Impact of Six Sigma in a developing economy: analysis on benefits drawn by Indian industries

Overall operational excellence is the key requirement of any business to have global competence and sustained growth. Indian industries are not the exception to this. Six Sigma has emerged as one of the most effective business improvement strategies world wide. Nothing much has been published so far illustrating an overall experience of Indian industries with Six Sigma. This paper presents an analysis of the impact of Six Sigma on developing economy like India. The paper provides an insight into what kind of benefits Indian industries are gaining from Six Sigma as a whole. The study further highlights similarity and differences of benefit gained by different scales and sectors of Indian industries through Six Sigma. This exhaustive analysis of the benefits drawn by Indian industries through Six Sigma can assist other industries in India as well as those in other developing countries, who have yet not experimented with Six Sigma, to become more focused regarding their expectations from this improvement drivePeer Reviewe

Impact of Six Sigma in a developing economy: analysis on benefits drawn by Indian industries

Overall operational excellence is the key requirement of any business to have global competence and sustained growth. Indian industries are not the exception to this. Six Sigma has emerged as one of the most effective business improvement strategies world wide. Nothing much has been published so far illustrating an overall experience of Indian industries with Six Sigma. This paper presents an analysis of the impact of Six Sigma on developing economy like India. The paper provides an insight into what kind of benefits Indian industries are gaining from Six Sigma as a whole. The study further highlights similarity and differences of benefit gained by different scales and sectors of Indian industries through Six Sigma. This exhaustive analysis of the benefits drawn by Indian industries through Six Sigma can assist other industries in India as well as those in other developing countries, who have yet not experimented with Six Sigma, to become more focused regarding their expectations from this improvement drivePeer Reviewe

Cerebral Developmental Abnormalities in a Mouse with Systemic Pyruvate Dehydrogenase Deficiency.

UNLABELLEDPyruvate dehydrogenase (PDH) complex (PDC) deficiency is an inborn error of pyruvate metabolism causing a variety of neurologic manifestations. Systematic analyses of development of affected brain structures and the cellular processes responsible for their impairment have not been performed due to the lack of an animal model for PDC deficiency.METHODSIn the present study we investigated a murine model of systemic PDC deficiency by interrupting the X-linked Pdha1 gene encoding the α subunit of PDH to study its role on brain development and behavioral studies.RESULTSMale embryos died prenatally but heterozygous females were born. PDC activity was reduced in the brain and other tissues in female progeny compared to age-matched control females. Immunohistochemical analysis of several brain regions showed that approximately 40% of cells were PDH(-). The oxidation of glucose to CO2 and incorporation of glucose-carbon into fatty acids were reduced in brain slices from 15 day-old PDC-deficient females. Histological analyses showed alterations in several structures in white and gray matters in 35 day-old PDC-deficient females. Reduction in total cell number and reduced dendritic arbors in Purkinje neurons were observed in PDC-deficient females. Furthermore, cell proliferation, migration and differentiation into neurons by newly generated cells were reduced in the affected females during pre- and postnatal periods. PDC-deficient mice had normal locomotor activity in a novel environment but displayed decreased startle responses to loud noises and there was evidence of abnormal pre-pulse inhibition of the startle reflex.CONCLUSIONSThe results show that a reduction in glucose metabolism resulting in deficit in energy production and fatty acid biosynthesis impairs cellular differentiation and brain development in PDC-deficient mice

Quantitation of number of the Purkinje cell nuclei in P35 control and PDC-deficient females.

<p>(A) Gaussian histogram of the Purkinje cell nuclei counts. (B) Average counts of the Purkinje cell nuclei. Twenty sections from 2 brains from each group were analyzed. Sections were spaced at 350 mm. Area of the Purkinje cell layer was randomly chosen, its length was 200 µm. Data are means ± S.D., *represents P<0.05.</p

Number of cells with PDH⁺ and PDH⁻ cells in brains of P35 control and PDC-deficient females.

a<p>Data are means ± S.D.</p>b<p>Significant difference (P<0.05) between the two groups of animals for a given type of cells examined.</p>c<p>PDH⁻ as percent of total cells.</p

Plot a shows the acoustic startle response.

<p>Plot b shows pre-pulse inhibition of the acoustic startle response as a function the intensity of the pre-pulse stimulus. Pre-pulse intensity was measured in decibels (dB). PDC-deficient mice had markedly decreased startle responses and evidence of impaired pre-pulse inhibition of the acoustic startle response at the highest pre-pulse stimulus intensity. Error bars indicate standard error of the mean. Data are reported as mean ± SEM (n = 4).</p

Genetic analysis of the <i>Pdha1</i> locus in control and PDC-deficient female progeny.

<p>(A) Depiction of wild-type (<i>Pdha1^wt)</i>, floxed (<i>Pdha1^flox8</i>), and null (<i>Pdha1</i>^Δ<i>ex8</i>) <i>Pdha1</i> alleles and the primers (arrows above the allele representations) used for genotypic analysis. (B) Genotypic analysis of the <i>Pdha1</i> locus in brain (B), liver (L), heart (H) and skeletal muscle (SM) tissues from a female offspring (genotye: <i>Pdha1</i>^Δ<i>ex8</i><i>/Pdha1^wt; Cre^all+</i>) produced from mating a floxed homozygous female with a <i>Cre</i> transgenic male. Upper gel [genotypes: wild-type allele (700 bp), floxed allele (800 bp), and null allele (400 bp)]. Lower gel: [genotype: <i>Cre</i> transgene (240 bp)]. − (minus) Lane: DNA from a wild-type female (700 bp), and+(plus) Lane: floxed allele (800 bp; upper gel) from a floxed female and null allele (240 bp; lower gel) from a PDC-deficient female included as negative and positive controls. M: DNA marker.</p

Immunostaining for BrdU and NeuN of the cerebella from P5 control and PDC-deficient females.

<p>BrdU was injected intraperitoneally (50 mg/kg body weight; 3 times 2 h apart), into 14-day pregnant dams. They were allowed to deliver pups naturally and nurse them. On P5 female progeny brain slices were immunolabeled with BrdU (red, upper panel) using rat anti-BrdU antibody (Oxford Biotechnology) and NeuN (green, middle panel) using mouse monoclonal antibody (Chemicon). Granule cell layer is marked by arrows. Bar is 50 µm.</p

PDC activities in brain, liver and skeletal muscle of control and PDC-deficient females.

<p>PDC activity was measured as described in the Methods section. PDC activity is expressed as munits/mg cellular protein. The results are means ± S.D. for 4–6 animals.</p

Photomicrograph of folia VIII (coronal section) from control and PDC-deficient females at different ages.

<p>Cryosections were immunostained using anti-calbindin D28K mouse monoclonal antibody (Sigma-Aldrich). Purkinje cells from PDC-deficient females at P5 showed fewer dendritic processes arising from cell body (yellow arrows in right column for P5) compared to age-matched control females. Purkinje cells from PDC-deficient females at P7 also showed fewer branches on dendrites (yellow arrows in right column for P7) compared to P7 control females. Purkinje cells from PDC-deficient females at P10 and P15 had shorter dendritic processes with fewer branches compared to controlled females. Bar is 10 µm.</p