miRNA sequences for AIF were designed using online software (BLOC

miRNA sequences for AIF were designed using online software (BLOCK-iT RNAi Designer from Invitrogen). The target sequence was 5′-GTGCCTATGCCTACAAGACTA-3′. This single-stranded oligonucleotide generated

a double-stranded oligonucleotide, which instructed into pcDNA™ 6.2-GW/EmGFP-miR vector. This vector contains EmGFP that allow identifying of the transfection efficiency using fluorescence microscopy. The construct pcDNA™ 6.2-GW/EmGFP-miR-LacZ was used as a control. Cells were transiently transfected with these plasmids using lipofectamine (Invitrogen). Statistical analysis The data are expressed as means ± SEM and the difference between two groups was evaluated using Student’s t-test. Multiple group comparison was done using one-way analysis of variance Selleck BIBW2992 followed by the Tukey post hoc test. A probability level of 0.05 was used to establish significance. Results and Discussion Effect of calpain inhibitor on silibinin-induced cell death Calpains are cytosolic Ca 2+ -activated neutral cysteine proteases and ubiquitously distributed in all animal cells, which play a critical role in regulating cell viability DAPT [11, 12]. Accumulating evidence suggests that calpain activation may contribute to cell death in certain cell types including thymocytes, monocytes, cardiomyocytes, and neuronal cells [13]. Since our previous study

showed that the calpain inhibitor Z-Leu-Leu-CHO at 0.5 μM significantly protected effectively against the silibinin-induced cell death [8], we observed in the present study the dose-dependency

of the inhibitor effect. The results showed that the calpain inhibitor exerted protective effect against the silibinin-induced cell death in a dose-dependent Plasmin manner with maximum potency at 0.5-1 μM (Figure 1A). Silibinin also induced calpain activation, which was blocked by EGTA and calpain inhibitor (Figure 1B). These results indicate that calpain activation plays a critical role in the silibinin-induced cell death in human glioma cells. Figure 1 Role of calpain in silibinin-induced cell death. (A) Cells were exposed to 30 μM silibinin for 36 h in the presence of various concentrations of calpain inhibitor (Z-CHO). Cell viability was estimated by MTT assay. Data are mean ± SEM of four independent experiments performed in duplicate. *p < 0.05 compared with silibinin alone. ( B ) Cells were exposed to 30 μM silibinin for 24 h in the presence of 2 mM EGTA and 0.5 μM Z-CHO. Calpain activity was measured by calpain assay kit. Data are mean ± SEM of four independent experiments performed in duplicate. *p < 0.05 compared with silibinin alone. Role of calpain and protein kinase C (PKC) activation in ROS generation and cell death induced by silibinin The silibinin-induced cell death was associated with ROS generation mediated by intracellular Ca2+ [8].

The interaction energies are calculated in the point-dipole appro

The interaction energies are calculated in the point-dipole approximation assuming a common linewidth for all transitions

of ∼80 cm−1. Screening by the protein is taken into account by a dielectric constant that was used a global free-fit parameter. The initial calculated dipole strength of 68.9 D 2 is thus reduced by a factor 2.4 leading to an effective dipole strength of 28.7 D 2, a value that is lower than that proposed by Pearlstein (1992). This value is close to a physically relevant value of the reduced dipole strength in the range of 25–40 D 2. In order to simulate the spectra, a minimum of free parameters was used to fit the essential features of the spectra. The authors proposed that the model can be improved by inclusion of vibrations, lifetime broadening of the highest energy Protein Tyrosine Kinase inhibitor INCB024360 concentration exciton states, and by allowing for different dipole strengths for the individual BChl a molecules and a variation of the dielectric constant over the protein. Simulations based on the same exciton model were performed by the following research groups: Vulto et al. (1998a, 1999), Wendling et al. (2000, 2002), and Iseri and Gülen (1999). Table 7 Exciton energies

of Prosthecochloris aestuarii in the monomer Exciton A B C D E 1 827.1–824.4 825.6 825.7 825.0 823.8 2 816.3 815.2 814.5 814.1 813.7 3 813.0 813.5 812.2 812.8 811.5 4 807.8 806.7 805.8 805.9 804.7 5 804.8 802.7 800.8 801.5 801.0 6 801.3 800.2 796.4 799.6 PJ34 HCl 797.8 7 793.6 791.5 793.0 791.5 789.4 Where A is from Johnson and Small (1991), B is from Louwe et al. (1997b), C is from Vulto et al. (1999), D is from Iseri and Gülen (1999), E is from Wendling et al. (2002) Nature of the lowest energy band The assignment of the bands in the absorption spectrum, especially of the band, the lowest in energy at 825 nm, has proven to be difficult. The number of excitonic states and their respective energies have been the subject of intense debate. Johnson and Small (1991) concluded that lower and higher spectral energy features flanking the hole-burning line can only be explained when excitonic interactions between the BChls are taken into account. Furthermore,

the results of spectral hole burning show the presence of eight states. Two of those eight identified exciton states, which have perpendicular symmetry, contribute to this lowest exciton band at 825 nm. Models excluding the interactions between the subunits of the trimer are not successful in describing this experimental data (Johnson and Small 1991). Therefore, Johnson and Small (1991) have developed a model in which this interaction is included leading to a maximum of 14 delocalized states (21 states in total, of which 14 are degenerate). This implies that the 825-nm band comprises of three, slightly shifted, bands of the subunits, of which two are degenerate. For the space group C 3, the states having E symmetry are degenerate while the states with A symmetry are not (Atkins 1995).

1 and 0 6 Figure 5 Phase diagram of ABC triblock copolymer with

1 and 0.6. Figure 5 Phase diagram of ABC triblock copolymer with χ AB N  =  χ BC N  = 13

and χ AC N  = 35 at grafting density σ  = 0.2. Dis represents the disordered phase. The red, blue, or black icons showing the parallel lamellar phases discern the different arrangement styles of the block copolymer with block A, block C, or block B adjacent to the brush layers, respectively. 4.  Comparison with ABC triblock copolymer thin film without polymer brush-coated substrates In this part, we give two cases for comparison between the ABC triblock copolymer thin film with and without polymer Osimertinib supplier brush-coated substrates (σ = 0.15) at χ AB N = χ BC N = χ AC N = 35. In order to simulate the similar interface environment with the ABC triblock copolymer thin film between polymer brush-coated substrates, we set the interaction parameters η AS N = η CS N = 35 and η BS N = 0 for the ABC triblock copolymer thin film between hard surfaces, which means the substrate is good for the middle block B. In principle, the effective film thickness for the ABC triblock copolymer thin film

confined between the polymer brush-coated substrates is like L z eff = L z  - 2aσP for σP 1/2 > 1 (where 2 is just for the upper and lower polymer grafted surfaces, brush height h = aσP for σP 1/2 > 1 [68]). When the ABC triblock copolymer is confined between two hard surfaces (without polymer brush-coated substrates), the corresponding effective film thickness is 22a in this case. The morphology comparison of ABC triblock copolymer confined between polymer-coated substrates and hard surfaces is listed in Figure  6. The first column is the composition Small molecule library supplier of ABC triblock copolymer. The second

column is the morphologies of the ABC triblock copolymer confined between the polymer brush-coated surfaces and the morphologies of the polymer brush. The third column is the morphologies of ABC triblock copolymer confined between hard surfaces (without polymer brush-coated) and the 3D isosurface for a clear view. The microphase patterns, displayed Clostridium perfringens alpha toxin in the form of density, are the red, green, and blue, assigned to A, B, and C, respectively. Similarly, the red, green, and blue colors in 3D isosurface graphs are assigned to blocks A, B, and C for a good correspondence, respectively. For the ABC triblock copolymer confined between polymer brush-coated substrates, the morphology of the grafted polymer on the lower substrate (polymer brush) is also shown below the morphology of ABC triblock copolymer. We only give the morphology of the grafted polymer on the lower substrate (polymer brush) due to the symmetry of the polymer brush (the two polymer brush-coated surfaces are identical). For the ABC triblock copolymer confined between the hard surfaces, the 3D isosurface is also shown below the morphology. Figure 6 Comparison of the morphology of ABC triblock copolymer confined between hard surfaces and polymer brush-coated substrates.

This is the first demonstration that tyramine can be produced fro

This is the first demonstration that tyramine can be produced from peptides containing tyrosine and therefore that free tyrosine is not the only precursor for tyramine production. We studied the expression of the tyrDC and tyrP genes to determine whether it was growth phase-dependent and/or nitrogen source dependent. tyrDC and tyrP expression The tyrDC and tyrP genes are co-transcribed in E. faecalis[13], L. brevis[15]

and Sporolactobacillus sp. [49]. A complete transcriptional analysis of the four genes of the operon was made in Lactobacillus SCH727965 price brevis IOEB 9809 [15]. Even if tyrDC tyrP transcripts were the most abundant, other polycistronic mRNA were described as: tyrS-tyrDC-tyrP-nhaC and tyrS-tyrDC, as well as tyrP-nhaC. So tyrDC and tyrP

can be transcribed from different manner. L. plantarum IR BL0076 tdc locus sequences was analysed using ARNold, an interface allowing localization of Rho-independent terminators in any bacterial sequence. (na.igmors.u-psud.fr/toolbox/arnold/). A predicted transcription terminator (−11.70 kcal/mol) localized at the 3′ end of TyrP coding region was identified. Erpin and RNAmotif programm predict the 5′ end position of this predicted transcription terminator at the nucleotide 3402 of the locus. To check the presence of a bicistronic tyrDC-tyrP in the IR BL0076 isolate, we used Reverse-Transcription-PCR experiments and primers tdcf and tyrPLpR located inside the tyrDC and tyrP genes respectively to study their expression Ku-0059436 solubility dmso in L. plantarum. An amplicon of 1,761 bp was obtained using cDNA obtained from RNA extracted from cultures on each medium selleck screening library 1 and medium 2 as the template. The length of the RT-PCR product indicates that tyrP is part of a polycistronic mRNA including tyrDC. As the four genes of the tyrosine decarboxylase operon

are part of a genetic island, as described for L. brevis[12], they have been disseminated through lactic acid bacteria via a horizontal gene transfer [49]. So it is expected that they are regulated in the same way in all enterococci and lactobacilli including L. plantarum. To study the tyrosine transport, expression tyrP and tyrDC was similarly analyzed by RT-qPCR. The expression of tyrP increased during growth in both medium 1 and medium 2, with a maximum at OD600nm = 1.8 (Figure 3a), and was significantly stronger during the stationary phase than during early exponential growth. The expression of tyrP paralleled the accumulation of tyramine in both media (Figure 1). This is coherent with what has been found for other bacteria producing biogenic amines, for example Streptococcus thermophilus[50], which produces histamine at the end of its growth, with an increase in the expression of the decarboxylase hdcA. The expression profile of tyrDC during growth was very similar to that of tyrP (Figure 3b). Both tyrDC and tyrP were significantly more strongly expressed during the early exponential growth phase in peptide medium (medium 2) than tyrosine medium (medium 1).

firmus GB1 In B subtilis levansucrases are induced by sucrose [

firmus GB1. In B. subtilis levansucrases are induced by sucrose [35] and levanases by low concentrations of fructose [35]. Based on this we analyzed biofilm formation by B. firmus GB1 and B. indicus HU36 in the presence of sucrose, fructose or STA-9090 clinical trial both sugars together. As shown in Figure 3B, while in HU36 cells production of the levan-based biofilm was not

significantly affected by the presence of fructose, sucrose or both carbohydrates, in GB1 cells biofilm synthesis was about two-fold induced by sucrose and this induction was reduced by the concomitantly presence of the two carbohydrates (Figure 3B). In our standard conditions (MSgg medium) B. indicus HU36 (grey bars) was more efficient than B. firmus GB1 (black bars) in producing a biofilm. The hydrolytic potential of B. firmus and B. indicus genomes correlate with mucin binding and degradation Mucins are a family of high molecular weight, heavily glycosylated proteins produced by epithelial cells and forming the viscoelastic gel-like layer that covers the epithelial surfaces in the mammalian GI-tract. The glycosidic part of mucin is formed by linear or branched oligosaccharides that form up to 85% of the molecule

by weight. Although chemically and structurally diverse, mucins invariably contain large quantities of galactose, amino sugars, fucose, have strongly PLX3397 nmr polar groups, such as neuraminic (sialic) acids and sulphate at the end of the polysaccharide moiety. Mucins can be degraded by several different hydrolytic enzymes to smaller oligomers, monosaccharides, and amino acids and used as carbon, nitrogen, and energy Paclitaxel manufacturer sources by colonic bacteria. It is commonly

accepted that the breakdown of mucins occurs as a cooperative activity in the gut microbiota with different bacteria able to synthesize the variety of hydrolytic enzymes (glycosidases, proteases, peptidases and sulfatases) needed for a complete degradation of mucins [37]. Also important in this regard is the action of deacetylases, enzymes needed to remove O-acetylated sugars that are present at the termini of host glycans to prevent direct cleavage by microbial glycoside hydrolases. Bacteria that have these enzymes therefore produce deacetylated sugars available for them and other components of the microbiota [37]. The CAZy annotation results are consistent with the ability of both pigmented Bacilli to adhere and degrade mucin. The B. firmus GB1 genome encodes a candidate polypeptide N-acetylgalactosaminyltransferase, belonging to the GT27 family (gb1_47520) and several candidate deacetylases (gb1_18820, gb1_34880, gb1_38420, gb1_07440, gb1_46210) of the CE4 family and a phosphate-deacetylase (gb1_66390) of the CE9 family (Additional file 1). The B.

The MIA PaCa-2, HPAC and Capan-2 cells were transfected with pcDN

The MIA PaCa-2, HPAC and Capan-2 cells were transfected with pcDNA3.1 mammalian expression vector containing full-length cDNA encoding human mesothelin, or with the empty pcDNA3.1 vector. After 2 weeks of selection with G418, mesothelin-expressing cells and vector control cells were obtained for each of the three pancreatic cancer cell lines. Mesothelin protein expression were measured by Western blot analysis (Figure 2C). All three mesothelin -expressing cells expressed high levels of mesothelin protein, whereas none of the three vector control cell lines expressed detectably increased levels of mesothelin protein Epacadostat (Figure 2C). Overexpression of mesothelin

increases cell proliferation in pancreatic cancer cells with wt-p53 by p53-dependent pathway To elucidate the role of mesothelin overexpression in pancreatic cancer cell proliferation, we used the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, comparing the cell growth rate among the mesothelin -overexpressing MIA PaCa-2 stable cell line, the empty vector MIA PaCa-2 stable cell line, and ZVADFMK the unrelated MIA PaCa-2 cell

line. The MTT assay showed that Mesothelin transfected cells proliferated almost 3.1 times faster than the control cells at day 3 (P < 0.05; Figure 3A), and almost 2.6 times faster at day 6 (P < 0.05; Figure 3A). To confirm the role of mesothelin in cell proliferation, we did the above assay with another stably mesothelin -overexpressing pancreatic cancer cell line, Capan-2. The similarity of the results provides further evidence for the role of mesothelin in inducing cell proliferation (Figure 3B). The similarity of the results was also found in HPAC cells (data not shown). Figure 3 Overexpression of mesothelin promotes pancreatic cancer cell survival and proliferation. A, Cell proliferation of MIA PaCa-2 and Capan-2 cells according to MTT assay. Stable mesothelin Thiamine-diphosphate kinase transfected MIA PaCa-2 and Capan-2 cells

and control cells were seeded in 96-well plates (2 × 103 cells/well), serum-starved (0% fetal bovine serum, FBS) for 24 h before changing to 2% FBS growth medium, and cultured for 6 day. Viability was measured with MTT. Relative increase in viability was measured by dividing viability at one time point by viability of the same cell at day 0 (day of addition of growth medium after initial serum starvation) and is plotted along the Y-axis. Points, mean of triplicate wells. B, cells grown in soft agar were counted. bars, SD. *, P < 0.05, relative to control or mock(at 14 days). C and D , Mesothelin increases bcl-2 and decrease Bax via p53-dependent pathway. Whole cell extract from cells were probed for western blot. E , Mesothelin increases bcl-2 and decrease Bax by p53-independent pathway. Whole cell extract from cells were detected for western blot.

(B) Multiple sequence alignment (MSA) of the first 15 amino acids

(B) Multiple sequence alignment (MSA) of the first 15 amino acids (aa) (given in the single letter code) after excision of a predicted 20 aa signaling peptide of MCFOs. The alignment was performed using CLUSTALW2 and displayed

with the Jalview editor (http://​www.​ebi.​ac.​uk/​Tools/​msa/​clustalw2/​). The selected proteins are: Fet3p [UniProtKB: Q59NF9], Fet31p [UniProtKB: Q59NF7], Fet33 [UniProtKB: Q5A503], Fet34p [UniProtKB: Q59NF5] Z-VAD-FMK cell line and Fet99p [UniProtKB: Q59NF8]. (C) SDS-PAGE analysis of MCFOs, which were extracted from cells grown in RPMI supplemented with different iron concentrations at 30°C for 3 h. Table 1 Peptide peaks obtained from MS-MALDI-TOF analysis Maraviroc mw of the MCFOs band Peptide peaks [m/z] MCFO 998.5 Fet3p 1384.7 Fet34p 1389.7 Fet3p 1399.7 Fet34p 1507.8 Fet3p, Fet31p 1726.9 Fet3p, Fet34p 1838.9 Fet34p 1867.0 Fet3p, Fet31p, Fet99p

Previous gene expression experiments in C. albicans had reported that FET34 expression was regulated by iron availability, as expression of this gene was induced under restricted iron compared to sufficient iron conditions [23, 43]. Thus, we further investigated the dependence of MCFOs expression on iron concentrations in the growth medium. According to information given by the supplier, RPMI medium does not contain iron salts and can be considered as medium with very low basal iron levels. Thus, the concentrations of FeCl3 added to this medium were taken as total Fe3+ concentration. Increasing ferric

iron concentrations led to significant decreases of MCFOs levels as determined by SDS PAGE and subsequent coomassie staining of proteins (Figure 3C). When iron concentrations equaled or exceeded 7.5 μM, hardly any protein band was visible. Taken together, these results confirm that the expression levels of extracted MCFOs were dependent on the iron ion concentration Clomifene in the growth medium. Deletion of HOG1 induced components of the HAIU pathway independent of iron availability Previously, de-repression of genes involved in iron uptake (FET34, FTR1, FRE10 and RBT5) was reported in the Δhog1 mutant by whole genome gene expression profiling of cells grown under sufficient iron conditions [27]. As the expression of these genes is usually repressed by sufficient iron conditions and only induced by restricted iron conditions [23] (for MCFOs see Figure 3), we investigated the function of Hog1p in the response of C. albicans to iron. We first confirmed elevated amounts of MCFO proteins in Δhog1 and Δpbs2 deletion mutants in comparison to the wild type (WT, SC5314) and the reference strain (DAY286) which was best seen in cells grown in YPD overnight (Figure 4A, see Additional file 2 for the complete gel). The identity of the MCFO proteins was proven by MS/MS analysis of the peptide at 1726.9 m/z (data not shown).

More recently, van Geel et al developed a fracture risk model in

More recently, van Geel et al. developed a fracture risk model in a cohort comprising postmenopausal women, inhabitants of the southern part of the Netherlands [27]. This clinical risk score is the simplest to use, as it only includes three risk factors in the final model. A major strength, compared to the other Dutch fracture models, is the consideration of the time window in which a prior fracture could have occurred. Like the model described by Pluijm et al., the van Geel model also is limited to women only and may Selleck PF2341066 not be representative for the entire country. A third model, introduced by the Dutch

Institute for Healthcare Improvement (CBO), aims to identify high-risk patients for fracture by calculating a fracture risk score based https://www.selleckchem.com/products/dabrafenib-gsk2118436.html on weighted widely recognized risk factors [28]. However, in contrast to the other Dutch fracture models, these weights are based on expert opinion and have not been developed and validated in clinical studies using Dutch patients’ data. Therefore,

these estimated weights may not reflect real-life weights. This CBO model is currently used in the national Dutch guidelines for fracture prevention [28]. The use of FRAX in these guidelines is limited: FRAX risk assessment is only recommended in patients with multiple clinical risk factors (CBO score ≥4), and a T-score between −2.0 SD and −2.5 SD, but without evidence of a recent fracture. The importance of calibrating FRAX to an individual country why is illustrated by the marked differences in lifetime risks of hip fracture in 50-year-old males and females between countries worldwide. In line with previous reports, we found much higher incidences for hip fracture in European countries (including the Netherlands), as compared to those in countries like China, Mexico, and those in the Mediterranean area [29–31]. Possible explanations for this decreased incidence rate in the latter countries as compared to the Netherlands include lower life expectancy, in particular in Latin America (as most hip fractures occur after the age of 65 years) [30], variations in reversible lifestyle factors, and genetics

[32, 33]. High prevalence rates in Scandinavian countries (including Sweden) may to some degree be explained by icy condition in the winter [34] and high smoking frequency/alcohol intake (in particular in Denmark) [35]. The use of FRAX as a clinical tool demands a consideration of intervention thresholds. These thresholds, determined by fracture probability, should be recommended based on clinical imperatives and validated by the cost-effectiveness of a possible FRAX-based strategy. In the UK, the National Osteoporosis Guideline Group has described management algorithms that are based on FRAX [36]. These guidelines describe fracture risk thresholds at which BMD assessment or osteoporosis treatment should be carried out.

An emergency operation to remove the hemorrhage was successfully

An emergency operation to remove the hemorrhage was successfully performed. Other patients recovered with conservative treatment. There were five major misinterpretations from the 77 cases (6.5%) of orbital plate fractures on face IWR-1 mouse CT, but none of the patients required surgical treatment or experienced persistent functional disorders. There were three major misinterpretations from the 272 cases (1.1%) of spinous process

fractures in the cervical spine, but surgical treatment was not required in any. There were 19 major misinterpretations (6.2%) out of the 306 cases that underwent chest CT (7 costal fractures, 4 transverse process fractures in the thoracic spine, 1 sternum fracture, 1 scapula fracture, 3 pulmonary contusions, 2 cases of pneumothorax, and 1 intercostal artery injury). The patient with intercostal artery trauma did not survive and was categorized as gravity level 3. Three patients with costal fractures and one patient with pneumothorax were categorized selleck as gravity level 2 because a chest drain was required. There were two major misinterpretations from the 295 cases (0.7%) that underwent abdominal CT (1 of liver trauma and 1 of kidney trauma). Neither required any surgical treatment. Anemia did not develop, and both recovered fully without intensive treatment. There were

three misinterpretations out of the 295 cases that underwent pelvic CT (1 each for fractures of the pubis, ischium, and neck of the femur). The patient with the femoral neck fracture was operated on by orthopedic surgeons, but the other two patients did not require any surgical treatment. Anemia did not develop in either case, and both recovered fully without intensive treatment. In the second period, 177 patients presented with blunt trauma, of whom 129 were male and 48 female. In total, emergency CT was used 820 times (171 times for the head, Montelukast Sodium 49 times for the face, 155 times for the neck, 151 times for the chest, 147 times for the abdominal area, and 147 times for the pelvic area). The

mean patient age was 50.3 ± 23.4 years (mean ± SD), and the mean ISS was 11.7 ± 9.1 (mean ± SD). There was no statistically significant difference in mean age or ISS compared with the first period. The cause of trauma was a traffic accident in 99 cases, a fall in 44 cases, and other mechanisms in 34 cases. The accuracy and outcomes of EPs’ interpretation in the second period are shown in Table  4. Of the 820 cases, 10 (1.2%) minor misinterpretations and two (0.2%) major misinterpretations were identified. The improvements between the first and second period were statistically significant. Minor misinterpretations occurred in 2.7% of cases (95% confidence interval, 1.9% to 3.5%) in the first period versus 1.2% of cases (95% confidence interval, 0.5% to 2.

Reprinted with permission from Müller et al [49] There are many

Reprinted with permission from Müller et al. [49]. There are many other II-VI and III-V semiconductor nanomaterials that deserve to be researched like ZnS,

GaN, ZnSe, and CdTe. One-dimensional nanomaterials have also been widely applied in the field of photocatalysis. Magnetic properties Several research about diluted magnetic semiconductor (DMS) have become much more attractive since Dietl et al. predicted that several wide bandgap semiconductors possibly have a room temperature Tc, including GaN and ZnO [53]. Low-dimensional DMS materials like nanowires have a significant application in spintronic nanodevices. The most important assignment is the synthesis of suitable DMS materials. Many papers reported that they can get room-temperature ferromagnetism through TM doping

in selleckchem the semiconductor FK506 materials, but some other researchers did not acquire room-temperature ferromagnetism through almost the same method. Ion implantation, as an effective doping method, plays an important role in the preparation of DMS. ZnO is the most fascinating II-VI semiconductor; room-temperature ferromagnetism of TM-doped ZnO has been reported [54, 55]. However, some other research did not reveal any ferromagnetism signal [56, 57]. There is also an argument about the origin of room-temperature ferromagnetism of these TM-doped materials. Jian et al. [58] reported that ferromagnetism of Co-implanted ZnO nanowires has a close connection with the structural order. In their work, the ZnO nanowire grew through thermal evaporation and then implanted by Co ions. In Figure 11a, the squares represent the as-implanted NWs, the circles represent the argon-annealed NWs, and Aurora Kinase the triangles represent vacuum-annealed NWs. After annealing, the implanted sample revealed an enhanced hysteresis loop, and as the annealing temperature increased, the hysteresis loop was squeezed. Jian, Wu et al. considered that it is related to the increased number of carriers;

the theory on carrier-mediated ferromagnetism may explain this phenomenon [59]. Annealing was performed once again in oxygen and argon atmosphere for the already annealed sample under high vacuum. The results reveal that the hysteresis loop of the oxygen-annealed sample has decayed and the argon-annealed sample almost has no change. Annealing in oxygen may cause the reduction of oxygen vacancies and concentration of carriers. Figure 11b shows the M-H curves of different doping quantity of nanowires; the hysteresis loops increase with the increasing concentration of Co ions. Shuai et al. [60] reported that the Cu+-implanted ZnO nanowires have room-temperature ferromagnetism. The ZnO nanowires were implanted with 100-keV Cu+ ions and then annealed at 600°C for 2 h in argon and oxygen atmosphere. They found that the oxygen-annealed samples have stronger ferromagnetism than the argon-annealed samples. Figure 11 Magnetization as a function of applied field at 2 K for Zn 0.