David A. Scott
· ProfessorVerifiedUniversity of California, Los Angeles · Art History
Active 1972–2025
About
David A. Scott is the author of the book "Art: Authenticity, Restoration, Forgery," which presents a detailed account of authenticity in the visual arts from the Paleolithic to the postmodern era. His work explores how the restoration of artworks can alter the perception of authenticity and may lead to the creation of fakes and forgeries. This book examines the complex interactions between authenticity, restoration, and forgery in the art world, providing a comprehensive study of these themes.
Research topics
- Microbiology
- Medicine
- Biology
Selected publications
Annals of Oncology · 2025-07-01
articleOpen accessNature Medicine · 2025-06-24 · 29 citations
articleOpen accessAbstract Tirzepatide induces weight reduction but the underlying mechanisms are unknown. This 6-week phase 1 study investigated early effects of tirzepatide on energy intake. Male and female adults without diabetes ( n = 114) and a body mass index from 27 to 50 kg per m 2 were randomized 1:1:1 to blinded once-weekly tirzepatide or placebo, or open-label once-daily liraglutide. The primary outcome was change from baseline to week 3 in energy intake during an ad libitum lunch with tirzepatide versus placebo. Secondary outcomes assessed self-reported ingestive behavior and blood-oxygenation-level-dependent functional magnetic resonance imaging with food photos. Tirzepatide reduced energy intake versus placebo at week 3 (estimated treatment difference −524.6 kcal (95% confidence interval −648.1 to −401.0), P < 0.0001). With regard to secondary outcomes versus placebo, tirzepatide decreased overall appetite, food cravings, tendency to overeat, perceived hunger and reactivity to foods in the environment but did not impact volitional restriction of dietary intake. At week 3 versus placebo, tirzepatide did not statistically significantly impact blood-oxygenation-level-dependent activation to highly palatable food photos (aggregated category of high-fat, high-sugar foods and high-fat, high-carbohydrate foods) but decreased activation to high-fat, high-sugar food photos in the medial frontal and cingulate gyri, orbitofrontal cortex and hippocampus. Our results suggest tirzepatide reduces food intake, potentially by impacting ingestive behavior. ClinicalTrials.gov registration: NCT04311411 .
2023-03-31
supplementary-materialsOpen access<p>PDF file - 164K</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file - 219K.</p><p><b>Please Note:</b> Supplementary Table 1 was updated 06/20/12. Please see the published <a href="http://dx.doi.org/10.1158/1055-9965.EPI-12-0618" target="_blank">correction notice</a> for details of modifications to the article made in order to correct author error.</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file - 219K.</p><p><b>Please Note:</b> Supplementary Table 1 was updated 06/20/12. Please see the published <a href="http://dx.doi.org/10.1158/1055-9965.EPI-12-0618" target="_blank">correction notice</a> for details of modifications to the article made in order to correct author error.</p>
Gastric Colonization by H. pylori
2023 · 6 citations
Senior authorCorresponding- Medicine
- Microbiology
- Biology
Treatment of Peptic Ulcer Disease: Yesterday, today and tomorrow
Proceedings for Annual Meeting of The Japanese Pharmacological Society · 2018-01-01
articleOpen accessThe edict “No Acid, No Ulcer” (Schwarz Beit Clin Chir 1910, led to efforts in the twentieth century to inhibit acid secretion. The most successful early intervention was vagotomy (Dragsted et al PSEBM 1943) which was then superseded by H2 antagonists (Black et al Nature 1972). These show uniform tolerance and short duration of action making them relatively ineffective but still were a major breakthrough in treatment. They were then replaced by PPIs that are acid activated covalent inhibitors of the gastric H,K ATPase (Fellenius et al Nature 1981) that show long duration of action and no tolerance. Omeprazole binds to cys813 and cys892 in the proton pathway (Besancon et al JBC 1997). However, the need for acid activation and a short plasma half-life restricts their efficacy even at bid dosing. The first potassium competitive inhibitor (PCAB) of the gastric H,K ATPase, SCH28080, had liver toxicity and was an imidazopyridine with a short plasma half-life and rapid dissociation (Wallmark et al JBC 1987) and many other imidazopyridine were tested and dropped. Recently a pyrrolopyridine (vonoprazan Hori et al JPET 2011) is on the market and others are in development with relatively long half-lives and immediate onset of action that likely will supersede PPIs. This compound's N-methylmethaneamine (pKa9.2) binds at glu343 blocking K binding and ATPase activity (Abe et al Nature 2018). It is now clear that infection by Helicobacter pylori is responsible for most peptic ulcer diseases where 1% of infected individuals succumb to the disease a rate 10 times higher than non-infected people and therefore eradication of the infection could be a new modality of treatment. Antibiotic resistance has made eradication difficult and generally unpredictable without measurement of antibiotic resistance. However, it appears that lengthy acid inhibition (pH >5.0 24hrs per day) stimulates bacterial division and hence amoxicillin sensitivity (Marcus et al APT 2012) and amoxicillin resistance is rare compared to resistance to other antibiotics. However, H. pylori expresses beta-lactamase so resistance may appear. Elevation of the organism's periplasmic pH is essential for acid survival and urease and periplasmic carbonic anhydrase are essential for this to occur. The elevation of periplasmic pH has been shown directly by measurement of eGFP fluorescence (Wen et al J Bact 20180 Expression of this carbonic anhydrase remains high at pH 3.0 in contrast to urease (Marcus et al Helicobacter 2018) suggesting its importance for gastric survival. An attractive eradication strategy would be then to use a long lasting carbonic anhydrase inhibitor with twice a day dosing to provide an antibiotic free means of eradication and this inhibitor is already available in the form of Diamox sequels. Treatment with Diamox resulted in a recurrence rate of 6% similar to that found after eradication of H. pylori compared to 43% following conventional medical therapy and with hindsight this is likely due to eradication of the infection (Puscas ANYAS 1984). It has indeed been shown that its periplasmic carbonic anhydrase is important for gastric survival of H. pylori and is required for neutralization of periplasmic pH in acid (Marcus et al J Bact 2005). So, today, the dictum might become “No Hp, no ulcer”.
Measurement of Internal pH in Helicobacter pylori by Using Green Fluorescent Protein Fluorimetry
Journal of Bacteriology · 2018-05-04 · 8 citations
articleABSTRACT Helicobacter pylori is an organism known to colonize the normal human stomach. Previous studies have shown that the bacterium does this by elevating its periplasmic pH via the hydrolysis of urea. However, the value of the periplasmic pH was calculated indirectly from the proton motive force equation. To measure the periplasmic pH directly in H. pylori , we fused enhanced green fluorescent protein (EGFP) to the predicted twin-arginine signal peptides of HydA and KapA from H. pylori and TorA from Escherichia coli . The fusion proteins were expressed in the H. pylori genome under the control of the cagA promoter. Confocal microscopic and cell fractionation/immunoblotting analyses detected TorA-EGFP in the periplasm and KapA-EGFP in both the periplasm and cytoplasm, while the mature form of HydA-EGFP was seen at low levels in the periplasm, with major cytoplasmic retention of the precursor form. With H. pylori expressing TorA-EGFP, we established a system to directly measure periplasmic pH based on the pH-sensitive fluorimetry of EGFP. These measurements demonstrated that the addition of 5 mM urea has little effect on the periplasmic pH at a medium pH higher than pH 6.5 but rapidly increases the periplasmic pH to pH 6.1 at an acidic medium pH (pH 5.0), corresponding to the opening of the proton-gated channel, UreI, and confirming the basis of gastric colonization. Measurements of the periplasmic pH in an HP0244 (FlgS)-deficient mutant of H. pylori expressing TorA-EGFP revealed a significant loss of the urea-dependent increase in the periplasmic pH at an acidic medium pH, providing additional evidence that FlgS is responsible for recruitment of urease to the inner membrane in association with UreI. IMPORTANCE Helicobacter pylori has been identified as the major cause of chronic superficial gastritis and peptic ulcer disease. In addition, persistent infection with H. pylori , which, if untreated, lasts for the lifetime of an infected individual, predisposes one to gastric malignancies, such as adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. A unique feature of the neutralophilic bacterium H. pylori is its ability to survive in the extremely acidic environment of the stomach through its acid acclimation mechanism. The presented results on measurements of periplasmic pH in H. pylori based on fluorimetry of fully active green fluorescent protein fusion proteins exported with the twin-arginine translocase system provide a reliable and rapid tool for the investigation of acid acclimation in H. pylori .
Erratum: Electric discharge during electrosurgery
Scientific Reports · 2018-03-19
erratumOpen accessScientific Reports 5: Article number: 9946; published online: 16 April 2015; updated: 19 March 2018. The original PDF version of this Article contained a typographical error in the volume number ‘5’ was incorrectly given as ‘4’. This error has now been corrected in the PDF version; the HTML version was correct from the time of publication.
Helicobacter · 2018-04-25 · 35 citations
articleSenior authorCorrespondingAbstract Background The pathogen Helicobacter pylori encounters many stressors as it transits to and infects the gastric epithelium. Gastric acidity is the predominate stressor encountered by the bacterium during initial infection and establishment of persistent infection. H. pylori initiates a rapid response to acid to maintain intracellular pH and proton motive force appropriate for a neutralophile. However, acid sensing by H. pylori may also serve as a transcriptional trigger to increase the levels of other pathogenic factors needed to subvert host defenses such as acid acclimation, antioxidants, flagellar synthesis and assembly, and CagA secretion. Materials and Methods Helicobacter pylori were acid challenged at pH 3.0, 4.5, 6.0 vs nonacidic pH for 4 hours in the presence of urea, followed by RNA ‐seq analysis and qPCR . Cytoplasmic pH was monitored under the same conditions. Results About 250 genes were induced, and an equal number were repressed at acidic pH s. Genes encoding for antioxidant proteins, flagellar structural proteins, particularly class 2 genes, T4 SS / Cag ‐ PAI , F o F 1 ‐ ATP ase, and proteins involved in acid acclimation were highly expressed at acidic pH . Cytoplasmic pH decreased from 7.8 at pH out of 8.0 to 6.0 at pH out of 3.0. Conclusions These results suggest that increasing extracellular or intracellular acidity or both are detected by the bacterium and serve as a signal to initiate increased production of protective and pathogenic factors needed to counter host defenses for persistent infection. These changes are dependent on degree of acidity and time of acid exposure, triggering a coordinated response to the environment required for colonization.
Frequent coauthors
- 197 shared
George Sachs
Providence College
- 108 shared
Elizabeth A. Marcus
- 65 shared
David L. Weeks
Elmhurst Hospital Center
- 32 shared
Yi Wen
Simon Fraser University
- 21 shared
Klaus Melchers
- 21 shared
Andrew G. Glass
Kaiser Permanente Center for Health Research
- 19 shared
Brenda B. Rush
- 19 shared
Attila T. Lörincz
Magyar Agrár- és Élettudományi Egyetem
Awards & honors
- Prize from the Association of American Publishers for the bo…
- Resume-aware match score
- Save to shortlist
- AI-drafted outreach
See your match with David A. Scott
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
- Free to start
- No credit card
- 30-second signup