Nat Nanotechnol 2008, 3:210–215 CrossRef 40 Stampfer C, Molitor

Nat Nanotechnol 2008, 3:210–215.CrossRef 40. Stampfer C, Molitor F, Graf D, Ensslin K, Jungen A, Hierold C, Ensslin K: Raman imaging of doping domains in graphene on SiO(2). Appl Phys Lett 2007, 91:241907.CrossRef Competing interests The authors declare

that they have no competing interests. Authors’ contributions C-H and B-JL carried on the experimental parts: the acquisition of data and analysis and interpretation of data. C-H also had been involved in drafting the manuscript. H-YL and C-HH analyzed and interpreted the data. They also had been involved in revising the manuscript. F-YS and W-HW (Institute of Atomic and Molecular Sciences, Academia Sinica) prepared the INCB028050 in vivo samples, suspended graphene using by micromechanical learn more method, and captured the OM and AFM images. C-YL have made substantial contributions MK-4827 chemical structure to the conception and design of the study and revising it critically for important intellectual content. H-CC, the corresponding author, had made substantial contributions to the conception and design of the study and had been involved in drafting the manuscript and revised it critically for important intellectual content. All authors read and approved the final manuscript.”
“Background

Scanning tunneling microscopy (STM) [1] and atomic force microscopy (AFM) [2] have revolutionized surface sciences by enabling the study of surface topography and other surface Sitaxentan properties at the angstrom-to-micrometer scale. The three major functions of AFM include imaging, spectroscopy (i.e., force-distance curve), and manipulation (nanolithography).

AFM techniques employ a very sharp tip as a probe to scan and image surfaces. Spectroscopic information is acquired through forces generated between the tip and the sample when the probe is brought into proximity with the sample surface, according to Hooke’s law. Xie et al. [3] classified nanolithographic techniques into two groups: force-assisted and bias-assisted nanolithography. In AFM, the interactive force between the tip of the probe and the sample surface is determined according to the deflection of a microfabricated cantilever with the tip positioned at the free end. Modifying the probe enables researchers to explore a range of surface characteristics. AFM probes with individual microparticles or nanoparticles attached to the cantilever/tip have been widely used to measure surface forces in AFM and near-field scanning optical microscopy (NSOM) [4] as the geometry and composition of the particle can be well controlled. Ducker et al. [5, 6] were pioneers in the attachment of microspheres to a tipless AFM cantilever with resin. Their colloidal probe technique employed a laser-pulled micropipette attached to an optical microscope. Mak et al.

Briefly, tissue sections were baked, deparaffinized and microwave

Briefly, tissue sections were baked, deparaffinized and microwaved at 98°C for 10 minutes in citrate buffer (0.01 M citric acid, pH6.0). After blocking the endogenous peroxidase by immersed the

sections in 3% H2O2, the sections were incubated with primary antibodies directing against human RhoA (sc-32039, 1:50; Santa Cruz) and RhoC (sc-12116, 1:50; Santa Cruz). Expression of RhoA or RhoC protein in tissue sections was detected with Anti-goat IgG/HRP Detection Kit(PV-6003; Zhongshan Biotechnology Limited Company, Beijing, China). The tissue sections were then counterstained with hematoxylin. Terminal Deoxynucleotidyl Transferase-mediated dUTP Nick End-labeling (TUNEL) Assay Assessment of cell death was performed by TUNEL GSK461364 in vivo method using an in situ cell death detection kit conjugated with horse-radish peroxidase (POD) (Roche Applied Science, Indianapolis, IN, USA), according to the manufacturer’s instructions. Five equal-sized fields in tissue sections were randomly chosen and analyzed under the Leica

DMI 4000B(Leica, Germany) light microscope. Density was evaluated in each positive staining field, yielding the density of dead cells (cell death index). Statistical Analysis All data were shown by mean Blebbistatin ± SD. Statistical analyses were performed using SPSS statistical software (SPSS Inc., Chicago, Illinois). Differences between two groups were assessed using a t test. A P value less than 0.05 was considered statistically significant. Results Ad-RhoA-RhoC-siRNA Inhibits Tumor Development in Nude Mice Tumors in the nude mice could be seen at 5th day from the implantation of HCT116 cells and Amylase all tumors had reached 5-7 mm in size at 9th day. The successful rate

of tumor implantation was 100%(Figure 1). After intratumorally injection, the growth speed of tumors in the three group was quite different. As shown in figure 2, the tumors in NS and Ad-HK group grew rapidly. In contrast, tumors in Ad-RhoA-RhoC group were significantly see more delayed. The dissected tumors in the NS and Ad-HK group had volumes of (699.62 ± 190.56)mm3 and (678.81 ± 155.39)mm3, which were 5.05 ± 0.48-fold and 4.58 ± 0.94-fold larger than the starting volume, whereas in the Ad-RhoA-RhoC group, the tumors had a volume of (441.38 ± 63.03)mm3, increased only 2.38 ± 0.56-fold (Figure 3). Tumor growth delay was statistically significant (P < 0.05). In addition, the mean tumor weight in NS, Ad-HK and Ad-RhoA-RhoC group was (0.75 ± 0.22) g, (0.78 ± 0.22) g and (0.36 ± 0.13) g, respectively. These data demonstrated that injection of Ad-RhoA-RhoC was able to slow down the growth of HCT116-derived xenografts. Figure 1 Tumor-bearing nude mice with 100% of tumor implantation rate. Figure 2 Growth curve of subcutaneous implanted tumors in nude mice treated with NS, Ad-HK, or Ad-RhoA-RhoC. Tumor volume is plotted against time elapsed. A significant delay in tumor growth is seen in the group treated with Ad-RhoA-RhoC.

Valdivielso P, et al Nephrology (Carlton) 2003;8:61–4 (Level 4

Valdivielso P, et al. Nephrology (Carlton). 2003;8:61–4. (Level 4)   4. Gazarin S, et al. J Nephrol. 2002;15:690–5. (Level 4)   5. Matzkies FK, et al. Am J Nephrol. 1999;19:492–4. (Level 4)   6. Olbricht CJ, et Necrostatin-1 al. Kidney Int 1999;71 (Suppl):S113–6. (Level 2)   7. Brown CD, et al. Am J Kidney Dis. 1995;26:170–7. (Level 3)   8. Thomas ME, et al. Kidney Int. 1993;44:1124–9. (Level 2)  

9. Shibasaki T, et al. Nihon Jinzo Gakkai Shi. 1993;35:1243–8. (Level 4)   10. Dogra GK, et al. Kidney Int. 2002;62:550–7. (Level 4)   11. Resh M, et al. Thromb Res. 2011;127:395–9. (Level 4)   Are RAS inhibitors recommended for patients with idiopathic membranous nephropathy and hypertension? Hypertension often occurs as a complication of membranous nephropathy and is a risk factor for the progression of CKD. To treat such hypertension, restriction of sodium intake and administration of anti-hypertensive agents have been recommended. The anti-proteinuric effect of RAS inhibitors on diabetic

and non-diabetic nephropathies is well known. Polanco et al. reported that treatment with RAS inhibitors was associated with a significantly increased probability of spontaneous Selleckchem GSK872 remission of membranous nephropathy. RAS inhibitors are preferred as the first-line antihypertensive therapy and are expected to reduce urine protein and Osimertinib solubility dmso slow the progression of membranous nephropathy. Bibliography 1. Polanco N, et al. J Am Soc Nephrol. 2010;21:697–704. (Level 4)   2. Kosmadakis G, et al. Scand J Urol Nephrol. 2010;44:251–6. (Level Exoribonuclease 2)   3. Iimura O, et al. Nihon Jinzo Gakkai Shi. 2003;45:439–44. (Level 4)   4. Prasher PK, et al. J Assoc Physicians India. 1999;47:180–2. (Level 4)   5. Ruggenenti P, et al. Am J Kidney Dis. 2000;35:381–91. (Level 4)

  6. Praga M, et al. Nephrol Dial Transplant. 1997;12:2576–9. (Level 4)   7. Rostoker G, et al. Nephrol Dial Transplant. 1995;10:25–9. (Level 4)   8. Gansevoort RT, et al. Nephrol Dial Transplant. 1992;7(Suppl1):91–6. (Level 3)   9. Thomas DM, et al. Am J Kidney Dis. 1991;18:38–43. (Level 4)   10. Kincaid-Smith P, et al. Nephrol Dial Transplant. 2002;17:597–601. (Level 2)   Is treatment with high-dose corticosteroid alone recommended for inducing remission in FSGS? An important prognostic indicator of FSGS is the initial response to therapy. Aggressive immunosuppressive therapy aimed at inducing remission is recommended because sustained nephrotic range proteinuria is a risk factor for progression to ESKD, and, conversely, responders to initial therapy have better long-term outcomes. There are no RCTs comparing corticosteroid or other agents to placebo as the first-line therapy for idiopathic FSGS. Observational studies have shown that high-dose corticosteroid could efficiently induce remission. Therefore, as the first-line therapy, steroid therapy aimed at inducing remission is recommended for patients with FSGS.

parvum Moredun Cervine (passaged in calves) Scotland C parvum    

parvum Moredun Cervine (passaged in calves) Scotland C parvum     Ch2 Human Yorkshire, England C hominis C. hominis GQ983348 IbA10G2 GQ983356 Ch3 Human North Wales C hominis C. hominis GQ983350 IbA10G2 GQ983358 Ch4 Human Cumbria, England C hominis C.

hominis GQ983352 IbA10G2 GQ983360 Cp2 Human Devon, England C parvum Sapanisertib cost C parvum GQ983349 IIaA18G3R1 GQ983357 Cp3 Human Cumbria, England C parvum C parvum GQ983351 IIaA17G1R1 GQ983359 Cp4 Human Grampian, Scotland C parvum C. parvum GQ983353 IIaA15G2R1 GQ983361 W7265 (W65) Human Leicestershire, England C parvum C. parvum GU971620 IIcA5G3 GU971624 W7266 (W66) Human Leicestershire, England C parvum C. parvum GU971621 IIcA5G3 GU971625 W7267 (W67) Human Leicestershire, England C parvum C. parvum GU971622 IIcA5G3 GU971626 W7270 (W70) Human Leicestershire, England C parvum

C. parvum GU971623 IIcA5G3 GU971627 W17330 (rabbit 1) Human Northampton-shire, England C hominis Rabbit genotype FJ262726 VaA18 FJ262732 W18455 (rabbit 2) Human Shropshire, selleck chemical England C hominis Rabbit genotype PD0332991 GU971628 VaA23 GU971631 W17525 (rabbit 3) Human Suffolk, England C hominis Rabbit genotype GU971629 VaA32 GU971632 (W17435 (rabbit 4) Human Essex, England C hominis Rabbit genotype GU971630 VaA22 GU971633 Details of the host, the geographical origin and the genotyping data of C. parvum and C. hominis isolates and reference strains, which DNA was tested during this study. Table 3 PCR results of other Cryptosporidium species.   C. andersoni C. felis Cervine genotype C. meleagridis C. baileyi Cgd2_80 – - – + – Cgd2_2430 + – - – - Cgd6_200 – - – + – Cgd6_5020 – + – + – Cgd8_2370 – - – + – Chro.20156 – - – - – Chro.50317 – - – + -

Chro.50330 – - – + – Chro.30149 – - + + – Chro.50457 – - – + – DNA from C. andersoni, C. felis, cervine genotype, C. meleagridis and C. baileyi was tested by PCR using the newly designed primers. Figure 1 Amplification of Cryptosporidium DNA from clinical isolates and reference strains. A: amplification of 266 bp of Cgd2_80 gene, B: amplification of 368 bp of Chro.50330 gene. Both Cryptosporidium species and all isolates were PCR positive. MW: molecular weight, 1: Cp2, 2: Cp3, 3: Cp4, 4: Ch2, 5:Ch3, 6: Ch4, 7: Iowa, 8: Moredun, 9: Dimethyl sulfoxide TU502, NTC: non template control. Interestingly, for Cgd2_2430 gene, only C. andersoni DNA was amplified by PCR. For Cgd6_5020, only C. felis DNA was PCR positive and for Chro.30149 primers, cervine genotype DNA was amplified. C. andersoni, cervine genotype and C. felis DNA was amplified by 10% (1/10) of primers tested. C. baileyi DNA was not amplified by any of the primers tested (Table 3). All positive PCR products were sequenced. PCR product sequences are available online [GenBank: GU904212-GU904405]. The alignments of PCR product sequences for each gene are shown [additional file 1]. One PCR product of C. meleagridis DNA using Chro.50330 primers did not generate good sequence and was therefore excluded from the analysis. In addition, PCR products for C.

Increased density of sensory nerve fibres in the endometriotic le

Increased density of sensory nerve fibres in the endometriotic lesions and in the eutopic endometrium have also been found [6]. Pertubation comprises passing solution through the uterine cavity and the fallopian tubes into the peritoneal cavity via a cuffed intra-cervical balloon catheter. Earlier studies have shown that pertubations with lignocaine hydrochloride can improve fertility and reduce dysmenorrhoea in patients with endometriosis [7–9]; the highest dosage

of lignocaine in these studies has been 10 mg. In total, more than 400 pertubations with lignocaine have been carried out without any lignocaine-related adverse events. Local anaesthetics in low concentrations have anti-inflammatory check details properties, and the clinical effect seen on pain and fertility might be due to decreased inflammation in the peritoneal cavity [2]. The adverse Raf inhibitor effects of lignocaine have been well investigated and manifest most commonly on the central nervous

system (CNS) and cardiovascular systems [10, 11]. Plasma concentrations of lignocaine above 5 μg/ml can cause adverse effects (i.e. nausea, dysphoria, drowsiness, cardiovascular instability), but concentrations of lignocaine above 10 μg/ml are needed to produce serious toxicity. Serum levels above 10 μg/ml can cause disorientation, GSK461364 respiratory depression, seizures and even coma, but serum levels exceeding 20 μg/ml are needed to cause cardiovascular collapse [10]. Serum levels of local anaesthetics after non-vascular administration correspond with the vascularity of the tissue [12]. The surface area of the peritoneum is about equal to that of the skin, i.e. >2 m2. Small molecules diffuse rapidly and the diffusion rates decrease with the molecular weight to become extremely slow for molecules Rebamipide with a molecular weight of

100,000 Da [13–15]. Lignocaine hydrochloride has a molecular weight of 271 Da. A review of systemic levels of local anaesthetics after intra-peritoneal application was conducted in 2010; nine trials in which lignocaine was used were found [11]. The dosage used varied from 100 to 1,000 mg, and serum levels were detected as early as 5 min after application, with a time to maximum concentration (T max) ranging from 5 to 40 min for plain lignocaine. The addition of adrenaline prolonged the T max. Mean concentration maximum (C max) ranged from 1.01 to 4.32 μg/ml, and the highest observed value was detected after intraperitoneal administration of 80 ml lignocaine 0.5 % (400 mg) [16]. No report of serum or clinical toxicity was found in any of the reviewed studies [11]. We have previously reported a randomized controlled trial that was carried out to evaluate the effect of pertubation with lignocaine 10 mg on dysmenorrhoea and quality of life in patients with endometriosis.

2d, e, g), which

2d, e, g), which H 89 supplier was NSC23766 supplier followed by a decrease (SSF 650/6; Fig. 2d) or return to the initial level (SSF 1250/12 and SSF 1250/6; Fig. 2e, g) by day 7. We note that the picture

in Fig. 2 remained essentially the same when the QA reduction state was estimated by another parameter (1-ql; data not shown), which takes into account the connectivity among PSII complexes for light energy transfer (Kramer et al. 2004). Fig. 2 Reduction state of Q A (1–qP) during light induction. The measurement protocol and the abbreviations of the light regimes are as described in the legend to Fig. 1. Data are means of five plants (±SE) Inverse patterns were found for ETR (Fig. 3), which is a proxy for the rate of electron transport at PSII. In the C 50 plants, ETR nearly reached saturation at around 80 μmol m−2 s−1 during 8-min illumination at 1,000 μmol photons m−2 s−1 (Fig. 3a). All plants that showed enhancement of QA oxidation during the 7-day acclimation (i.e., C 85, C 120, and LSF 650) also had increasing ETR; on day 7 the ETR values at the end of the

illumination were ca. 100 μmol m−2 s−1 in C 85 and LSF 650 and 120 μmol m−2 s−1 in C 120 (Fig. 3b, c and f). Similarly, the increasing 1-qp detected in the SSF plants (Fig. 2d, e, g) was accompanied by decreasing ETR (Fig. 3d, e, g). The ETR values of these plants were the lowest on day 3 (ca. 60 μmol m−2 s−1), but recovered to 90 (SSF 650/6) or 70 μmol m−2 s−1 (SSF 1250/12 and SSF 1250/6) by day 7. It needs to be reminded, however, that the calculation of ETR based on constant light absorption and equal turnover Selleck Tofacitinib of PSII and PSI (see “Materials and methods”) may not be uniformly applicable to plants undergoing acclimation to different light regimes. Fig. 3 Electron transport rate (ETR) during light induction. The values were calculated from the effective PSII efficiency measured under 1,000 μmol photons m−2 s−1 as described in the legend to Fig. 1. Data are means of five

plants (±SE) Carbohydrate accumulation under different sunfleck conditions In order to see whether the observed changes in PSII activity were reflected in the carbohydrate status of these plants, Glutamate dehydrogenase non-structural carbohydrate was analyzed in mature leaves harvested in the evening (after 10 h of illumination by the different light regimes) on day 2 and 5 (Fig. 4). The concentrations of soluble sugars (the sum of glucose, fructose, and sucrose) varied in leaves under the different light regimes (Fig. 4a), yet the differences between C 50 and other treatments were not significant. Higher starch levels were found in C 85 and C 120 on day 2 (Fig. 4b); especially, the leaf starch content in C 120 was more than three times that of C 50. The starch levels then declined in both C 85 and C 120 by day 5 although the plants in C 120 still had twice as much starch as in C 50. None of these changes in starch was accompanied by similar changes in soluble sugar (Fig. 4a).

We enrolled 20 patients with type 2 diabetes complicated by diabe

We enrolled 20 patients with type 2 diabetes complicated by diabetic nephropathy stage III to IV. Patients with diabetic nephropathy were classified by the Ministry of Health, Labour and Welfare of Japan [9]. The 20 patients consisted of 11 males and 9 females, ranging in age from 34 to 80 years [median age 61.6 years]. Patients previously treated with NSAIDs

or with a history of hypersensitivity to NSAIDs were excluded. We also excluded those who underwent knee or spine surgery, and patients with hematologic disease, liver cirrhosis, heart failure or malignancy. Adhesive skin patches containing 100 mg loxoprofen (LX-P; Loxonin® tape) Selleck Daporinad were applied to the back or knee of each patient, depending on the site of pain, for 24 h per day for five consecutive days (one patch per day). The degree of pain was assessed using a visual analogue scale (VAS) [10], consisting of a straight 10-cm line, presenting a continuum of pain intensity, with ‘no pain’ at the bottom and ‘pain as bad as it can be’ at the top. Blood pressure was measured by an aneroid sphygmomanometer in the supine position before breakfast. The mean

blood pressure values of 2 consecutive days Wee1 inhibitor before treatment were used as the baseline and the mean blood pressure value of days 4 and 5 were used as the end-point. Blood and urine samples were obtained under fasting ACP-196 conditions at baseline and at the end of the 5-day study period. The estimated glomerular filtration rate (eGFRcre) of each patient was calculated using the simplified equation of the Japanese Society of Nephrology, a version of the Modification of

Diet in Renal Disease study equation modified for Japanese patients [11]. GFR was also estimated from serum cystatin C concentrations (eGFRcys), as recently recommended by the Japanese Society of Nephrology [12]. HbA1c was measured using high-performance liquid chromatography and expressed as the National Glycohemoglobin Standardization Program (NGSP) equivalent value (%), as recommended by the Japanese Diabetes Society. Serum concentrations of loxoprofen and its active, trans-OH metabolite were measured by liquid chromatography coupled with tandem mass spectrometry (LC/MS/MS) (Sumika Chemical Analysis Service, Ltd., Osaka, Japan). Urinary PGE2 concentrations 5-FU cost were measured by a chemiluminescence immunoassay (SRL, Inc., Tokyo, Japan). The study protocol was approved by the Ethics Committee of Shiga University of Medical Science (approval number: 22-83-1), and all participants provided written informed consent. Statistical analysis Data were analyzed using SPSS version 17.0 (SPSS, Tokyo, Japan). The distribution of variables was analyzed by checking histograms and normal plots of the data, and normality was tested using the Kolmogorov–Smirnov and Shapiro–Wilk tests. Student’s t test was used to compare values at different time points.

It is therefore possible that other resistance mechanisms, such a

It is therefore possible that other resistance mechanisms, such as ParE polymorphisms, other horizontally acquired resistance genes (such as oqxAB and aac(6 ‘ )-Ib for example), over-active efflux, or even novel mechanisms are present in some of the isolates. Resistance patterns in pathogens often mirror those in commensals. This is borne out by our recent documentation of quinolone resistance in Vibrio cholerae isolates recovered in the same time frame as the E. coli strains presented in this report

[21]. Fifteen of the 40 QREC isolates identified in this study belonged to ST10, Wortmannin or were single- or double-locus variants of this ST, pointing to the possibility of clonal expansion.

ST10-selleck inhibitor complex strains were isolated in all three years and therefore over-representation of these STs in our sample cannot be explained PD-1/PD-L1 Inhibitor 3 research buy by short-term, localized clustering. There are four major E. coli phylogenetic clades: ECOR A, B1, B2 and D. Few studies have looked at the geographical variance in the distribution of these groups but overall, QREC from Ghana were predominantly drawn from ECOR group A. Of the STs identified in this study that are classified into ECOR clades at the E. coli MLST database, ST10 complex (14 isolates) belong to ECOR group A, ST131 (1 isolate) to ECOR B2, STs101 and 410 (3 isolates) to ECOR B1 and STs 156, 206 and 210 (4 isolates) are hybrids of ECOR A and B1, that is AxB1. Available Methane monooxygenase data appear to suggest that ECOR A strains are highly prevalent in Africa, compared to some other world regions [22]. However, when we compared the sequence types of quinolone-resistant and -susceptible strains from Ghana only, we still found that resistant strains were over-represented in the ST10 complex. Pandemic clonal expansion of some QREC lineages has been reported in the literature [23–28]. For example, ST131 is a globally disseminated multi-resistant clone and was detected once among the QREC in this study. Recent reports suggest

that isolates from Europe and North America that belong to ST10- or ST131- clonal complexes may be less likely to carry virulence factors for invasive disease, but more likely to be fluoroquinolone resistant [24–28]. However it is equally likely that mutations to fluoroquinolone resistance are more likely to be stably inherited in a specific genetic background. Our own data also appear to suggest that, although horizontally acquired, qnrS1 is associated with ST10 complex. A recent paper by Davidson et al suggests that the antimalarial chloroquine may select for fluoroquinolone-resistant fecal bacteria in malaria endemic areas and proposes that chloroquine-mediated selection accounts for high levels of QREC in fecal flora in villages in South America [29].

Diverticulitis Sigmoid diverticulitis is a common disease of the

Diverticulitis Sigmoid diverticulitis is a common disease of the Western World and results in a significant number of hospital admissions. Antibiotics are the standard of care for uncomplicated diverticulitis. Percutaneous drainage is the intervention of choice for simple uniloculated abscesses. It has a success

rate of more than 80%, but it may have a high failure rate in cases of complex multiloculated or inaccessible abscesses [49]. The use of antibiotics and percutaneous drainage in the management of diverticular abscesses Selleckchem INCB28060 facilitates single stage operation to perform subsequently an elective sigmoidectomy. Ambrosetti et al. [50] studied retrospectively 73 patients with diverticular abscesses with a follow up of 43 months and found that 59% of the patients needed surgery either during the acute admission or as an elective procedure. The other patients

did not need surgical intervention after conservative treatment either with or without percutaneous drainage. The study also compared the mesocolic abscesses with the pelvic ones. Pelvic abscesses exhibited an aggressive behaviour and therefore needed to be rapidly drained selleck products percutaneously and were likely to require surgery. Brandt et al. [51] retrospectively compared patients with CT confirmed abscesses, GSK-3 inhibitor treated by antibiotics alone and patient treated by antibiotics with percutaneous drainage. The patients treated with antibiotics alone achieved an outcome similar to patients treated with percutaneous drainage. The average abscess size was 4 cm in the antibiotic only group and 6 cm in percutaneous group. Failure rate of percutaneous drainage in this series was 33%. Siewert et al. [52] reported that antibiotics alone were effective in resolving acute symptoms for abscess size less than 3 cm. Urgent surgery for colonic diverticula perforations is indicated in patients with large or/and multiloculated diverticular abscesses inaccessible to percutaneous drainage or in whom clinical symptoms persist after CT guided percutaneous drainage, diverticulitis associated with free perforation and purulent or

fecal diffuse peritonitis. There is still controversy about the optimal surgical management of colonic diverticular disease, complicated by peritonitis. Hartmann’s resection PI-1840 has been considered the procedure of choice in patients with generalized peritonitis and remains a safe technique for emergency colectomy in perforated diverticulitis, especially in elderly patients with multiple co-morbidities [53]. More recently, some reports have suggested that primary resection and anastomosis is the preferred approach to diverticulitis, even in the presence of diffuse peritonitis [54, 55]. In 2006 a sistematic review by Constantinides et al. [56] about primary resection with anastomosis vs. Hartmann’s procedure in nonelective surgery for acute colonic diverticulitis was published.

(DOCX 661 KB) References 1 Kiely CJ, Fink J, Brust M, Bethell D,

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