Are we saving water? Simple methods for assessing the effectiveness of groundwater conservation measures

Substantial storage reductions by irrigation pumping in many of the world’s major aquifers jeopardize future food production. As a result, new conservation measures are being utilized to reduce pumping and extend aquifer lifespans. The key question is how effective are these practices in attaining true water conservation (i.e., water use reduction) for a given area? Relationships between pumping and precipitation help provide an answer, as precipitation explains most of the variation in annual irrigation water use for aquifers in semi-arid to sub-humid climates when surface water supplies are limited. Our objective is to utilize correlations between radar precipitation and irrigation groundwater use at a range of spatial scales to assess the effectiveness of conservation approaches in the High Plains aquifer in the central USA. Linear regressions between pumping and precipitation for a conservation area established in 2013 in northwest Kansas indicate that water use and water use per irrigated area were over 27 % less and 25 % less, respectively, during 2013–2021 compared to the same climatic conditions during 2005–2012. Similar regressions found over a 38 % reduction and 23 % reduction in irrigation water use and use per irrigated area, respectively, during 2018–2021 compared to the same conditions during 2005–2017 in a west-central Kansas county with conservation areas. A decrease in irrigated area accounted for most of the difference between these reductions. Higher R2 values after conservation area establishment imply that irrigation tracks precipitation better due to use of soil moisture sensors and other measures as part of increased irrigation efficiency and enhanced water management. The precipitation and water use relationships, which are statistically significant for a wide range of spatial scales, have great potential for assessing the effectiveness of conservation practices in areas with high-quality water use and precipitation data

Importance of a sound hydrologic foundation for assessing the future of the High Plains Aquifer in Kansas

This is the published version. Copyright National Academy of SciencesSteward et al. (1) assess the hydrologic and agricultural future of the High Plains Aquifer. We have many concerns about hydrologic aspects of their study and describe the most significant here. The authors state “…the lines of recharge plus storage in Fig. 1C very closely approximate the recent data points of metered groundwater pumping….” That is not correct, as is clear from a comparison of reported pumping data (diamonds) and the authors’ calculated groundwater use (solid line) for the SW region. There is a systematic deviation (authors’ calculated use is increasing, whereas reported metered pumping data are decreasing), which persists even when uncertain pre-1990 pumping data are neglected. The authors’ groundwater use is also markedly inconsistent with common experiences in western Kansas (2). The 2020–2025 (SW) and 2025–2030 (NW) peaks in the authors’ groundwater use are simply a product of their logistic function representation (maximum use at normalized thickness of 0.5) and are in dramatic contrast to recorded pumping trends. Given that calculated groundwater use is input into the agricultural models, we question all of the agricultural projections. The authors provide no objective basis for accepting the logistic function as an accurate tool for projecting water level declines. The comparisons in their table S1 do little to substantiate the use of the function given that the authors (i) adjust two parameters per well; (ii) adjust parameters at each well independently of the other 1,600 wells; and (iii) in aggregate, only assess the first 30% of depletion. A number of alternative functions could be found that would produce similar agreement with existing data but markedly different future projections. We note the circularity of including extrapolated 2060 values in the dataset used to develop logistic curves that are then used to make future projections. The authors state “…and measurement points were added at 1930 and 2060 from a linear extrapolation of observations while keeping these points within the saturated aquifer.” We are concerned about the sensitivity of future projections to inclusion of 1930 and 2060 “measurements” and to the process (unexplained) for “keeping these points within the saturated aquifer.” The authors state that “We computed recent recharge rates to preserve conservation of mass….” That cannot be correct, as is clear from a comparison of reported pumping data (diamonds) and the authors’ calculated change in storage plus recharge (solid line) for the SW region in their figure 1C; a conservation of mass calculation would produce a line through the center of mass of the reported 1981–2009 data. The calculated recharge values appear to have been adjusted in an unexplained manner. Given that, we also question the significance of the match obtained for the groundwater-supported corn plot in their figure 3A. The comparisons in their table S3 do little to substantiate the authors’ recharge estimates because of the above concerns and the lack of consistency with more recent process-based modeling investigations (3, 4). We conclude that this is an interesting, but highly flawed, mathematical exercise that has little bearing on future conditions in the High Plains Aquifer in western Kansas

CAG repeat length in the androgen receptor gene is related to age at diagnosis of prostate cancer and response to endocrine therapy, but not to prostate cancer risk

The length of the polymorphic CAG repeat in the N-terminal of the androgen receptor (AR) gene is inversely correlated with the transactivation function of the AR. Some studies have indicated that short CAG repeats are related to higher risk of prostate cancer. We performed a case–control study to investigate relations between CAG repeat length and prostate cancer risk, tumour grade, tumour stage, age at diagnosis and response to endocrine therapy. The study included 190 AR alleles from prostate cancer patients and 186 AR alleles from female control subjects. All were whites from southern Sweden. The frequency distribution of CAG repeat length was strikingly similar for cases and controls, and no significant correlation between CAG repeat length and prostate cancer risk was detected. However, for men with non-hereditary prostate cancer (n = 160), shorter CAG repeats correlated with younger age at diagnosis (P = 0.03). There were also trends toward associations between short CAG repeats and high grade (P = 0.07) and high stage (P = 0.07) disease. Furthermore, we found that patients with long CAG repeats responded better to endocrine therapy, even after adjusting for pretreatment level of prostate-specific antigen and tumour grade and stage (P = 0.05). We conclude that short CAG repeats in the AR gene correlate with young age at diagnosis of prostate cancer, but not with higher risk of the disease. Selection of patients with early onset prostate cancer in case–control studies could therefore lead to an over-estimation of the risk of prostate cancer for men with short CAG repeats. An association between long CAG repeats and good response to endocrine therapy was also found, but the mechanism and clinical relevance are unclear. © 1999 Cancer Research Campaig

Non-Hodgkin's lymphoma, obesity and energy homeostasis polymorphisms

A population-based case–control study of lymphomas in England collected height and weight details from 699 non-Hodgkin's lymphoma (NHL) cases and 914 controls. Obesity, defined as a body mass index (BMI) over 30 kg m−2 at five years before diagnosis,, was associated with an increased risk of NHL (OR=1.5, 95% CI 1.1–2.1). The excess was most pronounced for diffuse large B-cell lymphoma (OR=1.9, 95% CI 1.3–2.8). Genetic variants in the leptin (LEP 19G>A, LEP −2548G>A) and leptin receptor genes (LEPR 223Q>R), previously shown to modulate NHL risk, as well as a polymorphism in the energy regulatory gene adiponectin (APM1 276G>T), were investigated. Findings varied with leptin genotype, the risks being decreased with LEP 19AA (OR=0.7, 95% CI 0.5–1.0) and increased with LEP −2548GA (OR=1.3, 95% CI 1.0–1.7) and −2548AA (OR=1.4, 95% CI 1.0–1.9), particularly for follicular lymphoma. These genetic findings, which were independent of BMI, were stronger for men than women

Axonal Regeneration and Neuronal Function Are Preserved in Motor Neurons Lacking ß-Actin In Vivo

The proper localization of ß-actin mRNA and protein is essential for growth cone guidance and axon elongation in cultured neurons. In addition, decreased levels of ß-actin mRNA and protein have been identified in the growth cones of motor neurons cultured from a mouse model of Spinal Muscular Atrophy (SMA), suggesting that ß-actin loss-of-function at growth cones or pre-synaptic nerve terminals could contribute to the pathogenesis of this disease. However, the role of ß-actin in motor neurons in vivo and its potential relevance to disease has yet to be examined. We therefore generated motor neuron specific ß-actin knock-out mice (Actb-MNsKO) to investigate the function of ß-actin in motor neurons in vivo. Surprisingly, ß-actin was not required for motor neuron viability or neuromuscular junction maintenance. Skeletal muscle from Actb-MNsKO mice showed no histological indication of denervation and did not significantly differ from controls in several measurements of physiologic function. Finally, motor axon regeneration was unimpaired in Actb-MNsKO mice, suggesting that ß-actin is not required for motor neuron function or regeneration in vivo

Wine and other alcohol consumption and risk of ovarian cancer in the California Teachers Study cohort

OBJECTIVE: Whether alcohol consumption influences ovarian cancer risk is unclear. Therefore, we investigated the association between alcohol intake at various ages and risk of ovarian cancer. METHODS: Among 90,371 eligible members of the California Teachers Study cohort who completed a baseline alcohol assessment in 1995–1996, 253 women were diagnosed with epithelial ovarian cancer by the end of 2003. Multivariate Cox proportional hazards regression analysis was performed to estimate relative risks (RRs) and 95% confidence intervals (CIs). RESULTS: Consumption of total alcohol, beer, or liquor in the year prior to baseline, at ages 30–35 years, or at ages 18–22 years was not associated with risk of ovarian cancer. Consumption of at least one glass per day of wine, compared to no wine, in the year before baseline was associated with increased risk of developing ovarian cancer: RR = 1.57 (95% CI 1.11–2.22), P(trend) = 0.01. The association with wine intake at baseline was particularly strong among peri-/post-menopausal women who used estrogen-only hormone therapy and women of high socioeconomic status. CONCLUSIONS: Alcohol intake does not appear to affect ovarian cancer risk. Constituents of wine other than alcohol or, more likely, unmeasured determinants of wine drinking were associated with increased risk of ovarian cancer

Menopausal hormone use and ovarian cancer risk: individual participant meta-analysis of 52 epidemiological studies

Background Half the epidemiological studies with information about menopausal hormone therapy and ovarian cancer risk remain unpublished, and some retrospective studies could have been biased by selective participation or recall. We aimed to assess with minimal bias the effects of hormone therapy on ovarian cancer risk. Methods Individual participant datasets from 52 epidemiological studies were analysed centrally. The principal analyses involved the prospective studies (with last hormone therapy use extrapolated forwards for up to 4 years). Sensitivity analyses included the retrospective studies. Adjusted Poisson regressions yielded relative risks (RRs) versus never-use. Findings During prospective follow-up, 12 110 postmenopausal women, 55% (6601) of whom had used hormone therapy, developed ovarian cancer. Among women last recorded as current users, risk was increased even with <5 years of use (RR 1·43, 95% CI 1·31–1·56; p<0·0001). Combining current-or-recent use (any duration, but stopped <5 years before diagnosis) resulted in an RR of 1·37 (95% CI 1·29–1·46; p<0·0001); this risk was similar in European and American prospective studies and for oestrogen-only and oestrogen-progestagen preparations, but differed across the four main tumour types (heterogeneity p<0·0001), being definitely increased only for the two most common types, serous (RR 1·53, 95% CI 1·40–1·66; p<0·0001) and endometrioid (1·42, 1·20–1·67; p<0·0001). Risk declined the longer ago use had ceased, although about 10 years after stopping long-duration hormone therapy use there was still an excess of serous or endometrioid tumours (RR 1·25, 95% CI 1·07–1·46, p=0·005). Interpretation The increased risk may well be largely or wholly causal; if it is, women who use hormone therapy for 5 years from around age 50 years have about one extra ovarian cancer per 1000 users and, if its prognosis is typical, about one extra ovarian cancer death per 1700 users

Variants in genes encoding small GTPases and association with epithelial ovarian cancer susceptibility

Epithelial ovarian cancer (EOC) is the fifth leading cause of cancer mortality in American women. Normal ovarian physiology is intricately connected to small GTP binding proteins of the Ras superfamily (Ras, Rho, Rab, Arf, and Ran) which govern processes such as signal transduction, cell proliferation, cell motility, and vesicle transport. We hypothesized that common germline variation in genes encoding small GTPases is associated with EOC risk. We investigated 322 variants in 88 small GTPase genes in germline DNA of 18,736 EOC patients and 26,138 controls of European ancestry using a custom genotype array and logistic regression fitting log-additive models. Functional annotation was used to identify biofeatures and expression quantitative trait loci that intersect with risk variants. One variant, ARHGEF10L (Rho guanine nucleotide exchange factor 10 like) rs2256787, was associated with increased endometrioid EOC risk (OR=1.33, p=4.46 x 10-6). Other variants of interest included another in ARHGEF10L, rs10788679, which was associated with invasive serous EOC risk (OR=1.07, p=0.00026) and two variants in AKAP6 (A-kinase anchoring protein 6) which were associated with risk of invasive EOC (rs1955513, OR=0.90, p=0.00033; rs927062, OR =0.94, p=0.00059). Functional annotation revealed that the two ARHGEF10L variants were located in super-enhancer regions and that AKAP6 rs927062 was associated with expression of GTPase gene ARHGAP5 (Rho GTPase activating protein 5). Inherited variants in ARHGEF10L and AKAP6, with potential transcriptional regulatory function and association with EOC risk, warrant investigation in independent EOC study populations