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Embassy of Good Science: Scenario in Research Ethics and Research Integrity on Authorship

Traumatic brain injury (TBI) affects millions of people worldwide. Despite numerous preclinical and clinical research of pathophysiology and therapy of TBI, it remains the most significant cause of mortality and long-term disability, especially in previously healthy young people. One of the possible reasons why there is no effective neuroprotective agent proven to improve outcomes in TBI patients could be the complex and heterogenous pathobiology of TBI. That includes different cellular, molecular, biochemical and metabolic events that lead to progressive tissue damage and associated cell death. Because the primary injury is irreversible and cannot be pharmacologically affected, novel pharmacological options have been focused on the secondary injury. The recent pharmacological investigations are directed mainly toward multifunctional drugs that could affect different harmful pathomechanisms included in TBI. Here, our studies on the effects of the multifunctional compound, a peroxisome proliferator-activated receptor γ agonist, pioglitazone, on the different parameters of the rat brain damage will be presented. This work was supported by University of Rijeka, project uniri- biomed-18-204 to Ž.G. (from 2021 to D.P.).

Introduction: Traumatic brain injury (TBI) represents a burden to healthcare due to limited management options and long-term consequences. The latter are underrepresented and contribute to naming TBI a “silent epidemic“. Neuroinflammation appears to have a significant role in the development of secondary brain injury, involving processes affecting both resolution and persistence of inflammation. The purpose of this study was to illustrate the early activation of the cell-mediated response in experimental model of TBI. Methods: Lateral fluid percussion injury (LFPI), a TBI model causing both focal cortical lesion and diffuse damage in the ipsilateral hemisphere, was induced in adult male Wistar rats. Sham-operated rats were used as a control group. Animals were sacrificed 1, 3, or 7 days following the procedure. Markers of the cellular arm of adaptive immunity, CD+ cells, were evaluated by quantitative and qualitative immunohistochemical and immunofluorescent analyses of the brain tissue. Results: The results of this study demonstrate the invasion of CD3+, CD4+, and CD8+ cells in the ipsilateral cortices of the brain-injured animals. The number of CD3+ cells significantly increased 1 day after the trauma and has decreased towards the 8th day. Furthermore, CD4+ cells were most abundantly present in the cortex 3 days after the injury. Invasion of CD8+ cells was also noted not only in the cortex but also in the ipsilateral subpial space. Conclusion: Reported results show that LFPI elicits cellular immune response in the first days following TBI, which could modulate secondary events following the trauma and determining recovery outcome. This work was fully supported by project uniri- biomed-18-204 to Prof Gordana Župan.

Traumatic brain injury (TBI) is considered a major epidemiological and socioeconomic issue of the modern age, due to traffic accidents, sports, or warfare injuries. Although there are several established animal models of TBI that portray different patterns of injury caused by brain trauma and that shed light upon pathophysiological sequelae, much is still unknown about the link between immune response and TBI. The aim of this research was to investigate the infiltration of T cells, indicating activation of the adaptive immunity in the brain tissue, within the first week after experimental TBI in the rat. Lateral fluid percussion injury (LFPI), a model of TBI causing both focal cortical lesion and diffuse damage in the ipsilateral hemisphere, was induced in male Wistar rats. Experiments were divided into two parts. One experiment was conducted to evaluate the time course of neuroimmune mechanisms, with animals being sacrificed at 1, 3, or 7 days post-TBI. The other arm consisted of the application of the enoxaparin (1 mg/kg), low molecular weight heparin to the rats exposed to LFPI. After the injury, animals were administered with vehicle or enoxaparin over the course of 48 hours. Sham craniotomy and vehicle treatment were performed on the control group. The results of this study show the invasion of CD3+, CD4+, and CD8+ cells in the cortices of the brain-injured animals. Enoxaparin treatment did not affect CD3+ or CD4+ cell numbers in the cortices of injured animals as it also had no significant effect on the TBI-induced neuromotor impairment. In conclusion, the results of this study indicate that the LFPI model of TBI can elicit a cellular immune response, although significant effects of enoxaparin were not observed., Sažetak Traumatska ozljeda mozga (engl. traumatic brain injury, TBI) smatra se znatnim epidemiološkim i socioekonomskim problemom modernoga doba, uslijed prometnih nesreća, sportskih ili ratom uzrokovanih ozljeda. Iako je afirmirano nekoliko životinjskih modela traume mozga koji pobliže razjašnjavaju različite patofiziološke mehanizme, i dalje se ne zna mnogo o poveznici između adaptivne imunosti i traume mozga. Cilj ovog istraživanja bio je istražiti infiltraciju T stanica u prvome tjednu nakon eksperimentalne trauma mozga u štakora, što upućuje na aktivaciju mehanizama stanične imunosti u moždanome tkivu. Lateralna ozljeda tlakom tekućine (engl lateral fluid percussion injury, LFPI) vrsta je TBI koja uzrokuje žarišnu kortikalnu leziju i difuzno oštećenje u ipsilateralnoj hemisferi. LFPI uzrokovana je na Wistar štakorima muškog spola. Pokusi su podijeljeni u 2 dijela. Prvi je pokus planiran za evaluaciju vremenskog slijeda neuroimunih mehanizama gdje su životinje žrtvovane 1, 3, odnosno 7 dana nakon traume. U drugome su pokusu dani enoksaparin (1 mg/kg), niskomolekularni heparin, ili vehikul tijekom 48 sati životinjama kojima je inducirana LFPI. Lažno žrtvovane, kraniotomiji podvrgnute životinje kojima je apliciran vehikul, sačinjavale su kontrolnu skupinu. Rezultati ovog istraživanja pokazuju invaziju CD3, CD4, i CD8 pozitivnih stanica u korteksima ozlijeđenih životinja.. Tretman enoksaparinom nije utjecao na broj CD3+ i CD4+ stanica u korteksima ozlijeđenih životinja , niti je pokazao značajan utjecaj na traumom uzrokovan deficit u motornim funkcijama. Navedeni rezultati govore u prilog aktivacije mehanizama stanične imunosti u LFPI modelu, iako nisu uočeni značajni učinci enoksaparina.

"Slagalica nasljeđa" - priručnik za opismenjavanje iz medicinske genetike ima tri namjene. Prije svega, on je edukativna slikovnica za studente, liječnike i pacijente, ali i druge zainteresirane pojedince jer su u njoj kroz ilustracije objašnjene osnove genetike čovjeka, kao i osnove medicinske genetike. Od toga kako prepoznati osobu s genetičkim poremećajem, kako nastaju i koje vrste genetičkih poremećaja postoje pa sve do toga na koji ih način možemo dijagnosticirati. Nadalje, nakon svake ilustracije na pojedinoj stranici nalaze se definicije 79 pojmova iz medicinske genetike koje čine tezaurus za studente, liječnike i pacijente koji se na bilo koji način susreću s genetičkim poremećajima. Naposljetku, ova knjiga sadrži i primjere rečenica u koje su ubačeni stručni pojmovi iz medicinske genetike, a koji su namijenjeni studentima prilikom savladavanja komunikacijskih vještina na kolegiju Medicinska genetika, ali i liječnicima prilikom informiranja svojih pacijenata o (mogućem) genetičkom poremećaju. Uz kreatoricu ideje i urednicu izdanja, doc. dr. sc. Ninu Perezu, autori izdanja su studenti šeste godine Integriranog preddiplomskog i diplomskog sveučilišnog studija Medicina i prof. dr. sc. Saša Ostojić.

Introduction: Traumatic brain injury (TBI), being one of the leading causes of death and disabilities worldwide, represents an immense problem from a socio-economical and epidemiological aspect. The adequate neuroprotective therapy that could ameliorate neuroinflammation processes is still lacking and in the focus of the preclinical research. A PPAR-γ agonist, pioglitazone, has been shown to attenuate neuronal damage, cortical loss and microglial activation in some rodent models of TBI. Aim of the study: We investigated whether pioglitazone, administered twice daily, affects the microglial morphology as well as the expression of some microglia activation markers in the parietal cortex and the hippocampus of rats following TBI. Materials and methods: Experiments were performed on adult male Wistar rats divided into three groups. Single moderate lateral fluid percussion injury was carried out over the left parietal cortex. Following the injury, animals were administered with pioglitazone or vehicle in the peritoneal cavity in two doses, first one 10 minutes and second 12 hours after injury. Sham-operated, vehicle-treated animals were used as a control group. Twenty-four hours after the injury induction, animals were sacrificed and their brains were extracted and processed for the immunohistological and the Western blot analyses. Results: Digital reconstruction and the analyses of the cells labeled with microglial- specific marker Iba-1 indicated that the brain trauma caused changes in the cellular morphological features such as the extent of the process branching. The application of the tested drug did not affect these morphological changes. However, our results suggest that pioglitazone caused a decrease in the hippocampal expression of TLR- 2, microglia activation marker. Conclusion: Preliminary results of our study imply that pioglitazone could affect some features of the posttraumatic microglial reaction after TBI in the rat. This work was fully supported by project uniri-biomed-18-204 to Ž.G.

Introduction: One of the leading causes of death and disability throughout the world, traumatic brain injury (TBI), still lacks clinically effective neuroprotective therapy. Previously it was found that, in the TBI in rats, application of a single dose of pioglitazone, a peroxisome proliferator- activated receptor-γ (PPARγ) agonist, had some limited beneficial effects on trauma-induced oxidative hippocampal damage and neurodegeneration. The aim of this study was to examine the effects of pioglitazone, applied twice daily, on the microglial activation and the expressions of inflammation (COX-2) and cell stress (HSP70) markers in the rat hippocampus following lateral fluid percussion injury (LFPI). Materials and methods: Moderate brain trauma was performed over the left parietal cortex by the LFPI method in adult male Wistar rats. Pioglitazone or vehicle were administered i.p. 10 min and 12 h after the injury. Sham- operated, vehicle treated animals were used as the control group. Rats were sacrificed 24 h after TBI and their hippocampi were prepared for the histological and western blotting analyses. Results: Pioglitazone significantly decreased TBI-induced microglial activation in the dentate gyrus of the hippocampus. TBI caused an increase in the expressions of COX-2 and HSP70, but the applied PPARγ agonist did not have an effect on the levels of these proteins. Conclusions: Our study showed that pioglitazone, applied twice daily, reduced microglial reaction in the hippocampus after TBI in the rat, but did not influence the levels of measured inflammatory and cell stress markers. This work was supported by the University of Rijeka, Croatia, project number uniri-biomed- 18-204 to Ž.G.

Dipeptidyl peptidase IV (DPP IV/CD26) is a multifunctional protein and serine protease which plays crucial roles in physiological and pathological conditions. Neuropeptide Y (NPY) is considered to have a role in the regulation of immune and inflammatory events. Vasoactive intestinal peptide (VIP) has potential protective effect on intestinal mucosa. Both VIP and NPY are gut-brain peptides and DPP IV substrates. A causal connection between DPP IV/CD26 and inflammatory events has been proposed but mechanisms of this interactions are still unclear. Our hypothesis was that DPP IV/CD26 could affect the neuroimmune response at the systemic and local levels during colitis development and resolution in mice. Our aim was to evaluate the possible role of DPP IV/CD26 and the relevance of the gut-brain axis in a colitis model in mice. A model of Crohn’s disease has been induced in CD26 deficient and wild type (C57BL/6) mice using 2, 4, 6-trinitrobenzenesulfonic acid (TNBS). Experimental animals were monitored daily and sacrified on crucial days of colitis. NPY and VIP concentrations and protein expressions likewise DPP IV/CD26 enzymatic activity have been determined among the gut-brain axis, on local and systemic levels, by ELISA and Western blot techniques. Our study revealed constitutionally significantly (p

The quality of life has been at the center of attention of numerous researchers and scientists for years. WHO defines it as “an individual's perception of position in life within the context of culture and set of values they live in, and relating to their goals, expectations, standards, and worries.” Aphasia is an acquired language impairment that results from damage to specific brain regions, affecting one or more aspects of language, typically caused by stroke. Aphasia undoubtedly affects the quality of one’s life, but it yet remains unknown in which aspects and how to measure it. The main issue of measuring the quality of life in people with aphasia is that self-assessment often requires understanding and production of language and process of information recall. On the other hand, trying to overcome these obstacles by using significant others in the assessment of quality of life of people with aphasia is problematic. That is because quality of life represents the subjective construct interpreted differently by every individual. Besides mentioned problems, it is unknown how aware are the clinicians of the necessity to assess the quality of life in planning therapy and its outcomes for people with aphasia. Even the ones willing to implement quality of life assessment in their clinical work feel they lack practice, knowledge, resources, and/or time to do so. However, despite the obstacles, scientists and clinicians should have in mind that assessment of quality of life enables the preparation of efficient therapy and the estimation of its effectiveness. Due to the speech and language difficulties commonly found in people with aphasia, big importance lies within the speech therapists, professionals who can adjust the particles in assessment of quality of life and so ease the stressful situation. All of the above implies the necessity of education of speech therapists in this field.

Aphasia is an acquired language impairment typically caused by stroke. It occurs as a result of damage to specific brain regions, affecting one or more aspects of language. Traumatic brain injury (TBI) is an injury caused by external physical force or violent movement of the head. TBI often results in cognitive, physical, behavioral, and communication difficulties. Discourse analysis, including the study of coherence, can provide information needed to understand the language manifestation of aphasia and TBI. Coherence refers to the ability to maintain thematic unity and semantic connectedness of discourse at the propositional level. The notion of impaired coherence in discourse of people with TBI is widely accepted. On the other hand, there has been considerable debate of whether such deficits exist in discourse of people with aphasia. This research studied the global coherence in narrative discourse of people with aphasia and TBI assuming that no difference would be found. The study included the analysis of transcripts of 6 subjects (3 with aphasia and 3 with TBI). All of them were patients in The Special Hospital for Medical Rehabilitation in Krapinske Toplice. Data analysis was performed in the CLAN, using a 4-point subjective scale to measure global coherence. Statistical data processing was done in IBM SPSS Statistic – version 26 (t-test). No statistically significant difference was found in the coherence of discourse of the participants with aphasia and participants with TBI (p> 0, 05). That confirmed the initial hypothesis. Therefore, it seems possible that different background difficulties are manifested in the same way. In other words, language pathology in people with aphasia and deficits of executive functions in people with TBI both result in impaired narrative organization and production. However, due to a small sample of participants and lack of control of the sociodemographic and clinical factors, caution in generalization of results is needed.