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BACKGROUND: The inhabitants of 3 different types of population centers in Israel were assessed as to stress-related symptomatology during 2003 and 2004. These centers have been exposed to 2 distinct forms of violence-sporadic, large-scale terror attacks in the metropolitan areas in the heart of Israel and daily "war-zone" conditions in the settlements beyond the 1967 borders of Israel. METHOD: A semistructured interview and questionnaire survey of a random sample of 314 inhabitants of a suburb of Tel-Aviv, a settlement in the West Bank (Kiryat-Arba), and the Gush-Katif settlement cluster in the Gaza Strip was performed. Symptoms of acute stress and chronic (posttraumatic) stress as well as symptoms of general psychopathology and distress were assessed. RESULTS: The inhabitants of Gush-Katif, in spite of firsthand daily exposure to violent attacks, reported the fewest and least severe symptoms of stress-related complaints, the least sense of personal threat, and the highest level of functioning of all 3 samples. The most severely symptomatic and functionally compromised were the inhabitants of the Tel-Aviv suburb, who were the least frequently and least directly affected by exposure to violent attacks. Because the Gush-Katif population is exclusively religious, the data were reassessed according to religiousness. The religious inhabitants of Kiryat-Arba had almost the same symptom profile as the Gush-Katif population, whereas secular inhabitants of Kiryat-Arba reported faring worse than did either population in the Tel-Aviv suburb. CONCLUSION: Deeply held belief systems affecting life-views may impart significant resilience to developing stress-related problems, even under extreme conditions. Religiousness combined with common ideological convictions and social cohesion was associated with substantial resilience as compared to a secular metropolitan urban population.  相似文献   
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Eighteen carbapenem-resistant, OXA-48-positive enterobacterial isolates recovered from Turkey, Lebanon, Egypt, France, and Belgium were analyzed. In most isolates, similar 70-kb plasmids carrying the carbapenemase gene blaOXA-48 were identified. That gene was located within either transposon Tn1999 or transposon Tn1999.2, which was always inserted within the same gene. This work highlights the current plasmid-mediated dissemination of the OXA-48 carbapenemase worldwide.Carbapenem-hydrolyzing β-lactamases belonging to Ambler classes A, B, and D have been reported worldwide among Enterobacteriaceae (22). The extensive spread of Ambler class A carbapenemases of the KPC type highlights that carbapenemases may rapidly become threatening (17). Acquired class D ß-lactamases possessing carbapenemase properties have been reported previously, being identified mainly in Acinetobacter sp. (18, 21) and occasionally in Enterobacteriaceae. The chromosome-encoded oxacillinase OXA-23 was previously described for Proteus mirabilis (4), and the oxacillinase OXA-48 was first identified in a Klebsiella pneumoniae isolate from Turkey (20). Since then, several other OXA-48-producing isolates of various enterobacterial species (Citrobacter freundii and Escherichia coli) have been reported, mainly from Turkey (1, 6, 11, 16) but also from Belgium (8), from Lebanon (15), and more recently from the United Kingdom (14, 23a), India (3a), and Argentina (6a). So far, the blaOXA-48 gene has been found to be plasmid borne and located between two identical insertion sequences, IS1999, forming the composite transposon Tn1999 (3). We have analyzed here the genetic backgrounds associated with the blaOXA-48 gene among Enterobacteriaceae isolates collected from different countries.The study included 18 OXA-48-positive clinical isolates of K. pneumoniae (13 isolates), Enterobacter cloacae (2 isolates), Providencia rettgeri (1 isolate), C. freundii (1 isolate), and E. coli (1 isolate). Isolates were mainly from the Turkish cities Istanbul, Ankara, and Izmir (n = 14) (Table (Table1).1). Among the 13 K. pneumoniae isolates, at least Kp11978 (20) and KpB had been sources of nosocomial outbreaks (6). A single K. pneumoniae isolate (KpBEL) was recovered from Brussels, Belgium (8); another K. pneumoniae isolate (KpL) from Beirut, Lebanon (15); another K. pneumoniae isolate from the Bicêtre Hospital (KpBIC), Paris, France (this study); and another K. pneumoniae isolate from Gizah, Egypt (KpE) (8a). Samples were isolated from blood (KpI1, KpI2, KpB, and Enc1), urine (PR, KpBEL, KpL, Kp11978, and KpBIC), cerebrospinal fluid (Enc2), and catheter (KpE). Isolates from Belgium, France, Egypt, and Lebanon were from patients who did not report recent travel history.

TABLE 1.

MICs of β-lactams for the 18 isolates of Enterobacteriaceae and their transconjugants and/or transformants (pOXA-48) E. coli J53 and E. coli TOP10
β-Lactam(s)aMIC (μg/ml) of β-lactam forb:
MIC (μg/ml) of β-lactam forb:
Kp11978 (Istanbul; OXA-48, SHV-2a, TEM-1)E. coli J53(pA-1)KpB (Istanbul; OXA-48, CTX-M-15)E. coli J53(pBb)Kp3A (Ankara; OXA-48)E. coli J53(p3A)Kp4A (Ankara; OXA-48, CTX- M-15), Kp5A (Ankara; OXA-48, SHV-5), Kp6A (Ankara; OXA-48, TEM-150)E. coli J53(p4A, p5A, p6A)Kp7A (Ankara; OXA-48)E. coli J53(p7A)KpI-1 and KpI-2 (Izmir; OXA- 48, CTX-M-15)E. coli J53(pI-1, pI-2)KpBIC (Paris; OXA-48)E. coli TOP10(pBIC)KpE (Gizah; OXA-48, CTX-M-15)E. coli J53(pE)KpBEL (Brussels; OXA-48)E. coli J53(pBEL)KpL (Beirut; OXA-48)E. coli J53(pL)PR (Izmir; OXA-48, TEM-101)E. coli TOP10(pPR)Enc1 (Istanbul; OXA-48, SHV-5)E. coli J53(pEnc1)Enc2 (Istanbul; OXA-48, SHV-2a)E. coli J53(pEnc2)CF (Istanbul; OXA-48, VEB-1)E. coli J53(pCF)EcA (Ankara; OXA-48, TEM-150)E. coli J53(pEcA)E. coli J53E. coli TOP10
Imipenem642160.5>320.75>320.38>320.75240.50.50.5220.750.75>164>321.50.50.50.750.75>320.75240.750.060.06
Ertapenem640.19>320.25>320.25>320.12>320.19240.2520.53342>164>320.750.50.1250.750.19>320.25>320.250.060.06
Meropenem640.25320.12>320.12>320.094>320.12160.0940.50.5220.50.5>160,19>320.250.50.0940.750.12>320.12240.190.060.06
Amoxicillin>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25644
Amoxicillin + clav. acid>512128>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25644
Ticarcillin>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25624
Ticarcillin + clav. acid>512128>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25624
Piperacillin>5128>512>512>512512>512>512>512>512>512512>512>512>512512>2561289664>256128>512>512>512>512>512>512>25612812
Piperacillin + tazobactam5124>512>512>512512>512>512>512>512>512512>512>512>512512>2561289664>256128>512>512>512>512>512>512>25612812
Cephalotin>5120.5>51216>51216>51216>51216>51216>51216>512161616328>51216>51216>51216>512>512>5121644
Cefotaxime640.06>5120.510.5640.120.50.5640.120.50.5640.120.120.121.50.256432>5120.255120.25640.12640.120.060.06
Ceftazidime5120.12>51210.250.255120.120.120.125120.120.120.125120.1210.750.750.75512512>5120.75320.755120.755120.750.060.06
Cefepime320.06>512<0.50.50.12320.120.50.5320.120.50.5320.120.120.120.120.06320.540.12320.12320.12320.120.030.06
Aztreonam5120.06>512<0.120.060.065120.060.060.065120.060.060.065120.060.060.060.060.065120.06>5120.065120.065120.065120.060.030.06
Cefoxitin12821284221282128212821282128222821284>512251221282128224
Open in a separate windowaclav. acid, clavulanic acid.bKp, K. pneumoniae; Enc, E. cloacae; CF, C. freundii; PR, P. rettgeri; Ec, E. coli.Antibiotic susceptibility of the isolates was determined by the disk diffusion method (7). MICs of β-lactams were determined using Etest strips (AB bioMérieux, Solna, Sweden). All isolates were resistant to penicillins. Fourteen of the 18 isolates were resistant to carbapenems according to the CLSI guidelines (Table (Table1)1) (7). The four remaining isolates (KpBIC, KpE, Enc1, and Enc2) exhibited MICs of carbapenems remaining in the intermediate or in the susceptible range. Resistance to broad-spectrum cephalosporins was observed for most of the isolates. However, isolates Kp3A, Kp7A, KpBEL, KpL, and KpBIC remained susceptible to broad-spectrum cephalosporins (Table (Table1).1). All isolates were resistant to fluoroquinolones, except isolates Kp6A, Enc1, and Enc2. All isolates were resistant to aminoglycosides and sulfamethoxazole, except isolate CF, which remained susceptible to the latter antibiotic.Carbapenemase- and extended-spectrum-β-lactamase (ESBL)-encoding genes were identified by PCR experiments using previously designed primers (6, 8), followed by sequencing. Additional ESBL production was detected by synergy tests as described previously (12). Positive results for ESBL production were observed for isolates EcA, Enc1, Enc2, Kp4A, Kp5A, Kp6A, KpI-1, KpI-2, and KpE. Several ESBL determinants were identified, including CTX-M-15, SHV-5, SHV-2a, TEM-101, TEM-150, and VEB-1 (Table (Table11).Isolates belonging to the same species (13 K. pneumoniae isolates or two E. cloacae isolates) were compared by pulsed-field gel electrophoresis (PFGE) as described previously (6). Ten pulsotypes were identified among the 13 K. pneumoniae isolates. The two K. pneumoniae isolates from Izmir were clonally related, and the three K. pneumoniae isolates from Ankara (Kp4A, Kp5A, and Kp6A) shared very similar PFGE patterns. The two E. cloacae isolates recovered from Istanbul were not clonally related (Fig. (Fig.11).Open in a separate windowFIG. 1.Pulsed-field gel electrophoresis patterns of the 13 OXA-48-producing K. pneumoniae isolates and the two OXA-48-producing E. cloacae isolates. (A) Lane 1, Kp3A; lane 2, Kp4A; lane 3, Kp5A; lane 4, Kp6A; lane 5, Kp7A; lane 6, KpI-1; lane 7, KpI-2; lane 8, unrelated K. pneumoniae isolate (included as a comparative strain); lane 9, Enc1; lane 10, Enc2; lane 11, unrelated E. cloacae isolate (included as a comparative strain); lane M, molecular size marker. (B) Lane 1, Kp3A; lane 2, Kp11978; lane 3, Kp4A; lane 4, Kp7A; lane 5, KpI-1; lane 6, KpL; lane 7, KpB; lane 8, KpBEL; lane 9, KpE; lane 10, KpBIC; lane M, molecular size marker.Transferability of the blaOXA-48 gene was studied by conjugation experiments as described previously (6). When conjugation experiments failed, plasmid DNA extract was used for transformation as described previously (20). Transformants were selected on LB agar containing ticarcillin (50 μg/ml). Transconjugants and transformants with decreased susceptibility to carbapenems were obtained for all isolates (Table (Table1),1), and MICs for the transconjugants/transformants remained in the susceptible range. The E. coli transformant obtained from the P. rettgeri isolate exhibited reduced susceptibility to carbapenems associated with resistance to cefotaxime and ceftazidime.Plasmids were analyzed by using the Kieser technique (13). A 70-kb plasmid was identified in all transconjugants/transformants (data not shown). However, a 150-kb plasmid was identified in the blaOXA-48-positive transformant obtained with the PR isolate. The blaOXA-48 and blaTEM-101 genes were codetected on the same 150-kb plasmid, as confirmed by Southern blot hybridization as described previously (20) (data not shown), explaining the resistance to all β-lactams of the PR isolate and its transformant (Table (Table1).1). Plasmid restriction profiles were compared as described previously (10) (data not shown), and very similar restriction patterns (suggesting highly related structures) were obtained for all of the 70-kb plasmids but not for the 150-kb plasmid pPR.PCR mapping was used to assess the presence of insertion sequence IS1999 upstream of the blaOXA-48 gene, to confirm the presence of transposon Tn1999, and to identify the transposon insertion site for all of the OXA-48-positive isolates (3, 20). In all isolates, the blaOXA-48 gene was flanked by two copies of IS1999, as described previously (3). The prototype IS1999 located at the left extremity of transposon Tn1999 was identified in isolates Kp3A, Kp4A, Kp5A, Kp6A, Kp7A, CF, PR, Enc1, and Enc2. Insertion of IS1R into IS1999 as described for KpB (6) and giving rise to Tn1999.2 was identified for isolates EcA, KpBIC, KpI, KpL, KpBEL, and KpE (Fig. (Fig.2).2). In isolate Kp11978, transposon Tn1999 had been identified to be inserted into the tir gene, being functionally homologous to the F3 gene encoding the factor F involved in the plasmid replicative machinery (23). By use of a primer located upstream of Tn1999 inserted into the tir gene, insertion of Tn1999 at the same target site was evidenced in all of the blaOXA-48-positive plasmids except for the pPR plasmid (Fig. (Fig.2).2). Inverse PCR performed as described previously (3) was used for identifying the blaOXA-48-surrounding structures in isolate PR. Sequencing of the obtained amplicons indicated that Tn1999 had targeted a gene encoding a phosphoadenosine phosphosulfate reductase (ΔPPR).Open in a separate windowFIG. 2.Genetic environments of the blaOXA-48-carrying plasmids identified among the 18 OXA-48-positive Enterobacteriaceae isolates. (A) Structure described for pA-1, p3A, p4A, p5A, p6A, p7A, pCF, pEnc1, and pEnc2. (B) Structure of the 150-kb pPR plasmid. (C) Structure described for pBb, pI, pL, pBEL, pEcA, pBIC, and pE.Attempts to identify the incompatibility group of the 70-kb OXA-48-positive plasmids failed using a PCR-based replicon typing method as described previously (5). Since rep genes are often located close to the hot spots for resistance gene integration, cloning experiments were performed to study these plasmids further. A gene encoding phage replication protein P (RepP) was identified upstream of the blaOXA-48 gene. Primers specific for the repP gene were designed (RepPA, 5′-AATGGTTAACTTTGACTGTG-3′; RepPB, 5′-GCACGATTTAGAGGTCTAC-3′), and positive results were obtained for all 70-kb plasmids. Association of the repP gene with the blaOXA-48 gene on the 70-kb plasmid was confirmed by hybridization with a specific RepP probe (data not shown). However, the repP gene could not be detected on the 150-kb plasmid identified from isolate PR. Our study showed the spread of a blaOXA-48-carrying plasmid among different enterobacterial species, being identified first in Turkey and later in other European countries and in the Middle East. The present work indicates that dissemination of the blaOXA-48 gene is not driven by the dissemination of a single K. pneumoniae clone. Since the blaOXA-48-carrying plasmid confers by itself a low level of resistance to carbapenems, clinical laboratory detection of OXA-48-producing strains may be difficult. Since the reservoir of blaOXA-48 has been identified in the waterborne Gram-negative organism Shewanella oneidensis (19), it is likely that the process leading to the dissemination of this gene may be the consequence of a wide interspecies exchange. In addition, since plasmids belonging to the RepP group have been described among Pseudomonas sp., phytopathogenic Xanthomonas sp., and samples from soils and sludges (2, 9, 24), it may be hypothesized that the blaOXA-48 gene could also be identified in those species. This work underlines that besides class B (VIM and IMP) and class A (KPC) carbapenemases, the class D carbapenemase OXA-48 type might contribute significantly to carbapenem resistance in Enterobacteriaceae.  相似文献   
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OBJECTIVE: To report a multicenter analysis after laparoscopic radical nephroureterectomy for pathologically confirmed upper tract transitional cell carcinoma. MATERIALS AND METHODS: A total of 116 patients (72 males; mean age 68 years) underwent laparoscopic radical nephroureterectomy at five international institutions: 51 transperitoneally, 65 retroperitoneally. Location of the primary tumor was pelvicalyceal in 70 patients (60%), ureteral in 27 (23%), and multifocal in 19 (17%). In 18 patients (15%), transurethral resection was performed for concomitant bladder tumor. The median follow-up time was 25 months (range 3-93). A minimum follow-up of 1 and 2 years was available in 77 and 41 patients, respectively. RESULTS: Five patients (4%) were converted to open surgery. The specimen was extracted intact in all 116 patients: using an Endocatch bag in 78 patients, a Lapsac in 5, and manually in 33. Pathologic staging was pTis in 5 (4%), pTa in 41 patients (35%), pT1 in 31 (26%), pT2 in 18 (15%), pT3 in 16 (13%), and pT4 in 5 (4%). Pathological grade was grade I in 26 patients (23%), grade II in 41 (35%), grade III in 34 (29%) and grade IV in 15 (12%). Histopathology revealed a positive surgical margin in five patients (4.5%): renal hilum (one), periureteral soft tissue (two), distal edge of the ureter/ bladder cuff (two). Local recurrence was noted in two patients (1.7%). Bladder recurrence was noted in 28 patients (24%) with a mean time to recurrence of 13.9+/-11.5 months. Distant metastases occurred in 11 patients (9%): lung (5), liver (3), bones (2), adrenal (1); mean time to metastasis was 13 months. Overall, 23 patients (20%) died. One-year and 2-year cancer-specific survival was 92% and 87%, respectively. Two-year cancer-specific survival according to pathologic stage was 89% for patients with pT1 disease, 86% for pT2, 77% for pT3, and 0% for pT4 (p=0.0001). Two-year survival according to pathologic grade was 88% for grade I, 90% for grade II, 80% for grade III, and 90% for grade IV (p>0.05). CONCLUSION: Laparoscopic radical nephroureterectomy appears to be an effective minimally invasive treatment for select patients with upper tract transitional cell carcinoma. Although the 2-year survival data reported herein are encouraging, longer follow-up is needed before laparoscopy can be considered as a standard treatment.  相似文献   
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Vesico-uterine fistulae (VUF) lead to an abnormal breech between the bladder and the womb. They are responsible for urinary incontinence and/or cyclic hematuria. They are rare and, in most cases, lead to complications following caesarean deliveries. We report observations of 3 vesico-uterine fistulae treated over a 5 years period at university maternity based at Casablanca, Morocco; they all occurred following caesarean deliveries. These patients were consulted for urinary leakage occurring few weeks up to many years following surgical traumatism. Diagnosis was evoked clinically in all cases and confirmed by intravenous urography and/or hysterography. These VUF were successfully treated by simple breech suture at laparotomy. Treatment is very simple and efficient when the diagnosis is made early and fistula simple. Surgery is recommended after medical treatment failure aiming at fistula drainage.  相似文献   
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HCC is a common cancer and HBV and AFB(1) are well-documented, major risk factors. Epidemiologic studies have documented that cigarette smoking also contributes to the development of HCC. PAHs are ubiquitous environmental pollutants and products of incomplete combustion. They are present in both mainstream and sidestream cigarette smoke. PAHs are metabolically activated by phase I enzymes, including CYP1A1, into electrophilic reactants (diol epoxides), which covalently bind to DNA to form adducts. Diol epoxides are also substrates for phase II detoxifying enzymes, including GSTM and GSTP. To examine the association between PAH-DNA adducts and HCC, adduct levels were determined in liver tissue by relative staining intensity with an immunoperoxidase method using a polyclonal antiserum against BPDE-modified DNA. Subjects were also genotyped for polymorphism in several genes involved in the metabolism of PAH, including GSTM1 and GSTP1. Liver tissue was collected from patients with histologically confirmed HCC (n = 105) and from non-HCC controls (n = 37). There was a significant positive correlation (r = 0.3, p < 0.01) between adducts in tumor and adjacent nontumor tissues among HCC cases. The risk of HCC was higher after adjustment for age, sex and HBsAg in the group with the highest tertile tissue levels of PAH-DNA adducts (mean relative nuclear staining intensity of tumor and nontumor tissue > 344) than in the group with the lowest tertile (staining < 241, OR = 3.9, 95% CI = 1.0-14.9). Among non-HCC controls, there were no significant associations between adduct levels and cigarette smoking, GSTM1 null genotype and HBsAg positivity. A strikingly increased HCC risk was observed (OR = 20.3, 95% CI = 5.0-81.8) among HBsAg-positive subjects whose PAH-DNA adduct levels were high (mean relative nuclear staining intensity of tumor and nontumor tissue > 301, median of control tissues) compared to HBsAg-negative subjects who had low PAH-DNA adduct levels. 4-ABP- and AFB(1)-DNA adducts had been measured previously in these same tissues. Subjects with elevated DNA adduct levels of PAH, 4-ABP and AFB(1) had a significantly higher HCC risk with an OR of 36.7 (95% CI 7.2-187.2) compared to those who had low DNA adduct levels. These results suggest that PAHs may play a role in human hepatocarcinogenesis in conjunction with HBsAg carrier status, GSTM1 and GSTP1 genotypes and exposure to 4-ABP and AFB(1).  相似文献   
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