This equation shows the physical equivalence to a situation with

This equation shows the physical equivalence to a situation with only one scattering time and two different oscillations frequencies for the MW-driven subbands: w/3 for the intra-subband and w for the inter-subband scattering rate [32, 33]. They demonstrate also the origin for the learn more regular and strong interference profile observed in experiments where the factor 1/3 is essential to obtain the interference effect regularly spaced affecting only valleys and peaks.

A different factor would produce a totally distinct interference and also distinct R x x response. This factor comes from the calculation of the squared magnitude of the corresponding form factors which eventually determine the different scattering rates between the intra-subband and the inter-subband processes. Nutlin-3a research buy In physical terms,during the scattering jump, the electron perceives approximately three Crenolanib order times faster MW-driven oscillation

of the 2DES when is inter-subband with respect to the intra-subband. Then, we are going to obtain a MIRO profile made up of two different MW frequencies, as if the sample was illuminated by two different radiation sources at the same time. This gives rise to a clear interference effect reflected in the final R x x profile. To obtain R x x , we use the relation , where and σ x x ≪σ x y . In Figure 1, we present calculated R x x vs B for dark and MW situations and frequency f=w/2π=100 GHz. We can observe MISO peaks for the dark curve, MIRO for the MW curve, and the ZRS marked with an arrow. We observe the new features appearing regularly spaced in peaks and valleys for bilayer systems: two nearly symmetric shoulders in valleys and narrower peaks with respect to the single occupied subband case (see inset). According to our model, these new features

are results of the interference between the competing intra- and inter-subband scattering processes. In valleys, we observe a constructive interference see more effect giving rise to two shoulders, meaning more current through the sample; meanwhile, the narrower peaks mean a destructive interference and less current. Figure 1 Calculated R xx vs B for dark (no MW) and MW situations. The ZRS is marked with an arrow. The MW frequency is 100 GHz. We observe clearly the peculiar features for bilayer systems: shoulders at minima and narrower peaks regarding the single occupied subband case (see inset). Shoulders and narrow peaks are the outcomes of the interference between the intra- and inter-subband scattering processes. Conclusions In summary, we have theoretically studied the recently discovered microwave-induced resistance oscillations and zero resistance states in Hall bars with bilayer systems. Resistance presents a peculiar shape which appears to have an interference effect not observed before.

In fact, volunteers consumed less than one third of the current R

In fact, volunteers consumed less than one third of the current RDA for vitamin D both before and during training. Although sunlight exposure was not quantified during BCT, declines in serum ARN-509 nmr 25(OH)D levels observed in white volunteers coupled with suboptimal serum 25(OH)D levels in non-white volunteers throughout the study indicate that strategies to improve dietary intake of vitamin D and calcium during military training may be needed to improve vitamin D status. Further, sweat mineral losses were not quantified in the present study. Estimates

of mineral losses through sweat vary depending upon collection and assay techniques [36–38]. If significant calcium losses were to occur through sweating during military training, this could affect nutritional requirements and could affect bone health by stimulating PTH [39]. Conclusion In summary, this longitudinal

study determined vitamin D status during military training in females, to include interactions between vitamin D status and race. Serum 25(OH)D levels declined in white volunteers, and were lower in non-white volunteers as compared to white volunteers at all timepoints. Increases in PTH and indicators of bone turnover were observed during military training. Our findings indicate that efforts to improve the dining environment during military training should emphasize the consumption of foods containing vitamin D and calcium, as the cohort of Soldiers participating in the present study did not meet current recommended CRT0066101 ic50 intakes for either nutrient. Strengths of the study included the longitudinal design in an environment free of dietary supplements and other factors that may have affected the carefully controlled collection of dietary status and intake data. Weaknesses include the lack of functional data regarding bone health and injury outcomes Resveratrol and a lack of data quantifying

sun exposure. Future studies should determine whether the increased PTH and bone turnover observed during military training affect the vitamin D requirement, and whether vitamin D and calcium supplementation may be prudent for the prevention of injury, to include BV-6 price stress fracture. Acknowledgements We acknowledge the Soldier volunteers that participated in this study and the Command staff at Fort Jackson, SC, who provided access to potential volunteers. Research supported by the US Army Medical Research and Material Command. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Army or the Department of Defense. Any citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement of approval of the products or services of these organizations. References 1. DeLuca HF: Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr 2004,80(Suppl):1689S-1696S.PubMed 2.

Several microspheres were visually confirmed to be intracellular

Several microspheres were visually confirmed to be intracellular after the inoculation (Figure 2D). A significant increase in fluorescence was observed in wells containing PknD-coated microspheres relative to those containing their BSA-coated counterparts (P = 0.0002) (Figure 2E). Adherence of PknD-coated microspheres (but not BSA-coated microspheres) to HBMEC was significantly reduced by pre-incubation with anti-PknD serum, when compared

to incubation with naïve antiserum (P = 0.005) (Figure 2F). Figure 2 M. tuberculosis #https://www.selleckchem.com/products/jnk-in-8.html randurls[1|1|,|CHEM1|]# PknD is sufficient to trigger adhesion to HBMEC. A and B. Fluorescent microspheres were coated with either PknD sensor or BSA, inoculated into HBMEC, washed, and stained for actin. Confocal microscopy demonstrated that PknD sensor-coated microspheres (panel B) adhere to brain endothelia to a greater degree than those coated with BSA (panel A). C. Confocal images were assembled into a 3D reconstruction and examined under higher magnification. PknD sensor-coated microspheres appear to be largely enveloped by actin processes (arrows) indicating that PknD-induced uptake by host cells may be an active process. D. When confocal images are examined in multiple planes, it is clear that a number of microspheres exist intracellularly. E. Wells containing endothelial cells with microspheres were analyzed for fluorescence. Quantification

of fluorescence demonstrated a significant increase in the adherence of PknD-coated microspheres to the monolayer (P = 0.0002). F. Microspheres were pre-incubated with either custom anti-PknD serum or Milciclib cost naïve serum. Incubation with anti-PknD serum (1:250 dilution) significantly reduced adherence of PknD (P = 0.0007) but not BSA-coated microspheres (P = 0.6). Moreover, no reduction in adherence was noted for PknD or BSA-coated microspheres when incubated with naïve antiserum (BSA: P = 0.4; PknD: P = 0.1; ANOVA single factor). Fluorescence readings are presented as mean ± standard deviation. *Statistically significant difference. In order to determine whether microspheres were invading and present intracellularly, the above incubations were repeated, and cells

analyzed by flow cytometry. We observed that, in samples Liothyronine Sodium incubated with PknD-coated microspheres, 7.7 ± 0.4% of HBMEC contained fluorescent spheres, while only 0.6 ± 0.2% of cells incubated with BSA-coated microspheres were positive for fluorescence (Figure 3A-C). Microspheres were again incubated with anti-PknD serum, and internalization by HBMEC was significantly reduced when compared to incubation with naïve serum (P = 0.001) (Figure 3D). Together, these data indicate that M. tuberculosis PknD is sufficient to trigger uptake by brain endothelia. Figure 3 M. tuberculosis PknD triggers invasion of the brain endothelium. A. Brain endothelia were inoculated with either PknD sensor- or BSA-coated fluorescent microspheres, washed, and disrupted by trypsinization.

Stat3C) and their wild-type (WT) counter parts

Stat3C) and their wild-type (WT) counter parts Poziotinib chemical structure were used. K5.Stat3C mice express Stat3C, a constitutively active form of Stat3 and develop spontaneous lesions that resemble human psoriasis [11]. The expression of the Stat3C transgene in the basal cell layer of the selleck chemicals epidermis was driven by the bovine keratin 5 gene promoter, and hence the name K5.Stat3C. The mice were genotyped by PCR to detect the transgene and maintained in the breeding colony at LSUHSC-Shreveport. Effects of ACA, galanga extract, and FA on mouse epidermis following two weeks treatment with TPA in WT vs. K5.Stat3C mice The dorsal

skin of each mouse was shaved two days prior to the treatments. At 2 days post shaving, topical applications of respective treatments were Selleckchem BVD-523 administered on the dorsal surface of the mouse with the aid of a pipette, according to the two-week protocol reported previously for short-term tumor promoter experiments [8]. The mice were treated twice weekly for

two weeks as follows; treatment with either acetone vehicle, synthetic ACA (340 nmol), galanga extract (equivalent of 340 nmol ACA) or FA (2.2 nmol), followed by treatment with TPA (3.4 nmol). Mice were sacrificed 48 h after the last treatment application and tissues were harvested for further experimental analysis. The dorsal skin from the mice was excised and divided into three parts; one for wet weight analysis, one for histological analysis, and one for western blot analysis. For wet weight analysis, the underlying fat layer was dissected from one of the skin pieces and two holes were punched into the excised skin, one towards the rostral end and the other towards the caudal end. The punched biopsies Phosphoprotein phosphatase were then placed into vials and weighed on an analytical balance (AG135, Mettler-Toledo, Inc., Columbus, OH). The weights of the biopsies obtained from the rostral and caudal end were then averaged for each individual mouse and recorded. For histological analysis, one piece of skin was placed in 10% neutral buffered formalin, and at 24 hrs post fixation transferred into 50% ethanol and embedded in paraffin. The tissue sections were sliced crossectionally at

a thickness of 4 μm. Duplicate histology sections were stained with hemotoxylin and eosin for histopathological analysis. Epidermal thickness was measured using the hematoxylin and eosin stained histology slides. Digital images of the histology slides were captured using a Nikon Eclipse TE300 inverted microscope with an epi-fluorescence attachment. This was attached to Photometrics CoolSNAPfx monochrome 12-bit CCD camera and configured with imaging Software: IPLab 3.7 for Windows (Research Core Facility, LSUHSC). The procedure for measuring epidermal thickness reported by Li, Wheeler and colleagues was followed with slight modifications [39]. Digital pictures of 10 randomly selected fields were taken at 400X magnification. The sections were scored in a blinded fashion such that the slides only had a numerical identity.

Additional inflammation caused by surgery is seen as additional t

Additional inflammation caused by surgery is seen as additional trauma and has been considered as a possible risk factor for organ failure such as ARDS [18]. Much to our surprise the increased damage caused by IMN only partly induced changes in the systemic inflammatory response (only monocyte

HLA-DR expression in patients with isolated femur PF299 price fractures). Most striking was the absence of additional PMN activation after intramedullary nailing. This lack of change in PMN phenotype during IMN is in line with suggestions from a previously published report [19]. In that cohort, no increase was seen in MAC-1 expression on PMNs after bilateral femur fracture fixation. Thus, the extend of PMN activation appears mainly determined by the severity of initial trauma and is apparently not altered by intramedullary nailing. In contrast, plasma IL-6 levels and monocyte HLA-DR were significantly altered by intramedullary nailing. Thus, an impact of the surgical procedure can be measured by cytokines and the monocyte compartment. The blood samples were taken 1 hour prior to IMN and 18 hours after IMN, regardless of the interval between trauma and surgery. Although this affects the reproducibility of the results, it reflects daily care practice. 18 hours after IMN the peak of plasma IL-6 levels will be passed (max

at 6 hours post-operatively), but the changes in PMN phenotype will be selleck chemicals most defined. PMN phenotype behaved similarly in all patients, therefore, 38 patients were sufficient to state the conclusion. Because we analyzed the Bucladesine chemical structure functional phenotype of PMNs and monocytes, more information was obtained than merely static phenotypes. The inflammatory cellular response deficit to the development of ARDS appears to be mainly determined by the initial injuries

and not the additional insult by IMN. Acknowledgements This project was funded by the AO Foundation, grant S-06-14H. References 1. Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M, et al.: Incidence and outcomes of acute lung injury. N engl j med 2005, 20;353:1685–1693.CrossRef 2. Pape HC, Auf’m'kolk M, Paffrath T, Regel G, Sturm JA, Tscherne H: Primary intramedullary femur fixation Acetophenone in multiple trauma patients with associated lung contusion–a cause of posttraumatic ards? J trauma 1993, 34:540–547.PubMedCrossRef 3. Bosse MJ, Mackenzie EJ, Riemer BL, Brumback RJ, Mccarthy ML, Burgess AR, et al.: Adult respiratory distress syndrome, pneumonia, and mortality following thoracic injury and a femoral fracture treated either with intramedullary nailing with reaming or with a plate. A comparative study. J bone joint surg am 1997, 79:799–809.PubMed 4. Dunham CM, Bosse MJ, Clancy TV, Cole FJ, Coles MJ, Knuth T, et al.: Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients: the east practice management guidelines work group. J trauma 2001, 50:958–967.PubMedCrossRef 5.

Elegant studies by C Hill’s group on the effect of mutations in

Elegant studies by C. Hill’s group on the effect of mutations in 6 of the genes encoding PBPs (including lmo1438) on the susceptibility of L. monocytogenes to β-lactams, revealed that lmo0441 and lmo2229 (PBP4) contribute to the β-lactam

resistance of L. monocytogenes, but inactivation of lmo1438 did not result MK-8776 clinical trial in obvious changes to either the sensitivity to β-lactams or the cell morphology [8]. Taking into account the seemingly contradictory nature of the aforementioned reports and the fact that the gene encoding PBP3 has yet to be directly identified, plus the absence of reports regarding the physiological function of this protein, our study focused on gene lmo1438 (potentially encoding PBP3). Here we describe the use of the lactococcal nisin-controlled expression (NICE) system [10] for the overexpression of this gene. This strategy was chosen because in a recently described analysis, mutational inactivation of lmo1438 had no obvious physiological effect [8]. In the present study, it has been directly demonstrated that lmo1438 encodes L. monocytogenes PBP3. Overexpression of this protein, which was accompanied by a slight increase in PBP4 expression, Selleck S3I-201 resulted in growth

retardation, shortening of cells in the stationary phase of growth and minor changes in the susceptibility of L. monocytogenes to β-lactams. The observed changes in cell morphology indicate the involvement SIS3 of PBP3 in cell division. These novel data on the overexpression of gene lmo1438 provide a more comprehensive view of the physiological function of PBP3 and its significance in the susceptibility of L. monocytogenes to β-lactams. These findings also further our understanding of the mechanisms of L. monocytogenes susceptibility to β-lactams, which is of direct relevance to its antibiotic resistance, the use of antibiotic therapy to treat listeriosis, as well as the ability of this bacterium to form biofilms [2, 11]. Results and discussion Construction of plasmid pAKB carrying the nisin-controlled expression (NICE) system DAPT mouse and its application in

L. monocytogenes Given the contradictory reports on the significance of PBP3 in the susceptibility of L. monocytogenes to β-lactam antibiotics, it was decided to study the effects of overexpression of L. monocytogenes gene lmo1438. The lactococcal NICE system [10] was chosen for overexpression studies since it has previously been successfully used in a number of gram-positive genera, including L. monocytogenes [12–15]. This system consists of a two-component signal transduction system NisRK, which senses the presence of nisin and induces transcription from the promoter Pnis. Recently developed strategies for using the NICE system either place the nisRK genes on the host chromosome, which allows the use of a single-plasmid system with a nisA promoter [13], or place both nisRK and the nisA promoter on one plasmid [16]. The first strategy was successfully used in L. monocytogenes by Cotter et al.

Studies on skin

Studies on skin symptoms in relation to exposure Selleck PHA-848125 do exist (de Joode et al. 2007; Sripaiboonkij et al. 2009a, b), but even less information is available on the associations between exposure, skin, and respiratory symptoms as well as the relationship between skin and respiratory effects. Many occupational studies report the prevalence of both skin and respiratory symptoms but rarely explore the relationship between the two, or the prevalence of these symptoms coexisting. Lynde et al. (2009) reported that among male cleaners, those with skin symptoms were more likely to report respiratory symptoms. The mechanisms of

airborne and skin exposure are complex. Airborne and skin exposures can be related if they share sources, but these associations are

so far poorly studied (Schneider et al. 1999). Associations between skin and airborne exposures have been reported for bitumen and pyrene in road pavers, 1,6-hexamethylene diisocyanate (HDI) in spray painters, methylene bisphenyl isocyanate (MDI) in foundry works, solvents in spray painters, and nickel exposure in primary industries (McClean et al. 2004; Burstyn et al. 2002; Chang et al. 2007; Fent et al. 2008; Liljelind et al. 2010; Hughson and Cherrie. 2005). In two other studies, both involving pesticide exposure, there was no association found between skin and airborne exposure. The authors attribute this lack of association to the fact that the primary source of skin exposure was likely contact with contaminated foliage rather than the settling PLX3397 cost of airborne pesticide (Flack et al. 2008; Aprea et al. 2009). Bakery and auto body shop workers have both skin and respiratory exposures to known occupational allergens, making them good

candidates for further study of exposure–response relationships for skin symptoms, as well as the relationship between skin and respiratory symptoms. Loperamide Bakery and auto body shop workers are at increased risk of occupational asthma (OA) as well as occupational skin disease (OSD) due to their workplace exposures: flour dust and diisocyanates, respectively (McDonald et al. 2005, 2006). Flour dust is a common cause of occupational asthma in bakers. Flour dust, which includes wheat and α-amylase allergens among others, contains high molecular weight (HMW) antigens which act through an IgE-mediated (Type I) immunological pathway to cause OA and contact urticaria, and can also cause contact dermatitis through a Type IV (cell-mediated) mechanism (Nethercott and Holness 1989). Isocyanates are a heterogeneous group of compounds, including monomers and oligomers, categorized as low molecular weight (LMW) antigens. The mechanism of action leading to isocyanate-induced OA is not yet fully understood and though IgE (Type I)-mediated processes do appear to play a role in some cases, other unrevealed mechanisms play a role in respiratory sensitization (Target Selective Inhibitor Library Maestrelli et al. 2009; Wisnewski 2007).

European estimates suggest only 1 in 14 PKU centers monitor bone

European estimates suggest only 1 in 14 PKU centers monitor bone in children while 3 in 5 monitor bone in adults. Frequency of monitoring is

unreported in the U.S. This study aims to use clinical parameters collected in PKU patients to predict total bone mineral density (BMD). METHODS: Data were collected from early-treated PKU patients over 4 years of age at baseline of a clinical trial (n = 57). Demographic (age, sex, BMI), clinical (phe prescription, medical-food prescription), laboratory (plasma phe and tyrosine, lipids, vitamin D), genetic (AV sum, a genetic mutation severity score), and dietary data were included. Correlation coefficients adjusted for age, sex, BMI, phe, and medical food intake were calculated between each parameter and total BMD, a reproducible

measure reflecting www.selleckchem.com/products/ars-1620.html average density of multiple sites. Predictors that correlated significantly with BMD and interactions terms were considered in models. Final models PX-478 clinical trial with (1) all data, (2) routine clinic visit data (excluding vitamin D, lipids), and (3) routine + genetic data were selected considering r-square and MSE. Categories of actual and predicted BMD z-scores were compared: normal [>−1stadard deviation (SD) from reference], at-risk (−2.5 to −1SD), and low (<−2.5SD). Future studies will collect variables Captisol included in models to validate predicted BMD and DXA-measured BMD (total, axial, and peripheral). RESULTS: In the sample (mean age = 17.3; 60 % male), 16 (28 %) had at-risk BMD; 3 (5 %) had low BMD. BMD was correlated with age, BMI, medical food prescription, cholesterol, triglycerides, vitamin D, and AV sum (p < 0.05). R-square values for final models ranged from 0.75 to 0.86 suggesting good fit. Models’ estimated BMD correlated with actual BMD [correlation coefficients (1) 0.93, (2) 0.87, (3) 0.91; p-value <0.0001] and predicted z-scores agreed with actual z-scores (kappa = 1.00; p-value <0.0001). CONCLUSIONS: Nearly one-third of study participants had BMD 1 SD below normal, and 3 had BMD Metalloexopeptidase at least 2.5 SD below normal. Routinely collected parameters

can predict total BMD and z-score category (normal, low, at-risk) in individuals with PKU. Each of the models can be used to identify patients at-risk for bone abnormalities without DXA expense and radiation exposure. Partial research support by BioMarin Pharmaceuticals and in part by PHS Grant UL1 RR025008 from the Clinical and Translational Science Award program, National Institutes of Health, National Center for Research Resources P17 DISAGREEMENT IN THE DIAGNOSIS OF OSTEOPENIA/OSTEOPOROSIS BY DUAL ENERGY X-RAY ABSORPTIOMETRY MEASUREMENTS WITH NORLAND INSTRUMENTS, BETWEEN DEVICE REFERENCE CURVES AND SELF-DEVELOPED REFERENCE CURVES, IN THE SPANISH FEMALE POPULATION Juan D. Pedrera-Zamorano, PhD, Metabolic Bone Diseases Research Group. University of Extremadura, CACERES, Spain; Jesus M. Lavado-Garcia, PhD, Metabolic Bone Diseases Research Group.

8–1 2 pH units was

observed in solutions prepared

8–1.2 pH units was

observed in solutions prepared ABT888 in PP syringes compared with 0.9–1.2 units for those prepared in glass and 1.6–1.8 units for those prepared in PVC bags. The results are presented in Table 2. This decrease could be explained by the release of methanesulphonic acid that occurs during busulfan degradation. However, it should be noted that the pH values measured throughout the study remain compatible with intravenous administration. Table 2 Change over time in pH values of busulfan find more diluted in 0.9 % sodium chloride at a 0.55 mg/mL concentration Container Temperature (°C) Initial pHa pHa 6 h 12 h 18 h 24 h 30 h 36 h 42 h 48 h PP syringes 4 5.78 ± 0.01 5.39 ± 0.06 5,04 ± 0.01 5.09 ± 0.02 5.04 ± 0.03 4.99 ± 0.01 4.91 ± 0.01 4.93 ± 0.05 4.90 ± 0.08 13 5.70 ± 0.04 5.30 ± 0.02 5.08 ± 0.04 5.06 ± 0.05 5.09 ± 0.02 4.95 ± 0.04 4.99 ± 0.06 4.88 ± 0.06 4.99 ± 0.08 20 5.82 ± 0.07 5.23 ± 0.02 4.99 ± 0.02 5.03 ± 0.04 4.98 ± 0.03 4.87 ± 0.05 4.99 ± 0.08 4.85 ± 0.09 4.84 ± 0.02 PVC bags 4 6.77 ± 0,05 5.54 ± 0.14 5.44 ± 0.34 5.13 ± 0.03 5.12 ± 0.02 4.98 ± 0.06 5.05 ± 0.02 4.88 ± 0.10 5.02 ± 0.01 13 6.50 ± 0.11 5.33 ± 0.09 5.23 ± 0.21 5.15 ± 0.05

4.95 ± 0.04 4.88 ± 0.02 4.87 ± 0.02 4.86 ± 0.09 4.87 ± 0.04 20 6.49 ± 0.15 5.38 ± 0.05 5.04 ± 0.04 5.10 ± 0.06 4.86 ± 0.06 4.85 ± 0.06 4.87 ± 0.02 4.80 ± 0.07 4.87 ± 0.04 Glass bottles 4 6.10 ± 0.01 5.54 ± 0.02 5.17 ± 0.02 5.13 ± 0.03 5.14 ± 0.02 5.01 ± 0.06 4.93 ± 0.02 Raf inhibitor 4.88 ± 0.02 4.90 ± 0.05 13 5.97 ± 0.03 5.43 ± 0.08 5.15 ± 0.01 5.10 ± 0.02 5.12 ± 0.01 4.90 ± 0.03 4.94 ± 0.02 4.88 ± 0.06 4.94 ± 0.04 20 5.94 ± 0.02 5.41 ± 0.05 5.14 ± 0.05 5.04 ± 0.03 5.04 ± 0.03 4.87 ± 0.10 4.90 ± 0.04 Atazanavir 4.92 ± 0.01 5.04 ± 0.10

aValues presented as mean ± standard deviation (n = 4) PP polypropylene, PVC polyvinyl chloride Osmolarity changes (between 0 and 48 h) appear to be consistent with the stability described above: at 2–8 °C, there is no significant difference in osmolarity, regardless of the container used; at 13–15 °C, osmolarity is significantly different in PVC bags (p < 0.05, p = 0.002) and in glass bottles (p < 0.05, p = 0.003).

2004; Bloom and Chatterji 2009; Chowdhury and Santos 2010; Dees 2

2004; Bloom and Chatterji 2009; Chowdhury and Santos 2010; Dees 2009; Smith and Stevens 2010). The latter define upscaling as increasing the impact produced by a social-purpose organization to better match the magnitude of the social need or problem it seeks to address. They distinguish upscaling and deep KU55933 mw scaling. Upscaling refers to the growth in social value by expanding a current program to other geographic locations. This involves effort and costs in terms of building infrastructure, organizing and developing an ecosystem, obtaining licenses, and educating customers in a new region. Deep scaling refers to focusing energies and resources on achieving greater impact in the

same location where the enterprise was started by Ilomastat purchase engaging in activities like improving the quality of services, achieving greater penetration of the target population, Belnacasan finding new ways to serve people, extending services to new people, and developing innovative financial management approaches. Karamchandani

et al. (2009) and Klein (2008) have a somewhat different view. They refer to upscaling as the capacity of the enterprise to expand quickly, effectively, and efficiently. Upscaling can also mean expanding the capacity of the existing business, in the sense of developing resources, building a knowledge base, employing people, developing management systems, and even developing a culture. According to them, upscaling, thus, includes serving more people with the same product within the same region, as well as extending into new markets, i.e., different geographies. In a given situation, the meaning

of upscaling, to a large extent, depends on the motivation of the entrepreneur. Some enterprises may focus on developing a specific region in terms of new products and services before scaling geographically, while others may choose to scale into new geographies before venturing into new products and services. According to Dees et al. (2004), choosing the right path towards broader social impact is a complex matter, since it involves judgment, experimentation, and continuous learning. They develop an approach towards upscaling based on following five Rs, i.e., Readiness, Resources, Receptivity, Risk, and Return. Bloom and Chatterji (2009) Selleckchem Baf-A1 suggest the SCALERS model, i.e., Staffing, Communicating, Alliance-building, Lobbying, Earnings-generation, Replicating, and Stimulating market forces. Chowdhury and Santos (2010) suggest that successful upscaling can be achieved by disseminating information through the use of best-practice blueprints or intermediaries such as multilateral organizations and consulting firms. Since our study is set in an emerging economy with deep-rooted social inequality and poverty in addition to environmental problems, it is pertinent to also examine the literature about development projects, program, and non-governmental organizations (NGOs) for possibly useful insights about upscaling.