Measuring hyperemic response to light flicker stimulus using continuous laser speckle flowgraphy in mice.

Alterations in neurovascular coupling have been associated with various ocular, cerebral, and systemic vascular disorders. In the eye, changes in vessel caliber by dynamic vessel analysis have been used to measure neurovascular coupling following a light flicker stimulus. Here, we present a new protocol for quantifying light-flicker induced hyperemia in the C57/Bl6J mouse retina using laser speckle flowgraphy (LSFG).

Longitudinal Testing of Retinal Blood Flow in a Mouse Model of Hypertension by Laser Speckle Flowgraphy.

Purpose: The purpose of this study was to investigate the applicability of laser speckle flowgraphy (LSFG) for a longitudinal study of blood flow parameters in mice before, during, and after continuous infusion of angiotensin-II.

Methods: Normotensive C57BL/6J mice were imaged by LSFG at one (n = 22) or three sessions (n = 10). Two additional cohorts were imaged by LSFG before, during, and after continuous infusion of angiotensin-II by minipump for 2 or 4 weeks (n = 6 and 8, respectively).

Effects of long-term ethanol ingestion on hepatic iron metabolism in two mouse strains.

The mechanisms responsible for dysregulation of iron metabolism in response to ethanol ingestion are poorly understood. Relatively brief ethanol exposures in rodents are associated with reduced hepatic hepcidin expression without increases in hepatic iron content. This study evaluated the effects of long-term ethanol treatment on hepatic iron metabolism in two mouse strains.

Strain- and time-dependent alterations in hepatic iron metabolism in a murine model of nonalcoholic steatohepatitis.

Unlabelled: Nonalcoholic steatohepatitis is a common liver disease that is often accompanied by dysregulated iron metabolism. The aim of the study was to test the hypothesis that aberrant iron metabolism in nonalcoholic steatohepatitis is modulated by genetic susceptibility to inflammation and oxidative stress. Hepatic histology and iron content were assessed in 3 inbred strains of mice (C57BL/6, BALB/c, and C3H/HeJ) fed an atherogenic diet (AD).

Abnormal trigeminal sensory processing in obese mice.

Obesity is associated with several pain disorders including headache. The effects of obesity on the trigeminal nociceptive system, which mediates headache, remain unknown. We used 2 complementary mouse models of obesity (high-fat diet and leptin deficiency) to examine this.

Altered expression of iron regulatory genes in cirrhotic human livers: clues to the cause of hemosiderosis?

Hepatic iron deposition unrelated to hereditary hemochromatosis occurs commonly in cirrhosis but the pathogenesis of this condition is unknown. The aim of this study was to compare the expression of genes involved in the regulation of iron metabolism in cirrhotic (n=22) and control human livers (n=5). Transcripts were quantitated by real-time RT-PCR and protein levels were assessed by western blot.

Differential expression of stress-inducible proteins in chronic hepatic iron overload.

Introduction: Oxidative stress can trigger a cellular stress response characterized by induction of antioxidants, acute phase reactants (APRs) and heat shock proteins (HSPs), which are presumed to play a role in limiting tissue damage. In rodents, hepatic iron overload causes oxidative stress that results in upregulation of antioxidant defenses with minimal progressive liver injury. The aim of this study was to determine whether iron overload modulates expression of other stress-responsive proteins such as APRs and HSPs that may confer protection against iron-induced damage in rodent liver.

Increased hepatic telomerase activity in a rat model of iron overload: a role for altered thiol redox state?

Telomeres are repeated sequences at chromosome ends that are incompletely replicated during mitosis. Telomere shortening caused by proliferation or oxidative damage culminates in replicative arrest and senescence, which may impair regeneration during chronic liver injury. Whereas the effects of experimental liver injury on telomeres have received little attention, prior studies suggest that telomerase, the enzyme complex that catalyzes the addition of telomeric repeats, is protective in some rodent liver injury models.

Chronic iron overload stimulates hepatocyte proliferation and cyclin D1 expression in rodent liver.

Hepatomegaly is commonly observed in hepatic iron overload due to human hemochromatosis and in animal models of iron loading, but the mechanisms underlying liver enlargement in these conditions have received scant attention. In this study, male rats were treated with iron dextran or dextran alone for 6 months. Chronic iron loading resulted in a > 50-fold increase in hepatic iron concentration.

Expression of HSP47, a collagen-specific chaperone, in normal and diseased human liver.

HSP47 is a collagen-specific chaperone that is required for normal collagen synthesis. In animal models of liver injury, hepatic stellate cells (HSC) have been identified as a source of HSP47. Because expression of HSP47 has not been investigated in human liver, the aim of these studies was to characterize expression of HSP47 in human liver and to investigate its regulation in human HSC in vitro.

Intracerebroventricular calcitonin prevents stress-induced gastric dysfunction.

Background: Restraint stress produces gastric hypercontractility and acidity leading to stress ulceration. Intracerebroventricular (ICV) salmon calcitonin (sCT) decreases restraint injury and acidity, but its effects on restraint-induced hypercontractility are unknown.

Methods: Using stereotactic guidance, ICV catheters were placed into the lateral ventricle of adult male rats and calibrated gastric strain gauge transducers were implanted 5 days prior to restraint stress.