-Adrenergic receptor agonist induced hepatic steatosis in mice: modeling nonalcoholic fatty liver disease in hyperadrenergic states.

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of disorders ranging from hepatic steatosis [excessive accumulation of triglycerides (TG)] to nonalcoholic steatohepatitis, which can progress to cirrhosis and hepatocellular carcinoma. The molecular pathogenesis of steatosis and progression to more severe NAFLD remains unclear. Obesity and aging, two principal risk factors for NAFLD, are associated with a hyperadrenergic state.

Endocrine complications of celiac disease: a case report and review of the literature.

Purpose: The purpose of this article is to review recent literature regarding endocrine disorders related to celiac disease (CD).

Methods: We describe a case report and review existing literature on the endocrine manifestations of CD.

Results: CD is an autoimmune disorder characterized by intestinal inflammation in response to gluten.

Altered expression of hepatic β-adrenergic receptors in aging rats: implications for age-related metabolic dysfunction in liver.

Increased β-adrenergic receptor (β-AR)-mediated activation of adenylyl cyclase (AC) in rat liver during aging has been linked to age-related increases in hepatic glucose output and hepatosteatosis. In this study, we investigated the expression of β-ARs, individual receptor subtypes, and G protein-coupled receptor (GPCR) regulatory proteins in livers from aging rats. Radioligand-binding studies demonstrated that β-AR density increased by greater than threefold in hepatocyte membranes from senescent (24-mo-old) compared with young adult (7-mo-old) rats and that this phenomenon was blocked by food restriction, which is known to retard aging processes in rodents.

β2-Adrenergic receptor ablation modulates hepatic lipid accumulation and glucose tolerance in aging mice.

Catecholamines acting through β-adrenergic receptors (β(1)-, β(2)-, β(3)-AR subtypes) modulate important biological responses in various tissues. Our previous studies suggest a role for increased hepatic β-AR-mediated signaling during aging as a mediator of hepatic steatosis, liver glucose output, and insulin resistance in rodents. In the current study, we have utilized β(2)-AR knockout (KO) and wildtype (WT) control mice to define further the role of β(2)-AR signaling during aging on lipid and glucose metabolism.

Gene alterations and intestinal mucosal changes following growth factor and omega-3 exposure in a rat model of inflammatory bowel disease.

Background: We have previously shown that there is synergism between Hepatocyte Growth Factor (HGF) and Omega-3 (OM-3) enriched feeds using an immunologic model of inflammatory bowel disease (IBD). This combination decreased inflammation and cytokine levels and increased microvascular density and mucosal mass. This study evaluates the gene alterations that occurred using this same model.

Role of β-adrenergic receptors in regulation of hepatic fat accumulation during aging.

Excessive fat accumulation in liver (hepatic steatosis) predisposes to hepatic functional and structural impairment and overall metabolic risk. Previous studies noted an association between hepatic steatosis and age in humans and rodents. However, the mechanisms leading to age-associated hepatic fat accumulation remain unknown.

Vacuum-assisted closure in the treatment of extensive lymphangiomas in children.

Background: The management of lymphangiomas in children is a complex problem with frequent recurrence and infection. Vacuum-assisted closure (VAC) devices have been shown to accelerate the healing of open wounds. We hypothesized that VAC therapy might decrease complications after resection of lymphangiomas.

Hepatocyte growth factor and omega-3-enriched feeds have a synergistic effect on mucosal mass in an animal model of inflammatory bowel disease.

Background: Hepatocyte growth factor (HGF) decreases intestinal inflammation and cytokine levels in an animal model of inflammatory bowel disease (IBD). Luminal omega-3 (OM-3) is anti-angiogenic, reduces inflammation, and may decrease symptoms in patients with Crohn's disease. This study evaluates the synergism of HGF and OM-3.

Single-incision thoracoscopic surgery in children: equivalent results with fewer scars when compared with traditional multiple-incision thoracoscopy.

Background: Single-incision pediatric endosurgery is gaining popularity, especially for abdominal operations. Several reports in the literature support the feasibility of the single-incision approach in pediatric laparoscopy. Here we compare our experience with single-incision thoracoscopic surgery (SITS) to traditional multiple-incision video-assisted thoracoscopic surgery (VATS) in children.

Prophylactic antibiotics do not decrease the incidence of wound infections after laparoscopic pyloromyotomy.

Purpose: Although laparoscopic pyloromyotomy is considered to be a clean case, many surgeons administer prophylactic preoperative antibiotics. The aim of this study was to evaluate the impact of prophylactic antibiotics on the wound infection rate after laparoscopic pyloromyotomy.

Methods: We conducted a retrospective review of all patients who underwent laparoscopic pyloromyotomy at our institution between August 2002 and December 2009.

Chronology of the effect of massive small bowel resection and hepatocyte growth factor (HGF) on intestinal adaptation.

Background: We previously demonstrated that hepatocyte growth factor (HGF) increases mucosal protein and DNA content at single time points during intestinal adaptation in rats. This study evaluates mucosal changes after massive small bowel resection (MSBR) and with the addition of IV HGF measured over the timeframe of intestinal adaptation.

Methods: Sixty adult female Sprague-Dawley rats were divided into three groups and underwent massive small bowel resection (MSBR), MSBR+HGF (intravenous 150 mg/kg/d), or sham operation (control).

Impaired mitochondrial complex III and melatonin responsive reactive oxygen species generation in kidney mitochondria of db/db mice.

We have previously demonstrated that melatonin, at pharmacological concentrations, causes rapid reactive oxygen species (ROS) generation at the antimycin-A sensitive site of mitochondrial complex III (MC-3). In the current work, we used this melatonin response to investigate the role of mitochondrial dysfunction in the development of diabetic nephropathy. We find that the development of diabetic nephropathy, as indicated by hyperfiltration and histopathological lesions in the kidney of db/db mice, is associated with diminished melatonin-induced ROS generation and MC-3 activity, indicating impaired MC-3 at the antimycin-A site.

β-Adrenergic Responsive Induction of Insulin Resistance in Liver of Aging Rats.

INTRODUCTION. We previously demonstrated increases in β-adrenergic receptor (β-AR) density in rat liver, in association with increased β-AR-mediated stimulation of glucose output in rat hepatocytes, during senescent aging. We therefore hypothesized that pharmacologic β-adrenergic stimulation might induce insulin resistance and glucose output in liver of aging rats in vivo.

The effect of hepatocyte growth factor on gene transcription during intestinal adaptation.

Purpose: Previously, we investigated the physiologic effects of hepatocyte growth factor (HGF) on intestinal adaptation using a massive small bowel resection (MSBR) rat model. To correlate these altered physiologic changes with gene alterations, we used microarray technology at 7, 14, and 21 days after MSBR.

Methods: Forty-five adult female rats were divided into 3 groups and underwent 70% MSBR, MSBR + HGF (intravenous 150 μg/kg per day), or sham operation (control).

Dose variation of hepatocyte growth factor and its effects on an animal model of TPN-induced liver injury.

Background: Total parenteral nutrition (TPN) induced liver failure is the leading indication for transplantation in children. Our previous research demonstrated the benefit of a specific intravenous dose of hepatocyte growth factor (HGF) in the amelioration of TPN-induced liver injury. This study was designed to ascertain the optimum concentration of HGF in an animal model of TPN-induced liver injury.

Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition-associated liver disease.

Purpose: Dependence on total parenteral nutrition in intestinal failure or short bowel syndrome patients can lead to many complications. The most significant complication is progressive liver injury leading to liver failure. This study assesses the potential of hepatocyte growth factor (HGF) in modulating the hepatic response in a rat cholestatic liver injury model.

Role for Notch signaling in salivary acinar cell growth and differentiation.

The Notch pathway is crucial for stem/progenitor cell maintenance, growth and differentiation in a variety of tissues. The Notch signaling is essential for Drosophila salivary gland development but its role in mammalian salivary gland remains unclear. The human salivary epithelial cell line, HSG, was studied to determine the role of Notch signaling in salivary epithelial cell differentiation.

Reduced expression of epidermal growth factor receptors in rat liver during aging.

Proliferative responsiveness of hepatocytes to epidermal growth factor (EGF) declines during aging. The role of EGF receptors in mediating age-dependent changes of EGF-induced mitogenic signaling in liver remains incompletely understood. We assessed EGF receptor expression levels in whole liver specimens as well as in freshly isolated and cultured hepatocytes from young adult and senescent Fischer 344 male rats.

Of snakes and babies: intrathoracic stomach and vertebral rachischisis. A serpentine-like syndrome?

Snakes have intrathoracic stomachs and rachischisis-like spinal vertebrae. These anomalies are rare in babies and have not been previously described in combination in the English medical literature. Here we present 2 cases of total intrathoracic stomach with a foreshortened esophagus, cervical spine rachischisis, and splenic anomalies in newborns.

Distinct pathways of ERK activation by the muscarinic agonists pilocarpine and carbachol in a human salivary cell line.

Cholinergic-muscarinic receptor agonists are used to alleviate mouth dryness, although the cellular signals mediating the actions of these agents on salivary glands have not been identified. We examined the activation of ERK1/2 by two muscarinic agonists, pilocarpine and carbachol, in a human salivary cell line (HSY). Immunoblot analysis revealed that both agonists induced transient activation of ERK1/2.

Heat shock protein 90beta1 is essential for polyunsaturated fatty acid-induced mitochondrial Ca2+ efflux.

Nonesterified fatty acids may influence mitochondrial function by alterations in gene expression, metabolism, and/or mitochondrial Ca(2+) ([Ca(2+)](m)) homeostasis. We have previously reported that polyunsaturated fatty acids induce Ca(2+) efflux from mitochondria, an action that may deplete [Ca(2+)](m) and thus contribute to nonesterified fatty acid-responsive mitochondrial dysfunction. Here we show that the chaperone protein heat shock protein 90 beta1 (hsp90beta1) is required for polyunsaturated fatty acid-induced mitochondrial Ca(2+) efflux (PIMCE).

Mitogen-activated protein kinase up-regulation and activation during rat parotid gland atrophy and regeneration: role of epidermal growth factor and beta2-adrenergic receptors.

The rat secretory ductal obstruction model has been widely used to assess salivary gland injury, growth, and differentiation. In this study, a novel ductal obstruction and release procedure was used to explore the signaling pathways leading to salivary gland regeneration. Rats underwent bilateral parotid ductal obstruction in which the duct was occluded against a plastic disk subcutaneously and released by external ligature removal.

Expression of RUNX2 isoforms: involvement of cap-dependent and cap-independent mechanisms of translation.

RUNX2, a major regulator of skeletogenesis, is expressed as type-I and type-II isoforms. Whereas most eukaryotic mRNAs are translated by the cap-dependent scanning mechanism, translation of many mRNAs including type-I and type-II RUNX2 mRNAs has been reported to be initiated by a cap independent internal ribosomal entry site (IRES). Since the dicistronic plasmid assay used to demonstrate IRES has been questioned, we investigated the presence of IRES in RUNX2 mRNAs using dicistronic plasmid and mRNA assays.