A framework for the integration of green and lean six sigma for superior sustainability performance

Evidence suggests that Lean, Six Sigma and Green approaches make a positive contribution to the economic, social and environmental (i.e. sustainability) performance of organizations. However, evidence also suggests that organizations have found their integration and implementation challenging. The purpose of this research is therefore to present a framework that methodically guides companies through a five stages and sixteen steps process to effectively integrate and implement the Green, Lean and Six Sigma approaches to improve their sustainability performance. To achieve this, a critical review of the existing literature in the subject area was conducted to build a research gap, and subsequently develop the methodological framework proposed. The paper presents the results from the application of the proposed framework in four organizations with different sizes and operating in a diverse range of industries. The results showed that the integration of Lean Six Sigma and Green helped the organizations to averagely reduce their resources consumption from 20% to 40% and minimize the cost of energy and mass streams by 7-12%. The application of the framework should be gradual, the companies should assess their weaknesses and strengths, set priorities, and identify goals for successful implementation. This paper is one of the very first researches that presents a framework to integrate Green and Lean Six Sigma at a factory level, and hence offers the potential to be expanded to multiple factories or even supply chains

α-Adducin Gly460Trp Gene Mutation and Essential Hypertension in a Chinese Population: A Meta-Analysis including 10960 Subjects

BACKGROUND: The α-adducin Gly460Trp (G460W) gene polymorphism may be associated with susceptibility to essential hypertension (EH), but this relationship remains controversial. In an attempt to resolve this issue, we conducted a meta-analysis. METHODS: Twenty-three separated studies involving 5939 EH patients and 5021 controls were retrieved and analyzed. Four ethnicities were included: Han, Kazakh, Mongolian, and She. Eighteen studies with 5087 EH patients and 4183 controls were included in the Han subgroup. Three studies with 636 EH patients and 462 controls were included in the Kazakh subgroup. The Mongolian subgroup was represented by only one study with 100 EH patients and 50 controls; similarly, only one study with 116 EH patients and 326 controls was available for the She subgroup. The pooled and ethnic group odds ratios (ORs) along with the corresponding 95% confidence intervals (95% CI) were assessed using a random effects model. RESULTS: There was a significant association between the α-adducin G460W gene polymorphism and EH in the pooled Chinese population under both an allelic genetic model (OR: 1.12, 95% CI: 1.04-1.20, P = 0.002) and a recessive genetic model (OR: 1.40, 95% CI: 1.16-1.70, P = 0.0005). In contrast, no significant association between the α-adducin G460W gene polymorphism and EH was observed in the dominant genetic model (OR: 0.88, 95% CI: 0.72-1.09, P = 0.24). In stratified analysis by ethnicity, significantly increased risk was detected in the Han subgroup under an allelic genetic model (OR: 1.13, 95% CI: 1.04-1.23, P = 0.003) and a recessive genetic model (OR: 1.43, 95% CI: 1.17-1.75, P = 0.0006). CONCLUSIONS: In a Chinese population of mixed ethnicity, the α-adducin G460W gene polymorphism was linked to EH susceptibility, most strongly in Han Chinese

On the pathogenetic mechanism of hypercalciuria in genetically hypertensive rats of the Milan strain

The aim of this study was to investigate the pathogenesis of hypercalciuria in the Milan strain of genetically hypertensive rats. Dietary calcium intake and urinary and fecal calcium output were measured simultaneously with indices of sodium and phosphate homeostasis in male rats of the Milan hypertensive and normotensive strains. In addition, urinary calcium and creatinine excretion rates, calcium, phosphate and creatinine serum concentrations, and bone calcium content were also measured in these rats after an overnight fast. Under fed steady-state conditions dietary calcium, sodium, and phosphate intakes, were similar in the two groups of rats, but hypertensive rats had twofold higher urinary calcium excretion and normal urinary excretion of sodium and phosphate. Fecal calcium output was slightly but significantly higher in the adult hypertensive rats while fecal sodium and phosphate excretion was normal. Because of increased urinary and fecal calcium loss, net calcium balance was significantly less positive in hypertensive than in control rats. Under fasting conditions hypertensive rats were confirmed to have hypercalciuria despite normal serum calcium concentrations and normal creatinine clearance. In accordance with balance data and fasting hypercalciuria, bone calcium content was found to be significantly reduced in hypertensive rats. These findings confirm that hypercalciuria in the Milan hypertensive rats is explained by an altered renal calcium handling; it is also associated with a slightly increased fecal calcium output and, therefore, with a less positive calcium balance and reduced bone calcium content

Red cell sodium-proton exchange is increased in Dahl salt-sensitive hypertensive rats.

Red cell sodium-proton exchange is increased in Dahl salt-sensitive hypertensive rats. To investigate the relationship between red blood cell Na+/H+ exchange (EXC) and genetic factors in hypertension, we studied the maximal rate of the antiporter (mmol/liter cell × hr; flux units = FU) in three strains of genetically hypertensive rats. Salt-resistant Dahl rats (DR) were normotensive under low (0.02%) and high (8%) NaCl diets, while salt-sensitive Dahl rats (DS) became markedly hypertensive after four weeks on the high-NaCl diet. Na+/H+ exchange did not differ between DR and DS rats when both were fed with the low-NaCl diet (mean ± SE, 31 ± 3, N = 15, vs. 29 ± 3 FU, N = 14). On the high-NaCl diet, the DR strain did not exhibit significant changes in blood pressure and antiporter activity, but the DS rats significantly increased their blood pressure and Na+/H+ exchange (57 ± 4 FU, N = 13) versus DR rats (38 ± 3 FU, N = 15, P < 0.02). DS rats also significantly increased blood pressure and antiporter activity when fed with high-NaCl diet for one week. These data indicate that high NaCl intake per se does not increase Na+/H+ EXC because the control DR strain did not exhibit transport and blood pressure alterations as observed in the DS strain. Milan hypertensive and spontaneously hypertensive rats (Charles River substrain) had higher blood pressures than Milan and Wystar-Kyoto normotensive rats when they were maintained for four weeks on a 1.5% NaCl diet; however, no differences were seen among normotensive and hypertensive strains in Na+/H+ exchange activity. When the four strains were fed for four weeks with a low-NaCl diet, blood pressure and Na+/H+ exchange activity did not change in any of these strains. Na+/H+ exchange activity in the three hypertensive strains did not correlate with previously reported measurements in kidney brush border membrane vesicles, a finding suggesting that measurements in intact cells reveal antiporter regulatory mechanisms. Our data indicate that elevated Na+/H+ exchange is not due solely to hypertension or high-NaCl diet per se, since these alterations were not shared by all genetic rat models of hypertension. The development of hypertension with a high-NaCl intake in the DS strain followed by a stimulation of RBC Na+/H+ exchange indicate that the antiporter is up-regulated by salt-sensitive elevation of blood pressure

The glutamate transporter excitatory amino acid carrier 1 associates with the actin-binding protein alpha-adducin

Abstract—Excitatory amino acid carrier 1 (EAAC1) belongs to the family of the Na+-dependent glutamate carriers. Although the association between defective EAAC1 function and neurologic disease has been repeatedly studied, EAAC1 regulation is not yet fully understood. We have reported that in C6 glioma cells both the activity and membrane targeting of EAAC1 require the integrity of actin cytoskeleton. Here we show that, in the same model, EAAC1 partially co-localizes with actin filaments at the level of cell processes. Moreover, perinuclear spots in which EAAC1 co-localizes with the actin binding protein alpha-adducin are observed in some cells and, consistently, faint co-immunoprecipitation bands between EAAC1 and alpha-adducin are detected. Co-localization and partial co-immunoprecipitation of EAAC1 and adducin are still detectable after cell treatment with phorbol esters, a condition that leads to a protein kinase C (PKC)-dependent increase of EAAC1 expression on the membrane and to the phosphorylation of adducin. A co-immunoprecipitation band was also detected in protein extracts of rat hippocampus. The amount of adducin co-immunoprecipitated with EAAC1 increases after the treatment of C6 cells with retinoic acid, a differentiating agent that induces EAAC1 overexpression in this cell model. Moreover, in clones of C6 cells transfected with a hemagglutinin (HA)-tagged adducin, the bands of EAAC1 immunoprecipitated by an anti-HA antiserum were proportional to EAAC1 expression. These results suggest the existence of a pool of EAAC1 transporters associated with the actin binding protein alpha-adducin in a PKC-insensitive manner

alpha-adducin may control blood pressure both in rats and humans

1. Previous studies on the pathogenetic mechanisms of hypertension in the Milan hypertensive strain of rat (MHS) showed that a polymorphism within the alpha-adducin gene is responsible for up to 50% of the blood pressure difference between MHS and their MNS normotensive control strain. A case-control study has shown also in humans an association between alpha-adducin locus and hypertension using 4 multiallelic markers surrounding the alpha-adducin locus. 2. With a multiple regression approach we provide an estimate of the contribution of the genotype for each marker to the blood pressure variability in comparison to that provided by sex, body mass index and age. 3. While sex, body mass index and age contributed by about 40-45% to the overall blood pressure variability, the inclusion of the genotype for the marker closer to the alpha-adducin locus provided a further increase of the variability explained of about 5%. 4. The contribution independently provided by the other markers decreased exponentially with the increase of distance from alpha-adducin locus