Evaluation of an oral health training program for school nurses

Pediatric dental disease is a silent epidemic (Committee on Health, Education, Labor, and Pensions, 2002). Dental decay is commonly unrecognized and under-treated, and can affect children\u27s growth and development as well as their ability to perform in school. Effective interventions to prevent dental decay include water fluoridation, dental sealants, pediatric dental screenings, and dental health education programs. This pre-experimental design study evaluated the effectiveness of an oral health training program for school nurses. This training program was designed based on the First 5 California \u3c;\u3eral Health Training Program (2003). A non-randomized sample of fourteen (N=l4) school nurses participated in the presentation. Pre and post test results indicated a statistically significant (p\u3c.O I) increase in oral health knowledge among the participants. As a result of this study, the researchers recommend that school nurses receive formal training in dental health assessments to effectively contribute to the improvement of pediatric oral health in the school setting

Membrane transport of camptothecin: facilitation by human P-glycoprotein (ABCB1) and multidrug resistance protein 2 (ABCC2)

BACKGROUND: The purpose of the present study was to continue the investigation of the membrane transport mechanisms of 20-(S)-camptothecin (CPT) in order to understand the possible role of membrane transporters on its oral bioavailability and disposition. METHODS: The intestinal transport kinetics of CPT were characterized using Caco-2 cells, MDCKII wild-type cells and MDCKII cells transfected with human P-glycoprotein (PGP) (ABCB1) or human multidrug resistance protein 2 (MRP2) (ABCC2). The effects of drug concentration, inhibitors and temperature on CPT directional permeability were determined. RESULTS: The absorptive (apical to basolateral) and secretory (basolateral to apical) permeabilities of CPT were found to be saturable. Reduced secretory CPT permeabilities with decreasing temperatures suggests the involvement of an active, transporter-mediated secretory pathway. In the presence of etoposide, the CPT secretory permeability decreased 25.6%. However, inhibition was greater in the presence of PGP and of the breast cancer resistant protein inhibitor, GF120918 (52.5%). The involvement of additional secretory transporters was suggested since the basolateral to apical permeability of CPT was not further reduced in the presence of increasing concentrations of GF120918. To investigate the involvement of specific apically-located secretory membrane transporters, CPT transport studies were conducted using MDCKII/PGP cells and MDCKII/MRP2 cells. CPT carrier-mediated permeability was approximately twofold greater in MDCKII/PGP cells and MDCKII/MRP2 cells than in MDCKII/wild-type cells, while the apparent K(m )values were comparable in all three cell lines. The efflux ratio of CPT in MDCKII/PGP in the presence of 0.2 μM GF120918 was not completely reversed (3.36 to 1.49). However, the decrease in the efflux ratio of CPT in MDCKII/MRP2 cells (2.31 to 1.03) suggests that CPT efflux was completely inhibited by MK571, a potent inhibitor of the Multidrug Resistance Protein transporter family. CONCLUSIONS: The current results provide evidence that PGP and MRP2 mediate the secretory transport of CPT in vitro. However, the involvement of other transporters cannot be ruled out based on these studies. Since these transporters are expressed in the intestine, liver and kidney variations in their expression levels and/or regulation may be responsible for the erratic oral absorption and biliary excretion of CPT observed in human subjects

Updates in Gastrointestinal Oncology – insights from the 2008 44th annual meeting of the American Society of Clinical Oncology

We have reviewed the pivotal presentations rcelated to colorectal cancer (CRC) and other gastrointestinal malignancies from 2008 annual meeting of the American Society of Clinical Oncology (ASCO). We have discussed the scientific findings and the impact on practice guidelines and ongoing clinical trials. The report on KRAS status in patients with metastatic CRC receiving epidermal growth factor receptor (EGFR) targeted antibody treatment has led to a change in National Comprehensive Cancer Network guideline that recommends only patients with wild-type KRAS tumor should receive this treatment. The results of double biologics (bevacizumab and anti-EGFR antibody) plus chemotherapy as first-line treatment in patients with metastatic CRC has shown a worse outcome than bevacizumab-based regimen. Microsatellite Instability has again been confirmed to be an important predictor in patients with stage II colon cancer receiving adjuvant treatment

Evaluation of a manufacturer's sales representative training program

Includes bibliographical references

The design and implementation of a leadership development program for Greenheck Fan Corporation

Includes bibliographical references

Investigating the Effects of a Novel Fibronectin Mutation: The Role of ER Stress and Collagen Fibrillogenesis in the Pathogenesis of Spondylometaphyseal Dysplasia

Spondylometaphyseal dysplasia (SMD) is a group of skeletal disorders characterized by deformities of the spine and long bones. While the etiology of many SMDs are unknown, the discovery of a novel fibronectin mutation (FNC97W) has been recently linked to an individual with SMD. Fibronectin (FN) is a vital extracellular matrix (ECM) protein that assembles into a fibrillar matrix and regulates cellular activities, including matrix assembly of other ECM proteins such as type I collagen (COL1). Proper assembly of the ECM is essential for normal cell and tissue development, providing organization, developmental signals, and structural support to cells. Mutations in COL1 and other ECM proteins have been linked to skeletal disease through a number of different mechanisms, including deregulated matrix assembly and perturbations in cellular function caused by protein misfolding and subsequent ER stress, suggesting pathways by which our novel FN mutation may lead to SMD. Analyses of primary dermal fibroblasts heterozygous for the FNC97W mutation reveal abnormal accumulation of FN within the ER of the cells, which suggests ER stress and activation of the unfolded protein response (UPR), as well as lower levels of FN in the culture medium, revealing a defect in FN secretion. The cells also assemble a reduced FN matrix and fail to assemble a COL1 matrix. These results provide new insights into the effects of a FN mutation on cellular function, highlighting the importance of FN and COL1 matrix assembly in skeletal development and elucidating their potential role in the pathogenesis of SMD

060. John 1:29-42a.mp3

Chapel Sermon by Mark Drengler from John 1:29-42a on Friday, January 20, 2017

The Stereochemistry and Mechanism of The Biosynthesis of Ent-Sandaracopimaradiene and Related Diterpenes

198 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1980.The stereochemistry and mechanism of the cyclization of copalyl pyrophosphate to (+)-sandaracopimaradiene by enzyme extracts from R. cummunis was investigated. (S)-Geranyl-geraniol-1-d was prepared by enzymatic reduction of geranyl-geranial-1-d with horse liver alcohol dehydrogenase and NAD('+) with ethanol as a proton source. Inspection of the vinyl region of the ('1)H NMR spectrum of sandaracopimaradiene biosynthesized from (S)-geranylgeranyl pyrophosphate-1-d indicated that the deuteriovinyl group had the E configuration. The S(,N') cyclization of copalyl pyrophosphate to sandaracopimaradiene therefore proceeds with anti stereochemistry.The question as to whether the pro-E or pro-Z hydrogen at C-17 of copalyl pyrophosphate is eventually eliminated during the last step of sandaracopimaradiene was ascertained using (17E)-copalyl pyrophosphate-17-d. The exocyclic double bond of copalol was labelled by halogen-metal exchange on (17E)-bromo copalyl tetrahydropyranyl ether and hydrolysis with deuterium oxide. The E stereochemistry at C-17 was established by a stereospecific intramolecular cyclopropanation reaction of a side chain diazo ketone onto the exocyclic methylene of a partially degraded sample obtained from copalol-17-d. Inspection of the coupling constant between the two residual hydrogens on the cyclopropane ring confirmed the assigned stereochemistry.Integration of the NMR spectrum of (+)-sandaracopimaradiene biosynthesized from (17E)-copalyl pyrophosphate-17-d established that the C-17 pro-Z hydrogen was stereoselectively removed. The results are also consistent with cyclization between C-17 and C-13 of copalyl pyrophosphate occurring from the si face of C-17.The mechanism of the S(,N') reaction was probed by studying the incorporation of structural analogues of copalyl pyrophosphate. A mixture of ent-manool and ent-13-epimanool was prepared by selective epoxidation of the allylic double bond of copalol, conversion to the mesylate, and reductive opening of the epoxide ring coupled with cleavage of the mesylate group. 16-Nor-copalol was prepared by a Wittig condensation between trimethyl phosphonoacetate and the aldehyde derived from partial degradation of the side chain of copalol. cis-Copalol was prepared by reduction of cis-copalal obtained as a side product from the activated manganese dioxide oxidation of trans-copalol.The pyrophosphate esters of the analogues were incubated with cell free enzyme extracts from R. communis and M. macrocarpus. All the analogues except 16-norcopalyl pyrophosphate were efficiently incorporated into the diterpene hydrocarbons. The results indicate either the presence of an isomerase activity capable of interconverting all the analogues or that the pyrophosphate binding pocket of the diterpene cyclases is capable of ionizing the pyrophosphate group from several positions on the allylic system. The mechanism of the S(,N') reaction appears to proceed by ionization of the pyrophosphate group to an ion pair followed by condensation to close the C-ring.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD