Current drug metabolism最新文献

In recent years, the development of medical technologies leveraging nanomedicine has witnessed remarkable progress, particularly in areas such as targeted drug delivery, controlled drug release, tissue engineering, and in vitro diagnostics. This review explores the transformative impact of nanotechnology on medical imaging, focusing on developing novel contrast agents. Diagnostic imaging techniques, including Positron Emission Tomography (PET), Computed Tomography, and Magnetic Resonance Imaging, have become indispensable tools in modern healthcare. Contrast agents play an important role in enhancing the sensitivity of these imaging modalities, enabling the detection of previously undetectable anomalies. Nanotechnology offers unprecedented opportunities to revolutionize contrast agent design, leading to improved imaging modalities and diagnostic accuracy. Due to their high X-ray attenuation coefficients, metal-based inorganic nanoparticles, such as gold, bismuth, and lanthanide-based nanomaterials, exhibit significant potential as CT contrast agents. Furthermore, the pharmacokinetic properties and drug metabolism profiles of these nanomaterials are critical in ensuring their safety, efficacy, and optimal performance in clinical applications. Moreover, nanomaterials with integrated diagnostic and therapeutic capabilities are emerging as promising candidates for real-time disease detection and image-guided treatment. This review highlights the properties of nanomaterials that make them suitable for use as contrast agents. It discusses the challenges and opportunities in developing multifunctional nanomaterials for medical and diagnostic purposes. Overall, nanotechnology-enabled contrast agents have the potential to redefine the landscape of medical imaging, paving the way for more precise diagnosis and personalized treatment strategies.

Introduction: Polypharmacy is frequently practiced in the management of schizophrenia due to its chronic nature, recurrent relapses, and associated comorbidities. While combining psychotropic medications may benefit patients with treatment-resistant symptoms, it poses risks such as drug-drug interactions (DDIs), adverse effects, and reduced medication adherence. The absence of uniform prescribing standards further complicates clinical decision-making.

Methods: This narrative review was conducted using a scoping methodology. Databases including Pub- Med, Scopus, and Web of Science were searched for English-language publications from 2000 to 2024. Search terms included "schizophrenia," "polypharmacy," "drug-drug interactions," "clinical outcomes," and "pharmacogenetics." Eligible sources included clinical trials, observational studies, systematic reviews, and treatment guidelines. Exclusion criteria were non-English articles, gray literature, and individual case reports.

Results: Polypharmacy is reported in 30-60% of individuals with schizophrenia, especially in institutionalized or treatment-resistant populations. Treatment regimens often involve multiple antipsychotics along with adjunctive antidepressants or mood stabilizers. This approach is associated with increased risks of metabolic syndrome, cardiovascular events (e.g., QT prolongation), extrapyramidal symptoms, and decreased adherence. Interindividual variability in pharmacogenetics further affects drug efficacy and safety. Innovative approaches like genotype-guided therapy and computerized clinical decisionsupport systems are promising but not yet widely implemented.

Discussion: Although polypharmacy may offer symptomatic relief in specific scenarios, it requires careful management due to its potential to cause harm. Rational prescribing, close monitoring, and attention to individual patient factors such as pharmacogenetic profiles are essential to optimize therapy.

Conclusion: Ensuring a balance between therapeutic benefit and adverse effects is crucial when employing polypharmacy in schizophrenia treatment. Integrating personalized medicine strategies, regular monitoring, and deprescribing practices when feasible can enhance clinical outcomes and patient safety.

Physiologically based pharmacokinetic (PBPK) modeling is a computational technique that uses the physicochemical properties of drugs and physiological information to simulate plasma and tissue concentrations. PBPK modeling has become a mainstream approach in drug research and development, frequently employed to support regulatory packages for new drug applications. Understanding the pharmacokinetic characteristics of anti-HIV drugs is essential for successful treatment. In recent decades, PBPK modeling has been commonly used in the development and clinical therapy of anti-HIV medications. This review discusses the prevalence and application of PBPK modeling in the pharmacokinetics of anti-HIV drugs. Among the articles retrieved for this review, PBPK modeling was predominantly employed for anti-HIV drugs in contexts, such as pregnancy, drug-drug interactions, and pediatrics. The most commonly used software programs for this model are Simcyp, MATLAB, and PK-sim. This review will provide insights for researchers in applying PBPK models to manage patients with HIV infection, aiming to enhance the efficacy of anti-HIV drug therapy and prevent undesirable adverse effects.

Objective: Di-2-ethylhexylphthalate (DEHP) is utilized as a plasticizer in polyvinylchloride products (PVC). When medical devices like blood bags, tubes, and syringes are employed, DEHP leaches out of the PVC polymers and enters biological fluids through non-covalent binding. The presence of DEHP in peripheral blood leads to contamination of bone marrow. Previous research has demonstrated that this chemical induces oxidative stress, which adversely affects the viability and osteo-differentiation of bone marrow mesenchymal stem cells (BMSCs). Hence, our current study aims to utilize gallic acid (GA), a natural antioxidant, to alleviate the inhibitory effects of DEHP on BMSCs' osteogenic differentiation.

Materials and methods: In osteogenic media, BMSCs extracted from Wistar rats were treated with 0.25 μM of GA and 100 μM of DEHP individually and in combination for 20 days. Then viability, total protein, malondialdehyde (MDA), total antioxidant capacity (TAC), catalase (CAT) and superoxide dismutase (SOD), alkaline phosphatase activity, production of collagen1A1 protein as well as expression of Bmp2 and 7, Smad1, Runx2, Oc, Alp, Col-1a1 genes were investigated.

Results: The viability and differentiation ability of BMSCs was significantly (p<0.0001) decreased by DEHP, while GA significantly (P<0.0001) ameliorated the effect of DEHP. DEHP caused a significant decrease (P<0.0001) in the total protein and collagen-1A1 concentration, TAC and activity of antioxidant enzymes, but significantly (P<0.001) increased MDA level. In addition, DEHP caused a significant decrease in the expression of osteo-related genes. In the co-treatment group, GA mitigated the toxic effects of DEHP compared to the control group by inhibiting DEHP-induced oxidative stress and enhancing cell viability and osteo-differentiation properties.

Conclusion: These results confirm that GA reduces the negative effects of DEHP on the osteo-differentiation of BMSCs at the cellular level. However, further studies are necessary to validate these findings.

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