Chemical and biological structure of Lake Mead sediments

Lake Mead has undergone a serious decline since Glen Canyon Dam was constructed 450 km upstream in 1963. State fisheries management agencies are concerned that the decline was caused by water level fluctuations and more severe drawdowns during the bass spawning season, when the operation of Hoover Dam was altered during the post-Lake Powell period. The construction of Glen Canyon Dam and formation of Lake Powell in 1963 drastically altered the natural discharge and temperature cycles and decreased suspended sediment and nutrient loading in the Colorado River inflow to Lake Mead. Recent studies indicate that these changes in nutrient loading have caused a decrease in the fertility and productivity of Lake Mead, and this, in turn, could have contributed to the decline in the largemouth bass fishery. The Water and Power Resources Service initiated a detailed investigation of the chemical and biological properties of Lake Mead sediments in order to: (i) resolve questions regarding historical changes in fertility and productivity of the reservoir, (ii) better assess the cause(s) for the decline in the largemouth bass fishery and (iii) predict future impacts associated with the proposed power modifications to Hoover Dam and operation of pump-storage hydroelectric units. Sediment cores were collected with a Vibra-corer by a commercial, oceanographic drilling firm in non-delta areas of the inner Las Vegas Bay, middle Las Vegas Bay, Boulder Basin, Virgin Basin, Bonelli Bay and the Overton Arm. Sediments were dated by 137Cs assays and analyzed for organic content, organic carbon, total nitrogen, total phosphorus, organic phosphorus, NaOH -extractable phosphorus, calcium carbonate, bulk density and water of hydration. Individual-basin (Lower and Upper Basins) and reservoir-wide sedimentation rates were estimated for autochthonous and allochthonous organic carbon and calcium carbonate, nitrogen and phosphorus and dry weight during three periods (\u3c1954, 1955-1962, \u3c1963) of Lake Mead history. Autochthonous organic carbon sedimentation in the post-Lake Powell period was used with recent measurements of phytoplankton productivity to develop a regression model for predicting historic rates of productivity. Reservoir-wide sedimentation rates and productivity in Lake Mead were relatively low during the period prior to 1954. Increased nutrient loading in years of high runoff during the 1955-1962 period caused a sharp increase in reservoir-wide sedimentation and productivity. The Upper Basin was especially productive during this period due to large inputs of suspended sediments and phosphorus. Phosphorus loading in the Colorado River decreased by over 90% in the post-Lake Powell period and caused a severe reduction in productivity in the Upper Basin. Increased phosphorus loading from the discharges of secondary-treated sewage effluents into Las Vegas Bay, combined with relatively high nitrogen loading from the Colorado River, elevated productivity in the Lower Basin. However, this was not sufficient to offset reductions that occurred in the Upper Basin, and reservoir-wide productivity decreased by 77% during the post-Lake Powell period and was equivalent to productivity in the period prior to 1954. This decline in productivity was accompanied by a decrease in abundance of zooplankton, which comprise the principal food source for largemouth bass fry. Survival of bass fry appears to have decreased in the face of low zooplankton abundance, and this may be the cause for the historic decline of the largemouth bass fishery. The fertility and productivity of Lake Mead could be improved to benefit the bass fishery if: (i) Hoover Dam were operated from a surface, rather than deep, discharge, (ii) pump-storage hydroelectric units were operated to recirculate nutrients in the reservoir, (iii) nutrient loading from Las Vegas Wash were maintained at current levels or allowed to increase with some type of diffuser system to minimize the point source problem in the inner Las Vegas Bay

Z', new fermions and flavor changing processes, constraints on E6_6 models from μ\mu --> eee

We study a new class of flavor changing interactions, which can arise in models based on extended gauge groups (rank $>$4) when new charged fermions are present together with a new neutral gauge boson. We discuss the cases in which the flavor changing couplings in the new neutral current coupled to the $Z^\prime$ are theoretically expected to be large, implying that the observed suppression of neutral flavor changing transitions must be provided by heavy $Z^\prime$ masses together with small $Z$-$Z^\prime$ mixing angles. Concentrating on E$_6$ models, we show how the tight experimental limit on $\mu \rightarrow eee$ implies serious constraints on the $Z^\prime$ mass and mixing angle. We conclude that if the value of the flavor changing parameters is assumed to lie in a theoretically natural range, in most cases the presence of a $Z^\prime$ much lighter than 1 TeV is unlikely.Comment: plain tex, 22 pages + 2 pages figures in PostScript (appended after `\bye'), UM-TH 92-1

Selective Small-Molecule Agonists of G Protein–Coupled Receptor 40 Promote Glucose-Dependent Insulin Secretion and Reduce Blood Glucose in Mice

OBJECTIVE— Acute activation of G protein–coupled receptor 40 (GPR40) by free fatty acids (FFAs) or synthetic GPR40 agonists enhances insulin secretion. However, it is still a matter of debate whether activation of GPR40 would be beneficial for the treatment of type 2 diabetes, since chronic exposure to FFAs impairs islet function. We sought to evaluate the specific role of GPR40 in islets and its potential as a therapeutic target using compounds that specifically activate GPR40

BMI is an important driver of beta-cell loss in type 1 diabetes upon diagnosis in 10 to 18-year-old children.

OBJECTIVE: Body weight-related insulin resistance probably plays a role in progression to type 1 diabetes, but has an uncertain impact following diagnosis. In this study, we investigated whether BMI measured at diagnosis was an independent predictor of C-peptide decline 1-year post-diagnosis. DESIGN: Multicentre longitudinal study carried out at diagnosis and up to 1-year follow-up. METHODS: Data on C-peptide were collected from seven diabetes centres in Europe. Patients were grouped according to age at diagnosis (5 years 10 years 18 years, n=410). Linear regression was used to investigate whether BMI was an independent predictor of change in fasting C-peptide over 1 year. Models were additionally adjusted for baseline insulin dose and HbA1c. RESULTS: In individuals diagnosed between 0 and 5 years, 5 and 10 years and those diagnosed >18 years, we found no association between BMI and C-peptide decline. In patients aged 10-18 years, higher BMI at baseline was associated with a greater decline in fasting C-peptide over 1 year with a decrease (beta 95% CI; P value) of 0.025 (0.010, 0.041) nM/kg per m(2) higher baseline BMI (P=0.001). This association remained significant after adjusting for gender and differences in HbA1c and insulin dose (beta=0.026, 95% CI=0.0097, 0.042; P=0.002). CONCLUSIONS: These observations indicate that increased body weight and increased insulin demand are associated with more rapid disease progression after diagnosis of type 1 diabetes in an age group 10-18 years. This should be considered in studies of beta-cell function in type 1 diabetes

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

Palmitate-Induced β-Cell Dysfunction Is Associated with Excessive NO Production and Is Reversed by Thiazolidinedione-Mediated Inhibition of GPR40 Transduction Mechanisms

BACKGROUND: Type 2 diabetes often displays hyperlipidemia. We examined palmitate effects on pancreatic islet function in relation to FFA receptor GPR40, NO generation, insulin release, and the PPARgamma agonistic thiazolidinedione, rosiglitazone. PRINCIPAL FINDINGS: Rosiglitazone suppressed acute palmitate-stimulated GPR40-transduced PI hydrolysis in HEK293 cells and insulin release from MIN6c cells and mouse islets. Culturing islets 24 h with palmitate at 5 mmol/l glucose induced beta-cell iNOS expression as revealed by confocal microscopy and increased the activities of ncNOS and iNOS associated with suppression of glucose-stimulated insulin response. Rosiglitazone reversed these effects. The expression of iNOS after high-glucose culturing was unaffected by rosiglitazone. Downregulation of GPR40 by antisense treatment abrogated GPR40 expression and suppressed palmitate-induced iNOS activity and insulin release. CONCLUSION: We conclude that, in addition to mediating acute FFA-stimulated insulin release, GPR40 is an important regulator of iNOS expression and dysfunctional insulin release during long-term exposure to FFA. The adverse effects of palmitate were counteracted by rosiglitazone at GPR40, suggesting that thiazolidinediones are beneficial for beta-cell function in hyperlipidemic type 2 diabetes