schenckii. Conclusion We have shown the presence of a new G protein α subunit in S. schenckii, SSG-2. The cDNA sequence Selleckchem GSK1838705A of the ssg-2 gene encoded a 355 amino acid Gα subunit of 40.90 kDa containing the 5 consensus domains present in all Gα subunits. The genomic sequence has four introns, whose positions are conserved in the other fungal homologues of this gene. Yeast two-hybrid analysis using the complete amino acid sequence of SSG-2 identified a PLA2 homologue as an interacting partner of this G protein subunit. This 846 amino acid protein was encoded by an intronless

gene. The 92.62 kDa protein encoded by this gene contained all the domains and amino acid residues that characterize cytosolic phospholipase A2. PLA2 and other phospholipases in fungi have very diverse roles not only as virulence factors but also in membrane homeostasis and signal transduction. Inhibitor studies showed that this PLA2 homologue and its interaction with SSG-2 were necessary

for the re-entry of S. MI-503 supplier schenckii yeast cells into the budding cycle suggesting a role for this important virulence factor in the control of dimorphism in this fungus and for the expression of the yeast form. The effects of PLA2 on the yeast cell cycle could be viewed as resulting from the generation of lipid messenger molecules or from membrane remodelling that affects the G1->S transition and G protein activity. The relationship reported here between these two proteins, SSG-2 and SSPLA2, constitutes Cyclosporin A molecular weight the first report of the interaction of a fungal phospholipase and a G protein subunit and the possible involvement of G protein in fungal virulence and morphogenesis. Methods Strains and culture conditions S. schenckii (ATCC 58251) was used for all experiments. The yeast form of this fungus was obtained as described [2]. S. cerevisiae strains AH109 and Y187 were supplied with the MATCHMAKER Two-Hybrid System 3 (Clontech Laboratories Inc., Palo Alto, CA). Nucleic acids isolation DNA and RNA

Farnesyltransferase were obtained from S. schenckii yeast cells as described previously using the methods of Sherman [58], and Chomczynski & Sacchi [59], respectively. Poly A+ RNA was obtained from total RNA using the mRNA Purification Kit from Amersham Biosciences (Piscataway, NJ, USA). Sequencing the ssg-2 gene Polymerase chain Reaction and Rapid amplification of cDNA ends (RACE) S. schenckii DNA (100 ng) was used as template for polymerase chain reaction (PCR) with primers (100–200 ng) targeted to conserved motifs in Gα subunits. The primers used were: GESGKST (fw) 5′ ggtgc(c/t)ggtga(a/g)tc(a/c)gg(a/t)aa(a/g)tc 3′; KWIHCF (rev) 5′ aagcag tgaatccacttc 3′; TQATDT (rev) 5′gtatcggtagcttgggtc 3′; MGACMS (fw) 5′ atggg ggcttgcatgagt 3′ and KDSGIL (rev) 5′ taggataccggaatctttg 3′.

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L, Struck check details D, Young R: Rz/Rz1 lysis gene equivalents in pahges of Gram-negative hosts. J Mol Biol 2007, in press. 72. Savva CG, Dewey JS, Deaton J, White RL, Struck DK, Holzenburg A, Young R: The holin of bacteriophage lambda forms rings with large diameter. Mol Microbiol 2008,69(4):784–793.PubMedCrossRef 73. Grundling A, Smith DL, Blasi U, Young R: Dimerization between the holin and holin inhibitor of phage lambda. Journal of bacteriology 2000,182(21):6075–6081.PubMedCrossRef 74. Ranade K, Poteete AR: Superinfection exclusion (sieB) genes of bacteriophages P22 and lambda. J Bacteriol 1993,175(15):4712–4718.PubMed 75. Ranade K, Poteete AR: A switch in translation mediated by an antisense RNA. Genes Dev 1993,7(8):1498–1507.PubMedCrossRef 76. Sergueev K, Court D, Reaves L, Austin S: E.coli cell-cycle regulation by bacteriophage lambda. J Mol Biol 2002,324(2):297–307.PubMedCrossRef 77. Stayrook S, Jaru-Ampornpan P, Ni J, Hochschild A,

Lewis M: Crystal structure of the lambda repressor and a model for pairwise cooperative operator binding. Nature 2008,452(7190):1022–1025.PubMedCrossRef 78. Jain D, BIBW2992 Kim Y, Maxwell KL, Beasley S, Zhang R, Gussin GN, Edwards AM, Darst SA: Crystal structure of bacteriophage lambda cII and its DNA complex. Mol Cell 2005,19(2):259–269.PubMedCrossRef 79. Datta AB, Roy S, Parrack P: Role of C-terminal residues in oligomerization and stability of lambda CII: implications for lysis-lysogeny decision of the phage. J Mol Biol 2005,345(2):315–324.PubMedCrossRef 80. Hall BM, Roberts SA, Heroux A, Cordes MH: Two structures of a lambda Cro variant highlight dimer flexibility but disfavor major dimer distortions upon Anacetrapib specific binding of cognate

DNA. J Mol Biol 2008,375(3):802–811.PubMedCrossRef 81. Newlove T, Atkinson KR, Van Dorn LO, Cordes MH: A trade between Rabusertib price similar but nonequivalent intrasubunit and intersubunit contacts in Cro dimer evolution. Biochemistry 2006,45(20):6379–6391.PubMedCrossRef 82. Iwai H, Forrer P, Pluckthun A, Guntert P: NMR solution structure of the monomeric form of the bacteriophage lambda capsid stabilizing protein gpD. J Biomol NMR 2005,31(4):351–356.PubMedCrossRef 83. Chang C, Pluckthun A, Wlodawer A: Crystal structure of a truncated version of the phage lambda protein gpD. Proteins 2004,57(4):866–868.PubMedCrossRef 84. Kovall R, Matthews BW: Toroidal structure of lambda-exonuclease. Science 1997,277(5333):1824–1827.PubMedCrossRef 85. Maxwell KL, Yee AA, Arrowsmith CH, Gold M, Davidson AR: The solution structure of the bacteriophage lambda head-tail joining protein, gpFII. J Mol Biol 2002,318(5):1395–1404.PubMedCrossRef 86.

By direct contrast the MLVA PI3K Inhibitor Library in vitro analysis of 49 isolates belonging to the A.Br.008/009 sub-group revealed a more complex pattern with 14 different MLVA15 genotypes (Nei Diversity Index = 0.143, Figures 1 and 3c). This is a remarkable finding because it indicates that a variety of MLVA genotypes are persisting in

the different soils from which the A.Br.008/009 isolates were recovered. These results are an indication that A.Br.008/009, a major sub-group in Europe and Asia [5], has had an extensive history in China. It is difficult to determine the precise origins of the A.Br.008/009 subgroup (e.g. China versus Europe) at this point because rapidly evolving MLVA markers are subject selleck products to homoplasy and potentially inaccurate phylogenetic reconstructions. These issues can eventually

be resolved using additional whole genome sequencing and phylogenetic inference to more accurately predict the origins of the buy PXD101 A.Br.008/009 sub-group. The Ames sub-lineage appears to have descended from the A.Br.001/002 sub-group, a sub-group that has 106 isolates in our worldwide collection [5]. Seventy-four of these accessions were isolated from outbreaks in China and the remaining 32 isolates were recovered in the UK, other parts of Europe, North America and other parts of Asia. The large number of MLVA15 genotypes (n = 32) among the 74 Chinese isolates and a wide distribution throughout the Country indicates that the A.Br.001/002 sub-group is a major part of the B. anthracis population structure in this region (Figure 5a). This sub-group also appears to be basal to the Ames sub-lineage, indicating that 8 isolates from China and 11 isolates from Texas may share common ancestors that originated in China (Figure 5b and [10]). How then did the Ames lineage come to Texas and why is this lineage not found in Europe? This is still not known and subject to considerable speculation. By several accounts, it is believed that anthrax was introduced into the Gulf Coast States (Louisiana and Texas) by early settlers from Europe. Stein

[14, 15] indicates that the first recorded episodes of anthrax in livestock in Louisiana Vildagliptin occurred in 1835, 1851 and 1884; and in Texas in 1860 and 1880. By 1916, when a first national survey was conducted to obtain nation-wide information on the incidence of anthrax, Texas already had 41 counties reporting infections. A composite of outbreaks compiled after the 4th National Survey by the U.S. Department of Agriculture between 1916–1944 (Figure 6) indicates three major outbreak pockets: one in California, one in the Dakotas/Nebraska and the third along the coastal regions of Texas and Louisiana [15]. Figure 6 Historical Anthrax Incidences between 1915–1944 in Texas/Louisiana and The Dakotas/Nebraska/Iowa. Adapted from Stein (1945, [15]). Darker colors represent severe outbreaks and the lighter colors represent sporadic outbreaks.

9±5.5, 36.4±9.6, 35.0±10.2, 33.1±6.1 kcal/kg/day; p=0.20) or fat intake (34±10, 34±6, 34±6, 34±7 %; p=0.97). Protein intake significantly increased from baseline (1.7±0.4, 2.4±0.8, 2.3±0.6, 2.4±0.5 g/kg; p=0.002)

while carbohydrate intake significantly decreased (3.5±1.2, 3.3±0.6, 2.8±1.2, 2.3±0.9 g/kg; p=0.02); corresponding to an increase in percentage of protein (22±6, 26±3, 28±10, 29±6 %; p=0.03) and a decrease in percentage of carbohydrates (45±15, 38±8, 31±10, 28±9 %; p=0.003). After 4, 8 and 12 weeks, respectively, a significant increase in lean mass was observed (1.3±1.7, 2.1±1.8, 2.2±2.1 kg; p=0.001) with no significant effect on body fat percentage (14.3±2.7, XAV-939 in vivo 15.0±3.3, 14.7±3.5, 15.1±3.5 %; p=0.34). Bench press 1RM (-2±6, 3±6, 9±5 %; p=0.001) and

squat 1RM (14±10, 33±14, 43±18 %; p=0.001) increased from baseline. Conclusion Nutritional counseling prior to engaging in a resistance-training program that included post exercise supplementation increased dietary protein intake and resulted in positive training adaptations despite a reduction in carbohydrate intake. Additional nutritional guidance may be necessary to ensure adequate carbohydrate intake particularly in athletes engaged in heavy training. Funding Supported by National Strength and Conditioning Association. Supplements provided by CytosportTM, Inc.”
“Background this website Breast Linsitinib cell line cancer is one of the most prevalent diseases affecting women [1]. In Egypt, breast cancer represents 18.9% of total cancer cases among the Egypt National Cancer Institute during the year 2001 [2]. Breast cancer is the most common cause of cancer related deaths among women worldwide [3]. The etiology of breast cancer involves environmental factors, inherited genetic susceptibility, genetic changes during progression and interaction among these factors, with the relative importance of each ranging from strongly genetic or strongly environmental [4]. In the process associated with Edoxaban the development of breast cancer, it is known that malignant transformation involves genetic and epigenetic changes that result in uncontrolled cellular proliferation and/or abnormal programmed cell death or apoptosis.

These cellular abnormalities, i.e. cancer cells; arise through accumulation of mutations that are frequently associated with molecular abnormalities in certain types of genes, such as proto-oncogenes and tumor-suppressor genes, as a result of genetic predisposition and/or exposure to physical, chemical, biological or environmental factors [2]. These mutations are either inherited (germline) or acquired (somatic). Somatic mutation may determine the phenotype of a particular breast cancer and may be of clinical value in determining prognosis. However, only germline mutations can predetermine an individual’s risk of developing breast cancer. Two classes of inherited susceptibility genes are considered in the etiology of breast and other common cancers.

The MLVA band profiles may be resolved by different techniques ranging from low cost manual agarose gels to the more expensive capillary electrophoresis sequencing systems. The most frequently used method is the agarose gel. Recently, a more rapid and inexpensive method based on the

Lab on a chip technology has been proposed [31]. This miniaturized platform for electrophoresis applications is able to size and quantify PCR fragments, and was previously used for studying the genetic variability of Brucella spp. [32]. Recently a new high throughput micro-fluidics system, the LabChip 90 equipment (Caliper Life Sciences), was developed. This platform can be considered particularly useful when dealing with a large number of samples in short time. Therefore we evaluated the LabChip 90 system for MLVA Screening Library typing of Brucella strains applying the selected subset of 16 loci proposed by Al-Dahouk et al. [12] to fifty-three field isolates and ten DNA samples provided in 2006 for Brucella suis ring-trial. Furthermore, twelve DNA samples, provided in 2007 for a MLVA VNTR ring trial and seventeen human Brucella isolates whose MLVA fingerprinting profiles were previously resolved [32, 33], were de novo genotyped. Results By means of MLVA-16 on LabChip 90 (Caliper

Life Sciences) sixty-three DNA samples, fifty-three field isolates of Brucella (Table 1) and ten DNA provided for Brucella suis ring-trial, were analysed for investigating https://www.selleckchem.com/products/ganetespib-sta-9090.html a broader number of loci. In order to set up the system, Adenosine DNA samples, previously genotyped by sequencing system and Agilent technology [32, 33], were reanalyzed. DNA from all ninety-two isolates was amplified at 16 loci (MLVA-16 typing assay) to generate multiple band profiles. The LabChip 90 equipment acquires the sample in less than a minute and the analysis of 96 samples in less than an hour. After PCR amplification 5 μl of each phosphatase inhibitor library reaction was loaded into a 96-well plate and the amplification product size estimates were obtained by the LabChip Gx Software. The data produced by

the Caliper system showed band sizing discrepancies compared with data obtained from other electrophoresis platforms. Therefore a conversion table that would allow the allocation of the correct alleles to the range of fragment sizes was created. The table contained for each locus the expected size, the range of observed sizes, including arithmetical average ± standard deviation, and the corresponding allele (Table 2). The variability range for each allele was established experimentally by the analysis of different strain amplification products. Furthermore, in order to look at intra- and interchip variability, each allele was analyzed by repeating five times the analysis on the same chip and different chips.

On physical examination, a subtle swelling of the left upper quadrant was noted. The abdomen was soft but markedly tender to palpation diffusely with mild guarding. Laboratory studies revealed an initial hematocrit of 42.8%, and urine toxicology was positive for cocaine. Computed tomography (CT) scan of the abdomen and pelvis with oral and intravenous contrast showed learn more no evidence of free peritoneal air or injury to any solid organs or bones including the ribs, but did reveal fluid around the spleen, in the left paracolic gutter, and layering in the pelvis (Figures 1, 2 and 3). There was no evidence of active contrast extravasation, no vascular

blushes or aneurysms, no findings of portal hypertension, and no suspicion for malignancy. These radiographic findings pointed to a splenic source for hemoperitoneum.

Six hours after presenting to the ED, the patient’s hematocrit had dropped to 36.6%, and repeat CT scan revealed a focal collection of fluid surrounding the spleen. Given that the patient remained hemodynamically stable, he was admitted for non-operative management in the surgical intensive care unit, where he had serial abdominal examinations and blood count monitoring. Figure 1 Axial, contrast-enhanced CT image demonstrates moderate SIS3 clinical trial hemoperitoneum in left upper quadrant centered around the spleen. Figure 2 Sagittal, contrast-enhanced CT Selleck Venetoclax image demonstrates perisplenic hematoma. Figure 3 Axial, contrast-enhanced CT image of the pelvis demonstrates large hemoperitoneum. The patient did not require transfusion as his hematocrit remained

stable between 36% and 38% throughout his hospital course. During that time, infectious etiologies including Epstein-Barr virus and cytomegalovirus were ruled out as 4-Hydroxytamoxifen clinical trial possible causes. A human immunodeficiency virus test performed two weeks prior to this admission was negative. Additionally, hematologic malignancy was excluded with a peripheral blood smear. The patient’s symptoms significantly improved and he was discharged on hospital day four. On follow-up ten days after initial presentation, the patient’s symptoms had resolved and his vital signs were stable. An abdominal ultrasound revealed a subcapsular splenic hematoma at the tip of the spleen tracking anteriorly with interim resolution of free fluid in the pelvis, confirming a splenic etiology for hemoperitoneum (Figure 4). Although the patient’s CT scan did not show a blush suggestive of a pseudoaneurysm, the diagnosis of a splenic artery pseudoaneurysm could have been investigated further with a splenic angiogram. Figure 4 2D gray scale ultrasound image demonstrates small degree of subcapsular splenic hematoma. Conclusions Splenic rupture in the absence of trauma is exceedingly rare.

However, many genes previously reported to be virulence associated were not up-regulated in the presence of serum.

Expression of these genes may require additional signals that were absent from our study. Alternatively, these genes may be expressed transiently in particular host niches, expressed constitutively or the proteins may be regulated at the translational level. In addition, microarray analyses are also limited in that transcripts which are unstable or have a short half-life are unlikely to be measured accurately. However, our results serve to advance our understanding A-769662 mouse of genes which may be important in pathogenesis. Genes of unknown function are over represented in the set of genes HDAC inhibitor unique to pathogenic Leptospira spp. [45], consistent with the notion that Leptospira possesses unique virulence factors. Accordingly, such genes of unknown function that are differentially regulated upon serum exposure warrant further investigation to gain a better insight into their roles in the

pathogenesis of leptospirosis. Methods Bacterial growth and conditions Pathogenic L. interrogans serovar Copenhageni strain L533, and non-pathogenic L. biflexa serovar Patoc strain L41 were grown in EMJH broth medium at 30°C under aerobic conditions. Leptospires were grown to exponential phase at an approximate density of 5-8 × 108cells/ml before harvesting by centrifugation at 8000 × g. Complement and heat-inactivated sera CYC202 molecular weight Normal guinea pig serum (NGS) (Sigma, St Louis, MO) was obtained lyophilized and stored at -80°C until use. Serum was reconstituted in 1 or 5 ml of sterile ice-cold deionized water according to the manufacturer’s instructions. To maintain selleck products consistency, the same batch of serum was used throughout. Heat-inactivated serum (HIS) was obtained by incubating NGS at 56°C for 30 min. Sera were freshly prepared before use or stored at -80°C until use. Serum was prewarmed at 37°C for 30 min before incubating with leptospires. Serum bactericidal assay Serum bactericidal

assays were performed as described previously with minor modification [38]. Pathogenic leptospires were grown to exponential phase and diluted in liquid EMJH medium to a density of 2 × 108cells/ml before use. 1 × 107 bacteria were incubated with 50% NGS in a final volume of 100 μl at 37°C for up to 2 h. HIS was used as a control. Samples were taken at different time points and viable spirochetes were enumerated by dark-field microscopy using a Petroff-Hausser counting chamber. The percentage of viable leptospires was calculated by comparison with those incubated with 50% HIS which were considered as 100% viability. The assay was performed in triplicate. The non-pathogenic, complement-sensitive L. biflexa serovar Patoc was used in parallel under the same conditions as a control for serum killing. Microarray construction Microarrays were constructed based on a revised annotation of the whole genome sequence of L.

8% in our control subjects. This frequency is also similar to the frequencies see more found in other studies that analyzed GSTP1 polymorphism [18–20]. Some studies have reported a relationship GS-9973 between GST variants and risk of prostate cancer [9, 10, 12, 13, 21]. Investigation of the GSTP1 gene did not reveal any significant association between heterozygous GSTP1 genotype (Ile/Val) and prostate cancer. However, our results suggest that Val/Val genotype of GSTP1

gene could modulate the risk of prostate cancer, even if this association did not reach statistical significance. It should be kept in mind that the inability to reject the null hypothesis could be due to low power of the test because of a relatively selleck products small sample size. Therefore, the lack of significance does not necessarily mean equality of the distributions. It is plausible that polymorphism at the GSTP1 locus can play an important role in the susceptibility to different types of cancer. Association of the GSTP1 Val allele with cancer could be expected since the conversion of the amino acid at codon 105 from isoleucine to valine substantially lowers activity of the altered enzyme. It has been predicted

from molecular modelling that the amino acid at this site lies in a hydrophobic binding site for electrophile substrates and thus affects the substrate binding [22]. On the other hand, there are also studies which did not prove any independent effect of this type of polymorphism on the susceptibility for prostate cancer [23–25]. In the present study, we did not observe significantly different crude rates of the GSTM1 and GSTT1 null genotypes in the men diagnosed with prostate cancer and those in the control group. Our

data and the data published by other research groups suggest that differences in the GST frequencies between prostate cancer patients and the control group are relatively small, which therefore makes it difficult to separate the groups from each other cAMP based on statistical data analysis. Once again, the high variability in the groups could mask statistical differences due to low power. The easiest way to improve precision is to increase the number of subjects and patients in the experimental design. However, this may not be applicable to all research conditions due to such factors as additional costs, poorer availability of resources, lower population, which compromises the number of subjects eligible for investigation. In order to achieve a power of at least 80%, we have to identify other explanatory variables and the control for them, and/or apply meta-analysis in order to increase sample size.

Complementation of mutants The construction of plasmids to complement tat and

bro2 mutant strains was achieved as follows. Plasmid DNA (pRB.TatA.5, pRB.TatB.1, pRB.TatC.2, pRB.Tat.1, pRN.Bro11, pTS.BroKK.Ec) was digested with BamHI to release the cloned M. catarrhalis genes from the vector pCC1. Gene fragments were purified from agarose gel slices using the High Pure PCR Product Purification Kit (Roche Applied Science), ligated into the BamHI site of the M. catarrhalis/Haemophilus Lazertinib research buy influenza-compatible shuttle vector pWW115 [95], and electroporated into H. influenzae strain DB117. Spectinomycin resistant (spcR) colonies were screened by PCR using the pWW115-specific primers P17 (5′-TACGCCCTTTTATACTGTAG-3′) and P18 (5′-AACGACAGGAGCACGATCAT-3′), which flank the BamHI cloning site, to identify clones containing inserts of the appropriate size for the tat and bro2 genes. This process produced plasmids pRB.TatA, pRB.TatB, pRB.TatC, pRB.TAT, pTS.Bro, and pTS.BroKK. The O35E.TA mutant was naturally transformed with plasmids pWW115, pRB.TatA, and pRB.TatABC. The plasmids pWW115, pRB.TatB, and pRB.TAT were introduced in the O35E.TB mutant by

Rigosertib supplier natural transformation. The tatC mutants O35E.TC and O12E.TC were naturally transformed with the vector pWW115 and plasmid pRB.TatC. The plasmids pWW115, pTS.Bro, and pTS.BroKK were electroporated into the bro-2 mutant strain O35E.Bro. The successful introduction of these plasmids into the indicated strains was verified by PCR analysis of spcR transformants with the pWW115-specific primers P17 and P18, and by restriction endonuclease analysis of plasmid DNA purified from each strain. Growth rate experiments Moraxella. catarrhalis strains were first cultured onto agar plates supplemented with appropriate antibiotics. These plate-grown bacteria were used to inoculate 500-mL sidearm flasks containing 20-mL of broth (without antibiotics) to an optical density (OD) of 50 Klett units. The cultures were then incubated with shaking (225-rpm) at a temperature

of 37°C for 7-hr. The OD of each culture was determined every 60-min using a Klett™ Colorimeter (Scienceware®). These experiments were repeated on at least three separate occasions for each strain. In some experiments, aliquots were taken out of each culture after recording the optical density, Selinexor nmr diluted, and spread onto agar Histone demethylase plates to determine the number of viable colony forming units (CFU). Carbenicillin sensitivity assays Moraxella catarrhalis strains were first cultured onto agar plates supplemented with the appropriate antibiotics. These plate-grown bacteria were used to inoculate sterile Klett tubes containing five-mL of broth (without antibiotics) to an OD of 40 Klett units. Portions of these suspensions (25 μL) were spotted onto agar medium without antibiotics as well on plates supplemented with carbenicillin, and incubated at 37°C for 48-hr to evaluate growth. Each strain was tested in this manner a minimum of three times.

Due to the interaction between

Belnacasan cell line the surface of c-ZnO NWs and moisture solution, the radial concentration of Zn2+ ion would be changed because Zn2+ ions gradually dissolve and diffuse from the original c-ZnO NWs surface into the moisture solution. When the concentration of Zn2+ ion in moisture solution meets the saturation condition, the Zn2+ ions start to segregate out from the moisture solution; the a-ZnO NBs cause to grow from the main body of the original c-ZnO NWs, which can be seen in Figure 2b. If the dimension of the original c-ZnO NWs is sufficient, the dissolving and diffusing effects can be maintained for a long period; the a-ZnO NBs will keep growing and forming ultra-long a-ZnO NBs. Normally, a-ZnO NBs would be spontaneously grown from specific size of c-ZnO NWs, such as around hundreds of nanometers. In high humidity, however, Ipatasertib it is difficult for a-ZnO NBs to segregate from

the moisture solution, which means that the Zn2+ ion concentration in moisture solution is not high enough to meet the condition of saturation forming a-ZnO NBs. That is why the ultra-long a-ZnO NBs cannot be seen in high humidity (90% ± 2.5%). Figure 2 The spontaneous reaction mechanism of a-ZnO NBs is illustrated. (a) A uniform c-ZnO NWs (dark green rod) placed in the moisture environment surrounded by H2O molecules (light blue bubbles). The c-ZnO NW has uniform ZnO concentration which can be seen from the inset (ZnO concentration versus radius). (b) After H2O molecules learn more absorbed at the surface of c-ZnO NWs, the Zn2+ ions would be dissolved from the surface of c-ZnO NWs and became aqueous solution diffused away from the c-ZnO NWs. When the Zn2+ ions and the ZnO NBs start to segregate out from the moisture solution and cause to grow from the main body of the original ZnO NWs, respectively (inset). (c, d) The surface potential Cyclic nucleotide phosphodiesterase was measured before and after moisture treatment. (1) (2) (3) The main reactions can be understood by the previous equations [27–29]; there are several reactive intermediates like Zn(OH)4 2−, Zn(OH)2, or Zn(OH)3 −, which depend

on the specific parameters such as the concentration of Zn2+ ion, the amount of H2O molecules, and the pH value. Further investigation, the spontaneous growth mechanism of a-ZnO NBs can be studied through the c-ZnO NWs surface potential measurement by using Kelvin probe force microscope (KPFM) tapping mode. The surface potential of c-ZnO NWs can be changed due to the humidity absorption. Before humidity treatment, the surface morphology and potential were smooth and almost constant (around 10 to 25 mV variation) by SEM and KPFM analysis, respectively (Figure 2c). After humidity treatment, the surface morphology and potential were rough and varied (around 198.26 mV variation), respectively (Figure 2d). This surface potential variation might induce the a-ZnO NBs spontaneous growth.