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Abstract Background A minority of European countries have participated in international comparisons with high level data on lung cancer. However, the nature and extent of data collection across the continent is simply unknown, and without accurate data collection it is not possible to compare practice and set benchmarks to which lung cancer services can aspire. Methods Using an established network of lung cancer specialists in 37 European countries, a survey was distributed in December 2014. The results relate to current practice in each country at the time, early 2015. The results were compiled and then verified with co-authors over the following months. Results Thirty-five completed surveys were received which describe a range of current practice for lung cancer data collection. Thirty countries have data collection at the national level, but this is not so in Albania, Bosnia-Herzegovina, Italy, Spain and Switzerland. Data collection varied from paper records with no survival analysis, to well-established electronic databases with links to census data and survival analyses. Conclusion Using a network of committed clinicians, we have gathered validated comparative data reporting an observed difference in data collection mechanisms across Europe. We have identified the need to develop a well-designed dataset, whilst acknowledging what is feasible within each country, and aspiring to collect high quality data for clinical research.

Scientific communication has become global and almost instantaneous, and as the Editor in Chief, I feel that it is my duty to present you with the BJBMS as one of the main platforms highlighting the increasing advancements in the basic medicine. The BJBMS aims to cover the broadness of basic medical science and also make the link between the basic research and clinical studies and vice versa. In this we fully depend on you, as potential authors submitting manuscripts to our Journal. But the mainstay of the Journal is top-quality original science. Which studies receive the highest priority? This obviously strongly depends on novelty, the relevance of the research question, and on the strength of the design and data. We also feature strong cell biology and animal studies, which provide the scientific basis of the clinical sciences. As many of you know, we love novel technology, so new molecular methods, imaging and proof-of-concept therapy receive relatively high priority in our Journal. The BJBMS reaches out to you through the web, at www.bjbms.org and of course in its printed form, which arrives on your doors every three months. We were pleasantly surprised to find that the electronic BJBMS has about 1500 visits per month! It’s twice more than in the same time last year. The largest number of visitors is from Bosnia & Herzegovina, USA, Serbia, Turkey, India, Croatia, etc. We will continue to make a positive selection of the best papers, which at the time being means we accept one in five/six submitted manuscripts. Based on the above, we will adjust our 2007 instructions to authors at our journal. This is based on the uniform requirements for manuscripts submitted to biomedical journals1. Please read it, because it is meant to assist you in getting your manuscripts up to the currently advocated international quality standards. All this illustrates a delightful balance between dynamics and innovation on the one hand, and consistency and experience on the other. This is the way we like it; this is our BJBMS.

This retracts the article "EVALUATION OF CARCINOGENIC EFFECTS OF ELECTROMAGNETIC FIELDS (EMF)" on page 245. The Editor-in-chief of the Bosnian Journal ofBasic Medical Sciences has decided to retract the article from Bayazit V et al. [1] entitled as: “Evaluation of carcinogenic effects of electromagnetic fields (EMF)” published in Bosn J Basic Med Sci. 2010 Aug;10(3):245-50.After the editorial office was alerted of possible plagiarism in the article, it conducted thorough investigation and concluded that the article apparently represents plagiarized material from two World Health Organization reports, one European Commission report and other sources. Since this is considered scientific plagiarism and scientific misconduct, Editor-in-chief has decided to withdraw the article. The authors have agreed with the editorial office decision.

Aim To examine whether preoperative tumour size may serve as a biomarker for the occurrence of lymphovascular invasion (LVI) in centrally and peripherally located lung adenocarcinoma. Method The study included 261 patients surgically treated for diagnosed lung adenocarcinoma. A ROC curve was used to determine the biomarker potential of tumour size relative to the occurrence of LVI. Binary logistic regression was used to show changes of tumour size impact on the status of LVI. Result Tumour prevalence according to localization had no statistical significance (p=0.464), while the presence of LVI in central, as well as peripheral positions, was statistically significantly different (p

The aim of the study was to detect prevalence of MBL2 exon 1 (codons 52, 54 and 57) genetic polymorphism in postmenopausal women in Bosnia and Herzegovina and its possible role as genetic risk factor for susceptibility to occurrence of osteoporosis in this study group. Also, we investigated association between MBL serum concentrations and osteoporosis in postmenopausal women. Genetic codons’ variations were determined by PCR-RFLP and MBL in serum was measured by ELISA method in 75 postmenopausal women (37 with osteoporosis and 38 apparently healthy, non-osteoporotic women serving as a control). Serum MBL levels were not significantly different between osteoporosis and control group (492 (37-565.1) and 522.6 (477-559.4) ng/mL respectively, p=0.206). Genotype frequencies were not significantly different (p=0.997) between the studied groups of postmenopausal women. Genotype frequencies A/A, A/o and o/o in osteoporosis group were 0.576; 0.405; 0.018 and in control group 0.562; 0.412; 0.026, respectively. Frequencies of A and o allele were 0.78 and 0.22 in osteoporosis and 0.77 and 0.23 in control group. The results do not suggest association of functional polymorphism of MBL2 gene and MBL serum concentration with osteoporosis in postmenopausal females.

The most vital part of a scientific journal is the Editorial board and Advisory board. So, it is never good that the composition of these boards lasts longer than 2-3 years. With the first number of BJBMS in 2014, a new composition of the Editorial board and Advisory Board of this journal was published. They consist of eminent scientists with adequate qualifications from nine countries and who can actively contribute to the good management of the journal and its further development. Their tasks will be: - Supporting and promotion of the journal (being true ambassadors of the journal), - Writing editorials, reviews and commentaries on works from the field of their expertise, - Giving opinions and suggestions on the management and policy of the journal, with the timely identification of the upcoming challenges. Commitment to upholding the ethics of publishing with impartiality and confidentiality, the fight against plagiarism and multiple or simultaneous publication of articles will remain a priority in the work of the Editorial Board and Advisory Board of BJBMS. Also, the newly appointed boards will continue to work in the way of protection of copyright for authors who were victims of plagiarism. In this sense, the editor in chief, together with the Editorial Board will take measures in accordance with the guidelines of the Committee for Ethics in publishing [1]. Quality assurance in publishing and also in BJBMS is focused on the detection of forged data, images, and plagiarized articles. In its future work Editorial Board of BJBMS is obliged to pay attention to supporting academic integrity, ensuring the integrity of academic records and intellectual property. This latter implies: - Request for evidence of ethics for the approved research, that is, authors will be asked to prove that they obtained the consent of the patient for the study or in the case of experiments on animals, which methods were used so the animals would not suffer? - Ensuring that reports of clinical trials are in accordance with the Declaration of Helsinki [2], good clinical practice [3] and other relevant guides secure participation, - Ensuring that the reports of experiments and animal studies provided in accordance with the guide of healthy and humane service care and the use of laboratory animals [4] and of other relevant guides, - Adopting systems for detecting plagiarism in submitted works, - Supporting the authors whose copyright has been infringed or who were victims of plagiarism, - Readiness in the defence of the rights of authors (i.e. demanding the withdrawal or removal of materials from websites, journals, etc.) Regarding the above mentioned members of the new Editorial Board and Advisory Board, I wish them to achieve equally good results in forthcoming work, such as those achieved by their predecessors in the period of 2010 – 2013.

Until today, traditional clinical diagnosis and disease management was focused on the individual patient’s clinical symptoms and signs, medical and family history, data from laboratory and imaging evaluation that led to diagnose and treatment of illnesses. This is often a reactive approach to treatment, i.e., treatment starts after the symptoms and signs appear. Advances in medical genetics have enabled a more detailed understanding of the impact of genetics in diseases. It was the main reason for developing a so called personalized medicine. Large collaborative research projects (for example, the Human genome project) have laid the groundwork for the understanding of the roles of genes in human development and physiology. Even that revealed single nucleotide polymorphisms that pointed to some of the genetic variabilities between individuals. Important biological functions: growth, death, cellular movement and localization, differentiation, etc. are controlled by a process called signal transduction. This process is nearly entirely epi-genetic and governed by protein enzyme activity. Diseases such as cancer, based on genomic mutations, are functionally manifest as dysfunctional protein signal transduction. Historically, the pharmaceutical industry has developed medications based on empiric observations and more recently, on known disease mechanisms. For example, medications for diabetes aim to improve insulin release from the pancreas and the sensitivity of the muscle cells and fat tissues on the effect of insulin. Drugs for high cholesterol, affect the absorption, metabolism, and generation of cholesterol. It means that medications are developed based on mechanisms of disease that have been extensively studied over the past century. We hope that recent advancements in the genetic etiologies of common diseases will improve pharmaceutical development. Today we discovered that information about a patient’s proteomic, genetic and metabolic profile could be used to tailor medical care to that individual’s needs. One idea of this medical model is the development of diagnostics, whereby molecular assays that measure levels of proteins, genes or specific mutations are used to provide a specific therapy for an individual’s condition by stratifying disease status, selecting the proper medication and tailoring dosages to that patient’s specific needs. Besides that, many scientists and practitioners estimate that such methods might be used to assess a patient’s risk factor for a number of conditions and tailor individual preventative treatments such as nutritional immunology approaches. Contemporary potential applications of personalized medicine include pharmacogenetics, pharmacometabolomics and cancer management. Examples of pharmacogenetics include: Genotyping for single nucleotide polymorphisms in genes involved in the action and metabolism of warfarin. This medication is used clinically as an anticoagulant but requires periodic monitoring and is associated with adverse side effects. Recently, genetic variants in the gene encoding Cytochrome P450 enzyme CYP2C9, which metabolizes warfarin 1, and the Vitamin K epoxide reductase gene (VKORC1), a target of coumarins2, have led to commercially-available testing that enables more accurate dosing based on algorithms that take into account the age, gender, weight, and genotype of an individual. Examples of personalized cancer management include: Testing for disease-causing mutations in the BRCA1 and BRCA2genes, which are implicated in familial breast and ovarian cancer syndromes. Discovery of a disease-causing mutation in a family can inform “at-risk” individuals as to whether they are at higher risk for cancer and may prompt individualized prophylactic therapy including mastectomy and removal of the ovaries. More detailed molecular stratification of breast tumors may pave the way for future tailored treatments3. Targeted therapy is used for medications’ designing which targets epidermal grow factor receptors (EGFR) in a subset of patients with Non-Small Cell Lung Cancer (NSCLC). For example, Tyrosine kinase inhibitors such as erlotinib and gefitinib have been developed to treat NSCLC, where the mutation of the epidermal growth factor receptor gene (exon 19 - 21) in lung cancer cells was detected. These medications specifically inhibit the intracellular domain of this receptor, this way making blockade of intracellular signal transduction cascade which is responsible for cellular proliferation, invasion, metastasis, angiogenesis and inhibition of apoptosis. In the future, tissue-derived molecular information might be combined with an individual’s personal medical history, family history, data from imaging, and other laboratory tests to develop more effective treatments for a wider variety of conditions.

Genetics in psychiatry is based on the application of the achievements and methods of population’s genetics, immunogenetics, cytogenetics, molecular genetics and pharmacogenetics. Methods of genealogy are already known, and so are the twins method, methods of adoption. Especially present are the methods of DNA recombination discovering the location of genes on chromosomes and creating genetic maps. For now, it can be said that chromosomes 6, 22 and 8 are in the center of attention of geneticists examining the genetic background of schizophrenia[1]. Some studies also suggest an association could be made between HLA-A9 and paranoid schizophrenia. The manic-depressive disorders are more associated with a gene on the short arm of chromosome 11 and the X chromosome. Mental disorders are polygenic and conditioned multifactorial. It is because of the interaction of a number of genetic and environmental factors. The conclusion of most studies is that for the repetition of psychiatric disorders in families heritable factors are more deserving than environmental factors (e.g. studies in families with adopted children), although it is impossible to clearly separate the effects of genetic factors from the effects of environmental factors. The first studies that have attempted to detect predisposition genes for complex diseases were studies of genetic connectivity. They were based on the search of loci - markers in families, which were passed on through generations in the same way as the disease. In the search for the association of complexed hereditary diseases and certain variations of genes in a candidate, the evaluation of endofenotyp can be of a great benefit. Complexed diseases are characterized by a very diverse clinical picture and valuable data could be obtained if we individually evaluate each isolated characteristic of phenotype. The aim of the evaluation of endophenotype in the case of psychiatric disorders, is to penetrate into the mechanisms of the brain functioning and connect them with the hereditary basis. An important advantage of the endophenotype evaluation is also, that it can work in small groups of respondents. Endophenotype evaluation includes an assessment of cognitive deficits, EEG abnormalities, and data obtained by the method of neuroimaging. Considering the current cognition about the genetics of psychiatric disorders, especially schizophrenia [2], it can be said that no single gene by itself causes brain dysfunction. Many gene variants that have proved to be risky for psychiatric disorders have also been found in many healthy individuals. Strength of correlation of the detected genetic polymorphisms is estimated to be relatively low. This means: • COMT genes’ polymorphisms (catecho-O-methyltransferase), but also many other genes, modulate cognitive functions, but they do not represent the primary cause of disease[3], • genetic risk variants for psychiatric disorders are also found in many healthy people, • “Strength” of correlation of detected genetic polymorphisms and diseases is estimated as relative. Except for the primary sequence of nucleotides in our genome, there is also likely a hidden genetic code, which does not determine the sequence of amino acids in proteins, but it determines the time when a gene turns on or off (rewrites or not). The problem with this code is that it is more or less changeable. It is because of the modification of the genome (DNA). The modification with metillization of cytosine in CpG dinucleotide turns off the gene, whereas the acetylation of histones alters the structure of chromatin and turns on the genes. Epigenetics studies[4] such modifications of genomes. Epigenetics may explain the large variability of phenotypes in human population, and why monozygotic twins are not quite identical. They do not differ in the sequence of nucleotides in DNA, but they have different modifications of DNA, because they occur and change by the effect of environmental factors. Changes of epigenetic sample are the result of the effect of environmental factors, especially nutrition, as well as chemicals that we are exposed to, social contacts, family relationships, etc. Effects of environmental factors alter epigenetic pattern in our genome and may induce abnormal gene function. Except for epigenetic modifications, there is recently recognized the importance of functional DNA sequences that do not code proteins. These sequences encode small RNA molecules that have a regulatory role – they modulate posttranslational the level of gene expression. It is assumed that functional non coding DNA sequences make up 3-4% of the human genome, as opposed to coding, which make up only 1-2%. Micro RNAs are the products of non coding genes and are complementary to specific mRNA molecules that regulate[5]. Binding with mRNA creates double-stranded complexes that degrade or inactivate. The importance of this mechanism is particularly evident in neurons considering their morphology. Body of the cell is significantly away from the synaptic endings, so these ends must have supplies of mRNA molecules that could be translated into proteins if necessary. New mRNA’s synthesized in the nucleus travel at a specified speed along the nerve fibers and dendrites. Lipids and their mediators are involved in the regulation of gene expression[6]. The brain in its dry state consists almost exclusively of lipids. Some of the lipids are particularly abundantly present in the brain and we need to discover the mechanisms by which the brain is able to retain such amount of certain lipid molecules. Lipidomics could provide a molecular list of cellular signaling pathways of complexed diseases. Signaling by lipids is extremely complexed and very difficult to study. Lipids and their mediators in the brain are represented as: • - long-chain unsaturated fatty acids AA and DHA (they determine the dynamic properties of neuronal membranes, regulate ion channels and signal transduction, activate transcription factors and regulate gene expression), • - endocannabinoids (they regulate behavior, sedation, euphoria, appetite, memory), • - sterols (cholesterol) (they regulate the dynamics of lipid rafts - signal transduction), • - sphingolipids (myelin), • - gangliosides (vitally important but an unknown role). The enzymes that metabolize the membrane’s phospholipids are related to the cell membrane and they colocalize with monoaminergic receptors, and are therefore crucial for signal transmission, but also for the creation of long-term memory.

The most widely used classification of mammalian cell death recognizes two types: apoptosis and necrosis. Autophagy, which has been proposed as a third mode of cell death allows a starving cell, or in situations when cell is deprived of growth factors, to survive. Apoptosis, autophagy and necrosis, a particular mode of cell death may predominate, depending of the injury and the type of cell. [1] One very important characteristic of all multicellular organisms is apoptosis, the controlled death of cells. In necrosis, early loss of integrity of the plasma membrane resultant with swelling of the cell and its organelles. A key morphologic feature of apoptosis is collapses of cell and its subcellular components.[2] The distinction between apoptosis and necrosis is due in part to differences in how the plasma membrane participates in these processes. In apoptosis, plasma membrane integrity persists until late in the process. In necrosis, early loss of integrity of the plasma membrane allows an influx of extracellular ions and fluid, with resultant swelling of the cell and its organelles. During that time, on the inside of cell there occurs the cleavage of cytoskeletal proteins by aspartate specific proteases, which thereby collapses subcellular components. Other characteristic features are chromatin condensation, nuclear fragmentation and the formation of plasma membrane blebs. The type and intensity of noxious signals, ATP concentration, cell type, and other factors determine how cell death occurs. Acute myocardial ischemia induces necrosis (because the ischemia precipitates rapid and profound decreases of ATP), whereas chronic congestive heart failure induces apoptosis (with more modest and chronic decreases of ATP). The blockade of a particular pathway of cell death may not prevent the destruction of the cell but may instead recruit an alternative path: antiapoptotic caspase inhibitors cause hyperacute necrosis of hepatocytes and kidney tubular cells induced by TNF-α. The over expression of antiapoptotic proteins may allow injured cells to survive, and autophagy may assist by providing critical metabolites. Apoptotic cells induce anergy or an immunosuppressive phenotype, whereas necrotic cells augment inflammation, in part by binding the receptor C-type lectin domain family 9 on dendritic cells. Clinical implications of apoptosis are consist in more than 50% of neoplasm’s that have defects in the apoptotic machinery mutations in the tumor-suppressor gene TP53, that is called the “guardian of the genome,” initiates apoptosis in response to DNA damage induced by radiation, chemical agents, oxidative stress, and other agents.[3] Abnormalities in apoptosis can increase susceptibility to autoimmune diseases.[4] There is growing evidence that neuronal apoptosis plays a key role in neonatal brain disorders.[5] Hepatocytes are particularly prone to apoptosis in response to various types of stress, including infections.[6] Necrosis predominates in ischemic injury, but often there are apoptotic cells in the hypoxic penumbra in myocardial infarction and stroke and in globally hypoxic zones after reperfusion injury. Sepsis is perhaps the most remarkable clinical setting in which apoptosis occurs. Massive apoptosis of immune effectors’ cells and gastrointestinal epithelial cells develops in patients with sepsis.[7] The profound loss of immune effectors’ cells in sepsis inhibits the ability of the immune system to eradicate the primary infection and renders the patient susceptible to nosocomial infections. Finally, why apoptosis is good? Because without apoptosis, 2 tons of bone marrow and lymph nodes and a 16-km intestine would probably accumulate in a human by the age of 8o.[8]

A person’s reaction to trauma depends on the traumatic situation itself, personality characteristics of the person exposed to trauma, and posttraumatic social environment. Stressor must be extreme event that is extremely dangerous or fatal nature, and which is outside normal human experience [1]. Studies investigating psychological consequences of military and civil trauma confirmed the correlation between the nature and intensity of trauma, previous traumatic experience, and psychological consequences. Stress causes the autonomic nervous system hyperactivity. If the stress is extreme or constant symptoms of hyperactivity, increased heart rate, increased respiration, sweating, muscle tension, insomnia and increased anxiety are becoming significant for the prolonging the symptoms of PTSD. Our cells are well adapted to exposure to a mild stress for a short time. In contrast there are potentially serious consequences of exposure to the prolonged stress[2]. Various damages arising from the war in Bosnia (1992 - 1995) are almost undetectable, and the consequences for the mental health of the population of Bosnia and Herzegovina are long and painful. It is estimated that in Bosnia and Herzegovina there are 1.75 million people who have some stress-related mental disorders, of which 1 million in the Federation. PTSD may be represented by mutations that must be carried by many genes. There may even be epigenetic reasons for the disorder that have nothing to do with heritable mutations per se. Epigenetic means related to functional changes in the genome that can be regulated by external environmental events that do not involve alterations in the genetic code. One epigenetic mechanism is called “methylation,” a molecular process that affects the activity of a large percentage of genes. Epigenetic investigations say that methylation may be involved in the development of stress regulation in early life[3]. A number of longitudinal studies have looked at independent variables spanning the entire course of the illness. A 10-year follow-up study in Holocaust survivors clearly demonstrated decline in stress hormone levels for those patients in whom PTSD developed or in whom PTSD was chronic. No such decline was shown for those survivors who did not present with PTSD. Indeed, they showed a relative increase in hormone levels [4]. Hippocampal volume has also been studied (using the same types of experiments as the twin studies described previously). Hippocampal volume can be quite variable. It can change as a result of environmental exposure, duration of certain illnesses, and even the age of the subject. As noted, shrunken hippocampal volume has been shown in PTSD patients, but most of these are younger cohorts. When one examines PTSD in older cohorts, the differences in volume evaporate, and no linkage with disease is observed [5]. Microarray analysis is a powerful way to look at global gene expression profiles in tissues which can identify relevant molecular processes. On that way we have enough tools on hand to find the genes responsible for the disorder. Studying such genes can lead to creating effective treatments, including designing medications that are not only specific to the disorder but also specific to an individual’s experience with the disorder.

A major requirement both of national and international ethical codes for human experimentation, and of national legislation in many cases, is that new substances or devices should not be used for the first time on human beings unless previous tests on animals have provided a reasonable presumption of their safety. That is so called: Good Clinical Praxis (GCP). There are two international ethical codes intended principally for the guidance of countries or institutions that have not yet formulated their own ethical requirements for human experimentation: The Declaration of Helsinki of the World Medical Association and The Proposed International Guidelines for Biomedical Research Involving Human Subjects of the Council for International Organizations of Medical Sciences and the World Health Organization[1]. Animal experimentation is fundamental to the biomedical sciences, not only for the advancement of specific vital processes, but also for the improvement of methods of prevention, diagnosis, and treatment of disease both in man and in animals. The use of animals is also indispensable for testing the potency and safety of biological substances used in human and veterinary medicine, as well as for determining the toxicity of the rapidly growing number of molecules that never existed before in nature and which may represent a hazard to health. This extensive exploitation by man of animals implies philosophical and moral problems that are not peculiar to their use for scientific purposes, and there are no objective ethical criteria by which to judge claims and counterclaims in such matters[2]. However, there is a consensus that „deliberate cruelty is repugnant”. While many countries have general laws or regulations imposing penalties for ill-treatment of animals, relatively few make specific provision for their use for scientific purposes. Because of differing legal systems and cultural backgrounds there are varying approaches to the use of animals for research, testing, or training in different countries. In the few that have done so, the measures adopted vary widely: on the one hand, legally enforceable detailed regulations with licensing of experimenters and their premises together with an official inspectorate; on the other, entirely voluntary self-regulation by the biomedical community, with lay participation. Many variations are possible between these extremes, one intermediate situation being a legal requirement that experiments or other procedures involving the use of animals should be subject to the approval of ethical committees of specified composition. The International Guiding Principles are the product of the collaboration of a representative sample of the international biomedical community, including experts of the World Health Organization, and of consultations with responsible animal welfare groups. The International Guiding Principles have already gained a considerable measure of acceptance internationally. European Medical Research Councils (EMRC), an international association that includes all the West European medical research councils, fully endorsed the Guiding Principles in 1984. Here we bring the basic bioethical principles for using animals in biomedical research[3]: • Methods such as mathematical models, computer simulation and in vitro biological systems should be used wherever appropriate, • Animal experiments should be undertaken only after due consideration of their relevance for human or animal health and the advancement of biological knowledge, • The animals selected for an experiment should be of an appropriate species and quality, and the minimum number required to obtain scientifically valid results, • Investigators and other personnel should never fail to treat animals as sentient, and should regard their proper care and use and the avoidance or minimization of discomfort, distress, or pain as ethical imperatives, • Procedures with animals that may cause more than momentary or minimal pain or distress should be performed with appropriate sedation, analgesia, or anesthesia in accordance with accepted veterinary practice. Surgical or other painful procedures should not be performed on unanesthetized animals paralyzed by chemical agents, • Where waivers are required in relation to the provisions of article V, the decisions should not rest solely with the investigators directly concerned but should be made, with due regard to the provisions of articles IV, and V, by a suitably constituted review body. Such waivers should not be made solely for the purposes of teaching or demonstration, • At the end of, or, when appropriate, during an experiment, animals that would otherwise suffer severe or chronic pain, distress, discomfort, or disablement that cannot be relieved should be painlessly killed, • The best possible living conditions should be maintained for animals kept for biomedical purposes. Normally the care of animals should be under the supervision of veterinarians having experience in laboratory animal science. In any case, veterinary care should be available as required, • It is the responsibility of the director of an institute or department using animals to ensure that investigators and personnel have appropriate qualifications or experience for conducting procedures on animals. Adequate opportunities shall be provided for in-service training, including the proper and humane concern for the animals under their care. Also see Draft CIOMS Guiding Principles 2011 to be used by the international scientific community to guide the responsible use of vertebrate animals in scientific and/or educational activities[4]. Go to: Alternatives for animal in biomedical research There remain many areas in biomedical research which, at least for the foreseeable future, will require animal experimentation. An intact live animal is more than the sum of the responses of isolated cells, tissues or organs; there are complex interactions in the whole animal that cannot be reproduced by biological or non-biological “alternative” methods. The term “alternative” has come to be used by some to refer to a replacement of the use of living animals by other procedures, as well as methods which lead to a reduction in the numbers of animals required or to the refinement of experimental procedures. The experimental procedures that are considered to be “alternatives” include biological and non-biological methods. The biological methods include the use of micro-organisms, in vitropreparations (subcellular fractions, short-term cellular systems, whole organ perfusion, and cell and organ culture) and under some circumstances, invertebrates and vertebrate embryos. The non-biological methods include mathematical modeling of structure-activity relationships based on the physico-chemical properties of drugs and other chemicals, and computer modeling of other biological processes. In addition to experimental procedures, retrospective and prospective epidemiological investigations on human and animal populations represent other approaches of major importance. There no need specialy underline that the adoption of “alternative” approaches is viewed as being complementary to the use of intact animals and their development and use should be actively encouraged for both scientific and humane reasons.

Translational medicine is a medical practice based on interventional epidemiology. It is regarded by its proponents as a natural progression from Evidence-Based Medicine. It integrates research from the basic sciences, social sciences and political sciences with the aim of optimizing patient care and preventive measures which may extend beyond healthcare services. In short, it is the process of turning appropriate biological discoveries into drugs and medical devices that can be used in the treatment of patients.[1] Scientific research and the development of modern powerful techniques are crucial for improving patient care in a society that is increasingly demanding the highest quality health services.[2] Indeed, effective patient care requires the continuous improvement of knowledge on the pathophysiology of the diseases, diagnostic procedures and therapeutic tools available. To this end, development of both clinical and basic research in health sciences is required. However, what is most effective in improving medical knowledge, and hence patient care, is the cross-fertilization between basic and clinical science. This has been specifically highlighted in recent years with the coining of the term “translational research”.[3] Translational research is of great importance in all medical specialties. Translational Research is the basis for Translational Medicine. It is the process which leads from evidence based medicine to sustainable solutions for public health problems.[4] It aims to improve the health and longevity of the world’s populations and depends on developing broad-based teams of scientists and scholars who are able to focus their efforts to link basic scientific discoveries with the arena of clinical investigation, and translating the results of clinical trials into changes in clinical practice, informed by evidence from the social and political sciences. Clinical science and ecological support from effective policies can’t continue to be regarded as independent disciplines. Integrated training in translational research methods is needed for clinicians, guideline writers, grant awarding bodies, and policy makers, in order to redress current biases in funding and research publications, in order to reflect better the balance of research efforts which are necessary for better assessment of complex evidence-bases, to integrate effective and sensitive interventions with supporting environmental changes, and to encourage continuous improvement of evidence based public policies.[5] There are three major obstacles to effective translational medicine. The first is the challenge of translating basic science discoveries into clinical studies. The second hurdle is the translation of clinical studies into medical practice and health care policy.[6] A third obstacle to effective translational medicine is also philosophical. It is a fact that the available standard therapies for most common diseases are less efficacious than they are believed by the Public to be and significant funds are allocated to maintain this “placebo” effect through standard care. Proportionately, very little is spent to identify truly effective therapies. Finally, it may be a mistake to think that basic science, without observations from the clinic and without epidemiological findings of possible associations between different noxes and disease, will efficiently produce the novel therapies that we are eager to test. To pursue the promotion of translational research, the Editorial Board strongly supports basic scientific work and such that is a combination of basic research and clinical praxis.

Cigarette smoking affects all phases of atherosclerosis from endothelial dysfunction to acute occlusive clinical events. The problem is, whether the length of the period of cigarette smoking has a more reflection to the status of lipids and illnesses of cardiovascular system or the bigger number of smoked cigarettes in a shorter time-period? The observed sample has constituted of two groups of smokers, both gender, age 25-64 years old. The first group consisted of 210 examinees divided in 7 subgroups according to a number of years they have been smoking. The second group consisted of 150 examinees, which was divided in 5 subgroups, according to average number of cigarettes smoked daily. The average values of serum cholesterol (6.98 vs. 6.13 mmol/L), triglycerides (3.15 vs. 3.13 mmol/L) and LDL-cholesterol (3.80 vs. 3.64 mmol/L) were always higher in a group of smokers according to a number of daily smoked cigarettes. Average value of smoking consumption period was higher in a group of smokers according to the length of smoking consumption period than in a group of smokers according to a number of cigarettes smoked daily (20.34 y vs. 13.55 y.). Hypertension (72% vs. 30.9%), angina pectoris (44.6% vs. 20.4%), CHD (30.6% vs. 22.8%) and myocardial infarction (16% vs. 11.4%) appeared much more in the group of smokers according to a number of cigarettes smoked daily. More reflection to the status of lipids and illnesses of cardiovascular system has the bigger number of smoked cigarettes daily than the length of the period of cigarette smoking.

HeadHER1/EGFR is known to play a pivotal role in tumorigenesis and is overexpressed in up to 80% of NSCLCs. The study of an Expanded Access Clinical Program of Erlotinib in NSCLC is a phase IV openlabel, non-randomized, multicenter trial in patients with advanced (inoperable stage IIIb/IV) NSCLC who were eligible for treatment with erlotinib but had no access to trial participation. Patients for the study from Bosnia and Herzegovina (B&H) were selected from two Clinical centres (Sarajevo and Banja Luka). The aim of study was to evaluated efficacy and tolerability of erlotinib monotherapy in this setting. All patients who received at least one dose of erlotinib and data were entered in the database as of the CRF cut-off date of 14th May 2008 were included in analysis of data (n = 19). This population is defined as the Intent to Treat (ITT) population and includes all patients who had at least one dose of erlotinib regardless of whether major protocol violations were incurred. The findings are consistent with the results of the randomized, placebo-controlled BR.21 study. Indicating that erlotinib is an effective option for patients with advanced NSCLC who are unsuitable for, or who have previously failed standard chemotherapy. In B&H group of patients DCR was almost 84%, and PFS was approximately 24,7 weeks (compared with 44% and 9,7 weeks for erlotinib reported in phase III). Almost three quarter of the patients received erlotinib as their second line of therapy. Overall, erlotinib was well tolerated; there were no patients who withdrew due to a treatment-related AE (mainly rash) and there were few dose reductions. 24% of patients experienced an SAE (most commonly gastrointestinal (GI) disorders).

There is the question about the role of fixed combination of inhalatory corticosteroids and long acting β2 agonists in the treatment of patients admitted in hospital due to AECOPD. The objective of this study is to determine the frequency of etiologic factors of AECOPD, to research the length of recovery time and the time free from exacerbation due to AECOPD at the patients treated with fixed combination inhalers containing F/S versus patients who were not treated with this combination. This is retrospective-prospective, randomized, clinical study with a sample size of 70 patients who admitted to hospital due to AECOPD type I or II. Patients are randomized in two groups. Prospective group from 36 patients have been treated with oral or parenteral corticosteroids 7 - 14 days, other medications and fixed combination inhalers containing a F/S. Second, retrospective group from 34 patients have been treated with oral or parenteral corticosteroids 7 - 14 days (in time when we didn’t have fixed combination inhalers containing a F/S) and other medications. In both groups (prospective and retrospective) the most frequent etiological factors of AECOPD was bacterial infection, after that viral infection, other factors as well as congestive heart failure. Average recovery time for symptoms of AECOPD was statistically significant shorter in group patients treated with fixed combination inhalers containing F/S (prospective group) than in group treated without this fixed combination. There are also significant differences in average number of days need for recovery in subgroups of patients by etiological factors of AECOPD, except in cases of AECOPD onset because of congestive heart failure. Average free time from exacerbation at the patients treated with fixed combination inhalers was statistically significant longer than in group of patients who were not treated with this combination. In this study has demonstrated the presence of pathogenic bacteria in 53% our patients hospitalized due to AECOPD. There were 26% patients whose exacerbation is signed as viral origin. 11% cases had congestive heart failure. Average recovery time for non-viral AECOPD was 14,8 days and for exacerbations of viral origin 27,4 days. Average free time from exacerbation at the patients treated with fixed combination inhalers containing a F/S was statistically significant longer than in group of patients who were not treated with this combination. There were no statistically significant differences in average number of exacerbation during the year, between observed groups.