Introduction: Neutrophil-lymphocyte count ratio (NLCR) is a simple and low-cost marker of inflammatory response. NLCR has shown to be a sensitive marker of clinical severity in inflammatory-related tissue injury, and high value of NLCR is associated with poor outcome in traumatic brain injured (TBI) patients. The purpose of this study was to retrospectively analyze NLCR and its association with outcome in a cohort of TBI patients in relation to the type of brain injury. Methods: Adult patients admitted for isolated TBI with Glasgow Coma Score lower than eight were included in the study. NLCR was calculated as the ratio between the absolute neutrophil and lymphocyte count immediately after admission to the hospital, and for six consecutive days after admission to the intensive care unit (ICU). Brain injuries were classified according to neuroradiological findings at the admission computed tomography (CT) as DAI—patients with severe diffuse axonal injury; CE—patients with hemispheric or focal cerebral edema; ICH—patients with intracerebral hemorrhage; S-EH/SAH—patients with subdural and/or epidural hematoma/subarachnoid hemorrhage. Results: NLCR was calculated in 144 patients. Admission NLCR was significantly higher in the non-survivors than in those who survived at 28 days (p < 0.05) from admission. Persisting high NLCR value was associated with poor outcome, and admission NLCR higher than 15.63 was a predictor of 28-day mortality. The highest NLCR value at admission was observed in patients with DAI compared with other brain injuries (p < 0.001). Concussions: NLCR can be a useful marker for predicting outcome in TBI patients. Further studies are warranted to confirm these results.

Spinal cord injury (SCI) initiates a severe, destructive inflammation with pro-inflammatory, CD68+/CD163−, phagocytic macrophages infiltrating the area of necrosis and hemorrhage by day 3 and persisting for the next 16 weeks. Inhibition of macrophage infiltration of the site of necrosis that is converted into a cavity of injury (COI) during the first week post-SCI, should limit inflammatory damage, shorten its duration and result in neuroprotection. By sustained subdural infusion we administered Serp-1, a Myxoma virus-derived immunomodulatory protein previously shown to improve neurologic deficits and inhibit macrophage infiltration in the COI in rats with the balloon crush SCI. Firstly, in a 7 day long study, we determined that the optimal dose for macrophage inhibition was 0.2 mg/week. Then, we demonstrated that a continuous subdural infusion of Serp-1 for 8 weeks resulted in consistently accelerated lowering of pro-inflammatory macrophages in the COI and in their almost complete elimination similar to that previously observed at 16 weeks in untreated SCI rats. The macrophage count in the COI is a quantitative test directly related to the severity of destructive inflammation initiated by the SCI. This test has consistently demonstrated anti-inflammatory effect of Serp-1 interpreted as neuroprotection, the first and necessary step in a therapeutic strategy in neurotrauma.

Post cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. The control of gas exchange, and in particular oxygenation and carbon dioxide levels, is fundamental in mechanically ventilated patients after resuscitation, as arterial blood gases derangement might have important effects on the cerebral blood flow and systemic physiology.In particular, the pathophysiological role of carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and oxygen demand. Hypo/hypercapnia, as well as mechanical ventilation during and after resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and catecholamine levels. The developing hypocapnia can nullify the beneficial effects of the hypothermia. The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest.According to our findings, the optimal ventilator strategies in post cardiac arrest patients are not fully understood, and oxygen and carbon dioxide targets should take in consideration a complex pattern of pathophysiological factors. Further studies are warranted to define the optimal settings of mechanical ventilation in patients after cardiac arrest.

IntroductionNickel and iron are very commonly occurring metals. Nickel is used in industry, but nowadays it is also used in medical biomaterials. Iron is an element necessary for cell metabolism and is used in diet supplements and biomaterials, whence it may be released along with nickel.Material and MethodsBALB/3T3 and HepG2 cells were incubated with iron chloride or nickel chloride at concentrations ranging from 100 to 1,400 μM. The following mixtures were used: iron chloride 200 μM plus nickel chloride 1,000 μM, or iron chloride 1,000 μM plus nickel chloride 200 μM. The cell viability was determined with MTT, LHD, and NRU tests.ResultsA decrease in cell viability was observed after incubating the BALB/3T3 and HepG2 cells with iron chloride or nickel chloride. A synergistic effect was observed after iron chloride 1,000 μM plus nickel chloride 200 μM treatment in all assays. Moreover, the same effect was observed in the pair iron chloride 200 μM plus nickel chloride 1,000 μM in the LDH and NRU assays.ConclusionsIron (III) and nickel (II) decrease cell viability. Iron chloride at a concentration of 200 μM protects mitochondria from nickel chloride toxicity.

IntroductionTumours connected with head and neck comprise about 5% of all tumours. The most frequent histological type of laryngeal carcinoma is squamous cell carcinoma. Different research projects suggest that the role of T lymphocytes might be significant in tumour development. iNKT cells are a new subpopulation of T cells and show cytotoxic activity against tumours. iNKT cells participate in modulating the function of other cells which have anti-tumour properties and secrete cytokines, which have pro-inflammatory and anti-inflammatory effects. In animal models the significance of iNKT cells in various diseases including cancer was shown.Aim of the studyThe aim of this study was to determine the percentages of iNKT cells, CD161+ cells, CD161– cells, iNKT CD4+ cells, and iNKT CD8+ cells, NK cells, NKT-like cells, and T cells subsets present in peripheral blood of patients with laryngeal cancer before and two months after the tumour resection, in comparison to healthy volunteers.Materials and methodsThis study included material from laryngeal patients who were treated at the Department of Otolaryngology and Laryngological Oncology (Medical University of Lublin) between 2012 and 2013. A total of 50 patients (40 men and 10 women) aged between 45 and 77 years (median age: 60 years) were enrolled. Based on the TNM classification, the patients were classified as having stage I-IV laryngeal cancer. The control group was composed of 15 healthy volunteers (12 men and three women) aged between 43 and 82 years (median age: 61 years). The protocol of the study was approved by the Local Bioethical Committee at the Medical University of Lublin.Peripheral blood samples (15 ml) from the basilic vein were collected by venipuncture using sterile, sodium heparin-treated tubes (20 units per ml of blood) and used for cytometric analyses.ResultsiNKT cells were analysed among T CD3+ cells. The percentage of CD3+ and CD3+CD4+ T cells before tumour resection was higher than in the control group, but the increase of CD3+ T cells was not significant. The T CD3+CD4+ / T CD3+CD8+ cell ratio was significantly higher than in healthy donors. After tumour resection a decreased percentage of CD3+CD4+ T cells but an increased percentage of CD8+CD3+T cells was noted. The T CD3+CD4+ / T CD3+CD8+ cell ratio was significantly higher in patients before and after the surgery than in the control group. The amount of NKT-like cells increased after resection and was significantly higher than in the control group.ConclusionsOur study exhibited the change in percentage of iNKT, NK, NKT-like cells, and T lymphocytes after tumour resection in patients with laryngeal cancer. The research explains the contribution of those cells in immunological response against tumour.

BackgroundFingolimod is a drug administered orally to adult patients treated for relapsing remitting course of multiple sclerosis (MS). Mode of action of fingolimod is based on intense S1P1 receptor stimulation and “arresting” lymphocytes in lymphatic organs. Objective of the research was to assess changes in the frequencies of basic lymphocyte subsets in patients treated for multiple sclerosis with the use of fingolimod.Material and methodsStudy group comprised of 25 previously untreated adult patients with MS. Venous blood samples were collected from each patient before and one month, three months and six months after treatment initiation. Peripheral blood lymphocyte immunophenotype was assessed with a set of monoclonal antibodies bounded to appropriate fluorochromes and flow cytometer FACSC alibur. Statistical analysis of the results was conducted using Statistica 9.0 software.ResultsBefore fingolimod administration median of lymphocyte subsets percentage in each patient was in reference range. After 1 month of treatment we noticed significant changes in frequencies of following lymphocyte subsets: NK cells – 51.22% (p = 0.016), T CD4+ cells – 11.58% (p = 0.01), T CD4+:T CD8+ cells ratio – 0.61 (p = 0.005). After 3 and 6 months of treatment there was further increase of deviation from normal state.ConclusionsThe use of fingolimod is associated with profound changes in lymphocyte subsets distribution, which might bear a risk of the development of cellular immune deficiency symptoms.

Delirium, an acute alteration in mental status characterized by confusion, inattention and a fluctuating level of arousal, is a common problem in critically ill patients. Delirium prolongs hospital stay and is associated with higher mortality. The pathophysiology of delirium has not been fully elucidated. Neuroinflammation and neurotransmitter imbalance seem to be the most important factors for delirium development. In this review, we present the most important pathomechanisms of delirium in critically ill patients, such as neuroinflammation, neurotransmitter imbalance, hypoxia and hyperoxia, tryptophan pathway disorders, and gut microbiota imbalance. A thorough understanding of delirium pathomechanisms is essential for effective prevention and treatment of this underestimated pathology in critically ill patients.

No abstract