Exploring the Integration of Artificial Intelligence in Clinical Laboratory Diagnostics Education: Opportunities and Challenges

The rapid development of Artificial Intelligence (AI) is reshaping various sectors, particularly healthcare and education. This article explores the integration of AI in Clinical Laboratory Diagnostics Education and its potential to transform teaching and learning paradigms. AI enables personalized instruction, immersive virtual laboratories, and intelligent teaching management systems, thereby enhancing educational effectiveness and efficiency. Additionally, AI supports clinical decision-making through advanced diagnostic algorithms and multi-dimensional data analysis. Nonetheless, its implementation faces considerable challenges, including high infrastructure costs, data privacy concerns, and ethical implications. This review summarizes the current landscape, identifies critical barriers, and discusses future directions. A balanced and responsible adoption strategy is essential to maximize AI's benefits while addressing associated risks, ultimately cultivating a new generation of healthcare professionals proficient in both clinical diagnostics and AI technologies

Wheat plant height locus RHT25 encodes a PLATZ transcription factor that interacts with DELLA (RHT1)

Plant height is an important agronomic trait with a significant impact on grain yield, as demonstrated by the positive effect of the REDUCED HEIGHT (RHT) dwarfing alleles (Rht1b) on lodging and harvest index in the “Green Revolution” wheat vari eties. However, these gibberellic acid (GA)-insensitive alleles also reduce coleoptile length, biomass production, and yield potential in some environments, triggering the search for alternative GA-sensitive dwarfing genes. Here we report the identification, validation, and characterization of the gene underlying the GA-sensitive dwarfing locus RHT25 in wheat. This gene, designated as PLATZ-A1 (TraesCS6A02G156600), is expressed mainly in the elongating stem and developing spike and encodes a plant-specific AT-rich sequence- and zinc-binding protein (PLATZ). Natural and induced loss-of-function mutations in PLATZ-A1 reduce plant height and its over expression increases plant height, demonstrating that PLATZ-A1 is the causative gene of RHT25. PLATZ-A1 and RHT1 show a significant genetic interaction on plant height, and their encoded proteins interact with each other in yeast and wheat protoplasts. These results suggest that PLATZ1 can modulate the effect of DELLA on wheat plant height. We identified four natural truncation mutations and one promoter insertion in PLATZ-A1 that are more frequent in modern varieties than in landraces, suggesting positive selection during wheat breeding. These mutations can be used to fine-tune wheat plant height and, in combination with other GA-sensitive dwarfing genes, to replace the GA-insensitive Rht1b alleles and search for grain yield improvements beyond those of the Green Revolution varieties.Fil: Zhang, Junli. University of California. Department of Plant Sciences; Estados UnidosFil: Li, Chengxia. University of California. Department of Plant Sciences; Estados UnidosFil: Zhang, Wenjun. University of California. Department of Plant Sciences; Estados UnidosFil: Zhang, Xiaoqin. University of California. Department of Plant Sciences; Estados UnidosFil: Mo, Youngjun. University of California. Department of Plant Sciences; Estados UnidosFil: Tranquilli, Gabriela E. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Recursos Biológicos; ArgentinaFil: Vanzetti, Leonardo Sebastian. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Marcos Juárez. Grupo Biotecnología y Recursos Genéticos; ArgentinaFil: Dubcovsky, Jorge. University of California. Department of Plant Sciences; Estados Unidos. Howard Hughes Medical Institute; Estados Unido

Stigma experience and coping strategies in stroke survivors: a qualitative study

AimTo investigate the true experiences of stigma and changes in stroke survivors and explore how they manage their symptoms.BackgroundStroke is a serious disease that threatens human health with increasing mortality and disability rates. Declining self-care ability and excessive external dependence can easily lead to stigma. However, there is a lack of studies on real stigma experiences and coping styles among stroke survivors.DesignA descriptive qualitative study.MethodsFourteen participants were recruited across inpatient stroke settings in China. Semi-structured face-to-face interviews were conducted with participants to collect data. Audio-recorded data were transcribed. The data were analyzed using the seven-step Colaizzi method for phenomenological analysis, adhering to the principles of Phenomenological research methodology. The study adheres to SRQR EQUATOR checklist.FindingsFourteen semi-structured interviews were conducted, revealing three main themes and ten sub-themes: (1) Non-adaptive emotion regulation in response to stigma, including sub-themes of remorse, shame, sadness, perceived disaster, depression, and reduced self-worth; (2) Adaptive emotion regulation in response to stigma, including positive reappraisal, positive adjustment, acceptance, and support systems; (3) Origins of stigma, including sources such as relatives, friends, oneself, and medical staff.ConclusionThe findings have the potential to inform the development and implementation of strategies to reduce the experience of stigma in early-stage clinical settings. Medical professionals must prioritize the comprehensive examination of genuine instances of stigma encountered by stroke survivors. Timely identification of stigma is imperative to mitigate the risk of patients adopting inaccurate beliefs and maladaptive coping mechanisms post-stroke. Strategies aimed at diminishing stigma should consider personal, familial, policy-related, societal, institutional, and environmental dimensions

FLOWERING LOCUS T2 regulates spike development and fertility in temperate cereals

FLOWERING LOCUS T2 (FT2) is the closest paralog of the FT1 flowering gene in the temperate grasses. Here we show that overexpression of FT2 in Brachypodium distachyon and barley results in precocious flowering and reduced spikelet number, while down-regulation by RNA interference results in delayed flowering and a reduced percentage of filled florets. Similarly, truncation mutations of FT2 homeologs in tetraploid wheat delayed flowering (2-4 d) and reduced fertility. The wheat ft2 mutants also showed a significant increase in the number of spikelets per spike, with a longer spike development period potentially contributing to the delayed heading time. In the wheat leaves, FT2 was expressed later than FT1, suggesting a relatively smaller role for FT2 in the initiation of the reproductive phase. FT2 transcripts were detected in the shoot apical meristem and increased during early spike development. Transversal sections of the developing spike showed the highest FT2 transcript levels in the distal part, where new spikelets are formed. Our results suggest that, in wheat, FT2 plays an important role in spike development and fertility and a limited role in the timing of the transition between the vegetative and reproductive shoot apical meristem

Study on rooting characteristics and occurrence model of adventitious roots in cuttage of Aronia melanocarpa

Abstract [Objective] The aim of the study is to investigate the origin and development of the adventitious roots in cuttage of Aronia melanocarpa as well as to understand its mechanism. [Methods] Taking the semi-lignified cuttings of ‘Fukangyuan No.1’ as materials, the changes in internal structure and external morphology of the cuttings during the formation of adventitious roots were observed by hydroponic cutting technology and paraffin section method. [Results] The results showed that the rooting period of IBAtreated cuttings was 30-40 d under hydroponic conditions. During the cutting process, the adventitious roots were appeared at the lenticel at 10-15 d and at at the cutting incision 15-20 d, and the rooting speed, number, and root length were better than the control. The number of adventitious roots in the cuttings was the largest and the rooting was fast. Exogenous induction significantly improved rooting rate and quality. There was no latent root primordium in the cuttings before cutting, which was formed after cutting. The adventitious roots were formed into callus rooting type and internal meristem rooting type. The adventitious roots produced in the bark were originated from vascular cambium, phloem parenchyma cells, or cortex, while the adventitious roots produced by the callus were specialized by the parenchymal cells. Leaf gaps or branch gaps were the main areas for the formation of adventitious root primordia and the formation of callus. [Conclusion] The rooting of cuttings belongs to the multi-site mode and the induced rooting type

miR-486-5p attenuates tumor growth and lymphangiogenesis by targeting neuropilin-2 in colorectal carcinoma

Increasing evidence suggests that microRNAs are associated with many important biologic processes in carcinogenesis. Despite ample research revealing the dysregualtion of miR-486-5p in various cancers, little is known about the roles of miR-486-5p in colorectal carcinoma (CRC). In this study, we investigated the biological functions and molecular mechanisms of miR-486-5p in CRC growth and invasion, discussing the potential of using miR-486-5p as a biomarker for colorectal cancers. Our data revealed that miR-486-5p was significantly downregulated in CRC tissues compared with the paracancer tissue by quantitative real-time polymerase chain reaction and that miR-486-5p was downregulated to a greater extent in advanced stage cancer (stage III and IV) as compared to early stage cancer (stage I and II). Luciferase reporter assay verified that neuropilin-2 was a direct functional target of miR-486-5p in the CRC cells, and upregulation of miR-486-5p in CRC cells negatively correlated with the expression of neuropilin-2. Furthermore, overexpression of miR-486-5p inhibited the tumor growth and lymphangiogenesis in nude mice, which was reversed by overexpression of neuropilin-2. Taken together, our study suggested miR-486-5p might be a suppressor of CRC

Case Report: Perivascular epithelioid tumors of the gastrointestinal tract

BackgroundPerivascular epithelioid cell tumor of the gastrointestinal tract (GI PEComa) is a rare mesenchymal neoplasm. GI PEComa is mostly observed in the colon and has a marked middle-aged female predominance. PEComa has no typical clinical or imaging manifestations or endoscopic characteristics. Therefore, the diagnosis of this disease mostly relies on pathological findings. HMB-45 is a sensitive immune marker of PEComa.Case presentationWe reported a case of a middle-aged female with sigmoid colon PEComa. To exclude carcinogenesis, the large basal polyp in the sigmoid colon was removed by endoscopic mucosal resection (EMR). Immunohistochemistry analysis results showed that this lesion expressed HMB-45, which is a characteristic melanin marker of PEComa. Finally, the lesion was diagnosed as sigmoid colon PEComa. At the time of submission of this report, surgical resection was the primary treatment for PEComa. Though the characteristics of tumor biology and clinical behavior in PEComa are not clear, the boundary is clear, and the tumor can be completely removed. However, close follow-up is required after the surgery because of the lesion’s undetermined benign and malignant nature.ConclusionThe present case study emphasizes the importance of pathological diagnosis. Therefore, upon finding gastrointestinal polyps with a mucosal ulcer under endoscopy, the GI PEComa diagnosis should be considered. It is necessary to detect the characteristic melanin markers of PEComa. Due to the rarity of these cases, challenges are faced in diagnosing and treating PEComa

Genetic identification and molecular modeling characterization reveal a novel PROM1 mutation in Stargardt4-like macular dystrophy.

Stargardt disease-4 (STGD4) is an autosomal dominant complex, genetically heterogeneous macular degeneration/dystrophy (MD) disorder. In this paper, we used targeted next generation sequencing and multiple molecular dynamics analyses to identify and characterize a disease-causing genetic variant in four generations of a Chinese family with STGD4-like MD. We found a novel heterozygous missense mutation, c.734T>C (p.L245P) in the PROM1 gene. Structurally, this mutation most likely impairs PROM1 protein stability, flexibility, and amino acid interaction network after changing the amino acid residue Leucine into Proline in the basic helix-loop-helix leucine zipper domain. Molecular dynamic simulation and principal component analysis provide compelling evidence that this PROM1 mutation contributes to disease causativeness or susceptibility variants in patients with STGD4-like MD. Thus, this finding defines new approaches in genetic characterization, accurate diagnosis, and prevention of STGD4-like MD

Genetic Identification and Molecular Modeling Characterization Reveal a Novel PROM1 Mutation in Stargardt4-like Macular Dystrophy

Stargardt disease-4 (STGD4) is an autosomal dominant complex, genetically heterogeneous macular degeneration/dystrophy (MD) disorder. In this paper, we used targeted next generation sequencing and multiple molecular dynamics analyses to identify and characterize a disease-causing genetic variant in four generations of a Chinese family with STGD4-like MD. We found a novel heterozygous missense mutation, c.734T\u3eC (p.L245P) in the PROM1 gene. Structurally, this mutation most likely impairs PROM1 protein stability, flexibility, and amino acid interaction network after changing the amino acid residue Leucine into Proline in the basic helix-loop-helix leucine zipper domain. Molecular dynamic simulation and principal component analysis provide compelling evidence that this PROM1 mutation contributes to disease causativeness or susceptibility variants in patients with STGD4-like MD. Thus, this finding defines new approaches in genetic characterization, accurate diagnosis, and prevention of STGD4-like MD

Identification of a Novel Heterozygous Missense Mutation in the CACNA1F

Background. Retinitis pigmentosa (RP) is an inherited retinal degenerative disease, which is clinically and genetically heterogeneous, and the inheritance pattern is complex. In this study, we have intended to study the possible association of certain genes with X-linked RP (XLRP) in a Chinese family. Methods. A Chinese family with RP was recruited, and a total of seven individuals were enrolled in this genetic study. Genomic DNA was isolated from peripheral leukocytes, and used for the next generation sequencing (NGS). Results. The affected individual presented the clinical signs of XLRP. A heterozygous missense mutation (c.1555C>T, p.R519W) was identified by NGS in exon 13 of the CACNA1F gene on X chromosome, and was confirmed by Sanger sequencing. It showed perfect cosegregation with the disease in the family. The mutation at this position in the CACNA1F gene of RP was found novel by database searching. Conclusion. By using NGS, we have found a novel heterozygous missense mutation (c.1555C>T, p.R519W) in CACNA1F gene, which is probably associated with XLRP. The findings might provide new insights into the cause and diagnosis of RP, and have implications for genetic counseling and clinical management in this family