BACKGROUND & AIMS: OBJECTIVE:There has been an exponentially increasing interest in intraabdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) over the last decade, and different definitions have been suggested. Nevertheless, there has been an impetus from experts in the field to modify these definitions to reflect our current understanding of the pathophysiology of these syndromes. An international multidisciplinary group of interested doctors met with the goal of agreeing on a set of definitions that could be applied to patients with IAH and ACS. The goal of this consensus group was to provide a conceptual and practical framework to further define ACS, a progressive injurious process that falls under the generalized term 'IAH' and that includes IAH-associated organ dysfunction. DESIGN:In total, 21 North American, Australasian and European surgical, trauma and critical care specialists agreed to standardize the current definitions for IAH, ACS and related conditions in preparation for the second World Congress on Abdominal Compartment Syndrome (WCACS). The WCACS-meeting was endorsed by the European Society of Intensive Care Medicine (ESICM) and the World Society on Abdominal Compartment Syndrome (WSACS). METHODS:The consensus conference (Noosa, Australia; December 7, 2004) was attended by 21 specialists from Europe, Australasia and North America and approximately 70 other congress participants. In advance of the conference, a blueprint for the various definitions was suggested. After the conference the participants corresponded electronically with feedback. A writing committee was formed at the conference and developed the final manuscript based on executive summary documents generated by each participant. The final report of the 2004 International ACS Consensus Definitions Conference has recently been published. This article will describe the long road towards this final publication with the evolution of the different definitions and recommendations from the initial suggestions in 2004 to the further refinement and final publications in 2006 and 2007. It will try to explain how we got there and will also give the percentage of agreement with each proposed definition by the participants. RESULTS:New definitions were offered for some terms, while others were discarded and not kept in the final manuscript. Different cut-offs for defining IAH and ACS were given, as well as broad definitions of primary, secondary and recurrent IAH/ACS. A classification system was introduced taking into account the duration, origin, and etiology of IAH. The use of an organ severity scoring method, by means of the Sequential Organ Failure Assessment (SOFA) score when dealing with ACS patients was not recommended as an adjunctive tool to assess morbidity in the final publication. CONCLUSION:This document reflects a process whereby a group of experts and opinion leaders suggested definitions for IAH and ACS. This document should be used as a reference for the next consensus definitions conference in March 2007.

背景与目标：

BACKGROUND & AIMS: :Atherogenesis is a complex inflammatory process stemming from the accumulation and oxidation of low density lipoproteins (LDL). IgM autoantibodies against phosphorylcholine (anti-PC) bind to the PC epitope on oxidized LDL (OxLDL), inhibiting the uptake of oxLDL by macrophages in atherosclerotic lesions. Anti-PC autoantibodies have been reported to be protective against atherothrombosis. We investigated the relationship of anti-PC concentrations with cardiovascular outcomes in patients with acute coronary syndromes (ACS). We measured anti-PC levels within 7 days of an ACS in 3,356 patients enrolled in the ATLAS ACS-TIMI 46 trial, a randomized dose ranging study of rivaroxaban versus placebo. The primary endpoint was death, myocardial infarction (MI), stroke, or severe recurrent ischemia (SRI) requiring revascularization during 6 months. The median baseline anti-PC concentration was 40.9 U/mL (25th, 75th percentiles: 25.4, 67.4). There was no significant association between anti-PC levels and the primary endpoint (Q1: 6.8 %, Q2: 4.2 %, Q3: 7.8 %, Q4: 5.4 %, p-trend = 0.87), all-cause mortality (Q1: 1.4 %, Q2: 0.7 %, Q3: 2.4 %, Q4: 0.9 %, p-trend = 0. 96), or any of the other individual endpoint components (MI: p-trend = 0.87, Stroke: p-trend = 0.43, SRI: p-trend = 0.66). Using the previously reported anti-PC cutpoint of 17 U/mL did not reveal a significant relationship between anti-PC concentrations and cardiovascular outcomes (<17 U/mL: 8.1 % vs. ≥17 U/mL: 5.8 %; p = 0.11). Similarly, evaluation of anti-PC as a continuous variable did not reveal a significant association (p = 0.30). In this study of patients early after ACS undergoing intensive secondary preventive therapy, IgM anti-PC titers did not exhibit a significant relationship with cardiovascular outcomes.

背景与目标： : 动脉粥样硬化是一个复杂的炎症过程，源于低密度脂蛋白 (LDL) 的积累和氧化。针对磷酸胆碱的IgM自身抗体 (抗PC) 与氧化LDL (OxLDL) 上的PC表位结合，从而抑制动脉粥样硬化病变中巨噬细胞对oxLDL的摄取。据报道，抗PC自身抗体可预防动脉粥样硬化血栓形成。我们研究了急性冠脉综合征 (ACS) 患者抗PC浓度与心血管结局的关系。我们在参加ATLAS ACS-TIMI 46试验的3,356名患者中测量了ACS 7天内的抗PC水平，该试验是利伐沙班与安慰剂的随机剂量范围研究。主要终点是死亡，心肌梗死 (MI)，中风或需要在6个月内进行血运重建的严重复发性缺血 (SRI)。基线抗PC浓度中位数为40.9 U/mL (第25，75个百分位数: 25.4，67.4)。抗PC水平与主要终点 (Q1: 6.8%，Q2: 4.2%，Q3: 7.8%，Q4: 5.4%，p-趋势 = 0.87)，全因死亡率 (Q1: 1.4%，Q2: 0.7%，Q3: 2.4%，Q4: 0.9%，p-趋势 = 0.96)，或任何其他单独的终点分量 (MI: p-趋势 = 0.87，冲程: p-趋势 = 0.43，SRI: p-趋势 = 0.66)。使用先前报道的17 u/mL的抗PC切点未揭示抗PC浓度与心血管结局之间的显着关系 (<17 u/mL: 8.1% vs. ≥ 17 u/mL: 5.8%; p = 0.11)。类似地，作为连续变量的抗PC评价没有显示出显著的关联 (p = 0.30)。在这项研究中，ACS接受强化二级预防治疗后的早期患者，IgM抗PC滴度与心血管结局没有显着关系。

BACKGROUND & AIMS: BACKGROUND:The surgical care of patients with metastatic gastric cancer (GC) remains debated. Despite level 1 evidence showing lack of survival benefit, surgery may be used for symptoms prevention or palliation. This study examined short-term postoperative outcomes of non-curative gastrectomy performed for metastatic GC. METHODS:A multi-institutional retrospective cohort study was conducted using the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry, including gastrectomies for GC (2007-2015). The primary outcome was 30-day major morbidity. Multivariable analysis examined the association between metastatic status and outcomes adjusted for relevant demographic and clinical covariates. RESULTS:Of 5341 patients, 377 (7.1%) had metastases. Major morbidity was more common with metastases (29.4 vs. 19.6%; p < 0.001), driven by a higher rate of respiratory events. Prolonged hospital length of stay (beyond the 75th percentile: 11 days) was more likely with metastases than with no metastases (41.9 vs. 28.3%; p < 0.001). After adjustment, metastatic status was associated with major morbidity (odds ratio [OR], 1.49; 95% confidence interval [CI], 1.16-1.90). This association remained for respiratory events (OR, 1.58; 95% CI, 1.07-2.33), 30-day mortality (OR, 2.19; 95% CI, 1.38-3.48), and prolonged hospital stay (OR, 1.65; 95% CI, 1.31-2.07). CONCLUSION:Non-curative gastrectomy for metastatic GC was associated with significant major morbidity and mortality as well as a prolonged hospital stay, longer than expected for gastrectomy for non-metastatic GC. These data can inform decision making regarding non-curative gastrectomy, helping surgeons to weigh the risks of morbidity against the potential benefits and alternative therapeutic options.

背景与目标：

BACKGROUND & AIMS: AIMS:This randomized controlled trial (RCT) evaluated whether a process with single combined testing of copeptin and troponin at admission in patients with low-to-intermediate risk and suspected acute coronary syndrome (ACS) does not lead to a higher proportion of major adverse cardiac events (MACE) than the current standard process (non-inferiority design). METHODS AND RESULTS:A total of 902 patients were randomly assigned to either standard care or the copeptin group where patients with negative troponin and copeptin values at admission were eligible for discharge after final clinical assessment. The proportion of MACE (death, survived sudden cardiac death, acute myocardial infarction (AMI), re-hospitalization for ACS, acute unplanned percutaneous coronary intervention, coronary artery bypass grafting, or documented life threatening arrhythmias) was assessed after 30 days. Intention to treat analysis showed a MACE proportion of 5.17% [95% confidence intervals (CI) 3.30-7.65%; 23/445] in the standard group and 5.19% (95% CI 3.32-7.69%; 23/443) in the copeptin group. In the per protocol analysis, the MACE proportion was 5.34% (95% CI 3.38-7.97%) in the standard group, and 3.01% (95% CI 1.51-5.33%) in the copeptin group. These results were also corroborated by sensitivity analyses. In the copeptin group, discharged copeptin negative patients had an event rate of 0.6% (2/362). CONCLUSION:After clinical work-up and single combined testing of troponin and copeptin to rule-out AMI, early discharge of low- to intermediate risk patients with suspected ACS seems to be safe and has the potential to shorten length of stay in the ED. However, our results need to be confirmed in larger clinical trials or registries, before a clinical directive can be propagated.

背景与目标：

BACKGROUND & AIMS: AIM:The objective of this report was to present histological characteristics and gene expression profile of newly formed bone following horizontal augmentation of the atrophic anterior maxilla using recombinant human bone morphogenetic protein-2 in an absorbable collagen sponge carrier (rhBMP-2/ACS) versus an autogenous bone graft (ABG). METHODS:Bone core biopsies from 24 subjects participating in a randomized clinical trial were obtained at dental implant placement, 6 months following alveolar ridge augmentation using rhBMP-2/ACS (rhBMP-2 at 1.5 mg/ml; total dose 4.2 mg) or a particulate ABG harvested from the mandibular retro-molar region. A titanium mesh was used to provide wound stability and space for bone formation. Analysis included histological/histometric observations and gene expression profile of the newly formed bone. RESULTS:rhBMP-2/ACS yielded bone marrow rich in capillaries, undifferentiated cells and bone lining cells compared with the ABG (p = 0.002). Whereas no significant differences were observed in total bone fraction (p = 0.53), non-vital bone particles trapped in lamellar vital bone were observed in the ABG group (p < 0.001). Real-time PCR showed greater BMP-2 and RUNX2 expression for rhBMP-2/ACS over the ABG (p = 0.001 and 0.0021, respectively), while the ABG exhibited greater expression of RANKL:OPG, BSP and OPN over rhBMP-2/ACS (p = 0.01, 0.005 and 0.0009, respectively). CONCLUSIONS:Our observations suggest that formative biological processes explain bone formation following implantation of rhBMP-2/ACS, whereas remodelling, resorptive/formative processes, characterizes sites receiving ABGs.

背景与目标：

BACKGROUND & AIMS: :The vocational reintegration of patients after an acute coronary syndrome is a crucial step towards complete convalescence from the social as well as the individual point of view. Return to work rates are determined by medical parameters such as left ventricular function, residual ischaemia and heart rhythm stability, as well as by occupational requirement profile such as blue or white collar work, night shifts and the ability to commute (which is, in part, determined by physical fitness). Psychosocial factors including depression, self-perceived health situation and pre-existing cognitive impairment determine the reintegration rate to a significant extent. Patients at risk of poor vocational outcomes should be identified in the early period of rehabilitation to avoid a reintegration failure and to prevent socio-professional exclusion with adverse psychological and financial consequences. A comprehensive healthcare pathway of acute coronary syndrome patients is initiated by cardiac rehabilitation, which includes specific algorithms and assessment tools for risk stratification and occupational restitution. As the first in its kind, this review addresses determinants and legal aspects of reintegration of patients experiencing an acute coronary syndrome, and offers practical advice on reintegration strategies particularly for vulnerable patients. It presents different approaches and scientific findings in the European countries and serves as a recommendation for action.

背景与目标： : 从社会和个人的角度来看，急性冠状动脉综合征后患者的职业重返社会是迈向完全康复的关键一步。工作回报率取决于医学参数，例如左心室功能，残余缺血和心律稳定性，以及职业需求状况，例如蓝领或白领工作，夜班和通勤能力 (部分取决于身体健康)。心理社会因素，包括抑郁，自我感知的健康状况和先前存在的认知障碍，在很大程度上决定了重返社会的速度。应在康复的早期确定有不良职业结局风险的患者，以避免重返社会失败，并防止社会职业排斥带来不良的心理和经济后果。心脏康复启动了急性冠状动脉综合征患者的全面医疗保健途径，其中包括用于风险分层和职业恢复的特定算法和评估工具。作为同类产品中的第一篇，本综述探讨了患有急性冠状动脉综合征的患者重返社会的决定因素和法律方面，并提供了有关重返社会策略的实用建议，尤其是针对弱势患者。它提出了欧洲国家的不同方法和科学发现，并作为行动建议。

BACKGROUND & AIMS: :Intestinal occlusion is defined as an independent predictive factor of intra-abdominal hypertension (IAH) which represents an independent predictor of mortality. Baggot in 1951 classified patients operated with intestinal occlusion as being at risk for IAH ("abdominal blow-out"), recommending them for open abdomen surgery proposed by Ogilvie. Abdominal surgery provokes IAH in 44.7% of cases with mortality which, in emergency, triples with respect to elective surgery (21.9% vs 6.8%). In particular, IAH is present in 61.2% of ileus and bowel distension and is responsible for 52% of mortality (54.8% in cases with intra-abdominal infection). These patients present with an increasing intra-abdominal pressure (IAP) which, over 20-25 mmHg, triggers an Abdominal Compartment Syndrome (ACS) with altered functions in some organs arriving at Multiple Organ Dysfunction Syndrome (MODS). The intestine normally covers 58% of abdominal volume but when there is ileus distension, intestinal pneumatosis develops (third space) which can occupy up to 90% of the entire cavity. At this moment, Gastro Intestinal Failure (GIF) can appear, which is a specific independent risk factor of mortality, motor of "Organ Failure". The pathophysiological evolution has many factors in 45% of cases: intestinal pneumatosis is associated with mucosal and serous edema, capillary leakage with an increase in extra-cellular volume and peritoneal fluid collections (fourth space). The successive loss of the mucous barrier permits a bacterial translocation which includes bacteria, toxins, pro-inflammatory factors and oxygen free radicals facilitating the passage from an intra-abdominal to inter-systemic vicious cyrcle. IAH provokes the raising of the diaphragm, and vascular and visceral compressions which induce hypertension in the various spaces with compartmental characteristics. These trigger hypertension in the renal, hepatic, pelvic, thoracic, cardiac, intracranial, orbital and lower extremity areas, giving a critical clinical condition of Polycompartment Syndrome. The monitoring of Abdominal Perfusion Pressure (APP) is more correct than the measurement of IAP because it reveals hydrodynamic alterations in the abdominal compartment. The APP (MAP-IAP) depends on arterial flow, venous outflow and capacity of the abdominal compartments response to increased internal volumes. The medical therapy used to decrease IAH and to contrast ACS is intestinal decompression with gastric and rectal tube; colonic endoscopic detention; correction of electrolytic abnormalities and prokinetic agents. Surgery, besides being decompressive and resolutive, must prevent a recurrence of ACS through the "tension-free closure" procedure.

背景与目标： : 肠阻塞被定义为腹内高血压 (IAH) 的独立预测因素，代表死亡率的独立预测因素。Baggot 1951年将肠闭塞手术的患者归类为有IAH (“腹部爆裂”) 风险的患者，建议他们进行Ogilvie提议的开腹手术。腹部手术在44.7% 病例中引起IAH死亡，在紧急情况下，与择期手术相比增加了两倍 (21.9% 比6.8%)。特别是，IAH存在于肠梗阻和肠扩张的61.2% 中，并且负责死亡率的52% (54.8% 在腹腔感染的情况下)。这些患者的腹内压力 (IAP) 增加，超过20-25 mmHg，会触发腹腔室综合征 (ACS)，某些器官的功能改变会导致多器官功能障碍综合征 (MODS)。肠道通常覆盖58% 的腹腔容积，但当有肠梗阻扩张时，会出现肠内积气 (第三空间)，其可以占据整个腔的90%。此时，可以出现胃肠道功能衰竭 (GIF)，这是死亡率，运动性 “器官衰竭” 的特定独立危险因素。在45% 情况下，病理生理演变有许多因素: 肠积气与粘膜和浆液性水肿，毛细血管渗漏与细胞外体积增加和腹膜积液 (第四间隙) 有关。粘液屏障的连续丢失允许细菌易位，其中包括细菌，毒素，促炎因子和氧自由基，从而促进了从腹腔内到全身恶性循环的通过。IAH会引起diaphragm肌的升高，以及血管和内脏的压迫，从而在具有隔室特征的各个空间中诱发高血压。这些会触发肾脏，肝脏，盆腔，胸腔，心脏，颅内，眼眶和下肢区域的高血压，从而导致多室综合征的严重临床状况。腹部灌注压 (APP) 的监测比IAP的测量更正确，因为它揭示了腹腔室的水动力变化。APP (MAP-IAP) 取决于动脉流量，静脉流出和腹部隔室对内部容积增加的反应。用于减少IAH和对比ACS的药物疗法是用胃和直肠管进行肠减压; 结肠内窥镜滞留; 纠正电解异常和促动力剂。手术除了减压和缓解外，还必须通过 “无张力闭合” 程序防止ACS复发。

BACKGROUND & AIMS: BACKGROUND:Many trials have shown that 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors reduce the incidence of cardiovascular events and mortality. One method of decreasing the incidence of cardiovascular events could be to reduce the progression of coronary atherosclerosis, and a recent study found that atorvastatin can cause coronary plaque to regress. To generalize this finding, using conventional HMG-CoA reductase inhibitors at many Japanese centers, randomized trials of pitavastatin and atorvastatin will be conducted with patients with acute coronary syndrome (ACS). METHODS AND RESULTS:Patients with ACS who have undergone successful percutaneous coronary intervention under intravascular ultrasound guidance will be studied. They will be randomly allocated to pitavastatin or atorvastatin groups and followed up for 8-12 months. The primary endpoint will be the percent change in coronary plaque volume, and secondary endpoints will include absolute changes in coronary plaque volume, serum lipid levels and inflammatory markers. The safety profile will also be evaluated. CONCLUSIONS:This study will examine the ability of HMG-CoA reductase inhibitors to regress coronary plaque in Japanese patients with ACS and the findings should help to improve the prognosis of such patients and clarify the involved mechanisms.

背景与目标：

BACKGROUND & AIMS: BACKGROUND/OBJECTIVES:The prognostic difference between STEMI and NSTE-ACS after coronary stent placement remains unclear. We aimed to compare the short- and long-term event rates in patients presenting with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation acute coronary syndrome (NSTE-ACS) after percutaneous coronary intervention (PCI) with either bare-metal stents (BMS) or drug-eluting stents (DES). METHODS:Between 2000 and 2005 a total of 1749 STEMI and 1921 NSTE-ACS patients received either a BMS or DES in consecutive real world cohorts. Descriptive statistics and multivariate survival analyses were applied to compare the event rates in STEMI and NSTE-ACS during 4 years follow-up. RESULTS:NSTE-ACS patients had significantly higher clinical and angiographic risk profiles at baseline and were treated with less optimal medical therapy during follow-up. At 4 years follow-up, all-cause mortality was significantly higher in STEMI compared to NSTE-ACS after coronary stent placement (17.4% vs. 14.3%; HR 1.60, 95% CI 1.24-2.07). In a landmark analysis no difference was seen in all-cause mortality among STEMI en NSTE-ACS between 1 month and 4 years follow-up (HR 1.10, 95% CI 0.81-1.51). Cardiac death was more prevalent in STEMI patients, while the 4-year cumulative incidences of any myocardial infarction, any coronary revascularization, target lesion revascularization and definite stent thrombosis were similar in both ACS groups. CONCLUSIONS:Patients presenting with STEMI have a worse long-term prognosis compared to NSTE-ACS after coronary stent placement, due to higher short-term death rates. However, after the first month STEMI and NSTE-ACS patients have a comparable long-term survival.

背景与目标：

BACKGROUND & AIMS: BACKGROUND:Glycoprotein IIb/IIIa blockers reduce procedure-related thrombotic complications of percutaneous coronary intervention, and the risk of death and myocardial infarction in patients with acute coronary syndromes. The effect on risk of death and myocardial infarction is particularly apparent in patients undergoing early percutaneous coronary interventions. We did a randomised, multicentre trial to study the effect of the glycoprotein IIb/IIIa blocker abciximab on patients with acute coronary syndromes who were not undergoing early revascularisation. METHODS:We enrolled 7800 patients who were admitted to hospital with chest pain and either ST-segment depression or raised troponin T or I concentrations. 2598 were randomly assigned placebo, 2590 an abciximab bolus and 24 h infusion, and 2612 an abciximab bolus and 48 h infusion; all patients received aspirin and either unfractionated or low-molecular-weight heparin. The primary endpoint was death or myocardial infarction at 30 days after randomisation. Analysis was by intention to treat. FINDINGS:There were no drop-outs. 209 (8.0%) patients on placebo, 212 (8.2%) on 24 h abciximab, and 238 (9.1%) on 48 h abciximab died or had a myocardial infarction before day 30 (odds ratio 1.0 [95% CI 0.83-1.24], for difference between placebo and 24 h abciximab, and 1.1 [0.94-1.39] for difference between placebo and 48 h abciximab). The lack of benefit from treatment with abciximab was consistent in most subgroups investigated; in particular, no benefit was seen in patients with raised cardiac troponin T or I concentrations at enrolment, although these patients did have a strongly increased risk of subsequent events. Bleeding rates were low, but increased with abciximab, particularly when continued for 48 h. Additionally, thrombocytopenia was more frequent with abciximab than with placebo. INTERPRETATIONS:Although the explanations for our findings are unclear, this study indicates that abciximab is not beneficial as first-line medical treatment in patients admitted with acute coronary syndromes.

背景与目标：

BACKGROUND & AIMS: STUDY OBJECTIVE:Point-of-care testing reduces time to cardiac marker results in patients evaluated for acute coronary syndromes, yet evidence this translates to a decreased length of stay is lacking. We hypothesized that point-of-care testing decreases length of stay in patients being evaluated for acute coronary syndromes in the emergency department (ED). METHODS:Patients being evaluated for possible acute coronary syndromes at 4 EDs in the United States were randomized to having point-of-care markers as well as central laboratory markers, or central laboratory markers only (laboratory arm). Point-of-care markers were obtained using early serial testing at presentation and at 90, 180, and 360 minutes as required by the treating physician. Evaluation, treatment, and disposition decisions were at the treating physician's discretion. Length of stay was from presentation to the time of departure from the ED, either to an inpatient setting or to home. RESULTS:There were 1,000 patients in each study arm. There were 520 patients discharged home from the ED. Median (interquartile range) time to discharge home was 4.6 hours (3.5 to 6.1 hours) in laboratory patients and 4.5 hours (3.5 to 6.1 hours) in point-of-care patients. Median (interquartile range) time to transfer to an inpatient setting for admitted patients was 5.5 hours (4.2 to 7.5 hours) in laboratory patients, and 5.4 hours (4.1 to 7.3 hours) in point-of-care patients. At one site, time to transfer to the floor was reduced in the point-of-care arm compared with the laboratory arm (difference in medians 0.45 hours; 95% confidence interval [CI] -0.14 to 1.04 hours). At one site, time to ED departure for discharged patients was higher in the point-of-care arm than the laboratory arm (difference in medians 1.25 hours; 95% CI 0.13 to 2.36 hours). CONCLUSION:The effect of point-of-care testing on length of stay in the ED varies between settings. At one site, point-of-care testing decreased time to admission, whereas at another, point-of-care testing increased time to discharge. Potential effects of point-of-care testing on patient throughput should be considered in the full context of ED operations.

背景与目标：

BACKGROUND & AIMS: BACKGROUND:The benefits of laparoscopic (LC) versus open (OC) colectomy for symptomatic colonic diverticulosis as an elective operation remain unclear. METHODS:Using the American College of Surgeons-National Surgical Quality Improvement Project (ACS-NSQIP) participant-user file, patients were identified who underwent elective colon resection for symptomatic colonic diverticulosis, between 2005 and 2008. Demographic, clinical, intraoperative variables, and 30-day morbidity and mortality were collected. Logistic regression analysis was performed to determine the association between the surgical approach (LC vs. OC) and risk-adjusted overall mortality, overall morbidity, serious morbidity, and wound complications. RESULTS:A total of 7,629 patients were identified who underwent colon resection for symptomatic diverticulosis. They were subdivided into two groups: OC (3,870 (50.7%)) and LC (3,759 (49.3%)). Patients who underwent OC were significantly older (59.0 vs. 55.7 years, P < 0.0001) with more comorbidities compared with those who underwent LC. After risk-adjusted analysis, it was noted that the patients treated with LC were significantly less likely to experience overall morbidity (11.9% vs. 23.2%), serious morbidity (4.6% vs. 10.9%), and wound complications (9.1% vs. 17.5%), but not mortality (0.3% vs. 0.8%). Operative duration was significantly longer with LC (176.64 vs. 166.70 min, P < 0.0001), but the length of stay was significantly shorter (4.77 vs. 7.68 days, P < 0.0001). Using logistic regression analysis, patients with history of peripheral vascular disease, percutaneous coronary interventions, current steroid use, and hypertension requiring medication were at an increased risk of morbidity and mortality at 30 days. Patients with history of chronic obstructive pulmonary disease and smoking experienced more wound complications at 30 days. CONCLUSIONS:In the elective setting for symptomatic diverticulosis, LC seems to be associated with lower 30-day morbidity and complication rates compared with OC.

背景与目标：

BACKGROUND & AIMS: :The Arabidopsis ethylene-overproducing mutants eto1, eto2, and eto3 have been suggested to affect the post-transcriptional regulation of 1-aminocyclopropane-1-carboxylic acid synthase (ACS). Here, we present the positional cloning of the gene corresponding to the dominant eto3 mutation and show that the eto3 phenotype is the result of a missense mutation within the C-terminal domain of ACS9, which encodes one isoform of the Arabidopsis ACS gene family. This mutation is analogous to the dominant eto2 mutation that affects the C-terminal domain of the highly similar ACS5. Analysis of purified recombinant ACS5 and epitope-tagged ACS5 in transgenic Arabidopsis revealed that eto2 does not increase the specific activity of the enzyme either in vitro or in vivo; rather, it increases the half-life of the protein. In a similar manner, cytokinin treatment increased the stability of ACS5 by a mechanism that is at least partially independent of the eto2 mutation. The eto1 mutation was found to act by increasing the function of ACS5 by stabilizing this protein. These results suggest that an important mechanism by which ethylene biosynthesis is controlled is the regulation of the stability of ACS, mediated at least in part through the C-terminal domain.

背景与目标： : 已建议拟南芥乙烯过量生产突变体eto1，eto2和eto3影响1-氨基环丙烷-1-羧酸合酶 (ACS) 的转录后调控。在这里，我们介绍了与显性eto3突变相对应的基因的位置克隆，并表明eto3表型是ACS9 C末端域内错义突变的结果，该突变编码拟南芥ACS基因家族的一个同工型。该突变类似于影响高度相似acs5的C末端结构域的显性eto2突变。对转基因拟南芥中纯化的重组ACS5和表位标记的ACS5的分析表明，eto2在体外或体内均不增加酶的比活性; 相反，它增加了蛋白质的半衰期。以类似的方式，细胞分裂素治疗通过至少部分独立于eto2突变的机制增加了ACS5的稳定性。发现eto1突变通过稳定该蛋白来增强ACS5的功能而起作用。这些结果表明，控制乙烯生物合成的重要机制是调节ACS的稳定性，至少部分通过C末端结构域介导。

BACKGROUND & AIMS: :Low-density lipoprotein-cholesterol (LDL-C) is a well-accepted causal risk factor for athero-thrombotic cardiovascular disease, as demonstrated in large epidemiological studies, including Mendelian randomization data. Several randomized controlled trials and meta-analyzes have shown that lipid lowering therapies, such as statins and more recently the non-statin agents ezetimibe and Proprotein Convertase Subtilisin Kexin type 9 (PCSK9) monoclonal antibodies (mAb), reduce cardiovascular events across a broad range of baseline LDL-C levels. Over time, the recommended target for LDL-C has become more stringent, moving from 2.6 mmol/l to 1.8 mmol/l in very high-risk patients. It is currently recommended to start high intensity statin treatment immediately after acute coronary syndromes (ACS) to maximally and rapidly reduce LDL-C. The novel treatment options enable the achievement of very low LDL-C levels below 1 mmol/l, with no reported safety issues, in particular with regard to neurocognitive events. However, current evidence supports the use of PCSK9 mAb treatment in ACS patients only after an initial 2-3 month run-up treatment adaptation period with maximally tolerated statin. The use of PCSK9 mAb immediately in the acute phase of ACS (<1 month) remains to be studied. Some data suggest that circulating PCSK9 increases coronary plaque vulnerability, inflammation as well as platelet aggregation in the acute phase of ACS, potentially justifying earlier PSCK9 mAb treatment initiation. As the use of novel treatment combinations in ACS is further explored to widen the perspectives of a more personalized approach for the management of ACS based on individual patient risk profile and baseline LDL-C values, their relative cost-effectiveness will also need to be assessed.

背景与目标： : 低密度脂蛋白胆固醇 (ldl-c) 是动脉粥样硬化血栓性心血管疾病的公认因果危险因素，包括孟德尔随机化数据在内的大型流行病学研究证明。一些随机对照试验和荟萃分析表明，降脂疗法，例如他汀类药物和最近的非他汀类药物依折麦贝和前蛋白转化酶枯草杆菌蛋白酶Kexin 9型单克隆抗体 (mAb)，可减少心血管事件广泛的基线ldl-c水平。随着时间的推移，ldl-c的推荐目标变得更加严格，在高危患者中从2.6  mmol/l变为1.8  mmol/l。目前建议在急性冠状动脉综合征 (ACS) 后立即开始高强度他汀类药物治疗，以最大程度地快速降低ldl-c。新的治疗方案使ldl-c水平低于1 mmol mmol/l，没有安全性问题的报道，特别是关于神经认知事件。然而，目前的证据支持在ACS患者中使用PCSK9 mAb治疗仅在初始2-3个月的启动治疗适应期后使用最大耐受他汀类药物。在ACS急性期 (<1个月) 立即使用PCSK9 mAb仍有待研究。一些数据表明，在ACS急性期，循环PCSK9会增加冠状动脉斑块的脆弱性，炎症以及血小板聚集，这可能证明较早开始PSCK9 mAb治疗是合理的。随着在ACS中使用新型治疗组合的进一步探索，以扩大基于个体患者风险状况和基线ldl-c值的更加个性化的ACS管理方法的观点，还需要评估其相对成本效益。

BACKGROUND & AIMS: The cellular distribution of Ca(2+)-inhibitable adenylyl cyclase (AC) type 5 and type 6 mRNAs in rat outer medullary collecting duct (OMCD) was performed by in situ hybridization. Kidney sections were also stained with specific antibodies against either collecting duct intercalated cells or principal cells. The localization of type 5 AC in H(+)-ATPase-, but not aquaporin-3-, positive cells demonstrated that type 5 AC mRNA is expressed only in intercalated cells. In contrast, type 6 AC mRNA was observed in both intercalated and principal cells. In microdissected OMCDs, the simultaneous superfusion of carbachol and PGE(2) elicited an additive increase in the intracellular Ca(2+) concentration, suggesting that the Ca(2+)-dependent regulation of these agents occurs in different cell types. Glucagon-dependent cAMP synthesis was inhibited by both a pertussis toxin-sensitive PGE(2) pathway (63.7 +/- 4.6% inhibition, n = 5) and a Ca(2+)-dependent carbachol pathway (48.6 +/- 3.3%, n = 5). The simultaneous addition of both agents induced a cumulative inhibition of glucagon-dependent cAMP synthesis (78.2 +/- 3.3%, n = 5). The results demonstrate a distinct cellular localization of type 5 and type 6 AC mRNAs in OMCD and the functional expression of these Ca(2+)-inhibitable enzymes in intercalated cells.

背景与目标： 通过原位杂交进行了大鼠外髓质收集管 (OMCD) 中Ca(2) 抑制腺苷酸环化酶 (AC) 5型和6型mrna的细胞分布。肾脏切片也用针对收集导管插层细胞或主要细胞的特异性抗体染色。5型AC在H(+)-ATPase-而非aquaporin-3-阳性细胞中的定位表明5型AC mRNA仅在插层细胞中表达。相反，在插层细胞和主细胞中均观察到6型AC mRNA。在显微解剖的OMCDs中，卡巴胆碱和PGE(2) 的同时融合引起细胞内Ca(2) 浓度的增加，表明这些试剂的Ca(2) 依赖性调节发生在不同的细胞类型中。胰高血糖素依赖性cAMP合成被百日咳毒素敏感的PGE(2) 途径 (63.7 +/- 4.6% 抑制，n = 5) 和Ca(2 +) 依赖性卡巴胆碱途径 (48.6 +/- 3.3%，n = 5) 抑制。两种药物的同时加入诱导了胰高血糖素依赖性cAMP合成的累积抑制 (78.2 +/- 3.3%，n = 5)。结果表明，OMCD中5型和6型AC mrna具有明显的细胞定位，并且这些Ca(2) 抑制酶在插入细胞中的功能表达。