Cyclophosphamide (CP) is an alkylating chemotherapeutic agent commonly used in cancer treatments. In this study, we aimed to investigate the effects of 4-Hydroperoxy cyclophosphamide (4-HC), which is active form of CP, on glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), phospho-protein kinase R (PKR)-like endoplasmic reticulum (ER) kinase (p-PERK), phospho-inositol-requiring enzyme 1 alpha (p-IRE1α), eukaryotic translation initiation factor 2 alpha (eIF2α), and caspase-3 messenger ribonucleic acids (mRNAs) and proteins that play roles in the ER stress pathway and apoptosis in U87 and T98 human glioblastoma cell lines. U87 and T98 human glioblastoma cell lines were divided into control and 4-HC-treated groups. Cell viability assay was used to detect the half maximal inhibitory concentration (IC50) for 24 hours of 4-HC. Immunocytochemistry and quantitative polymerase chain reaction (qPCR) methods were used to evaluate the levels of proteins and their mRNAs. The IC50 values of U87 and T98 cells were calculated as 15.67±0.58 μM and 19.92±1 μM, respectively. The levels of GRP78, ATF6, p-PERK, p-IRE1α, eIF2α, and caspase-3 protein expressions in the 4-HC-treated group compared to that in the control group. These increased protein expressions also were correlated with the mRNA levels. The ER stress signal pathway could be active in 4-HC-induced cell death. Further studies of ER-related stress mechanisms in anticancer treatment would be important for effective therapeutic strategies.

Artificial intelligence (AI) is a field within computer science that has vast applications and has transformed medical technologies. It is often regarded to be the branch of computer science that can handle complicated problems with minimal theory and many applications. AI is utilized to assist researchers in the analysis of large data sets, enabling precision medicine and assisting physicians in improving patient outcomes. New techniques in AI can bring together various types of data to make sense of new information obtained from multiomics datasets. Analyzing high-quality data combined with machine learning, a subset of AI, can help modify patients' unhealthy behaviors, predict risk or recurrence of chronic diseases after a surgical and curative treatment, prediction of progression and survival rates of patients with chronic diseases, therapeutic need, generation of improved clinical trial interpretations and identification of new targets. Howeveri, to effectively implement precision medicine in healthcare, a more user-friendly interface would be required. If AI technologies are applied correctly, fairly and robustly, in close cooperation with human intelligence, it is expected to open up new possibilities for effective and personalised healthcare services worldwide. In this review, the general outlines of AI technology, its application areas in healthcare and its future are overviewed.

Aim: Duchenne Muscular Dystrophy (DMD) results in a deficiency of dystrophin expression in patient muscle fibers, leading to progressive muscle degeneration. Treatment of DMD has undertaken current transformation with the advancement of novel gene therapy and molecular biology techniques, which are secure, well-tolerated, and effective therapeutic approaches. Introduction: DMD gene therapies have mainly focused on young DMD patients as in vivo animal model trials have been performed in 0–1-month DMD mice. However, it has not yet been answered how micro-dystrophin encoding lentiviral treatment affects Dystrophin expression and DMD symptoms in 10-month mdx mice. Methods: We planned to integrate the micro-Dystrophin gene sequence into the muscle cells by viral transfer, using micro-Dystrophin-encoding lentivirus to reduce the dystrophic pathology in late-stage dmd mice. The histopathological and physiological-functional regeneration activities of the lentiviralmicro- Dystrophin gene therapy methods were compared, along with changes in temporal Dystrophin expression and their functionality, toxicity, and gene expression level. Results: Here, we showed that the micro-dystrophin transgene transfers intramuscularly and intraperitoneally in late-stage dmd-mdx-4cv mice restored dystrophin expression in the skeletal and cardiac muscle (p <0.001). Furthermore, motor performance analysis, including hanging and tracking tests, improved statistically significantly after the treatment (p <0.05). Conclusion: Consequently, this study suggests that patients in the late stages of muscular dystrophy can benefit from lentiviral micro-dystrophin gene therapies to present an improvement in dystrophic muscle pathology.

Selinexor (SLX), a selective inhibitor of nuclear export (SINE), has been shown to interfere with nuclear export mechanisms and to exert antitumor effects

Three new Zn (II), Cu (II) and Mn (II) complexes have been synthesized from 5‐hydroxy‐1,4‐naphthoquinone (HNQ). Elemental analysis, magnetic susceptibility, UV–Vis, IR and Mass spectrometry have all been used to explore the structural characterization of these compounds. When the electronic spectra of these compounds are examined, they correspond to π → π* transitions in the 261–262 nm range, n → π* transitions in the 316–354 nm range, and charge transfer transitions in the 417–423 nm range. Also, in vitro cytotoxic activities of both juglone ligand and its metal complexes against A549 lung cancer and HT‐29 colon cancer cells have been investigated. The Mn (II)‐Juglone complex showed better cytotoxic activity than juglone ligand and other metal complexes in both cell lines. Moreover, molecular docking analyses demonstrated that the Mn (II)‐Juglone complex exhibited stronger binding interactions with both DNA and the anti‐apoptotic protein Bcl‐2 compared to the free Juglone ligand. Annexin V/PI double staining results using flow cytometry showed that there were more total apoptotic cells in the Mn (II)‐Juglone complex‐treated groups than in the ligand‐treated groups in both cell lines. In addition, it was found that Cas‐3 and Bax immunoreactivity increased significantly and Bcl‐2 immunoreactivity decreased significantly in Mn (II)‐Juglone complex‐treated groups compared to the control and ligand groups.