Transient receptor potential vanilloid (TRPV-1) promotes neurogenic inflammation in the pancreas via activation of the neurokinin-1 receptor (NK-1R).

Objectives: The transient receptor potential vanilloid 1 (TRPV-1) is an ion channel found on primary sensory afferent neurons. Activation of TRPV-1 leads to the release of the proinflammatory neuropeptide substance P (SP). SP then binds to the neurokinin-1 receptor (NK1-R) on endothelial cells and promotes extravasation of plasma and proteins into the interstitial tissue and neutrophil infiltration, a process called neurogenic inflammation.

Preferential attachment of human gingival fibroblasts to the resin ionomer Geristore.

The resin ionomer Geristore has been used extensively for root perforation repairs. The purpose of this study was to evaluate oral in vitro biocompatibility of the resin ionomer Geristore compared to two other dental perforation repair materials, Ketac-Fil and Immediate Restorative Material (IRM). Growth and morphology of human gingival fibroblasts (HGFs) was determined using scanning electron microscopy (SEM) of HGFs cells grown on test materials as well as cytotoxicity assays using eluates from test materials.

Medical versus surgical management of biliary tract disease in pregnancy.

Background: The management of symptomatic cholelithiasis during pregnancy remains controversial. We compared outcomes after medical versus surgical management of biliary tract disease in pregnant patients.

Methods: We reviewed the clinical course of patients with symptomatic cholelithiasis during pregnancy from 1992 to 2002 at two university hospitals.

p38 MAPK regulates IL-1beta induced IL-6 expression through mRNA stability in osteoblasts.

Osteoblast-derived IL-6 functions in coupled bone turnover by supporting osteoclastogenesis favoring bone resorption instead of bone deposition. Gene regulation of IL-6 is complex occurring both at transcription and post-transcription levels. The focus of this paper is at the level of mRNA stability, which is important in IL-6 gene regulation.

Differential regulation of MMP-13 by chemical modified tetracyclines in osteoblasts.

Tetracyclines have been shown to regulate matrix metalloproteinase (MMP) expression in numerous cell types with various periodontal disease models. MMP-13, or collagenase-3, has been shown to be induced by a number of osteotropic cytokines and hormones in osteoblastic cells. In this study, we studied MMP-13 gene expression and regulation in osteoblasts by chemically modified tetracyclines (CMTs).

Pancreatic resection in the elderly.

Background: Elderly patients undergoing pancreatic resection present unique challenges in postoperative care. Although mortality rates among elderly patients after pancreatectomy at high-volume centers is known to be low, the anticipated decline in functional status and nutritional parameters has received little attention. Functional decline is an unrecognized but critically important consequence of pancreatic resection in older patients.

Activation of nociceptive neurons in T9 and T10 in cerulein pancreatitis.

Mechanisms of pain transduction in acute pancreatitis are poorly understood. Increased Fos expression in the spinal cord is a marker of activation of nociceptive neurons. We hypothesized that cerulein pancreatitis leads to increased Fos expression at T9 and T10, which receive sensory input from the pancreas.

Update on antibiotics used to treat orofacial infections.

Odontogenic infections are most often composed of many different bacteria. The pathogenesis of odontogenic infections depends on the relationship between anaerobic and aerobic bacteria within the infection. Historically, penicillins have been used to treat odontogenic infections.

Functional cooperation between interleukin-17 and tumor necrosis factor-alpha is mediated by CCAAT/enhancer-binding protein family members.

Interleukin (IL)-17 is a recently described cytokine involved in the amplification of inflammatory responses and pathologies. A hallmark feature of IL-17 is its ability to induce expression of other cytokines and chemokines. In addition, IL-17 potently synergizes with tumor necrosis factor-alpha (TNFalpha) to up-regulate expression of many target genes, particularly IL-6.

Chemically modified tetracyclines selectively inhibit IL-6 expression in osteoblasts by decreasing mRNA stability.

In bone biology, interleukin (IL)-6 is an autocrine/paracrine cytokine which can induce osteoclasts formation and activation to help mediate inflammatory bone destruction. Previous studies have shown that tetracycline and its derivatives have potentially beneficial therapeutic effects in the prevention and treatment of metabolic bone diseases by modulating osteoblast and osteoclast activities. Our previous studies indicated that non-antimicrobial chemically modified tetracyclines (CMTs) can dose-dependently inhibit IL-1 beta-induced IL-6 secretion in osteoblastic cells.

Gene expression profile of tissue engineered skin subjected to acute barrier disruption.

The main function of the skin is to protect the body from infection, dehydration, and other environmental insults by creating an impermeable barrier of cornified cell layers, the stratum corneum. In contrast to cells in culture, tissue-engineered skin equivalents contain well-developed basal, spinous, granular, and cornified cell layers providing an excellent model to study the tissue response to barrier disruption. After 7 d of culture at the air-liquid interface the barrier of the tissues was disrupted by short exposure to acetone and the global gene expression profile of the tissues was evaluated using DNA microarrays.

Cementoblasts maintain expression of osteocalcin in the presence of mineral trioxide aggregate.

This study investigated the effects of mineral trioxide aggregate on cementoblast growth and osteocalcin production in tissue culture. For cellular morphology studies, cementoblasts on mineral trioxide aggregate, IRM, and amalgam were incubated for 48 h then fixed for scanning electron microscopic analysis. For gene expression on mineral trioxide aggregate and IRM, reverse transcriptase polymerase chain reaction was performed using primer sets for glyceraldehyde-3-phosphate dehydrogenase, type I collagen, alkaline phosphatase, osteocalcin, and bone sialoprotein after 3 and 5 days.

In vitro mineralization studies with substrate-immobilized bone morphogenetic protein peptides.

Understanding the factors that control osteoblastic behavior is centrally important in establishment of successful osseointegration. Pharmacogenetic control of the osteoblast to increase the mineral content around dental implants may offer a unique advantage to clinicians in improving osseointegration success and decreasing time before mechanical loading. This in vitro pilot study has screened for bioactive peptides derived from bone morphogenetic protein 7 (BMP-7) (also called osteogenic protein 1 [OP-1]).

The prevention of preterm labour -- corticotropin releasing hormone type 1 receptors as a target for drug design and development.

The role of the corticotropin releasing hormone in the onset of labour and the subsequent medicinal chemistry implications of CRH antagonists for the prevention of premature birth, and identification of the CRH type 1 receptor as the target for this drug design, are reviewed here.

Lovastatin alters biliary lipid composition and dissolves gallstones: a long-term study in prairie dogs.

Lovastatin, an inhibitor of the rate-limiting enzyme in cholesterol biosynthesis, is widely used to treat hypercholesterolemia. We investigated the long-term effects of lovastatin alone and in combination with ursodeoxycholic acid on biliary lipid composition and gallstone dissolution. Forty-two prairie dogs were fed 1.

Recombinant human neutral endopeptidase ameliorates pancreatic elastase-induced lung injury.

Background: Genetic deletion of neutral endopeptidase (NEP), a cell-surface metalloprotease that degrades proinflammatory peptides, exacerbates lung injury induced by pancreatic elastase in a model of pancreatitis-associated lung injury. We tested 3 hypotheses: (1) genetic deletion of NEP prolongs lung recovery after elastase injections; (2) elastase-mediated lung injury is associated with down-regulation of NEP; and (3) pretreatment of NEP (-/-) and (+/+) animals with recombinant human NEP (rhNEP) reduces pulmonary damage in this model.

Methods: NEP (+/+) or (-/-) mice were injected with pancreatic elastase (0.

Pathophysiology of gallstone pancreatitis.

Gallstone pancreatitis was first recognized as an entity by Opie in 1901 (1), and since then has generated volumes of literature which have attempted to explain its pathophysiology. Multiple animal experiments and human clinical studies in the past thirty years have led to a better understanding of both macro- and microscopic events which lead to pancreatic inflammation in the setting of a passing or impacted gallstone. Evidence suggests that pancreatic duct outflow obstruction is the initial event.

Deletion of neutral endopeptidase exacerbates intestinal inflammation induced by Clostridium difficile toxin A.

Toxin A (TxA) of Clostridium difficile induces acute inflammation of the intestine initiated by release of substance P (SP) and activation of the neurokinin-1 receptor. However, the mechanisms that terminate this response are unknown. We determined whether the SP-degrading enzyme neutral endopeptidase (NEP, EC 3.

NK-1 receptor desensitization and neutral endopeptidase terminate SP-induced pancreatic plasma extravasation.

Substance P (SP) induces plasma extravasation and neutrophil infiltration by activating the neurokinin-1 receptor (NK1-R). We characterized the mechanisms regulating this response in the rat pancreas. Anesthetized rats were continuously infused with SP, and plasma extravasation was quantified using Evans blue (EB) dye.

Substance P is a determinant of lethality in diet-induced hemorrhagic pancreatitis in mice.

Background: The neuropeptide substance P (SP) induces plasma extravasation and neutrophil infiltration by activating the neurokinin 1-receptor (NK1-R). SP-induced neurogenic inflammation is terminated by the cell surface enzyme neutral endopeptidase (NEP), which degrades SP. We determined whether genetic deletion of the NK1-R reduces mortality and, conversely, whether genetic deletion of NEP increases mortality in a lethal model of hemorrhagic pancreatitis.

The consistency of neuropsychological assessments performed via telecommunication and face to face.

Previous studies have suggested that cognitive assessments of adult psychiatric patients can be carried out as reliably via teleconsultation as they can face to face. However, the designs of these studies have often been less than satisfactory. The present study used videoconferencing at 128 kbit/s for the cognitive assessment of individuals with a history of alcohol abuse.

Substance P mediates inflammatory oedema in acute pancreatitis via activation of the neurokinin-1 receptor in rats and mice.

Pancreatic oedema occurs early in the development of acute pancreatitis, and the overall extent of fluid loss correlates with disease severity. The tachykinin substance P (SP) is released from sensory nerves, binds to the neurokinin-1 receptor (NK1-R) on endothelial cells and induces plasma extravasation, oedema, and neutrophil infiltration, a process termed neurogenic inflammation. We sought to determine the importance of neurogenic mechanisms in acute pancreatitis.

IL-1 beta increases type 1 inositol trisphosphate receptor expression and IL-6 secretory capacity in osteoblastic cell cultures.

Acute IL-6 secretion from osteosarcoma cells induced by the PI-linked hormones PTH(1-34) and endothelin-1 is potentiated by IL-1 beta. The present findings indicate that this potentiation is accompanied by increased signal transduction capacity. Specifically, IL-1 beta (30 pM) increased the B(max) of InsP(3) receptor binding (2.