NC_003869; [25]) and Thermotoga maritima (GenBank Accession No. NC_000853; [26]) microorganisms. The protein sequences of the proteins under scrutiny share a 26-70% identity and a 46-75% similarity with the E. coli K12 SSB, a 21-53% identity and 38-66% similarity with the Shewanella woodyi SSB, a 21-31% identity and 37-48% similarity with the B. subtilis SSB, a 21-36% identity and

36-53% similarity with the Thermoanaerobacter LY2606368 supplier tengcongensis SSB3, and a 19-31% identity and 34-52% similarity with the Thermotoga maritima (Table  2). The similarity between these proteins refers

primarily to the N-terminal domain and the LBH589 solubility dmso four or five terminal amino acids of C-terminal domain which are common in all the known bacterial SSB proteins. Figure 1 The multiple amino acid alignment of the SSB proteins under study, with the SSBs from psychrophilic, mesophilic and thermophilic bacteria. The alignments were performed by dividing the amino acids into six similarity groups: group 1 V, L, I, M, group 2 W, F, Y, group 3 E, D, group 4 K, R, group 5 Q, D, and group 6 S, T. The capital letters represent single amino acid codes. White fonts on black boxes represent 100% similarity, white fonts on grey boxes denote <80% similarity, and black fonts

on grey boxes show <60% similarity. Abbreviations: DpsSSB Desulfotalea psychrophila (NCBI Reference Sequence: WP_011189820.1), FpsSSB Flavobacterium psychrophilum (NCBI Reference Sequence: WP_011963776.1), ParSSB Psychrobacter arcticus (NCBI Reference Sequence: AAZ19531.1), PcrSSB Psychrobacter cryohalolentis (NCBI Reference Sequence: ABE75735.1), Flavopiridol (Alvocidib) PinSSB Psychromonas ingrahamii (NCBI Reference Sequence: WP_011771629.1), PprSSB Photobacterium profundum (NCBI Reference Sequence: WP_011219846.1), PtoSSB Psychroflexus torquis (NCBI Reference Sequence: WP_015023871.1), SwoSSB Shewanella woodyi (NCBI Reference Sequence: WP_012323283.1), EcoSSB Escherichia coli K12 (NCBI Reference Sequence: YP_492202.1), BsuSSB Bacillus subtilis (NCBI Reference Sequence: NP_391970.1), TteSSB3 Thermoanerobacter tengcongensis MB4 (NCBI Reference Sequence: AAM25884.1), and TmaSSB Thermotoga maritima MSB8 (NCBI Reference Sequence: WP_004081225.1). An arrow indicates the boundary between the N-and C-terminal domains.

Electrochemical experiments GDC-0449 in vitro were carried out with a CHI-660B electrochemical workstation (Shanghai, China). Measurements were performed at least three times on a glassy carbon

electrode (GCE). A conventional three-electrode system was employed, comprising a GCE (3-mm diameter) as the working electrode, a platinum wire as the auxiliary electrode, and an Ag/AgCl (saturated KCl) as the reference electrode. Voltammetric responses were recorded in 50 ml of substrate solutions prepared in PBS buffer solution. First, the modified electrode was activated by several successive voltammetric cycles from -0.20 to 0.80 V. Second, cycle voltammograms (CVs) at the rate of 50 mV · s-1 were carried out from -0.20 to 0.80 V after subtracting the background. Finally, the GCE was regenerated by 10 successive cyclic voltammetric sweeps in the blank solution. After several measurements, the GCE should be repolished. All the electrochemical measurements were carried out at room temperature. Preparation of SmBO3 nanocrystals Precursor-laminated SmBO3 multilayers were synthesized by solid-state-hydrothermal method. In a typical synthesis, 0.6 mmol Sm2O3, 0.72 mmol H3BO3, 14 ml deionized

water are mixed in a 20-ml-capacity Teflon-lined autoclave. The autoclave is sealed and maintained at 200°C constantly for 36 h and then cooled to room temperature naturally. The precipitation is centrifuged and washed with deionized water several times. Finally, as-obtained check details products are dried under vacuum at 60°C for 4 h. We propose that the formation processes of SmBO3 in the solid-state-hydrothermal system at 200°C can be assigned to two stages: Sm2O3 is first transformed into hydroxide, Sm(OH)3, then the hydroxide

interacts with H3BO3 to form products. The formation reactions of SmBO3 are proposed and shown in Figure 1. Figure 1 Formation mechanism of SmBO 3 in the S-S-H route. Immobilization of laccase on SmBO3 nanocrystals The SmBO3 multilayers were employed as carriers for the immobilization however of laccase, and the laccase was immobilized on these materials by the physical adsorption method. In a typical procedure, 100 mg of SmBO3 support was suspended in 10 ml of phosphate buffer (pH = 7.0) containing a certain amount of laccase (about 20 mg). The mixture of the supports and laccase solution was slowly stirred at room temperature for 12 h. Subsequently, the laccase immobilized on SmBO3 was separated by a centrifuge. Then the samples were washed with 10 ml of buffer solution by shaking for 5 min and separated quickly using a centrifuge. The washing procedure was repeated several times until no protein was detected in the supernatant. Finally, the laccase immobilized by SmBO3 were stored at 4°C before using. The percentage of the immobilized laccase on the SmBO3 samples is in the range of 10.7% ~ 15.2%.

Campylobacter concisus is a heterogeneous species complex comprised of several phenotypically indistinguishable but genetically distinct taxa (“”genomospecies”"). Numerous methods can be used to genetically separate the genomospecies, including PCR analysis

of the 23S rRNA gene [11] and cluster analysis of amplified fragment length polymorphism (AFLP) or random amplified polymorphic DNA (RAPD) profiles [1, 2]. Based on these typing methods, at MLN2238 mw least two main C. concisus genomospecies have been identified [1, 2, 4, 11]. Differences in pathogenicity amongst distinct genomospecies of some bacterial taxa [12, 13] support the notion that certain C. concisus genomospecies may be more likely than others to cause intestinal disease. While an early study by Van Etterijck et al. [10] concluded that C. concisus was not pathogenic given similar isolation rates from diarrheic and healthy children, genetic diversity of the isolates with respect to clinical presentation was not considered.

A more recent study showed that isolates from healthy individuals were genetically distinct from those of diarrheal origin; however, differences in epithelial cytotoxicity between the two groups were not evident [2]. Additionally, cluster analysis of diarrheic isolate AFLP profiles delineated two main C. concisus Selleck Fer-1 genomospecies (designated genomospecies 1 and 2), which where characterized by type strains of oral and diarrheal origin, respectively [1]. Genomospecies 2 isolates were more frequently isolated from the stool of patients presenting with diarrhea in which no other pathogens were found, and bloody diarrhea was associated only with genomospecies 2 isolates. While

these studies suggest that distinct C. concisus genomospecies may vary in their pathogenic ability, this has yet to be empirically examined. Our understanding of Campylobacter pathogenesis is based primarily on C. jejuni. Its small, spiral shape coupled with flagella-mediated motility, allow C. jejuni to penetrate intestinal mucus [14] where it can then adhere to and invade intestinal epithelial cells. This bacterium can also translocate across the intestinal epithelium via a paracellular mechanism involving disruption of epithelial Meloxicam tight junctions [15, 16] or via a lipid raft-mediated transcellular mechanism [17]. C. jejuni also causes cellular cytotoxicity through the production of various toxins; cytolethal distending toxin (CDT) is a well-characterized toxin produced by most strains. The cytolethal distending toxin blocks cell proliferation in the G2/M phase resulting in cellular distension leading to the induction of apoptotic cell dealth [18]. This bacterium also induces intestinal epithelial secretion of interleukin-8 (IL-8), a pro-inflammatory chemoattractant that recruits neutrophils to the site of infection [19]. Cytolethal distending toxin-like activity has been reported for a majority of clinical C.

Bcl-x gene was cloned by Boise[8] in 1993 by screening a chicken lymphocyte cDNA library using mouse Bcl-2 cDNA as the probe. Bcl-x has dual regulatory roles after activation. It is localized at 20q11.21 and a different splicing site at the 5′ terminus of its 1st mRNA exon leads to two fragments: a longer fragment Bcl-xl and a shorter fragment Bcl-xs. In recent years, expression of Bcl-x gene products (Bcl-xl and Bcl-xs)

in some tumors has been reported in domestic and foreign studies. However, the expression status in endometrial carcinoma tissue has rarely been characterized yet. Expression of Bcl-xl in endometrial carcinoma tissue and the significances Bcl-xl contains 241 amino acids and BH1-BH4 4 homologous sequences. Its sequence is 43% identical to that of Bcl-2 and their

click here functions are similar too. Bcl-xl could inhibit cell apoptosis through forming heterodimer with Bax in cytosol. Studies found that Bcl-xl could inhibit apoptosis in a Bcl-2-independent manner. It could inhibit cell apoptosis mediated by many apoptosis-inducing factors, which was far upstream in regulation of apoptosis. Bcl-xl protein was highly expressed Small molecule library ic50 in some tumors with low level of Bcl-2. Some researchers believed that Bcl-xl protein might have substituted the function of Bcl-2 in some tumors. Under certain condition, this protein has stronger apoptosis-inhibitory effect over Bcl-2, indicating the key role of Bcl-xl in the process of cell transformation. Studies showed that tumor cell apoptosis could be induced by lowering the Bcl-xl expression in human prostate cancer tissue[9]. Furthermore, Methocarbamol researches demonstrated that induction of tumor cell apoptosis could be achieved through inhibiting the expression of Bcl-xl in malignant pleural mesothelioma[10]. Boehmdenf et al. [11]also showed that Bcl-xl expression in head and neck squamous cell carcinoma was significantly different among different types of pathological grading, while the expression of Bcl-xl protein in human prostate cancer specimens was closely correlated with the Gleason scoring

and metastasis of human prostate cancers[12]. Therefore, Bcl-xl plays an important role in pathogenesis of tumor as an anti-apoptotic factor, and chemotherapy-resistance of the tumor cell may be associated with high level of Bcl-xl expression [13, 14]. Our study found that expressions of Bcl-xl mRNA and protein were slightly increased in simple hyperplasia and atypical hyperplasia endometrial tissues, while significantly increased in endometrial carcinoma tissue. In addition, Bcl-xl expression was correlated with the pathological grading of endometrial carcinoma, suggesting that elevation in Bcl-xl disrupted the regulation of signal transduction and normal gene expression, while it led to abnormal endometrial cell proliferation differentiation and eventually endometrial carcinoma.

In contrast, elements carbon

(C) (Figure 4B) and copper (Cu) (Figure 4E) were distributed both inside and outside of cells because cells were embedded by carbon-contained plastic Epon before section in order to maintain the cell shape, as well as sectional samples were coated by copper grids to support thin slicing of bio-samples. However, strong signals of selenium as shown by orange color were only observed outside of cells whereas the color in cells was black background even the white dots in cells signaling pathway suspected to be SeNPs were not similar to SeNPs outside of cells (Figure 4D), indicating that SeNPs were only formed outside of cells rather than inside of cells. The EDS map of elemental selenium was consistent with TEM-EDX result focusing on high density particles, i.e., SeNPs did not occur in the interior of C. testosteroni S44 cells. In addition, it was clear that small SeNPs aggregated into bigger particles outside of cells (Additional file 1: Figure S1). Figure 3 EDX analysis of electron dense particles formed by cultures of C. testosteroni S44 amended with 1.0 mM sodium selenite. (A) Extracellular particles pointed out by arrows. The emission lines for selenium are shown at 1.37 keV (peak

SeLα), 11.22 keV (peak SeKα) and 12.49 keV (peak SeKβ). (B) Intracellular particles pointed out by arrows. No emission peaks of Se. Figure 4 Localization of selenium particles using EDS Elemental Mapping. (A) The box showed the check details mapping area of B-E, where the K series peaks of the elements was used for mapping. The arrow points to an extracellular selenium particle. B, C, D and E show the distribution of different elements of C (from cell and Epon), Cl, Se and Cu (from Cu grids), respectively. Tungstate inhibited Se(VI) but not Se(IV) reduction Tungsten has been used as

an inhibitor of the molybdoenzymes, since it replaces molybdenum (Mo) in the Mo-cofactor (MoCo) of these enzymes. Tungstate did not affect Astemizole reduction of Se(IV) (Figure 5A) since the same red color of the SeNPs could be observed whether tungstate was added to cells of C. testosteroni S44 or not. In contrast, addition of tungstate and Se(VI) resulted in no development of red colored nanoparticles as in the negative control with no added Se(VI) and tungstate. In contrast, addition of Se(VI) without tungstate resulted in red-colored colonies on LB agar plates (Figure 5B). Therefore, tungstate only inhibited molybdenum-dependent Se(VI) reduction and subsequent reduction to elemental selenium and formation of nanoparticles. Similar results were obtained in different media such as LB, TSB and CDM. Figure 5 Comparison of Se(IV) and Se(VI) reduction and tungstate inhibition in C. testosteroni S44. Cultures were amended with 0.2 mM Se(IV) (A), 5.0 mM Se(VI) (B), respectively, and with or without 10 mM tungstate.

Br J Cancer 2007, 96: 457–463.CrossRefPubMed 23. Davidson JD, Ma L, Flagella M, Geeganage S, Gelbert LM, Slapak CA: An increase in the expression of ribonucleotide reductase large subunit 1 is associated with gemcitabine resistance in non-small cell lung cancer cell lines. Cancer Res 2004, 64: 3761–3766.CrossRefPubMed 24. Bergman AM, Eijk PP, Ruiz van Haperen VW, Metformin order Smid K, Veerman G, Hubeek I, van den Ijssel P, Ylstra B, Peters GJ: In vivo induction of resistance to gemcitabine results in increased expression of ribonucleotide reductase subunit M1 as the major determinant. Cancer

Res 2005, 65: 9510–9516.CrossRefPubMed 25. Nakahira S, Nakamori S, Tsujie M, Takahashi Y, Okami J, Yoshioka S, Yamasaki M, Marubashi S, Takemasa I, Miyamoto A, Takeda Y, Nagano H, Dono K, Umeshita K, Sakon M, Monden M: Involvement of ribonucleotide reductase M1 subunit overexpression in gemcitabine resistance of human pancreatic cancer. Int J Cancer. 2006, 120 (6) : 1355–1363.CrossRef 26. Itoi T, Sofuni A, Fukushima N, Itokawa F, Tsuchiya T, Kurihara T, Moriyasu F, Tsuchida A, Kasuya K: Ribonucleotide reductase subunit M2 mRNA expression in pretreatment

biopsies obtained from unresectable pancreatic carcinoma. J Gastroenterol 2007, 42: 389–394.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions RA and BN have made substantial CH5424802 contributions to conception, design, data analysis, interpretation of data, and drafting the manuscript. MS, NM, AS, and KY have made substantial contributions to patients sample collection and acquisition of data. KH and TA have made contributions to revising the manuscript critically for important intellectual content. All authors read and approved the final manuscript.”
“Background Colorectal cancer (CRC) is the second leading cause PLEKHM2 of cancer-related deaths in the US and the incidence is increasing rather rapidly in developing countries including China [1]. Traditional treatments for colorectal cancer such as surgical resection and chemotherapy

do not increase the survival rate satisfactory enough. There are still 50% patients died from tumor recurrence and metastasis. It is of great importance to find a new therapeutics against colorectal cancer. Survivin, a member of the inhibitor of apoptosis protein (IAP) family, is expressed highly in most human tumors and fetal tissues, but is barely detectable in terminally differentiated cells [2]. The Survivin protein functions to inhibit caspase activation by interacting with caspases via baculovirus IAP repeat domains, therefore leading to negative regulation of apoptosis [3]. There was evidence by cDNA microarray that Survivin plays an important role in pathogenesis of colorectal cancer [4]. Several reports had successfully inhibited cancer cell growth by applying Survivin antagonists, antisense oligonuceotides or Survivin RNA interferences [5–7]. Thus Survivin is considered as an ideal target for colorectal cancer gene therapy [8].

Ballif M, Harino P, Ley S, Carter R, Coulter C, Niemann S, Borrell S, Fenner L, Siba P, Phuanukoonnon S, Gagneux S, Beck H-P: Genetic diversity of Mycobacterium tuberculosis in Madang, Papua New Guinea. The international journal of tuberculosis and lung disease: the official journal of the International Union against Tuberculosis and Lung Disease 2012, 16:1100–1107.

5. Gagneux S, DeRiemer K, Van T, Kato-Maeda M, de Jong BC, Tigecycline Narayanan S, Nicol M, Niemann S, Kremer K, Gutierrez MC, Hilty M, Hopewell PC, Small PM: Variable host-pathogen compatibility in Mycobacterium tuberculosis. Proc Natl Acad Sci U S A 2006, 103:2869–2873.PubMedCrossRef 6. Zhang Y, Yew WW: Mechanisms of drug resistance in Mycobacterium tuberculosis [State of the art series. Drug-resistant tuberculosis. Edited by C-Y. Chiang. Number 1 in the series]. The International Journal of Tuberculosis and Lung Disease 2009, 13:1320–1330.PubMed 7. Müller B, Streicher EM, Hoek KGP, Tait M, Trollip A, Bosman ME, Coetzee GJ, Chabula-Nxiweni EM, Hoosain E: Gey van Pittius NC, Victor TC, van Helden PD, Warren RM: inhA promoter mutations: a gateway to extensively drug-resistant tuberculosis in South Africa? Int. J. Tuberc. Lung Dis 2011, 15:344–351.PubMed 8. Sandgren A, Strong M, Muthukrishnan P, Weiner BK, Church GM, Murray MB: Tuberculosis Drug Resistance Mutation Database. PLoS Med 2009, 6:e1000002.CrossRef 9. Hazbón MH, Brimacombe M: Bobadilla del Valle M, Cavatore

M, Guerrero MI, Varma-Basil M, Billman-Jacobe H, Lavender C, Fyfe J, García-García L, León CI, Bose learn more M, Chaves F, Murray M, Eisenach KD, Sifuentes-Osornio J, Cave MD, Ponce de León A, Alland D: Population Genetics Study of Isoniazid Resistance Mutations and Evolution of Multidrug-Resistant Mycobacterium tuberculosis. Antimicrob Agents Chemother 2006,

50:2640–2649.PubMedCrossRef 10. Sherman DR, Mdluli K, Hickey MJ, Arain TM, Morris SL, Barry CE: Stover CK: Compensatory ahpC gene expression in isoniazid-resistant Mycobacterium tuberculosis. Science Interleukin-2 receptor 1996, 272:1641–1643.PubMedCrossRef 11. Gagneux S, Burgos MV, DeRiemer K, Enciso A, Muñoz S, Hopewell PC, Small PM, Pym AS: Impact of Bacterial Genetics on the Transmission of Isoniazid-Resistant Mycobacterium tuberculosis. PLoS Pathog 2006, 2:e61.PubMedCrossRef 12. Telenti A, Imboden P, Marchesi F, Lowrie D, Cole S, Colston MJ, Matter L, Schopfer K, Bodmer T: Detection of rifampicin-resistance mutations in Mycobacterium tuberculosis. Lancet 1993, 341:647–650.PubMedCrossRef 13. Van Deun A, Barrera L, Bastian I, Fattorini L, Hoffmann H, Kam KM, Rigouts L, Rüsch-Gerdes S, Wright A: Mycobacterium tuberculosis strains with highly discordant rifampin susceptibility test results. J Clin Microbiol 2009, 47:3501–3506.PubMedCrossRef 14. van Ingen J, Aarnoutse R, de Vries G, Boeree MJ, van Soolingen D: Low-level rifampicin-resistant Mycobacterium tuberculosis strains raise a new therapeutic challenge. Int. J. Tuberc. Lung Dis 2011, 15:990–992.PubMedCrossRef 15.

Cautions against oversimplifications from gene sampling and potential losses are valid and are growing (Archibald 2009; Bodyl et al. 2009; Howe et al. 2008; Inagaki et al. 2009; Stiller 2007; Stiller et al. 2009), though not always popular with the current multitude who continue to try to find the right place(s) for Cinderella’s slipper. Transitory and constant

associations There are multiple extant states of symbiotic associations between aquatic animals and photosynthetic organisms, both at the single cell level and multicellular levels. Many of them provide clues that might be useful in alternate considerations of how plastids differentiated and spread. An elaboration of many such examples is illustrated in the chapter by Johnson (2010) dealing with this website adaptive strategies in hosting cells and their organelles. These

adaptive strategies are mutualistic and are generally Stem Cell Compound Library driven by the sharing of basic metabolic resources. Dinoflagellate associations with coral tissue appear to be rather common, as are hydra and green algal associations (Trench 1979). To what extent there has been gene transfer between host and symbiont is generally not known. However, gene transfers between two very different Chl a/b algae to sea slug hosts have been demonstrated (Rumpho et al. 2008; Pierce et al. 2007). Another example from Stoecker’s laboratory (Johnson et al. 2007) highlights a ciliate that “fed” on flagellated cryptophytes and retained transcriptionally active cryptophyte nuclei. Such examples clearly suggest that transfer of genetic content is not uncommon among algal IKBKE groups and hosts. Yet, these associations, whether transitory or relatively stable, do not necessarily lead to evolutionary progressions as has been so commonly inferred for chloroplast lineage(s), especially among the collection of algae placed in the

chromalveolate group. Summary opinion The assumption of a one-time chloroplast origin and subsequent dispersals via specific hosts is clearly under threat from new data and multiple interpretations. With ever increasing examples of gene transfers (HGT, EGT) among prokaryotes and eukaryotes, of fungi to animals (Moran and Jarvick 2010), and between algae and animals, it is difficult to cling to some of the presently strongly held concepts of strictly linear progressions on which widely accepted models for the evolution of photosynthesis are based. It seems very unlikely that there was a straight linear progression to a PSI–PSII progenitor and one endosymbiotic cyanobacteria to chloroplast occurrence. Many phylogenomic applications have narrowed, rather than broadened, our views of evolutionary progressions.

The accuracy of secondary data sources in capturing cases has been explored with results varying upon the source selected Sirolimus solubility dmso and gold standard used [6–9]. In the study from Penberthy et al., the Virginia Cancer Registry (CR) and a statewide

hospital discharge file (HDF) were both tested for accuracy in correctly identifying a cancer and its site of origin. Data from inpatient medical records were used as the gold standard. Based on the conclusions stated, nor the CR neither the HDF was sufficient independently to allow the complete capture of incident cancer cases. However, HDF accuracy in capturing incident cancer cases was high, with the overall positive predictive value being 94% and site specific values ranging from 86% (cervix) to 98% (breast) [9]. In Italy, the government supports cancer surveillance throughout a network of population-based local CRs included in the Italian Association of Cancer Registries (AIRTUM). Currently, the AIRTUM covers 33.8% of the Italian population, namely 19 million people out of 61 million inhabitants. A notable disproportion in CRs coverage exists among Northern, Central and Southern areas of Italy (i.e., 50.2%, 25.5% and check details 17.9%, respectively) [10]. We have previously underlined the need to integrate data from the Italian CRs with additional sources and identified the National

Hospital Discharge Records (NHDRs) as a potential tool [11]. In this study we aimed to evaluate the burden of breast cancer in Italian women by analyzing data from the NHDRs through a non-model-based methodology with a specific focus on major surgical procedures. Compared to our previous work, data have been updated to reflect a larger time window (2001–2008 vs. 2000–2005) and methods refined to overcome some of the limitations from our previous study. Materials and methods Data source We used the NHDR database which includes records

from all the Italian public and private hospitals. Data were made available by the Italian Ministry of Health relatively to the time frame between 2001 and 2008. These data were subject to a systematic quality assessment performed at a Regional and central level. The matching with the National Institute for Statistics (ISTAT) by social security code showed a percentage of correct fantofarone linkage increasing from 95.6% in 2001 (50,921 records matched out of 53,226) to 99.8% in 2008 (58,367 records matched out of 58,492) [12, 13]. The years 1999 and 2000 were excluded due to incomplete data. Breast cancer cases were identified on the basis of the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) [14, 15]. We considered patients diagnosed with invasive breast cancer (i.e., malignant neoplasm of breast, ICD-9CM codes: 174.0-174.9 and 175.0-175.9). Data related to patients with in situ breast carcinoma (ICD-9-CM major diagnosis 233) were also included.

Brazil first launched her nanotechnology program in 2005 with a budget of about US$31 million with 10 research networks involving about 300 PhD researchers [27]. Their focus has been on nanoparticles, nanophotonics, nanobiotechnology, CNTs, nanocosmetics, and simulation and modeling of nanostructures. Brazil has a strong collaboration link in her plan 2007 to 2013 with BAY 73-4506 research buy European Union, South Africa, and India, which has strengthened

their nanotechnology capabilities. TERI [28] reported that active Nanoscience and Technology Initiative (NSTI) started in India when its government launched her 5-year plan 2007 to 2012 with a budget estimate of US$254 million (approximately Re1,000 crore). The plan was aimed at developing centers Ibrutinib supplier of excellence (COEs) targeting laboratories, infrastructure, and human resource development. They have strong collaboration with foreign stakeholders. Many of her states are participating actively in nanotechnology

programs such as Karnataka, Trivandrum and Tamilnadu engaging in biotechnology and health-related activities, respectively. The India Department of Science and Technology (DST) is the agency responsible for both basic and applied research in nanotechnology, with their areas of focus include nanotubes, nanowire, DNA chips, and nanostructured alloys/systems, among others. Molapisi [29] reported that South Africa is at the forefront and had strategically started her nanotechnology activities with a budget of US$2.7 million in 2005 and has spent a total sum of about US$77.5 million (2005 to 2012). South Africa nanotechnology is powered by her DST focusing on human capital development through students on researcher support program, establishment of nanoscience centers, equipment acquisition Bcl-w program, and establishment of nanotechnology platform and two nanotechnology innovation centers that will encourage patent and prototype products [26]. South Africa has a strong collaboration with foreign partners especially Brazil and India.

Today, South Africa has gone into applied research stage focusing on nanocatalyst, nanofilters, nanowires, nanotubes, and quantum dots [28]. Malaysia started her nanotechnology campaign in 2001 and categorized it as a strategic plan under her IRPA (8MP) 2001 to 2005. A more robust plan was made for a 15-year period from 2005 to 2020 with more than 150 local researchers focusing on nanotechnology for advance materials and biotechnology to encourage the development of new companies and new products [30]. Wiwut [31] reported that in Thailand, the National Nanotechnology Center (NANOTEC) was approved in 2003 with National Science and Technology Development Agency under Ministry of Science and Technology supervising with a mandate to promote industrial clusters in nanotechnology through human resource capitals and robust infrastructural development.