Uridine-Modified Ruthenium(II) Complex as Lysosomal LIMP-2 Targeting Photodynamic Therapy Photosensitizer for the Treatment of Triple-Negative Breast Cancer.

Lysosome-targeted photodynamic therapy, which enhances reactive oxygen species (ROS)-responsive tumor cell death, has emerged as a promising strategy for cancer treatment. Herein, a uridine (dU)-modified Ru(II) complex (RdU) was synthesized by click chemistry. It was found that RdU exhibits impressive photo-induced inhibition against the growth of triple-negative breast cancer (TNBC) cells in normoxic and hypoxic microenvironments through ROS production.

Preparation, Characterization, and Antioxidant Activities of Extracts from L. Flowers.

A novel water-soluble L. flowers polysaccharide (APL) was successfully isolated and purified from L. flowers by hot water extraction.

Ruthenium(II) Complexes Coupled by Erianin via a Flexible Carbon Chain as a Potential Stabilizer of G-Quadruplex DNA.

Herein, two novel ruthenium(II) complexes coupled by erianin a flexible carbon chain, [Ru(phen)(L-(CH)-erianin)](ClO) (L = 2-(2-(tri-fluoromethyphenyl))-imidazo [4,5][1-10]phenanthroline (1) and [Ru(phen)(L-(CH)-eria)](ClO) (L = 2-(4-(tri-fluoromethyphenyl))-imidazo [4,5][1,10]phenanthroline (2), have been synthesized and investigated as a potential G-quadruplex(G4) DNA stabilizer. Both complexes, especially 2, can bind to G4 DNA with high affinity by electronic spectra, and the binding constant calculated for 1 and 2 is about 15.1 and 2.

Novel Chiral Ru(II) Complexes as Potential c-myc G-quadruplex DNA Stabilizers Inducing DNA Damage to Suppress Triple-Negative Breast Cancer Progression.

Currently, effective drugs for triple-negative breast cancer (TNBC) are lacking in clinics. c-myc is one of the core members during TNBC tumorigenesis, and G-rich sequences in the promoter region can form a G-quadruplex conformation, indicating that the c-myc inhibitor is a possible strategy to fight cancer. Herein, a series of chiral ruthenium(II) complexes ([Ru(bpy)(DPPZ-R)](ClO), -1: R = -H, -2: R = -Br, -3: R = -C≡C(CH)NH) were researched based on their interaction with c-myc G-quadruplex DNA.

Injury risk in professional boxing.

Objective: Although a popular endeavor, boxing has fallen under increased scrutiny because of its association with traumatic brain injury. However, few studies have investigated the overall epidemiology of boxing injuries from representative samples, and no study has ever documented the incidence of injuries in female boxers. This study is a review of professional boxing data from the state of Nevada from September 2001 through March 2003.

Intraperitoneal injection induces a delayed preconditioning-like effect in mice.

We hypothesized that intraperitoneal injections of anaesthetics or fluid per se might evoke a delayed preconditioning-like response in mice hearts isolated and Langendorff perfused 24 h later. To test this, mice were given opioid anaesthesia by intraperitoneal injections or sham treated and the hearts were harvested and subjected to global ischaemia and reperfusion 24 h later in series 1. In series 2, mice were subjected to intraperitoneal injection of Ringer, sham needle prick procedure, or no intervention 24 h before heart isolation.

Myocardial protection by remote preconditioning: the role of nuclear factor kappa-B p105 and inducible nitric oxide synthase.

Objective: Adaptation to ischemia by brief episodes of ischemia and reperfusion (preconditioning) of the heart protects the heart against sustained ischemia, where the transcription factor nuclear factor kappa-B (NFkappaB) appears crucial for the protection. Preconditioning of the heart may even be evoked by brief episodes of ischemia and reperfusion in other organs. The present study investigates a possible role for NFkappaB and inducible nitric oxide synthase (iNOS) in adaption to ischemia by remote, delayed protection.

Cocaine induces apoptosis in fetal rat myocardial cells through the p38 mitogen-activated protein kinase and mitochondrial/cytochrome c pathways.

Cocaine induces apoptosis in fetal rat myocardial cells (FRMCs). However, the mechanisms are not clear. The present study examined the role of p38 mitogen-activated protein kinase (MAPK) and cytochrome c release in the cocaine-induced apoptosis in primary culture of FRMCs prepared from the fetal heart of gestational age of 21 days.

Effect of prenatal hypoxia on heat stress-mediated cardioprotection in adult rat heart.

Fetal programming has profound effects on cardiovascular function in later adult life. We tested the hypothesis that chronic hypoxic exposure during fetal development downregulates endogenous cardioprotective mechanisms in adult rats. Time-dated pregnant rats were divided between normoxic and hypoxic (10.

Mechanisms of myocardial ischemic preconditioning are age related: PKC-epsilon does not play a requisite role in old rabbits.

Data obtained from adult cohorts have implicated activation/translocation of protein kinase C (PKC)-epsilon as an important cellular mediator of myocardial infarct size reduction with ischemic preconditioning (PC). Age-related alterations in cellular signaling may, however, confound the extrapolation of mechanistic insight derived from adults to the aging population, the specific subset in which cardioprotection is undoubtedly most relevant. Accordingly, our aim was to investigate the role of PKC-epsilon as a mediator of infarct size reduction with PC in old vs.

Effect of fetal hypoxia on heart susceptibility to ischemia and reperfusion injury in the adult rat.

Objective: Epidemiologic studies showed an association between adverse intrauterine environment and ischemic heart disease in the adult. We tested the hypothesis that prenatal hypoxia increased the susceptibility of adult heart to ischemia-reperfusion (I-R) injury.

Methods: Time-dated pregnant rats were divided between normoxic and hypoxic (10.

Effect of maternal chronic hypoxic exposure during gestation on apoptosis in fetal rat heart.

Chronic hypoxia during pregnancy is one of the most common insults to fetal development. We tested the hypothesis that maternal hypoxia induced apoptosis in the hearts of near-term fetal rats. Pregnant rats were divided into two groups, normoxic control and continuous hypoxic exposure (10.

The gap junction uncoupler heptanol abrogates infarct size reduction with preconditioning in mouse hearts.

Background: Emerging evidence suggests that gap junction-mediated intercellular transmission of ions, metabolites and/or second messengers may serve as important determinants of myocyte viability. Our aim was to determine, using isolated buffer-perfused mouse hearts, whether the cardioprotection achieved with ischemic preconditioning (PC) is due in part to: (i) disruption of cell-cell coupling (manifest as a loss in the primary gap junction protein, connexin 43 [Cx43]) and resultant impaired transmission of a 'death' messenger, or conversely, (ii) transfer of a humoral 'survival' factor via existing gap junctions.

Methods: To explore the first possibility, we employed immunostaining to visualize and quantify Cx43 in hearts subjected to 212 min of PC ischemia or a matched control period.

Relationship between no reflow and infarct size as influenced by the duration of ischemia and reperfusion.

No reflow after acute myocardial infarction is an important predictor of infarct size and clinical outcome. However, the exact relationship between no reflow and infarct size remains to be determined, particularly because no reflow may progress during the time course of reperfusion. Control groups of five previous protocols using the anesthetized, open-chest rabbit model of coronary artery occlusion and reperfusion were retrospectively analyzed with respect to the correlation between regional myocardial blood flow (RMBF; radioactive microspheres) and infarct size (triphenyltetrazolium chloride) in the course of reperfusion.