Publications by authors named "Nichole Miller"

Background And Aims: Fecal microbiota transplantation (FMT) has recently been shown to be a promising therapy for recurrent and refractory Clostridium difficile infections (CDI) despite lack of protocol standardization. Patients with inflammatory bowel disease (IBD) present a particular challenge to CDI therapy as they are reported to have worse clinical outcomes, including higher colectomy rates and increased mortality. We aimed to assess the outcomes of FMT for recurrent CDI in patients with IBD at our healthcare system.

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Background: Several publications have reported an increase in nonspecific reactions when automated technologies such as solid phase are used for the detection of red blood cell alloantibodies. However, there is little known about patient-specific factors associated with these reactions and the clinical importance of these nonspecific reactions.

Study Design And Methods: We performed a 6-year retrospective review of our blood bank records and all newly reported unidentified (UID) reactivity using a test tube polyethylene glycol (t-PEG) and solid-phase method for the detection and identification of alloantibodies was recorded.

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Article Synopsis
  • Clostridium difficile infection (CDI) poses significant healthcare challenges, but fecal microbiota transplantation (FMT) shows a much higher success rate (80-90%) compared to traditional antibiotic treatments for recurrent cases.
  • In a study of 201 patients undergoing FMT, the failure rate was 12.4%, with predictors of failure including being female, previous hospitalizations, and surgeries before the transplant.
  • The overall mortality rate was 9.0%, and failure of FMT significantly increased the risk of death, emphasizing the need for awareness of risk factors associated with FMT outcomes.
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Oxidative stress is thought to contribute to disease pathogenesis in the central nervous system (CNS) disease multiple sclerosis (MS). Myeloperoxidase (MPO), a potent peroxidase that generates toxic radicals and oxidants, is increased in the CNS during MS. However, the exact mechanism whereby MPO drives MS pathology is not known.

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) mediated by T helper (h)1 and/or Th17 CD4 T cells that drive inflammatory lesion development along with demyelination and neuronal damage. Defects in immune regulatory mechanisms are thought to play a role in the pathogenesis of MS. While an early clinical trial indicated that IFN-γ administration was detrimental to MS, studies in the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), indicated that IFN-γ exhibits a number of anti-inflammatory properties within the CNS.

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The signaling lymphocyte activation molecule (SLAM) family plays important roles in adaptive immune responses. Herein, we evaluated whether the SLAM family member 2B4 (CD244) plays a role in immune cell development, homeostasis and antibody responses. We found that the splenic cellularity in Cd244-/- mice was significantly reduced due to a reduction in both CD4 T cells and follicular (Fo) B cells; whereas, the number of peritoneal cavity B cells was increased.

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R-Ras is a member of the Ras superfamily of small GTPases, which are regulators of various cellular processes, including adhesion, survival, proliferation, trafficking, and cytokine production. R-Ras is expressed by immune cells and has been shown to modulate dendritic cell (DC) function in vitro and has been associated with liver autoimmunity. We used Rras-deficient mice to study the mechanism whereby R-Ras contributes to autoimmunity using experimental autoimmune encephalomyelitis (EAE), a mouse model of the CNS autoimmune disease multiple sclerosis.

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Article Synopsis
  • - MS is an autoimmune and neurodegenerative disease that causes inflammation and damage to neurons in the central nervous system, but the mechanism behind how the immune system contributes to neuronal damage is still not fully understood.
  • - Previous research has shown that certain immune cells, like CD4 T-cells, can cause early damage to neurons, and this study extends those findings by showing that activated immune cells can destabilize microtubules in neuronal structures without direct contact.
  • - The study found that this microtubule destabilization occurs in axons (the long projections of neurons) before any cell death signs, highlighting the ability of immune cells to disrupt neuronal function independently from killing the neurons.
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The molecular packing in a polymer: fullerene bimolecular crystal is determined using X-ray diffraction (XRD), molecular mechanics (MM) and molecular dynamics (MD) simulations, 2D solid-state NMR spectroscopy, and IR absorption spectroscopy. The conformation of the electron-donating polymer is significantly disrupted by the incorporation of the electron-accepting fullerene molecules, which introduce twists and bends along the polymer backbone and 1D electron-conducting fullerene channels.

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Underage drinking, or binge drinking, has become a major concern in U.S. society.

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The generalized anatomic and physiologic immaturity of preterm infants of very low birth weight (VLBW) ( View Article and Find Full Text PDF