Sara M. Hoffman

ORCID: 0009-0007-9546-8077
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About
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Research Areas
  • Complement system in diseases
  • Helicobacter pylori-related gastroenterology studies
  • Artificial Intelligence in Healthcare and Education
  • Cell Adhesion Molecules Research
  • Immune Response and Inflammation
  • Eosinophilic Esophagitis
  • Nitric Oxide and Endothelin Effects
  • Caveolin-1 and cellular processes
  • Urticaria and Related Conditions
  • Receptor Mechanisms and Signaling
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Blood Coagulation and Thrombosis Mechanisms
  • Liver Disease and Transplantation
  • T-cell and B-cell Immunology
  • Monoclonal and Polyclonal Antibodies Research
  • Pharmacological Effects of Natural Compounds
  • Platelet Disorders and Treatments
  • Hydrogen's biological and therapeutic effects
  • Biotin and Related Studies
  • Reproductive System and Pregnancy
  • Glycosylation and Glycoproteins Research
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Dietary Effects on Health
  • Organ Transplantation Techniques and Outcomes
  • SARS-CoV-2 and COVID-19 Research

Harvard University
2024

Kansas State University
2010

Medical University of South Carolina
2010

Versiti Blood Center of Wisconsin
2002

University of Wisconsin–Madison
2001

Drawing from real-life scenarios and insights shared at the RAISE (Responsible AI for Social Ethical Healthcare) conference, we highlight critical need in health care (AIH) to primarily benefit patients address current shortcomings systems such as medical errors access disparities. The embodying a sense of responsibility urgency, emphasized that AIH should enhance patient care, support professionals, be accessible safe all. discussions revolved around immediate actions leaders, adopting...

10.1056/aip2400036 article EN NEJM AI 2024-02-22

Abstract Reperfusion of ischemic tissue induces significant damage in multiple conditions, including myocardial infarctions, stroke, and transplantation. Although not as common, the mortality rate mesenteric ischemia/reperfusion (IR) remains >70%. complement naturally occurring Abs are known to mediate during IR, target Ags intracellular molecules. We investigated role serum protein, β2-glycoprotein I an initiating Ag for Ab recognition (β2-GPI) peptides a therapeutic IR. The time...

10.4049/jimmunol.1002520 article EN The Journal of Immunology 2010-10-19

Intestinal ischemia-reperfusion (IR)-induced damage requires complement receptor 2 (CR2) for generation of the appropriate natural Ab repertoire. Pathogenic Abs recognize neoantigens on ischemic tissue, activate complement, and induce intestinal damage. Because C3 cleavage products act as ligands CR2, we hypothesized that CR2(hi) marginal zone B cells (MZBs) require pathogenic Abs. To explore ability splenic CR2(+) to generate damaging repertoire, adoptively transferred either MZBs or...

10.4049/jimmunol.1002059 article EN The Journal of Immunology 2010-12-28

Our previous study indicated that normal serum contains complement-fixing natural IgM antibodies reacting with a large variety of randomly generated protein carboxy-termini. Here we show the "carboxy-terminal" (C-IgM) specifically react short peptide sequences located immediately at carboxy-terminus. The specificity C-IgM-peptide interactions is tentatively defined by three to four amino acid residues. All carboxy-terminal peptides in library apparently C-IgM antibodies. Immobilized...

10.1006/mthe.2001.0340 article EN cc-by-nc-nd Molecular Therapy 2001-06-01

Abstract Helicobacter species are common laboratory pathogens which induce intestinal inflammation and disease in susceptible mice. Since vitro studies indicate that products activate macrophages, we hypothesized vivo infection regulates the inflammatory response of muscularis macrophages from C57Bl/6 hepaticus increased surface expression macrophage markers F4/80, CD11b MHC‐II within whole muscle mounts. However, constitutive cytokine chemokine production by isolated infected mice...

10.1002/cbf.1709 article EN Cell Biochemistry and Function 2010-11-23

Hemorrhage and hemorrhagic shock instigate intestinal damage inflammation. Multiple components of the innate immune response, including complement neutrophil infiltration, are implicated in this pathology. To investigate interaction activation other response during hemorrhage, we treated mice after hemorrhage with CR2-fH, a targeted inhibitor alternative pathway assessed inflammation 2 h hemorrhage. In wild-type mice, CR2-fH attenuated hemorrhage-induced, midjejunal as determined by...

10.1097/shk.0b013e3181ed8ec9 article EN Shock 2010-06-24

With more than half of the world population infected, Helicobacter infection is an important public health issue associated with gastrointestinal cancers and inflammatory bowel disease. Animal studies indicate that complement oxidative stress play a role in infections. Hemorrhage (HS) induces tissue damage attenuated by blockade either activation or products. Therefore, we hypothesized chronic hepaticus would modulate HS-induced intestinal inflammation. To test this hypothesis, examined...

10.1097/shk.0b013e3181dc077e article EN Shock 2010-03-23

Ischaemia-reperfusion-induced intestinal injury requires both Toll-like receptor 4 (TLR4) signalling through myeloid differentiation primary response gene (88) (MyD88) and complement activation. As a common Gram-negative pathogen, Helicobacter hepaticus signals TLR4 upregulates the inhibitor, decay accelerating factor (DAF; CD55). Since ischaemia-reperfusion (IR) is dependent, we hypothesized that infection may alter IR-induced damage. Infection increased DAF transcription subsequently...

10.1113/expphysiol.2010.055426 article EN Experimental Physiology 2010-11-06
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