Publications by authors named "Tolani F Olonisakin"

Background: Thymic stromal lymphopoietin (TSLP) plays an important role in mediating the type-2-inflammatory response. This study examined how TSLP and interleukin (IL)-4 levels in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) correlated with clinical and postoperative outcomes.

Methods: Solid-phase sandwich ELISA was used to analyze TSLP and IL-4 levels in mucus (n = 47), plasma (n = 17), polyp (n = 30), inferior (n = 25), and middle (n = 26) turbinate tissue collected during functional endoscopic sinus surgery (FESS) in CRSwNP patients (n = 76) and controls (n = 11).

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  • - The study focused on KPC-Kp bloodstream infections, which are deadly, and aimed to understand how these bacteria resist a key defense mechanism in our blood, called complement.
  • - Researchers tested various KPC-Kp isolates from patients, discovering that 27% of them resisted killing by human serum; a specific gene mutation (wcaJ) linked to capsule production contributed to this resistance.
  • - This mutation resulted in less capsule presence, paradoxically increasing the bacteria's ability to bind complement proteins while also improving their survival against immune responses, potentially allowing them to thrive in the bloodstream without being overly virulent in tissues.
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  • *Researchers found that 27% of KPC-Kp isolates showed increased resistance to human serum, linked to a mutation that reduces capsule content and helps the bacteria evade immune responses.
  • *The mutation allows KPC-Kp to survive better in the bloodstream while being less virulent in tissues, highlighting a complex interaction that aids the bacteria's persistence in the host.
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  • Elevated levels of IL-5, IL-13, IL-33, and CCL2 are linked to lower scores on the University of Pennsylvania Smell Identification Test (UPSIT) in patients with Chronic Rhinosinusitis (CRS) and Aspirin-Exacerbated Respiratory Disease (AERD).
  • Higher levels of IL-5, IL-13, TNF-α, CCL2, and CXCL-8 are associated with increased scores on the Sino-Nasal Outcome Test (SNOT-22) in the same patient populations.
  • These findings suggest a complex relationship between inflammatory markers and the severity of nasal symptoms and smell function in CRS and AERD patients.
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Purpose: Neoadjuvant targeted therapy provides a brief, preoperative window of opportunity that can be exploited to individualize cancer care based on treatment response. We investigated whether response to neoadjuvant therapy during the preoperative window confers survival benefit in patients with operable head and neck squamous cell carcinoma (HNSCC).

Patients And Methods: A pooled analysis of treatment-naïve patients with operable HNSCC enrolled in one of three clinical trials from 2009 to 2020 (NCT00779389, NCT01218048, NCT02473731).

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Background: Fractional exhaled nitric oxide (FeNO) is a cost-effective, noninvasive point-of-care test that has proven valuable in identifying patients with lower airway inflammation and predicting the likelihood of responsiveness to inhaled corticosteroid therapy in asthma. The utility of FeNO in upper airway disease, specifically in CRS, remains to be determined.

Objective: The goal of this study was to test whether FeNO could serve as a noninvasive marker of sinonasal mucosal inflammation in CRS patients.

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  • - SARS-CoV-2 viral RNA (vRNA) was found in the blood of COVID-19 patients, with detection rates varying significantly across different patient groups: 100% in ICU patients, around 52.6% for non-ICU hospitalized, and only 11.1% in outpatients.
  • - Higher levels of vRNA in the blood were linked to worse health outcomes, such as higher WHO scores at admission and increased mortality risk, particularly with levels above 6000 copies/mL.
  • - The presence of virus particles in plasma confirms that the detected vRNA is partly due to viremia, and while it correlates with disease severity and some inflammatory markers, it does not correlate with neutralizing antibody
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Interleukin-36γ (IL-36γ), a member of the IL-1 cytokine superfamily, amplifies lung inflammation and impairs host defense during acute pulmonary infection. To be fully active, IL-36γ is cleaved at its N-terminal region by proteases such as neutrophil elastase (NE) and cathepsin S (CatS). However, it remains unclear whether limiting extracellular proteolysis restrains the inflammatory cascade triggered by IL-36γ during infection.

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  • Macrophages play a crucial role in managing heme metabolism and increase in number during the breakdown of damaged red blood cells (RBCs) in the liver, which is linked to their immune function.
  • The study reveals that an increase in RBC disposal by macrophages during a pulmonary infection with Klebsiella pneumoniae leads to an immunosuppressive state, resulting in increased bacterial growth outside the lungs and poorer survival rates in infected mice.
  • This immunosuppression is related to a decrease in the STAT1 pathway and interferon responses, primarily influenced by the porphyrin component of heme, rather than by the iron it contains, indicating a complex relationship between heme metabolism and immune response during severe infections.
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Complement is crucial for host defense but may also drive dysregulated inflammation. There is limited understanding of alternative complement function, which can amplify all complement activity, during critical illness. We examined the function and key components of the alternative complement pathway in a series of critically ill patients and in a mouse pneumonia model.

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Irreproducibility of preclinical biomedical research has gained recent attention. It is suggested that requiring authors to complete a checklist at the time of manuscript submission would improve the quality and transparency of scientific reporting, and ultimately enhance reproducibility. Whether a checklist enhances quality and transparency in reporting preclinical animal studies, however, has not been empirically studied.

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Klebsiella pneumoniae remains an important cause of intrapulmonary infection and invasive disease worldwide. K. pneumoniae can evade serum killing and phagocytosis primarily through the expression of a polysaccharide capsule, but its pathogenicity is also influenced by host factors.

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