Early and precise diagnosis of cancer is pivotal for effective therapeutic intervention. Traditional diagnostic methods, despite their reliability, often face limitations such as invasiveness, high costs, labor-intensive procedures, extended processing times, and reduced sensitivity for early-stage detection. Electrochemical biosensing is a revolutionary method that provides rapid, cost-effective, and highly sensitive detection of cancer biomarkers. This review discusses the use of electrochemical detection in biosensors to provide real-time insights into disease-specific molecular interactions, focusing on target recognition and signal generation mechanisms. Furthermore, the superior efficacy of electrochemical biosensors compared to conventional techniques is explored, particularly in their ability to detect cancer biomarkers with enhanced specificity and sensitivity. Advancements in electrode materials and nanostructured designs, integrating nanotechnology, microfluidics, and artificial intelligence, have the potential to overcome biological interferences and scale for clinical use. Research and innovation in oncology diagnostics hold potential for personalized medicine, despite challenges in commercial viability and real-world application.

Type 2 Diabetes (T2D) and Alzheimer’s Disease (AD) share common risk factors that can be seen through T2D nearly doubling an individual’s likelihood of developing AD. Some AD patients show signs of metabolic dysfunction as well. This review focuses on the potential mechanisms associated with these two diseases, like insulin resistance, inflammation, oxidative damage, mitochondrial injury, and cell death. One of the notable elements in this connection is the “brain insulin resistance,” most frequently named as “type 3 diabetes,” which impairs glucose metabolism and facilitates amyloid beta (Aβ) plaque synthesis while reducing the action of insulin-degrading enzyme (IDE). Moreover, the overactivity of glycogen synthase kinase-3 beta (GSK-3β) also triggers taurine protein pathology. Raised concentrations of glucose in blood can produce advanced glycation end products (AGEs), which further exacerbate neuroinflammation in tandem with the mitigation of neurotoxic Aβ oligomers. Inflammation and subsequent damage to mitochondria lead to the dissolution of synapses. Current vascular insults include the breakdown of the blood-brain barrier (BBB) and decreased brain perfusion, along with other contributory factors to conditions conducive to neurotoxicity. Recently, novel therapies are emerging, including GLP-1 agonists, intranasal insulin, and mitochondrial antioxidants, that show surprising results for treating both conditions, but on the contrary, bioavailability and the timing of interventions remain a big challenge in the management of these diseases. Eventually, further research should center on understanding the mechanisms of integration along with the development of molecular biology, neuroimaging, and outcome-driven treatment strategies. Comprehensive strategies that exist between T2D-AD for integration and preservation of brain and metabolic health are addressed in this review. Graphical abstract

Background: Tenecteplase (TNK) is a novel thrombolytic agent gaining attention as an alternative to alteplase for treating acute ischemic stroke (AIS). This meta‐analysis evaluates the safety and efficacy of various TNK doses compared to alteplase, integrating recent randomized controlled trials (RCTs) and employing a frequentist network meta‐analysis to identify the optimal dose while addressing existing evidence gaps.Methods: Up until December 2024, PubMed, Cochrane Central, and ScienceDirect were searched. Using Review Manager 5.4.1 for pairwise meta‐analysis, the Risk Ratios (RR) with 95% Confidence Intervals (CI) were pooled under the random effects model. Additionally, R version 4.3.2 and the “netmeta” package were used to conduct a network meta‐analysis for various dosages of the two thrombolytic drugs.Results: Thirteen RCTs, pooling 9,044 patients, were included in the quantitative synthesis. TNK was associated with a statistically significant improvement in the excellent functional outcome (mRS 0–1) (RR = 1.04; 95% CI: [1.00, 1.08]; p = 0.03) compared to alteplase. No significant differences were observed between TNK and alteplase in terms of good functional outcome (mRS 0–2), poor functional outcome (mRS 5–6), major neurological improvement within 72 h, symptomatic intracranial hemorrhage (sICH), or mortality at 90 days. On network analysis, TNK 0.25 mg/kg showed significant improvement in excellent functional outcome (RR = 1.05, 95% CI: [1.01, 1.10]) and TNK 0.32 mg/kg in good functional outcome (1.30, 95% CI: [1.15, 1.48]) compared to alteplase. According to the P‐score ranking, TNK 0.25 mg/kg was ranked as the best for achieving an excellent outcome (P‐score = 0.86), and TNK 0.1 mg/kg as the worst (P‐score = 0.16). For symptomatic intracranial hemorrhage (sICH), alteplase 0.9 mg/kg was ranked as the best (P‐score = 0.71), and TNK 0.4 mg/kg as the worst (P‐score = 0.17).Conclusion: TNK (0.25‐0.32 mg/kg) demonstrates superior efficacy compared to alteplase in achieving functional outcomes for AIS, while alteplase remains safer regarding sICH. Optimal dosing favors TNK 0.25 mg/kg for efficacy, but safety considerations highlight the need for individualized thrombolytic selection.

Background: Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, has emerged as a novel therapeutic option for the management of patients with diabetes, chronic kidney disease, or heart failure. We seek to summarize the evidence on the drug's effectiveness regarding cardiovascular (CV) outcomes.Methods: We conducted a literature search of Pubmed, Cochrane CENTRAL, Embase, and ClinicalTrials.gov from inception to September 2024. Trials exploring the effects of finerenone on CV outcomes were extracted and analyzed. The results of pooled analyses were presented as risk ratios (RRs) with 95% confidence intervals (CIs).Results: A total of eight trials, incorporating 21 200 patients, were included. The pooled analysis demonstrated a significant reduction in all‐cause death (RR 0.92, 95% CI: 0.85–0.99), major adverse CV events (RR 0.85, 95% CI: 0.81–0.90), heart failure‐related hospitalizations or unplanned hospital visits (RR 0.82, 95% CI: 0.76–0.87) with finerenone administration compared to control. Finerenone use was associated with a trend of reduced risk of CV death without reaching statistical significance (RR 0.90, 95% CI: 0.81–1.00). The risk of myocardial infarction (RR 0.91, 95% CI: 0.74–1.12), adverse events (RR 0.96, 95% CI: 0.89–1.03), adverse events leading to discontinuation (RR 1.06, 95% CI: 0.96–1.17) remained comparable across both groups. However, an increased risk of hyperkalemia (RR 2.07, 95% CI: 1.88–2.27) was observed with finerenone therapy compared to the control group.Conclusion: Finerenone administration was associated with improved CV outcomes in the CV‐renmetabolic conditions compared to the control group.

The effectiveness of glucagon‐like peptide‐1 receptor agonists in facilitating weight loss among patients with diabetes is widely recognized. However, there are limited data available on the relative effectiveness and safety of once‐weekly semaglutide versus once‐daily liraglutide. We conducted a systematic review and meta‐analysis of randomized controlled trials (RCTs) identified through a comprehensive search of the Cochrane Library, PubMed, and ScienceDirect databases from inception until July 2024. Statistical analysis was conducted using R version 4.4.1 with the “meta” package, employing a random effects model. Three RCTs with a total of 922 patients were included in our meta‐analysis. The results indicated that OW semaglutide significantly reduced body weight (WMD: −4.55; 95% CI: −6.43, −2.67, p < 0.01), HbA1c (WMD: −0.46; 95% CI: −0.84, −0.08; p = 0.02), and fasting plasma glucose levels (WMD: −1.23; 95% CI: −1.51, −0.95; p < 0.01) in comparison to OD liraglutide. The risk of severe adverse effects (OR, 1.66; 95% CI, 0.53–5.16; p = 0.38) and gastrointestinal adverse effects (OR, 1.84; 95% CI, 0.82–4.14; p = 0.14) was comparable between both groups. Once‐weekly semaglutide therapy results in a more pronounced loss in body weight, HbA1c, and fasting glucose levels compared to once‐daily liraglutide.

Introduction: Inclisiran, a small interfering RNA (siRNA), reduces the levels of low‐density lipoproteins (LDL) in the body by preventing the hepatic synthesis of proprotein convertase subtilisin/kexin type 9 (PCSK9). However, there is limited pooled data regarding the efficacy and safety of inclisiran in patients with hypercholesterolemia.Methods: PubMed/MEDLINE, Embase and the Cochrane Library were searched by investigators from inception till July 2024 to identify randomised controlled trials (RCTs) that investigated inclisiran in patients with hypercholesterolemia. Weighted mean differences (MDs) for continuous outcomes and risk ratios (RRs) for the dichotomous outcomes were pooled. The analysis was conducted using the random effects model, and a p‐value of < 0.05 was considered statistically significant.Results: A total of 8 RCTs reporting data for 5016 patients were included in the pooled analysis. Our pooled analysis demonstrated that inclisiran was associated with a significant decline in the % of LDL‐C levels (MD = −50.42, 95% CI: −56.15 to −44.70), % of PCSK9 levels (MD = −78.57, 95% CI: −81.64 to −75.50), % of total cholesterol levels in the body (MD = −31.22, 95% CI: −33.08.15 to −29.37), and apo B levels (MD = −41.47, 95% CI: −44.83 to −38.11) when compared with the control group. The risk of all‐cause death, cardiovascular death, major adverse cardiovascular events, myocardial infarction, stroke, and serious adverse events remained comparable (p > 0.05) across the two groups.Conclusion: Inclisiran reduces LDL‐C, PCSK9, cholesterol and apo‐B levels in the body without increasing the risk of serious adverse events.