Introduction: Semaglutide 2.4 mg is the reference pharmacotherapy for weight management, yet many patients do not reach ambitious weight-loss targets. CagriSema, a fixed-dose combination of cagrilintide and semaglutide, may offer additional benefit through complementary mechanisms. We quantified its incremental efficacy and safety against semaglutide 2.4 mg monotherapy in adults with overweight or obesity, with and without type 2 diabetes. Methods: This PRISMA 2020–compliant review (PROSPERO CRD420261380458) searched PubMed, Embase, Cochrane CENTRAL, ScienceDirect, ClinicalTrials.gov and WHO ICTRP to 30 June 2026 for randomised controlled trials comparing CagriSema with semaglutide 2.4 mg or placebo. Effects were pooled within two prespecified comparator strata using random-effects models with restricted maximum likelihood estimation of τ² and a Hartung–Knapp–Sidik–Jonkman small-sample adjustment, with prediction intervals, leave-one-out and phase-3a-restricted sensitivity analyses, trial sequential analysis. Results: Five trials (4,746 unique participants) were included. Versus semaglutide 2.4 mg, CagriSema produced greater weight loss (mean difference −6.89 percentage points, 95% CI −8.70 to −5.06; I² = 33%; prediction interval −8.91 to −4.86), a greater absolute reduction in body weight (−7.16 kg, 95% CI −9.15 to −5.17) and in body-mass index (−2.41 kg/m², 95% CI −2.83 to −1.99), and roughly twice the likelihood of reaching a 20% reduction (RR 2.10, 95% CI 1.78 to 2.47). Waist circumference fell further (−4.07 cm, 95% CI −5.10 to −3.04). No incremental glycaemic benefit was detected, with intervals for glycated haemoglobin (−0.07, 95% CI −0.14 to 0.01) and fasting plasma glucose lying entirely within prespecified minimal important differences. Injection-site reactions were more frequent (RR 3.14, 95% CI 1.42 to 6.96); gastrointestinal adverse events were not significantly increased under the primary model (RR 1.09, 95% CI 0.97 to 1.21). Conclusion: CagriSema produces clinically meaningful additional weight loss and modest improvements in surrogate cardiometabolic measures compared with semaglutide 2.4 mg alone, at the cost of more frequent injection-site reactions and, at most, modestly more frequent gastrointestinal events. The evidence is insufficient to determine whether serious adverse events or neoplasms differ between treatments, and long-term durability, cardiovascular outcomes and body composition remain undetermined. Systematic review registration: https://www.crd.york.ac.uk/prospero/ , identifier CRD420261380458.

Triple-negative breast cancer (TNBC) continues to resist the therapeutic gains achieved in other breast cancer subtypes, and much of that resistance, it turns out, is less about the drugs themselves than about where they end up in the body. Passively targeted nanocarriers were meant to solve this, yet a substantial body of preclinical work now shows that only a median of roughly 0.7% of an intravenously administered nanoparticle dose ever reaches tumor tissue — a figure that helps explain why so much laboratory promise has struggled to survive contact with the clinic. This review draws together evidence on the biological barriers responsible for that shortfall, including mononuclear phagocyte clearance, desmoplastic stroma, elevated interstitial fluid pressure, and an immunosuppressive tumor microenvironment, before turning to the engineering strategies designed to work around them. We examine organic, inorganic, and biomimetic nanocarrier platforms; ligand-based active targeting of biomarkers such as MUC1, CD44, EGFR, and Trop-2; and stimuli-responsive systems that exploit tumor acidosis, redox imbalance, hypoxia, or externally applied triggers to release payload precisely where it is needed. Multimodal strategies — chemo-immunotherapy, phototherapy, radiosensitization — are considered alongside the practical obstacles, GMP scalability, immunogenicity, and preclinical model fidelity chief among them, that continue to slow clinical translation. Rather than treating these as separate literatures, we attempt to place barrier biology, carrier engineering, and translational hurdles into a single, coherent narrative, one that we hope clarifies where the field has made genuine progress and where the delivery efficiency gap remains stubbornly, and instructively, open.

Triple-negative breast cancer (TNBC) has long resisted targeted therapy, largely because it lacks the estrogen, progesterone, and HER2 receptors that give clinicians a molecular handle elsewhere in breast cancer. That absence left oncologists relying on broadly cytotoxic chemotherapy and a slow, hypothesis-driven discovery process that struggles against so heterogeneous and unstable a tumor. This review asks a direct question: has artificial intelligence actually changed that picture, or is enthusiasm running ahead of the evidence? Drawing on eighty peer-reviewed sources spanning dermatological and oncological applications of machine learning, deep learning, and computer-aided drug design, we trace how computational methods are reshaping early-stage target identification in TNBC, while situating that work within the broader AI-oncology landscape from which many of its methods originated. The synthesis points to a genuinely convergent picture: phenotypic screening, transcriptomic feature selection, digital pathology, and generative chemistry, developed independently across research groups, keep arriving at an overlapping shortlist of biologically plausible targets — AKT, FGFR2, MFGE8, TGFβR1, and BRCA1/2-linked synthetic lethal networks among them. At the same time, the translational picture is not as settled as some performance metrics suggest; dataset bias, algorithmic opacity, and a shortage of prospective clinical validation remain real constraints on how much of this promise has reached patients. What this review offers, ultimately, is less a verdict than a structured accounting of where the evidence is strong, where it is preliminary, and what a more explainable, federated, clinically validated AI ecosystem would need to look like before TNBC target discovery moves from the computer screen to the clinic.

The purpose of this study was to see how Saraswata Churna (SC) affected the cognition of 4-month-old adult male Wistar rats who had epilepsy. One of the most common epilepsy symptoms is memory impairment. The elevated plus maze (EVPM) and Morris water maze (MWM) tests were used to assess the effect of SC on rat learning and memory. Pilocarpine (270 mg/kg BW, i.p.) was used to induce epilepsy. Saraswata Churna's effect on pilocarpine-induced epilepsy was evaluated. Saraswata Churna (300 mg/kg b.w. orally) improved the rats' cognitive performance, as shown by reduced latency in the EVPM, decreased escape latency during training, and more time spent in the target zone during recovery in the MWM. Saraswata Churna (300 mg/kg b.w. oral) has memory-enhancing action comparable to phenytoin (30 mg/kg b.w. i.p.). Saraswata Churna demonstrated memory-improving efficacy in rats, most likely because to its phytoconstituents, which have anti-inflammatory, antioxidant, and anticonvulsive properties.

The aim of our present study was to assess Saraswata Churna's anxiolytic and anti-depressant efficacy in a Pilocarpine-induced epilepsy rat model. Depression and anxiety are major psychological symptoms in epilepsy patients, and they have a significant impact on health-related quality of life. Many cases of neurological problems have been treated using Saraswata Churna, an ayurvedic medicine. The elevated plus maze (EVPM) was used to assess anxiolytic action, while the forced swimming test (FST) was used to assess antidepressant activity. The EVPM test has been shown to be effective in determining the anxiolytic effects of pharmaceuticals and various steroid as well as non-steroid hormones, as well as identifying the brain locations and mechanisms that underpin anxiety-related behaviour in rodents. Saraswata churna was reported to be effective in reducing anxiety and depression in rats at a dosage of 500 mg/kg.b.w by increasing open arm time and decreasing closed arm entrance in the EVPM paradigm and increasing the duration of immobility in the FST model. As a result, Saraswata Churna could be used as an effective therapeutic agent for anxiety and depression.