962 resultados para LEAN MASS
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Obesity and osteoporosis are important global health problems characterized by increasing prevalence with high impact on morbidity and mortality. The objective of this review was to determine whether excess weight during adolescence interferes with bone mass accumulation. If bone mineral gain can be optimized during puberty, adults are less likely to suffer from the devastating complications of osteoporosis. The increased fracture risk in obese children has also been attributed to a lower bone mass for weight compared to non-obese children. Thus, adiposity present in this age group may not result in the protection of bone mass, in contrast to what has been observed in adults. However, studies involving adolescents have reported both protective and detrimental effects of obesity on bone. The results and mechanisms of these interactions are controversial and have not been fully elucidated, a fact highlighting the extreme relevance of this topic and the need to monitor intervening and interactive variables. © 2013 by the authors; licensee MDPI, Basel, Switzerland.
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BACKGROUND: Oxidative killing is the primary defense against surgical pathogens; risk of infection is inversely related to tissue oxygenation. Subcutaneous tissue oxygenation in obese patients is significantly less than in lean patients during general anesthesia. However, it remains unknown whether reduced intraoperative tissue oxygenation in obese patients results from obesity per se or from a combination of anesthesia and surgery. In a pilot study, we tested the hypothesis that tissue oxygenation is reduced in spontaneously breathing, unanesthetized obese volunteers. METHODS: Seven lean volunteers with a body mass index (BMI) of 22 +/- 2 kg/m(2) were compared to seven volunteers with a BMI of 46 +/- 4 kg/m(2). Volunteers were subjected to the following oxygen challenges: (1) room air; (2) 2 l/min oxygen via nasal prongs, (3) 6 l/min oxygen through a rebreathing face mask; (4) oxygen as needed to achieve an arterial oxygen pressure (arterial pO(2)) of 200 mmHg; and (5) oxygen as needed to achieve an arterial pO(2) of 300 mmHg. The oxygen challenges were randomized. Arterial pO(2) was measured with a continuous intraarterial blood gas analyzer (Paratrend 7); deltoid subcutaneous tissue oxygenation was measured with a polarographic microoxygen sensor (Licox). RESULTS: Subcutaneous tissue oxygenation was similar in lean and obese volunteers: (1) room air, 52 +/- 10 vs 58 +/- 8 mmHg; (2) 2 l/min, 77 +/- 25 vs 79 +/- 24 mmHg; (3) 6 l/min, 125 +/- 43 vs 121 +/- 25 mmHg; (4) arterial pO(2) = 200 mmHg, 115 +/- 42 vs 144 +/- 23 mmHg; (5) arterial pO(2) = 300 mmHg, 145 +/- 41 vs 154 +/- 32 mmHg. CONCLUSION: In this pilot study, we could not identify significant differences in deltoid subcutaneous tissue oxygen pressure between lean and morbidly obese volunteers.
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A fundamental combustion model for spark-ignition engine is studied in this report. The model is implemented in SIMULINK to simulate engine outputs (mass fraction burn and in-cylinder pressure) under various engine operation conditions. The combustion model includes a turbulent propagation and eddy burning processes based on literature [1]. The turbulence propagation and eddy burning processes are simulated by zero-dimensional method and the flame is assumed as sphere. To predict pressure, temperature and other in-cylinder variables, a two-zone thermodynamic model is used. The predicted results of this model match well with the engine test data under various engine speeds, loads, spark ignition timings and air fuel mass ratios. The developed model is used to study cyclic variation and combustion stability at lean (or diluted) combustion conditions. Several variation sources are introduced into the combustion model to simulate engine performance observed in experimental data. The relations between combustion stability and the introduced variation amount are analyzed at various lean combustion levels.
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Total body water (TBW) is reduced in adult GH deficiency (GHD) largely due to a reduction of extracellular water. It is unknown whether total blood volume (TBV) contributes to the reduced extracellular water in GHD. GH and insulin-like growth factor I (IGF-I) have been demonstrated to stimulate erythropoiesis in vitro, in animal models, and in growing children. Whether GH has a regulatory effect on red cell mass (RCM) in adults is not known. We analyzed body composition by bioelectrical impedance and used standard radionuclide dilution methods to measure RCM and plasma volume (PV) along with measuring full blood count, ferritin, vitamin B12, red cell folate, IGF-I, IGF-binding protein-3, and erythropoietin in 13 adult patients with GHD as part of a 3-month, double blind, placebo-controlled trial of GH (0.036 U/kg.day). TBW and lean body mass significantly increased by 2.5 +/- 0.53 kg (mean +/- SEM; P < 0.004) and 3.4 +/- 0.73 kg (P < 0.004), respectively, and fat mass significantly decreased by 2.4 +/- 0.32 kg (P < 0.001) in the GH-treated group. The baseline RCM of all patients with GHD was lower than the predicted normal values (1635 +/- 108 vs. 1850 +/- 104 mL; P < 0.002). GH significantly increased RCM, PV, and TBV by 183 +/- 43 (P < 0.006), 350 +/- 117 (P < 0.03), and 515 +/- 109 (P < 0.004) mL, respectively. The red cell count increased by 0.36 +/- 0.116 x 10(12)/L (P < 0.03) with a decrease in ferritin levels by 39.1 +/- 4.84 micrograms/L (P < 0.001) after GH treatment. Serum IGF-I and IGF-binding protein-3 concentrations increased by 3.0 +/- 0.43 (P < 0.001) and 1.3 +/- 0.15 (P < 0.001) SD, respectively, but the erythropoietin concentration was unchanged after GH treatment. No significant changes in body composition or blood volume were recorded in the placebo group. Significant positive correlations could be established between changes in TBW and TBV, lean body mass and TBV (r = 0.78; P < 0.04 and r = 0.77; P < 0.04, respectively), and a significant negative correlation existed between changes in fat mass and changes in TBV in the GH-treated group (r = -0.95; P < 0.02). We conclude that 1) erythropoiesis is impaired in GHD; 2) GH stimulates erythropoiesis in adult GHD; and 3) GH increases PV and TBV, which may contribute to the increased exercise performance seen in these patients.
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To compare the effects of deflazacort (DEFLA) vs. prednisone (PRED) on bone mineral density (BMD), body composition, and lipids, 24 patients with end-stage renal disease were randomized in a double blind design and followed 78 weeks after kidney transplantation. BMD and body composition were assessed using dual energy x-ray absorptiometry. Seventeen patients completed the study. Glucocorticosteroid doses, cyclosporine levels, rejection episodes, and drop-out rates were similar in both groups. Lumbar BMD decreased more in PRED than in DEFLA (P < 0.05), the difference being particularly marked after 24 weeks (9.1 +/- 1.8% vs. 3.0 +/- 2.4%, respectively). Hip BMD decreased from baseline in both groups (P < 0.01), without intergroup differences. Whole body BMD decreased from baseline in PRED (P < 0.001), but not in DEFLA. Lean body mass decreased by approximately 2.5 kg in both groups after 6-12 weeks (P < 0.001), then remained stable. Fat mass increased more (P < 0.01) in PRED than in DEFLA (7.1 +/- 1.8 vs. 3.5 +/- 1.4 kg). Larger increases in total cholesterol (P < 0.03), low density lipoprotein cholesterol (P < 0.01), lipoprotein B2 (P < 0.03), and triglycerides (P = 0.054) were observed in PRED than in DEFLA. In conclusion, using DEFLA instead of PRED in kidney transplant patients is associated with decreased loss of total skeleton and lumbar spine BMD, but does not alter bone loss at the upper femur. DEFLA also helps to prevent fat accumulation and worsening of the lipid profile.
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Many persons in the U.S. gain weight during young adulthood, and the prevalence of obesity has been increasing among young adults. Although obesity and physical inactivity are generally recognized as risk factors for coronary heart disease (CHD), the magnitude of their effect on risk may have been seriously underestimated due to failure to adequately handle the problem of cigarette smoking. Since cigarette smoking causes weight loss, physically inactive cigarette smokers may remain relatively lean because they smoke cigarettes. We hypothesize cigarette smoking modifies the association between weight gain during young adulthood and risk of coronary heart disease during middle age, and that the true effect of weight gain during young adulthood on risk of CHD can be assessed only in persons who have not smoked cigarettes. Specifically, we hypothesize that weight gain during young adulthood is positively associated with risk of CHD during middle-age in nonsmokers but that the association is much smaller or absent entirely among cigarette smokers. The purpose of this study was to test this hypothesis. The population for analysis was comprised of 1,934 middle-aged, employed men whose average age at the baseline examination was 48.7 years. Information collected at the baseline examinations in 1958 and 1959 included recalled weight at age 20, present weight, height, smoking status, and other CHD risk factors. To decrease the effect of intraindividual variation, the mean values of the 1958 and 1959 baseline examinations were used in analyses. Change in body mass index ($\Delta$BMI) during young adulthood was the primary exposure variable and was measured as BMI at baseline (kg/m$\sp2)$ minus BMI at age 20 (kg/m$\sp2).$ Proportional hazards regression analysis was used to generate relative risks of CHD mortality by category of $\Delta$BMI and cigarette smoking status after adjustment for age, family history of CVD, major organ system disease, BMI at age 20, and number of cigarettes smoked per day. Adjustment was not performed for systolic blood pressure or total serum cholesterol as these were regarded as intervening variables. Vital status was known for all men on the 25th anniversary of their baseline examinations. 705 deaths (including 319 CHD deaths) occurred over 40,136 person-years of experience. $\Delta$BMI was positively associated with risk of CHD mortality in never-smokers, but not in ever-smokers (p for interaction = 0.067). For never-smokers with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 1.62, 1.61, and 2.78, respectively (p for trend = 0.010). For ever-smokers, with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 0.74, 1.07, and 1.06, respectively (p for trend = 0.422). These results support the research hypothesis that cigarette smoking modifies the association between weight gain and CHD mortality. Current estimates of the magnitude of effect of obesity and physical inactivity on risk of coronary mortality may have been seriously underestimated due to inadequate handling of cigarette smoking. ^
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Upwardpropagation of a premixed flame in averticaltubefilled with a very leanmixture is simulated numerically using a single irreversible Arrhenius reaction model with infinitely high activation energy. In the absence of heat losses and preferential diffusion effects, a curved flame with stationary shape and velocity close to those of an open bubble ascending in the same tube is found for values of the fuel mass fraction above a certain minimum that increases with the radius of the tube, while the numerical computations cease to converge to a stationary solution below this minimum mass fraction. The vortical flow of the gas behind the flame and in its transport region is described for tubes of different radii. It is argued that this flow may become unstable when the fuel mass fraction is decreased, and that this instability, together with the flame stretch due to the strong curvature of the flame tip in narrow tubes, may be responsible for the minimum fuel mass fraction. Radiation losses and a Lewis number of the fuel slightly above unity decrease the final combustion temperature at the flame tip and increase the minimum fuel mass fraction, while a Lewis number slightly below unity has the opposite effect.
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Recent data have identified leptin as an afferent signal in a negative-feedback loop regulating the mass of the adipose tissue. High leptin levels are observed in obese humans and rodents, suggesting that, in some cases, obesity is the result of leptin insensitivity. This hypothesis was tested by comparing the response to peripherally and centrally administered leptin among lean and three obese strains of mice: diet-induced obese AKR/J, New Zealand Obese (NZO), and Ay. Subcutaneous leptin infusion to lean mice resulted in a dose-dependent loss of body weight at physiologic plasma levels. Chronic infusions of leptin intracerebroventricularly (i.c.v.) at doses of 3 ng/hr or greater resulted in complete depletion of visible adipose tissue, which was maintained throughout 30 days of continuous i.c.v. infusion. Direct measurement of energy balance indicated that leptin treatment did not increase total energy expenditure but prevented the decrease that follows reduced food intake. Diet-induced obese mice lost weight in response to peripheral leptin but were less sensitive than lean mice. NZO mice were unresponsive to peripheral leptin but were responsive to i.c.v. leptin. Ay mice did not respond to subcutaneous leptin and were 1/100 as sensitive to i.c.v. leptin. The decreased response to leptin in diet-induced obese, NZO, and Ay mice suggests that obesity in these strains is the result of leptin resistance. In NZO mice, leptin resistance may be the result of decreased transport of leptin into the cerebrospinal fluid, whereas in Ay mice, leptin resistance probably results from defects downstream of the leptin receptor in the hypothalamus.
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Perilipin coats the lipid droplets of adipocytes and is thought to have a role in regulating triacylglycerol hydrolysis. To study the role of perilipin in vivo, we have created a perilipin knockout mouse. Perilipin null (peri−/−) and wild-type (peri+/+) mice consume equal amounts of food, but the adipose tissue mass in the null animals is reduced to ≈30% of that in wild-type animals. Isolated adipocytes of perilipin null mice exhibit elevated basal lipolysis because of the loss of the protective function of perilipin. They also exhibit dramatically attenuated stimulated lipolytic activity, indicating that perilipin is required for maximal lipolytic activity. Plasma leptin concentrations in null animals were greater than expected for the reduced adipose mass. The peri−/− animals have a greater lean body mass and increased metabolic rate but they also show an increased tendency to develop glucose intolerance and peripheral insulin resistance. When fed a high-fat diet, the perilipin null animals are resistant to diet-induced obesity but not to glucose intolerance. The data reveal a major role for perilipin in adipose lipid metabolism and suggest perilipin as a potential target for attacking problems associated with obesity.
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A Mass Customisation model is discussed as a competitive positioning strategy in the marketplace adding value to the customer’s end-use. It includes the user as part of the construction process responding to the customer’s demands and wishes. To the present day, almost all proposals for Mass Customisation have been focused on the design phase and single family houses. The reality is that the processes carried out in the work execution are so inefficient that the costs of the Mass Customisation models are assumed by the customer and they do not offer solutions that support the change management. Furthermore, this inefficiency often makes Mass Customisation unfeasible in terms of deadlines and site management. Therefore, the present proposal focuses on achieving the paradigm of Mass Customisation in the traditional residential construction complementary to the existing proposals in the design phase. All this through the proposal of a framework for the integral management in the work execution, which will address change management introduced by the users offering an efficient and productive model that reduces costs in the process. This model will focus on the synergy between different strategies, techniques and technologies currently used in the construction management (such as Lean Construction or Six Sigma), together with, other strategies and technologies that have proven to be valid solutions in other fields (such as Business Process Management, Service Oriented Architecture, etc.).
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Background: Lean bodyweight (LBW) has been recommended for scaling drug doses. However, the current methods for predicting LBW are inconsistent at extremes of size and could be misleading with respect to interpreting weight-based regimens. Objective: The objective of the present study was to develop a semi-mechanistic model to predict fat-free mass (FFM) from subject characteristics in a population that includes extremes of size. FFM is considered to closely approximate LBW. There are several reference methods for assessing FFM, whereas there are no reference standards for LBW. Patients and methods: A total of 373 patients (168 male, 205 female) were included in the study. These data arose from two populations. Population A (index dataset) contained anthropometric characteristics, FFM estimated by dual-energy x-ray absorptiometry (DXA - a reference method) and bioelectrical impedance analysis (BIA) data. Population B (test dataset) contained the same anthropometric measures and FFM data as population A, but excluded BIA data. The patients in population A had a wide range of age (18-82 years), bodyweight (40.7-216.5kg) and BMI values (17.1-69.9 kg/m(2)). Patients in population B had BMI values of 18.7-38.4 kg/m(2). A two-stage semi-mechanistic model to predict FFM was developed from the demographics from population A. For stage 1 a model was developed to predict impedance and for stage 2 a model that incorporated predicted impedance was used to predict FFM. These two models were combined to provide an overall model to predict FFM from patient characteristics. The developed model for FFM was externally evaluated by predicting into population B. Results: The semi-mechanistic model to predict impedance incorporated sex, height and bodyweight. The developed model provides a good predictor of impedance for both males and females (r(2) = 0.78, mean error [ME] = 2.30 x 10(-3), root mean square error [RMSE] = 51.56 [approximately 10% of mean]). The final model for FFM incorporated sex, height and bodyweight. The developed model for FFM provided good predictive performance for both males and females (r(2) = 0.93, ME = -0.77, RMSE = 3.33 [approximately 6% of mean]). In addition, the model accurately predicted the FFM of subjects in population B (r(2) = 0.85, ME -0.04, RMSE = 4.39 [approximately 7% of mean]). Conclusions: A semi-mechanistic model has been developed to predict FFM (and therefore LBW) from easily accessible patient characteristics. This model has been prospectively evaluated and shown to have good predictive performance.
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Aim: N-3 fatty acids, especially eicosapentaenoic acid (EPA), may possess anticachectic properties. This trial compared a protein and energy dense supplement enriched with n-3 fatty acids and antioxidants (experimental: E) with an isocaloric isonitrogenous control supplement (C) for their effects on weight, lean body mass (LBM), dietary intake, and quality of life in cachectic patients with advanced pancreatic cancer. Methods: A total of 200 patients (95 E; 105 C) were randomised to consume two cans/day of the E or C supplement (480 ml, 620 kcal, 32 g protein ± 2.2 g EPA) for eight weeks in a multicentre, randomised, double blind trial. Results: At enrolment, patients' mean rate of weight loss was 3.3 kg/month. Intake of the supplements (E or C) was below the recommended dose (2 cans/day) and averaged 1.4 cans/day. Over eight weeks, patients in both groups stopped losing weight (Δweight E: -0.25 kg/month versus C: -0.37 kg/month; p=0.74) and LBM (ΔLBM E: +0.27 kg/month versus C: +0.12 kg/month; p=0.88) to an equal degree (change from baseline E and C, p<0.001). In view of evident non-compliance in both E and C groups, correlation analyses were undertaken to examine for potential dose-response relationships. E patients demonstrated significant correlations between their supplement intake and weight gain (r=0.50, p<0.001) and increase in LBM (r=0.33, p=0.036). Such correlations were not statistically significant in C patients. The relationship of supplement intake with change in LBM was significantly different between E and C patients (p=0.043). Increased plasma EPA levels in the E group were associated with weight and LBM gain (r=0.50, p<0.001; r=0.51, p=0.001). Weight gain was associated with improved quality of life (p<0.01) only in the E group. Conclusion: Intention to treat group comparisons indicated that at the mean dose taken, enrichment with n-3 fatty acids did not provide a therapeutic advantage and that both supplements were equally effective in arresting weight loss. Post hoc dose-response analysis suggests that if taken in sufficient quantity, only the n-3 fatty acid enriched energy and protein dense supplement results in net gain of weight, lean tissue, and improved quality of life. Further trials are required to examine the potential role of n-3 enriched supplements in the treatment of cancer cachexia.
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Oxidised biomolecules in aged tissue could potentially be used as biomarkers for age-related diseases; however, it is still unclear whether they causatively contribute to ageing or are consequences of the ageing process. To assess the potential of using protein oxidation as markers of ageing, mass spectrometry (MS) was employed for the identification and quantification of oxidative modifications in obese (ob/ob) mice. Lean muscle mass and strength is reduced in obesity, representing a sarcopenic model in which the levels of oxidation can be evaluated for different muscular systems including calcium homeostasis, metabolism and contractility. Several oxidised residues were identified by tandem MS (MS/MS) in both muscle homogenate and isolated sarcoplasmic reticulum (SR), an organelle that regulates intracellular calcium levels in muscle. These modifications include oxidation of methionine, cysteine, tyrosine, and tryptophan in several proteins such as sarcoplasmic reticulum calcium ATPase (SERCA), glycogen phosphorylase, and myosin. Once modifications had been identified, multiple reaction monitoring MS (MRM) was used to quantify the percentage modification of oxidised residues within the samples. Preliminary data suggests proteins in ob/ob mice are more oxidised than the controls. For example SERCA, which constitutes 60-70% of the SR, had approximately a 2-fold increase in cysteine trioxidation of Cys561 in the obese model when compared to the control. Other obese muscle proteins have also shown a similar increase in oxidation for various residues. Further analysis with complex protein mixtures will determine the potential diagnostic use of MRM experiments for analysing protein oxidation in small biological samples such as muscle needle biopsies.
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The maintenance of normal body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time. Prior to the onset of AN, premorbid body mass index (BMI) spans the entire range from underweight to obese. After recovery, patients have reduced rates of overweight and obesity. As such, loci involved in body weight regulation may also be relevant for AN and vice versa. Our primary analysis comprised a cross-trait analysis of the 1000 single-nucleotide polymorphisms (SNPs) with the lowest P-values in a genome-wide association meta-analysis (GWAMA) of AN (GCAN) for evidence of association in the largest published GWAMA for BMI (GIANT). Subsequently we performed sex-stratified analyses for these 1000 SNPs. Functional ex vivo studies on four genes ensued. Lastly, a look-up of GWAMA-derived BMI-related loci was performed in the AN GWAMA. We detected significant associations (P-values <5 × 10(-5), Bonferroni-corrected P<0.05) for nine SNP alleles at three independent loci. Interestingly, all AN susceptibility alleles were consistently associated with increased BMI. None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2: CARF and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previously been associated with AN or obesity. Sex-stratified analyses revealed that the strongest BMI signal originated predominantly from females (chr. 10 rs1561589; Poverall: 2.47 × 10(-06)/Pfemales: 3.45 × 10(-07)/Pmales: 0.043). Functional ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fasting. Hypothalamic expression of Ctbp2 was increased in diet-induced obese (DIO) mice as compared with age-matched lean controls. We observed no evidence for associations for the look-up of BMI-related loci in the AN GWAMA. A cross-trait analysis of AN and BMI loci revealed variants at three chromosomal loci with potential joint impact. The chromosome 10 locus is particularly promising given that the association with obesity was primarily driven by females. In addition, the detected altered hypothalamic expression patterns of Ctbp2 and Nbeal1 as a result of fasting and DIO implicate these genes in weight regulation.
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La filosofia del lean thinking ha dimostrato in numerose occasioni, dalla sua nascita ad oggi, di poter apportare reali e consistenti benefici all’interno degli ambienti aziendali rivoluzionando a volte non solo il modo di produrre delle aziende ma anche quello di pensare, generando un profondo cambiamento culturale. La filosofia lean nasce come esigenza di riadattamento del sistema produttivo in contrapposizione a quello della mass production per questo molti dei testi di riferimento storici sul lean thinking citano prassi e casi aziendali che toccano esclusivamente l’ambito della produzione, tuttavia tale ambito rappresenta solamente uno dei tanti che si possono osservare in ambito aziendale. Successivamente si è compreso come il lean thinking rappresenti in realtà un sistema, composto da: principi, tecniche, metodi e strumenti in grado di garantire il miglioramento dei processi. Si tratta di fatto di un framework adattabile alle diverse funzioni aziendali e che per massimizzare la propria efficacia deve essere assimilato dall’intera organizzazione e non solo dall’ambiente produttivo. Negli anni infatti l’aggettivo “lean” è stato accostato agli ambiti più vari: lean sales, lean accounting, lean services, lean managment, lean organization, lean enterprise, lean office e molti altri. Tuttavia raramente ci si imbatte nel termine “lean warehousing” e ancora più raramente ci si imbatte in casi di applicazioni di strumenti lean in ambito logistico o a testi di riferimento che trattino l’argomento. In un mercato sempre più̀ competitivo è fondamentale per qualsiasi azienda avere una logistica efficiente e flessibile che consenta di offrire un alto livello di servizio per il cliente. Il magazzino rappresenta il punto di arrivo e di partenza per ogni flusso logistico e data la rilevanza che ancora oggi la sua funzione detiene per le aziende risulta fondamentale per il successo dell’interno sistema implementare anche in questa divisione la filosofia lean.