Hidratación con Ringer Lactato combinado con diclofenaco rectal en la prevención de pancreatitis poscolangiopancreatografía retrógrada endoscópica

ObjectiveDifferent measures are recommended to reduce pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP). We conducted a study in patients with ERCP treated with rectal diclofenac or lactated Ringer's solution, or both interventions, to assess whether there is a decrease in the number of cases of post-ERCP pancreatitis.Material and methodsA mixed cohort study involving 1,896 patients from 2009 to 2018. Up to June 2012 without treatment (Group I). Subsequently, 100 mg of rectal diclofenac (Group II). Since 2016, lactated Ringer's solution 200 ml/hour during the procedure and 4 hours after it, in addition to 500 ml over 30 minutes when the pancreas was cannulated (Group III). Since 2017, lactated Ringer's solution plus Diclofenac (Group IV). There were 725 patients in group I, and 530, 227 and 414 patients in groups II, III and IV, respectively. Factors predisposing to post-ERCP pancreatitis and post-ERCP pancreatitis cases that were defined by consensus criteria have been collected.ResultsThere were 65 cases of post-ERCP pancreatitis (3.4%); 2.9%, 3.4%, 3.1% and 4.3% in groups I, II, III and IV, respectively (P = .640). In group I, there was 4.2% of post-ERCP pancreatitis in naïve papillae and 4%, 4.9% and 6.3% in groups II, III and IV, respectively (P = .585). The severity of post-ERCP pancreatitis and adverse effects were similar in all groups. 38.4% were high-risk patients. There were also no differences in post-ERCP pancreatitis in this group (P = .501).ConclusionIn this work, no benefit was obtained with diclofenac plus hydration in reducing the number and severity of cases of post-ERCP pancreatitis nor with the other prophylactic measures.     

Utilidad de la cápsula endoscópica en el diagnóstico de la enfermedad injerto contra huésped gastrointestinal

Introduction and aimGraft-versus-host disease (GvHD) is a complication of hematopoietic cell transplantation, and the small bowel is one of the main targets in the gastrointestinal tract. Capsule endoscopy is a safe procedure and can be useful in the diagnosis of GvHD. The aim of the present study was to compare the diagnostic yield of capsule endoscopy with the histopathologic findings in GvHD.Materials and methodsA retrospective diagnostic test study included all the patients with suspected GvHD that underwent gastroscopy and colonoscopy, with histopathologic evaluation of the biopsies taken, and capsule endoscopy, within the time frame of July 2015 and July 2019. Capsule endoscopy findings were compared with the histopathologic diagnosis, considered the gold standard.ResultsTwenty-one patients with GvHD (7 [33%] women; 37 ± 11.9 years of age) were included, 20 (95%) of whom had acute GvHD. The median gastric transit time of the capsule was 55 minutes (20-113) and the median small bowel transit time was 261 minutes (238-434). The entire small bowel was visualized through capsule endoscopy in 17 cases (80.95%). The histopathologic findings and capsule endoscopy findings resulted in the diagnosis of GvHD in 17 and 16 cases, respectively. There was agreement between the histopathologic and capsule endoscopy findings in 18 cases (15 positive and 3 negative). Sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic yield of capsule endoscopy were 88%, 75%, 94%, 60%, and 85%, respectively.ConclusionsCapsule endoscopy is a safe tool for the diagnosis of GvHD, with high sensitivity and positive predictive value, as well as moderate agreement with histopathologic findings.     

广州市某三甲医院护士睡眠质量状况

目的:研究广州市某三甲医院护士睡眠质量的状况,分析影响其睡眠质量的因素,提出相应的对策,从而提高护士的睡眠质量,促进护士的身心健康。方法:采用匹兹堡睡眠质量指数量表(PSQI)及自制一般情况调查表,以广州市某三甲医院护士为研究对象,采用整群抽样方法对该院206名在职护士进行问卷调查资料收集,并进行统计学分析。结果:1该院PSQI7分者共69人(33.5%),PSQI平均得分(6.72±3.27),与常模比较差异显著(t=20.84,P0.05);2不同科室的护士在入睡时间、睡眠障碍、日间功能障碍及PSQI总分差异显著(F=3.903,5.543,2.448,3.079;P0.05),其他4个因子的比较上,差异均无统计学意义(P0.05)。结论:该院临床护士整体睡眠质量差,应采取有效措施进行干预,以提高他们的身心健康水平。     

Epidemiological and Survival Trends of Pediatric Cardiac Arrests in Emergency Departments in Korea: A Cross-sectional,Nationwide Report

Cardiac arrest (CA) in children is associated with high mortality rates. In Korea, cohort studies regarding the outcomes of pediatric CAs are lacking, especially in emergency departments (EDs) or in-hospital settings. This study was conducted to examine the trends in epidemiology and survival outcomes in children with resuscitation-attempted CAs using data from a cross-sectional, national, ED-based clinical registry. We extracted cases in which cardiopulmonary resuscitation and/or manual defibrillation were performed according to treatment codes using the National Emergency Department Information System (NEDIS) from 2008 to 2012. The total number of ED visits registered in the NEDIS during the 5-yr evaluation period was 20,424,530; among these, there were 2,970 resuscitation-attempted CAs in children. The annual rates of pediatric CAs per 1,000 ED visits showed an upward trend from 2.81 in 2009 to 3.62 in 2012 (P for trend = 0.045). The median number of estimated pediatric CAs at each ED was 7.8 (25th to 75th percentile, 4 to 13) per year. The overall rates for admission survival and discharge survival were 35.2% and 12.8%, respectively. The survival outcome of adults increased substantially over the past 5 yr (11.8% in 2008, 11.7% in 2010, and 13.6% in 2012; P for trend = 0.001); however, the results for children did not improve (13.6% in 2008, 11.4% in 2010, and 13.7% in 2012; P for trend = 0.870). Conclusively, we found that the overall incidence of pediatric CAs in EDs increased substantially over the past 5 yr, but without significantly higher survival outcomes.

Graphical Abstract

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Postoperative survival for patients with thymoma complicating myasthenia gravis—preliminary retrospective results of the ChART database

Background

It is so far not clear that how myasthenia gravis (MG) affected the prognosis of thymoma patients. The aim of this assay is to compare the postoperative survival between patients with thymoma only and those with both thymoma and MG.

Methods

The Chinese Alliance for Research in Thymomas (ChART) registry recruited patients with thymoma from 18 centers over the country on an intention to treat basis from 1992 to 2012. Two groups were formed according to whether the patient complicated MG. Demographic and clinical data were reviewed, patients were followed and their survival status were analyzed.

Results

There were 1,850 patients included in this study, including 421 with and 1,429 without MG. Complete thymectomy were done in 91.2% patients in MG group and 71.0% in non-MG group (P<0.05). There were more percentage of patients with the histology of thymoma AB, B1, or B2 (P<0.05) in MG group, and more percentage of patients with MG were in Masaoka stage I and II. The 5- and 10-year overall survival (OS) rates were both higher in MG group (93% vs. 88%; 83% vs. 81%, P=0.034) respectively. The survival rate was significantly higher in patients with MG when the Masaoka staging was 3/4 (P=0.003). Among patients with advanced stage thymoma (stage 3, 4a, 4b), the constituent ratios of 3, 4a, 4b were similar between MG and non-MG group. Histologically, however, there were significantly more proportion of AB/B1/B2/B3 in the MG group while there were more C in the non-MG group (P=0.000). Univariate analyses for all patients showed that MG, WHO classification, Masaoka stage, surgical approach, chemotherapy and radiotherapy and resectability were significant factors, and multivariate analysis showed WHO classification, Masaoka stage, and resectability were strong independent prognostic indicators.

Conclusions

Although MG is not an independent prognostic factor, the survival of patients with thymoma was superior when MG was present, especially in late Masaoka stage patients. Possible reasons included early diagnosis of the tumor, better histologic types, an overall higher R0 resection and less recurrence.     

Unidentified Bright Objects on Brain Magnetic Resonance Imaging Affect Vestibular Neuritis

Objectives

The aim of this study was to investigate the differences in clinical manifestations of in two groups of vestibular neuritis (VN) patients with or without unidentified bright objects (UBOs).

Methods

A prospective, observational study with 46 patients diagnosed with VN between May 2013 and November 2013 was executed. A caloric test, a cervical vestibular-evoked myogenic potentials (cVEMPs) test, brain magnetic resonance imaging (MRI), spontaneous nystagmus test, head impulse test, and head-shaking nystagmus test were performed.

Results

Of the patients, 56.5% (n=26) were classified as UBO-positive by MRI. These showed lower caloric weakness and more prominent cVEMP asymmetry compared with the UBO-negative group (P<0.05). Total VN (TVN) was the most common in the UBO-positive group (45.0%), followed by superior VN (SVN, 30.0%), and inferior VN (IVN, 25.0%). However, in the UBO-negative group, SVN (75.0%) was the most common, followed by TVN and IVN (P<0.05). The recovery rate was not influenced by UBOs (P>0.05).

Conclusion

UBOs on T2-weighted or fluid attenuated inversion recovery MRI may affect the patterns of the vestibular nerve in patients with VN.     

Muscarinic acetylcholine receptor activation induces Ca2+ mobilization and Na+/K+-ATPase activity inhibition in eel enterocytes

The effect of carbachol (Cch) on intracellular calcium concentration ([Ca2+]i) in eel enterocytes was examined using the fluorescent Ca2+ indicator fura-2. Cch caused a biphasic increase in [Ca2+]i, with an initial spike followed by a progressively decreasing level (over 6 min) to the initial, pre-stimulated, level. The effect of Cch was dose-dependent with a 7.5-fold increase in [Ca2+]i over basal level induced by the maximal dose of Cch (100 microM). In Ca2+-free/EGTA buffer the effect of Cch was less pronounced and the [Ca2+]i returned rapidly to basal levels. The increment of [Ca2+]i was dose-dependently attenuated in cells pre-treated with U73122, a specific inhibitor of phospholipase C, suggesting that the Cch-stimulated increment of [Ca2+]i required inositol triphosphate formation. In the presence of extracellular Ca2+, thapsigargin (TG), a specific microsomal Ca2+-ATPase inhibitor, caused a sustained rise in [Ca2+]i whereas in Ca2+-free medium the increase in [Ca2+]i was transient; in both cases, subsequent addition of Cch was without effect. When 2 mM CaCl2 were added to the cells stimulated with TG or with Cch in Ca2+-free medium, a rapid increase in [Ca2+]i was detected, corresponding to the capacitative Ca2+ entry. Thus, both TG and Cch depleted intracellular Ca2+ stores and stimulated influx of extracellular Ca2+ consistent with capacitative Ca2+ entry. K+ depolarization obtained with increasing concentrations of KCl in the extracellular medium induced a dose-related increase in [Ca2+]i which was blocked by 2 microM nifedipine, a non-specific L-type Ca2+ channel blocker. Nifedipine also changed significantly the height of the Ca2+ transient, and the rate of decrement to the pre-stimulated [Ca2+]i level, indicating that Ca2+ entry into enterocytes also occurs through an L-type voltage-dependent calcium channel pathway. We also show that isolated enterocytes stimulated with increasing Cch concentrations (0.1-1000 microM) showed a dose-dependent inhibition of the Na+/K+-ATPase activity. The threshold decrease was at 1 microM Cch; it reached a maximum at 100 microM (50.5% inhibition) and did not decrease further with the use of higher dose. The effect of Cch on Na+/K+-ATPase activity was dependent on both protein kinase C (PKC) and protein phosphatase calcineurin activation since the PKC inhibitor calphostin C abolished Cch effects, while the calcineurin inhibitor FK506 augmented Cch effect. Collectively, these data establish a functional pathway by which Cch can modulate the activity of the Na+/K+-ATPase through a PKC-dependent (calphostin C-sensitive) pathway and a calcineurin-dependent (FK506-sensitive) pathway.     

Microarray analysis of endothelial differentially expressed genes in liver of cirrhotic rats

BACKGROUND & AIMS: There is a long-standing interest in the identification of endothelial-specific pathways for therapeutic targeting in cirrhosis. Therefore, the aim of this study was to evaluate differences in gene expression patterns between liver endothelial cells (LECs) from control and cirrhotic rats by using microarrays. METHODS: LECs were obtained by isopycnic centrifugation. LECs gene expression was then analyzed on high-density oligonucleotide microarrays. RESULTS: Analysis of gene expression revealed that most of the differentially expressed mRNA in cirrhosis are associated with extracellular matrix remodeling, inflammation, antioxidant/stress response, and cell signaling. CONCLUSIONS: The collective expression changes observed within some functional groups of genes indicate that LECs in cirrhotic livers may contribute to lymphangiogenesis, enhancement of fibrogenesis and inflammatory processes, changes in cell-cell interaction with up-regulation of adherens junction proteins, and alterations in the intrahepatic vascular tone because of the down-regulation of genes involved in vasodilatation.     

Immune evasion in HPV− head and neck precancer–cancer transition is driven by an aneuploid switch involving chromosome 9p loss

An aneuploid-immune paradox encompasses somatic copy-number alterations (SCNAs), unleashing a cytotoxic response in experimental precancer systems, while conversely being associated with immune suppression and cytotoxic-cell depletion in human tumors, especially head and neck cancer (HNSC). We present evidence from patient samples and cell lines that alterations in chromosome dosage contribute to an immune hot-to-cold switch during human papillomavirus-negative (HPV⁻) head and neck tumorigenesis. Overall SCNA (aneuploidy) level was associated with increased CD3⁺ and CD8⁺ T cell microenvironments in precancer (mostly CD3⁺, linked to trisomy and aneuploidy), but with T cell-deficient tumors. Early lesions with 9p21.3 loss were associated with depletion of cytotoxic T cell infiltration in TP53 mutant tumors; and with aneuploidy were associated with increased NK-cell infiltration. The strongest driver of cytotoxic T cell and Immune Score depletion in oral cancer was 9p-arm level loss, promoting profound decreases of pivotal IFN-γ-related chemokines (e.g., CXCL9) and pathway genes. Chromosome 9p21.3 deletion contributed mainly to cell-intrinsic senescence suppression, but deletion of the entire arm was necessary to diminish levels of cytokine, JAK-STAT, and Hallmark NF-κB pathways. Finally, 9p arm-level loss and JAK2-PD-L1 codeletion (at 9p24) were predictive markers of poor survival in recurrent HPV⁻ HNSC after anti–PD-1 therapy; likely amplified by independent aneuploidy-induced immune-cold microenvironments observed here. We hypothesize that 9p21.3 arm-loss expansion and epistatic interactions allow oral precancer cells to acquire properties to overcome a proimmunogenic aneuploid checkpoint, transform and invade. These findings enable distinct HNSC interception and precision-therapeutic approaches, concepts that may apply to other CN-driven neoplastic, immune or aneuploid diseases, and immunotherapies.

The genetic bases for predisposition, and neoplastic transformation, to cancer have been increasingly well described. However, it remains less clear how early, precancer cells employ these genetic alterations to acquire the characteristic features and properties (1) of malignant disease. For example, studies of the immune landscape led to breakthrough trials of programmed death-1 (PD-1) inhibitors for recurrent, metastatic head and neck squamous cell carcinoma (HNSC) therapy (2–4). This underscores the importance of immune modulation in these tumors, despite a still suboptimal overall response rate of less than 20% in advanced cancers. Immune response within tumors has been observed to be strongest at the earliest neoplastic stages, as reported recently in lung adenocarcinoma precursors (5). As such, new, immune-based strategies could be developed to reduce the high global burden of HNSC, by intercepting the most common precursor of the most common HNSC presentation: HPV⁻ oral squamous cell carcinomas (6–8).Studies of chromosome somatic copy-number (CN) alteration (SCNA) profiles have reported the impact of 3p14, 9p21, or 17p13 loss in molecular models of HNSC progression (9) and risk (10–15). Early studies reported that patients with oral precancers harboring 9p21 and/or 3p14 loss were at significantly greater cancer risk than those with retention at these loci (10, 16). A comprehensive, prospective validation study examined the relative contribution of six candidate chromosome-arm regions. 9p21 loss had the greatest influence on cancer risk (13). The mechanism underlying the association between CN and malignant transformation of precancers, however, is unclear (17–20). Studies of CN-altered neoplastic cells have shown that SCNAs can trigger a cytotoxic response in experimental precancer systems (21, 22) but, paradoxically, were associated with immune evasion (23) and suppression (24) in computational studies of naturally occurring human cancers. The latter, in melanoma, found that nonresponders to PD-1 and CTLA-4 blockade had higher CN alteration and loss burdens, which correlated with immunologically cold tumors, characterized by cytotoxic-cell, marker, and metric reductions, and suppressive microenvironment cell, network, and signal increases (23–26). This SCNA-cold association was particularly strong in our previous, pan-The Cancer Genome Atlas (TCGA) computational study in HNSC (23). These data point to a putative in vivo switch from immune hot-to-cold in the precancer–cancer transition, and raise the hypothesis that SCNAs in precursor lesions contribute to malignant transformation through genomic events and mechanisms that enable the acquisition of immune-suppressive, evasive properties. To test this hypothesis, we evaluated CN influence on immune profiles and outcomes in a large prospective oral precancer patient cohort, and HPV⁻ HNSC (tissue specimens and cell lines) and anti–PD-1–treated recurrent-disease cohorts.     

IMPACT Trial: angiographic and intravascular ultrasound observations of the first human experience with mycophenolic acid-eluting polymer stent system.

The purpose of the study was to examine the safety and efficacy of two different formulations of mycophenolic acid (MPA)-eluting Duraflex stents on coronary de novo lesions. Recent data indicate that local delivery of MPA in the porcine overstretch coronary model significantly reduces neointimal hyperplasia (NIH). Patients were divided into three consecutive groups. The first (n=50) and second (n=55) groups received moderate- and slow-release MPA-eluting Duraflex stent, respectively. The last group (n=50) received the bare metal Duraflex stent. Clinical, angiographic, and intravascular ultrasound analysis were performed at 6-month follow-up. All stents were successfully deployed and patients were discharged home without clinical events. Compared to controls, 6-month in-lesion and in-stent minimum luminal diameter as well as late lumen loss were not significantly different in the moderate- and slow-release treatment groups. At follow-up, percentage obstruction and NIH volume were also similar between the three groups. At 30 days and 6 and 12 months, there were no differences noted between the three groups with respect to major adverse cardiac events as well as the individual rates of mortality, myocardial infarction, or repeat revascularization. There were no cases of subacute or late thrombosis. In this feasibility trial, the MPA-eluting Duraflex stents in either slow- or moderate-release formulations were well tolerated, but showed no benefit for treatment of coronary lesions when compared to controls. Further testing with different drug dosing or delivery rate might improve these results.