Metal loads and biomarker suite responses in a tropical carnivorous fish indicative of anthropogenic impacts in a Southeastern Brazilian lagoon.

Tropical coastal lagoons are highly productive environments exhibiting high biodiversity. However, the use of these ecosystems by local communities is of concern, since this generally leads to environmental degradation. The Imboassica coastal lagoon, located in Macaé city, in Northern Rio de Janeiro, is an important ecosystem in the state, however, already displaying signs of anthropogenic impacts. Carnivorous fish Hoplias malabaricus specimens were sampled from this impacted site, as well as from a reference area. Fish from Imboassica Lagoon presented lower condition factor, lower cholinesterase activity, and higher percentage of erythrocyte micronuclei when compared to fish from the reference site. Metals in fish from Imboassica Lagoon were always higher than Encantada Lagoon, with some seasonal differences, where some metals were higher in the rainy season compared to the dry season in muscle tissue, with the exception of Cu, Fe, Sr, and Zn; and in the liver, except for Ba, Cd, Cr, Ni, and Sr. Cr and Mn in the edible muscle portion of the fish were higher than the limits established by Brazilian and International legislations as permissible for human consumption, thus leading to concerns regarding public health risks for the local population that use fish as their main protein source.

Erratum to: The management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for management of intra-abdominal infections.

[This corrects the article DOI: 10.1186/s13017-017-0141-6.].

Erratum to: Antimicrobials: a global alliance for optimizing their rational use in intra-abdominal infections (AGORA).

[This corrects the article DOI: 10.1186/s13017-016-0089-y.].

Paracetamol and salicylic acid removal from contaminated water by microalgae.

The biomass growth, pharmaceutical removal and light conversion efficiency of Chlorella sorokiniana under the presence of paracetamol (PC) and salicylic acid (SaC) were assessed and compared at two different concentrations of these pharmaceuticals (I: 25 mg l-1, II: 250 mg l-1). Microalgae were resistant to these concentrations and, moreover, their growth was significantly stimulated (p ≤ 0.05) under these drugs (biomass concentration increased above 33% PCI, 35% SaCI, 13% PCII and 45% SaCII, as compared with the respective positive controls). At the steady state of the semicontinuous culture, C. sorokiniana showed removal efficiencies above 41% and 69% for PCI and PCII, respectively; and above 93% and 98% for SaCI and SaCII, respectively. Under an irradiance of 370 µE m-2 s-1, higher quantum yields were reached by microalgae under the presence of drugs, either at dose I or II, than by the respective positive controls. These results point to C. sorokiniana as a robust strain for the bioremediation of paracetamol and salicylic acid concentrated wastewaters.

Erratum to: 2016 WSES guidelines on acute calculous cholecystitis.

[This corrects the article DOI: 10.1186/s13017-016-0082-5.].

2016 WSES guidelines on acute calculous cholecystitis.

Acute calculus cholecystitis is a very common disease with several area of uncertainty. The World Society of Emergency Surgery developed extensive guidelines in order to cover grey areas. The diagnostic criteria, the antimicrobial therapy, the evaluation of associated common bile duct stones, the identification of "high risk" patients, the surgical timing, the type of surgery, and the alternatives to surgery are discussed. Moreover the algorithm is proposed: as soon as diagnosis is made and after the evaluation of choledocholitiasis risk, laparoscopic cholecystectomy should be offered to all patients exception of those with high risk of morbidity or mortality. These Guidelines must be considered as an adjunctive tool for decision but they are not substitute of the clinical judgement for the individual patient.

Inter-site and inter-scanner diffusion MRI data harmonization.

We propose a novel method to harmonize diffusion MRI data acquired from multiple sites and scanners, which is imperative for joint analysis of the data to significantly increase sample size and statistical power of neuroimaging studies. Our method incorporates the following main novelties: i) we take into account the scanner-dependent spatial variability of the diffusion signal in different parts of the brain; ii) our method is independent of compartmental modeling of diffusion (e.g., tensor, and intra/extra cellular compartments) and the acquired signal itself is corrected for scanner related differences; and iii) inter-subject variability as measured by the coefficient of variation is maintained at each site. We represent the signal in a basis of spherical harmonics and compute several rotation invariant spherical harmonic features to estimate a region and tissue specific linear mapping between the signal from different sites (and scanners). We validate our method on diffusion data acquired from seven different sites (including two GE, three Philips, and two Siemens scanners) on a group of age-matched healthy subjects. Since the extracted rotation invariant spherical harmonic features depend on the accuracy of the brain parcellation provided by Freesurfer, we propose a feature based refinement of the original parcellation such that it better characterizes the anatomy and provides robust linear mappings to harmonize the dMRI data. We demonstrate the efficacy of our method by statistically comparing diffusion measures such as fractional anisotropy, mean diffusivity and generalized fractional anisotropy across multiple sites before and after data harmonization. We also show results using tract-based spatial statistics before and after harmonization for independent validation of the proposed methodology. Our experimental results demonstrate that, for nearly identical acquisition protocol across sites, scanner-specific differences can be accurately removed using the proposed method.

Nutrients and pharmaceuticals removal from wastewater by culture and harvesting of Chlorella sorokiniana.

This work aimed to study both the removal of nutrients and pharmaceuticals, namely salicylic acid or paracetamol, from water by the culture of Chlorella sorokiniana. The removal of nutrients was nearly complete at the end of the batch culture; above 70% for nitrates and 89% for phosphates in the semicontinuous culture. The pharmaceuticals removal kinetics were 2.3 times greater for the salicylic acid than paracetamol, reaching volumetric efficiencies above 93% for salicylic acid in the semicontinuous culture. Finally, to separate the microalgae biomass from treated water, metal salts, synthetic polyelectrolytes and a biopolymer were tested as coagulants-flocculants. The best flocculation results were achieved with AlCl3 (95.23% with 200mgg(-1), 1min incubation time). However, given that resulting flocs had different characteristics, flocculants must be chosen on the basis of the subsequent use of the biomass.

Ataxia and myoclonic epilepsy due to a heterozygous new mutation in KCNA2: proposal for a new channelopathy.

We have recently performed exome analysis in a 7 year boy who presented in infancy with an encephalopathy characterized by ataxia and myoclonic epilepsy. Parents were not consanguineous and there was no family history of the disease. Exome analysis did not show any pathogenic variants in genes known to be associated with seizures and/or ataxia in children, including all known human channelopathies. However, we have identified a mutation in KCNA2 that we believe to be responsible for the disease in our patient. This gene, which encodes a member of the potassium channel, voltage-gated, shaker-related subfamily, has not been previously described as a cause of disease in humans, but mutations of the orthologous gene in mice (Kcna2) are known to cause both ataxia and convulsions. The mutation is c.890C>A, leading to the amino acid substitution p.Arg297Gln, which involves the second of the critical arginines in the S4 voltage sensor. This mutation is characterized as pathogenic by five different prediction programs. RFLP analysis and Sanger sequencing confirmed the presence of the mutation in the patient, but not in his parents, characterizing it as de novo. We believe that this discovery characterizes a new channelopathy.

The epidemic of pre-injury oral antiplatelet and anticoagulant use.

BACKGROUND: As the population ages, an increasing number of trauma patients are taking antiplatelet and anticoagulant medications (ACAP) prior to their injuries. These medications increase their risk of hemorrhagic complications, particularly intracerebral hemorrhage. Clopidogrel and warfarin are common and their mechanisms well understood, but optimal reversal methods continue to evolve. The novel direct thrombin and factor Xa inhibitors are less well described and do not have existing antidotes. METHODS: This article reviews the relevant literature on traumatic outcomes with use of ACAP medications, as well as data on ideal reversal strategies. Suggested algorithms are introduced, and future research directions discussed. RESULTS: Although they are beneficial in preventing clot formation, once bleeding occurs ACAP medications contribute to increased morbidity and mortality, particularly in geriatric patient populations. The efficacy of clopidogrel reversal with platelet transfusions and DDAVP remains unclear. Warfarin use is best treated with the algorithm-driven use of plasma, vitamin K, prothrombin complex concentrates (PCCs) and possibly recombinant factor VIIa depending upon specific patient and injury factors. Optimal treatment for direct thrombin and factor Xa inhibitors has yet to be developed, but PCCs are promising for rivaroxaban and apixaban while dabigatran is best treated with medication cessation and the possible addition of activated PCCs or hemodialysis. CONCLUSION: New developments in reversal of the ACAP medications are promising, particularly PCCs for warfarin and the factor Xa inhibitors. Function assays and clear antidotes are needed for the thrombin and Xa inhibitors. Research on outcomes and appropriate treatments is actively ongoing.

Planned re-laparotomy and the need for optimization of physiology and immunology.

Planned re-laparotomy or damage control laparotomy (DCL), first described by Dr. Harlan Stone in 1983, has become a widely utilized technique in a broad range of patients and operative situations. Studies have validated the use of DCL by demonstrating decreased mortality and morbidity in trauma, general surgery and abdominal vascular catastrophes. Indications for planned re-laparotomy include severe physiologic derangements, coagulopathy, concern for bowel ischemia, and abdominal compartment syndrome. The immunology of DCL patients is not well described in humans, but promising animal studies suggest a benefit from the open abdomen (OA) and several human trials on this subject are currently underway. Optimal critical care of patients with OA's, including sedation, paralysis, nutrition, antimicrobial and fluid management strategies have been associated with improved closure rates and recovery.

Nutritional support in patients following damage control laparotomy with an open abdomen.

INTRODUCTION: Damage control laparotomy (DCL) and the open abdomen have been well accepted following either severe abdominal trauma or emergency surgical disease. As DCL is increasingly utilized as a therapeutic option, appropriate management of the post-DCL patient is important. Early caloric support by enteral nutrition (EN) in the critically ill patient improves wound healing and decreases septic complications, lung injury, and multi-system organ failure. However, following DCL, nutritional strategies can be challenging and, at times, even daunting. CONCLUSIONS: Even though limited data exist, the use of early EN following DCL seems safe, provided that the patient is not undergoing active resuscitation or the bowel is not in discontinuity. It is unknown as to whether EN in the open abdomen reduces septic complications, prevents enterocutaneous fistula (ECF), or alters the timing of definitive abdominal wall closure. Future investigation in a prospective manner may help elucidate these important questions.

Early ghrelin treatment attenuates disruption of the blood brain barrier and apoptosis after traumatic brain injury through a UCP-2 mechanism.

Ghrelin has been shown to be anti-inflammatory and neuroprotective in models of neurologic injury. We hypothesize that treatment with ghrelin will attenuate breakdown of the blood brain barrier (BBB) and apoptosis 24h following traumatic brain injury (TBI). We believe this protection is at least in part mediated by up-regulation of UCP-2, thereby stabilizing mitochondria and preventing up-regulation of caspase-3. A weight drop model was used to create severe TBI. Balb/c mice were divided into 3 groups. Sham: no TBI or ghrelin treatment; TBI: TBI only; TBI/ghrelin: 20µg (IP) ghrelin at the time of TBI. BBB permeability to 70kDa FITC-Dextran was measured 24h following injury and quantified in arbitrary integrated fluorescence (afu). Brain tissue was subjected to TUNEL staining and TUNEL positive cells were quantified. Immunohistochemistry was performed on injured tissue to reveal patterns of caspase-3 and UCP-2 expression. TBI increased cerebral vascular permeability by three-fold compared to sham. Ghrelin treatment restored vascular permeability to the level of shams. TUNEL staining showed that ghrelin mitigated the significant increase in apoptosis that follows TBI. TBI increased both caspase-3 compared to sham. Treatment with ghrelin significantly increased UCP-2 compared to TBI alone and this increase in UCP-2 expression was associated with a decrease in expression of caspase-3. Early ghrelin treatment prevents TBI induced BBB disruption and TBI mediated apoptosis 24h following injury. These results demonstrate the neuroprotective potential of ghrelin as a therapy in TBI.

Acute lower GI bleeding for the acute care surgeon: current diagnosis and management.

Lower gastrointestinal bleeding is a common cause for hospital admission that results in significant morbidity and mortality. After initial resuscitation of the patient, the diagnosis and treatment of lower gastrointestinal bleeding remains a challenge for acute care surgeons. Identifying the source of bleeding can be difficult since many patients bleed intermittently or stop bleeding spontaneously. It is therefore important for the acute care surgeon to be familiar with the different diagnostic and therapeutic modalities and their advantages and disadvantages in order to guide the management of the acutely bleeding patient. This review summarizes the current methods available for the diagnosis and treatment of acute lower gastrointestinal bleeding and proposes an algorithm for the management of these patients.

A 20-year experience with portal and superior mesenteric venous injuries: has anything changed?

OBJECTIVES: To identify predictive factors causing mortality in patients with injuries to the portal (PV) and superior mesenteric veins (SMV). DESIGN: Retrospective analysis of prospectively collected data. MATERIALS AND METHODS: Adults admitted with blunt or penetrating PV and SMV injuries at an academic level I trauma center during a 20-year period. RESULTS: Of 26,387 major trauma victims admitted from 1987 through 2006, 26 sustained PV or SMV injuries (PV=15, SMV=11). Mechanism of injury was penetrating in 19 (73%) and 20 were in shock. Active hemorrhage occurred in 21. Most patients had associated injuries (2.9+/-1.8/patient). Mean Injury Severity Score (ISS) was 27.8+/-16.8. All PV injuries underwent suture repair and 27% of SMV injuries were ligated. Overall mortality was 46% (PV=47%, SMV=45%). Stab wounds had a lower mortality (31%) compared to gunshot wounds (67%) and blunt injuries (57%). Nonsurvivors had a higher ISS (35.8 vs. 20.9; p=0.02), more associated injuries (3.7 vs. 2.2; p=0.02), were older, and had active hemorrhage. Active hemorrhage (p=0.04) was independently related to death while shock on admission (odds ratio=6.1, p=0.61) trended toward higher mortality. CONCLUSION: Despite improvements in trauma care, mortality of PV and SMV injuries remains high. Shock, active hemorrhage, and associated injuries were predictive of increased mortality.

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain.

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5 degrees C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 +/- 1.14 to 73.62 +/- 8.99%, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 +/- 5.02 vs 63.26 +/- 11.97%, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5°C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 ± 1.14 to 73.62 ± 8.99 percent, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 ± 5.02 vs 63.26 ± 11.97 percent, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.

On the kinetics and energetics of one-electron oxidation of 1,3,5-triazines.

One-electron oxidation of 1,3,5-triazines is observed with both excited uranyl ion (*UO2(2+)) and sulfate radical anion (SO4.-) in aqueous solution, but not with Tl2+, indicating that the standard reduction potentials E degree of 1,3,5-triazine radical cations are = 2.3 +/- 0.1 V vs. NHE, consistent with theoretical calculations; this suggests that if triazines inhibit electron transfer during photosynthesis, they would need to act on the reductive part of the electron transport chain.