Medical review (Berlin, Germany)最新文献

The diagnosis and prognosis of Prostate cancer (PCa) have undergone a significant transformation with the advent of prostate-specific membrane antigen (PSMA)-targeted positron emission tomography (PET) imaging. PSMA-PET imaging has demonstrated superior performance compared to conventional imaging methods by detecting PCa, its biochemical recurrence, and sites of metastasis with higher sensitivity and specificity. That transformation now intersects with rapid advances in artificial intelligence (AI) - including the emergence of generative AI. However, there are unique clinical challenges associated with PSMA-PET imaging that still need to be addressed to ensure its continued widespread integration into clinical care and research trials. Some of those challenges are the very wide dynamic range of lesion uptake, benign uptake in organs that may be adjacent to sites of disease, insufficient large datasets for training AI models, as well as artifacts in the images. Generative AI models, e.g., generative adversarial networks, variational autoencoders, diffusion models, and large language models have played crucial roles in overcoming many such challenges across various imaging modalities, including PET, computed tomography, magnetic resonance imaging, ultrasound, etc. In this review article, we delve into the potential role of generative AI in enhancing the robustness and widespread utilization of PSMA-PET imaging and image analysis, drawing insights from existing literature while also exploring current limitations and future directions in this domain.

Current two-dimensional (2D) cell models for effective drug screening suffer from significant limitations imposed by the lack of realism in the physiological environment. Three-dimensional (3D) organoids models hold immense potential in mimicking the key functions of human organs by overcoming the limitations of traditional 2D cell models. However, current techniques for preparation of 3D organoids models had limitations in reproducibility, scalability, and the ability to closely replicate the complex microenvironment found in vivo. Additionally, traditional 3D cell culture systems often involve lengthy and labor-intensive processes that hinder high-throughput applications necessary for a large-scale drug screening. Advancements in 3D bioprinting technologies offer promising solutions to these challenges by enabling precise spatial control over cell placement and material composition, thereby facilitating the creation of more physiologically relevant organoids than current techniques. This review provides a comprehensive summary of recent advances in 3D bioprinting technologies for creating organoids models, which begins with an introduction to different types of 3D bioprinting techniques (especially focus on volumetric bioprinting (VBP) technique), followed by an overview of bioinks utilized for organoids bioprinting. Moreover, we also introduce the applications of 3D bioprinting organoids in disease models, drug efficiency evaluation and regenerative medicine. Finally, the challenges and possible strategies for the development and clinical translation of 3D bioprinting organoids are concluded.

The advancement of catheter-based interventional techniques represents a significant evolution in cardiovascular medicine. However, traditional methods that rely on fluoroscopic guidance present considerable limitations including radiation exposure and contrast agent-related risks and the heavy load-caused lead suits. In response, zero or low X-ray emerge, including percutaneous and non-fluoroscopical (PAN) procedure coming as a transformative solution, particularly in treating congenital heart disease, valvular disease, and arrhythmias. These methods minimize the risk of iatrogenic injuries associated with radiative procedures. Innovative PAN procedures and methodologies have been developed to enhance imaging, transcatheter interventions, safety, and accuracy, overcoming previous limitations. By eliminating radiation and expanding accessibility, PAN procedures offer a safe, effective, and economically viable alternative to traditional methods, ushering in a new era of minimally invasive cardiovascular treatment.

Introduction: With the popularity of yoga increasing as a means to improve overall well-being, this umbrella review aimed to evaluate the potential effects of yoga on chronic disease outcomes by synthesizing previously published systematic reviews, including meta-analyses, of randomized controlled trials in adult populations.

Content: PubMed, Scopus, Cochrane, Web of Science, and CINAHL for systematic reviews published up to 31st March 2023. Systematic reviews examining the effectiveness of yoga interventions compared with controllable groups on chronic disease outcomes were searched from adults aged above 18 years old. Fifty-one systematic reviews, of which 34 were with meta-analyses, were eligible. The included reviews yielded 579 individual studies with 28403 reported participants. Most studies (n=45, 86.5 %) were conducted with general adult participants, other six studies were with women diagnosed with breast cancer. Yoga interventions had strong effects on depression, blood pressure, blood glucose, and fatigue management, while weak evidence was found for pain management and arthritis.

Summary: Yoga intervention may have an effect on improvements on depression, hypertension, type 2 diabetes, and fatigue management but not beneficial for physically disordered chronic diseases.

Outlook: Future studies with larger sample sizes and longer durations are necessary to validate the effect of yoga on chornic diseases. Further exploration on yoga implementation are expected.

Primary funding source: JIF201036Y and JIF201018Y (PROSPERO: CRD42023417841).

Selenium (Se) is an essential trace mineral crucial for human health. Nearly a dozen human clinical trials with seleno-methionine (SeMet) and selenized-yeast (contains mostly SeMet) for the prevention of non-cutaneous solid organ cancers in North America and European countries conclusively refuted their utility. We have articulated two lessons from these trials: (1) the anti-oxidant hypothesis was tested in inappropriate Se-adequate populations, and (2) the selection of these Se forms was not supported by cell culture and animal efficacy data. Nevertheless, preclinical studies of proximal methylselenol precursors ("methyl Se") have shown many desirable attributes, involving crucial molecules and pathways in cancer epithelial cells, vascular endothelial, immune and inflammatory cells in the tumor microenvironment, for potential use as chemopreventive and therapy agents. Methylseleninic acid and Se-methylselenocysteine are prototypical methyl-Se, yet not equal in their targets. Selenate, selenite and selenious acid had been recently studied in human clinical trials, providing novel safety data, but, missing critical genotoxicity assessments. Given the popularity of Se-enriched foods in China and a continued presence of nutritional Se deficiency in many localities, we discuss recommendations for clinical studies of Se forms for cancer therapy or chemoprevention in China and other countries with similar Se nutrition predicament.

Organoid technology has significantly transformed biomedical research by providing exceptional prospects for modeling human tissues and disorders in a laboratory setting. It has significant potential for understanding the intricate relationship between genetic mutations, cellular phenotypes, and disease pathology, especially in the field of genetic diseases. The intersection of organoid technology and genetic research offers great promise for comprehending the pathophysiology of genetic diseases and creating innovative treatment approaches customized for specific patients. This review aimed to present a thorough analysis of the current advancements in organoid technology and its biomedical applications for genetic diseases. We examined techniques for modeling genetic disorders using organoid platforms, analyze the approaches for incorporating genetic disease organoids into clinical practice, and showcase current breakthroughs in preclinical application, individualized healthcare, and transplantation. Through the integration of knowledge from several disciplines, such as genetics, regenerative medicine, and biological engineering, our aim is to enhance our comprehension of the complex connection between genetic variations and organoid models in relation to human health and disease.

Alzheimer's disease (AD) is a chronic neurodegenerative disorder for which there are currently no effective treatment options. Increasing evidence suggests that AD is a systemic disease closely associated with the immune system, not merely a central nervous system (CNS) disorder. Immune cells play crucial roles in the onset and progression of AD. Microglia and astrocytes are the primary inflammatory cells in the brain that can sensitively detect changes in the internal environment and transform into different phenotypes to exert differing effects at various stages of AD. Peripheral immune cells, such as T cells, B cells, monocytes/macrophages, and neutrophils can also be recruited to the CNS to mediate the inflammatory response in AD. As such, investigating the role of immune cells in AD is particularly important for elucidating its specific pathogenesis. This review primarily discusses the roles of central innate immune cells, peripheral immune cells, and the interactions between central and peripheral immune cells in the development of neuroinflammation in AD. Furthermore, we listed clinical trials targeting AD-associated neuroinflammation, which may represent a promising direction for developing effective treatments for AD in the future.

Lactate is the end product of glycolysis, and extensive research has shown that lactate participates in various pathophysiological processes. Along with associated hydrogen ions, lactate typically functions as an immunosuppressive negative factor and plays a crucial role in tumor metabolic reprogramming. The recently discovered lactylation is a novel epigenetic modification that, similar to other epigenetic modifications, modifies histones to alter chromatin spatial configuration, thereby affecting DNA accessibility and regulating gene expression. More importantly, the degree of lactylation is closely related to local lactate concentrations, establishing a link between epigenetics and metabolic reprogramming. During cellular metabolism, lactate accumulation promotes histone lysine lactylation in cancer cells and immune cells such as macrophages and T cells, playing an essential role in tumor immune evasion and resistance to immunotherapy. This paper details the role of lactylation modifications in cancer immune evasion and resistance to immunotherapy, providing novel therapeutic directions and targets for cancer treatment.

Fragile X syndrome (FXS) is a genetic disorder caused by a mutation in the FMR1 gene on the X chromosome, leading to a range of developmental and intellectual disabilities. FXS is characterized by intellectual disability, behavior challenges, and distinct physical features such as an elongated face, large ears, and hyperflexible joints; FXS remains the most common inherited cause of intellectual disability. Behavioral manifestations often include attention deficits, hyperactivity, anxiety, and features of autism spectrum disorder. The prevalence of FXS in the South Asian population is not well-documented, but existing studies suggest it may be comparable to global prevalence rates, which are approximately 1 in 4,000 males and 1 in 8,000 females. Accurate diagnosis of FXS in South Asians is crucial due to the implications for early intervention and treatment, which can significantly improve the quality of life and developmental outcomes for affected individuals. Early diagnosis also facilitates genetic counselling and family planning, helping to reduce the risk of recurrence in families. Increased awareness and screening in South Asian communities are essential to address the diagnostic gap and ensure timely support for individuals with FXS or disorders associated with the premutation of FMR1.