Malnutrition in critically ill children: from admission to 6 months after discharge

BACKGROUND & AIMS: Little is known about the nutritional status of critically ill children during hospitalisation in and after discharge from an intensive care unit. We set up a prospective, observational study to evaluate the nutritional status of children in an intensive care unit from admission up to 6 months after discharge. A secondary aim was identifying patient characteristics that influence the course of the various anthropometric parameters. METHODS: The nutritional status of 293 children--104 preterm neonates, 96 term neonates and 93 older children--admitted to our multidisciplinary tertiary pediatric and neonatal intensive care unit was evaluated by anthropometry upon and during admission, at discharge and 6 weeks and 6 months following discharge. RESULTS: Upon admission, 24% of all children appeared to be undernourished. Preterm and term neonates, but not older children, showed a decline in nutritional status during admission. At 6 months after discharge almost all children showed complete recovery of nutritional status. Length of stay and history of disease were the parameters that most adversely affected the nutritional status of preterm and term neonates at discharge and during follow-up. CONCLUSION: While malnutrition is a major problem in pediatric intensive care units, most children have good long-term outcome in terms of nutritional status after discharge.     

The spatial extent of contaminants and the landscape scale: an analysis of the wildlife, conservation biology, and population modeling literature

Many contaminant releases to the terrestrial environment are of small areal extent. Thus, rather than evaluating the ecological impact on species in the immediate vicinity of the release, it may be more ecologically meaningful to determine if population impacts occur at the landscape level. In order to do this, the cumulative impact of all releases in the landscape under consideration must be evaluated. If the release sites are viewed as localized areas that are no longer available for use by ecological receptors (i.e., no longer part of the habitat), this can be thought of as a form of habitat fragmentation. Habitat fragmentation is typically viewed as the loss of large areas of habitat within a landscape, leaving small isolated patches of intact habitat within a hostile matrix. Small-scale contaminant releases, on the other hand, result in small uninhabitable areas within a primarily intact habitat. With this consideration in mind, we analyzed the wildlife and conservation biology literature to determine if information on habitat size requirements such as home-range or critical patch size could inform us about the potential for impact at the landscape level from release sites based on the size of the release alone. We determined that evaluating the impact of release size had to be conducted within a contextual basis (considering the existing state of the landscape). Therefore, we also reviewed the population modeling literature to determine if models could be developed to further evaluate the impact of the spatial extent of chemical releases on the landscape. We identified individual-based models linked to geographic information systems to have the greatest potential in investigating the role of release size with respect to population impacts at the landscape level.     

Errors in search strategies were identified by type and frequency

OBJECTIVE: Errors in the electronic search strategy of a systematic review may undermine the integrity of the evidence base used in the review. We studied the frequency and types of errors in reviews published by the Cochrane Collaboration. STUDY DESIGN AND SETTING: Data sources were MEDLINE searches from reviews in the Cochrane Library, Issue 3, 2002. To be eligible, systematic reviews must have been of randomized or quasi-randomized controlled trials, reported included and excluded studies, and used one or more sections of the Cochrane Collaboration's Highly Sensitive Search Strategy. MEDLINE search strategies not reported in enough detail to be assessed or that were duplicates of a search strategy already assessed for the study were excluded. Two librarians assessed eligibility and scored the eligible electronic search strategies for 11 possible errors. Dual review with consensus was used. RESULTS: Of 105 MEDLINE search strategies examined, 63 were assessed; 31 were excluded because they were inadequately reported, and 11 were duplicates of assessed search strategies. Most (90.5%) of the assessed search strategies contained > or =1 errors (median 2, interquartile range [IQR] 1.0-3.0). Errors that could potentially lower recall of relevant studies were found in 82.5% (median 1, IQR 1.0-2.0) and inconsequential errors (to the evidence base) were found in 60.3% (median 1, IQR 0.0-1.0) of the search strategies. The most common search errors were missed MeSH terms (44.4%), unwarranted explosion of MeSH terms (38.1%), and irrelevant MeSH or free text terms (28.6%). Missed spelling variants, combining MeSH and free text terms in the same line, and failure to tailor the search strategy for other databases occurred with equal frequency (20.6%). Logical operator error occurred in 19.0% of searches. CONCLUSION: When the MEDLINE search strategy used in a systematic review is reported in enough detail to allow assessment, errors are commonly revealed. Additional peer review steps are needed to ensure search quality and freedom from errors.     

Effects of cyclooxygenase-2 (COX-2) inhibition on plasma and renal renin in diabetes

COX-2-derived prostaglandins (PG) have been suggested to be important modulators of renin release and expression. However, the role of COX-2 in various high-renin states is still being debated. In the present studies we explored the role of COX-2-derived PG on basal and angiotensin converting enzyme inhibitor (ACEI)-stimulated plasma and renal renin concentrations (PRC and RRC, RIA), and mRNA expression (RmRNA, RNAse protection assay) in experimental diabetes (DM). Groups of moderately hyperglycemic (n = 5, approximately 350 mg/dl), streptozotocin-diabetic rats (D) after 3 weeks of DM were treated with a selective COX-2 inhibitor, MF-tricyclic (MF, 5 mg/kg/day for 10 days in food), the combination of MF and the ACEI enalapril (3 mg/kg/day), enalapril alone, or vehicle (MF-free chow), for 10 days. Non-diabetic control rats, fed MF-free chow, were also studied. All groups of diabetic rats demonstrated similar glycemic control. Treatment with ACEI resulted in significant elevations in PRC, RRC and RmRNA as compared to non-ACEI treated groups of diabetic and control rats. A similar rise in these parameters was observed in the rats treated with the combination of ACEI and MF. Furthermore, in diabetic rats treated with MF alone, PRC and RRC were similar to vehicle-treated animals. Diabetic rats demonstrated higher urinary PG as compared to controls. MF-treated rats demonstrated a significant reduction in urinary PG excretion. In summary, selective COX-2 inhibition influenced neither basal renin status nor ACEI-induced renin release and expression in diabetic rats. These findings do not support a significant role for COX-2 in mediating renin status in diabetes.     

Relationship of medial arterial calcinosis to autonomic neuropathy and adverse outcomes in a diabetic veteran population

STATEMENT OF THE PROBLEM: Medial arterial calcinosis (MAC) is associated with neuropathy, amputation, and mortality through an unknown mechanism. We hypothesized that MAC was a marker of autonomic neuropathy rather than a risk factor and that the outcomes were due to autonomic neuropathy. METHODS: All subjects in an ongoing prospective study of diabetic foot conditions in a diabetic veteran cohort who received a foot radiograph between 11/7/90 and 11/5/93 were included. Autonomic neuropathy measured as either heart rate variability with timed respiration or postural hypotension. A logistic model predicted the presence of MAC at baseline and Cox proportional models assessed the relative contribution of autonomic neuropathy and traditional risk factors for the outcomes of ulceration, amputation, and death. RESULTS: MAC was identified in 181 subjects, no MAC in 253 subjects, and 39 were excluded due to disagreement between observers. Both measures of autonomic neuropathy were independent predictors of MAC at baseline, even after adjustment for vibration sensation loss in a logistic model. MAC was associated with an increased risk for ulceration (hazards ratio, HR: 2.1, 95% confidence intervals, CI, 1.4-3.1), amputation (HR 3.3, 95% CI 1.5-7.4), and mortality (HR 1.6, 95% CI 1.1-2.2). The addition of either autonomic measure of neuropathy did not change the MAC HR or significantly improved the fit of the model. CONCLUSIONS: Our hypothesis that the excess mortality, amputation, and ulceration in persons with MAC could be explained by autonomic neuropathy measured as postural hypotension or heart rate variability with measured respiration was not supported.     

Response of plasma matrix metalloproteinase-9 to conventional abdominal aortic aneurysm repair or endovascular exclusion: implications for endoleak

PURPOSE: Matrix metalloproteinases are enzymes capable of breaking down all of the components of the extracellular matrix and have been implicated in the development of aneurysm formation. Because matrix metalloproteinase-9 (MMP-9) levels are elevated in aortic aneurysmal tissue and in that patient plasma, we hypothesized that plasma MMP-9 levels should decrease significantly after conventional and endovascular infrarenal abdominal aortic aneurysm (AAA) repair but that plasma MMP-9 levels would remain elevated in patients with endoleaks. METHODS: A sandwich enzyme-linked immunosorbent assay was used to measure plasma levels of MMP-9 in patients with AAA who underwent conventional (n = 26; mean age, 71.5 years) and endovascular (n = 25; mean age, 76.4 years) AAA repair. Levels were drawn before surgery and at 1 month and 3 months after surgery. Eight patients for endovascular repair had endoleaks identified on postoperative computed axial tomographic scans. RESULTS: No correlation existed between preoperative plasma MMP-9 levels when compared with age, gender, or aneurysm diameter. No significant difference in preoperative plasma MMP-9 levels or AAA diameter was identified between patients with conventional repair compared with endovascular repair. Of the 51 patients, 33 had follow-up samples available for analysis. A significant increase in mean plasma MMP-9 levels was noted 1 month (149.5 +/- 40.1 ng/mL) after conventional AAA repair compared with preoperative levels (83.9 +/- 26.1 ng/mL; P <.05) and remained elevated 3 months after surgery (129.8 +/- 56.6 ng/mL). In those patients who underwent endovascular aneurysm exclusion without endoleak, a significant decrease in mean plasma MMP-9 levels was noted at 3 months (27.4 +/- 5.2 ng/mL) when compared with preoperative values (60.8 +/- 8.8 ng/mL; P <.01). In contrast, patients with endoleak after endovascular exclusion did not have a significant decrease in plasma MMP-9 levels at 3 months. CONCLUSION: Plasma MMP-9 levels remain elevated for as much as 3 months after conventional AAA repair, whereas successful endovascular exclusion of an AAA results in decreased plasma MMP-9 levels by 3 months. MMP-9 may have clinical value as an enzymatic marker for endoleak after endovascular AAA exclusion.     

应用GINI检出微卫星不稳定型大肠癌中新的突变基因

目的 应用GINI筛选微卫星不稳定型大肠癌中新的突变基因.方法 采用NMD抑制药物emetine(依米丁)联合actmomycin D(放线菌素D),分别处理高度微卫星不稳定型(MSI-H)大肠癌细胞株HCT116和微卫星稳定(MSS)的大肠癌细胞株HT29,以及对照的MSS乳腺癌细胞株,以全基因组cDNA芯片检测经药物处理和不经药物处理的细胞株的mRNA表达变化.经过芯片数据分析筛选在HCT116细胞中mRNA表达量特异性升高的基因,以DNA直接测序法检测突变,并在22个大肠癌细胞株及30例原发癌组织中验证.结果 在MSI-H大肠癌细胞株HCT116中筛选出新的突变基因ARV1和ZNF294,并在8个MSI-H细胞株中验证其突变率分别为37.5%和87.5%,在20例MSI-H原发大肠癌组织中突变率均为35%.结论 基于NMD抑制的新的基因筛选方法GINI,能够相对快速、有效的检出发生突变的基因.