Targeting synthetic lethality between the SRC kinase and the EPHB6 receptor may benefit cancer treatment.

Application of tumor genome sequencing has identified numerous loss-of-function alterations in cancer cells. While these alterations are difficult to target using direct interventions, they may be attacked with the help of the synthetic lethality (SL) approach. In this approach, inhibition of one gene causes lethality only when another gene is also completely or partially inactivated.

Ultrasonography reveals in vivo dose-dependent inhibition of end systolic and diastolic volumes, heart rate and cardiac output by nesfatin-1 in zebrafish.

Nesfatin-1 is an 82 amino acid peptide that inhibits food intake in rodents and fish. While endogenous nesfatin-1, and its role in the regulation of food intake and hormone secretion has been reported in fish, information on cardiovascular functions of nesfatin-1 in fish is in its infancy. We hypothesized that cardiac NUCB2 expression is meal responsive and nesfatin-1 is a cardioregulatory peptide in zebrafish.

Comparison of the acute effects of benzo-a-pyrene on adult zebrafish (Danio rerio) cardiorespiratory function following intraperitoneal injection versus aqueous exposure.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants. PAH exposure causes developmental toxicity in multiple fish species, while acute adult fish toxicity is thought to be minimal. The literature increasingly suggests sublethal PAH effects may occur, but differences in exposure route may confound conclusions.

Acute effects of β-naphthoflavone on cardiorespiratory function and metabolism in adult zebrafish (Danio rerio).

Aryl hydrocarbon receptor (AhR) agonists are known to cause lethal cardiovascular deformities in fish after developmental exposure. Acute adult fish toxicity of AhR agonists is thought to be minimal, but limited evidence suggests sublethal effects may also involve the cardiac system in fish. In the present study, adult zebrafish (Danio rerio) were aqueously exposed to solvent control or three nominal concentrations of the commonly used model AhR agonist, β-naphthoflavone (BNF), for 48 h.

The risk of heart failure and cardiometabolic complications in obesity may be masked by an apparent healthy status of normal blood glucose.

Although many obese individuals are normoglycemic and asymptomatic of cardiometabolic complications, this apparent healthy state may be a misnomer. Since heart failure is a major cause of mortality in obesity, we investigated the effects of heme-oxygenase (HO) on heart failure and cardiometabolic complications in obese normoglycemic Zucker-fatty rats (ZFs). Treatment with the HO-inducer, hemin, reduced markers of heart failure, such as osteopontin and osteoprotegerin, abated left-ventricular (LV) hypertrophy/fibrosis, extracellular matrix/profibrotic proteins including collagen IV, fibronectin, TGF-β1, and reduced cardiac lesions.