Integrating Care: The Primary Care Provider’s Role in Age-Related Macular Degeneration in Eastern Maine

Objectives: To assess general patient knowledge of age-related macular degeneration (AMD), including risk factors, early signs, treatment options, and low-vision resources. We also aimed to assess primary care provider practice patterns including early detection, timely referral to ophthalmology, and management after diagnosis of AMD. Methods: A 20-point patient questionnaire was distributed to all adult patients at check-in by front office staff at the Center for Family Medicine office in Bangor, ME. Additionally, a looping waiting room slideshow and informational exam room flyer were created for patient education. A 10-point online questionnaire was distributed to residents and faculty at the Center for Family Medicine and three other local primary care offices. A care management summary document was distributed to residents and faculty at each practice. Results: Our sample included 46 adult patients and 23 primary care providers. 18% of patients reported adequate or expert knowledge of early signs and symptoms; 50% reported poor to no knowledge. Similarly, 18% of patients reported adequate knowledge of risk factors; 50% reported poor to no knowledge. 64% of patients did not know what AMD was, but 74% wish they knew more about the disease. Patients with AMD in one or both eyes, or who have family members with AMD, were more likely to be knowledgeable of signs, symptoms and risk factors. 70% of providers routinely ask about vision at Well-visits. However, 43% of providers somewhat or completely disagree that they can comfortably perform a fundus exam. 52% of providers somewhat or completely disagree that they can comfortably perform and interpret the Amsler grid test. 39% of providers wish they knew more about the risk factors for AMD, while 34% considered themselves to have adequate or expert knowledge of the risk factors. 43% of providers wish they knew more of early signs and symptoms of AMD, while 53% considered themselves adequate or expert. Conclusions and Recommendations: Our study suggests that knowledge of AMD risk factors, signs and symptoms are lacking in the general adult population. However, the vast majority of patients desire to know more about the disease. While the majority of primary care providers inquire about vision at well-visits, the majority of providers felt that their ability to perform funduscopic exams and Amsler grid testing were inadequate. Additionally, the majority of providers expressed inadequate knowledge of risk factors, early signs, and referral guidelines; subsequently, an even higher percentage or providers expressed a desire to know more. Furthermore, most providers lacked knowledge of low-vision behavioral modifications and community resources to support patients with existing AMD. This demonstrates the value and need for additional AMD education for primary care providers and the general patient population.https://scholarworks.uvm.edu/fmclerk/1163/thumbnail.jp

Vermonters’ Opinions on Low-Dose CT Lung Cancer Screening

Introduction: Lung cancer is the number one cause of cancer death among men and women in Vermont and the United States. Smoking increases the risk of lung cancer—nearly 90% of lung cancer is due to smoking. Frequently, lung cancers do not present clinically until they are advanced stage and therefore prognosis is poor. However, if detected early lung cancers are more operable and patients have better outcomes. In December 2013 the US Preventive Services Task Force released new guidelines for lung cancer screening among current and former smokers ages 55 to 80. It is recommended that current and former (within 15 years of quitting) smokers of 30 pack years receive an annual low-dose CT scan. The objective of this project was to assess the level of knowledge and attitudes towards lung cancer screening with low-dose CT scanning among Vermonters in the Burlington area.https://scholarworks.uvm.edu/comphp_gallery/1205/thumbnail.jp

of the Boston Keratopros-thesis

Purpose: We tested the feasibility of using titanium to enhance adhesion of the Boston Keratoprosthesis (B-KPro), ultimately to decrease the risk of implant-associated complications. Methods: Cylindrical rods were made of poly(methyl methacrylate) (PMMA), PMMA coated with titanium dioxide (TiO 2 ) over a layer of polydopamine (PMMA TiO2 ), smooth (Ti) and sandblasted (Ti SB ) titanium, and titanium treated with oxygen plasma (Ti ox and Ti SBox ). Topography and surface chemistry were analyzed by scanning electron microscopy (SEM), atomic force microscopy (AFM), and X-ray photoelectron spectroscopy (XPS). Adhesion force between rods and porcine corneas was measured ex vivo. Titanium sleeves, smooth and sandblasted, were inserted around the stem of the B-KPro and implanted in rabbits. Tissue adhesion to the stem was assessed and compared to an unmodified B-Kpro after 1 month. Results: X-ray photoelectron spectroscopy demonstrated successful deposition of TiO 2 on polydopamine-coated PMMA. Oxygen plasma treatment did not change the XPS spectra of titanium rods (Ti and Ti SB ), although it increased their hydrophilicity. The materials did not show cell toxicity. After 14 days of incubation, PMMA TiO2 , smooth titanium treated with oxygen plasma (Ti ox ), and sandblasted titanium rods (Ti SB , Ti SBox ) showed significantly higher adhesion forces than PMMA ex vivo. In vivo

Multiple duties for spindle assembly checkpoint kinases in meiosis

Cell division in mitosis and meiosis is governed by evolutionary highly conserved protein kinases and phosphatases, controlling the timely execution of key events such as nuclear envelope breakdown, spindle assembly, chromosome attachment to the spindle and chromosome segregation, and cell cycle exit. In mitosis, the spindle assembly checkpoint (SAC) controls the proper attachment to and alignment of chromosomes on the spindle. The SAC detects errors and induces a cell cycle arrest in metaphase, preventing chromatid separation. Once all chromosomes are properly attached, the SAC-dependent arrest is relieved and chromatids separate evenly into daughter cells. The signaling cascade leading to checkpoint arrest depends on several protein kinases that are conserved from yeast to man. In meiosis, haploid cells containing new genetic combinations are generated from a diploid cell through two specialized cell divisions. Though apparently less robust, SAC control also exists in meiosis. Recently, it has emerged that SAC kinases have additional roles in executing accurate chromosome segregation during the meiotic divisions. Here, we summarize the main differences between mitotic and meiotic cell divisions, and explain why meiotic divisions pose special challenges for correct chromosome segregation. The less-known meiotic roles of the SAC kinases are described, with a focus on two model systems: yeast and mouse oocytes. The meiotic roles of the canonical checkpoint kinases Bub1, Mps1, the pseudokinase BubR1 (Mad3), and Aurora B and C (Ipl1) will be discussed. Insights into the molecular signaling pathways that bring about the special chromosome segregation pattern during meiosis will help us understand why human oocytes are so frequently aneuploid

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival

All in the Family

A previously healthy 2-year-old male presented to neuro-ophthalmology clinic for a head turn that started 1.5 months ago and his left eye began turning in over the last 2 weeks

All in the Family

A previously healthy 2-year-old male presented to neuro-ophthalmology clinic for a head turn that started 1.5 months ago and his left eye began turning in over the last 2 weeks

All in the Family

A previously healthy 2-year-old male presented to neuro-ophthalmology clinic for a head turn that started 1.5 months ago; and his left eye began turning in over the last 2 weeks. He had no recent infections, vaccinations, or illnesses. With the birth; of his new baby sister 6 weeks prior the family said they attributed the head turn to a new behavior from stress of a new; sibling. He had no headache or weakness noticed in the face or extremities and no drooling or dysphagia. He had a large; head that was consistently tracking on his own growth curve and followed closely by his pediatrician, who was his paternal; grandfather. Family history was notable for a maternal grandfather with multiple sclerosis and mother with history of optic; neuritis 10 years ago without recurrence. His maternal great grandmother had strabismus and his paternal great uncle had; strabismus requiring surgery. There is otherwise no family history of developmental delay, seizures or other neurologic; disorders. The exam showed a left abduction deficit with an esotropia of 55 prism diopters in primary gaze, 25 prism; diopters in right gaze, and increasing to >55 in left gaze. The anterior segments of both eyes were normal. There was very; subtle blurring of the optic disc margin in the left eye on quick view due to cooperation and the left optic nerve could not; be viewed due to the large esotropia. An urgent brain MRI with and without contrast was ordered and he was instructed to; begin patching the right eye due to amblyopia risk.Non