No systematic data

on spot removal chemicals used in dry-cleaning shops or elsewhere were available. In Sweden, PER has been used almost exclusively for dry-cleaning since the 1950s (Kemikalieinspektionen 1990; Johansen et al. 2005). National regulation and structural changes within learn more the industry (reductions in demand and improvements in efficiency) have led to a dramatic (~95%) reduction in the consumption (sales) of PER from around 5,000 tonnes/year in the early 1970s to 300 tonnes/year three decades later (R Wettström, personal communication 1993; Swedish Chemicals Agency 2009). No exposure measurements of PER or other dry-cleaning agents were available from the companies in the present study, but in an exhaustive

search for historical data from Nordic dry-cleaning establishments, it was concluded that PER exposure levels in the 1970s were of the order of 100–200 mg/m3 (15–30 ppm) (Johansen et al. 2005). Additional information from click here contemporary Swedish studies indicates that exposure to PER in the early 1980s was variable within and between various dry-cleaning establishments with the 8-h average exposure level rarely exceeding 50 ppm (Andersson et al. 1981; Lindberg and Bergman 1984; Arbetarskyddsstyrelsen 1988). In the 21st century, this remains the permissible level for occupational PER exposure for several industrialised countries (Institut für Arbeitsschutz der Deutschen Gesetzlichen Unfallversicherung 2010). Originally,

10,389 subjects were reported by the companies (“washing establishments”), but 677 (6.5%) were excluded for either not fulfilling the original inclusion criteria or other reasons pertaining to the present study design and 272 (2.6%) were lost in the identification process, Demeclocycline leaving 9,440 individuals (2,810 men and 6,630 women) to follow-up (Table 1). The vital status as of 31 December 2006 of each cohort member was obtained using a PIN-based match to the national population register and the national cause-of-death register. Dates of emigration, if any, were obtained by reference to the national emigration register. Person-years were counted from 1 January 1985 until 85 years old, death, emigration or the end of the observation period, whichever came first. Emigrants returning to Sweden during the observation period were reintroduced into the study from the day of re-entry and followed up as described. For subjects with several separate episodes of employment in the industry, the total duration was obtained by summing each component period. Incident cases of malignant tumours in the cohort, coded to the 7th revision of the International Classification of Diseases (ICD-7), were obtained by matching to the national cancer register for the period 1985–2006.

The PCR conditions were 95 °C for 5 min, followed by 50 cycles of 95 °C for 30 sec, 55 °C for 30 sec, and 72

°C for 30 sec. The expression of β-actin gene was also quantified in a similar way for normalization. Comparative delta-delta CT method was used to analyze the results where expression level of the respective gene at the corresponding time point in non-transfected cells was regarded as one [39, 40]. Each experiment was performed in triplicate. Enzyme-linked immunosorbent assay (ELISA) measurement of TGF-β2 protein level Cell culture supernatant was collected at 24 hours post-infection for the analysis of TGF-β2 expression. The total TGF-β2 protein level was measured by enzyme-linked immunosorbent assay (Emax® ImmunoAssay System, Promega, Madison, WI, USA) according to the manufacturer’s procedures. this website Each experiment was performed in triplicate. Reverse transfection of a mimic or an inhibitor of miR-141 The cells were transfected in suspension after trypsinisation with 60 nM anti-miR, pre-miR or negative control (Applied Biosystems). For the assay, 1×105 cells per mL were transfected per well of a 24-well plate. Transfection complexes were prepared in OptiMEM (Invitrogen) with 1.5 μL/24-well of siPORT NeoFx transfection agent (Ambion, Austin, TX, USA). At 24 hours post-transfection, the cells were lysed for qRT-PCR analysis or EX 527 purchase subjected

to H1N1 or H5N1 virus infection. The transfection efficiency was calculated from the percentage of fluorescent cells that were observed using florescence microscopy after the transfection of fluorescein isothiocyanate (FITC)-labeled short nucleotide primers in separate controls. The transfection efficiency was about 78.2 ± 6.3% Interleukin-2 receptor (mean ± SD), which was considered to be adequate for the functional analyses. The human miR-1 miRNA was also used as a positive control. In this control, the human miR-1 miRNA mimic effectively down-regulated the expression of twinfilin-1 (also known as PTK9) by 80% at the mRNA level as detected by real-time PCR using TaqMan® Gene Expression Assays (Applied Biosystems) for PTK9. This positive control proved

the effective delivery and activity of Pre-miR miRNA Precursor. We therefore used this model in further functional experiments. Each experiment was performed in triplicate. Acknowledgements This study was supported by the Research Fund for the Control of Infectious Diseases, Food and Health Bureau, Hong Kong Special Administrative Region. We thank Prof. Pilaipan Puthavathana for the provision of A/Thailand/1(KAN-1)/2004(H5N1) isolate. References 1. World Health Organization: 26 April 2013, posting date. Cumulative number of confirmed human cases of avian influenza A/(H5N1) reported to WHO. Geneva, Switzerland: World Health Organization; 2003–2013. 2. Chan PK: Outbreak of avian influenza A(H5N1) virus infection in Hong Kong in 1997. Clin Infect Dis 2002,34(Suppl 2):S58-S64.PubMedCrossRef 3.

An allele-specific real-time PCR (AS Kinetic PCR) method was developed to interrogate these high-D SNPs [29]. SNP interrogation is an efficient means of classifying E. faecalis and E. faecium into groups that are concordant GW786034 price with the population structure of these organisms [29]. In this study we have applied this rapid SNP genotyping method to determine the diversity of enterococci in the Coomera River, South East Queensland, Australia

over a period of two years and also investigated the antibiotic resistance determinants associated with E. faecalis and E. faecium SNP genotypes. Methods Study site The Pimpama-Coomera watershed is located in South East Queensland, Australia and is used intensively for agriculture and

recreational purposes and has a strong anthropogenic impact. The main water source is the Coomera River, which flows for 90 km from its headwaters in the Lamington National Park. The upper reaches of the river passes through mainly rural areas Lazertinib order comprising crops and cattle grazing. In the middle to lower reaches, land uses include farming and cropping. In the 1970s and 1980s the river was widened 20 km upstream from the mouth as a consequence of sand and gravel extraction operations. The lower reaches of the Coomera River passes through highly developed areas including canal estates such as Santa Barbara, Hope Island, Sanctuary Cove and the Coomera Mooring Marina. Most of the sewage system collection is gravity fed and follows natural catchment drainage lines until the wastewater is treated at the central treatment plant. After treatment, the water is released into the Gold Coast Seaway located Arachidonate 15-lipoxygenase south of the Coomera River estuary. Despite the existence of such an effective treatment system, high numbers of coliforms were observed over a long period of time in the

estuary. Sampling Environmental water samples were collected during four seasonal trips at the same time each day from six designated sites of the Coomera River, from May 2008 to July 2009. Hot-spots selected for sampling included: Coomera Marina (C1), Santa Barbara (C2), Sanctuary Cove (C3), Jabiru Island (C4), Paradise Point (C5) and Coombabah (C6). These sites were suggested by the Gold Coast City Council as being problematic sites with a history of high numbers of faecal coliforms. The positions of these sampling sites are shown in Figure 1. The exact location and characteristics of sampling sites are summarised in Table 1. Figure 1 Water sampling sites along the Coomera River, South-East Queensland, Australia.

Low reflectivity in the UV to green light wavelength range gives promise find more for multi-junction solar cells if more junctions are requested especially for high-band gap subcells. Figure 4 Reflectance values of bare T-J solar cell and T-J solar cells with Si 3 N

4 and ZnO nanotube coating, respectively. The photovoltaic I-V characteristics were measured under one sun AM1.5 (100 mW/cm2) solar simulator. The device parameters of open-circuit voltage (V oc), short-circuit current (I sc), fill factor (FF) conversion efficiency (η), and quantum efficiency (QE) were measured. Figure 5a shows the I-V characteristics of T-J solar cells with and without a Si3N4 and ZnO nanotube structure. The efficiencies BIRB 796 concentration of a T-J solar cell with and without a Si3N4 and ZnO nanotube structure are 19.3, 22.5, and 24.2%, respectively, as shown in Table 1. The short-circuit current density (J sc) increased from 12.5 to 13.2 and 13.2 to 13.9 mA/cm2 after the addition of a Si3N4 and ZnO nanotube on the solar cell, and the J sc was improved 5.3% in enhancement in overall

power conversion efficiency. The largest efficiency and J sc values were obtained for the T-J solar cell with ZnO nanotube. The reason for this is that a ZnO nanotube decreases the reflectance and increases the short-circuit current. The quantum efficiency of a solar cell is defined by the following equation: Figure 5 I-V characteristics of T-J solar cells and External quantum efficiency. (a) Photovoltaic I-V characteristics of T-J solar cell with and without Si3N4and ZnO nanotube structure, respectively. (b) External quantum efficiency of bare triple-junction (T-J) solar cell and T-J solar cell with Ureohydrolase SiN4 and ZnO nanotube coating, respectively. Table 1 Measured illuminated electrical properties of bare triple (T-J) solar cell and T-J solar cell with SiN 4 and ZnO nanotube coating, respectively Sample V oc (V) J sc(mA/cm 2) FF (%) Efficiency (%) Bare T-J solar cell 2.2 12.5 71.2 19.3 With SiNx AR coating 2.3 13.2 74.5 22.5 With ZnO NW AR coating 2.3 13.9 74.8 24.2 (1) where

J sc (λ) is the total photogenerated short-circuit current density at a given wavelength λ, ϕ(λ) is the photon flux of the corresponding incident light, and q is the elementary charge [18]. We measured the spectral response of the external quantum efficiency (EQE), in which a xenon lamp and a halogens lamp were used as the illumination source sources. The EQE of the T-J solar cell device with SiN4 and ZnO nanotube coating, respectively, are presented in Figure 5b. Physically, EQE means the ability to generate electron-hole pairs caused by the incident photon [19]. The cell with ZnO nanotube coating shows an enhanced EQE in a range from of 350 to 1800 nm. The average EQE enhancements (△EQE) of the top and middle cells were 2.5 and 6.6%, respectively. This is due to the low reflection between the wavelength 350 to 500 nm, in respect to the solar cell coated with a ZnO nanotube.

The supernatant was collected as IM fraction and the pellet, containing the OM, was resuspended in 20 mM Tris–HCl, pH 7.5. SDS-PAGE electrophoresis with NuPage 4-12% Bis-Tris gels (Invitrogen) and Western blot analysis were performed according to standard procedures. Opa proteins were detected by monoclonal antibody 4B12, kindly provided MK0683 by M. Achtman. Pili were detected by monoclonal antibody

SM1, kindly provided by M. Virji. OpaB protein was detected by polyclonal antisera against NG0070 His-tagged protein; purification of the protein and mice immunization were performed as described before. Bands were visualized with Super Signal Chemiluminescent Substrate (PIERCE). Two-dimensional gel electrophoresis and image analysis 200 μg of proteins were precipitated with 0.015% sodium deoxycholate and 48% trichloroacetic acid and dissolved in 7 M urea, 2 M thiourea, 2% CHAPS, 2% ASB14, 1% DTT, 2 mM tributylphosphine, 20 mM Tris and 2% carrier ampholyte.

Proteins were absorbed overnight onto Immobiline DryStrips (7 cm; pH-gradient 3–10 non linear) and the first dimension was run using a IPGphor Isoelectric Focusing Unit (Ge Healthcare), applying sequentially 150 V for 1 hour, 500 V for 35 min, 1000 V for 30 min, 2600 V for 10 min, 3500 V for 15 min, 4200 V for 15 min and finally 5000 V to reach 12kVh. For the second dimension, strips GSI-IX were equilibrated as described and proteins were separated on linear 4–12% polyacrylamide gels. Bidimensional gel was acquired with a Personal Densitometer

SI (Molecular Dynamics) and images were analyzed with the software Image Master 2D v2003.02 (Ge Healthcare). In-gel protein digestion and MALDI-TOF mass spectrometry analysis Protein spots were excised from the gels, washed with 50 mM ammonium bicarbonate/acetonitrile 50/50 (v/v) and air-dried. Dried spots were digested for 2 hours at 37°C with sequencing grade modified trypsin in 5 mM ammonium bicarbonate, loaded on a matrix PAK5 prespotted Anchorchip (PAC 384 HCCA, Bruker-Daltonics, Bremen, Germany), air-dried and washed with 70% ethanol, 0.1% trifluoracetic acid. Mass spectra were acquired on an ultraflex MALDI TOF mass spectrometer (Bruker-Daltonics). Spectra were externally calibrated by using the combination of standards present on the PAC (Bruker-Daltonics). Monoisotopic peptide matching and protein search were performed automatically by MASCOT software. Cell culture Ectocervical and Endocervical cells (Ect1/E6E7 and End1/E6E7 from ATCC) were maintained in keratinocyte serum-free medium (KSFM, Gibco) supplemented with 50 μg/mL bovine pituitary extract, 0.1 ng/mL epidermal growth factor, 0.4 mM CaCl2 and antibiotics at 37°C in 5% CO2. Transformed urethral epithelial cells (kindly provided by M.

BC-ER cells showed lower Bcl-2 expression and higher Bax expression

than BC-V cells in the presence of E2 We investigated the mechanism of the resistance of BC-ER cells to chemotherapeutic agents. Western blot was performed to determine the protein expression of Bcl-2 and Bax in BC-ER and BC-V cells in the presence or absence of E2. In contrast to the effect of E2 on Bcl-2 expression in T47D cells, treatment with E2 for 12 days decreased the expression level of Bcl-2 significantly. BC-ER cells had lower Bcl-2 expression than BC-V A-1210477 purchase cells when treated with E2 for 12 days. Low Bax expression levels were detected in both BC-ER and BC-V cells; however, treatment with E2 induced an increase of Bax expression in BC-ER cells (Figure 5). Figure 5 Bcl-2 and Bax protein expression in BC-ER and BC-V cells.

BC-ER cells showed lower Bcl-2 expression and higher Bax expression than BC-V cells in the presence of E2 (western blot). Treatment of BC-ER cells with E2 for 12 days downregulated Bcl-2 and upregulated the Bax expression. BC-ER cells showed a lower Bcl-2/Bax ratio than BC-V MCC950 molecular weight cells in the presence of E2, which did not contribute much to greater resistance of BC-ER cells than BC-V cells. BC-ER cells grew more slowly than BC-V cells in the presence of E2 Since the Bcl-2/Bax apoptotic pathway did not contribute to the chemoresistance of BC-ER cells, we investigated the role of cell growth rate in the development of chemoresistance in BC-ER cells. In contrast to the effect of E2 on T47D cells, E2 treatment for 16 hours increased the percentage of BC-ER cells in the G1 phase and decreased the percentage of cells in the S and G2/M phases. E2 treatment for 12 days led to a marked accumulation of cells in the G1 phase. E2 treatment had no obvious influence on cell cycle distribution of BC-V cells. The percentages of BC-ER cells in the Inositol monophosphatase 1 S and G2/M phases were significantly lower than those of BC-V cells. E2 inhibited the proliferation of BC-ER cells as demonstrated by the growth curve. However, the growth of BC-V cells was not influenced by E2 treatment (Figure 6). In the presence of E2, BC-ER cells had lower growth potential

than BC-V cells, which may have induced the resistance of BC-ER cells to chemotherapeutic agents. Figure 6 BC-ER cells grew more slowly than BC-V cells in the presence of E2. (A, B) Cell cycle status of the BC-ER and BC-V cells. (A) Cells were treated with E2 for 16 hours before being analyzed by flow cytometry. (B) Cells were treated with E2 for 12 days. (C) The growth curve of the BC-ER and BC-V cells was plotted for 6 days of cell culture. Discussion Several studies have reported the relationship between ERα and resistance to chemotherapeutic agents in breast cancer cells [2, 10–14]. Most papers have reported the activation of ERα by E2 upregulated expression of Bcl-2, which leads to resistance to chemotherapeutic agents in breast cancer cells.

5% alcohol. Results are presented in Table 2, with only the most significantly affected genes shown. Interestingly, one gene observed to be affected by alcohol and Nm23 in the opposite manner was fibronectin receptor subunit integrin alpha 5 (ITGA5). In cells overexpressing Nm23,

alcohol treatment was no longer able to increase ITGA5 expression (Table 2). Additionally, alcohol exposure increased the expression of ITGA5 nine-fold; however, this effect was eliminated by the overexpression of Nm23 (Figure 4A and Table 2), suggesting that Nm23 blocked the effects of alcohol. Thus, our data suggests that the effects of alcohol on ITGA5 are Nm23-dependent. Table 2 Effects of alcohol and Nm23 overexpression on extracellular matrix and adhesion proteins expression Gene Name 0.5% EtOH Nm23-H1 0.5% EtOH RG7420 + Nm23-H1 VCAN 4.1125 3.1514 4.359 COL8A1 -18.2522 -18.6875 -8.9755 CTGF -4.3772 -5.712 -4.1296 CTNNA1 -15.455 A-1210477 -20.1681 -14.5808 CTNNB1 5.6569 5.5251 5.9134 CTNND1 -69.551 -18.9483 -26.4647 CTNND2 16.9123 12.9601 17.9262 ITGA1 -1.7777 -2.3168 -1.6771 ITGA2 -6.4531 -8.421 -6.0881 ITGA4 -5.3889 -7.0323 -5.0841 ITGA5 9.3827 -12.0754 -9.038 ITGA6 -1.1408 -1.4886 -1.0762 ITGA7 -8.1681 -7.5371 -5.4869 ITGAL -6.3643 -8.3051 -6.0043 ITGAV -2.042 -2.6647 -1.9265 ITGB1 -3.0314 -3.2355 -1.554

ITGB2 -2.3295 -3.0398 -2.1977 ITGB3 -5.2416 -4.8032 -3.8798 ITGB4 -1.021 1.8226 1.6066 ITGB5 -19.4271 -15.3908 -3.62 KAL1 1.454 1.1142 1.5411 LAMA1 1.1096 -1.1761 1.1761 MMP1 4.1487 -1.136 1.2176 MMP10 -12.5533 -11.3451 -5.191 MMP13 24.761 18.9746 26.2455 MMP16 4.1989 4.1583 5.6334 MMP2 3.249 1.7363 2.3685 NCAM1 -3.8106 -4.9726 -3.595 PECAM1 -13.4543 -17.5573 -12.6933 SELE 1.2483 -1.0454 1.3232 SELL 7.0128 5.374 7.4333 SELP -7.1107 -9.2792 -6.7085 SGCE 1.021 -1.2781 1.0822 SPG7 10.4107 6.0043 8.2477 CLEC3B -1.4641 -1.9106 -1.3813 TNC -3.9177 -5.1124 -3.6961 VCAM1 1.0281 1.325 1.0898 Figure

4 Nm23 down-regulates ITGA5 expression. Nm23 regulates cell invasion through ITGA5 expression. (A) ITGA5 mRNA levels were determined by qRT-PCR in T47D cells treated with 0.5% v/v ethanol and overexpressing Nm23, independently and in combination. Alcohol promotes ITGA5 mRNA expression approximately Florfenicol nine-fold. This effect was blocked by the overexpression of Nm23. (B) Western blot shows Nm23 and ITGA5 protein level in T47D cells with ethanol treatment, Nm23 overexpression, and in combination. (C) Western blots show Nm23 and ITGA5 protein level in MCF-7 (left) and MDA-MB-231 (right) cells following various doses of ethanol treatment. (*p < 0.05, as compared to the control cells transfected with empty vector). To determine the relationship between Nm23 and ITGA5 in alcohol-treated T47D breast cancer cells, we knocked down each gene separately and in combination, using small interfering RNA (siRNA), and subsequently measured cell invasion.

g., the lumbar spine versus total hip) and the specialist additionally indicated an overall fracture risk, the overall risk assessment only was compared to the assessment made by the research team. Concordance between assessments made by reading specialists and the research team was measured using Cohen’s kappa [14, 15]. Raw kappa statistics were calculated as well as linearly MX69 cost weighted kappas,

with weights structured to penalize disagreements separated by two categories of risk more than those separated by one category. Diagnostic categorization review Collected reports were also reviewed to determine if CAR’s standards of diagnostic categorization, published in 2005 [11], were used on the BMD reports. The CAR’s categorizations differ from the WHO’s in that they distinguish post-menopausal women (“normal”, “osteopenia,” and “osteoporosis”) from pre-menopausal women and 4SC-202 men (“normal” or “reduced bone density”). To assign CAR diagnostic categorizations, the research team abstracted the gender, age, and lowest T-score results from the following sites: lumbar spine, total hip, trochanter, and femoral neck.

These data as well as menopausal status were then used to categorize participants according to CAR criteria. Diagnostic categories assigned by the research team were then compared to categories presented by reading specialists. Where the reading specialists assigned several competing diagnoses to different imaged regions (e.g., the lumbar spine versus

total hip), it was assumed that the specialist’s overall diagnosis for the patient was the one based on the lowest T-score present. This diagnosis was then compared to the assessment made by the research team. To assess prevalence of standards, we report the percentage of reports that agree with CAR diagnostic criteria. Inositol monophosphatase 1 Conformation to CAR’s 2005 reporting recommendations Finally, collected reports were reviewed to determine their overall conformation to CAR’s 2005 report format recommendations. Specifically, the 2005 recommendations suggest that all baseline reports include patient identifiers, a DXA scanner identifier, BMD raw results (in g/cm2), T-scores, a diagnostic category, and, for patients over age 50, a fracture risk category. For serial scans, additional information is suggested for inclusion: a statement as to whether BMD change was statistically significant and the BMD test center’s least significant change (LSC) for each skeletal site (in g/cm2) [11]. To determine the degree to which 2008 reports conformed to 2005 format recommendations, the presence of the informational elements listed above was counted in the collected reports. Information could appear anywhere in the reports to be counted, including in attachments from DXA machines. A report including the brand of the DXA scanner used met the criteria for DXA scanner identifier.

Deissler, the director of the Marburg Consultation Group and one of the pioneers of systemic and postmodern forms of consultation and therapy in Germany; Maurizio Andolfi, SHP099 order a professor of psychology at La Sapienza (University of Rome) and the director of the Accademia di Psicoterapia Familiare in Rome, Italy; Gill Gorell Barnes, a senior lecturer at the London Tavistock Clinic; Alan Cooklin, an honorary senior lecturer at University College London; Eia Asen,

a consultant child psychiatrist and psychotherapist who has been the director at Marlborough Family Service for many years and a consultant psychotherapist at the Maudsley Hospital; Hugh Jenkins, a psychotherapist and a member of the Institute of Family Therapy in London; Florence Kaslow, a visiting professor of psychology at the Florida CDK inhibitor Institute of Technology; Manfred Cierpka, a professor of psychosomatic and family therapy at the Göttingen University; and Michael Wirshing, the medical director and chairman of the Department of Psychosomatic Medicine and Psychotherapy at Albert-Ludwigs-University in Freiburg, Germany. It is important to emphasize the exceptional importance of the

Flavopiridol (Alvocidib) cooperation with the Institute of Family Therapy (IFT) in London, which enabled IFT therapists to conduct workshops regularly in Poland and Polish therapists to visit institutions in London

that practiced family therapy. This exchange of experiences was extremely inspiring, especially for those who were entering the field. Cooperation with Klaus Deissler, who came each year for several years for consultations on a reflecting team model, was substantial and important. In June of 1989, Satu Stierlin from Heidelberg was invited to run the first group on the family of origin of the therapist. This very important event encouraged Polish family therapists to use this method. After October of 1989, two other groups were formed, and since then, genogram work has been included in routine training for therapists who practice family therapy. Since 1989, family therapy has been used as the main method for treating children and adolescents in the Department of Child and Adolescent Psychiatry at the Institute of Psychiatry and Neurology in Warsaw. The systemic training used live supervision and the one-way mirror. At the same time, family therapy has also become the main treatment paradigm in some outpatient units for emotionally and mentally ill patients.

doi:10.1007/s00464–013–3257–0. PubMed PMID: 24178863 71. Collins D, Winter DC: Elective resection for diverticular disease: an evidence-based review. World J Surg 2008,32(11):2429–2433. RG7112 molecular weight doi:10.1007/s00268–008–9705–7. PubMed PMID: 18712563PubMedCrossRef 72. Broderick-Villa G, Burchette RJ, Collins JC, Abbas MA, Haigh PI: Hospitalization for acute diverticulitis does not mandate routine elective colectomy. Arch Surg 2005,140(6):576–581. discussion 81–3. doi:10.1001/archsurg.140.6.576. PubMed PMID: 15967905PubMedCrossRef 73. Pittet O, Kotzampassakis N, Schmidt S, Denys A, Demartines N, Calmes JM: Recurrent left colonic diverticulitis episodes: more severe than the initial

diverticulitis? World J Surg 2009,33(3):547–552. doi:10.1007/s00268–008–9898–9. PubMed PMID: 19148697PubMedCrossRef 74. Klarenbeek BR, Samuels M, van der Wal MA, van der Peet DL, Meijerink WJ, Cuesta

MA: Indications for elective sigmoid resection in diverticular disease. Ann Surg 2010,251(4):670–674. doi:10.1097/SLA.0b013e3181d3447d. PubMed PMID: 20224374PubMedCrossRef 75. Reissfelder C, Buhr HJ, Ritz JP: What is the optimal time of surgical intervention after an acute attack of sigmoid diverticulitis: early or late elective laparoscopic resection? Dis Colon Rectum 2006,49(12):1842–1848. doi:10.1007/s10350–006–0730-z. PubMed PMID: 17036202PubMedCrossRef 76. Margolin AZD1390 chemical structure DA: Timing of elective surgery for diverticular disease. Clin Colon Rectal Surg 2009,22(3):169–172. doi:10.1055/s-0029–1236161. PubMed PMID: 20676260; PubMed Central PMCID: PMC2780261PubMedCentralPubMedCrossRef 77. Constantinides

VA, Tekkis PP, Senapati A, Association of Coloproctology of Great Britain I: Prospective multicentre evaluation of adverse outcomes following treatment for complicated diverticular disease. Br J Surg 2006,93(12):1503–1513. doi:10.1002/bjs.5402. PubMed PMID: 17048279PubMedCrossRef 78. Demetriades D, Pezikis A, Melissas J, Parekh D, Pickles G: Factors influencing the morbidity of colostomy closure. Am J Surg 1988,155(4):594–596. PubMed PMID: 3354784PubMedCrossRef 79. Khalid MS, Moeen S, Khan AW, Arshad R, Khan AF: Same admission colostomy Pregnenolone closure: a prospective, randomised study in selected patient groups. Surg: J Roy Coll Surg Edinb Ireland 2005,3(1):11–14. PubMed PMID: 15789787 80. Roe AM, Prabhu S, Ali A, Brown C, Brodribb AJ: Reversal of Hartmann’s procedure: timing and operative technique. Br J Surg 1991,78(10):1167–1170. PubMed PMID: 1958975PubMedCrossRef 81. Iwashyna TJ, Ely EW, Smith DM, Langa KM: Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA: J Am Med Assoc 2010,304(16):1787–1794. doi:10.1001/jama.2010.1553. PubMed PMID: 20978258; PubMed Central PMCID: PMC3345288CrossRef 82. Iwashyna TJ, Cooke CR, Wunsch H, Kahn JM: Population burden of long-term survivorship after severe sepsis in older Americans. J Am Geriatr Soc 2012,60(6):1070–1077. doi:10.1111/j.1532–5415.2012.03989.x.