5 mM for SAL respectively The formation of the biofilms was obse

5 mM for SAL respectively. The formation of the biofilms was observed by determination of total counts on Columbia blood agar (CBA) plates at 5 time points during the incubation time. The final structure,

as well as the thickness of the biofilms at 5 time points during the incubation time, was determined by confocal laser scanning microscopy (CLSM). The experiments confirmed and extended our previous finding [11] that the composition of the growth medium has a major effect on the development, stability and composition of the biofilms. The iHS medium delayed biofilm formation by 20 h compared to mFUM4 this website (Figure 1). 4 h after inoculation in mFUM4, the discs were densely colonized by cocci. Based on the observation that most of these cocci appeared as chains, they can be assumed to be streptococci. However, after 4 h of incubation in iHS, cocci were observed to appear almost exclusively as dense microcolonies, while rods (morphologically Fusobacterium nucleatum, Prevotella intermedia, or Tannerella forsythia) in low abundance colonized the majority of the disc. Incubation in SAL medium Temsirolimus supplier led to a similar observation as in mFUM4: The disc was colonized mainly by cocci (Figure 2). Figure 1 Time course of biofilm growth comparing

SAL, mFUM4, and iHS as growth media. Total counts determined by plating on CBA agar plates (T. denticola and T. forsythia are not cultivable on CBA). Each box PIK3C2G represents N = 9 independent biofilms from three independent triplicate experiments. The boxes

represent the inter quartile range of the data points, the bar indicates the median. The whiskers cover the data points within the 1.5x inter quartile range. Dots are outliers within 1.5 and 3 box lengths outside the interquartile range. Figure 2 Bacterial attachment to the disc surface under different nutritional conditions 4 h after inoculation. Comparison of the growth media mFUM4 (A), iHS (B) and SAL (C). green: DNA staining using YoPro-1 + Sytox. The disc surface is visualized in grey colour. The images show representative areas of one disc each. Scale bars: 15 μm (A/B) and 10 μm (C). The high concentration of human serum in iHS improved biofilm stability in terms of firm attachment to the disc (less cell loss during dip washing and the FISH staining procedure), and further the average thickness of the biofilms was significantly increased after 64.5 h when compared to biofilms grown in mFUM4, or SAL respectively (Figure 3A). However, the total counts of bacteria per biofilm did not show significant differences between the three growth media (Figure 3B). Figure 3 Thickness (A) and total counts (FISH/IF) (B) of biofilms grown for 64.5 h in SAL, mFUM4, and iHS growth medium. Thickness was determined by CLSM, total counts were calculated from the species specific quantification by visual microscopic counting following FISH- or IF from N=9 independent biofilms from three independent experiments.

0, 200 mM NaCl) The imidazole in the eluent was removed using a

0, 200 mM NaCl). The imidazole in the eluent was removed using a Centrifuge Biomax-5 column (Millipore, Billerica, MA, USA), and the AirR protein solution was supplemented with 30% glycerol and stored at −80°C until use. The full-length airS ORF was amplified using PCR with the e-airS-f and e-airS-r primers from S. aureus NCTC8325 genomic DNA, cloned into the expression vector pET28a (+), and transformed selleckchem into E. coli BL21 (DE3). Purification of 6-His-tagged AirS was performed following

the procedures of AirR purification except an overnight induction of 0.5 mM IPTG at 16°C. The purity of the proteins was determined by SDS-PAGE, and the protein concentration was determined using the BCA assay with bovine serum albumin as the standard. AirR phosphorylation in vitro For AirR phosphorylation

in vitro, we used lithium potassium acetyl phosphate as phosphoryl group donor. Briefly, 10 μM AirR was equilibrated in buffer containing 50 mM Tris at pH 7.4, 50 mM KCl, 5 mM MgCl2, and 10% glycerol (phosphorylation buffer). Lithium potassium acetyl phosphate (Sigma-Aldrich, St. Louis, MO, USA) was added to a final concentration of 50 mM, and this mixture was incubated for 60 min at 37°C [27]. We also used AirS for AirR phosphorylation in vitro. Briefly, 10 μl phosphorylation buffer containing 2 μM AirS and 10 mM ATP was used to initiate the autophosphorylation of AirS. After incubation at 25°C for 5 min, 10 μM AirR was added and the incubation was continued for another 10 min [22]. Electrophoretic mobility shift assay The DNA fragments containing

the promoter region were amplified from the S. aureus NCTC8325 Selleckchem Peptide 17 genomic DNA. The PCR products were labeled using a digoxigenin (DIG) gel shift kit (Roche, Indianapolis, IN, USA) according to the manufacturer’s instructions. The labeled fragment was incubated at 25°C for 15 min with various amounts of AirR in 10 μl of incubation buffer (10 mM Tris–HCl, pH 8.0, 100 mM NaCl, 1 mM EDTA). After incubation, the mixtures were electrophoresed in a 5% native polyacrylamide gel in 0.5 × Tris-borate-EDTA (TBE) buffer. The band shifts were detected and analyzed according to the manufacturer’s instructions. The images were obtained using ImageQuant Fossariinae LAS 4000 mini (GE, Piscataway, NJ, USA). The unlabeled fragments of each promoter were added to the labeled fragments at a ratio of approximately 50:1, respectively, as specific competitors (SCs). The unlabeled fragments of the pta ORF region (50-fold) were added as non-specific competitors (NCs). Statistics The data were analyzed using the T-test analysis of variance, with a P value of < 0.05 considered significant (one asterisk), P < 0.01 (two asterisks). Results Transcriptional profile of the airSR mutated strain To investigate the function of AirSR, we performed a cDNA microarray analysis using total RNA from the exponential growth stage. The microarray results indicated that approximately 190 genes were up-regulated (ratio > 2.0) and 290 genes were down-regulated (ratio < −2.0).


Conversely, DAPT a sedentary lifestyle would be associated with an increased risk of colon cancer in men and women [8]. Fermented food is an important component of traditional diets, both for its nutritional value and its prophylactic and therapeutic properties [13]. However, its consumption

in Brazil remains at a low level, due probably to the relatively high price of such products [14]. Research has also demonstrated that the commensal lactic acid bacterium from the human gut, Enterococcus (formerly Streptococcus) Caspase cleavage faecium CRL 183, if consumed in a fermented soy product, has several beneficial effects on the health. These include appreciable cholesterol-reducing activity, stimulation of the immune system, anticarcinogenic activity and inhibition of post-menopausal osteoporosis [15–19]. In view of the

possible benefits of ingesting E. faecium and the potential role of physical exercise in the prevention of certain types of cancer, we decided to test the effects of consuming soy product fermented with E. faecium CRL 183, while engaging (or not) in physical exercise (moderate or intense), on the formation of ACF in rats injected with DMH. Methods Animal maintenance and administering of products Eighty 4-week-old male Wistar SPF rats, average weight 200 g, were obtained from the central

animal facility at the State University of Campinas (CEMIB, UNICAMP-SP, Brazil). The animals were housed for 8 weeks in boxes Phospholipase D1 within a vivarium cabinet (Alesco®, Brazil) equipped with air filtration, controlled temperature (22 ± 1°C) and a dark:light cycle of 12:12 h. During the experiment, the rats had free access to sterile water and sterilized commercial rat chow (Purina®, Brazil), with the following composition: 23% protein, 49% carbohydrate, 4% fat, 5% fiber, 7% ash and 6% vitamin C. The products being tested were administered daily by gavage, at 3 mL/kg body weight (b.w.) per day, throughout the 8-week period. All animal procedures were submitted to the Research Ethics Committee of the School of Pharmaceutical Sciences, UNESP at Araraquara (SP, Brazil), who approved the experimental protocol.

2%) than in Tau-positive (52 4%) Our results differ from those o

2%) than in Tau-positive (52.4%). Our results differ from those obtained in the studies on breast cancer, where co-expression of Tau protein and estrogen receptor was considered as good prognostic factor [8, 11, 15]. This divergence might be caused by Tau significance evaluation in different cancer sites. Hormone-dependent breast cancer is associated with good prognosis and chemo resistance. Tau genes are regulated by estrogens and tamoxifen so Tau protein expression is associated with hormones. On the other

hand, in ER-negative breast cancer patients group prognostic value of Tau protein was not confirmed. In other study prognostic value of Tau protein in breast cancer was not observed [13]. The only independent parameter significantly influencing on OS in multivariate analysis was sensitivity GW-572016 nmr to first-line chemotherapy (HR 22.59; p<0.0001), defined as no progression or recurrent disease in 6 months from the end of treatment. The aim of adjuvant chemotherapy is prolongation of OS

as well as PFS. The effect is possible to achieve if malignancy is prone to drugs. Thus, chemosensitivity is a good prognostic factor. Conclusions Many studies confirm prognostic value of time duration between chemotherapy ending and disease progression in ovarian cancer [16–18]. Everolimus purchase Extension of this period might be caused by tumor susceptibility to cytostatics as well as maximal cytoreduction during surgery. Mechanisms affecting chemosensitivity are complex. Tau expression is a single factor, influencing sensitivity to paclitaxel. Platinum analogue (the other component of standard regimen in ovarian cancer) effectiveness is modified by numerous factors such as epigenic changes in cancer cells, expression of multidrug resistance proteins (for example: P-gp, MRP1, MRP2, LRP), p53 gene mutations and GST-pi increase [19]. The processes are intricate, thus identification of single factors seems to be complicated, especially in polichemotherapy. Better response to paclitaxel related to negative status of Tau protein in primary tumors

in ovarian cancer is conducive to extension of PFS, and therefore to the improvement of prognosis in ovarian cancer patients. Although sample size in our analysis was not great and the data were evaluated retrospectively, the results of our study may direct successive researches in ovarian cancer. Significance of Tau Megestrol Acetate protein expression requires evaluation in prospective studies with larger group of patients, including assessment of the other predictive and prognostic parameters in paclitaxel and platinum-based chemotherapy. Acknowledgements This study was supported by grant from budget resources for science in the years 2010–2011 as a research project. References 1. McGuire WP, Hoskins WJ, Brady MF: Cyclophosphamide and cisplatin compared with paclitaxel and cisplatin in patients with stage III and stage IV ovarian cancer. N Engl J Med 1996, 334:1–6.PubMedCrossRef 2.

Furthermore, the gene integrity has to be proven To correlate vi

Furthermore, the gene integrity has to be proven. To correlate virulence with the expression of gtf, fimB and pilB, these factors have to be deleted by the construction of knock-out mutants to determine difference in the ability to form biofilms, the adherence to and invasion of host cells and the adherence to ECM proteins. This will show the impact of these factors on binding to host cells and most likely correlate with the bacterial

potential to cause IE. In addition, the determined virulence factors reflected only a small proportion of the presumably Napabucasin order high quantity of possible virulence factors in S. gallolyticus. Accordingly, the absence of a correlation between the potential to adhere to as well as to invade cells and the number of the existing putative virulence genes most likely could also be explained by these reasons. The role of biofilm formation in IE remains ambiguous. Several studies demonstrated an association between biofilm formation and streptococcal IE [45–47],

whereas another study indicated AZD4547 cell line that the ability to form biofilms in vitro is not associated with endocarditis virulence [30]. The results of our study support the lack of association between biofilm formation and adherence to or invasion of endothelial cells and adherence to ECM proteins. Most IE patients have valve abnormalities, resulting in the exposure of ECM proteins, the production of tissue factor and the deposition of fibrin and platelets promoting bacterial colonization. Streptococcal adherence to endothelial matrix proteins has previously been shown to be an important factor for the infection of host tissues [32–37, 48]. Recently, Sillanpää et al. analyzed endocarditis-derived human isolates of S. gallolyticus and, according to the results obtained in our study, binding to collagen I was found to be the most common phenotype, followed by collagen type IV, fibrinogen and fibronectin [2]. In contrast,

both studies revealed a weak binding to fibronectin, which PAK6 is contradictory to studies observing a direct connection between adherence to fibronectin and the applicability of S. sanguis to induce IE [49]. This observation possibly indicates a different pathogenesis of S. gallolyticus IE. Interestingly, a study of animal isolates of S. gallolyticus revealed no adherence to collagen I [12]. Further analysis of the draft genome sequence of an ECM protein-adherent S. gallolyticus strain by Sillanpää et al. revealed 11 predicted LPXTG-type cell-wall-anchored proteins with characteristics of MSCRAMMs (microbial surface components recognizing adhesive matrix molecules), including the “”adhesin to collagen of the S. bovis group”" (acb) gene [50]. Remarkably, a recombinant Acb protein showed high affinity binding to immobilized collagen. Cell surface expression of Acb correlated with the presence of acb and collagen adherence of different isolates.

Therefore their role will not be further discussed Suffice here

Therefore their role will not be further discussed. Suffice here to remember that the antifracture efficacy is better for a daily intake of 1,000–1,200 mg

calcium and 800–880 IU vitamin D [19]. Excesses in sodium intake have a negative impact on calcium balance by increasing the urinary calcium excretion. There is, however, an interindividual differences in salt sensitivity. Obligatory urinary calcium losses are correlated selleck products with urinary sodium excretion [20]. For every 100 mmol of sodium excreted, approximately 1 mmol loss of urinary calcium is observed [20]. It has been suggested, however, that enough calcium in the diet could overcome the salt deleterious effect. There could be 2-fold differences in sodium-induced calciuria with low and high

calcium intakes. In a recent study, as compared with a low salt diet (3.9 g/day), a high salt intake (11.2 g/day), corresponding to upper intakes in postmenopausal women on a Western-style INK 128 clinical trial diet provoked a significant increase in urinary calcium excretion (+36%). The negative bone calcium balance was not counteracted by a high calcium diet (1,284 mg/day). Paradoxically, the negative bone calcium balance induced by both high and low salt diets was less marked with a low calcium intake. There was a significant increase in the levels of parathyroid hormone (+11.4%) and of urinary N-telopeptide (+19%) in response to the high sodium diet [21]. In previous studies such as the Framingham

study, in a 12-year follow-up, the risk of hip fracture over each 2-year period was found significantly increased by the consumption of ≥2.5 units of caffeine per day (one cup of coffee = one unit of caffeine, and one cup of tea = 0.5 unit of caffeine) [22]. There is a theoretical explanation to Obatoclax Mesylate (GX15-070) the fragilization of bone by caffeine intake: caffeine increases urinary and faecal calcium losses and may provoke a negative calcium balance in presence of a low calcium diet [23]. Caffeine at a dose of 330 mg/day (i.e. four cups (600 ml)) possibly might be associated with a modestly increased risk of osteoporotic fractures (Hazards ratio, 1.20 (95% confidence interval (CI), 1.07–1.35)), compared with a low caffeine intake (<200 mg/day) [24]. However, this deleterious effect of caffeine seems to be offset by increasing calcium intake (by 40 mg calcium for every 177.5 ml serving of caffeine-containing coffee, i.e. ∼1 cup) [25]. This positive calcium effect greatly minimizes a potential role for caffeine in BMD maintenance and bone strength. No study has been done with decaffeinated coffee. High phosphorus intakes are associated with lower levels of calcium urinary excretion, but a slightly higher intestinal calcium excretion. These opposite effects neutralize themselves and does not seem to negatively impact on calcium balance [26, 27]. The role of protein intake remains controversial in the development of osteoporosis.

CrossRefPubMed 31 Abramovitz JN, Baston RA, Yablon JS: Vertebral

CrossRefPubMed 31. Abramovitz JN, Baston RA, Yablon JS: Vertebral osteomyelitis, the surgical management of neurologic complications. Spine 1986, 11:418–20.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions

DV participated in the data collection in the analysis of the data, reviewed and revised the manuscript. DA participated in the data collection and prepared the manuscript. FF participated in the data collection and in the analysis of the data. KSF reviewed and revised the manuscript and has given final approval of the version to be published. All authors read and approved the final manuscript.”
“Background End-to-end anastomoses after resection of injured arteries were described in the United States as early as 1897, however it was not until the later stages of World War

II, and then the Korean War that they became Panobinostat an acceptable solution for the management of acute vascular injuries [1–4]. Although Carrel and Guthrie are credited with describing an end-to-end anastomosis using triangulation with 3 equidistant sutures [5], other techniques have since been published [6]. These include, but are not limited to, interrupted and continuous suturing with, or without “”parachuting”" of the graft and/or vessel [6]. A simple and rapid method for end-to-end anastomosis after limited segmental resection of an injured femoral artery is described in this report. Case presentation A 22-year old, otherwise healthy, male presented following a single gunshot wound to the left groin. On examination, the patient Kinase Inhibitor Library purchase was hemodynamically stable, but had no palpable lower extremity pulses on the injured side (dorsalis pedis or posterior tibial). The ankle-brachial index confirmed an arterial injury (<0.9). On immediate exploration, a transacted superficial

3-oxoacyl-(acyl-carrier-protein) reductase left femoral artery was identified. Following debridement of the contused ends of the vessel, as well as moderate mobilization, a primary repair was completed using the technique described. The patient was discharged home on post-operative day 3 with normal extremity function. Discussion of technique As with most vascular anastomoses, a synthetic, nonabsorbable monofilament suture on an atraumatic needle (6-0 polypropylene) was employed. Basic principles of vascular repair were followed. These included debridement of contused or lacerated vessel, proper orientation, and an absence of tension on the anastomosis. We did not require an autalogous graft (reversed saphenous vein). This technique of vascular anastomosis requires a double-armed polypropylene suture placed in a continuous fashion with perpendicular bites located 1 mm from the vessel edge and 1 mm apart. The anastomosis begins at the position opposite the operator (3 or 9 o’clock depending on the patient side) where the first 2 bites are placed from inside to outside the vessel using both arms of the suture (Fig. 1).

The therapeutic potential of octreotide is further stressed by th

The therapeutic potential of octreotide is further stressed by the fact that BCLC stage-matched patients receiving no active treatment had a shorter survival time than patients

with TACE treatment as expected from the well known fact of a survival benefit of TACE therapy [19, 20]. And yet, TACE treatment was not better than octreotide treatment. Along the same line, the study of Plentz et al [23] showed a similar survival of patients treated with octreotide compared to patients treated with TACE. Treatment with long-acting octreotide [Sandostatin LAR] was excellently tolerated except for a few episodes of soft stools presumably due to the effect of reduced exocrine pancreatic output. This could easily be corrected either with supplementation of pancreatin containing capsules or with loperamid tablets. No intramuscular haematoma formation was observed after i.m. administration of LDK378 mouse long-acting octreotide

[Sandostatin LAR] despite reduced coagulation capacitiy. The interpretation of our data might be limited by the retrospective non-randomised nature of our study and the long time period of recruitment of patients which results in a considerable heterogeneity of the study groups. Although, we tried to match the patients in the study groups according to HIF-1 activation the BCLC system, the best available prognostic staging system, residual heterogeneity in the study population might have influenced the results. In addition, patients under octreotide treatment tended to have lower MELD scores than patients undergoing other treatment modalities although there was no overall difference in MELD score between the various groups. In summary, this retrospective analysis of survival of BCLC stage-matched patients with HCC showed that octreotide

treatment produces a similar survival benefit as TACE or multimodal therapy as compared to no active treatment. Given the few side effects of long-acting octreotide [Sandostatin LAR] this treatment seems to Megestrol Acetate be a therapeutic option for patients with HCC and needs further randomised controlled studies in BCLC stage-matched patients. References 1. Schoniger-Hekele M, Muller C, Kutilek M, Oesterreicher C, Ferenci P, Gangl A: Hepatocellular carcinoma in Central Europe: prognostic features and survival. Gut 2001, 48 (1) : 103–9.CrossRefPubMed 2. Llovet JM, Brú C, Bruix J: Prognosis of hepatocellular carcinoma: the BCLC staging classification. Semin Liver Dis 1999, 19 (3) : 329–38.CrossRefPubMed 3. Okuda K, Ohtsuki T, Obata H, et al.: Natural history of hepatocellular carcinoma and prognosis in relation to treatment. Study of 850 patients. Cancer 1985, 56: 918–28.CrossRefPubMed 4. The Cancer of Liver Italian Program (CLIP) Investigators: A new prognostic system for hepatocellular carcinoma: a retrospective study of 435 patients.

456** 0 462** V MF Total 0 744** 0 700** 0 427** 0 581** 0 717**

456** 0.462** V MF Total 0.744** 0.700** 0.427** 0.581** 0.717** SurMF 0.739** 0.700** 0.408** 0.583** 0.704** CurvMF 0.692** 0.666** 0.380** Metformin mouse 0.571** 0.657** EulMF 0.675** 0.670** 0.429** 0.663** 0.673** The lin./qua.fuzziness and log./exp.entropy in the neck is n.s. The highest values in each parameter group are rendered in italics n.s. not significant *p < 0.05; **p < 0.01 BMC of the total proximal femur (total BMC) showed the highest correlation with FL (r = 0.802; Fig. 2). By adjusting FL to BH and age, differences between highest BMC and highest BMD correlation coefficients decreased (Δr = 0.015 and

Δr = 0.008, respectively; Table 3). After adjustment of FL to BW and measures of femoral bone size, highest correlations were observed for BMD and not for BMC. The highest correlation coefficient of FL and all adjusted FL parameters with BMC or BMD did not significantly differ from the highest of the trabecular structure parameters (p > 0.05). Fig. 2 Total BMC versus FL, app.TbSp (head) versus FL/HD, f-BF (head) versus FL/HD, neck \( m_P_\left( \alpha \right) \) (SIM) versus FL/HD and Proteasome assay V MF versus FL. Solid lines display the regression curves App.TbSp in the femoral head showed the highest correlation of all morphometric parameters with

FL and all adjusted FL parameters (up to r = −0.743 for FL/HD; Fig. 2). By adjusting FL to BH and measures of femoral bone size, higher correlation coefficients were achieved for app.TbSp in the head (Table 3). Correlation of FL/HD with app.TbSp in the head was even higher than those with BMC and BMD. After adjustment of FL to BH, measures of femoral bone Amino acid size and age, correlation coefficients of fuzzy logic parameters and SIM-derived \( m_P_\left( \alpha \right) \) remained almost unchanged (Table 3). Fuzzy logic parameters and \( m_P_\left( \alpha \right) \) had lower correlations with FL and all adjusted FL parameters than the morphometric parameters. Highest correlations were observed for f-BF in the head (up to r = 0.506

for FL/HD; Fig. 2) and for the neck \( m_P_\left( \alpha \right) \) with FL/HD (r = 0.493; Fig. 2). The highest correlation of all MF with FL was found for V MF (r = 0.744; Fig. 2). Adjusted FL parameters showed lower correlations with MF (Table 3), but the respective highest correlation coefficient did not significantly differ from the overall highest correlation coefficient achieved by BMC, BMD, or app.TbSp in the head (p > 0.05). The best DXA and best multiple regression models for FL and all adjusted FL parameters are listed in Table 4. Structure parameters of the trabecular bone could add significant information in the multiple regression models. The best multiple regression model for FL and each adjusted FL parameter showed significantly higher R adj than the respective model of the best DXA parameter alone (p < 0.05).

Moreover, it is also demonstrated that strong polymer-filler inte

Moreover, it is also demonstrated that strong polymer-filler interaction could modify the molecular configuration of the polymer chains in the vicinity of the filler to the formation of localized amorphous regions. This would inhibit and retard the crystalline development of the CS chains. It became more pronounced when the CDHA content exceeds 30 wt.%. However, the crystallinity of CDHA seems to be enhanced by the addition of

CS. The full-width at half maximum of the XRD peak of the CS-CDHA nanocomposites was observed to be lower than that of the pristine CDHA, thereby displaying sharper peak (better crystallinity). Thus, we suggest that the CS chains might induce the crystallinity of CDHA. Figure 2 shows the TEM images of the pristine CDHA (a), CS37 (b), CS55 (c), and CS73 (d) nanocomposites. The pristine CDHA exhibited click here needle-like structure of nanorods (5 to 20 nm in diameter and 50 to 100 nm in length). The CS-CDHA nanocomposites exhibited homogenously dispersed nanorods in the CS networks, especially in the CS73,

as illustrated in Figure 2b,c,d. The reason is that the electrostatic attraction between the NH3 + group (positive charge of the CS chains) and the PO4 3- group (negative charge of the CDHA nanorods) served as the stable force for the colloid suspension, favoring the dispersion of CDHA. Moreover, the structure of the CS-CDHA nanocomposites (CS73) became denser with the increase of the CS content due to the better compatibility Obeticholic Acid mw and stable network of high molecular weight of CS. In contrast, CS55 and CS37 exhibited less dense morphologies. A comparison of the chemical binding energy change of the pristine CDHA, pristine CS, and CS37 nanocomposites was shown in Lepirudin the ESCA spectra. The ESCA analysis shows that the surface was mainly composed of N, Ca, and P atoms, which could represent the chemical structure and interaction of CS (N atom) and CDHA (Ca and P atoms). Figure 3a shows the ESCA data of N1s scan spectra in CS, CDHA, and CS37. The N1s peak in the pristine CS was found at 402.3 eV, implying the amino group of CS

(no peak existing in the pristine CDHA). However, the NH2 peak was shifted from 402.3 to 400.0 eV in the CS37, implying the complex formation of CS and CDHA. Two Ca2p peaks of the pristine CDHA were observed with the binding energy of 347.8 eV (2p 3/2) and 351.4 (2p 1/2), as indicated in Figure 3b. Two peaks (2p 3/2 348.0 eV and 2p3/2 351.6 eV) were exhibited in CS37 and displayed 0.2 eV chemical shift compared to the pristine CDHA, suggesting the formation of CDHA in the CS37 and some chemical interaction between CS and CDHA (no additional peak in the pristine CS). Similar with the ESCA spectrum of Ca2p , 0.8 eV (133.1-eV shift to 133.9 eV) chemical shifts were found between the pristine CDHA and CS37 in the P2p spectrum. These results indicate that the CDHA nanorods were grown in the CS matrix through in situ precipitated process.