Antihypertensive treatment of end-stage renal disease patients on hemodialysis does not alter circulating ACE and ACE2 activity and angiotensin peptides.

Cardiovascular diseases (CVD) are the main causes of death in hemodialysis patients, representing a public health challenge. We investigated the effect of different antihypertensive treatments on circulating levels of renin-angiotensin system (RAS) components in end-stage renal disease (ESRD) patients on hemodialysis. ESRD patients were grouped following the prescribed antihypertensive drugs: ß-blocker, ß-blocker+ACEi and ß-blocker+AT1R blocker. ESDR patients under no antihypertensive drug treatment were used as controls. Blood samples were collected before hemodialysis sessions. Enzymatic activities of the angiotensin-converting enzymes ACE and ACE2 were measured through fluorescence assays and plasma concentrations of the peptides Angiotensin II (Ang II) and Angiotensin-(1-7) [Ang-(1-7)] were quantified using mass spectrometry (LC-MS/MS). ACE activity was decreased only in the ß-blocker+ACEi group compared to the ß-blocker+AT1R, while ACE2 activity did not change according to the antihypertensive treatment. Both Ang II and Ang-(1-7) levels also did not change according to the antihypertensive treatment. We concluded that the treatment of ESRD patients on hemodialysis with different antihypertensive drugs do not alter the circulating levels of RAS components.

Development of an automated, high-throughput assay to detect angiotensin AT2-receptor agonistic compounds by nitric oxide measurements in vitro.

Angiotensin AT2-receptor (AT2R) agonists have shown a wide range of protective effects in many preclinical disease models. However, the availability of AT2R-agonists is very limited due to the lack of high-throughput assays for AT2R-agonist identification. Therefore, we aimed to design and validate an assay for high-throughput screening of AT2R-agonist candidates. The assay is based on nitric oxide (NO) release measurements in primary human aortic endothelial cells (HAEC), in AT2R-transfected CHO cells (AT2R-CHO) or in non-transfected CHO cells (Flp-CHO) using the fluorescent probe DAF-FM diacetate. It is run in 96-well plates and fluorescence signals are semi-automatically quantified. The assay was tested for sensitivity (recognition of true positive results), selectivity (recognition of true negative results), and reliability (by calculating the repeatability coefficient (RC)). The high-throughput, semi-automated method was proven suitable, as the NO-releasing agents C21, CGP42112A, angiotensin-(1-7) and acetylcholine significantly increased NO release from HAEC. The assay is sensitive and selective, since the established AT2R-agonists C21, CGP42112A and angiotensin II significantly increased NO release from AT2R-CHO cells, while the non-AT2R-agonists angiotensin-(1-7) and acetylcholine had no effect. Assay reliability was shown by high-throughput screening of a library comprised of 40 potential AT2R-agonists, of which 39 met our requirements for reliability (RC ≤ 20% different from RC for C21). Our newly developed high-throughput method for detection of AT2R-agonistic activity was proven to be sensitive, selective, and reliable. This method is suitable for the screening of potential AT2R-agonists in future drug development programs.

Functional assay for assessment of agonistic or antagonistic activity of angiotensin AT2 receptor ligands reveals that EMA401 and PD123319 have agonistic properties.

With the discovery of the protective arm of the renin-angiotensin system (RAS), interest has grown in protective RAS-related receptors such as the angiotensin AT2-receptor [AT2R] as potential new drug targets. While it is known that AT2R couple to Gi, it is also apparent that they do not signal via inhibition of adenylyl cyclase/decrease in cAMP, as do many Gi-coupled receptors. Thus, standard commercially-available assays cannot be applied to test for agonistic or antagonistic properties of AT2R ligands. This lack of standard assays has hampered the development of new drugs targeting the AT2R. Therefore, we aimed at developing a reliable, technically easy assay for the determination of intrinsic activity of AT2R ligands, primarily for distinguishing between AT2R agonists and antagonists. We found that measurement of NO release by DAF-FM fluorescence in primary human aortic endothelial cells (HAEC) or in AT2R-transfected CHO cells is a reliable assay for the characterization of AT2R ligands. While testing the assay, we made several novel findings, including: a) C21 is a full agonist at the AT2R (with the same efficacy as angiotensin II); b) C21 has no intrinsic activity at the receptor Mas; c) AT2R-transfected HEK-293 cells are unresponsive to AT2R stimulation; d) EMA401 and PD123319, which are commonly regarded as AT2R antagonists, are partial agonists at the AT2R. Collectively, we have developed and tested an assay based on the measurement and quantification of NO release in HAEC or in AT2R-CHO cells that is suitable for the characterisation of novel and established AT2R ligands.

Oral supplementation of nicotinamide riboside alters intestinal microbial composition in rats and mice, but not humans.

The gut microbiota impacts systemic levels of multiple metabolites including NAD+ precursors through diverse pathways. Nicotinamide riboside (NR) is an NAD+ precursor capable of regulating mammalian cellular metabolism. Some bacterial families express the NR-specific transporter, PnuC. We hypothesized that dietary NR supplementation would modify the gut microbiota across intestinal sections. We determined the effects of 12 weeks of NR supplementation on the microbiota composition of intestinal segments of high-fat diet-fed (HFD) rats. We also explored the effects of 12 weeks of NR supplementation on the gut microbiota in humans and mice. In rats, NR reduced fat mass and tended to decrease body weight. Interestingly, NR increased fat and energy absorption but only in HFD-fed rats. Moreover, 16S rRNA gene sequencing analysis of intestinal and fecal samples revealed an increased abundance of species within Erysipelotrichaceae and Ruminococcaceae families in response to NR. PnuC-positive bacterial strains within these families showed an increased growth rate when supplemented with NR. The abundance of species within the Lachnospiraceae family decreased in response to HFD irrespective of NR. Alpha and beta diversity and bacterial composition of the human fecal microbiota were unaltered by NR, but in mice, the fecal abundance of species within Lachnospiraceae increased while abundances of Parasutterella and Bacteroides dorei species decreased in response to NR. In conclusion, oral NR altered the gut microbiota in rats and mice, but not in humans. In addition, NR attenuated body fat mass gain in rats, and increased fat and energy absorption in the HFD context.

Quantitative Phosphoproteomics of the Angiotensin AT2-Receptor Signaling Network Identifies HDAC1 (Histone-Deacetylase-1) and p53 as Mediators of Antiproliferation and Apoptosis.

BACKGROUND: Angiotensin AT2-receptor signaling is atypical for a G-protein coupled receptor and incompletely understood. To obtain novel insights into AT2-receptor signaling, we mapped changes in the phosphorylation status of the entire proteome of human aortic endothelial cells in response to AT2-receptor stimulation. METHODS: Phosphorylation status of human aortic endothelial cells after stimulation with C21 (1 µM; 0, 1, 3, 5, 20 minutes) was determined utilizing time-resolved quantitative phosphoproteomics. Specific changes in protein phosphorylation and acetylation were confirmed by Western Blotting. Functional tests included resazurin assay for cell proliferation, and caspase 3/7 luminescence assay or FACS analysis of annexin V expression for apoptosis. RESULTS: AT2-receptor stimulation significantly altered the phosphorylation status of 172 proteins (46% phosphorylations, 54% dephosphorylations). Bioinformatic analysis revealed a cluster of phospho-modified proteins involved in antiproliferation and apoptosis. Among these proteins, HDAC1 (histone-deacetylase-1) was dephosphorylated at serine421/423 involving serine/threonine phosphatases. Resulting HDAC1 inhibition led to p53 acetylation and activation. AT2-receptor stimulation induced antiproliferation and apoptosis, which were absent when cells were co-incubated with the p53 inhibitor pifithrin-α, thus indicating p53-dependence of these AT2-receptor mediated functions. CONCLUSIONS: Contrary to the prevailing view that AT2-receptor signaling largely involves phosphatases, our study revealed significant involvement of kinases. HDAC1 inhibition and resulting p53 activation were identified as novel, AT2-receptor coupled signaling mechanisms. Furthermore, the study created an openly available dataset of AT2-receptor induced phospho-modified proteins, which has the potential to be the basis for further discoveries of currently unknown, AT2-receptor coupled signaling mechanisms.

Dietary Protein Restriction Improves Metabolic Dysfunction in Patients with Metabolic Syndrome in a Randomized, Controlled Trial.

Dietary restriction (DR) reduces adiposity and improves metabolism in patients with one or more symptoms of metabolic syndrome. Nonetheless, it remains elusive whether the benefits of DR in humans are mediated by calorie or nutrient restriction. This study was conducted to determine whether isocaloric dietary protein restriction is sufficient to confer the beneficial effects of dietary restriction in patients with metabolic syndrome. We performed a prospective, randomized controlled dietary intervention under constant nutritional and medical supervision. Twenty-one individuals diagnosed with metabolic syndrome were randomly assigned for caloric restriction (CR; n = 11, diet of 5941 ± 686 KJ per day) or isocaloric dietary protein restriction (PR; n = 10, diet of 8409 ± 2360 KJ per day) and followed for 27 days. Like CR, PR promoted weight loss due to a reduction in adiposity, which was associated with reductions in blood glucose, lipid levels, and blood pressure. More strikingly, both CR and PR improved insulin sensitivity by 62.3% and 93.2%, respectively, after treatment. Fecal microbiome diversity was not affected by the interventions. Adipose tissue bulk RNA-Seq data revealed minor changes elicited by the interventions. After PR, terms related to leukocyte proliferation were enriched among the upregulated genes. Protein restriction is sufficient to confer almost the same clinical outcomes as calorie restriction without the need for a reduction in calorie intake. The isocaloric characteristic of the PR intervention makes this approach a more attractive and less drastic dietary strategy in clinical settings and has more significant potential to be used as adjuvant therapy for people with metabolic syndrome.

Harmonic Focus Versus Conventional Electrocautery for Femoral Artery Exposure: a "Direct" Comparison on the Same Patients.

Surgical access complications during endovascular aneurysm repair (EVAR) are reported relatively frequent. HARMONIC FOCUS® (HF; Ethicon Endo-Surgery Inc., Cincinnati, Ohio, USA) is a device developed to improve bleeding control and reduce heat-related damage stemming from surgical preparation. The aim of this study was to evaluate outcomes and safety of HF versus conventional haemostasis with electrocautery, both techniques used in the same patient. Five patients developed bilateral wound's thickening (13.9%) demonstrated at the CT scan, two of whom had no clinical manifestation while in three cases the thickening was associated with lymphocele (4.54%), 2 of which were in the side where the EC was used (5.5%), and 1 case (2.7%), in the HF applied side. One isolated lymphocele occurred at the left groin (2.7%) (tables n.2-3). A Fisher's exact test was conducted between EC and HF on the occurrence of wound healing complications (3/36 for EC and 1/36 for HF) that resulted statistically significant at p<0.05. Focus Harmonic Scalpel has certain advantages than conventional haemostasis in avoiding surgical access complications.

Double-Microcatheter Technique through Tortuous Anatomy for Coil Embolization of a Saccular $plenic Aneurysm: a Technical Report.

We report on a case of an asymptomatic splenic artery aneurysm (SAA) with a large neck in a 53-year-old female with an extreme vessel tortuosity which was treated with a Double Microcatheter Technique. This endovascular procedure consists of embolization of the aneurysm using detachable coils with no application of any glue, stent or balloon. At the end of procedure, no complications occurred. At the three-month follow-up an MRI showed the aneurysm's complete exclusion and patency of the splenic artery.

Standard Carotid Endarterectomy versus Carotid Artery Stenting with Closed-Cell Stent Design and Distal Embolic Protection: does the age matter?

Carotid artery endarterectomy (CEA) is considered the gold standard for treatment of symptomatic and asymptomatic carotid disease. Carotid artery stenting (CAS) is a less invasive approach and therefore could be considered a viable alternative to CEA, especially in high-risk patients or those with relative contraindications to CEA (i.e. actinic stenosis, post-CEA restenosis, previous neck or tracheostomy surgery, contralateral laryngeal nerve paralysis, etc.). METHODS: The aim of this study is to evaluate the short- and medium-term outcomes of CAS performed with a single type of closed-cell stent design and distal filter protection by comparing the procedure with CEA based upon 3 endpoints: overall survival rate, stroke free survival rate and restenosis free survival rate.The same endpoints were also evaluated in 2 different age groups, more and less than 70 years, to show possible age-based differences on outcomes.Among 105 patients (77 males, 28 females), 74 were submitted to CEA and 31 were subject to CAS.In all cases the same self-expanding stent with closed-cell design (XACT Carotid Stent, Abbott Vascular) and the same distal embolic protection device (Emboshield NAV, Abbott Vascular) were employed. RESULTS: At 12 months, no statistically significant difference was observed in overall survival rates (CEA 93.2% vs CAS 93.5%, p=0.967) and restenosis free survival rates (CEA 94.5% vs CAS 96.8%, p=0.662).An increased stroke free survival rate was observed in the CEA group when compared to the CAS group (CEA 100.0% vs CAS 93.5%, p=0.028).The age-based endpoints didn't show any significant difference. CONCLUSION: These results suggest that CEA still remains the gold standard of treatment for carotid stenosis given its greater efficacy in the prevention of stroke CAS. However, CAS could be considered as an alternative treatment to CEA to be used in select cases only.

Genetic deletion of the alamandine receptor MRGD leads to dilated cardiomyopathy in mice.

We have recently described a new peptide of the renin-angiotensin system, alamandine, a derivative of angiotensin-(1-7). Mas-related G protein-coupled receptor member D (MrgD) was identified as its receptor. Although similar cardioprotective effects of alamandine to those of angiotensin-(1-7) have been described, the significance of this peptide in heart function is still elusive. We aimed to evaluate the functional role of the alamandine receptor MrgD in the heart using MrgD-deficient mice. MrgD was localized in cardiomyocytes by immunofluorescence using confocal microscopy. High-resolution echocardiography was performed in wild-type and MrgD-deficient mice (2 and 12 wk old) under isoflurane anesthesia. Standard B-mode images were obtained in the right and left parasternal long and short axes for morphological and functional assessment and evaluation of cardiac deformation. Additional heart function evaluation was performed using Langendorff isolated heart preparations and inotropic measurements of isolated cardiomyocytes. Immunofluorescence indicated that the MrgD receptor is expressed in cardiomyocytes, mainly in the membrane and perinuclear and nuclear regions. Echocardiography showed left ventricular remodeling and severe dysfunction in MrgD-deficient mice. Strikingly, MrgD-deficient mice presented a pronounced dilated cardiomyopathy with a marked decrease in systolic function. Echocardiographic changes were supported by the data obtained in isolated hearts and inotropic measurements in cardiomyocytes. Our data add new evidence for a major role for alamandine/MrgD in the heart. Furthermore, our results indicate that we have identified a new gene implicated in dilated cardiomyopathy, unveiling a new target for translational approaches aimed to treat heart diseases. NEW & NOTEWORTHY The renin-angiotensin system is a key target for cardiovascular therapy. We have recently identified a new vasodepressor/cardioprotective angiotensin, alamandine. Here, we unmasked a key role for its receptor, Mas-related G protein-coupled receptor member D (MrgD), in heart function. The severe dilated cardiomyopathy observed in MrgD-deficient mice warrants clinical and preclinical studies to unveil its potential use in cardiovascular therapy.

Identification of protein phosphatase involvement in the AT2 receptor-induced activation of endothelial nitric oxide synthase.

The Angiotensin II type 2 receptor (AT2R) promotes vasodilation by nitric oxide (NO) release from endothelial cells. However, the mechanisms underlying the AT2R-induced stimulation of endothelial NO synthase (eNOS) is still not completely understood. Therefore, we investigated whether in addition to the known AT2R-mediated phosphorylation of eNOS at Ser1177, activation of phosphatases and dephosphorylation of eNOS at Tyr657 and Thr495 are also involved. Human aortic endothelial cells (HAEC) were stimulated with the AT2R-agonist Compound 21 (C21) (1 µM) in the presence or absence of either PD123319 (10 µM; AT2R antagonist), l-NG-Nitroarginine methyl ester (l-NAME) (10 µM; eNOS inhibitor), MK-2206 (100 nM; protein kinase B (Akt) inhibitor) sodium fluoride (NaF) (1 nM; serine/threonine phosphatase inhibitor) or sodium orthovanadate (Na3VO4) (10 nM; tyrosine phosphatase inhibitor). NO release was estimated by quantifying 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate (DAF-FM) fluorescence. The phosphorylation status of activating (eNOS-Ser1177) or inhibitory eNOS residues (eNOS-Tyr657, eNOS-Thr495) was determined by Western blotting. Phosphorylation of Akt at Ser473 was measured to estimate Akt activity. AT2R stimulation significantly increased NO release from HAEC, which was blocked by PD123319, l-NAME and both phosphatase inhibitors. Intracellular calcium transients were not changed by C21. AT2R stimulation resulted in phosphorylation of eNOS-Ser1177 and dephosphorylation of eNOS-Tyr657 and eNOS-Thr495 Phosphorylation at eNOS-Ser1177 was prevented by inhibition of Akt with MK-2206. From these data, we conclude that AT2R stimulation in human endothelial cells increases eNOS activity through phosphorylation of activating eNOS residues (eNOS-Ser1177) by Akt, and through dephosphorylation of inactivating eNOS residues (eNOS-Tyr657, eNOS-Thr495) by serine/threonine and tyrosine phosphatases, thus increasing NO release.

Immunoglobulin heavy and light chains and T-cell receptor beta and gamma chains PCR assessment on cytological samples. A study comparing FTA cards and cryopreserved lymph node fine-needle cytology.

OBJECTIVES: To evaluate and compare the DNA yield and quality extracted from lymph node fine needle cytology (FNC) samples stored on FTA cards to those cryopreserved, and to assess the immunoglobulin heavy and light chains (IGHK) and T-Cell receptor beta and gamma chains (TCRBG) PCR tests. METHODS: DNA extractions were performed on FNC of 80 non-Hodgkin lymphomas (NHL), four myelomas and 56 benign reactive hyperplasias (BRH) cryopreserved and stored on FTA cards. The JAK2 gene was amplified to assess the DNA integrity and the IGHK/TCRBG clonality status was tested. RESULTS: IGHK monoclonality was found in 99% of B-cell NHL and 100% of myeloma. TCRBG monoclonality was found in 100% of T-cell NHL. TCRBG polyclonality was detected in 97% of B-cell NHL, 100% of myeloma and 96% of BRH. IGHK/TCRBG PCR data were confirmed by histological and/or follow-up controls. No differences were found in the DNA quality between cryopreservation and FTA cards storage methods. CONCLUSIONS: IGHK/TCRBG PCR of the lymphoproliferative process on FTA cards is comparable to those cryopreserved. FTA cards can be used to store lymph node FNC for further molecular investigations.

Effect of young sibling visitation on respiratory syncytial virus activity in a NICU.

OBJECTIVE: To determine whether the restriction of young sibling (<13 years) visitation in the neonatal intensive care unit (NICU) during the respiratory syncytial virus (RSV) season was associated with a reduction in the rate of RSV infection among NICU patients. STUDY DESIGN: A retrospective chart review of all RSV positive infants from the 2001-2010 RSV seasons. The 2001-2006 RSV seasons (group 1) contained 639 admissions and the 2007-2010 (group 2, with sibling restriction) contained 461 admissions. Groups were compared by using the Fisher's Exact Test. RESULTS: There was a reduction of RSV positive infants from 6.7% in Group 1 to 1.7% in Group 2 (P<0.0001). There was a reduction of symptomatic infants from the number of infants with symptomatic RSV infection from 23/639 infants with young sibling visitation to 2/461 (P<0.001). CONCLUSION: Exclusion of young sibling visitors <13 years of age during RSV season was associated with a significant reduction in the number of RSV positive infants in the NICU.

Fine needle aspiration cytology of lymphoproliferative lesions of the oral cavity.

OBJECTIVE: Oral cavity non-Hodgkin lymphoma (OCL) is a rare condition that may be clinically and radiologically indistinguishable from other pathologies of the mouth. A complete excision or adequate biopsy of the OCL may be difficult. Fine needle aspiration (FNA) cytology has been successfully utilized in the pre-operative diagnosis of oral masses and in lymphoma involving other anatomical areas. Our experience with FNA pre-operative cytological diagnosis of 16 OCLs is reported herein. METHODS: The results of FNA cytology on 16 consecutive lymphoproliferative lesions of the oral cavity collected over an 8-year period in three institutions were retrieved. Sampled lesions were submucosal masses of different sizes bulging into the oral cavity. Rapid on-site evaluation (ROSE) and routine cytological staining were performed. Immunocytochemistry (ICC), flow cytometry (FC) and polymerase chain reaction (PCR) of the IGH (immunoglobulin heavy) locus were performed on additional passes according to ROSE. RESULTS: Fourteen OCLs, one myeloma and one florid reactive lymphoid hyperplasia (FRLH) were diagnosed by FNA. OCLs were diagnosed as large B-cell (eight cases) and small B-cell (six cases) lymphomas. Histology revealed eight diffuse large B-cell lymphomas (DLBCL), four lymphomas of mucosa-associated lymphoid tissue (MALT), two follicular lymphomas and one FRLH; no false-negative or false-positive results were diagnosed, but accurate subclassification was obtained in four cases only. CONCLUSIONS: FNA diagnosis of OCLs may be hampered by the rare incidence, anatomical context and difficulties in obtaining a sufficient amount of cells. Ancillary techniques should be used according to ROSE; a pre-operative FNA cytology diagnosis can avoid unnecessary extensive surgery and speed up the institution of therapeutic procedures.

[The use in routine of mass spectrometry in a hospital microbiology laboratory]. / Bilan de l'utilisation en routine de la spectrométrie de masse dans un laboratoire hospitalier de microbiologie.

OBJECTIVES: Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) has recently been introduced in diagnostic microbiology laboratories for the identification of microorganisms. The mass fingerprint obtained by analyzing the ribosomal proteins and proteins associated with membranes is compared to spectra and superspectra of database. Microbiological Laboratory of Mulhouse acquired this system 1 year ago. METHOD: The MALDI-TOF MS analyses of all strains were performed on Axima(®) (Shimadzu), data analysis with Saramis(®) software (Anagnostec) and integration with SirWeb(®) software (I2A society). RESULTS: Rapidly, laboratory technicians and biologists are able to turn the system after a few days of training. The data prospectively gathered in the present study demonstrated that MALDI-TOF mass spectrometry identification is an efficient method included fastidious bacteria. Exactly 98.8 % of 10,000 isolates were identified in genus and species levels. Use of identification techniques was seldom necessary for a few clinical relevant isolates. The database is in constant evolution. The superspectra contain characteristic signals of genus, species allowing reliable microorganism identifications with high confidence. CONCLUSION: In conclusion, our results show that MALDI-TOF MS is a fast and reliable technique for identification of most bacterial strains routinely isolated in a clinical microbiology. Identification and susceptibility testing with a single cell colony are more often possible. The simple tests, such as Gram staining and oxidase and catalase tests are usually performed in our laboratory.

Effect of autonomic nervous system dysfunction on sudden death in ischemic patients with anginal syndrome died during electrocardiographic monitoring in Intensive Care Unit.

AIM: The aim of this study was to investigate the role of sympathovagal imbalance in patients with ''ischemic'' sudden death (arrhythmic death preceded by ST segment shift). Although heart rate variability is a powerful tool for risk stratification after myocardial infarction, the mechanism precipitating sudden death is poorly known. METHODS: We analyzed the records of 10 patients who had ischemic sudden death during ECG Holter monitoring. Thirty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computed interactive Holter system. RESULTS: In 8 patients the sudden death was induced by ventricular fibrillation; in 2 by atrioventricular block followed by sinus arrest. All 10 patients showed ST segment shift. ST depression (maximal change 0.54+/-0.16 mV) occurred in 6 patients and ST elevation (maximal change 0.65+/-0.24 mV) in 4. The standard deviation of normal RR intervals (SDNN) was 92+/-30 ms during total Holter monitoring period vs 70+/-10 ms and 46+/-8 ms in epoch 1 and epoch 2 respectively. The SDNN was lower before the occurrence of ischemic sudden death: 54+/-12 ms (P< 0.005) in epoch 3 and 26+/-5 (P<0.005) in epoch 4 (i.e. 5 min before the onset of fatal ST segment shift). In controls the SDNN was 108+/-30 ms during total Holter monitoring period, whereas is measured 58+/-28 ms 5 min before the most significant episode of ST shift vs 26+/-5 in the group with sudden death (P<0.001). CONCLUSION: Sympathovagal imbalance, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These findings suggest that transient autonomic dysfunction may facilitate, during acute myocardial ischemia, fatal arrhythmias precipitating in sudden death.

Ascitis quilosa y síndrome de maltrato infantil / Chylous ascites and syndrome maltratation infant

La ascitis quilosa (AQ) es una entidad rara asociada a la patología del sistema linfático. El primer caso pediátrico fue reportado por Morton en 1683 en un paciente con tuberculosis. Puede producirse por una malformación linfática congénita, una obstrucción o trauma

Ascitis quilosa y síndrome de maltrato infantil / Chylous ascites and syndrome maltratation infant

La ascitis quilosa (AQ) es una entidad rara asociada a la patología del sistema linfático. El primer caso pediátrico fue reportado por Morton en 1683 en un paciente con tuberculosis. Puede producirse por una malformación linfática congénita, una obstrucción o trauma