A new group of antidiabetic drugs, sodium-glucose cotransporter 2 inhibitors (SGLT-2 inhibitors), have recently been shown to have anticancer effects and their expression has been confirmed in many cancer cell lines. Given the metabolic reprogramming of these cells in a glucose-based model, the ability of SGLT-2 inhibitors to block the glucose uptake by cancer cells appears to be an attractive therapeutic approach. In addition to tumour cells, SGLT-2s are only found in the proximal tubules in the kidneys. Furthermore, as numerous clinical trials have shown, the use of SGLT-2 inhibitors is well-tolerated and safe in patients with diabetes and/or heart failure. In vitro cell culture studies and preclinical in vivo studies have confirmed that SGLT-2 inhibitors exhibit antiproliferative effects on certain types of cancer. However, the mechanisms of this action remain unclear. Even in those tumour cell types in which SGLT-2 is present, there is sometimes an SGLT-2-independent mechanism of anticancer action of this group of drugs. This article presents the current state of knowledge of the potential mechanisms of the anticancer action of SGLT-2 inhibitors and their possible future application in clinical oncology.

Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a protein that regulates low-density lipoprotein (LDL) cholesterol metabolism by binding to the hepatic LDL receptor (LDLR), ultimately leading to its lysosomal degradation and an increase in LDL cholesterol (LDLc) levels. Treatment strategies have been developed based on blocking PCSK9 with specific antibodies (alirocumab, evolocumab) and on blocking its production with small regulatory RNA (siRNA) (inclisiran). Clinical trials evaluating these drugs have confirmed their high efficacy in reducing serum LDLc levels and improving the prognosis in patients with atherosclerotic cardiovascular diseases. Most studies have focused on the action of PCSK9 on LDLRs and the subsequent increase in LDLc concentrations. Increasing evidence suggests that the adverse cardiovascular effects of PCSK9, particularly its atherosclerotic effects on the vascular wall, may also result from mechanisms independent of its effects on lipid metabolism. PCSK9 induces the expression of pro-inflammatory cytokines contributing to inflammation within the vascular wall and promotes apoptosis, pyroptosis, and ferroptosis of cardiomyocytes and is thus involved in the development and progression of heart failure. The elimination of PCSK9 may, therefore, not only be a treatment for hypercholesterolaemia but also for atherosclerosis and other cardiovascular diseases. The mechanisms of action of PCSK9 in the cardiovascular system are not yet fully understood. This article reviews the current understanding of the mechanisms of PCSK9 action in the cardiovascular system and its contribution to cardiovascular diseases. Knowledge of these mechanisms may contribute to the wider use of PCSK9 inhibitors in the treatment of cardiovascular diseases.

Objectives: The COVID-19 pandemic has forced emergency services to implement new standards of practice around the world. The dynamic and unpredictable nature of many clinical situations has placed emergency service personnel in direct danger of contracting the disease. This work uses a...

Objectives: The variety of clinical presentation on the topic of carbon monoxide (CO) intoxication ranges from slight headache to coma or death. YouTube allows patients to search not only for entertainment but also medical advice. Therefore, the aim of this study was to evaluate the content and...

Background: Maintaining highly effective cardiopulmonary resuscitation (CPR) can be particularly difficult when artificial ventilation using a bag-valve-mask device, combined with chest compression have to be carried out by one person. The aim of the study is to compare the quality of CPR conducted by one paramedic using chest compression from the patient’s side with compression conducted from the ‘over-the-head’ position. Methods: The subject of the study were two methods of CPR – ‘standard’ (STD) and ‘over-the-head’ (OTH). The STD method consisted of cycles of 30 chest compressions from the patient’s side, and two attempts at artificial ventilation after moving round to behind the patient’s head. In the OTH method, both compressions and ventilations were conducted from behind the patient’s head. Results: Both CPR methods were conducted by 38 paramedics working in medical response teams. Statistical analysis was conducted on the data collected, giving the following results: the average time of the interruptions between compression cycles (STD 9.184 s, OTH 7.316 s, p < 0.001); the depth of compression 50–60 mm (STD 50.65%, OTH 60.22%, p < 0.001); the rate of compression 100–120/min. (STD 46.39%, OTH 53.78%, p < 0.001); complete chest wall recoil (STD 84.54%, OTH 91.46%, p < 0.001); correct hand position (STD 99.32%, OTH method 99.66%, p < 0.001). A statistically significant difference was demonstrated in the results to the benefit of the OTH method in the above parameters. The remaining parameters showed no significant differences in comparison to reference values. Conclusions: The higher quality of CPR in the simulated research using the OTH method by a single person justifies the use of this method in a wider range of emergency interventions.

An out-of-hospital cardiac arrest requires early recognition, prompt and quality clinical interventions, and coordination between different clinicians to improve outcomes. Clinical team leaders and clinical teams have high levels of cognitive burden. We aimed to investigate the effect of a dedicated Cardio-Pulmonary Resuscitation (CPR) Quality Officer role on team performance. This multi-centre randomised control trial used simulation in universities from the UK, Poland, and Norway. Student Paramedics participated in out-of-hospital cardiac arrest scenarios before randomisation to either traditional roles or assigning one member as the CPR Quality Officer. The quality of CPR was measured using QCPR® and Advanced Life Support (ALS) elements were evaluated. In total, 36 teams (108 individuals) participated. CPR quality from the first attempt (72.45%, 95% confidence interval [CI] 64.94 to 79.97) significantly increased after addition of the CPR Quality role (81.14%, 95% CI 74.20 to 88.07, p = 0.045). Improvement was not seen in the control group. The time to first defibrillation had no significant difference in the intervention group between the first attempt (53.77, 95% CI 36.57–70.98) and the second attempt (48.68, 95% CI 31.31–66.05, p = 0.84). The time to manage an obstructive airway in the intervention group showed significant difference (p = 0.006) in the first attempt (168.95, 95% CI 110.54–227.37) compared with the second attempt (136.95, 95% CI 87.03–186.88, p = 0.1). A dedicated CPR Quality Officer in simulated scenarios improved the quality of CPR compressions without a negative impact on time to first defibrillation, managing the airway, or adherence to local ALS protocols.