Eurotium cristatum (E. cristatum), commonly known as “golden flower”, is the dominant strain in the microbial fermentation process of Fu brick tea. E. cristatum has favorable biological characteristics, including enzyme production, antimicrobial properties, immune regulation, antitumor properties, fat reduction capabilities, and weight loss benefits. With its probiotic characteristics, E. cristatum can be combined with different varieties of tea substrates to make a variety of fermented teas. More importantly, in the process of tea fermentation, E. cristatum can secrete a variety of extracellular enzymes, including some hydrolytic enzymes and oxidoreductases. They metabolize and transform various chemical components in tea through a series of reactions such as oxidation, degradation, and condensation, which significantly affect the quality of tea. In this review, by summarizing its basic functional characteristics as well as its application in fermented tea, an in-depth analysis of the key problems existing in the fermentation application of E. cristatum is described and some beneficial suggestions are presented in order to provide a rich theoretical basis for the development and utilization of E. cristatum to a greater extent.

The genome editing technology based on clustered regularly interspaced short palindromic repeats/CRISPR-associated protein-9 (CRISPR/Cas9), is revolutionizing research, particularly in the context of human neurodegenerative disorders. This review examines recent advancements in CRISPR/Cas9 and its potential to address the protein misfolding mechanisms underlying these diseases. Proteins, the fundamental units of life, can misfold due to various changes, resulting in aggregation and contributing to devastating illnesses such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis, and Huntington’s disease. Understanding the pathology of these disorders and the methods used for their detection is vital for developing effective treatments. CRISPR/Cas9 offers a powerful tool for combating neurodegenerative disorders at the molecular level. Its groundbreaking gene-editing capabilities are advancing preclinical and animal studies, paving the way for potential human trials and innovative therapeutic strategies. This review explores the complex challenge of protein misfolding and highlights how CRISPR technology could provide a crucial breakthrough in the fight against neurodegenerative disorders. It offers a synthesis of CRISPR advancements for neurodegenerative disorders. However, it is essential to be aware of the review’s limitations, including potential selection bias, the risk of oversimplification, and possible obsolescence in rapidly changing research fields. Despite these considerations, the transformative promise of CRISPR in understanding and potentially treating neurodegenerative diseases warrants continued research and thorough analysis.

This article explores the significant improvements in manufacturing of monoclonal antibodies (mAbs) and antibody-drug conjugates (ADCs) enabled by the microgravity environment in orbiting space vehicles. mAbs, which are extensively incorporated into modern cancer treatments based on their ability to specifically target and kill tumor cells, traditionally require intravenous (IV) delivery. However, the inconvenience, potential risks of infection, and adverse systemic effects associated with IV administration have led to a move towards subcutaneous (SC) self-administration formulations. Current limitations hindering the development of SC injections are high viscosity and limited solubility of mAbs at high concentrations. The microgravity environment of space provides potential solutions to these challenges by promoting the formation of colloidal crystalline protein suspensions of low-viscosity and high concentration suitable for SC injection. Although conducting research and manufacturing in microgravity poses its own set of challenges, the benefits of improving the delivery, storage, and stability of mAbs are substantial. SpacePharma has developed novel, autonomous, remote-controlled, microfluidics-based lab-on-chip microgravity systems as a platform for the rapid screening and improved growth of crystallized monoclonal antibodies inside micron-size droplets. The advancements in this field have significant potential to improve patient care by enabling large-scale manufacturing of crystallized mAb therapies in the emerging space economy.

Splenic venous hypertension or left-sided portal hypertension is a rare condition caused by an obstruction of the splenic vein. Usually, it presents with upper gastrointestinal bleeding in the absence of liver disease. Etiologies can be classified based on the mechanism of development of splenic vein hypertension: compression, stenosis, inflammation, thrombosis, and surgically decreased splenic venous flow. Diagnosis is established by various imaging modalities and should be suspected in patients with gastric varices in the absence of esophageal varices, splenomegaly, or cirrhosis. The management and prognosis vary depending on the underlying etiology but generally involve reducing splenic venous pressure. The aim of this review was to summarize the etiologies of splenic venous hypertension according to the mechanism of development.

The incidence and prevalence of inflammatory bowel diseases (IBD), including ulcerative colitis and Crohn’s disease, are rapidly increasing. Currently, colonoscopy is the gold standard for diagnosing and monitoring the course of IBD. However, the recently implemented “treat-to-target” strategy, which involves meticulously pursuing multiple therapeutic objectives, has opened avenues for non-invasive diagnostic and monitoring tools. These tools aim to assess disease activity and predict the likelihood of recurrence. Research studies into serum and fecal biomarkers in IBD have been ongoing for several years. Among the most relevant biomarkers, fecal calprotectin and C-reactive protein have shown the best accuracy, with good-to-optimal correlation with endoscopic, histologic, or transmural activity. Numerous studies have explored the potential advantages of using multi-target tools that combine serum and fecal biomarkers with clinical activity indexes to enhance diagnostic and monitoring effectiveness. Encouraging findings have emerged for fecal lactoferrin, autoantibodies, micro-RNA, gene expression, and many other serological and fecal markers. However, limited evidence has hindered their widespread adoption in routine clinical practice. This review aimed to summarize the available data on the utilization of biomarkers in IBD.

The burgeoning integration of machine learning (ML) and automation in laboratory medicine marks a significant shift, propelling the sector towards enhanced diagnostic accuracy and operational efficiency. This critical analysis investigates the technological paces being made to enhance the analytical precision and the efficient interpretation of complicated clinical/laboratory-based datasets. The beginning of automation, coupled with ML, ushers in an era where algorithmic expertise and predictive analytics supplement significantly elevating established diagnostic methods, thereby setting higher standards for reliability and quality in clinical laboratory testing. However, this technological advancement is not without its challenges. This review highlights several concerns about data privacy, the need for rigorous validation procedures, the difficulty of integrating new technology into primitive systems, and the continuous struggle to comply with guidelines. Financial constraints exacerbate these issues, particularly in settings with limited resources in developing and underdeveloped countries. To address these challenges, the review presents several strategic methods, including the development of international guidelines for algorithmic validation, interdisciplinary collaborations to match technology developments to healthcare demands, workforce training campaigns, and the implementation of ethical guidelines for the usage of ML approaches in lab environments. The review provides a concise yet comprehensive analysis of the current situation, highlighting challenges and possible solutions associated with automation and ML in laboratory medicine. It establishes the foundation for a future anticipated to have advanced diagnostics that are also more tailored to personalized patient care.

Iron overload is a significant complication commonly observed in individuals with β-thalassemia, resulting from enhanced iron absorption due to ineffective erythropoiesis and frequent blood transfusions. Iron overload can lead to severe tissue damage and organ dysfunction, significantly impacting the quality of life for those affected. Additionally, recent research indicates that iron overload may also adversely impact mitochondrial function, further exacerbating the pathophysiology of this disease. Excessive iron accumulation in mitochondria can impair the electron transport chain, reduce adenosine tri phosphate synthesis, and increase the generation of reactive oxygen species, resulting in elevated tissue damage and clinical complications. Emerging evidence suggests that specific mitochondrial DNA (mtDNA) mutations may further contribute to the severity of iron overload in β-thalassemia patients. Currently, the clinical management of iron overload in patients with β-thalassemia primarily relies on conventional iron chelation therapies, aiming to reduce iron burden and prevent tissue damage. However, cases involving mtDNA mutations introduce additional complexities, necessitating personalized treatment approaches. Advances in gene therapy and mitochondrial replacement strategies offer promising avenues for potential targeted interventions. This review provides a comprehensive overview of the mechanisms underlying iron overload in β-thalassemia and its association with mtDNA mutations. It discusses the clinical manifestations, diagnostic challenges, and current treatment options for managing iron overload, while also highlighting emerging research directions and potential therapeutic targets for improved patient care. Ultimately, a better understanding of the complex interplay between iron overload and mtDNA mutations in β-thalassemia will pave the way for innovative strategies to alleviate the disease burden.

Infectious diseases caused by pathogenic strains of bacteria are a global cause of morbidity and mortality. Hospital-acquired infections caused by Klebsiella pneumonia and Pseudomonas aeruginosa were found vulnerable during the COVID-19 pandemic. They are also responsible for the onset of certain life-threatening infectious diseases such as cystic fibrosis, endocarditis, bacteremia, and sepsis. Looking into the importance of these two superbugs there is a strong need for extensive comparative differential gene expression analysis among the wild-type and mutant for betterment of intensive care unit patients especially as such pathogenic bacterial strains have a dangerous role in the intensive care unit.

This study revealed the RNA microarray gene expression profiles of GSE24688, GSE4026, and GSE117438. The study compared all genes from three different datasets and all drug resistance genes from two divergent organisms, Klebsiella pneumonia and Pseudomonas aeruginosa.

10 numbers of shared significant genes and five drug resistance genes were obtained in this study. These putative genes may show intriguing patterns of connection with resistance mechanisms and can be used in the field of diagnostics and treatment. Our divergent analysis also revealed a very clear distinct relation between Klebsiella pneumoniae and Pseudomonas aeruginosa at the genetic level, though they both function under antimicrobial resistance.

This study enhances the understanding of the genetic basis, providing valuable knowledge for the development of new strategies to combat antibiotic resistance and enhance the efficacy of existing antibiotics.

Hepatocellular carcinoma (HCC) cases with small nodules are commonly treated with radiofrequency ablation (RFA), but the recurrence rate remains high. This study aimed to establish a blood signature for identifying HCC with metastatic traits pre-RFA.

Data from HCC patients treated between 2010 and 2017 were retrospectively collected. A blood signature for metastatic HCC was established based on blood levels of alpha-fetoprotein and des-γ-carboxy-prothrombin, cell-free DNA (cfDNA) mutations, and methylation changes in target genes in frozen-stored plasma samples that were collected before RFA performance. The HCC blood signature was validated in patients prospectively enrolled in 2021.

Of 251 HCC patients in the retrospective study, 33.9% experienced recurrence within 1 year post-RFA. The HCC blood signature identified from these patients included des-γ-carboxy-prothrombin ≥40 mAU/mL with cfDNA mutation score, where cfDNA mutations occurred in the genes of TP53, CTNNB1, and TERT promoter. This signature effectively predicted 1-year post-RFA recurrence of HCC with 92% specificity and 91% sensitivity in the retrospective dataset, and with 87% specificity and 76% sensitivity in the prospective dataset (n=32 patients). Among 14 cases in the prospective study with biopsy tissues available, positivity for the HCC blood signature was associated with a higher HCC tissue score and shorter distance between HCC cells and microvasculature.

This study established an HCC blood signature in pre-RFA blood that potentially reflects HCC with metastatic traits and may be valuable for predicting the disease’s early recurrence post-RFA.

Hepatitis B virus (HBV) infection is a major risk factor for cirrhosis and liver cancer, and its treatment continues to be difficult. We previously demonstrated that a dopamine analog inhibited the packaging of pregenomic RNA into capsids. The present study aimed to determine the effect of dopamine on the expressions of hepatitis B virus surface and e antigens (HBsAg and HBeAg, respectively) and to elucidate the underlying mechanism.

We used dopamine-treated HBV-infected HepG2.2.15 and NTCP-G2 cells to monitor HBsAg and HBeAg expression levels. We analyzed interferon-stimulated gene 15 (ISG15) expression in dopamine-treated cells. We knocked down ISG15 and then monitored HBsAg and HBeAg expression levels. We analyzed the expression of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway factors in dopamine-treated cells. We used dopamine hydrochloride-treated adeno-associated virus/HBV-infected mouse model to evaluate HBV DNA, HBsAg, and HBeAg expression. HBV virus was collected from HepAD38.7 cell culture medium.

Dopamine inhibited HBsAg and HBeAg expression and upregulated ISG15 expression in HepG2.2.15 and HepG2-NTCP cell lines. ISG15 knockdown increased HBsAg and HBeAg expression in HepG2.2.15 cells. Dopamine-treated cells activated the JAK/STAT pathway, which upregulated ISG15 expression. In the adeno-associated virus-HBV murine infection model, dopamine downregulated HBsAg and HBeAg expression and activated the JAK-STAT/ISG15 axis.

Dopamine inhibits the expression of HBsAg and HBeAg by activating the JAK/STAT pathway and upregulating ISG15 expression.