Comparison of safety and effectiveness of micropulse transscleral cyclophotocoagulation and "slow cook" diode laser transscleral cyclophotocoagulation in patients with refractory open-angle glaucoma

ABSTRACT Purpose: This study aimed to compare the safety and effectiveness of intraocular pressure reduction between micropulse transscleral cyclophotocoagulation and "slow cook" transscleral cyclophotocoagulation in patients with refractory primary open-angle glaucoma. Methods: We included patients with primary open angle glaucoma with at least 12 months of follow-up. We collected and analyzed data on the preoperative characteristics and postoperative outcomes. The primary outcomes were a reduction of ≥20% of the baseline value (criterion A) and/or intraocular pressure between 6 and 21 mmHg (criterion B). Results: We included 128 eyes with primary open-angle glaucoma. The preoperative mean intraocular pressure was 25.53 ± 6.40 and 35.02 ± 12.57 mmHg in the micropulse- and "slow cook" transscleral cyclophotocoagulation groups, respectively (p<0.001). The mean intraocular pressure was reduced significantly to 14.33 ± 3.40 and 15.37 ± 5.85 mmHg in the micropulse- and "slow cook" transscleral cyclophotocoagulation groups at the last follow-up, respectively (p=0.110). The mean intraocular pressure reduction at 12 months was 11.20 ± 11.46 and 19.65 ± 13.22 mmHg in the micropulse- and "slow cook" transscleral cyclophotocoagulation groups, respectively (p<0.001). The median preoperative logMAR visual acuity was 0.52 ± 0.69 and 1.75 ± 1.04 in the micropulse- and "slow cook" transscleral cyclophotocoagulation groups, respectively (p<0.001). The mean visual acuity variation was −0.10 ± 0.35 and −0.074 ± 0.16 in the micropulse- and "slow cook" transscleral cyclophotocoagulation, respectively (p=0.510). Preoperatively, the mean eye drops were 3.44 ± 1.38 and 2.89 ± 0.68 drugs in the micropulse- and "slow cook" transscleral cyclophotocoagulation groups, respectively (p=0.017), but those were 2.06 ± 1.42 and 1.02 ± 1.46 at the end of the study in the "slow cook" and micropulse transscleral cyclophotocoagulation groups, respectively (p<0.001). The success of criterion A was not significant between both groups. Compared with 11 eyes (17.74%) in the "slow cook" transscleral cyclophotocoagulation group, 19 eyes (28.78%) in the micropulse transscleral cyclophotocoagulation group showed complete success (p=0.171). For criterion B, 28 (42.42%) and 2 eyes (3.22%) showed complete success after micropulse- and "slow cook" transscleral cyclophotocoagulation, respectively (p<0.001). Conclusion: Both techniques reduced intraocular pressure effectively.

Púrpura fulminante postinfecciosa: a propósito de un caso / Postinfectious purpura fulminans: A case report

La púrpura fulminante adquirida postinfecciosa es una entidad aguda y grave, poco frecuente, caracterizada por necrosis cutánea asociada a coagulopatía intravascular diseminada (CID), en ausencia de infección activa o alteraciones previas de la coagulación. Afecta fundamentalmente a la población pediátrica y, en el 90 % de los casos, está precedida por un proceso infeccioso. El mecanismo fisiopatológico es un déficit transitorio de proteína S mediado por autoanticuerpos que favorece un estado de hipercoagulabilidad. Se presenta el caso de un varón de 8 años previamente sano, con lesiones cutáneas purpúricas características de púrpura fulminante asociada a CID en ausencia de sepsis. Se constató deficiencia plasmática transitoria de proteína S. Requirió tratamiento sustitutivo con plasma fresco congelado y anticoagulación; la evolución fue favorable. La actividad de la proteína S permaneció disminuida durante 2 meses.

Acquired postinfectious purpura fulminans is a rare, acute, and severe disease characterized by skin necrosis associated with disseminated intravascular coagulation (DIC) in the absence of active infection or previous coagulation disorders. It mainly affects the pediatric population and, in 90% of cases, it is preceded by an infectious process. The pathophysiological mechanism is a transient autoantibodymediated protein S deficiency that favors a hypercoagulable state. Here we describe the case of a previously healthy 8-year-old boy with purpuric skin lesions typical of purpura fulminans associated with DIC in the absence of sepsis. A transient plasma protein S deficiency was confirmed. He required replacement therapy with fresh frozen plasma and anticoagulation; he had a favorable course. Protein S activity remained decreased for 2 months.

Mycotoxins and coccidiosis in poultry - co-occurrence, interaction, and effects.

Avian coccidiosis, a common disease caused by Eimeria species, results in significant losses in global poultry production. Mycotoxins are low-molecular-weight natural products (i.e., small molecules) produced as secondary metabolites by filamentous fungi and they have the potential to economically and significantly affect global poultry production. Little is known about the relationship between mycotoxins and avian coccidiosis, although they often co-occur in the field. This comprehensive review examines the intricate relationship between mycotoxins and avian coccidiosis, in particular how mycotoxins, including aflatoxins, ochratoxins, trichothecenes as well as Fusarium mycotoxins, compromise the health of the poultry flock and open the door to Eimeria parasites in the gut. In addition, this review sheds light on the immunosuppressive effects of mycotoxins, their disruption of cellular signaling pathways, and the consequent exacerbation of coccidiosis infections. The mechanisms of mycotoxin toxicity are also reviewed, emphasizing direct damage to intestinal epithelial cells, impaired nutrient absorption, inflammation, oxidative stress, and changes in the gut microbiota. Finally, the consequences for the prevention and treatment of coccidiosis when mycotoxins are present in the feed are discussed. This review emphasizes the need for effective management strategies to mitigate the combined risks of mycotoxins and coccidiosis and highlights the complexity of diagnosing and controlling these interrelated problems in poultry. The review advocates a holistic approach that includes strict feed management, disease prevention measures and regular monitoring to maintain the health and productivity of poultry against these significant challenges.

Protein C Pretreatment Protects Endothelial Cells from SARS-CoV-2-Induced Activation.

SARS-CoV-2 can induce vascular dysfunction and thrombotic events in patients with severe COVID-19; however, the cellular and molecular mechanisms behind these effects remain largely unknown. In this study, we used a combination of experimental and in silico approaches to investigate the role of PC in vascular and thrombotic events in COVID-19. Single-cell RNA-sequencing data from patients with COVID-19 and healthy subjects were obtained from the publicly available Gene Expression Omnibus (GEO) repository. In addition, HUVECs were treated with inactive protein C before exposure to SARS-CoV-2 infection or a severe COVID-19 serum. An RT-qPCR array containing 84 related genes was used, and the candidate genes obtained were evaluated. Activated protein C levels were measured using an ELISA kit. We identified at the single-cell level the expression of several pro-inflammatory and pro-coagulation genes in endothelial cells from the patients with COVID-19. Furthermore, we demonstrated that exposure to SARS-CoV-2 promoted transcriptional changes in HUVECs that were partly reversed by the activated protein C pretreatment. We also observed that the serum of severe COVID-19 had a significant amount of activated protein C that could protect endothelial cells from serum-induced activation. In conclusion, activated protein C protects endothelial cells from pro-inflammatory and pro-coagulant effects during exposure to the SARS-CoV-2 virus.

Partitioning purification, biochemical characterization, and milk coagulation efficiency of protease from a newly Streptomyces sp. isolate.

An actinobacteria strain was isolated from an olive waste mill and tested for protease production on skimmed milk media. The strain identification was achieved through both 16 S rDNA sequencing and phenotypic characterization. The enzyme was purified using the ammonium sulfate/t-butanol three-phase partitioning (TPP) method, followed by characterization to investigate the effect of pH, temperature, and various chemical agents. Subsequently, the enzyme was assessed for its milk coagulation activity. The strain belonging to the Streptomyces genera, exhibits significant phylogenetic and phenotypic differences from the aligned species, suggesting its novelty as a new strain. The enzyme was best separated in the TPP aqueous phase with a 5.35 fold and 56.25% yield. Optimal activity was observed at pH 9.0 and 60 °C, with more than half of the activity retained within the pH range of 7-10 over one hour. The protease demonstrated complete stability between 30 and 60 °C. While metallic ions enhanced enzyme activity, EDTA acted as an inhibitor. The enzyme displayed resistance to H2O2, SDS, Tween 80, and Triton X-100. Notably, it was activated in organic solvents (ethyl acetate, petroleum ether, and xylene), maintaining > 75% of its original activity in butanol, ethanol, and methanol. Additionally, the enzyme yielded high milk coagulant activity of 11,478 SU/mL. The new Streptomyces sp. protease revealed high activity and stability under a wide range of biochemical conditions. Its use in the dairy industry appears particularly promising. Further industrial process investigations will be valuable in determining potential uses for this enzyme.

Comprehensive genomic filtering algorithm to expose the cause of skewed X chromosome inactivation. The proof of concept in female haemophilia expression.

BACKGROUND: Exploring the expression of X linked disorders like haemophilia A (HA) in females involves understanding the balance achieved through X chromosome inactivation (XCI). Skewed XCI (SXCI) may be involved in symptomatic HA carriers. We aimed to develop an approach for dissecting the specific cause of SXCI and verify its value in HA. METHODS: A family involving three females (two symptomatic with severe/moderate HA: I.2, the mother, and II.1, the daughter; one asymptomatic: II.2) and two related affected males (I.1, the father and I.3, the maternal uncle) was studied. The genetic analysis included F8 mutational screening, multiplex ligation-dependent probe amplification, SNP microarray, whole exome sequencing (WES) and Sanger sequencing. XCI patterns were assessed in ectoderm/endoderm and mesoderm-derived tissues using AR-based and RP2-based systems. RESULTS: The comprehensive family analysis identifies I.2 female patient as a heterozygous carrier of F8:p.(Ser1414Ter) excluding copy number variations. A consistent XCI pattern of 99.5% across various tissues was observed. A comprehensive filtering algorithm for WES data was designed, developed and applied to I.2. A Gly58Arg missense variant in VMA21 was revealed as the cause for SXCI.Each step of the variant filtering system takes advantage of publicly available genomic databases, non-SXCI controls and case-specific molecular data, and aligns with established concepts in the theoretical background of SXCI. CONCLUSION: This study acts as a proof of concept for our genomic filtering algorithm's clinical utility in analysing X linked disorders. Our findings clarify the molecular aspects of SXCI and improve genetic diagnostics and counselling for families with X linked diseases like HA.

Hypocoagulability in severe yellow fever infection is associated with bleeding: results from a cohort study.

Background: Severe yellow fever infection (YFI) may be complicated by a hemorrhagic diathesis. However, the hemostasis profile of YFI has rarely been reported. Objectives: The aim of this study was to characterize the hemostatic features of YFI by using a rotational thromboelastometry (ROTEM). Methods: We evaluated clinical, laboratory, and ROTEM parameters in adults with severe YFI and their correlation with hemostatic variables according to bleeding and death. Results: A total of 35 patients were included (median age, 49 years). ROTEM was performed in 22 patients, of whom 21 (96%) presented bleeding and 4 (18%) died. All patients who died had major bleeding. Patients who died presented prolonged clotting time (CT; median, 2326 seconds; IQR, 1898-2986 seconds) and reduced alpha angle (median, 12°; IQR, 12°-15°) in comparison with patients who had minor (median CT, 644 seconds; IQR, 552-845 seconds and alpha angle, 47°; IQR, 28°-65°) and major (median CT, 719 seconds; IQR, 368-1114 seconds and alpha angle, 43°; IQR, 32°-64°) bleeding who survived. In patients who had bleeding, CT showed a strong negative correlation with factor (F)V (r = -.68), FIX (r = -.84), and FX (r = -.63) as well as alpha angle showed a strong negative correlation with FIX (r = -.92). In patients who died, the correlations were even stronger. A total of 19/21 (90%) patients presented hypocoagulability assessed by ROTEM. Conclusion: Hypocoagulabitity is the hallmark of the bleeding diathesis of severe YFI. Abnormal CT and alpha angle associated with death and could be used as potential predictors of adverse outcome in severe YFI.

Angiopoietin2 is associated with coagulation activation and tissue factor expression in extracellular vesicles in COVID-19.

Coagulation activation in immunothrombosis involves various pathways distinct from classical hemostasis, offering potential therapeutic targets to control inflammation-induced hypercoagulability while potentially sparing hemostasis. The Angiopoietin/Tie2 pathway, previously linked to embryonic angiogenesis and sepsis-related endothelial barrier regulation, was recently associated with coagulation activation in sepsis and COVID-19. This study explores the connection between key mediators of the Angiopoietin/Tie2 pathway and coagulation activation. The study included COVID-19 patients with hypoxia and healthy controls. Blood samples were processed to obtain platelet-free plasma, and frozen until analysis. Extracellular vesicles (EVs) in plasma were characterized and quantified using flow cytometry, and their tissue factor (TF) procoagulant activity was measured using a kinetic chromogenic method. Several markers of hemostasis were assessed. Levels of ANGPT1, ANGPT2, and soluble Tie2 correlated with markers of coagulation and platelet activation. EVs from platelets and endothelial cells were increased in COVID-19 patients, and a significant increase in TF+ EVs derived from endothelial cells was observed. In addition, ANGPT2 levels were associated with TF expression and activity in EVs. In conclusion, we provide further evidence for the involvement of the Angiopoietin/Tie2 pathway in the coagulopathy of COVID-19 mediated in part by release of EVs as a potential source of TF activity.

Trastornos de la coagulación: factor V Leiden, panorama biológico, clínico y epidemiológico / Coagulation Disorders: Factor V Leiden, Biological, Clinical, and Epidemiological Overview

Resumen El sistema de coagulación mantiene la sangre en estado fluido en todo momento y, por tanto, está incesantemente activa durante toda la vida. Sin embargo, en el momento en que ocurre una lesión del sistema vascular, el sistema de coagulación inmediatamente gira 180° y transforma la sangre en un cuerpo sólido perfectamente localizado, al que llamamos coágulo. Este proceso, mediante el cual se forma un coágulo, se conoce como hemostasia, que es uno de los componentes del sistema de coagulación. La importancia de la mutación Leiden del factor V se basa en lo siguiente: el factor V de la coagulación es una proteína que se sintetiza en el hígado y el gen que lo codifica está situado en la región 23 del brazo largo del cromosoma 1, este factor circula en sangre periférica de manera inactiva hasta que interactúa con el factor X activado, formando un complejo que convierte al factor II (protrombina) en trombina, que va a tener su acción sobre el fibrinógeno convirtiéndolo en fibrina. La regulación del factor V activado se da por la actividad de la proteína C activada, cuando el factor V tiene una mutación (nombrada Leiden) que es ocasionada por el cambio de una adenina por una guanina en el nucleótido 1691 del factor V (G1691A), que causa que se sustituya una arginina por una glutamina en el residuo 506 de la proteína factor V; la proteína resultante es un factor V anómalo, mismo que no puede inactivarse por la proteína C activada, por lo que el factor V continúa activado y no puede impedir que el proceso de coagulación se detenga. En nuestro país (considerando varias afecciones) se ha descrito en diversas publicaciones de investigadores mexicanos que las mutaciones Leiden del factor V y la G20210A de la protrombina no son frecuentes, como lo son en los países europeos.

Abstract The coagulation system always keeps the blood in a fluid state and is therefore incessantly active throughout life. However, the moment an injury to the vascular system occurs, the coagulation system immediately rotates 180° and transforms the blood into a perfectly localized solid body, which we call a clot. This process, by which a clot forms, is known as hemostasis, which is one of the components of the coagulation system. The importance of the Leiden mutation of factor V is based on the following: coagulation factor V is a protein that is synthesized in the liver and the gene that encodes it is located in region 23 of the long arm of chromosome 1, this factor circulates in peripheral blood inactively until it interacts with activated factor X forming a complex that converts factor II (prothrombin) into thrombin, which will have its action on fibrinogen turning it into fibrin. The regulation of activated factor V is given by the activity of activated protein C, when factor V has a mutation (named Leiden) that is caused by the exchange of an adenine for a guanine in the nucleotide 1691 of factor V (G1691A), which causes arginine to be replaced by a glutamine in the 506 residue of the factor V protein, the resulting protein is an abnormal factor V, which cannot be inactivated by activated protein C, so factor V remains activated and cannot prevent the clotting process from stopping. In our country (considering several conditions) it has been described in various publications of Mexican researchers that Leiden mutations of factor V and G20210A of prothrombin are not frequent, as they are in European countries.

Effectiveness of a natural coagulant based on common mallow (Malva sylvestris) in urban wastewater treatment.

This study evaluated the effectiveness of a natural coagulant based on common mallow (Malva sylvestris) to remove turbidity in urban wastewater. A 22 factorial design was selected to determine the optimal dose and the working pH of the natural coagulant. Its potential was studied in 50.0-450 mg/L and 4.00-10.0 ranges of doses and pH, respectively. A simplex lattice mixture evaluated its effectiveness as a coagulant aid combined with aluminum sulfate (conventional coagulant). Mixture proportions 0.000-1.00 were studied for each component, finding the proportion more effective. Results showed that the coagulation treatment could be feasible since a turbidity removal efficiency of 73.7% can be achieved under optimal conditions (50.0 mg/L and pH of 10.0). Likewise, a turbidity removal of 58.9% is obtained using 250 mg/L and maintaining wastewater pH (7.45). This efficiency can be increased using 31.0% natural coagulant mixed with 69.0% aluminum sulfate at 250 mg/L without modifying the wastewater pH. This improvement was associated with the natural coagulant's high molecular weight and long-chained structure since these properties enhance settling time, floc size and strength, and low sludge production. These results support using common mallow as a natural coagulant, making its use more feasible in alkaline water pH or as a coagulant aid combined with aluminum sulfate for urban wastewater treatment. A cost of USD 370/Kg of natural coagulant was estimated, which is higher than conventional coagulants. However, a cost-effectiveness analysis of its implementation should be performed since process scaling costs could significantly reduce its price.

Proteomic Insights into Biology of Bipolar Disorder: Implications for Health Complexity and Mortality.

OBJECTIVE: The present study has the following objectives: 1) identify differentially expressed proteins and pathways in blood samples of BD compared to healthy controls by employing high-throughput proteomics and bioinformatics and 2) characterize disease-related molecular signatures through in-depth analysis of the differentially expressed proteins and pathways. METHODS: Blood samples from BD patients (n=10) classified into high (BD+) or poor functioning (BD-), based on functional and cognitive status, and healthy controls (n=5) were analyzed using mass spectrometry-based proteomic analysis. Bioinformatics was performed to detect biological processes, pathways, and diseases related to BD. RESULTS: Eight proteins exclusively characterized the molecular profile of patients with BD+ compared to HC, while 26 altered proteins were observed in the BD- group. These altered proteins were mainly enriched in biological processes related to lipid metabolism, complement system and coagulation cascade, and cardiovascular diseases; all these changes were more prominent in the BD- group. CONCLUSION: These findings may represent systemic alterations that occur with the progression of the illness and a possible link between BD and medical comorbidities. Such comprehensive understanding provides valuable insights for targeted interventions, addressing mental and physical health aspects in subjects with BD. Despite these promising findings, further research is warranted, encompassing larger sample cohorts and incorporating biological validation through molecular biology methods.

Immunothrombosis and its underlying biological mechanisms

Abstract The evolutionary conserved link between coagulation and innate immunity is a biological process characterized by the thrombosis formation stimulus of immune cells and specific thrombosis-related molecules. In physiological settings, the relationship between the immune system and thrombosis facilitates the recognition of pathogens and damaged cells and inhibits pathogen proliferation. However, when deregulated, the interplay between hemostasis and innate immunity becomes a pathological process named immunothrombosis, which is at the basis of several infectious and inflammation-related thrombotic disorders, including coronavirus disease 2019 (COVID-19). In advanced stages, alterations in both coagulation and immune cell function due to extreme inflammation lead to an increase in blood coagulability, with high rates of thrombosis and mortality. Therefore, understanding underlying mechanisms in immunothrombosis has become decisive for the development of more efficient therapies to treat and prevent thrombosis in COVID-19 and in other thrombotic disorders. In this review, we outline the existing knowledge on the molecular and cellular processes involved in immunothrombosis, focusing on the role of neutrophil extracellular traps (NETs), platelets and the coagulation pathway. We also describe how the deregulation of hemostasis is associated with pathological conditions and can significantly aggravate a patient's condition, using COVID-19 as a clinical model.

Condiciones trombofilicas y su riesgo en una cohorte latinoamericana de gestantes, estudio observacional descriptivo / Thrombophilic conditions and their risk in a Latin American cohort of pregnant women, descriptive observational study

Objetivo: Evaluar las trombofilias asociadas a tromboembolismo venoso durante la gestación. Métodos: Estudio observacional descriptivo. Se analizaron las alteraciones clínicas y de laboratorio asi como la clasificación del perfil relacionado de una cohorte de gestantes latinoamericanas con eventos trombóticos durante la gestación y hasta el puerperio de 120 días. Se realizaron anticuerpos del síndrome antifosfolipídico, proteína C, S de la coagulación, antitrombina III, mutaciones contra el factor V de Leiden, mutaciones en la metilenetetrahidrofolato reductasa, hiperhomocisteinemia, mutación de la protrombina y elevación de los factores VIII, IX y XI. Resultados: La edad media fue de 24,5 + 7,6 años, de ellas 9 pacientes (10,3 %) tenían antecedente de tromboembolismo, 23 pacientes (26,4 %) habían tenido una pérdida fetal al menos. Se encontraron anticuerpos antifosfatidilserina elevados en 23 pacientes (26,4 %), anticuerpos contra la beta 2 glicoproteína elevado en 20 pacientes (22,9 %), anticoagulante lúpico positivo en 16 pacientes (18,3 %), factor VIII elevado en 13 pacientes (14,94 %), factor IX elevado en 15 pacientes (17,2 %), el factor XI elevado en 12 pacientes (13,7 %), la mutación de la protrombina en 7 pacientes (8,07 %) y las otras en menor proporción. Conclusiones: Los resultados aquí encontrados señalan la alta tasa de prevalencia de alteraciones trombofílicas subdiagnosticadas en las gestantes, aún falta evidencia de peso para analizar dicha relación con peores resultados durante la gestación(AU)

Objective: To evaluate thrombophilias associated with venous thromboembolism during pregnancy. Methods: Descriptive observational study. Clinical and laboratory alterations were analyzed, as well as the classification of the related profile of a cohort of Latin American pregnant women with thrombotic events during gestation and up to the 120-day puerperium. Antiphospholipid syndrome antibodies, coagulation protein C, S, antithrombin III, mutations against factor V Leiden, mutations in methylenetetrahydrofolate reductase, hyperhomocysteinemia, prothrombin mutation, and elevation of factors VIII, IX, and XI were performed. Results: The mean age was 24,5 + 7,6 years, of which 9 patients (10,3%) had a history of thromboembolism, 23 patients (26,4%) had had at least one fetal loss. Elevated antiphosphatidylserine antibodies were found in 23 patients (26,4%), elevated antibodies against beta2-glycoprotein in 20 patients (22,9%), positive lupus anticoagulant in 16 patients (18,3%), elevated factor VIII in 13 patients (14,94%), elevated factor IX in 15 patients (17,2%), elevated factor XI in 12 patients (13,7%), prothrombin mutation in 7 patients (8,07%) and the others to a lesser extent. Conclusions: The results found here point to the high prevalence rate of underdiagnosed thrombophilic disorders in pregnant women. There is still a lack of strong evidence to analyze this relationship with worse results during pregnancy(AU)

Are coagulation profiles in Andean highlanders with excessive erythrocytosis favouring hypercoagulability?

Chronic mountain sickness is a maladaptive syndrome that affects individuals living permanently at high altitude and is characterized primarily by excessive erythrocytosis (EE). Recent results concerning the impact of EE in Andean highlanders on clotting and the possible promotion of hypercoagulability, which can lead to thrombosis, were contradictory. We assessed the coagulation profiles of Andeans highlanders with and without excessive erythrocytosis (EE+ and EE-). Blood samples were collected from 30 EE+ and 15 EE- in La Rinconada (Peru, 5100-5300 m a.s.l.), with special attention given to the sampling pre-analytical variables. Rotational thromboelastometry tests were performed at both native and normalized (40%) haematocrit using autologous platelet-poor plasma. Thrombin generation, dosages of clotting factors and inhibitors were measured in plasma samples. Data were compared between groups and with measurements performed at native haematocrit in 10 lowlanders (LL) at sea level. At native haematocrit, in all rotational thromboelastometry assays, EE+ exhibited hypocoagulable profiles (prolonged clotting time and weaker clot strength) compared with EE- and LL (all P < 0.01). At normalized haematocrit, clotting times were normalized in most individuals. Conversely, maximal clot firmness was normalized only in FIBTEM and not in EXTEM/INTEM assays, suggesting abnormal platelet activity. Thrombin generation, levels of plasma clotting factors and inhibitors, and standard coagulation assays were mostly normal in all groups. No highlanders reported a history of venous thromboembolism based on the dedicated survey. Collectively, these results indicate that EE+ do not present a hypercoagulable profile potentially favouring thrombosis.

Concerns about the application of resistance exercise with blood-flow restriction and thrombosis risk in hemodialysis patients.

BACKGROUND: Hemodialysis (HD) per se is a risk factor for thrombosis. Considering the growing body of evidence on blood-flow restriction (BFR) exercise in HD patients, identification of possible risk factors related to the prothrombotic agent D-dimer is required for the safety and feasibility of this training model. The aim of the present study was to identify risk factors associated with higher D-dimer levels and to determine the acute effect of resistance exercise (RE) with BFR on this molecule. METHODS: Two hundred and six HD patients volunteered for this study (all with a glomerular filtration rate of <15 mL/min/1.73 m2). The RE + BFR session consisted of 50% arterial occlusion pressure during 50 min sessions of HD (intradialytic exercise). RE repetitions included concentric and eccentric lifting phases (each lasting 2 s) and were supervised by a strength and conditioning specialist. RESULTS: Several variables were associated with elevated levels of D-dimer, including higher blood glucose, citrate use, recent cardiovascular events, recent intercurrents, higher inflammatory status, catheter as vascular access, older patients (>70 years old), and HD vintage. Furthermore, RE + BFR significantly increases D-dimer after 4 h. Patients with borderline baseline D-dimer levels (400-490 ng/mL) displayed increased risk of elevating D-dimer over the normal range (≥500 ng/mL). CONCLUSION: These results identified factors associated with a heightened prothrombotic state and may assist in the screening process for HD patients who wish to undergo RE + BFR. D-dimer and/or other fibrinolysis factors should be assessed at baseline and throughout the protocol as a precautionary measure to maximize safety during RE + BFR.

Ascorbic acid prevents stress-induced hypercoagulability in overweight and obese individuals.

Ascorbic acid (AA) may contribute to restoring hemostatic balance after mental stress (MS) in overweight/obese adults. We aimed to determine the effects of AA administration on hemostatic responses to MS in overweight/obese men. Fourteen overweight/obesity men (27 ± 7 years; BMI: 29.7 ± 2.6 kg m-2) performed the Stroop color-word stress task for 5 min after non-simultaneous infusion of placebo (PL, 0.9% NaCl) and AA (3 g). Blood was collected at baseline, during MS, and 60 min after MS to measure: activated partial thromboplastin time, prothrombin time, and fibrinogen concentration, by coagulometer; platelet-derived microvesicles (PMV, mv/µL), by flow cytometry; nitrite (µM), by chemiluminescence. In PL session, MS led to decreases in PTs (stress, p = 0.03; 60 min, p < 0.001), PT-INR (stress, p < 0.001; 60 min, p < 0.01), aPTTs (60 min, p = 0.03), aPTT ratio (60 min, p = 0.04) and fibrinogen (60 min, p = 0.04), while increased PT activity (60 min, p = 0.01) when compared to baseline. Furthermore, AA increased PTs (60 min, p < 0.001), PT-INR (60 min, p = 0.03) and decreased PT activity (60 min, p < 0.001) and fibrinogen (stress, p = 0.04) when compared to PL. Nitrite was increased in response to stress during AA session (p < 0.001 vs PL). There was no difference in PMV. Ascorbic acid prevented the impaired hemostatic profile and improved nitrite response to stress in the overweight and obese adults.

ATR1 A1166C (rs5186), FII G20210A (rs1799963), FV G1691A (rs6025), FXIII 97G > T (rs11466016) and MTHFR A1298C (rs1801131) polymorphisms and the risk of ST-elevation myocardial infarction in young Mexican individuals.

BACKGROUND: Previous studies had identified genetic variants associated with Myocardial Infarction, but results are inconclusive. We examined the association between FII G20210A (rs1799963), FV G1691A (rs6025), FXIII 97G > T (rs11466016), ATR1 A1166C (rs5186) and MTHFR A1298C (rs1801131) polymorphisms and ST elevation Myocardial Infarction in young Mexican individuals. METHODS: We included a total of 350 patients with Myocardial Infarction <45 years old and 350 controls matched by age and gender. The polymorphisms were analyzed by PCR-RFLP using specific restriction enzymes. DNA fragments were separated by electrophoresis in 2% gel of agarose and visualized using SYBR green. RESULTS: The A1166C (p = 0.004) but not FXIII 97G > T (p = 0.19), G20210A (p = 0.32), G1691A (p = No significant) and A1298C (p = 0.21) polymorphisms were associated with increased risk for ST elevation Myocardial Infarction. Moreover, dyslipidemia, hypertension, smoking and family history of atherothrombotic disease were associated. CONCLUSIONS: We found that A1166C represented increased risk for ST elevation Myocardial Infarction. However, G20210A, G1691A, 97G > T, and A1298C were not associated. In addition, we had determined that Glu298Asp, PLA1/A2, TAFI Thr325Ile, ACE I/D, AGT M235T and PAI-1 4G/5G polymorphisms represented increased risk in the same group of patients. However, MTHFR C677T, AGT T174M, FV G1691A, TSP-1 N700S, MTHFR C677T and TAFI 174 M polymorphisms were no associated. Our results suggest that in young patients with ST Myocardial Infarction, those polymorphisms could contribute to premature endothelial dysfunction, atherothrombosis, vasoconstriction, increased platelet aggregation, muscle cell migration and proliferation. Further studies are required to try to better assess gene-gene and gene-modifiable factors interaction.

Treatment of effluents from Food Services Establishment (FSEs) by physico-chemical processes: a case study for Trinidad & Tobago.

BACKGROUND: Effluents from Food Services Establishments (FSEs) contain primarily Fats, Oil and Grease (FOG) which severely impact on sewers and the environment when released in high concentrations. In Trinidad & Tobago, it is estimated that approximately 231,304 kg/day of unaccounted for FOG bearing wastewaters from FSEs, are released into the environment with no viable treatment in the country. This research explored the optimization of physico-chemical processes for the treatment of FOGs for subsequent release into sewers. RESULTS: Bench-scale studies analysed the characteristics of FSE's effluents from three popular sources, conducted the treatment of these effluents using Jar Tests, and subsequently confirm results via a pilot plant study. Characterization showed the mean concentration of the parameters examined to be; FOG (511 mg/l ± 116 mg/l), Suspended Solids (446 mg/l ± 146 mg/l), Chemical Oxygen Demand (2229 mg/l ± 963 mg/l) and pH (6 ± 0.3). Jar Tests were conducted using Poly-aluminium Chloride (PACl) as coagulant, anionic and cationic polyelectrolytes as flocculant aids with suitable pH adjustments of samples to determine the isoelectric point for the coagulant. Effluent results showed FOG removal levels of 99.9% and final effluent concentration of 0.17 mg/l. This was attained using PACl concentration of 250 mg/l, a 0.1% low cationic polyelectrolyte (CP 1154) at 4 mg/l with the pH of sample adjusted to 8. The pilot plant achieved a 97.4% removal of FOG (residual of 16.8 mg/l) using the same coagulant dosing, and pH value, but increasing the strength of the flocculant aid to 0.1% medium cationic (CP1156) at 5 mg/l. CONCLUSION: Experimentation showed high concentrations of emulsified FOG can be efficiently removed to levels below the permissible requirements (20 mg/l) for entry into sewer systems in Trinidad and Tobago using coagulation, flocculation and sedimentation techniques. Pilot scale study also revealed that a higher strength and/or dose of the cationic polyelectrolyte and increased times in primary and final tanks were required to attain the desired results as in the bench level study, where equipment limitations in the flocculation tank were faced. This is in alignment with theory where factors critical for agglomeration is equipment type and density charge. It is, concluded that the optimum combination of chemicals and the respective dosages attained at the bench level study should prove effective should the right equipment be made available.

Postinfectious purpura fulminans: A case report. / Púrpura fulminante postinfecciosa: a propósito de un caso.

Acquired postinfectious purpura fulminans is a rare, acute, and severe disease characterized by skin necrosis associated with disseminated intravascular coagulation (DIC) in the absence of active infection or previous coagulation disorders. It mainly affects the pediatric population and, in 90% of cases, it is preceded by an infectious process. The pathophysiological mechanism is a transient autoantibody-mediated protein S deficiency that favors a hypercoagulable state. Here we describe the case of a previously healthy 8-year-old boy with purpuric skin lesions typical of purpura fulminans associated with DIC in the absence of sepsis. A transient plasma protein S deficiency was confirmed. He required replacement therapy with fresh frozen plasma and anticoagulation; he had a favorable course. Protein S activity remained decreased for 2 months.

La púrpura fulminante adquirida postinfecciosa es una entidad aguda y grave, poco frecuente, caracterizada por necrosis cutánea asociada a coagulopatía intravascular diseminada (CID), en ausencia de infección activa o alteraciones previas de la coagulación. Afecta fundamentalmente a la población pediátrica y, en el 90 % de los casos, está precedida por un proceso infeccioso. El mecanismo fisiopatológico es un déficit transitorio de proteína S mediado por autoanticuerpos que favorece un estado de hipercoagulabilidad. Se presenta el caso de un varón de 8 años previamente sano, con lesiones cutáneas purpúricas características de púrpura fulminante asociada a CID en ausencia de sepsis. Se constató deficiencia plasmática transitoria de proteína S. Requirió tratamiento sustitutivo con plasma fresco congelado y anticoagulación; la evolución fue favorable. La actividad de la proteína S permaneció disminuida durante 2 meses.

Chitosan in the treatment of mine spoil rainwater - An approach to protect the aquatic biota.

The mining industry suppresses vegetation, exposing large soil areas in its ordinary operation. Water pollution and turbidity are caused by the carrying of solids, mainly colloidal particles, to the watercourses due to the effect of rainfall events. Therefore, the discharge of those effluents will lead to failure with watercourse quality parameters. Thus, there is a need to treat drainages (rainwaters) from the mining industry. However, using common coagulants and flocculants can result in acute or chronic ecotoxicity for aquatic biota. In this scenario, this research aimed to evaluate using a natural coagulant, the biopolymer Chitosan, to remove turbidity from mining industry spoiled water through bio-coagulation. The ecotoxicity of the natural coagulant was compared to the commonly used coagulants. For this purpose, we used synthetic rainwater (SRW) from the dispersion of fine (colloidal) particles in natural waters. Materials (water and soil) were collected in the mining area's sumps (sedimentation basins). The turbidity of the produced SRW ranged from between 500 and 4000 NTU. Jar Tests using Chitosan (CTS), polyaluminum chloride (PAC®12), and Superfloc®N100 variable doses were carried out to compare the effects of the coagulating/flocculating agents on the SRW turbidity reduction. The obtained results demonstrated the efficiency of CHS on turbidity reduction. The results were encouraging for low turbidity samples (<1000 NTU), making it possible to meet the limit parameters recommended by the Brazilian legislation. In addition, it was possible to conclude both CHS and the effluents treated with this coagulant have lower toxicity to aquatic biota than the combination of PAC®12 and Superfloc®N100.