In addition, the non-substrate based inhibitors, such as small molecule inhibitors, showed significant inhibitory activities at low micromolar concentrations against the flavivirus proteases [31, 32]. Although several of these compounds are potent inhibitors of the dengue NS2b-NS3

protease, some showed poor stability in solution. Furthermore, several studies did not use cell-based assays to evaluate the toxicity and antiviral efficacy of the identified compounds [18]. The nature of the dengue protease, which possesses a flat and hydrophilic active site, decreases the possibility of identifying potent inhibitors to develop as antiviral therapeutics [18]. Based on the results of this EGFR inhibition study, we postulate that the hydrophobic residues of Ltc 1 are important for stabilising the binding to the hydrophilic active site of the dengue protease. In this study, the inhibitory potential of the Ltc 1 peptide against the dengue protease was further verified using cell based assays. Previously, other characteristics of the latarcin family peptides, such as anti-neoplastic cells activities [21], were examined. The latarcin peptides can alter the lipid bilayers of the cell membrane, may induce the apoptosis of mammalian cells [21]. Because of this, the possible GSK2126458 ic50 effect of the Ltc 1 peptide on cell proliferation was removed to avoid false interpretation

of selleck chemical the antiviral activity. Subsequently, the antiviral activity of the Ltc 1 peptide was evaluated at the doses with minimal effects on cell proliferation as determined by MTT assay and Real-Time Cellular Analysis (RTCA). The results of the immunostaining and western blot analyses showed that the Ltc 1 peptide significantly reduced the viral particles and non-structural protein NS1 in DENV-infected cells. Furthermore, the results of the time-of-addition assay showed that the Ltc 1 peptide inhibited dengue virus replication at both the simultaneous and post-treatments compared to the pre-treatment. The mechanism of antimicrobial activity of the latarcin peptides depends on the helix-hinge-helix structure that is important for lysing

bacterial cell membranes [35, 36]. This finding emphasised that the direct incubation of DENV with the Ltc 1 peptide during from the simultaneous treatment may led to lysis of the viral particles by the peptide. The results of the post-treatment and dose-response assays showed that the viral load was significantly deceased after treatment with the Ltc 1 peptide. Based on this finding, we hypothesise that the Ltc 1 peptide may interrupt the dengue life cycle in HepG2 cells during post-translational processing of the polyprotein by inhibiting the dengue serine protease. This inhibition may hinder flavivirus replication and virion assembly, as evidenced by the lack of infectious virion production in mutants carrying inactivating viral proteases [13].

Possible AZD8186 limitations of our meta-analysis includes relatively small number of studies, different heterogeneous matching factors, different countries and ethnicities, possible publication

bias, as well as possible interaction with other biologic and environmental factors. It is well documented that ethnic factor contributes to the lung cancer incidence. In our study, we included 2 U.S., 1 Chinese, 1 Japanese, 1 Finnish and 1 British studies. Therefore, heterogeneity by ethnicity needs to be taken into account when interpreting our data. Heterogeneous matching factors and differential adjustment for confounding factors are other sources of bias. The above limitations might have contributed to the low statistical power of our meta-analysis. Despite RSL3 clinical trial some limitations, our results based on nested case-control studies which represent of best study design. In addition, we obtained the results from dichotomous and continuous variable respectively, which made the results

more reliable. What’s more, heterogeneity and publication bias of the studies were not significant. Thus, the data of our study are reliability. Conclusion In summary, we found that association between circulating levels of IGF-I, IGFBP-3 and the risk of lung cancer are marginally and statistically significant, respectively. So it may be helpful in the diagnosis and treatment of lung cancer. Since circulating IGF-I and IGFBP-3 remain important factors in lung cancer, more studies Barasertib cell line need to be conducted to discern this association. And uniform adjustment of confounding factors across the studies will help in terms of interpretability and comparability. References 1. Spiro SG, Silvestri GA: One hundred years of lung cancer. Am J Respir Crit Care Med 2005, 172: 523–529.CrossRefPubMed 2. Chan JM, Stampfer MJ, Giovannucci E, Gann PH, Ma J, Wilkinson P, Hennekens CH, Pollak M: a prospective study. Science 1998, 279: 563–566.CrossRefPubMed 3. Hankinson SE, Willett WC, Colditz GA, Hunter DJ, Michaud DS, Deroo B, Rosner B, Speizer FE, Pollak M: Circulating concentrations of insulin-like growth factor-I and risk of breast cancer. Lancet 1998,

351: 1393–1396.CrossRefPubMed 4. Ma J, Pollak MN, Giovannucci E, Chan JM, Tao Y, Hennekens CH, Stampfer MJ: Prospective crotamiton study of colorectal cancer risk in men and plasma levels of insulin-like growth factor (IGF)-I and IGF-binding protein-3. J Natl Cancer Inst 1999, 91: 620–625.CrossRefPubMed 5. Yu H, Spitz MR, Mistry J, Gu J, Hong WK, Wu X: Plasma levels of insulin-like growth factor-I and lung cancer risk: a case-control analysis. J Natl Cancer Inst 1999, 91: 151–156.CrossRefPubMed 6. Yu H, Rohan T: Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst 2000, 92: 1472–1489.CrossRefPubMed 7. Giovannucci E: Insulin, insulin-like growth factors and colon cancer: a review of the evidence. J Nutr. 2001, 131 (11 Suppl) : S3109-S3120. 8.

On examination, he was GDC-0994 cost hypoxic (94% oxygen saturation), hypothermic (35.6°C) and tachycardic with new onset, fast atrial fibrillation (rate 142/minute), but normotensive. In addition, he was diffusely tender in the supra-pubic region and in both loins, especially on the right. Neurological examination was normal other than MRC grade 4/5 power in the lower limbs. Blood tests demonstrated a marked inflammatory response with raised CRP (373 mg/L) Selleck Adriamycin and predominantly neutrophilic

leucocytosis (20.5 × 109/L). Acute kidney injury (urea 31.4 mmol/L; creatinine 244 μmol/L) and mildy deranged liver function tests (alkaline phosphatase 343 IU/L; GGT 183 IU/L; ALT 52 IU/L; bilirubin 14 μmol/L) were evident. Arterial blood gases demonstrated a metabolic acidosis PU-H71 concentration (pH 7.32; base excess −8 mEq/L). A chest radiograph was normal. Urinalysis was positive for leucocytes and erythrocytes only. Blood cultures were taken and broad spectrum antibiotics were commenced for presumed urosepsis. 24 hours after admission, the right hand became diffusely swollen, erythematous and tender, and the patient continued to experience pyrexia. His urine cultures yielded Serratia marcescens sensitive to the antibiotics. Ultrasonography of the urinary tract failed to demonstrate hydronephrosis. Ultrasonography of the right

hand showed generalised soft tissue oedema with a 1 cm deep fluid filled collection containing echogenic material overlying the MCP joints.The following day, the acute kidney injury worsened (urea 43.4 mmol/L; creatinine 351 μmol/L). An urgent CT thorax/abdomen/pelvis demonstrated an unexpected finding of bilateral iliopsoas abscesses, most extensive on the right side which contained a considerable volume

of gas (Figures 1 and 2). Figure 1 Transverse view on CT of the bilateral iliopsoas abscesses. Figure 2 CT demonstrated Sagittal View of Abdomen and Pelvis demonstrating gas locules in Right Iliopsoas Region. The patient proceeded to theatre for drainage of the abscesses. During intubation the anaesthetist noted the oropharynx was sloughy and inflamed and accordingly biopsies were taken. Bilateral groin incisions were used to approach the iliopsoas muscles in the extra-peritoneal acetylcholine plane. On the right side the abscess cavity involved the entire length of the iliopsoas muscle and contained 100 ml of cream coloured pus as well as gas. On the left side an estimated 40 ml of pus was contained within the lower psoas muscle. There was no evidence of communication with the replaced hip joints on either side. Drains were placed into the cavities. The hand abscess was also drained and samples from all sites were sent to microbiology. The patient was then transferred post-operatively to ICU for inotropic support (noradrenaline) and ongoing fluid resuscitation. 72 hours after admission the blood cultures returned a yield of F. necrophorum and subsequently tazocin and metronidazole were commenced.

Typical fatigue behavior was seen in SHAM-ovariectomized as well as in ZOL-treated, ovariectomized rats. Fatigue properties, trabecular microarchitecture, and buy AZD5153 cortical thickness were similar in both groups. Previously, we showed that static compressive behavior was also similar in L3 vertebrae

of the same groups of rats [13]. Altogether, this suggests that ZOL treatment of ovariectomized rats results in the same vertebral bone mass and structure as SHAM, ovariectomized rats, as well as the same vertebral static and fatigue properties. For all vertebrae, force–displacement curves displayed typical fatigue behavior characterized by decreasing secant stiffness, increasing hysteresis, click here and increasing nonlinearity. This agrees with compressive, fatigue behavior previously reported for cortical and trabecular bone specimens [27, 31–33]. Also, the strong linear correlation between the log steady-state selleck chemicals llc creep rate and the log time to failure agrees with the literature [32, 33], which indicates the validity of the test. This also indicates that the integral fatigue behavior of cortical and trabecular bone in rats is similar to the two bone compartments assessed separately. We found an average apparent strain at failure of about 4% for both groups,

which is just slightly higher than the 3.4% and 2.8% reported for, respectively, human and bovine trabecular bone [31, 33]. Samples that did not fail during the test were removed from further analysis and showed a decreasing rather than an increasing Adenosine triphosphate apparent strain range per cycle during the test accompanied by an increasing secant stiffness. This behavior suggests that artifacts were present in these tests [41, 42], possibly due to vertebral ends that were not perfectly parallel. In this case, when the force range, leading to 0.75% apparent strain, was determined at the start of the test, the actual

area bearing the load would be smaller than the total bone area. During the test, the area bearing the load would then be compressed, resulting in the same load being born by the area of the whole vertebra and thus in lower strains. Improving the sawing procedure and specimen fixation in the loading device could possibly reduce the rate of exclusion of samples. The fatigue behavior in these whole vertebrae was comparable to the fatigue behavior found in studies on cortical and trabecular bone, though no fatigue data on rat bone are available. Although not determined in our study, it would be interesting to study whether failure starts in the cortical or trabecular bone. Most of the fatigue properties were unrelated to cortical or trabecular bone morphology, with the exception of weak relationships between trabecular bone morphology and apparent strain at failure.

In the

high-MOI infection, 11 genes and LAT peaked at 4 h find more within the 6-h examination period, while in the JAK inhibitor low-MOI infection only the us3 transcript had a slightly lower R value at 6 h than at 4 h pi. The us3 gene was the only one among the 70 PRV genes which was expressed at a higher level at 4 h than at 6 h pi in another study [1]. Intriguingly, the ep0 mRNAs reached a 3.5-fold higher level in the low-dose than in the high-dose infection in an average cell at 6 h pi. Furthermore, at 6 h pi the ul1 and ul51 genes were expressed at an approximately 10 times higher level under the low-MOI than under the high-MOI conditions. Gene expression kinetics within the 0 to 6-h infection period The expression of most PRV genes basically differed under the two infection conditions (Additional file

1c), which is in contrast with the case of rhesus monkey rhadinovirus (a γ-herpesvirus), whose lytic gene expression commences at a fixed pace in infected cells, regardless of the MOI [48]. Most genes were expressed at a lower level in a cell in the low-MOI experiment in the first 4 h of infection, but more than half of these gene products surpassed the high-MOI values by 6 h pi. The R values of 3 PRV genes (ie180, ul1 and ul30) were higher in the low-MOI than in the high-MOI infection at every examined time selleck chemicals point, while the opposite was true (the R values of high-MOI were always higher) in 13 genes: ul5, ul15, ul17,

ul19, ul23, ul24, ul44, ul49.5, ul54, us6, us9, us1 and us3 (Figure 3). These latter genes U0126 in vitro form clusters on the basis of their localization on the genome (genes in close vicinity are underlined), which suggests that the adjacent genomic sequences might be under common regulatory control. This observation is supported by the similarity of the Ra curves of adjacent genes (Additional file 1c). For example, the expression rates of the ul36, ul37 and ul38 genes were similar to each other in both experiments, but each of them exhibited an inverse expression pattern in the two infection conditions. All genes were expressed at a higher rate (Ra) within the 1 h to 6 h period of infection in the low-titre experiment, except for ie180 and the two antisense transcripts. The quantities of ie180 mRNAs were similar in the two experiments, except at 1 h pi, where the level of the transcripts was 2.8-fold higher in the low-MOI infection. Thus, the amount of total ie180 transcript in an infected cell appears to be under strict control, independently of the initial infection conditions. In contrast, the expression of the ep0 gene differed basically in the two experiments.

Figure 1 Intraoperative trans-cystic cholangiography. a) a biliary leakage appears on the left posterolateral aspect of the common bile duct, 1 cm below the biliary confluence; b) contrast material leakage is highlighted in green. Over the postoperative period,

the patient continued to improve steadily with gradual return of bowel function and oral feeding. On postoperative day 30, a T-tube cholangiography showed a normal biliary tree, without neither leakage nor stricture. The T-tube was subsequently removed and the patient was discharged from the intensive care unit. The patient had a complete selleckchem recovery. Discussion CBD injury occurs frequently at three LY2603618 in vivo areas of relative fixation of the biliary tract [20]: 1) the origin of the left hepatic duct, 2) the bifurcation of the hepatic ducts, 3) the pancreaticoduodenal junction. Different mechanisms, even in combination, may produce rupture of the common bile duct: compression of the ductal system against the vertebral column [21], sudden increase of intraluminal pressure in the gallbladder with a short and permeable cystic duct [22], and a “shearing force” producing avulsion

of the common duct at its fixed part at the junction with the pancreas [23]. The diagnostic modalities to be used and the order of testing depend greatly on the stability of the patient, risk, or suspicion of associated injuries, and other Phenylethanolamine N-methyltransferase indications that may necessitate operative exploration. Diagnosis may be performed in three different moments [24]: immediately in patients undergoing laparotomy for associated injuries, lately in stable patients with scant symptoms (>50% of cases), and because of

complications due to missed injuries at the time of the trauma. Common bile duct injury is often discovered during laparotomy when bile staining in the hepatoduodenal ligament area prompts exploration. The diagnosis is often more difficult with incomplete injuries that result in a delayed presentation. These cases may present days to months Apoptosis Compound Library postinjury, with nausea, vomiting, jaundice, and abdominal pain [25]. Such symptoms are caused by a stricture or bile leak from a direct injury or ischemic insult from injury resulting in devascularization of the extrahepatic biliary tree. The diagnosis of a bile duct injury is often difficult in the multiply injured patient and demands a high index of suspicion.

8) to detect 10% difference in the running time to exhaustion (G*Power, Franz Faul, Kiel University, Germany). The BAY 80-6946 in vivo supplementation experiment extended for a five-day period that began after an acclimatization period of one week. Test animals were twice placed on a rat treadmill (with at least a two-day interval to avoid a training effect) for 10 min at 10 m/min during acclimatization. The food was a standard rat chow (Fwusow, Taichung, Taiwan) mainly consisting mainly of carbohydrates (52%), protein (23.5%), fat (4.5%), water (12%), ash (10%), and fiber (8%). The average intake weights of the rat chow during the experimental click here period were 30.9

± 2.2, 37.4 ± 3.7, and 36.6 ± 3.3 g/day/rat for the C, Ex, and ExSCP groups respectively, with the last two groups consuming significantly more than the first group. The use of a rat model in this study was approved and conducted under the guidelines of the Animal Studies Committee of National Pingtung University of Science and Technology. SCP preparation and dosage The methods used in Charles and Huang [13] were adopted for isolating and preparing SCPs. The methods and procedures employed were, briefly, as follows: pellets were ground into cassava flour after preparatory procedures (i.e. the sweet cassava tuber was washed, peeled, and pelletized). The mixtures (250 g cassava flour with 500–750

g of water) were centrifuged at 14,300 g at 4°C for 20 min and the supernatants removed. Then, crude mucilage was produced when the supernatant DihydrotestosteroneDHT was filtered, concentrated, and lyophilized. Crude polysaccharides were fractioned by anion exchange chromatography with elution by NaCl at different concentrations (0.5, 1.0, 2.0, and 3.0 ml). The SCP was purified by Sephacryl S-400/HR gel filtration chromatography

after being pooled, concentrated, desalted, and freeze-dried. Test animals were fed a dose of 500 mg SCP/kg body weight/day. SCPs were given by gastric GNA12 intubation in two 250 mg/kg doses; one after the morning exercise and the other in the evening at approximately 1700–1800. The dosage of SCP was determined by the rat’s daily weight measurement in the morning, and the SCP was mixed with physiological saline at 100 mg/ml. On the sixth day, the same supplementation times were used as had been on the previous five days, but there was no exercise. Exhaustive running was completed on the morning of the seventh day after overnight fast, and gastrocnemius and soleus muscles, as well as blood samples from all rats were collected after anesthetization and sacrifice (Figure 1). Figure 1 Overview of the experimental procedure. Exercise model After one week of acclimatization, the Ex and ExSCP groups had one exercise bout each day for five days. The speed and duration of the first three days and the final two days were 20 m/min for 20 min and 25 m/min for 30 min respectively.

J Clin Oncol 2002, 20:1–9.CrossRef 10. Kim NW, Piatyszek MA, Prowse KR, Harley CB, West MD, Ho PL, Coviello GM, Wright WE, Weinrich SL, Shay JW: Specific association of human telomerase activity with immortal cells and cancer. Science 1994, 266:2011–2015.mTOR inhibitor PubMedCrossRef 11. Garcia-Aranda C, de Juan C, Diaz-Lopez A, Sanchez-Pernaute A, Torres A, Diaz-Rubio E, Balibrea J, Benito M, Iniesta P: Correlations of telomere length, telomerase activity, and telomeric-repeat binding factor

1 expression in colorectal carcinoma. Cancer 2006, 106:541–551.PubMedCrossRef this website 12. de Vos M, Schreiber V, Dantzer F: The diverse roles and clinical relevance of PARPs in DNA damage repair: current state of the art. Biochem Pharmacol Selleck Rabusertib 2012, 84:137–146.PubMedCrossRef 13. Rulten SL, Fisher AE, Robert I, Zuma MC, Rouleau M, Ju L, Poirier G, Reina-San-Martin B, Caldecott KW: PARP-3 and APLF function together to accelerate nonhomologous end-joining. Mol Cell 2011, 41:33–45.PubMedCrossRef 14. Yélamos J, Schreiber V, Dantzer F: Toward specific functions of poly (ADP-ribose) polymerase-2. Trends Mol Med 2008, 14:169–178.PubMedCrossRef 15. Smith S, de Lange T: Tankyrase promotes telomere elongation in human cells. Curr Biol 2000, 10:1299–1302.PubMedCrossRef 16. Lehtiö L, Jemth A, Collins R, Loseva O, Johansson A, Markova N, Hammarström M, Flores A, Holmberg-Schiavone L, Weigelt J, Helleday

T, Schüler H, Karlberg T: Structural basis for inhibitor specificity in human poly (ADP-ribose) polymerase-3. J Med Chem 2009, 52:3108–3111.PubMedCrossRef 17. Kyo S, Takakura M, Fujiwara T, Inoue M: Understanding and exploiting hTERT promoter regulation for diagnosis and treatment of human cancers. Cancer Sci 2008, 99:1528–1538.PubMedCrossRef 18. Horikawa I, Cable PL, Mazur SJ, Appella E, Afshari CA, Barrett JC: Downstream E-box-mediated regulation

of the human telomerase reverse transcriptase (hTERT) gene transcription: evidence for an endogenous mechanism of transcriptional repression. Mol Biol Cell 2002, 13:2585–2597.PubMedCentralPubMedCrossRef Competing Orotidine 5′-phosphate decarboxylase interests The authors declare that they have no competing interests. Authors’ contributions TFM and CF carried out most of the molecular studies, the statistical analysis, participated in interpretation of data, and were involved in drafting the manuscript. IP, CDJ and JH participated in molecular analysis and interpretation of data. AG, FH and JRJ participated in analysis and interpretation of data, as well as in advice on possible clinical implications of results from this work. MR supplied the PARP3 antibody and the SK-N-SH cells as control for Western-blot. EDR, AJT and MB have been involved in revising the manuscript. PI carried out the design and coordination of the study, and drafted the manuscript. All authors have read and approved the final manuscript.

Israel J Plant Sci 42:331–345 Smith TB, Kark S, Ro 61-8048 datasheet Schneider CJ, Wayne RK, Moritz C (2001) Biodiversity hotspots and beyond: the need for preserving environmental transitions. Trends Ecol Evol 16:431CrossRef Stebbins GL, Major J (1965) Endemism and speciation in the California flora. Ecol CX-5461 ic50 Monogr 35:1–35CrossRef Stoms DM, Comer PJ, Crist PJ, Grossman DH (2005) Choosing surrogates for biodiversity conservation in complex planning

environments. J Conserv Plan 1:44–63 Thorne JH, Kennedy JA, Quinn JF, McCoy M, Keeler-Wolf T, Menke J (2004) A vegetation map of Napa County using the manual of California vegetation classification and its comparison to other digital vegetation maps. Madroño 51:343–363 Thuiller W, Albert C, Araújo M, Berry PM, Cabeza M, Guisan A, Hickler T, Midgley GF, Patterson

J, Schurr FM, Sykes MT, AZ 628 Zimmerman N (2008) Predicting global change impacts on plant species’ distributions: future challenges. Perspect Plant Ecol Evol Syst 9:137–152CrossRef United States Census Bureau (2000) State and County Quick Facts. http://​www.​census.​gov. Cited July 2007 Viers JH, Thorne JH, Quinn JF (2006) CalJep: A spatial distribution database of Calflora and Jepson plant species. San Francisco Estuary & Watershed Science 4. Available via http://​repositories.​cdlib.​org/​cgi/​viewcontent.​cgi?​article=​1018&​context=​jmie/​sfews White J (1999) Rarity and the phylogeography of the large-flowered Piptolobi of Astragalus L. (Fabaceae). Doctor of Philosophy dissertation, Department of Botany and Plant Pathology, Michigan State University, Carnitine palmitoyltransferase II East Lansing, MI White J (2004) Range size, error rates, and the geometry of rare species distributions. Proceedings of the 2002 rare plant symposium: the ecology and management of rare plants of northwestern California. California Native Plant Society, Sacramento, CA Williams P, Gibbons D, Margules C, Rebelo A, Humphries C, Pressey R (1996) A comparison of richness hotspots, rarity hotspots, and complementary areas for conserving diversity

of British birds. Conserv Biol 10:155–174CrossRef World Conservation Union (IUCN) (2001) IUCN Red List Categories: Version 3.1. IUCN Species Survival Commission. IUCN, Gland, Switzerland. http://​www.​iucnredlist.​org/​static/​categories_​criteria_​3_​1. Cited 2005–2007″
“We are facing an unprecedented plant diversity crisis. If current trends in habitat conversion, over-exploitation, alien species invasions, and climate change continue, up to 50% of the world’s vascular plant flora is expected to become threatened with extinction within the twenty-first century (Pitman and Jørgensen 2002; Root et al. 2003; Hahns et al. 2009). Climate change seems to rapidly have become recognized as the primary threat to many plants. In Europe, more than half of the vascular plant flora may become endangered by the year 2080 as a result of climatic changes (Thuiller et al.

0) measures highly abundant proteins that are found in all microorganisms. The characteristic

patterns of these highly abundant proteins are used to reliably and accurately identify a particular see more microorganism by matching the respective pattern with an extensive open database to determine the identity of the microorganism down to the species level (Bruker). For identification of colonies using the MALDI-TOF MS; direct placing or placing on a steel target following extraction was done (according to the manufacturer’s instructions). Briefly, single colony from each plate was picked up and smeared as a thin film directly on a MALDI steel target. Microorganisms that could not be identified directly by MALDI-TOF MS underwent extraction and were retested. Pure colonies were transferred to a 1.5 ml tube (Eppendorf, Germany) mixed thoroughly in 300 μl of distilled water. Nine hundred micro liters Givinostat molecular weight (900 μl) of absolute ethanol were added, the mixture was centrifuged at 15,500 g for 2 min, and the supernatant was discarded. The pellet was air-dried at room temperature. Subsequently, 50 μl of formic acid (70% v/v) was added to the pellet and mixed thoroughly before the addition of 50 μl of acetonitrile. The mixture was centrifuged again at 15,500 g for 2 min. One microliter of the supernatant was placed onto a spot of the steel target and air-dried at room temperature. Following this, 1 μl

of matrix solution (20 mg/ml 3, 5-dimethoxy-4-hydroxycinnamic acid in acetonitrile (ACN): purified water: trifluoroacetic acid (TFA) (50:50:0.1)) was used to overlay the smeared PAK6 colonies on the steel target. The steel target was air-dried for 10 minutes and placed in the MALDI Biotyper for analysis. Measurements were done using

a Microflex Mass Spectrometer (Bruker Blasticidin S molecular weight Daltonik, Bremen, Germany) with FlexControl software (version 3.0). Spectra were recorded in the positive linear mode (laser frequency, 20 Hz; ion source 1voltage, 20 kV; ion source 2 voltage, 18.4 kV; lens voltage, 9.1 kV; mass range, 2,000 to 20,000 Da). For each spectrum 240 shots in 40-shot steps from different positions of the target spot (automatic mode) were collected and analysed. All colonies reported were above 1.80 score value. Identification of unknown microbes found in the hospital was classified using modified score values proposed by the manufacturer: a score of ≥2 indicated species identification; a score between 1.7 and 1.9 indicated genus identification and a score of <1.7 indicated not reliable identification [17]. Results and discussion Quantification of bacterial airborne contaminants During sampling rounds, bacterial counts obtained using settle plates and SAS-Super 90 in both the kitchen area and wards (male and female) ranged between ≥ 2 cfu/m-3 for the first sampling round, ≤ 3.0 × 101 cfu/m-3 for the second sampling round, ≤ 1.5 × 101 cfu/m-3 for the third sampling round and ≤ 6.0 × 101 cfu/m-3 in the fourth sampling round (Figure 1).