15 research outputs found
Chronic Wound Healing: A Review of Current Management and Treatments
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NO reduce cellular damage of reconstituted epidermal tissue infected with MR<i>SA</i>.
<p>(<b>A</b>) NO-np attenuate cellular damage of reconstituted epidermal tissue infected with MR<i>SA</i>. Reconstituted human epidermis control group had no bacteria or nanoparticles, reconstituted human epidermis infected with <i>SA</i>, and reconstituted human epidermis infected with <i>SA</i> and treated with NO-np. Scale bar, 10 µm. (<b>B</b>) Relative LDH activity measured in the tissue culture supernatant by reconstituted human epidermal tissue after 24 h co-culture with <i>SA</i> in the absence or presence of NO-np. Bars are the averages of the results for three measurements, and error bars denote standard deviations. Asterisks denote <i>P</i> value significance (*, <i>P</i><0.05 in comparing the MR<i>SA</i>+NO-np group with the control group; **, <i>P</i><0.001 in comparing the MR<i>SA</i> group with control group; #, <i>P</i><0.01 in comparing the MR<i>SA</i> group with MR<i>SA</i>+NO-np group) calculated by analysis of variance and adjusted by use of the Bonferroni correction.</p
NO-np prevents MR<i>SA</i> collagen degradation in subcutaneous abscesses.
<p>(<b>A</b>) Histological analysis of Balb/c mice untreated MR<i>SA</i>-infected, np-treated MR<i>SA</i>-infected, and MR<i>SA</i>-infected treated with NO-np, day 4. Mice were infected with 10<sup>7</sup> bacterial cells. The blue stain indicates collagen. Scale bar: 25 µm. (<b>B</b>) Quantitative measurement of collagen intensity in 20 representative fields of the same size for untreated MR<i>SA</i>-infected, np-treated MR<i>SA</i>-infected, and MR<i>SA</i>-infected treated with NO-np. Bars are the averages of the results, and error bars denote standard deviations. Asterisks denote <i>P</i> value significance (*, <i>P</i><0.05 in comparing MR<i>SA</i>-infected np and untreated control groups; **, <i>P</i><0.001 in comparing MR<i>SA</i>-infected NO-np and untreated control groups; #, <i>P</i><0.01 in comparing MR<i>SA</i>-infected np and NO-np groups) calculated by analysis of variance and adjusted by use of the Bonferroni correction.</p
NO-np decreases vascularization in the setting of MR<i>SA</i> abscesses.
<p>Histological analysis of untreated, np-treated and NO-np treated MR<i>SA</i>-infected Balb/c mice, day 4. Mice were infected with 10<sup>7</sup> MR<i>SA</i>. The brown staining indicates vascularization. Representative CD34-immunostained sections of the skin lesions are shown with the <i>Insets</i> representing Gram of MR<i>SA</i>. White arrows denote Gram positive cocci. Scale bars: 25 µm.</p
NO-np decreases subcutaneous abscess area in mice.
<p>(<b>A</b>) Abscesses of Balb/c mice untreated MR<i>SA</i>-infected, np-treated MR<i>SA</i>-infected, and MR<i>SA</i>-infected treated with NO-np, day 4. Arrows denote abscesses. <i>Inset</i> shows a representative purulent abscess 4 days after MR<i>SA</i> infection. Scale bar: 5 mm. (<b>B</b>) Abscess area analysis of Balb/c mice subcutaneous lesions. Abscesses were infected with MR<i>SA</i> and untreated or treated in the absence or presence of NO. Each point represents an abscess. Dashed lines are the averages of the results for fourteen measurements, and error bars denote standard deviations. Asterisks denote <i>P</i> value significance (** <i>P</i><0.001) calculated by analysis of variance and adjusted by use of the Bonferroni correction.</p
Cytokine levels in abscesses of mice.
<p><i>n</i> = 7 mice per group.</p>a<p>Value significantly greater than the value for control mice (<i>P</i><0.05).</p>b<p>Value significantly less than the value for control mice (<i>P</i><0.05).</p
NO-np inhibits MR<i>SA</i> growth <i>in vitro</i>.
<p>The effect of NO in MR<i>SA</i> growth kinetics after 24 h co-culture was determined using Bioscreen C analysis. MR<i>SA</i> was grown in the absence or presence of nanoparticles with NO (NO-np) or without NO (np). Each point represents the average of four measurements and error bars denote standard deviations.</p
NO-np killed MR<i>SA</i> in subcutaneous abscesses.
<p>(<b>A</b>) Abscess bacterial burden (CFU; colony forming units) in mice infected subcutaneously with 10<sup>7</sup> MR<i>SA</i> and treated with NO-np is significantly lower than untreated or np-treated mice (<i>n</i> = 20 abscesses per group). Each point represents an abscess. Dashed lines are the averages of the results and error bars denote standard deviations. Asterisks denote <i>P</i> value significance (** <i>P</i><0.001) calculated by analysis of variance and adjusted by use of the Bonferroni correction. (<b>B</b>) Histological analysis of Balb/c mice untreated MR<i>SA</i>-infected, np-treated MR<i>SA</i>-infected, and MR<i>SA</i>-infected treated with NO, day 4. Mice were infected with 10<sup>7</sup> MR<i>SA</i>. Representative H&E-stained sections of the skin lesions are shown with the <i>Insets</i> showing Gram staining of MR<i>SA</i>. Scale bars: 25 µm.</p
Topical clindamycin for acne vulgaris: analysis of gastrointestinal events
Purpose: Topical clindamycin, a lincosamide antibiotic, is commonly combined with benzoyl peroxide or a retinoid for acne vulgaris (AV) treatment. While oral and topical clindamycin carry warnings/contraindications regarding gastrointestinal (GI) adverse events (AEs), real-world incidence of GI AEs with topical clindamycin is unknown. This review provides background information and an overview of safety data of topical clindamycin for treating AV.Materials and Methods: Available safety data from published literature, previously unpublished worldwide pharmacovigilance data, and two retrospective cohort studies were reviewed.Results and Conclusions: According to pharmacovigilance data, the rate of GI adverse drug reactions with topical clindamycin-containing products was 0.000045% (64/141,084,533). Results from two retrospective medical record studies of patients with AV indicated that physicians prescribe topical clindamycin equally to patients with or without inflammatory bowel disease history, and that rates of pseudomembranous colitis in these patients were low. In 8 published pivotal clinical trials of topical clindamycin for AV, GI AEs were reported in 1.4% of participants. Limitations include under/inaccurate reporting of AEs or prescription data and limited generalizability. This review of published case reports, worldwide pharmacovigilance data, retrospective US prescription data, and clinical trials safety data demonstrates that the incidence of colitis in patients exposed to topical clindamycin is extremely low.</p
Mortality, Severe Acute Respiratory Infection, and Influenza-Like Illness Associated with Influenza A(H1N1)pdm09 in Argentina, 2009
<div><h3>Introduction</h3><p>While there is much information about the burden of influenza A(H1N1)pdm09 in North America, little data exist on its burden in South America.</p> <h3>Methods</h3><p>During April to December 2009, we actively searched for persons with severe acute respiratory infection and influenza-like illness (ILI) in three sentinel cities. A proportion of case-patients provided swabs for influenza testing. We estimated the number of case-patients that would have tested positive for influenza by multiplying the number of untested case-patients by the proportion who tested positive. We estimated rates by dividing the estimated number of case-patients by the census population after adjusting for the proportion of case-patients with missing illness onset information and ILI case-patients who visited physicians multiple times for one illness event.</p> <h3>Results</h3><p>We estimated that the influenza A(H1N1)pdm09 mortality rate per 100,000 person-years (py) ranged from 1.5 among persons aged 5–44 years to 5.6 among persons aged ≥65 years. A(H1N1)pdm09 hospitalization rates per 100,000 py ranged between 26.9 among children aged <5 years to 41.8 among persons aged ≥65 years. Influenza A(H1N1)pdm09 ILI rates per 100 py ranged between 1.6 among children aged <5 to 17.1 among persons aged 45–64 years. While 9 (53%) of 17 influenza A(H1N1)pdm09 decedents with available data had obesity and 7 (17%) of 40 had diabetes, less than 4% of surviving influenza A(H1N1)pdm09 case-patients had these pre-existing conditions (p≤0.001).</p> <h3>Conclusion</h3><p>Influenza A(H1N1)pdm09 caused a similar burden of disease in Argentina as in other countries. Such disease burden suggests the potential value of timely influenza vaccinations.</p> </div
