Last data update: Sep 23, 2024. (Total: 47723 publications since 2009)
Records 1-5 (of 5 Records) |
Query Trace: McLean CA [original query] |
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COVID-19 Stats: COVID-19 Incidence,* by Age Group
Duca LM , Xu L , Price SF , McLean CA . MMWR Morb Mortal Wkly Rep 2021 69 (5152) 1664 During late March–late May, COVID-19 incidence was highest among adults aged ≥80 years, with a peak in incidence in the week beginning April 12. In June, incidence increased in all age groups, with the most rapid rate of increase and highest overall incidence among young adults aged 18–24 years; the rate in this group continues to be the highest among all age groups. Incidence steadily increased among children and adolescents (aged 0–17 years). The incidence in high school–aged persons (aged 14–17 years) was markedly higher than that in younger children by early July, then decreased before increasing in September. During late September–early October, weekly incidence decreased among young adults aged 18–24 years only, then continued to steadily increase among all age groups through November 14. |
COVID-19 Stats: COVID-19 Incidence,* by Urban-Rural Classification
Duca LM , Coyle J , McCabe C , McLean CA . MMWR Morb Mortal Wkly Rep 2020 69 (46) 1753 Early in the pandemic, from mid-March to mid-May, COVID-19 incidence was highest among residents of large central and large fringe metropolitan areas. Beginning in mid-April, incidence in large metropolitan (central and fringe) areas declined and then increased similarly among all urban-rural areas. In September 2020, COVID-19 incidence sharply increased, and it remains highest among residents of medium/small metropolitan areas and micropolitan/noncore areas, indicating increased spread into rural communities. In October, weekly incidence was increasing steadily among all urban-rural areas. |
Iatrogenic Creutzfeldt-Jakob disease with amyloid-beta pathology: an international study
Cali I , Cohen ML , Hasmall yi Ukrainiank S , Parchi P , Giaccone G , Collins SJ , Kofskey D , Wang H , McLean CA , Brandel JP , Privat N , Sazdovitch V , Duyckaerts C , Kitamoto T , Belay ED , Maddox RA , Tagliavini F , Pocchiari M , Leschek E , Appleby BS , Safar JG , Schonberger LB , Gambetti P . Acta Neuropathol Commun 2018 6 (1) 5 The presence of pathology related to the deposition of amyloid-beta (Abeta) has been recently reported in iatrogenic Creutzfeldt-Jakob disease (iCJD) acquired from inoculation of growth hormone (GH) extracted from human cadaveric pituitary gland or use of cadaveric dura mater (DM) grafts.To investigate this phenomenon further, a cohort of 27 iCJD cases - 21 with adequate number of histopathological sections - originating from Australia, France, Italy, and the Unites States, were examined by immunohistochemistry, amyloid staining, and Western blot analysis of the scrapie prion protein (PrP(Sc)), and compared with age-group matched cases of sporadic CJD (sCJD), Alzheimer disease (AD) or free of neurodegenerative diseases (non-ND).Cases of iCJD and sCJD shared similar profiles of proteinase K-resistant PrP(Sc) with the exception of iCJD harboring the "MMi" phenotype. Cerebral amyloid angiopathy (CAA), either associated with, or free of, Thioflavin S-positive amyloid core plaques (CP), was observed in 52% of 21 cases of iCJD, which comprised 37.5% and 61.5% of the cases of GH- and DM-iCJD, respectively. If only cases younger than 54 years were considered, Abeta pathology affected 41%, 2% and 0% of iCJD, sCJD and non-ND, respectively. Despite the patients' younger age CAA was more severe in iCJD than sCJD, while Abeta diffuse plaques, in absence of Abeta CP, populated one third of sCJD. Abeta pathology was by far most severe in AD. Tau pathology was scanty in iCJD and sCJD.In conclusion, (i) despite the divergences in the use of cadaveric GH and DM products, our cases combined with previous studies showed remarkably similar iCJD and Abeta phenotypes indicating that the occurrence of Abeta pathology in iCJD is a widespread phenomenon, (ii) CAA emerges as the hallmark of the Abeta phenotype in iCJD since it is observed in nearly 90% of all iCJD with Abeta pathology reported to date including ours, and it is shared by GH- and DM-iCJD, (iii) although the contributions to Abeta pathology of other factors, including GH deficiency, cannot be discounted, our findings increase the mounting evidence that this pathology is acquired by a mechanism resembling that of prion diseases. |
Carrageenan-based gel retains limited anti-HIV-1 activity 8-24 hours after vaginal application by HIV-infected Thai women enrolled in a phase I safety trial
Haaland RE , Chaowanachan T , Evans-Strickfaden T , van de Wijgert JH , Kilmarx PH , McLean CA , Hart CE . J Acquir Immune Defic Syndr 2012 61 (5) e71-3 There is a need to improve in vitro testing to evaluate topical microbicide candidates that prevent acquisition of HIV. Many vaginal microbicides with different anti-HIV activities have undergone preclinical testing and a few of those have been selected for clinical safety and efficacy testing. Clinical efficacy trials of vaginal microbicide gels have yielded mixed results. Initial nonspecific entry inhibitors were shown to be ineffective in clinical efficacy trials,1–4 whereas more recent testing of microbicide gels containing the nucleoside reverse transcriptase inhibitor, tenofovir, has shown some level of protection in 1 of 2 clinical trials.5,6 Yet, nearly all preclinical testing outcomes predicted that products should significantly reduce sexual acquisition of HIV when used appropriately in a clinical trial. However, a recent report using ex vivo testing of the microbicide Pro2000 demonstrated that this product loses anti-HIV activity after vaginal application and sexual intercourse.7 Changes in anti-HIV activity over time after vaginal application have not been studied for most candidate vaginal microbicides. | We investigated the carrageenan-based vaginal gel Carraguard, an HIV entry inhibitor that failed in a clinical efficacy trial,1 for degradation and loss of anti-infective activity after vaginal application. Cervicovaginal lavages (CVLs) were collected from 16 HIV-infected Thai women participating in a randomized, controlled, 3-treatment (Carraguard, methylcellulose placebo, no product) crossover safety trial.8 Women applied each treatment daily for 7 days after menses. The order of the 3 treatments was randomized. CVLs (5 mL) were collected on the first clinic visit in each treatment cycle before gel application (T0), 15 minutes after gel application (T15min), and on day 7 clinic visit which was 8–24 hours after the final gel application (T8–24hr). Self-reported adherence was 98% overall, and participants reported that vaginal application of the gel was highly acceptable.9 |
HIV genital shedding and safety of Carraguard use by HIV-infected women: a crossover trial in Thailand
McLean CA , van de Wijgert JH , Jones HE , Karon JM , McNicoll JM , Whitehead SJ , Braunstein S , Achalapong J , Chaikummao S , Tappero JW , Markowitz LE , Kilmarx PH . AIDS 2010 24 (5) 717-22 OBJECTIVE: To evaluate the safety, including impact on genital HIV RNA shedding, of Carraguard vaginal gel in HIV-infected women. DESIGN: This is a randomized, controlled, crossover study of Carraguard in HIV-infected women in Thailand. METHODS: Each woman (CD4 cell count 51-500 cells/mul and not on antiretroviral therapy) used each treatment (Carraguard, methylcellulose placebo, and no-product) once daily for 7 days during each 1-month period (3-week wash-out). Women were randomized to one of the six possible treatment sequences. Safety assessments were conducted at baseline (pregel), 15 min postgel, day 7, and day 14, and included HIV RNA measurements in cervicovaginal lavage (CVL) specimens. RESULTS: Sixty women were enrolled, and 99% of scheduled study visits were completed. At baseline, median age (34 years), CD4 lymphocyte count (296 cells/mul), plasma HIV viral load (4.6 log10 copies/ml), CVL HIV viral load (3.1 log10 total copies per CVL), and sexual behaviors were similar among randomization groups. HIV viral load, leukocyte and hemoglobin levels, and epithelial cell counts in CVLs were lower 15 min after application of Carraguard or placebo compared with no product; CVL HIV viral load was still lower at day 7 but returned to baseline by day 14. Carraguard use was not associated with prevalent or incident genital findings or abnormal vaginal flora. CONCLUSION: Carraguard appears to be well tolerated for once-daily vaginal use by HIV-infected women. The observed reduction in CVL HIV viral load in the gel months may be clinically relevant but could have resulted from interference with sample collection by study gels. |
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