Evaporation-Induced Hierarchical Assembly of Rigid Silicon Nanopillars Fabricated by a Scalable Two-Level Colloidal Lithography Approach.

Periodic arrays of silicon nanowires/nanopillars are of great technological importance in developing novel electrical, optical, biosensing, and electromechanical devices. Here, we report a novel two-level colloidal lithography technology for making periodic arrays of single-crystalline silicon nanopillars (or nanocolumns) over large areas. Spin-coated monolayer silica colloidal crystals with unusual nonclose-packed structures are utilized as first-level etching masks in generating ordered polymer posts whose sizes can be much smaller than the templating silica microspheres.

Valproic Acid Inhibits Human Retinal Pigment Epithelial (hRPE) Cell Proliferation Via a P38 MAPK Signaling Mechanism.

Valproic acid (VPA) has been reported to inhibit cancer cell growth and has therapeutic use in retinal diseases. However, the mechanism of this action remains unclear. In order to explore this mechanism, primary human retinal pigment epithelial (hRPE) cell cultures were established.

Superhydrophobic hierarchical arrays fabricated by a scalable colloidal lithography approach.

Here we report an unconventional colloidal lithography approach for fabricating a variety of periodic polymer nanostructures with tunable geometries and hydrophobic properties. Wafer-sized, double-layer, non-close-packed silica colloidal crystal embedded in a polymer matrix is first assembled by a scalable spin-coating technology. The unusual non-close-packed crystal structure combined with a thin polymer film separating the top and the bottom colloidal layers render great versatility in templating periodic nanostructures, including arrays of nanovoids, nanorings, and hierarchical nanovoids.

Valproic Acid Induced Human Retinal Pigment Epithelial Cell Death as Well as its Survival after Hydrogen Peroxide Damage is Mediated by P38 Kinase.

Age-related macular degeneration (AMD) is a leading cause of legal blindness in developed countries. Several new drugs are now available to reduce the sight threatening complications of this disease, however, all are useful in only a small fraction of patients and none of them prevents disease development. An understanding of the pathogenesis of the retinal and macular degeneration is the first step in developing preventive and fully effective treatment options for this condition.

Skeletal developmental patterns in the acromial process and distal clavicle as observed by MRI.

Objective: To provide an MRI timeline of normal skeletal developmental patterns in the acromial process and distal clavicle in children up to 18 years of age.

Materials And Methods: Retrospective review of all shoulder MRIs obtained at our institution between January 2003 and March 2012, in children up to age 18, was performed. When available, radiographs and CT scans for these children were also reviewed.

Increased expression of the receptor for advanced glycation end-products in human peripheral neuropathies.

Background: Diabetic neuropathy and idiopathic neuropathy are among the most prevalent neuropathies in human patients. The molecular mechanism underlying pathological changes observed in the affected nerve remains unclear but one candidate molecule, the receptor for advanced glycation end-products (RAGE), has recently gained attention as a potential contributor to neuropathy. Our previous studies revealed that RAGE expression is higher in porcine and murine diabetic nerve, contributing to the inflammatory mechanisms leading to diabetic neuropathy.

Reduced expression of Munc13-1 in human and porcine diabetic peripheral nerve.

Peripheral neuropathy (PN) involves widespread peripheral nerve disorders affecting a large human population worldwide. In Europe and the United States, the first single most prominent cause of peripheral neuropathy is diabetes, affecting 60-70% patients with long-term diabetes followed by idiopathic neuropathy, peripheral nerve damage of unknown etiology, diagnosed in 10-40% of all patients admitted to hospitals with symptoms of peripheral nerve damage. The molecular mechanisms underlying the pathogenesis of this disorder are not yet fully understood, however a few potential molecular contributors, such as Munc13-1, have been recently suggested.

Impaired intracellular signaling may allow up-regulation of CTGF-synthesis and secondary peri-retinal fibrosis in human retinal pigment epithelial cells from patients with age-related macular degeneration.

Age-related macular degeneration (AMD) is a major sight-threatening ocular disorder in the United States of America and the world, yet its etiology is not clearly understood, preventing the development of effective prevention or therapy. Connective tissue growth factor (CTGF) has been implicated in the pathological synthesis of peri-retinal fibrous tissue in patients with AMD. Very little is known about the mechanism of this interaction.

MAP kinase pathway is involved in IGF-1-stimulated proliferation of human retinal pigment epithelial cells (hRPE).

Purpose: To investigate the mitogenic activity of insulin-like growth factor-1 (IGF-1) on the proliferation of human retinal pigment epithelial cells (hRPE) and to elucidate the role of vascular endothelial growth factor (VEGF) and MAP kinase (MAPK) in the IGF-1 signaling cascade.

Methods: Human RPE specimens were obtained from postmortem non-pathological eyes and cultured in vitro through several passages. Cellular proliferation in the presence of increasing concentrations of IGF-1 and IGF-1 + PD98059 (a known MAPK inhibitor) was measured by [(3)H]thymidine incorporation; trypan blue exclusion studies (T) verified cell viability.

Phenobarbital in comparison with carbon tetrachloride and phenobarbital-induced cirrhosis in rat liver regeneration.

Background: The simultaneous administration of carbon tetrachloride (CCl4) and phenobarbital in the rat produces one of the most common experimental models of liver cirrhosis. As phenobarbital also has a hepatotrophic effect, its role in liver regeneration following partial hepatectomy (HTX) is not elucidated.

Purpose: To examine the effect of long-term administration of phenobarbital in liver regeneration after HTX with regard to CCl4-induced cirrhotic rat model.

Treatment of cirrhotic rats with epidermal growth factor and insulin accelerates liver DNA synthesis after partial hepatectomy.

Prevention of postoperative hepatic failure is important after hepatic resection. In patients with cirrhosis, impaired liver function and regenerative capacity after major hepatic resection are associated with increased morbidity and mortality. In this study, a combination of epidermal growth factor (EGF) and insulin were used as hepatotrophic factors in an attempt to stimulate DNA synthesis after 70% hepatectomy (HTX).

Modulation of basic fibroblast growth factor effect by retinoic acid in cultured retinal pigment epithelium.

Purpose: We investigated the effect of retinoic acid (RA) on basic fibroblast growth factor (bFGF)-stimulated proliferation of cultured human retinal pigment epithelial (hRPE) cells and of 125I-bFGF-binding to the bFGF plasma membrane receptors of hRPE.

Methods: Proliferation of hRPE cells in the presence of increasing concentrations of bFGF and bFGF + RA was measured by 3H-thymidine incorporation into hRPE cells. To characterize bFGF receptors, hRPE cells were incubated at 4 degrees C with 125I-bFGF in the presence or absence of heparin.

Somatostatin inhibits bombesin-stimulated Gi-protein via its own receptor in rabbit colonic smooth muscle cells.

The effect of somatostatin on Bombesin-induced contraction of isolated rabbit colonic smooth muscle cells was examined. Preincubation of muscle cells with somatostatin 10(-6) M inhibited bombesin-induced contraction. To characterize somatostatin receptors, muscle cells (10(5) cells/tube) were incubated at 24 degrees C with 125I-Tyr0-SS-28.

Preferential suppression of insulin-stimulated proliferation of cultured hepatocytes by somatostatin: evidence for receptor-mediated growth regulation.

The role of somatostatin (SS-14) in the regulation of rat liver regeneration was examined by using thymidine incorporation into hepatocyte DNA labeled with tritiated thymidine, a nuclear-labeling index, and the binding of 125I-tyr11-SS-14 to hepatocytes isolated at various times after partial hepatectomy. The data demonstrated no suppressive effect of SS-14 on insulin and glucagon-stimulated thymidine incorporation into hepatocyte DNA as early as 2 h after partial hepatectomy. These data were substantiated by a nuclear labeling index studies.

Divergent mechanisms of insulin-like growth factor I and II on rat hepatocyte proliferation.

Insulin-like growth factors I and II are peptides with a structural homology for proinsulin, and are involved in hepatocyte proliferation. IGF-I and IGF-II, however, have different metabolic roles, and their mechanisms of action are incompletely known. We hypothesized that IGF-I and IGF-II act by different signal transduction pathways.

Impaired phorbol ester-induced hepatocyte proliferation in cirrhosis.

Cirrhotic livers are considered to regenerate less actively than normal livers after hepatic resection. Little is known about the mechanisms responsible for impaired capacity of regeneration in cirrhotic liver. In the present study, we investigated the effect of phorbol ester on hepatocyte proliferation in healthy and cirrhotic hepatocytes, using one of the phorbol esters, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), which has a direct effect on activation of protein kinase C (PKC).

Vasopressin stimulates DNA synthesis in cultured rat hepatocytes.

Liver regeneration following partial hepatectomy is significantly impaired in rats with hereditary vasopressin (AVP) deficiency. This suggested that AVP might have a direct effect on cultured rat hepatocytes. Hepatocytes from male Sprague-Dawley rats were isolated using a two-step collagenase perfusion technique and plated at a density of 10(5)/16-mm Primaria plate.

Molecular and functional studies of inhibitory G protein in RINm5F cells.

Inhibitory G proteins (Gi) play an important role in cell proliferation. In order to characterize Gi proteins in RINm5F (RIN) cells, we first established RIN cells in cell culture. Immunoblot analysis was performed on extracted G proteins using Western blot techniques and a Gi-specific antibody.

The effects of transforming growth factor alpha and somatostatin on regenerating hepatocytes in the rat.

Transforming growth factor alpha (TGF alpha) stimulates DNA synthesis in adult rat hepatocytes, and plays a physiological role after partial hepatectomy by an autocrine mechanism. Somatostatin (SS-14) is a potent inhibitor of gastrointestinal function and inhibits proliferation in various cell types. We examined the proliferative effect of TGF alpha and the inhibitory effect of SS-14 on hepatocytes isolated at various times after partial hepatectomy.

Hepatectomy impairs hepatic processing of somatostatin-14.

Somatostatin-14 (SS-14) inhibits the hepatotrophic effect of a variety of growth factors in cultured hepatocytes. We hypothesized that hepatic somatostatin processing might be altered during regeneration. Male Sprague-Dawley rats underwent the intraportal injection of radiolabeled SS-14 after sham or 70% hepatectomy.

Mechanisms of somatostatin action in RINm5F cells in culture: preliminary evidence for possible altered G protein function.

Octreotide (SMS), a somatostatin analogue, is an established antigrowth peptide, but it does not effectively inhibit the growth of insulinoma cells. In order to study the mechanisms that underlie this apparent lack of an antiproliferative effect on insulinoma tumor cells we established the rat insulinoma cell line, RINm5F, in culture. Cells in culture were tested by incubation in media with and without SMS.

Identification and partial characterization of a somatostatin-14 binding protein on rat liver plasma membranes.

Binding of somatostatin-14 to rat liver plasma membranes was characterized with 125-labeled[tyr11] somatostatin-14. Binding at 24 degrees C reached a plateau at 50 min and was reversible by synthetic somatostatin-14. Scatchard analysis revealed a single class of binding sites (affinity constant = 2.

Transforming growth factor-alpha (TGF-alpha) improves hepatic DNA synthesis after hepatectomy in cirrhotic rats.

Impaired liver regeneration in cirrhosis complicates the surgical treatment of liver tumors which arise in this setting. We developed a rat model to investigate the regenerative response of cirrhotic liver after hepatectomy and studied the effect of exogenous transforming growth factor-alpha (TGF-alpha), a potent liver mitogen. Micronodular cirrhosis was established by the simultaneous administration of CCl4 and phenobarbital.