Table of contentsP001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP effluxR. M. Bateman, M. D. Sharpe, J. E. Jagger, C. G. EllisP002 - Lower serum immunoglobulin G2 level does not predispose to severe flu.J. Solé-Violán, M. López-Rodríguez, E. Herrera-Ramos, J. Ruíz-Hernández, L. Borderías, J. Horcajada, N. González-Quevedo, O. Rajas, M. Briones, F. Rodríguez de Castro, C. Rodríguez GallegoP003 - Brain protective effects of intravenous immunoglobulin through inhibition of complement activation and apoptosis in a rat model of sepsisF. Esen, G. Orhun, P. Ergin Ozcan, E. Senturk, C. Ugur Yilmaz, N. Orhan, N. Arican, M. Kaya, M. Kucukerden, M. Giris, U. Akcan, S. Bilgic Gazioglu, E. TuzunP004 - Adenosine a1 receptor dysfunction is associated with leukopenia: A possible mechanism for sepsis-induced leukopeniaR. Riff, O. Naamani, A. DouvdevaniP005 - Analysis of neutrophil by hyper spectral imaging - A preliminary reportR. Takegawa, H. Yoshida, T. Hirose, N. Yamamoto, H. Hagiya, M. Ojima, Y. Akeda, O. Tasaki, K. Tomono, T. ShimazuP006 - Chemiluminescent intensity assessed by eaa predicts the incidence of postoperative infectious complications following gastrointestinal surgeryS. Ono, T. Kubo, S. Suda, T. Ueno, T. IkedaP007 - Serial change of c1 inhibitor in patients with sepsis – A prospective observational studyT. Hirose, H. Ogura, H. Takahashi, M. Ojima, J. Kang, Y. Nakamura, T. Kojima, T. ShimazuP008 - Comparison of bacteremia and sepsis on sepsis related biomarkersT. Ikeda, S. Suda, Y. Izutani, T. Ueno, S. OnoP009 - The changes of procalcitonin levels in critical patients with abdominal septic shock during blood purificationT. Taniguchi, M. OP010 - Validation of a new sensitive point of care device for rapid measurement of procalcitoninC. Dinter, J. Lotz, B. Eilers, C. Wissmann, R. LottP011 - Infection biomarkers in primary care patients with acute respiratory tract infections – Comparison of procalcitonin and C-reactive proteinM. M. Meili, P. S. SchuetzP012 - Do we need a lower procalcitonin cut off?H. Hawa, M. Sharshir, M. Aburageila, N. SalahuddinP013 - The predictive role of C-reactive protein and procalcitonin biomarkers in central nervous system infections with extensively drug resistant bacteriaV. Chantziara, S. Georgiou, A. Tsimogianni, P. Alexandropoulos, A. Vassi, F. Lagiou, M. Valta, G. Micha, E. Chinou, G. MichaloudisP014 - Changes in endotoxin activity assay and procalcitonin levels after direct hemoperfusion with polymyxin-b immobilized fiberA. Kodaira, T. Ikeda, S. Ono, T. Ueno, S. Suda, Y. Izutani, H. ImaizumiP015 - Diagnostic usefullness of combination biomarkers on ICU admissionM. V. De la Torre-Prados, A. Garcia-De la Torre, A. Enguix-Armada, A. Puerto-Morlan, V. Perez-Valero, A. Garcia-AlcantaraP016 - Platelet function analysis utilising the PFA-100 does not predict infection, bacteraemia, sepsis or outcome in critically ill patientsN. Bolton, J. Dudziak, S. Bonney, A. Tridente, P. NeeP017 - Extracellular histone H3 levels are in...

The aim of this research is to evaluate the current streptokinase thrombolytic treatment and to identify or improve new techniques that will base new approaches with a higher efficiency in this area of expertise. In order to be as realistic as possible a new method was set up using magnetic vectorized nanoparticles streptokinase and human blood thrombus. The experimental data confirm the maximum 83% thrombus lyses whenever increase streptokinase concentration. It is very probable to happen because of the presence of high concentration of antiplasmin in the blood that neutralizes around half of the thrombolytic potential of the sanguine plasminogen. The experiment shows also that only free serum plasminogen are available for streptokinase action in order to generate plasmin.

Background:Snakebite is a health issue specific to some parts of the world, especially in the tropical areas, where it produces many victims. The main clinical damage caused by snakebite involves haemotoxic, neurotoxic and myotoxic reactions. We report the case of a young woman suffering from snakebite who developed deep vein thrombosis and compartment syndrome.Case Report: We present the case of a 32-year-old Romanian woman who was injured by her own Crotalinae snake (also known as pit viper or rattlesnake) on her left forearm. When admitted to our Emergency Department, she was conscious with a Glasgow coma scale of 12/15, somnolent, febrile, suffering of headache, tachypnoea; the marks of the snakebite were located in the distal part of the anterior left forearm; she had pain and bleeding at the bite site and swelling of the left upper limb with lymphangitis up to the axilla. She experienced fasciotomy-requiring compartment syndrome of the upper limb and required unfractionated heparin and close monitoring using activated partial thromboplastin time evolution due to micro-thrombosis in the brachial vein. Local improvement was achieved in the next 4 days with progressive diminishment of local tenderness and swelling.Conclusion: Limb deep vein thrombosis might be induced by snakebite, despite the pro-haemorrhagic general condition induced by the envenomation. A high index of clinical suspicion is needed for early diagnosis and timely management, which can improve survival of these patients.

Mercury is a chemical element that has been known since prehistoric times and has been used over time as a component of paints, in the treatment of various diseases, and later in various industrial compounds. Mercury enters the body transcutaneously, by inhaling or by ingesting food contaminated with mercury. The most common cause of mercury poisoning is eating seafood, but people can get mercury poisoning from industrial processing, thermometers, dental work, and old paints. The most vulnerable are people at occupational risk due to chronic exposure, as well as fetuses in the intrauterine period. Mercury poisoning produces extremely serious effects on the nervous, renal, and gastrointestinal systems. The nature and extent of mercury poisoning depend on factors such as the route of exposure, the rate of exposure, the distribution and biotransformation of mercury in the body, the chemical form of mercury or the mercury compound. Both mercury in the blood and the urine should not exceed 10 μg/L. The critical values of mercury in the blood are >150 μg/L and the lethal ones exceed 800 μg/L. New diagnostic methods allow the rapid and accurate identification of the concentration of mercury in biological products. Treatment is based on the use of chelating agents. However, the prognosis of mercury poisoning is extremely variable, due to the potentially irreversible nature of the lesions.

Organophosphates (OP) are widely used in both agriculture and household settings as pesticides. Human exposure is mainly due to residues in food or living environment and the main mechanism of OP toxicity are the acetylcholinesterase (AChE) inhibition. Acute poisoning is associated with a high rate of mortality due to parasympathetic overstimulation. In long-term exposure, OP are linked to systemic damage occurrence like nervous, hepatic or renal dysfunction. These compounds are considered as potential endocrine disrupters, causing significant hormonal imbalance targeting the adrenals or thyroid glands. The aim of this article is to review current data in the literature regarding effects of both acute and chronic OP exposure on thyroid hormonal status.