Deficient Repair Mechanisms Research Articles

Study on the barriers and breakthroughs of resilience building in aging Urban communities from the perspective of risk management: A case study of Jin Guang Men community in Xi’an

The continuous escalation of social risks has exacerbated the challenges faced by aging urban communities. In this context, resilience building emerges as a critical approach, offering new perspectives and innovative solutions to address these issues. This paper applies the theories of risk society and resilience governance to establish an analytical framework for resilience governance, specifically examining the current status of resilience construction within the Jin Guang Men community in Xi’an. The findings indicate that resilience building within these aging urban communities is hindered by issues such as weak grassroots governance, deficient repair mechanisms, inadequate infrastructure, and a slow pace of information technology adoption. To effectively manage social risks, it is imperative to strengthen party leadership in governance, enhance community self-repair capacities, upgrade infrastructure, and accelerate the application of information technology. These measures are essential for bolstering the risk management capabilities of aging urban communities.

PARP inhibitor combinations in prostate cancer.

Polyadenosine-diphosphate-ribose polymerase (PARP) inhibitors cause deoxyribonucleic acid (DNA) damage that can be lethal to cells with deficient repair mechanisms. A number of PARP inhibitors are being tested as treatments for men with prostate cancer, both as monotherapies and in combinations that are based on purported synergies in treatment effect. While the initial single-agent development focused on men with identified deficiencies in DNA-repair pathways, broader patient populations are being considered for combination approaches. This review summarizes the current clinical development of PARP inhibitors and explores the rationale for novel combination strategies.

Cancer risk related to genetic polymorphisms in carcinogen metabolism and DNA repair.

Chemical carcinogenesis involves metabolism in the body of the carcinogen to the ultimate carcinogen and its interaction with DNA. There is considerable interindividual variation in the metabolic ability to activate as well as detoxify the carcinogens and in the ability to repair the carcinogen-DNA adducts. In many cases such differences occur as genetic polymorphisms and form the basis for variation in susceptibility to carcinogens and thereby to cancer risk. The activation mechanism is particularly related to the cytochromes P-450 (CYPs), and four of these are known to activate carcinogens: CYP1A1, CYP1A2, CYP2E1, and CYP3A4. Increased cancer risk has been related to polymorphisms in the CYPs and other activating enzymes. The DNA repair mechanisms show considerable complexity, and deficient repair mechanisms in certain human disorders are clearly related to increased cancer risk. Yet, there is no unambiguous epidemiological evidence available for cancer risk among individuals in general. In vivo methods have to be refined and developed for use in epidemiological studies.