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biological evaluations of its analogues. Chin J Org Chem 2012,32(1):1–12.CrossRef 21. Xu J, Caro-Diaz EJ, Batova A, Sullivan SD, Theodorakis EA: Formal synthesis of (-)-englerin A and cytotoxicity studies of truncated englerins. Chem Asian J 2012,7(5):1052–60.PubMedCrossRef 22. Sulzmaier FJ, Li Z, Nakashige ML, Fash DM, Chain WJ, Ramos JW: Englerin A selectively induces necrosis in human renal cancer cells. PLoS One 2012,7(10):e48032.PubMedCrossRef 23. Sourbier C, Scroggins BT, Ratnayake R, Prince TL, Lee S, Lee BIIB057 MJ, Nagy PL, Lee YH, Trepel JB, Beutler JA, Linehan WM, Neckers L: Englerin A stimulates PKCθ to inhibit insulin signaling and to simultaneously activate HSF1: pharmacologically induced synthetic lethality. Cancer Cell 2013,23(2):228–37.PubMedCrossRef 24. Huang Y, Fang Y, Wu J, Dziadyk JM, Zhu X, Sui M, Fan W: Regulation of Vinca alkaloid-induced apoptosis by NF-κB/IκB pathway in human tumor cells. Mol Cancer Ther 2004,3(3):271–277.PubMed learn more 25. Chandra D, Choy G, Deng X, Bhatia B, AZD9291 Daniel P, Tang DG: Association of active caspase 8 with the mitochondrial membrane during

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We have demonstrated that these peptides exert broad-spectrum activity against both gram-positive and gram-negative bacteria, and thus could be useful in the treatment of patients with polymicrobial wounds infections [6, 7]. Methods 5.1 Bacterial strains and media S.

aureus (ATCC 25923, American Type Culture Collection, Manassas, VA) was grown in Nutrient Broth (Difco Laboratories, Detroit, Mich.) at pH 7, 37°C, 24 h with shaking at 200 rpm. The overnight culture was frozen with 20% glycerol and stored buy E7080 at -80°C. The frozen stock was enumerated (CFU/ml) by dilution plating and growth on Nutrient Agar plates. 5.2 Peptides and Anti-microbial assays The sequences and net charges of the peptides are shown in Table 1. The molecular weight reported here for each peptide reflects the trifluoroacetic acid (TFA) salt form of the peptides. NA-CATH, NA-CATH:ATRA1-ATRA1, ATRA-1, ATRA-1A, ATRA-2 peptides (86.1 and 89.7, 97.2, 94.5, and 88.2%, respectively) (Genscript, Piscataway, NJ), LL-37 (95% purity) (AnaSpec 61302) and D-LL-37 (92.0% purity) (Lifetein, South Plainfield, NJ) were synthesized CP673451 clinical trial commercially. The anti-microbial activity of the NA-CATH and NA-CATH:ATRA1-ATRA1, the variations

on the ATRA peptides LL-37 and D-LL-37 against S. aureus were determined as previously described, with some modification [26, 29]. For anti-microbial assays, frozen enumerated aliquots were thawed and gently mixed immediately before use. In a 96-well plate (BD Falcon 353072), 1 × 105 CFU per well bacteria were incubated with different peptide concentrations (in serial dilutions of 1:10 across the plate) in a solution of buffer containing this website sterile 10 mM sodium phosphate (pH 7.4) and incubated (3 h, 37°C). Negative control wells contained bacteria with no peptide. Serial dilutions were then carried out in sterile 1x PBS (Fisher Scientific) (pH 7) and plated in triplicate on Nutrient Agar plates, incubated (37°C, 24 h) and counted. Bacterial survival at each peptide concentration was calculated as previously described [25, 26] based on the

LY294002 percentage of colonies in each experimental plate relative to the average number of colonies observed for assay cultures lacking peptide. The EC50 was calculated as previously described [26, 47]. Each experiment was repeated at least twice, and a representative experiment is shown, for clarity. Errors were reported based on the standard deviation from the mean of the log10 EC50 values [19]. 95% confidence intervals were used to determine whether points were statistically different at p = 0.05. 5.3 CD Spectroscopy Circular dichroism (CD) spectra of the peptides were collected using Jasco J-815 spectropolarimeter. Samples were allowed to equilibrate (10 min, 25°C) prior to data collection in a 0.1 cm path length cuvette, with a chamber temperature 25°C throughout each scan. Spectra were collected from 190 to 260 nm using 0.

Several molecular diversity surveys over different spatial scales ranging from centimeters to tens of thousands of kilometers have supported distance-decay relationships (effect of distance on spatial interactions) for microbial organisms, including bacteria (e.g. [26, 27]), archaea (e.g. [28]), fungi (e.g. [29]) and also protists (e.g. [30–32]). Even organisms with large population sizes and the potential to spread globally using spores, which were assumed to be cosmopolitan [13, 33], show significant 3-MA mw non-random spatial distribution patterns [34]. However, in our study of ciliate communities in these

DHABs, a similar distance-decay relationship was not observed (insignificant correlation between Bray-Curtis and geographic distances in Pearson correlation Avapritinib purchase and Mantel test). A potential explanation could be that the small number of compared locations may have masked true patterns. Alternatively, the presence of a metacommunity [35] within the Mediterranean Sea could cause the absence of a significant heterogeneous distribution [36, 37]. In limnic systems geographic distance has been found to influence asymmetric latitudinal genus richness patterns between 42° S and the pole [32]. However, this seems to be a fundamental difference between marine and “terrestrial”

(land-locked) Selleckchem AZD5582 systems. Furthermore, on a global scale, historical factors were significantly more responsible for the geographic patterns in community composition of diatoms than environmental conditions [32]. In other marine studies ciliates showed variations in taxonomic composition between closely related samples, which were explained by environmental factors rather than distance [38]. Similarly, in our study geographic distance could not explain the variations Glycogen branching enzyme observed between the ciliate communities. Instead, hydrochemistry explained some of the variation in observed ciliate community patterns, and there was a strong separation of halocline interface and brine communities (Figure

3). The DHAB interfaces are characterized by extremely steep physicochemical gradients on a small spatial scale typically less than a couple of meters (for example, only 70 cm in Medee, [39]). The concentrations of salt and oxygen are the most prominent environmental factors that change dramatically along the interfaces into the brines. In a recent metadata-analysis of environmental sequence data, these two factors were identified as strong selection factors for ciliates [40]. Also for bacterial communities, salt concentration emerged as the strongest factor influencing global distribution [41]. Likewise, the bacterioplankton community composition in coastal Antarctic lakes was weakly related with geographical distance, but strongly correlated with salinity [42]. Accordingly, Logares et al.

Blood was collected via finger prick method for measurement of blood glucose and participants completed a second POMS questionnaire. Participants then mounted an electronically-braked cycle ergometer (Velotron, RacerMate Inc., Seattle, WA) and completed 3 Wingate Anaerobic Tests (WAnT) lasting 30 s each, and utilizing a resistance equal to ~7% body weight, with 2.5 min passive recovery between each test. Peak

power KU55933 order and mean power were recorded for each WAnT. After each WAnT, participants continued pedaling at a resistance level and cadence of their choice for 2.5 min. During all WAnT, participants were given strong verbal encouragement. Following the third WAnT, participants were given a short time (~15 min) to recover, towel off and have post-exercise weight measured before

reporting their session-RPE. Additionally, a 2-item selleck chemical questionnaire was administered to assess the difficulty of the exercise session compared to participants’ normal workouts and to assess their beliefs regarding whether drinking the assigned beverage improved their performance ability. Each question was assessed using a 100-mm visual analog scale. The same investigator collected and recorded all glucose concentrations but was not actively involved in the performance tests to minimize the risk of unblinding remaining investigators and participants to beverage identity since it was expected that CE would increase blood glucose levels. Beverage treatments For the experimental trials, participants received 1 of 3 treatments during the 60-min submaximal exercise

Bcl-w bout: water, a grape-flavored 6% carbohydrate-electrolyte (CE) beverage, or a non-caloric grape-flavored beverage containing electrolytes (NCE) and sweetened with sucralose and acesulfame potassium. Beverage treatments were administered to participants in 3 equal aliquots, chilled and in a tinted unmarked bottle at minutes 0, 20, and 40 during the 60-min submaximal cycling bout. Participants were instructed to consume all fluid within a 10–minute period from the time the beverage was received. The mean total beverage volume was 847 ± 368 mL and was equivalent to that participant’s sweat losses based on the familiarization trial. Study staff and participants were blinded to the caloric and non-caloric beverages but could not be blinded to water. Participants were informed that they would be receiving water and 2 sport beverages during the familiarization session when the purpose of the study was explained, but no other information regarding the beverages was provided. Additionally, participants were instructed not to discuss the characteristics of the beverages with other participants. Data Ferroptosis mutation analysis One-way repeated measures analysis of variance was used to analyze differences among beverage trials for WBGT, average HR, peak power for the first WAnT, mean power for the first WAnT , mean power averaged across all 3 WAnT, S-RPE, and post-exercise questionnaire items.

Taken together, these data do not support a PKA-mediated ET effect on TEM. Figure 3 ET activates PKA in HMVEC-Ls. HMVEC-Ls were seeded onto 10 cm plates and allowed to reach Tipifarnib datasheet 80-90% confluence prior to (A) 6 h exposure to increasing doses of ET, or (B) increasing exposure times with ET (1000 ng/mL:1000 ng/mL). Lysates were collected and PKA activity assayed by ELISA. Each vertical bar represents mean (+/- SEM) absorbance at 450 nm. The n for each group is indicated in each bar. * indicates significantly increased compared to the simultaneous medium controls at p < 0.05. Figure 4 ET Inhibition of TEM in the Presence of PKA Inhibitors. (A) HMVEC-Ls were preincubated in the presence (+) or absence (-)

of H-89 (10 μM) or KT-5720 (10 μM), respectively, before being treated with ET (1000 ng/mL:1000 ng/mL) for 6 h and lysed. The lysates were processed for pCREB immunoblotting. To control for protein loading and transfer, blots were stripped and 17-AAG reprobed for β-tubulin. IB, immunoblot, IB*, immunoblot after stripping. (B) The pCREB signals in each blot described in (A) were quantified

by densitometry of pCREB and normalized to β-tubulin signal in the same lane in the same blot. (C) HMVEC-Ls cultured to confluence in assay chambers were pretreated with medium, H-89 (10 μM) or KT-5720 (10 μM), after which they were treated for 4 h with medium, ET, ET with H-89, or ET with KT-5720. The HMVEC-L monolayers were then inserted into wells containing NU7441 supplier Etoposide mouse either medium or IL-8 (10 ng/mL), after which calcein-AM-labeled PMNs were added to the upper compartment of each chamber. After 2 h, the contents of each lower compartment were fluorometrically assayed. Each vertical bar represents mean (+/- SEM) TEM of PMNs (%). The n for each group is indicated in each bar. * indicates significantly increased compared to the simultaneous medium only controls at p < 0.05. ** indicates significantly decreased compared to IL-8 alone at p < 0.05. Forskolin (FSK) and 3-isobutyl-1-methylxanthine (IBMX) fail to reproduce the ET effect on IL-8-driven TEM of PMNs To provide further evidence that ET does not decrease TEM of PMNs through cAMP or PKA activity,

two distinct interventions known to increase cAMP, FSK and IBMX, each were introduced. To confirm that FSK and IBMX increased PKA activity in HMVEC-Ls, we first examined FSK- and IBMX- stimulated phosphorylation of CREB at 6 h (Figure 5A). FSK (10 μM) and IBMX (1 mM) each increased phosphorylation of CREB normalized to β-tubulin when compared to the simultaneous medium control (Figures 5B). Previous investigators have demonstrated that FSK and IBMX cause maximal increases of cAMP at 0.5 h with a decrease by 4 h [36]; in our studies, phosphorylation of CREB normalized to β-tubulin was elevated but not significantly different from the effect at the later time point (Additional File 1: Figure S1A, B). Next, we investigated the effects of FSK and IBMX on IL-8-driven TEM.

The amplification efficiencies were determined

through serial tenfold dilutions of the DNA samples using the LightCycler 480 software and were shown to be similar for each target gene, namely glpk, cdsB and rep. The relative copy number N of pMyBK1 or pMG2B-1 plasmids was calculated by the following formula: N relative = (1+E)-ΔCt, where E and ΔCt represent the PCR amplification efficiency and the difference between the cycle threshold number (Ct) of glpk and cdsB or rep reaction, respectively. The experiment was performed in triplicate. DNA sequencing and sequence analyses Purified check details mycoplasma plasmids were linearized using a restriction enzyme (EcoRI, EcoRV or HindIII) and were then sub-cloned into the pBluescript vector linearized with the same enzyme. The resulting plasmids were sequenced using T7 and T3 universal primers or by primer-walking when necessary. When there was not a unique restriction site within the plasmid, multiple restriction fragments were individually sub-cloned and sequenced. The nucleotide sequences were determined by means of at least two overlapping reads on each strand of the whole plasmids. When

Selleckchem MK-8776 necessary, complementary plasmid sequences were obtained by direct sequencing of PCR products (for the list of PCR primers see Additional file 1: Table S1). The plasmid sequences determined in this study have been deposited in the GenBank database under the following accession numbers: JX294729 for pMG1A-1, JX294730 for pMG1C-1, JX294731 for pMG2B-1, JX294732 for pMG2F-1, JX294733 for pMG2C-1, JX294734 for pMG2E-1, JX294735 for pMG2A-1, JX294736

for pMG2D-1 and JX294737 for pMG1B-1 (Table 1). Coding sequences (CDSs) were searched using the AMIGene software ([32], http://​www.​genoscope.​cns.​fr/​agc/​tools/​amigene/​). Pyruvate dehydrogenase Database searches and comparisons of DNA sequences or DNA-derived protein sequences were carried out using BLAST programs (http://​www.​ncbi.​nlm.​nih.​gov/​blast/​). Conserved domains were detected by GF120918 clinical trial CD-Search against the CDD resource from NCBI [33]. Protein secondary structures were predicted from sequences using the SOPM method [34]. DNA repeats were identified using the software RepFind [35], nucleic acid folding and calculation of free energy for hairpin formation were determined using the Mfold program [36]. Multiple sequence alignments were performed with T-Coffee [37] or ClustalW2 softwares [38]. Subsequent phylogenetic analyses were performed with the Mega 5 software [10] using the neighbor-joining or the maximum likelihood method. Multiple-way pairwise comparisons of plasmid nucleic sequences were conducted with the Artemis Comparison Tool, ACT [39]. Southern blot hybridization and immunoblotting The detection of ssDNA intermediates was performed by Southern blot hybridization and S1 nuclease treatment as described previously by others [40]. Total M.

The present work concerns repABC replicons, which are present on large, low copy-number plasmids and on some secondary chromosomes in at least 19 α-proteobacterial genera. Some bacterial strains contain more than one repABC replicon, indicating that this plasmid family encompasses several incompatibility groups [5–7]. The basic replicon of repABC plasmids is compact because all of the elements required for replication and segregation are encoded in a single operon, the repABC operon [8, 9]. However, this operon is controlled by a complex regulatory mechanism. The first two genes of the

repABC operon encode for proteins belonging to a type Ia segregation system BMN 673 price [10]. RepA and RepB have been implicated in the negative transcriptional regulation of the repABC operon [9, 11]. RepC is a limiting replication factor and thus has been suggested to be the initiator protein [8, 12, 13]. The members of the repABC family contain a centromeric-like sequence (parS) in three possible locations: downstream of and close to the stop codon of repC [14, 15], between repA and repB, or upstream of repA [16, 17]. A conserved sequence between the repB and repC genes is present in all known repABC replicons and contains an antisense RNA (ctRNA) gene, the product of which negatively modulates the expression of RepC [18–20]. Regulatory role of the ctRNA depends on its pairing with the repABC mRNA. In the absence LCZ696 datasheet of the ctRNA, the

mRNA section corresponding to the repB-repC intergenic region folds into a large stem-loop structure so that the predicted repC Shine-Dalgarno (SD) sequence and the repC initiation codon remain single-stranded, allowing repC translation. In contrast, when the ctRNA hybridizes with the repABC mRNA, the repC leader sequence forms an intrinsic terminator, blocking repC transcription [21]. Many aspects of the biology of these plasmids remain unknown, click here especially the details of the replication or segregation

of these genetic elements. In this paper, Oxalosuccinic acid we demonstrate the following: A) RepC is the only element encoded in the repABC operon of the Rhizobium etli p42d plasmid (formally pRetCFN42d) that is necessary and sufficient for plasmid replication. B) RepC is an incompatibility factor. C) The RepC carboxy-terminal region is involved in the incompatibility phenotype. D) The origin of replication of the repABC plasmid resides in a large A+T-rich region located at the central section of the repC gene. Methods Plasmids, bacterial strains and growth conditions The bacterial strains and the plasmids used in this work are described in Table 1. E. coli strains were grown at 37°C in Luria-Bertani medium. Rhizobium strains were grown at 30°C in PY medium supplemented with 1 mM CaCl2 [22]. Nalidixic acid (20 μg/ml) and chloramphenicol (30 μg/ml) were added when required. Growth kinetics were made in 500 ml flasks containing, 50 ml of PY medium without antibiotics. Incubation was performed at 30°C and 250 rpm.

Values shown are mean ± SD for sextuple cultures from one experiment, representive of three independent experiments conducted. B: PcDNA3.1(IGFBP7)-RKO cells (500/well) were seeded into 0.3% Bacto-agar over a 0.6% agar bottom layer in triplicate in 6-well plates, with or without 1 μg/ml HSP60. After 3 weeks of incubation, colony number (>100 μm)were analyzed. Values are mean ± S.D for data from three

independent experiments. C: Colony size was also analyzed under microscopy. Representive size of the colony was photographed under high power microscopy (×100). Discussion Here we describe a proteomics study of two human colon cancer cell lines differing in the expression of IGFBP7, which is an important tumor suppressor gene well defined by our Selleck MK1775 previous studies[7]. To our knowledge, this is the first proteomic

LY2874455 clinical trial study on the alterations of IGFBP7 protein expression profiles in colon cancer cells. We were successful in identifying six IGFBP7-associated downstream target proteins, including ALB, HSP60, Actin cytoplasmic Selleckchem RAD001 1 or 2, PKM2, FARSB and hypothetical protein. These differentially expressed proteins represent candidate proteins that may be directly or indirectly regulated by IGFBP7. The comparation between the current findings at the translation level and our previous studies identifying the IGFBP7-induced genes at the transcriptional level detected by Affymetrix chip platform(unpublished data) resulted in some interesting points in agreement. The proteomics finding indicated that actin was influenced by IGFBP7. While the cDNA array studies also indicated that the actin binding proteins were greatly influenced by IGFBP7. These findings at both the transcriptional and the translational level suggested that IGFBP7 may possibly be an actin-binding associated gene, which need our further study to provide the direct evidence. However, there is little overlap of identified genes between our mRNA and protein data, consistent with the data reviewed by Sagynaliev and the colleagues that

among various gene expression studies only about 25% of differentially expressed proteins Astemizole were reflected by concomitant changes at the mRNA level in CRC [18]. This may be due to two reasons. First, the lower dynamic range of the 2D PAGE protocol allows less abundant proteins to escape detection [19]. With only around 1100 protein spots visible, this approach allows the analysis of only a fraction of the total number of proteins expressed in the cell. Second, from the transcriptional profiles, we found that IGFBP7 could influence the expression levels of many secretary genes. However, many of them could not be detected by the current proteomics approach in the cell lysates samples. Secretome studies performed in the supermedium of the cells will probably enlarge our finding [20]. Among the differentially expressed proteins induced by IGFBP7, HSP60 attracted our attention.

The charge–discharge curves of the αAZD2281 -Fe2O3 NP (shown in Figure 1b) electrode during the first and second cycles are shown in Figure 7b. In selleck products the first discharge curve, there was a weak potential slope located at 1.2 to 1.0 V and an obvious potential plateau at 0.9 to 0.8 V. The

capacity obtained above 0.8 V was 780 mAh·g−1 (4.6 mol of Li per mole of α-Fe2O3). After discharging to 0.01 V, the total specific capacity of the as-prepared α-Fe2O3 reached 887 mAh·g−1, corresponding to 5.3 mol of Li per mole of α-Fe2O3. During the second cycle, the discharge curve only showed a slope at 1.0 to 0.8 V, and the capacity was reduced to 824 mAh·g−1. Usually, the slope behavior during the discharge process of metal oxide anode materials was considered to be related with the irreversible formation of a nanocomposite of crystalline grains of metals and amorphous Li2O matrix. The comparison of the rate as well as cycling performances between Fe2O3 NPs and nanoarchitectures were also conducted, which were obtained by a 12.0-h hydrothermal treatment at 150°C with a molar ratio of FeCl3/H3BO3/NaOH as 2:0:4 (Figure 1b) and 2:3:4 (Figure 2e), respectively. The discharge and charge capacities in the first cycle at a current of 0.1 C were 1,129 and 887 mAh·g−1 for

Fe2O3 NPs (Figure 7c) and 1,155 and 827 mAh·g−1 for Fe2O3 nanoarchitectures. AZD8931 cell line For the second cycle, the discharge and charge capacities were 871 and 824 mAh·g−1 for Fe2O3 NPs and 799 and 795 mAh·g−1 for Fe2O3 nanoarchitectures. The Li-ion storage

capacitance of the current Fe2O3 NPs/nanoarchitectures reported in this work is higher than that of hematite nanorod (ca. 400 mAh·g−1 at 0.1 C) [68], nanoflakes selleck kinase inhibitor [69], hierarchial mesoporous hematite (ca. 700 mAh·g−1 at 0.1 C) [65], hollow nanospindles (457 mAh·g−1 at 0.2 mA cm−2) [37], hollow microspheres (621 mAh·g−1 at 0.2 mA cm−2) [37], and dendrites (670 mAh·g−1 at 1 mA cm−2) [70]. When the current increased, both the discharge and charge capacities decreased, especially for Fe2O3 NPs (Figure 7c,e). The discharge and charge capacities of Fe2O3 nanoarchitectures were larger than those of Fe2O3 NPs. For instance, when the current rate increased to 2.0 C, the charge and discharge capacities of Fe2O3 nanoarchitectures were 253 and 247 mAh·g−1, while those of Fe2O3 NPs were only 24 and 21 mAh·g−1. This indicated that the Fe2O3 nanoarchitectures presented much improved rate performance for the reason that the porous nature of Fe2O3 nanoarchitectures allow a fast Li-ion diffusion by offering better electrolyte accessibility and also accommodate the volume change of NPs during Li insertion/extraction. However, similar to many Fe2O3 nanostructures reported in literatures, the α-Fe2O3 nanoarchitectures exhibited a rapid capacity fading within the potential range of 0.01 to 3.

K. and U.S. osteoporosis treatment guidelines. J Clin Endocrinol Metab 95:1856–1860PubMedCrossRef”
“Introduction Vitamin D status has been found to be poor among nonwestern immigrant populations in European countries compared to indigenous European populations [1–4]. The lower serum 25(OH)D concentrations among nonwestern immigrants compared to indigenous European populations may lead to differences

in health. Consequences of vitamin D deficiency include bone- and muscle-related symptoms (e.g., bone and muscle pain), decreased muscle strength, and diseases (e.g., LCZ696 chemical structure rickets in children; osteomalacia in adults) [5, 6]. Other possible consequences are diabetes mellitus, infectious diseases, and cancer [7]. Direct sunlight stimulates the production of vitamin D in the skin from 7-dehydrocholesterol. Other sources of vitamin D include some natural foods (e.g., fatty fish), fortified foods (e.g., margarine), and supplements. The amount of vitamin D produced through exposure to UVB radiation depends on skin type: the darker the skin, the more sunlight is required to produce a given amount of vitamin D [8–10]. Nonwestern immigrants usually have darker skin than indigenous European subjects. Therefore, they

have a higher risk of lower serum 25-hydroxyvitamin D (25(OH)D) concentrations when living at the same latitude. The duration of UVB irradiation needed to produce a certain quantity of vitamin SCH772984 molecular weight D in a particular skin surface depends on season, time of day, and geographical location [11]. The higher the latitude, the lower the UVB intensity, and the fewer months and hours per day during which vitamin D is produced. Most European countries are located at a higher latitude than the countries of Selleckchem Epacadostat origin of nonwestern immigrants. The threshold for vitamin D deficiency should—ideally—be based on its consequences. However, most studies of the consequences of vitamin D deficiency

have been performed among older western populations in Europe Liothyronine Sodium and North America, rather than among adult nonwestern immigrant populations in these countries. Another means of establishing a deficiency threshold is through the use of reference values within a population [12]. For that purpose, a comparison of the vitamin D status of nonwestern immigrant populations with the populations in their countries of origin might be more suitable than a comparison with the indigenous western populations. Our aim was to compare the vitamin D status of nonwestern immigrant populations with both the populations in their countries of origin and the populations in the country they migrated to. Additionally, we wanted to identify what determinants were mentioned to explain differences in vitamin D status between subgroups in the studied populations. Methods We performed literature searches in the “PubMed” and “Embase” databases. The search profile consisted of terms referring to vitamin D or vitamin D deficiency, prevalence or cross-sectional studies, and countries or ethnicity.