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21.

Purpose

Studies show that conflict can negatively affect psychological health. The Syrian crisis is 8 years old and yet little is known about the impact of the conflict on the well-being of Syrians who remain. This gap was addressed by conducting an empirical study on the mental health burden of Syrian children in two areas of the country.

Methods

492 children between 8 and 15 years were randomly selected from schools in Damascus and Latakia. The incidence of psychological disorder symptoms was measured using self-report screening instruments, the Children’s Revised Impact of Event Scale (CRIES-8) and the Revised Children’s Anxiety and Depression Scale (RCADS-25). Simultaneously, sociodemographic and traumatic event information was collected. Binary logistic regression was used to identify factors that influence the development of post-traumatic stress disorder (PTSD) symptoms.

Results

In our sample, 50.2% of students were internally displaced and 32.1% reported a negative experience. 60.5% of those tested had at least one probable psychological disorder with PTSD the most common (35.1%), followed by depression (32.0%), and anxiety (29.5%). Binary logistic regression indicated that PTSD symptoms were predicted by: living in Damascus [odds ratio (OR) 2.36, 95% confidence interval (CI) 1.51–3.69], being female (1.54, 1.02–2.34), having depression and anxiety (2.55, 1.48–4.40), and the negative experiences; displacement and daily warzone exposure (1.84, 1.02–3.30 and 2.67, 1.08–6.60).

Conclusions

Syrian children are experiencing traumatic events and war-associated daily stresses that are hugely impacting psychological well-being. Our data offer guidance for mental health providers regarding risk factors and highlights the use of the school system to reach suffering children.
  相似文献   
22.
ObjectivesThis study aims to examine the outcome of end-stage renal disease (ESRD) patients admitted with sepsis to the intensive care unit (ICU).DesignSingle centre, retrospective cohort studySettingThe study was conducted in the Intensive Care Department of King Abdulaziz Medical City, Riyadh, Saudi Arabia.ParticipantsData were extracted from a prospectively collected ICU database from 2002 to 2017. Patients were considered to have sepsis based on the sepsis-3 definition and were stratified into 2 groups based on the presence or absence of ESRD.Primary and secondary outcomesThe primary outcome of the study was in-hospital mortality. Secondary outcomes included ICU mortality, ICU and hospital lengths of stay, and mechanical ventilation duration.ResultsA total of 8803 patients were admitted to the ICU with sepsis during the study period. 730 (8.3%) patients had ESRD. 49.04% of ESRD patients with sepsis died within their hospital stay vs. 31.78% of non-ESRD patients. ESRD septic patients had 1.44 greater odds of dying within their hospital stay as compared to septic non-ESRD patients (OR 1.44, 95% CI 1.03–1.53). Finally, the predictors of hospital mortality in septic ESRD patients were found to be mechanical ventilation (OR 3.36; 95% CI 2.27–5.00), a history of chronic liver disease (OR 2.26; 95% CI 1.26–4.07), and use of vasopressors (OR 1.74; 95% CI 1.19–2.54). Among patients with ESRD, hospital mortality was higher in subgroups of patients with chronic cardiac (OR 1.86 (1.36–2.53) vs. 1.19 (0.96–1.47)) and chronic respiratory illnesses (OR 2.20 (1.52–3.20) vs. 1.21 (0.99–1.48)).ConclusionESRD patients admitted to the intensive care unit with sepsis are at greater odds of mortality compared to patients with non-ESRD. This risk is particularly increased if these patients have a concomitant history of chronic cardiac and respiratory illnesses.

Key Messages

  • Sepsis and bacterial infections are very common in ESRD patients and following cardiovascular disease; sepsis is the second leading cause of death in patients with ESRD.
  • This study aims to examine the outcome of patients with end-stage renal disease (ESRD) patients admitted with sepsis to the intensive care unit (ICU).
  • The results of this study have shown that end-stage renal disease is associated with greater odds of ICU and hospital mortality among septic patients admitted to an intensive care unit.
  • ESRD patients were also more likely to be started on vasopressors and mechanical ventilation.
  相似文献   
23.
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   
24.
Cross-clamping of aorta is routinely performed in cardiac surgery. The objective of this study was to simulate cross-clamping of the aorta to elucidate the perturbation of stresses in the wall (solid mechanics) and lumen of the vessel (fluid mechanics). Models of the aorta and clamp were created in Computer Assisted Design and Finite Element Analysis packages. The vessel wall was considered as a non-linear anisotropic material while the fluid was simulated as Newtonian with pulsatile flow. The clamp was applied to produce total occlusion in approximately 1 s. A cylindrical and rectangular geometry for the clamp were considered. High jet speed and flow reversal were demonstrated during clamping. It was found that the clamp design and vessel wall anisotropy affected both the fluid wall shear stress (WSS) and solid stresses in vessel wall. The maximum wall stresses increased by about 170 and 220% during closure in the cases of plate and cylindrical clamps, respectively. The plate clamp design was superior for reduction of both solid stresses as well as fluid shear stresses. The cylindrical clamp causes much larger stresses than the plate clamp in each of the stress components; e.g., radial compression of −180 vs. −50 kPa. Vibrations, flow and WSS oscillations were detected immediately before total vessel occlusion. The present findings provide valuable insights into the mode of tissue injury during clamping and may also be useful for improving surgical clamp designs.  相似文献   
25.
Oxidative protein modification involving carbonylation has recently been identified as an important factor in skeletal muscle dysfunction in patients with chronic obstructive pulmonary disease (COPD). However, the exact identity of modified proteins inside limb muscles of patients with COPD remains unknown. We used 2D electrophoresis, immunoblotting, and mass spectrometry to identify carbonylated proteins in the vastus lateralis muscle of 12 patients with COPD and 6 control subjects. Both creatine kinase (CK) and carbonic anhydrase III (CAIII) were identified as being strongly carbonylated in this muscle in both groups of subjects. Total CK activity, CK protein expression, and the intensity of CK carbonylation were significantly greater in the muscles of patients with COPD as compared with control subjects, whereas CAIII protein expression and intensity of carbonylation were similar in the two groups. In patients with COPD, CK activity and protein expression correlated positively with FEV(1) and V O(2)max, whereas the intensity of CK carbonylation correlated negatively with the same parameters. These results indicate that oxygen radicals selectively target CK and CAIII inside limb muscles of humans. The observation that the intensity of CK carbonylation correlates negatively with CK activity in limb muscles of patients with COPD suggests that carbonylation may have a deleterious effect on CK activity, and may contribute to impaired CK function in the limb muscles of these patients.  相似文献   
26.
Immunogenicity and safety of ACWY-TT compared with licensed ACWY polysaccharide vaccine (MenPS) in healthy adults, and lot-to-lot consistency of three ACWY-TT lots were evaluated in a phase 3, open, controlled study. Adults aged 18-55 y were randomized to receive ACWY-TT (one of three lots) or MenPS. Serum bactericidal antibodies (rSBA) were measured pre- and 1 mo post-vaccination. Adverse events (AEs) were assessed 4 d (solicited symptoms) and 31 d (unsolicited symptoms) post-vaccination. Serious AEs were reported up to 6 mo after vaccination. The number of vaccinated subjects was 1247 (ACWY-TT, n = 935; MenPS, n = 312). ACWY-TT lot-to-lot consistency and non-inferiority of ACWY-TT as compared with MenPS groups were demonstrated according to pre-specified criteria. The percentages of subjects with a vaccine response (VR = rSBA titer ≥ 1:32 in initially seronegative; ≥ 4-fold increase in initially seropositive) to ACWY-TT vs. MenPS were 80.1%/69.8% (serogroup A), 91.5%/ 92.0% (C), 90.2%/85.5% (W-135), 87.0%/78.8% (Y). Exploratory analyses showed that for serogroups A, W-135 and Y, VR rates and GMTs were significantly higher for ACWY-TT compared with MenPS. For each serogroup, ≥ 98.0% of subjects had rSBA titers ≥ 1:128. Grade 3 solicited AEs were reported in ≤ 1.6% of subjects in any group. The immunogenicity of ACWY-TT vaccine was non-inferior to MenPS for all four serogroups in adults, with significantly higher VR rates to serogroups A, W-135 and Y and an acceptable safety profile. Consistency of 3 ACWY-TT production lots was demonstrated. These data suggest that, if licensed, ACWY-TT conjugate vaccine may be used for protection against invasive meningococcal disease in healthy adults. This study is registered at clinicaltrials.gov NCT00453986.  相似文献   
27.
28.
Embryonic stem cells have the capacity to differentiate into a wide range of cell types. We previously described that blastocyst injection of wild type (WT) embryonic stem cells (ESCs) into various knockout (KO) mouse models of human disease prevents disease from occurring. In this study we ask if the blastocyst approach can also correct defects in a mouse model of transgenic (Tg) overexpression of a pro-apoptotic factor. We injected ROSA26 (LacZ-marked) WT ESCs into human mammalian sterile 20 like-kinase 1 (Mst1) Tg blastocysts. Mst1 Tg mice overexpress Mst1, a pro-apoptotic factor, in a cardiac-specific manner. As a result, Mst1 Tg mice develop adult dilated cardiomyopathy driven by apoptosis, reduction in cell density and no hypertrophic compensation. Incorporation of WT ESCs generated WT/Mst1 chimeric mice with normal hearts at histological and functional levels. Accordingly, apoptosis and cell density parameters were normalized. The experiments suggest that an adult-onset cardiac myopathy induced by overexpression of the pro-apoptotic Mst1 can be reversed by developmental incorporation of WT ESCs. The findings also suggest that since forced expression of the Mst1 transgene is not abolished in the rescued chimeras, the WT ES-derived cells normalize pathways that lie downstream of Mst1. The results expand the therapeutic capability of the ESCs to mouse models that overproduce detrimental proteins.  相似文献   
29.
We sought to examine the role of genetics in the multifactorial disease, abdominal aortic aneurysm (AAA), by studying sequence variation in the BAK1 gene (BAK1) that codes for an apoptotic‐promoting protein, as chronic apoptosis activation has been linked to AAA development and progression. BAK1 abdominal aorta cDNA from AAA patients and nondiseased individuals were compared with each other, as well as to the BAK1 genomic sequence obtained from matching blood samples. We found specific BAK1 single nucleotide polymorphism (SNP) containing alleles in both aneurysmic (31 cases) and healthy aortic tissue (5 cases) without seeing them in the matching blood samples. These same BAK1 SNPs have been reported, although rarely (average frequency <0.06%), in reference BAK1 DNA sequences. Based on this and other similar observations, we propose a novel hypothesis postulating that multiple variants of genes may preexist in “minority” forms within specific nondiseased tissues and be selected for, when intra‐ and/or extracellular conditions change. Therefore, the fact that different BAK1 variants can exist in both diseased and nondiseased AA tissues compared to matching blood samples, together with the rare occurrence of these same SNPs in reference sequences, suggests that selection may be a significant factor in AAA ontogeny. Hum Mutat 30:1–5, 2009. © 2009 Wiley‐Liss, Inc.  相似文献   
30.
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