Nemzetközi kitekintés a post-mortem adatvédelemre = An International Perspective on Post-Mortem Data Protection

A huszonegyedik században, a keletkező nagy mennyiségű adat okán kiemelt figyelmet kell fordítanunk azok védelmére. Az életünk során hatalmas adathalmaz keletkezik rólunk, mely valós személyünktől akár teljesen elkülönülhet. Halálunkat követően ezek a rólunk tárolt információk, az online személyiségünk önállósodnak, tovább élnek, mely okot adhat az ezekkel kapcsolatos védelem kérdésének felvetésére. A cikkben egy nemzetközi kitekintést teszek, mely során megvizsgálom különböző külföldi államok jogszabályait, és a post-mortem adatvédelemre vonatkozó szabályozási megoldásait

A több detektorsoros komputertomográfia jelentősége a vascularis képalkotásban = The importance of multidetector computed tomography in the vascular imaging

A több detektorsoros spirál-CT-berendezések és a hozzájuk tartozó speciális rekonstrukciós szoftverek bevezetése lehetővé tette az erek jó minőségű CT-vizsgálatát. Cél és módszerek: A szerzők ismertetik a CT-angiográfiai vizsgálatok elvét, technikáját, amelyet az elmúlt három évben közel 700 saját betegükön végzett vizsgálataik eredményeivel, tapasztalataival egészítenek ki. Bemutatják a CT-angiográfia jelentőségét, valamint annak más vascularis képalkotó eljárások helyett vagy melletti alkalmazhatóságát. Következtetések: A CT-angiográfia gyors, noninvazív vizsgálati módszer, amellyel – önmagában vagy más vizsgálattal kiegészítve – pontos diagnózis állítható fel. | The introduction of multidetector CT and special post processing software has made an excellent image quality of vascular structures possible. Aim and methods: The authors present the method and technique of CT angiography, added their own experience acquired on 700 patients in the last 3 years. Beside other vascular imaging methods the importance of CT angiography and its usefulness is demonstrated. Conclusions: CT angiography is a fast, non-invasive method, and either in itself or combined with other ones it is suitable for a definitive diagnosis

Recent Progress in the Diagnosis and Management of Type 2 Diabetes Mellitus in the Era of COVID-19 and Single Cell Multi-Omics Technologies

Type 2 diabetes mellitus (T2DM) is one of the world’s leading causes of death and life-threatening conditions. Therefore, we review the complex vicious circle of causes responsible for T2DM and risk factors such as the western diet, obesity, genetic predisposition, environmental factors, and SARS-CoV-2 infection. The prevalence and economic burden of T2DM on societal and healthcare systems are dissected. Recent progress on the diagnosis and clinical management of T2DM, including both non-pharmacological and latest pharmacological treatment regimens, are summarized. The treatment of T2DM is becoming more complex as new medications are approved. This review is focused on the non-insulin treatments of T2DM to reach optimal therapy beyond glycemic management. We review experimental and clinical findings of SARS-CoV-2 risks that are attributable to T2DM patients. Finally, we shed light on the recent single-cell-based technologies and multi-omics approaches that have reached breakthroughs in the understanding of the pathomechanism of T2DM

Metabolic syndrome influences cardiac gene expression pattern at the transcript level in male ZDF rats

Background: Metabolic syndrome (coexisting visceral obesity, dyslipidemia, hyperglycemia, and hypertension) is a prominent risk factor for cardiovascular morbidity and mortality, however, its effect on cardiac gene expression pattern is unclear. Therefore, we examined the possible alterations in cardiac gene expression pattern in male Zucker Diabetic Fatty (ZDF) rats, a model of metabolic syndrome. Methods: Fasting blood glucose, serum insulin, cholesterol and triglyceride levels were measured at 6, 16, and 25 wk of age in male ZDF and lean control rats. Oral glucose tolerance test was performed at 16 and 25 wk of age. At week 25, total RNA was isolated from the myocardium and assayed by rat oligonucleotide microarray for 14921 genes. Expression of selected genes was confirmed by qRT-PCR. Results: Fasting blood glucose, serum insulin, cholesterol and triglyceride levels were significantly increased, glucose tolerance and insulin sensitivity were impaired in ZDF rats compared to leans. In hearts of ZDF rats, 36 genes showed significant up-regulation and 49 genes showed down-regulation as compared to lean controls. Genes with significantly altered expression in the heart due to metabolic syndrome includes functional clusters of metabolism (e.g. 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2; argininosuccinate synthetase; 2-amino-3ketobutyrate-coenzyme A ligase), structural proteins (e.g. myosin IXA; aggrecan1), signal transduction (e. g. activating transcription factor 3; phospholipase A2; insulin responsive sequence DNA binding protein-1) stress response (e.g. heat shock 70kD protein 1A; heat shock protein 60; glutathione S-transferase Yc2 subunit), ion channels and receptors (e.g. ATPase, (Na+)/K+ transporting, beta 4 polypeptide; ATPase, H+/K+ transporting, nongastric, alpha polypeptide). Moreover some other genes with no definite functional clusters were also changed such as e. g. S100 calcium binding protein A3; ubiquitin carboxy-terminal hydrolase L1; interleukin 18. Gene ontology analysis revealed several significantly enriched functional inter-relationships between genes influenced by metabolic syndrome. Conclusions: Metabolic syndrome significantly alters cardiac gene expression profile which may be involved in development of cardiac pathologies in the presence of metabolic syndrome

Spreading depolarization remarkably exacerbates ischemia-induced tissue acidosis in the young and aged rat brain

Spreading depolarizations (SDs) occur spontaneously in the cerebral cortex of subarachnoid hemorrhage, stroke or traumatic brain injury patients. Accumulating evidence prove that SDs exacerbate focal ischemic injury by converting zones of the viable but non-functional ischemic penumbra to the core region beyond rescue. Yet the SD-related mechanisms to mediate neurodegeneration remain poorly understood. Here we show in the cerebral cortex of isoflurane-anesthetized, young and old laboratory rats, that SDs propagating under ischemic penumbra-like conditions decrease intra and- extracellular tissue pH transiently to levels, which have been recognized to cause tissue damage. Further, tissue pH after the passage of each spontaneous SD event remains acidic for over 10 minutes. Finally, the recovery from SD-related tissue acidosis is hampered further by age. We propose that accumulating acid load is an effective mechanism for SD to cause delayed cell death in the ischemic nervous tissue, particularly in the aged brain