Can cross linking of collagen prevent contraction by cells?5 answersCrosslinking of collagen has been explored as a strategy to prevent contraction induced by cells. Various methods such as using low cytotoxic cross-linkers like genipin and EDC, controlled collagen crosslinking with inhibitors like β-aminopropionitrile (BAPN), and photochemical cross-linking with riboflavinhave shown promising results in inhibiting collagen contraction. These approaches have demonstrated reduced contraction of collagen gels, improved mechanical properties, enhanced cell viability, and altered cell behavior within the gel. Overall, crosslinking of collagen presents a viable method to mitigate gel contraction by cells, offering potential applications in tissue engineering and wound healing by maintaining the structural integrity of the extracellular matrix and regulating cellular microenvironments.
How many UV-crosslinks need to trap Topoisomerase 1 in DNA?4 answersTo trap Topoisomerase 1 (Top1) in DNA, at least one UV-crosslink is required. This is supported by the findings that UV-crosslinking Topoisomerase to bromocytosine-substituted DNA allows for the identification of the site of contact between the enzyme and the DNA sequence. Additionally, Top1 forms DNA-protein adducts with various DNA structures, including nicks and gaps induced by different sources, indicating its ability to interact with DNA at different sites. The interaction between Top1 and DNA is crucial for inducing DNA cleavage at specific sites, as demonstrated by the synthesis of polyamide-camptothecin conjugates designed to induce cleavage at predetermined DNA sites in the presence of Top1. Overall, these studies highlight the importance of UV-crosslinks in trapping Top1 at specific DNA sites for its catalytic activity.
What is mitoxantrone?5 answersMitoxantrone (MTX) is an anthracycline class synthetic anticancer drug that acts as a topoisomerase IIα inhibitor, preventing DNA re-ligations and causing DNA damage, ultimately leading to apoptosis in tumor cells. It is used in cancer therapy and refractory multiple sclerosis treatment, but its severe adverse effects, such as cardiotoxicity, are a concern. MTX has shown efficacy in reducing relapse rates and disability progression in multiple sclerosis patients, although long-term use may lead to adverse events like bone marrow suppression and hematological malignancies. Additionally, MTX can be locally administered for antitumor lymphatic metastasis, reducing toxic effects and targeting the lymphatic system to inhibit metastasis and improve patient quality of life.
Dose of mitomycin c injection scleral melting5 answersThe dose of mitomycin C injection used in pterygium excision surgeries has been associated with scleral melting and serious complications. Various concentrations and dosing schedules of mitomycin C need further definition to ensure safety and efficacy. Prolonged use of mitomycin C drops postoperatively after pterygium excision can lead to delayed complications such as corneal melting and scleral necrosis. Even a single intraoperative application of mitomycin C can result in corneoscleral perforation and iris prolapse, questioning the safety of this approach. Mitomycin C has also been implicated in scleral melting after trabeculectomy, with trauma and scleral necrosis being the main causes. A case study reported a patient who experienced recurrent pain and visual impairment after pterygium excision with mitomycin C adjuvant application, suggesting a potential association between the dose of mitomycin C and scleral melting.
How cytochrome transfer electrons?5 answersCytochrome proteins transfer electrons through various mechanisms. The investigation of electron-transfer mechanisms in cytochrome research has involved physicists, chemists, and biochemists, leading to the development of a theoretical framework for electron transfer. Heterogeneous electron transfer reactions of cytochrome c have been studied at clean metal surfaces, providing fundamental knowledge of the mechanisms involved. The reduction of cytochrome c at the d.m.e occurs in three stages, with the electrochemical reaction kinetics affected by the monolayer of irreversibly adsorbed protein. Cytochrome oxidase catalyzes the four-electron reduction of O2 to water and conserves the free energy in the form of a protonmotive force, involving a sequence of coupled electron and proton transfer reactions. Overall, the mechanisms of cytochrome electron transfer involve interdisciplinary research, studying reactions at metal surfaces, and understanding the kinetics and thermodynamics of the reactions.
How does antibiotic treatment induce C. difficile?5 answersAntibiotic treatment induces C. difficile through various mechanisms. One mechanism is the induction of persister-like non-spore cells, which are able to survive lethal antibiotic concentrations. Another mechanism involves the alteration of the intestinal microbiota, leading to metabolic imbalances and loss of colonization resistance, which allows for the proliferation of opportunistic pathogens like C. difficile. Additionally, inter-species interactions within the gut microbiota can impact C. difficile's response to antibiotics. For example, the production of hydrogen sulfide by Desulfovibrio piger increases C. difficile's tolerance to metronidazole. Furthermore, antibiotic treatment can lead to changes in the gut environment, such as a transient elevation of succinate levels, which C. difficile can exploit to expand in the perturbed intestine. Overall, antibiotic treatment disrupts the balance of the gut microbiota and creates conditions favorable for the growth and persistence of C. difficile.