In this work, we report the use of bilayer graphene (BLG) as an a

In this work, we report the use of bilayer graphene (BLG) as an atomically smooth contact in a molecular memory. Although various device structures based on graphene have been explored [12], our study is unique in the context of its use to improve reliability. BLG may prevent the electromigration of Ni atoms into the active material of the device. Furthermore, the use of BLG instead of monolayer or several-layer graphene is twofold. As compared to the monolayer, the probability of complete coverage with BLG is higher in the presence of defects. On the other hand, with the increasing number of layers, the transport properties of the device may be dominated by

the multilayer graphene itself. Thus, BLG tends to provide an optimum trade-off. Methods The device schematic with BLG contact is shown in Figure 1a. We synthesized BLG on a 300 nm Ni film deposited on a 300-nm thermally grown oxide on Si substrate. Ni was deposited by using electron-beam INCB28060 price evaporator (Angstrom Engineering, Kitchener, Ontario, Canada) at 1 Å/s rate under LY2874455 order < 7 × 10−7 Torr chamber pressure. Ni pallets were placed in an alumina boat (both supplied by International Advanced Materials, Spring Valley, NY, USA) to avoid any contamination or residues. Prior to Ni evaporation, Si/SiO2 substrate was cleaned with acetone for 10 min, methanol for 10 min, deionized (DI) water rinse for

10 min, then nanostrip for 20 min (commercial Piranha substitute), followed by DI water rinse for another 10 min. This sequence removes the impurities from the SiO2 surface and provides better Ni adhesion. After Ni evaporation, the check details sample was further processed in UV

ozone cleaner (Novascan PDS-UV; Novascan Technologies, Inc., Ames, IA, USA) to remove any organic impurities on the Ni surface. The sample was then loaded into a homemade CVD furnace (Lindberg/Blue 1-in. diameter quartz tube; Thermo Fisher Scientific Inc., Waltham, MA, USA) at room temperature under Ar ambient with 200 standard cubic centimeter (sccm) flow rate. After ramping the temperature to 1,000°C, the sample was annealed in H2:Ar (65, 200 sccm) ambient for 10 min. BLG was then synthesized by flowing CH4:Ar (23, 200 sccm) for 2 min, and moving the hot portion of the tube to the room temperature by ultrafast cooling Nintedanib (BIBF 1120) [13]. Research grade 5.0 (minimum purity 99.999%) process gasses supplied by Praxair Inc. (Danbury, CT, USA) were used. A 100 nm C60 film was deposited on the Ni/BLG structure, by using thermal evaporator (Edwards Coating System, E306A; Edwards Coating System, Sanborn, NY) at 1 Å/s rate under < 7 × 10−7 Torr chamber pressure. The commercial C60 powder was supplied by M.E.R Corporation (Tucson, AZ, USA). The use of C60 molecules ensures uniformity of the channel material constituents. Next, the sample was loaded in the electron-beam evaporator, and 5 nm of SiO2 was evaporated, followed by 90 nm of Cr by using a shadow mask. The evaporation rates of SiO2 and Cr were 0.

In women, Bartholin abscesses and vulval skin infections are the

In women, Bartholin abscesses and vulval skin infections are the most common causes of NF. Surgical management includes wide incision and debridement of all involved areas. As the involvement of deep fascia and muscles is rare with this syndrome, it is not necessary to continue the debridement into the healthy-looking tissue. The mortality ranges from 11% to 45% despite

the improvement in critical care, usage of broad-spectrum antibiotics and aggressive surgical debridement [13]. The types of necrotizing infections on the AW are numerous and the indication for AW reconstruction after serial RGFP966 molecular weight surgical debridements and necrectomies depends on the etiology, size and site of the defects. Complicated intra-abdominal infections such as appendicitis with perforation, infections after complex hernia repairing, perforated diverticulitis, cholecystitis, gastroduodenal perforations, small bowel perforations, obstructive colon cancer with perforation and complex trauma of the AW, are the main sources of NF in the AW and RS. Severe sepsis and septic shock can lead to multiple organ dysfunction syndromes (MODS). The defects of any size on the anterior AW may allow herniation of the viscera, which can lead into incarceration, and ultimately, strangulation. Any surgical incision can potentially result in ventral hernia, especially if a history of infection in that area is already present. Intra-abdominal

infections “”per se”" include many pathological conditions, ranging ARN-509 cell line from uncomplicated appendicitis to complicated fecal peritonitis [14, 15]. Generally speaking, the choice of the surgical procedure depends on the anatomical source

of infection, the degree of peritoneal and retroperitoneal inflammation, generalized septic response and patient’s general conditions. Retroperitoneal phlegmon with necrotizing fasciitis is an uncommon soft Wnt inhibitor tissue infection that may become fatal. It usually ensues in cases of immunocompromised patients or advanced neoplastic disease. The infection spreads quickly and any delay in surgical intervention is associated with increased mortality. Necrotizing fasciitis of the anterior AW or perineum usually manifests with erythema and induration of the overlying skin. Nevertheless, when the retroperitoneum is involved, Adenosine excision may be delayed due to the lack of clinical symptoms. Although the mortality rate of this infection is very high, survival is possible owing to the prompt and repeated wide surgical debridements and extensive necrectomy with proper broad spectrum antibiotic therapy [15, 16]. Risk factors The most common risk factor for the development of NSTI is diabetes mellitus, with an occurrence of 56% in all cases [7, 17] (Table 3). The other co-morbidities include obesity, alcohol abuse, immunodeficiency, chronic renal failure, liver cirrhosis, hypertension, peripheral vascular disease, and age above 60 years.

These distances were scaled

to 2 dimensions using the mul

These distances were scaled

to 2 Selleck ICG-001 dimensions using the multidimensional scaling function cmdscale in R [44] these dimensions being treated as x and y coordinates. The central coordinate in x and y space was calculated using the mean of all coordinates. R788 ic50 The Euclidian distance of each strain in the cluster to the centroid was calculated by Pythagorean mathematics using the x and y coordinates from the multiple dimensional scaling calculations. Sequencing Genomic DNA from pure bacterial cultures from each of the strains was sequenced using either 454 or Illumina technologies. The strains sequenced by 454 used the titanium chemistry in conjunction with 8 kb insert libraries. Those sequenced employing the Illumina technology used 50 bp read lengths in conjunction with either a paired end or mate-paired 3 kb insert library. Several strains were sequenced using both 454 and Illumina technologies (Table  see more 3). Assembly The 454 sequences were assembled using the Newbler software (version 2.5) from Roche. Default parameters were used for assembly and scaffolding. The Illumina reads were assembled using Velvet version 1.1.05 [45]. The process was optimised using the velvet optimizer script from the Victorian Bioinformatics

Consortium ( https://​github.​com/​Victorian-Bioinformatics-Consortium/​VelvetOptimiser) with a kmer range of 33 to 47. The additional options -shortMatePaired2 yes -ins_length2 2500 -ins_length2_sd 500 were specified for reads from the

3 kb mate pair libraries. Contigs were joined into scaffolds using the SSPACE tool [46]. Mapping and SNP calling In order to discover SNPs using a single method for Illumina reads, 454 reads or Clomifene complete sequences from GenBank, short ‘Illumina-style’ reads were simulated from 454 assemblies and GenBank-derived genomes. This was achieved using the wgsim program from the Samtools package [47] with these parameters -e 0 -r 0 -N 3000000 -d 250–1 50–2 50. This resulted in two fastq files representing 3 million paired end reads of 50 bp with an insert size of 250 bp equivalent to the reads from the paired end libraries from the experimental Illumina sequences. Simulated or experimental Illumina reads from all strains was mapped to the genome sequence of the Corby strain using bowtie 0.12.7 [48] using the –m1 parameter to exclude reads that map in more than one place on the reference sequence and tend to cause false positives when calling SNPs. The Sequence Alignment Map from the Bowtie mapping was sorted and indexed using samtools to produce a Binary Alignment Map (BAM). Samtools mpileup was used to create a combined Variant Call Format (VCF) file using each of the BAM file. The VCF file was further parsed using a simple script to extract only SNP positions that were of the high quality in all of the genomes and write out these SNPs into a multiple FASTA format file.

Oncologist 2007, 12: 51–67 CrossRef 145 Sheiner LB, Rubin DB: In

Oncologist 2007, 12: 51–67.CrossRef 145. Sheiner LB, Rubin DB: Intention-to-treat analysis and the goals of clinical trials. Clin Pharmacol Ther 1995, 57: 6–15.PubMedCrossRef 146. Pampallona S, von Rohr E, van Wegberg B, Bernhard J, Helwig

S, Heusser P, Huerny C, Schaad H, Cerny T: Socio-demographic and medical characteristics of advanced cancer patients using conventional or complementary medicine. Onkologie 2002, 25: 165–170.PubMedCrossRef 147. Concato J, Shah N, Horwitz RI: Randomized, controlled trials, observational studies, and the hierarchy of research designs. N Engl J Med 2000, 342: 1887–1892.PubMedCrossRef 148. Benson K, Hartz AJ: A comparison of observational studies and randomized, controlled trials. N Engl J Med 2000, 342: 1886.CrossRef 149. Kunz R, Oxman AD: The unpredictability paradox: review of empirical

comparisons of randomised and non-randomised clinical trials. BMJ. 1998, 317 (167) : 1185–1190.PubMed VX-680 150. Rothwell PM: External validity of randomised controlled trials: “”To whom do the results of this trials apply?”". Lancet 2005, 365: 82–93.PubMedCrossRef 151. Fritz P, Dippon J, Kierschke T, Siegle I, Mohring A, Moisa A, Murdter TE: Impact of mistletoe lectin binding in breast cancer. Anticancer Res 2004, 24: 1187–1192.PubMed 152. Frantz M, Jung M-L, Ribéreaulearn more -Gayon G, Anton R: Modulation of mistletoe ( Viscum album L.) lectins WH-4-023 price cytotoxicity by carbohydrates and serum glycoproteins. Arzneimittelforschung. 2000, 50 (5) : 471–478.PubMed 153. Olsnes S, Stripe F, Sandvig K, Pihl A: Isolation and characterization of Viscumin, a toxic lectin from Viscum album L. (mistletoe). Grape seed extract The Journal of Biological Chemistry 1982, 257: 13263–13270.PubMed 154. Seifert G, Jesse P, Längler A, Reindl T, Lüth M, Lobitz S, Henze G, Prokop

A, Lode HN: Molecular mechanisms of mistletoe plant extract-induced apoptosis in acute lymphoblastic leukemia in vivo and in vitro. Cancer Lett 2008, 264: 218–228.PubMedCrossRef 155. Thies A, Dautel P, Meyer A, Pfuller U, Schumacher U: Low-dose mistletoe lectin-I reduces melanoma growth and spread in a scid mouse xenograft model. Br J Cancer 2008, 98: 106–112.PubMedCrossRef 156. Pryme IF, Bardocz S, Pusztai A, Ewen SW: Suppression of growth of tumour cell lines in vitro and tumours in vivo by mistletoe lectins. Histol Histopathol 2006, 21: 285–299.PubMed 157. Rostock M, Huber R, Greiner T, Fritz P, Scheer R, Schueler J, Fiebig HH: Anticancer activity of a lectin-rich mistletoe extract injected intratumorally into human pancreatic cancer xenografts. Anticancer Res 2005, 25: 1969–1975.PubMed 158. Antony S, Kuttan R, Kuttan G: Inhibition of lung metastasis by adoptive immunotherapy using Iscador. Immunological Investigations 1999, 28: 1–8.PubMedCrossRef 159. Antony S, Kuttan R, Kuttan G: Role of natural killer cells in Iscador mediated inhibition of metastasis by apoptive immunotherapy.

To identify whether or not plasma total osteocalcin was independe

To identify whether or not plasma total osteocalcin was independently associated with the development of T2DM, we performed a multivariate logistic regression analysis with backward variable selection. Analysis was performed using SPSS (version 13.0; SPSS, Inc. Chicago, IL, USA), and p values of <0.05 were considered significant. Results We divided the study subjects according to glucose tolerance status, and compared the plasma total osteocalcin levels. The plasma

osteocalcin levels were significantly FDA-approved Drug Library molecular weight different between the groups (p < 0.001); however, no difference was noted in the osteocalcin levels between the NGT (18.4 ± 9.0 ng/ml) and pre-diabetes groups (19.1 ± 8.9 ng/ml). After the development of diabetes (15.3 ± 6.8 ng/ml), the plasma osteocalcin levels were decreased compared with the pre-diabetes group (Fig. 1). Next, we divided the subjects into tertiles

(lower, BMS345541 in vivo middle, and upper) by plasma osteocalcin levels; the glucose and HbA1c levels varied inversely with the osteocalcin tertiles, and the insulin secretory capacity, including the AUC insulin/glucose, HOMA-B%, insulinogenic index, and disposition index and insulin sensitivity index (Matsuda’s, Stumvoll’s, and OGIS indices), increased with the osteocalcin tertiles. In addition, the plasma adiponectin levels were increased with the osteocalcin tertiles; however, no difference was noted in the plasma leptin SU5402 cell line levels with the osteocalcin tertiles (Table 1). To determine whether or not plasma

osteocalcin level is independently associated with improved glucose tolerance and insulin sensitivity and secretory capacity, multiple linear regression analyses were performed. The plasma osteocalcin level was inversely associated with FPG and AUC glucose levels and positively associated with the disposition index and Stumvoll’s and OGIS indices after adjusting for age, gender, BMI, and other adipokines including adiponectin and leptin levels (Table 2). To investigate the independent Astemizole association between the osteocalcin level and diabetes, a multiple logistic regression analysis was performed. The analysis included age, gender, BMI, fasting plasma glucose level, and plasma adiponectin, leptin, and osteocalcin levels. Our results indicated that age and the fasting plasma glucose level appeared to be independently associated with the development of diabetes; the plasma osteocalcin level was inversely associated with the development of diabetes (OR, 0.955; 95% CI, 0.919–0.994, p = 0.023; Table 3). Fig. 1 Osteocalcin levels (means ± SDs) by glucose tolerance status. NGT normal glucose tolerance, Pre-DM pre-diabetes, DM diabetes. To convert osteocalcin levels to nanomoles per liter, multiply by 0.

[Govindjee has always greatly valued Bob Blankenship’s kind words

[Govindjee has always greatly valued Bob Blankenship’s kind words about the Advances in Photosynthesis and Respiration book series at the time volume 25 (Chlorophylls and GW3965 in vitro Bacteriochlorophylls) was released. He wrote: “Congratulations on another volume in the Advances in Photosynthesis and Respiration (AIPH) series. Govindjee’s mentor Eugene Rabinowitch wrote the story of photosynthesis

in the 1940s and 1950s. No one could ever hope to do that again; the amount of information is just too vast for any one person to ever hope to do a proper job of giving the real state of knowledge. However, Govindjee has really Barasertib datasheet duplicated Rabinowitch’s accomplishment in the only way it could be done nowadays, by enlisting editors who are experts in areas of the field and having them in turn enlist expert authors. When I look at the AIPH books on my shelf I am struck with how effectively they collectively summarize the field. I am continually impressed with how Govindjee has added new books to the series that make sense and really provide the level of detail that is needed” Source: ; see Fig. 4… JJE-R.] Bob Buchanan Professor, Department of Plant & Microbial Biology University of California Ro 61-8048 molecular weight Berkeley, CA Dear Govindjee Your contributions in making the work of Andrew Benson better known will be long

remembered. [It was Govindjee who spent many days with Andy Benson, the co-discoverer of Calvin-Benson cycle for carbon fixation, and brought to light Benson’s contributions; he brought Benson’s work to the attention of the BBC that has produced a video “Botany: A Blooming History, Episode 2: The Power of Plants”; it fully recognizes Benson’s contributions. There is also a entertaining chat by Govindjee with Benson at a web site; it was recorded by John Nishio; it can be seen at: http://​www.​life.​illinois.​edu/​govindjee/​index_​files/​Andy%20​Benson_​Asilomar_​2002.​mpg

… JJE-R.] Carl N. Cederstrand Retired from Beckman Instrument Company, Lives in Orange, CA It gives me much pleasure to comment on my association with Govindjee during the time I was at the photosynthesis laboratory at Exoribonuclease the University of Illinois at Urbana-Champaign. Govindjee had so much enthusiasm for understanding photosynthesis that I believe his enthusiasm could have made photosynthesis work without chlorophyll. [Carl Cederstrand’s PhD was done essentially under the guidance of Govindjee. It was at the time when they provided one of the first papers on fluorescence characteristics of the two photosystems and the existence of different spectral forms of chlorophyll a (Cederstrand and Govindjee 1961; Cederstrand et al. 1966a, b). It was Cederstrand who taught Govindjee how to drive a car and survived (see Eaton-Rye 2007b)… JJE-R.] Fred (W. S.

DNA amplification

was performed on 1 μl of purified genom

DNA amplification

was performed on 1 μl of purified genomic DNA in a final volume of 50 μl containing 0.1 μM of TR6 and 1 μM of TR10 primers, 200 μM of each deoxynucleoside triphosphate, 1× PeqLab PCR buffer Y (20 mM Tris-HCL, 16 mM (NH4)2SO4, 0.01% Tween 20, 2 mM MgCl2) and 1.25 units Hot Taq-DNA-Polymerase (PeqLab, Erlangen, Germany). After an initial denaturation of 96°C for 3 min, the protocol consisted of 35 cycles at 96°C for 45 s, 52°C for 45 s, and 72°C for 45 s following a final extension at 72°C for 7 Fludarabine research buy min. PCR products were prepared for sequencing using the QIAquick® PCR Purification Kit (QIAGEN, Hilden, Germany) and 0.35 μl of the purified products were applied for sequencing using the BigDye Terminator v3.1 Cycle Sequencing Kit (Applied Biosystems, Foster City, USA) with identical primers employed in the PCR. Automated sequence detection was performed on an ABI capillary sequencing system and GDC-0994 concentration sequences were analysed using the BioNumerics 5.10 software (Applied Maths, Belgium). Classification of TRST types, repeat alignment, and cluster analysis Data processing was performed with BioNumerics 5.10 by using a novel, dedicated “”Repeat Typing”" plugin that allowed automated batch assembly of trace files. The assignment of TRST sequence types was based on the successive occurrence of user-defined repeats in concatenated sequences from

both tandem repeat loci. A repeat distance matrix for matching and clustering were calculated based on the DSI model [47], a mutation model comprising

substitutions, indels (insertions or deletions), and duplications. Subsequent cluster analysis was performed based on the neighbor joining algorithm. Multilocus sequence typing Clostridium difficile isolates were typed by MLST as described previously [31]. Sequence data were submitted to the C. difficile MLST database http://​www.​pasteur.​fr/​recherche/​genopole/​PF8/​mlst/​Cdifficile.​html to assign allele profiles and the resulting sequence types. Sequence types were analysed by constructing a dendrogram based on the UPGMA Rucaparib (Unweighted Pair Group Method with Arithmetic mean) clustering algorithm using the multistate categorical similarity coefficient (tolerance 0%) available in the BioNumerics software. MLVA PU-H71 concentration Seven-locus MLVA was conducted as described previously [20, 22], except that the different loci were PCR-amplified individually and PCR products were sequenced for repeat copy number determination. To facilitate sequence analysis of MLVA locus C6 [20], two novel oligonucleotide primers were used: C6-F 5′-CCAAGTCCCAGGATTATTGC-3′ and C6-R 5′-AACATGGGGATTGGAATTGA-3′. Repeat copy numbers were determined manually using BioNumerics 5.10 software. The summed tandem-repeat difference was calculated where appropriate; it is the sum of repeat differences between two isolates at all seven MLVA loci [21].

GO (0 1 μg/mL) were incubated with DCs for up

GO (0.1 μg/mL) were incubated with DCs for up HDAC inhibitor to 24 h, and the viability of the cells was evaluated by the standard MTS assay. The Selleckchem LY2109761 results revealed no significant difference in the numbers of live cells between the GO-treated and control groups (Figure 5B). The data indicated that GO at the low concentration exhibited negligible toxicity against DCs, a result consistent with former toxicity studies of GO on

Hela cells [35]. Figure 5 Phenotype and cellular viability studies of the DCs after stimulation. (A) Flow cytometry evaluation of CD86, CD83, and HLA-DR expression on DCs treated with GO, Ag, or GO-Ag. (B) Viability of DCs after being treated with 0.1 μg/mL of GO for 1, 4, or 24 h (mean ± std, LY3023414 datasheet n = 6). Discussion The aim of the study was to investigate whether a two-dimensional nanomaterial, GO, could be utilized to modulate DC-mediated anti-glioma immune reactions. The results showed that pulsing DCs with free Ag generated a limited anti-glioma response compared to un-pulsed DCs (Figure 3A). Pulsing DCs with GO alone failed to produce obvious modulation effects. However, stimulating DCs with GO-Ag significantly enhanced the anti-glioma

immune reaction (p < 0.05), a finding that was further verified with the IFN-γ secretion experiments (Figure 3B). In addition, the enhanced immune response appeared to be relatively specific towards the target cells carrying the Ag peptide (Figure 4). Furthermore, at the concentration used in this study, GO exerted minimal toxicity to the DCs (Figure 5). very These data suggested that GO might have application potential for enhancing the DC-mediated immune reactions against glioma cells. The mechanisms of the observed immune enhancement are unclear at this stage. One hypothesis is that GO may serve as an immune adjuvant, which can activate the DCs and induce a more potent immune response. However, the data of this study showed that GO alone did not generate significant immune modulatory effects, a behavior inconsistent with

most immune adjuvants (Figure 3A). Another possible mechanism is that GO may function as a carrier of the antigens for crossing the cell membrane [36] and thus bring more antigen into the DCs. Presumably more glioma antigens will be processed within the DCs, leading to an improved DC-mediated anti-glioma response. Obviously, extensive future studies are still warranted to unveil the immune-modulating mechanisms of GO. The GO concentration used in this study was 0.1 μg/mL. At this concentration, we did not detect obvious GO toxicity against the DCs. This result was in agreement with prior toxicity studies of GO on Hela cells [35]. Interestingly, a recent study reported that high dosage of GO of 1 to 25 μg/mL suppressed antigen presentation in DCs and down-regulated the ability of DCs to activate antigen-specific T lymphocytes [37].

Conservation, multiplication and dissemination of such trees as c

Conservation, multiplication and dissemination of such trees as components of non-orchard landscapes could result in increased fruit yields and produce a supply of valuable timber and wood products for rural

landowners (Harvey et al. 2008). Fig. 1 Aerial photo of Las Juntas on the Rio Pescados near Llano Grande, Veracruz (12° 22′ 18.64′′ N, 96° 51′ 18.98′′ W), showing fragmentation of native forest in different successional status (red polygons) and the placement of these fragments with respect to orchards (white polygons), pastures, sugar cane and other crops (light green areas, not marked with polygons). Primary and secondary forest fragments are primarily located in rough or inaccessible areas such selleck screening library as canyons (blue lines). The landscape is crossed by a main road (yellow

line). Source Google Earth Interactions among Tephritidae, hymenopteran parasitoids and fruit trees Some fruit flies are among the world’s most damaging agricultural insect pests (Aluja and Mangan 2008). The economically important genera are Anastrepha, Bactrocera, Ceratitis, Rhagoletis, and Toxotrypana, all of which are represented in the subtropical and tropical regions of the Americas. Anastrepha species, the focus of our discussion, are distributed from the southern United States to northern Argentina (Hernández-Ortíz and Aluja 1993; Aluja 1994). In Latin America, many species of native plants in tropical dry and wet forests support fruit fly larvae of both economic (<5 %; 7 species) and non-economic importance (>95 %; >200 species) (Aluja et al. 2003 and references therein). In developed areas these same plants can

also be found as isolated individuals that have either survived agricultural practices or been planted as living fences or fruit or shade trees. Semi-Selleck Copanlisib commercial and commercial orchards in Mexico are often located near or even mixed into patches of native vegetation that include tephritid hosts, particularly if the adjacent sites, such Thiamine-diphosphate kinase as canyon walls, do not lend themselves readily to cultivation (Fig. 1). Movement between wild and cultivated hosts (described in detail by Aluja and Birke 1993; Aluja and Rull 2009) is typical of several important pest fruit fly species and is important to their population survival because: (1) no single host species fruits throughout the year; and (2) pest fruit flies do not diapause and adults survive for only limited periods; thus they have no mechanism to bridge fruit-free periods (Aluja et al. 1998, 2009). Anastrepha spp. control Toxic bait sprays have been used extensively to control pest Anastrepha species (Aluja 1994; Raga and Sato 2005). But the sterile insect technique (SIT) (Reyes et al. 2000), classical biological control (Eskafi 1990; Ovruski et al. 2000) and augmentative releases of parasitoids (Sivinski et al. 1996; Montoya et al. 2000, 2007) have resulted in complete or partial control of pest tephrtid populations at certain times and places.

Salo J, Lehenkari P, Mulari M, Metsikkö K, Väänänen HK: Removal o

Salo J, Lehenkari P, Mulari M, Metsikkö K, Väänänen HK: Removal of osteoclast bone resorption products by transcytosis. Science 1997, 276:270–273.CrossRef selleck compound 33. Smith ER, Hanssen E, McMahon

LP, Holt SG: Fetuin-A-containing calciprotein particles reduce mineral stress in the macrophage. PLoS One 2013, 8:e60904.CrossRef 34. Zhanga M, Kataokaa K: Nano-structured composites based on calcium phosphate for cellular delivery of therapeutic and diagnostic agents. Nano Today 2009, 4:508–517.CrossRef 35. Orrenius S, Zhivotovsky B, Nicotera P: Regulation of cell death: the calcium-apoptosis link. Nat Rev Mol Cell Biol 2003, 4:552–565.CrossRef 36. Zhivotovsky B, Orrenius S: Calcium and cell death mechanisms: a perspective from the cell death community. Cell calcium 2011, 50:211–221.CrossRef 37. Dorozhkin SV: Amorphous calcium (ortho)phosphates. Acta Biomater 2010, 6:4457–4475.CrossRef 38. Oceandy D, Mohamed TM, Cartwright EJ, Neyses L: Local signals with global impacts and clinical implications: lessons from the plasma membrane calcium pump (PMCA4). Biochim Biophys Acta 2011, 1813:974–978.CrossRef 39. Li J, Yang Y, Huang L: Calcium phosphate nanoparticles with an asymmetric lipid bilayer selleck chemicals coating for siRNA delivery to the tumor. J Control Release 2012, 158:108–114.CrossRef

40. Torchilin VP, Rammohan R, Weissig V, Levchenko TS: TAT peptide on the surface of liposomes affords their efficient intracellular delivery even at low temperature and in the presence of metabolic inhibitors. Proc Natl Acad Sci U S A 2001, 98:8786–8791.CrossRef SN-38 price 41. Torchilin VP, Levchenko TS, Lukyanov AN, Khaw BA, Klibanov AL, Rammohan R, Samokhin 3-oxoacyl-(acyl-carrier-protein) reductase GP, Whiteman KR: p-Nitrophenylcarbonyl-PEG-PE-liposomes: fast and simple attachment of specific ligands, including monoclonal antibodies, to distal ends of PEG chains via p-nitrophenylcarbonyl groups. Biochim Biophys Acta 2001, 1511:397–411.CrossRef 42. Low PS, Antony AC: Folate receptor-targeted drugs

for cancer and inflammatory diseases. Adv Drug Deliv Rev 2004, 56:1055–1058.CrossRef 43. Mamasheva E, O’Donnell C, Bandekar A, Sofou S: Heterogeneous liposome membranes with pH-triggered permeability enhance the in vitro antitumor activity of folate-receptor targeted liposomal doxorubicin. Mol Pharm 2011, 8:2224–2232.CrossRef 44. Pirollo KF, Chang EH: Does a targeting ligand influence nanoparticle tumor localization or uptake? Trends Biotechnol 2008, 26:552–558.CrossRef 45. Mishra A, Lai GH, Schmidt NW, Sun VZ, Rodriguez AR, Tong R, Tang L, Cheng J, Deming TJ, Kamei DT, Wong GC: Translocation of HIV TAT peptide and analogues induced by multiplexed membrane and cytoskeletal interactions. Proc Natl Acad Sci U S A 2011, 108:16883–16888.CrossRef 46. Li SD, Huang L: Nanoparticles evading the reticuloendothelial system: role of the supported bilayer. Biochim Biophys Acta 2009, 1788:2259–2266.CrossRef 47.