Influenza Vaccination of young children or Antibody Immune Response and Protection after Inactivated Influenza Vaccine in Children – A Literature Review

Influenza virus infection is a major cause of morbidity and mortality in at risk populations. Children, especially under the age of two, are at an increased risk of complications associated with influenza virus infection. Evidence suggests that a single dose of influenza vaccine does not adequately protect children against circulating influenza virus. The Centers for Disease Control and Prevention’s (CDC) Advisory Committee on Immunizations Practices (ACIP) recommends two doses of influenza vaccine, spaced at least four weeks apart, before the beginning of the influenza season for children between the ages of 6 months through 8 years receiving influenza vaccine for the first time. The initial dose is thought to prime the immune system, and the second dose is thought to mount a protective antibody response. We conducted a systematic literature review to summarize current evidence from randomized controlled trials (RCTs) and observational studies that compared immunogenicity and vaccine effectiveness (VE) after one or two doses of influenza vaccine in children to evaluate the evidence basis for the CDC recommendations. The search identified 727 unique articles and 82 were screened in full text for eligibility. A total of 26 studies met inclusion criteria, 16 immunogenicity and 10 VE studies. Overall, the evidence demonstrates increased immunogenicity and VE after two doses of influenz

Patient Guide to Access Quality Health Information Online

A large percentage of patients use online search engines to access health information. However, there is a large amount of health information online that is unregulated and not evidence-based. As a result patients may acquire health information that is incorrect which may negatively affect patient-provider relationships and patient\u27s healthcare. A brochure was created to highlight safe practices for accessing health information online.https://scholarworks.uvm.edu/fmclerk/1492/thumbnail.jp

Transportation Barriers to Healthcare in Adults 65+ in the Greater Burlington Area

Introduction. Missed appointments often lead to poorer health care outcomes for patients and pose a major economic burden on medical centers. Transportation is an obstacle to accessing medical care for elderly patients in Vermont and results in delayed medical appointments. Methods. We surveyed senior citizens in Chittenden county to determine both the type of transportation barriers and medical care missed due to the lack of transpor- tation. An original survey assessing the impact of transportation to health care was distributed in person and through an online platform. Participants were asked to identify the following in the past year: how often transportation was an issue for healthcare, specific barriers to transportation, and which specific health care appointments were missed due to lack of transportation. Ninety-six surveys out of a total of 251 collected were included in the analysis. Respondents were grouped into either having high transportation barriers, n=43, (always, often, sometimes had issues in the past year), or low transportation barriers, n=53, (rarely had issues). Results. The high barriers group reported more missed appointments, with eye appointments being the most frequent, and depended more on other modes of trans- portation. The low barriers group was able to drive themselves to their appointments more often. Conclusion. The results suggest a trend between barriers to transportation and a lack of access to healthcare appointments. Although more than half of the survey respondents indicated that they do not currently experience transportation barriers, many expressed concern about the transportation difficulties they could encounter in the future.https://scholarworks.uvm.edu/comphp_gallery/1263/thumbnail.jp

p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis.

Spatiotemporal activation of RhoA and actomyosin contraction underpins cellular adhesion and division. Loss of cell-cell adhesion and chromosomal instability are cardinal events that drive tumour progression. Here, we show that p120-catenin (p120) not only controls cell-cell adhesion, but also acts as a critical regulator of cytokinesis. We find that p120 regulates actomyosin contractility through concomitant binding to RhoA and the centralspindlin component MKLP1, independent of cadherin association. In anaphase, p120 is enriched at the cleavage furrow where it binds MKLP1 to spatially control RhoA GTPase cycling. Binding of p120 to MKLP1 during cytokinesis depends on the N-terminal coiled-coil domain of p120 isoform 1A. Importantly, clinical data show that loss of p120 expression is a common event in breast cancer that strongly correlates with multinucleation and adverse patient survival. In summary, our study identifies p120 loss as a driver event of chromosomal instability in cancer

Pharmacodynamic evaluation and safety assessment of treatment with antibodies to serum amyloid P component in patients with cardiac amyloidosis: an open-label Phase 2 study and an adjunctive immuno-PET imaging study.

BACKGROUND: In a Phase I study treatment with the serum amyloid P component (SAP) depleter miridesap followed by monoclonal antibody to SAP (dezamizumab) showed removal of amyloid from liver, spleen and kidney in patients with systemic amyloidosis. We report results from a Phase 2 study and concurrent immuno-positron emission tomography (PET) study assessing efficacy, pharmacodynamics, pharmacokinetics, safety and cardiac uptake (of dezamizumab) following the same intervention in patients with cardiac amyloidosis. METHODS: Both were uncontrolled open-label studies. After SAP depletion with miridesap, patients received ≤ 6 monthly doses of dezamizumab in the Phase 2 trial (n = 7), ≤ 2 doses of non-radiolabelled dezamizumab plus [89Zr]Zr-dezamizumab (total mass dose of 80 mg at session 1 and 500 mg at session 2) in the immuno-PET study (n = 2). Primary endpoints of the Phase 2 study were changed from baseline to follow-up (at 8 weeks) in left ventricular mass (LVM) by cardiac magnetic resonance imaging and safety. Primary endpoint of the immuno-PET study was [89Zr]Zr-dezamizumab cardiac uptake assessed via PET. RESULTS: Dezamizumab produced no appreciable or consistent reduction in LVM nor improvement in cardiac function in the Phase 2 study. In the immuno-PET study, measurable cardiac uptake of [89Zr]Zr-dezamizumab, although seen in both patients, was moderate to low. Uptake was notably lower in the patient with higher LVM. Treatment-associated rash with cutaneous small-vessel vasculitis was observed in both studies. Abdominal large-vessel vasculitis after initial dezamizumab dosing (300 mg) occurred in the first patient with immunoglobulin light chain amyloidosis enrolled in the Phase 2 study. Symptom resolution was nearly complete within 24 h of intravenous methylprednisolone and dezamizumab discontinuation; abdominal computed tomography imaging showed vasculitis resolution by 8 weeks. CONCLUSIONS: Unlike previous observations of visceral amyloid reduction, there was no appreciable evidence of amyloid removal in patients with cardiac amyloidosis in this Phase 2 trial, potentially related to limited cardiac uptake of dezamizumab as demonstrated in the immuno-PET study. The benefit-risk assessment for dezamizumab in cardiac amyloidosis was considered unfavourable after the incidence of large-vessel vasculitis and development for this indication was terminated. Trial registration NCT03044353 (2 February 2017) and NCT03417830 (25 January 2018)

Pharmacodynamic evaluation and safety assessment of treatment with antibodies to serum amyloid P component in patients with cardiac amyloidosis: an open-label Phase 2 study and an adjunctive immuno-PET imaging study.

BACKGROUND: In a Phase I study treatment with the serum amyloid P component (SAP) depleter miridesap followed by monoclonal antibody to SAP (dezamizumab) showed removal of amyloid from liver, spleen and kidney in patients with systemic amyloidosis. We report results from a Phase 2 study and concurrent immuno-positron emission tomography (PET) study assessing efficacy, pharmacodynamics, pharmacokinetics, safety and cardiac uptake (of dezamizumab) following the same intervention in patients with cardiac amyloidosis. METHODS: Both were uncontrolled open-label studies. After SAP depletion with miridesap, patients received ≤ 6 monthly doses of dezamizumab in the Phase 2 trial (n = 7), ≤ 2 doses of non-radiolabelled dezamizumab plus [89Zr]Zr-dezamizumab (total mass dose of 80 mg at session 1 and 500 mg at session 2) in the immuno-PET study (n = 2). Primary endpoints of the Phase 2 study were changed from baseline to follow-up (at 8 weeks) in left ventricular mass (LVM) by cardiac magnetic resonance imaging and safety. Primary endpoint of the immuno-PET study was [89Zr]Zr-dezamizumab cardiac uptake assessed via PET. RESULTS: Dezamizumab produced no appreciable or consistent reduction in LVM nor improvement in cardiac function in the Phase 2 study. In the immuno-PET study, measurable cardiac uptake of [89Zr]Zr-dezamizumab, although seen in both patients, was moderate to low. Uptake was notably lower in the patient with higher LVM. Treatment-associated rash with cutaneous small-vessel vasculitis was observed in both studies. Abdominal large-vessel vasculitis after initial dezamizumab dosing (300 mg) occurred in the first patient with immunoglobulin light chain amyloidosis enrolled in the Phase 2 study. Symptom resolution was nearly complete within 24 h of intravenous methylprednisolone and dezamizumab discontinuation; abdominal computed tomography imaging showed vasculitis resolution by 8 weeks. CONCLUSIONS: Unlike previous observations of visceral amyloid reduction, there was no appreciable evidence of amyloid removal in patients with cardiac amyloidosis in this Phase 2 trial, potentially related to limited cardiac uptake of dezamizumab as demonstrated in the immuno-PET study. The benefit-risk assessment for dezamizumab in cardiac amyloidosis was considered unfavourable after the incidence of large-vessel vasculitis and development for this indication was terminated. Trial registration NCT03044353 (2 February 2017) and NCT03417830 (25 January 2018)