Introduction: Trauma scoring systems in prehospital settings are supposed to ensure the most appropriate in-hospital treatment of the injured. Aim of the study: To determine the sensitivity and specificity of the CRAMS scale (circulation, respiration, abdomen, motor and speech), RTS score (revised trauma score), MGAP (mechanism, Glasgow Coma Scale, age, arterial pressure) and GAP (Glasgow Coma Scale, age, arterial pressure) scoring systems in prehospital settings in order to evaluate trauma severity and to predict the outcome. Materials and Methods: A prospective, observational study was conducted. For every trauma patient, a questionnaire was initially filled in by a prehospital doctor and these data were subsequently collected by the hospital. Results: The study included 307 trauma patients with an average age of 51.7 ± 20.9. Based on the ISS (injury severity score), severe trauma was diagnosed in 50 (16.3%) patients. MGAP had the best sensitivity/specificity ratio when the obtained values indicated severe trauma. The sensitivity and specificity were 93.4 and 62.0%, respectively, for an MGAP value of 22. MGAP and GAP were strongly correlated with each other and were statistically significant in predicting the outcome of treatment (OR 2.23; 95% Cl 1.06–4.70; p = 0.035). With a rise of one in the MGAP score value, the probability of survival increases 2.2 times. Conclusion: MGAP and GAP, in prehospital settings, had higher sensitivity and specificity when identifying patients with a severe trauma and predicting an unfavorable outcome than other scoring systems.
Patients suffering from cholelithiasis have an increased risk of developing cardiovascular complications, particularly ischemic myocardial disease. Ursodeoxycholic acid (UDCA), already used in clinical practice for the treatment of cholelithiasis and related conditions, has proven antioxidative, anti-inflammatory, and cytoprotective effects. Therefore, the aim of this study was to investigate the cardioprotective effect of UDCA pre-treatment on isoprenaline-induced myocardial injury in rats. Male Wistar albino rats were randomized into four groups. Animals were pre-treated for 10 days with propylene glycol + saline on days 9 and 10 (control), 10 days with propylene glycol + isoprenaline on days 9 and 10 (I group), 10 days with UDCA + saline on days 9 and 10 (UDCA group), and 10 days with UDCA + isoprenaline on days 9 and 10 (UDCA + I group). UDCA pre-treatment significantly reduced values of high-sensitivity troponin I (hsTnI) and aspartate aminotransferase (AST) cardiac markers (p < 0.001 and p < 0.01, respectively). The value of thiobarbituric acid reactive substances (TBARS) was also decreased in the UDCA + I group compared to the I group (p < 0.001). UDCA also significantly increased glutathione (GSH) levels, while showing a tendency to increase levels of superoxide dismutase (SOD) and catalase (CAT). The level of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) expression, a key regulatory gene of inflammation, was diminished when UDCA was administered. A reduction of cardiac damage was also observed in the UDCA pre-treated group. In conclusion, UDCA pre-treatment showed a cardioprotective effect on isoprenaline-induced myocardial injury in rats, primarily by reducing oxidative stress and inflammation.
The dose-response relationship of sildenafil effects on cardiac function is not completely elucidated. The aim of this study was to assess the effects of different doses of sildenafil on coronary flow and oxidative stress in isolated rat hearts. Coronary flow and markers of oxidative stress, including nitrite outflow, and superoxide anion production in coronary effluent, were determined for isolated rat hearts. The experiments were performed during control conditions and in the presence of sildenafil (10, 20, 50, 200 nM) alone or with Nω-nitro-L-arginine monomethyl ester (L-NAME) (30 μM). Sildenafil was shown to result in a significant increase in coronary flow at lower coronary perfusion pressure (CPP) values at all administered doses, whereas, with an increase in CPP, a reduction in coronary flow was observed. An increase in nitric oxide (NO) was most pronounced in the group treated with the lowest dose of sildenafil at the highest CPP value. After the inhibition of the NO-cyclic guanosine monophosphate (cGMP) signaling (NOS) system by L-NAME, only a dose of 200 nM sildenafil was high enough to overcome the inhibition and to boost release of O2−. That effect was CPP-dependent, with statistical significance reached at 80, 100 and 120 mmHg. Our findings indicate that sildenafil causes changes in heart vasculature in a dose-dependent manner, with a shift from a vasodilatation effect to vasoconstriction with a pressure increase. The highest dose administered is capable of producing superoxide anion radicals in terms of NOS system inhibition.
Background/Objectives: Pain is the most frequently reported symptom in over 90% of patients presenting with traumatic injuries, and three-quarters of patients are discharged from emergency departments experiencing moderate to severe pain. The objective of this study was to compare the frequency of analgesic administration between patients with chest pain presumed to be of cardiac origin and those with suspected bone fractures as well as to assess whether significant differences exist between these two groups. Methods: A retrospective, observational study was conducted. Patients were categorized into two groups: Group 1—patients with angina pectoris, acute myocardial infarction, or non-specific chest pain; and Group 2—patients with a preliminary diagnosis of bone fracture made by the attending physician at the scene. Results: A total of 1189 patients were included in this study, with 503 (42.3%) in Group 1 and 686 (57.7%) in Group 2 (χ2 = 28.166; p < 0.001). Analgesic administration was significantly more frequent among patients in Group 1 than in Group 2 (χ2 = 23.187; p < 0.001). Within Group 1, the highest rate of analgesic use was recorded in patients diagnosed with acute myocardial infarction. In Group 2, analgesics were administered to 36.4% of patients with suspected trunk bone fractures, while only 7.1% of patients with suspected cranial fractures received analgesic therapy. Pain intensity scores were not available for either group. Conclusions: The administration of analgesic treatment was significantly more common among patients presenting with chest pain of presumed cardiac origin than among those with suspected bone fractures, including fractures involving multiple body regions.
Peptide therapeutics occupy a unique position between small organic compounds and large protein biomolecules, combining high specificity, strong pharmacological efficacy, and favourable safety profiles. Consequently, they have emerged as important therapeutic agents for a wide range of diseases, including metabolic and oncological disorders. However, oral administration of peptide drugs remains a major challenge due to extensive enzymatic degradation, low intestinal permeability, mucus entrapment, and presystemic metabolism within the gastrointestinal tract. This review provides a comprehensive overview of contemporary strategies for improving oral peptide delivery, with special emphasis on emerging pharmaceutical formulation technologies, bioinspired delivery systems and ingestible device-assisted approaches. A qualitative literature search was conducted using major scientific databases and included relevant publications available up to May 2026. The analysis identified the main barriers responsible for low oral bioavailability of peptide drugs, as well as promising approaches to overcoming these obstacles, including peptide modification, enzyme inhibition, permeation enhancement, mucolytic strategies, and advanced carrier systems. Special attention is given to multifunctional carrier systems, ingestible medical devices and bile acid-inspired technologies as emerging directions in oral peptide delivery. The convergence of pharmaceutical sciences, bioinspired formulation strategies and biomedical engineering is expected to accelerate the clinical translation of oral peptide formulations and enable their therapeutic potential to be fully exploited.