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Bioethics was created in the 70s of the last century. From this period come works written by Van Resselaer Potter and André Hellegers, in which the authors raised the issue of the need to discuss the progress and to define a new reflection, they used for the first time in the scientific literature the term bioethics. In the United States of America, as well as in European countries, institutions began to emerge in which scientific bioethical reflection was realized. In Poland in the 1970s, the socio-political situation was not conducive to the integration of scientific circles or the freedom of exchange of views. Significant progress in the field of medicine, emerging new treatment options, posed questions that had to be answered. The questions were formulated in different environments, including by doctors who themselves participated in the progress of medical sciences, introducing, for example, new increasingly aggressive treatments, or saw new challenges emerging in the medical profession, which were not regulated by the hitherto applied principles of classical medical ethics. The article describes the achievements of prof. Jan Nielubowicz, prof. Józef Bogusz and prof. Tadeusz Kielanowski in the creation of Polish bioethical regulations in the field of experimental research in humans, the activity of prof. Kornel Gibińki in the formation of Bioethics Commisions, contribution of prof. Stefan Raszeja and prof. Marek Sych in bioethical education of the society and the role of prof. Krzysztof Szczygieł in the creation of the first Polish scientific bioethical unit., (© 2018 MEDPRESS.)

Significant recovery of discussion about the need for the formulation of criteria of death was provoked due to the progress of medicine. Development of anaesthesiology and intensive therapy, introduction of new resuscitation techniques and devices, which are increasingly better able to maintain and sometimes even replace functions of the respiratory or cardiovascular system, which are essential for the survival meant that existing for centuries, socially accepted classical criteria of death, based on cessation of breath and circulation, are no longer sufficient. The criteria of brain death developed by the Ad Hoc Committee - 12-experts commission at Harvard University, published in Journal of American Medical Association in August 1968 and were the breaking point. The concept has been adopted and accepted by society in many countries soon, while in Poland the process of formulating and introduction of criteria for brain death took much more time. Based on the available literature and preserved archival materials, this article describing the process of development of new death criteria, acceptance by the National Team of Specialists and publication in 1984 the announcement by the Minister of Health and Social Welfare about the criteria of brain death.

Cancer cells exhibit an altered metabolism characterized by enhanced glycolysis and glucose consumption. In glucose‑addicted cancer cells upregulation of glucose transport across the plasma membrane is mediated by a family of facilitated glucose transporter proteins, particularly glucose transporter 1 (GLUT1). The aim of the present study was to investigate the impact of GLUT1 expression on glucose uptake and viability of FTC-133 and 8305c thyroid cancer cells growing in hypoglycemic, normoglycemic and hyperglycemic conditions. The results showed that the total expression of GLUT1 was higher in the two cell types growing in low glucose compared to cells growing in normoglycemia or hyperglycemia and this was correlated with AKT Ser473 phosphorylation but not with the expression of hypoxia inducible factor α (HIF1α). However, the membrane expression of GLUT1 was correlated with HIF1α expression. HIF1α expression was positively correlated with the glucose concentration in FTC-133 cells, whereas this expression was inversely correlated in 8305c cells. Glucose uptake was dependent on the membrane level of GLUT1 but not total GLUT1 expression. Downregulation of GLUT1 expression by RNAi in FTC-133 cells caused a reduction in glucose uptake but did not significantly affect cell viability. In the case of 8305c cells showing low endogenous GLUT1 expression and lack of HIF1α expression in normoxic conditions GLUT1 RNAi impacted cell viability. These data suggested that GLUT1 may be part of an AKT1-dependent mechanism allowing cells to survive in low levels of glucose. Glucose concentration inversely affected HIF1α expression and the level of GLUT1 in membrane as well as glucose uptake in FTC-133 and 8305c cells. The extent of GLUT1 impact on cell viability was also cell-type-dependent.

First codes of medical ethics appeared between 18th and 19th century. Their formation was inspired by changes that happened in medicine, positive in general but with some negative setbacks. Those negative consequences revealed the need to codify all those ethical duties, which were formerly passed from generation to generation by the word of mouth and individual example by master physicians. 210 years has passed since the publication of "Medical Ethics" by Thomas Percival, yet essential ethical guidelines remain the same. Similarly, ethical codes published in Poland in 19 century can still be an inspiration to modem physicians.

Malignant cells are known to enhance glucose metabolism, to increase glucose uptake and to inhibit the process of oxidative phosphorylation. Accelerated glycolysis is one of the biochemical characteristics of cancer cells that allow them to compensate the inefficient extraction of energy from glucose in order to continue their uncontrolled growth and proliferation. Upregulation of glucose transport across the plasma membrane is mediated by a family of facilitated glucose transporter proteins named GLUT. Overexpression of GLUTs, especially the hypoxia-responsive GLUT1, has been frequently observed in various human carcinomas. Many studies have reported a correlation between GLUT1 expression level and the grade of tumor aggressiveness, which suggests that GLUT1 expression may be of prognostic significance. Therefore, GLUT1 is a key rate-limiting factor in the transport and glucose metabolism in cancer cells. This paper presents the current state of knowledge on GLUT1 regulation as well as its utility in the diagnosis and therapy of cancers.

O-GlcNAcylation is a common and dynamic modification of intracellular proteins in which β-N-acetyl-glucosamine moieties are attached to hydroxyl groups of serine or threonine residues (O-GlcNAc). Accumulating evidence suggests the critical role of protein O-GlcNAcylation in signal transduction, transcriptional control, cell cycle regulation and protein degradation. However, the exact role of O-GlcNAc modification in tumor pathogenesis or progression remains to be established. In the present study, we investigated the effect of increased O-GlcNAcylation of cellular proteins on IGF‑1 signaling in 8305C thyroid anaplastic cancer cells. The global O-GlcNAc level in the 8305C cells was increased by down-regulation of β-N-acetyl-D-glucosaminidase (O-GlcNAcase) activity, an enzyme which removes O-GlcNAc moieties. We demonstrated here that IGF‑1 stimulates Akt1 activity in 8305C cells, and down-regulation of O-GlcNAcase activity by the chemical inhibitor PUGNAc or RNA interference method enhances this effect. Increased Akt1 activation increased cell proliferation. In cells with down-regulation of O-GlcNAcase activity, kinase GSK3β phosphorylation and cyclin D1 levels were higher than those in control cells. Our findings suggest that increased proliferation of 8305C cells treated with PUGNAc or RNAi against O-GlcNAcase at least partially depends on the IGF‑1-Akt1-GSK3β-cyclin D1 pathway.

RNA interference is one of the most important discoveries in the field of molecular biology. To date, many studies have been reported which suggest that RNA interference takes part in various biological processes essential for the development of many diseases. On the other hand, owing to its high specificity and efficiency, RNA interference has become a powerful tool in gene therapy. However, introduction of small interfering RNAs (siRNAs) to a target tissue requires overcoming some critical biological barriers. This, in turn, contributes to searching for new effective vectors, which should selectively penetrate the tissue and be able to exclude the innate immune response. This study provides a brief overview of the application of RNA interference in the diagnosis and therapy of some human diseases.

Objectives: Noninvasive fetal RHD genotyping from maternal plasma of RhD(/-) pregnant women of Caucasian race may be used for predicting the risk of hemolytic disease because the RHD gene is usually absent in such populations. If detected in plasma of such women, the RHD gene originates from the RhD(+) fetus. The number of fetal copies of the gene in maternal plasma is extremely small. In the presented case of the RhD(/-) pregnant woman with anti-D it was impossible to give a fetal RHD result due to mother's RHD(+) genotype. The fetal RHD was determined from amniocytes., Aim: to present the difficulties related to the interpretation of results of invasive and noninvasive procedures., Material and Methods: whole blood, plasma and amniotic fluid of the RhD(-) woman with anti-D (14 week of pregnancy) as well as whole blood of the newborn. RHD and RHCE*c were genotyped by real-time PCR in DNA isolated from maternal plasma and amniocytes and the RHD and d-genotypes were tested by SSP methods in DNA isolated from whole blood and amniocytes., Results: RHD and RHCE*c were detected in DNA isolated from plasma. The high level of RHD suggested its origin from the mother's DNA therefore it was impossible to determine the fetal RHD. The d-little test identified a RHD(IVS3+ 1G>A) variant in the mother's genome. A weak signal of real-time PCR for the RHD was obtained in amniocytes but the RHD was not detected by SSP. The RHCE*c was detected by both methods. Results were inconclusive; the fetal RHD status remained unknown. The child was RhD(-) with RHD in its DNA undetected by either method., Conclusions: 1/The RHD(IVS3+ 1G>A) variant in the RhD(-) mother precluded formal noninvasive fetal RHD genotyping. 2/Real-time PCR is too sensitive for amniocyte testing and may lead to false results as it detects trace maternal DNA in amniotic fluid. 3/The frequency of RHD(IVS3+1G>A) occurrence in Poland requires further studies.

Diabetic retinopathy is one of the most common causes of blindness. The majority of studies concerning this problem were performed in patients with late stage of disease, demonstrating proliferative retinopathy, when malformations of retinal vessels became irreversible. Numerous angiogenic factors related to retinal angiogenesis have been described. Among them, VEGF is thought to be the major mediator of proliferative retinopathy. Our present study was performed on sera collected from patients with earlier stage of ocular complications, manifested as background retinopathy. We have believed that the knowledge of the earliest events leading to pathological angiogenesis may be valuable for establishing some prophylactic regimens. Sera of 22 persons with DM1, aged 33-70 years, 37 persons with DM2, aged 37-79 years, 51 healthy people, aged 22-80 years (as controls) were studied. Direct serum-induced cutaneous angiogenesis test in mice (SIA) was applied. VEGF concentration in sera was mesured by ELISA (R & D Systems) test. Angiogenic activity and VEGF concentration of DM1 patients sera were highly statistically lower than these parameters in DM2 patients and controls.

Galectin-3 is a 31 kDa member of a growing family of beta-galactoside-binding animal lectins. This protein is expressed in a variety of tissues and cell types and is mainly found in the cytoplasm, although, depending on cell type and proliferative state, a significant amount of this lectin can also be detected in the nucleus, on the cell surface or in the extracellular environment. Galectin-3 is secreted from cells by a novel and incompletely understood mechanism that is independent of the classical secretory pathway through the endoplasmic reticulum/Golgi network. Galectin-3 exhibits pleiotropic biological function, playing a key role in many physiological and pathological processes.

Diabetes is associated with a hypercoagulable state. Eighty percent of patients with diabetes mellitus die due to various thrombotic vascular complications. Disorder of coagulation and fibrynolysis is associated with diabetic retinopathy and nephropathy. Angiogenesis requires degradation of vascular basement membrane prior to migration and proliferation of endothelial cells. Various serine proteases play important role in this process. The homeostatic system is also the source of endogenous inhibitors of angiogenesis. Human serum contains various factors able to induce or suppress formation of new blood vessels. The aim of the present study was to evaluate the activity of some angiogenesis inhibitors, anti-proteases, anti-thrombin III, a1 anti-trypsin and a2 anti-plasmin in sera of patients with diabetes mellitus type 1 and 2 and non-proliferative retinopathy, and to correlate this activity to total angiogenic potential of these sera, measured by mice cutaneous test. Sera of 22 persons with DM1, aged 33-70 years, 35 persons with DM2, aged 37-79 years, and 51 healthy people, aged 22-80 years (as control group) were studied. Direct serum-induced cutaneous angiogenesis test in mice (SIA) was applied. Berichrom (ade Behring) tests and immunoturbidimetric method were used for evaluation of anti-proteases activity. Angiogenic activity of DM1 patients sera was statistically lower than this parameter in DM2 patients and in control group. Levels of anti-proteases were similar in DM1, DM2 and control group, with one exception: anti-thrombin level was lower in DM2 patients' sera than this in the control group. Analysis of correlation revealed important difference in behaviour of DM1 sera, as compared to other groups. Significant negative correlation was observed between angiogenic activity and anti-thrombin, as well as anti-trypsin level of DM1 patients' sera. On the other hand, correlation analysis performed for the sera of control group revealed significant positive correlation between their angiogenic activity and anti-thrombin level. No other correlations were found.

The critical steps of modern cardiopulmonary resuscitation had arrived in the middle of our 20th century. Mouth-to-mouth ventilation was rediscovered and proven more effective than the manual methods and was combined with external chest compression into what we know today as cardiopulmonary resuscitation.