofilament Ca2+ sensitization in age-dependent cerebrovascular myogenic tone.

In light of evidence that immature arteries contain a higher proportion of noncontractile smooth muscle cells than found in fully differentiated mature arteries, the present study explored the hypothesis that age-related differences in the smooth muscle phenotype contribute to age-related differences in contractility. Because Ca(2+) handling differs markedly between contractile and noncontractile smooth muscle, the present study specifically tested the hypothesis that the relative contributions of Ca(2+) influx and myofilament sensitization to myogenic tone are upregulated, whereas Ca(2+) release is downregulated, in immature [14 days postnatal (P14)] compared with mature (6 mo old) rat middle cerebral arteries (MCAs). Myofilament Ca(2+) sensitivity measured in ß-escin-permeabilized arteries increased with pressure in P14 but not adult MCAs. Cyclopiazonic acid (an inhibitor of Ca(2+) release from the sarcoplasmic reticulum) increased diameter and reduced Ca(2+) in adult MCAs but increased diameter with no apparent change in Ca(2+) in P14 MCAs. La(3+) (Ca(2+) influx inhibitor) increased diameter and decreased Ca(2+) in adult MCAs, but in P14 MCAs, La(3+) increased diameter with no apparent change in Ca(2+). After treatment with both La(3+) and CPA, diameters were passive in both adult and P14 MCAs, but Ca(2+) was decreased only in adult MCAs. To quantify the fraction of smooth muscle cells in the fully differentiated contractile phenotype, extents of colocalization between smooth muscle α-actin and SM2 myosin heavy chain were determined and found to be at least twofold greater in adult than pup MCAs. These data suggest that compared with adult MCAs, pup MCAs contain a greater proportion of noncontractile smooth muscle and, as a consequence, rely more on myofilament Ca(2+) sensitization and Ca(2+) influx to maintain myogenic reactivity. The inability of La(3+) to reduce cytosolic Ca(2+) in the pup MCA appears due to La(3+)-insensitive noncontractile smooth muscle cells, which contribute to the spatially averaged measurements of Ca(2+) but not contraction.

Postnatal maturation attenuates pressure-evoked myogenic tone and stretch-induced increases in Ca2+ in rat cerebral arteries.

Although postnatal maturation potently modulates agonist-induced cerebrovascular contractility, its effects on the mechanisms mediating cerebrovascular myogenic tone remain poorly understood. Because the regulation of calcium influx and myofilament calcium sensitivity change markedly during early postnatal life, the present study tested the general hypothesis that early postnatal maturation increases the pressure sensitivity of cerebrovascular myogenic tone via age-dependent enhancement of pressure-induced calcium mobilization and myofilament calcium sensitivity. Pressure-induced myogenic tone and changes in artery wall intracellular calcium concentrations ([Ca(2+)](i)) were measured simultaneously in endothelium-denuded, fura-2-loaded middle cerebral arteries (MCA) from pup [postnatal day 14 (P14)] and adult (6-mo-old) Sprague-Dawley rats. Increases in pressure from 20 to 80 mmHg enhanced myogenic tone in MCA from both pups and adults although the normalized magnitudes of these increases were significantly greater in pup than adult MCA. At each pressure step, vascular wall [Ca(2+)](i) was also significantly greater in pup than in adult MCA. Nifedipine significantly attenuated pressure-evoked constrictions in pup MCA and essentially eliminated all responses to pressure in the adult MCA. Both pup and adult MCA exhibited pressure-dependent increases in calcium sensitivity, as estimated by changes in the ratio of pressure-induced myogenic tone to wall [Ca(2+)](i). However, there were no differences in the magnitudes of these increases between pup and adult MCA. The results support the view that regardless of postnatal age, changes in both calcium influx and myofilament calcium sensitivity contribute to the regulation of cerebral artery myogenic tone. The greater cerebral myogenic response in P14 compared with adult MCA appears to be due to greater pressure-induced increases in [Ca(2+)](i), rather than enhanced augmentation of myofilament calcium sensitivity.