Adiaspiromicose humana. Relato de um caso tratado com cetoconazol

É descrito um caso de adiaspiromicose humana, da forma pulmonar disseminada, no qual se empregou o cetoconazol. O paciente, oriundo de Goianésia, GO, referia tosse produtiva, dispnéia e emagrecimento. Doente há dois meses, já fizera uso do esquema tríplice tuberculostático, devido a um radiograma do tórax ter acusado lesões sugestivas de tuberculose miliar. Esse tratamento não surtiu o efeito esperado, pelo que foi ele submetido a uma biópsia pulmonar a céu aberto. A medida permitiu o reconhecimento da natureza fúngica da doença. Passou-se, então, ao emprego do cetoconazol, quando o processo já completara três meses de evolução. Dois meses depois, foi o paciente novamente visto, para controle do tratamento: todas as manifestações respiratórias haviam cessado e um novo radiograma mostrou regressão completa das alterações pulmonares. Apesar disso, é discutida a eficácia do cetoconazol contra C. parvum var crescens, tendo-se em conta o fato de o microrganismo não se reproduzir no hospedeiro.<br>A case of human disseminated pulmonary adiaspiromycosis is reported. The patient, from Goianesia, GO, was admitted to the Brasilia University Hospital, in November 1992, with wet cough, dyspnea and weight loss3/4manifestations that had appeared two months before. Prior to admission, he had been treated for a suspected miliary tuberculosis, because a chest roentgenogram had shown a diffuse reticulonodular infiltrate in both lungs. This therapy brought no improvement to the patient status. An open chest biopsy was then performed, and the microscopic examination of the lung tissue revealed the fungal nature of the disease. Ketoconazole, 400mg/day, was started and the patient discharged from the hospital. He was seen again two months later: the respiratory manifestations had disappeared and a new chest roentgenogram showed complete resolution of the pulmonary lesions. The usefulness of ketoconazole is, however, questioned, since, as there is no multiplication of the fungus in the host organism3/4adiaspiromycosis. is believed to be, usually, a self-healing disease -, the efficacy of this imidazole derivative against the agent in animal tissues remains to be confirmed

Ablation of organic polymers by 46.9-nm-laser radiation

Includes bibliographical references (pages 034109-3).We report results of the exposure of poly(tetrafluoroethylene) -(PTFE), poly(methyl methacrylate)-(PMMA), and polyimide -(PI) to intense 46.9-nm-laser pulses of 1.2-ns-duration at fluences ranging from ~0.1 to ~10 J/cm2. The ablation rates were found to be similar for all three materials, ~80-90 nm/pulse at 1 J/cm2. The results suggest that the ablation of organic polymers induced by intense extreme ultraviolet laser radiation differs from that corresponding to irradiation with longer wavelengths

XUV-laser induced ablation of PMMA with nano-, pico-, and femtosecond pulses

Includes bibliographical references (page 932).For conventional wavelength (UV-vis-IR) lasers delivering radiation energy to the surface of materials, ablation thresholds, etch (ablation) rates, and the quality of ablated structures often differ dramatically between short (typically nanosecond) and ultrashort (typically femtosecond) pulses. Various very short-wavelength (λ < 100 nm) lasers, emitting pulses with durations ranging from ∼10 fs to ∼1 ns, have recently been placed into routine operation. This has facilitated the investigation of how ablation characteristics depend on the pulse duration in the XUV spectral region. Ablation of poly(methyl methacrylate) (PMMA) induced by three particular short-wavelength lasers emitting pulses of various durations, is reported in this contribution

Short-wavelength ablation of molecular solids: pulse duration and wavelength effects

As liver fibrosis is the result of persistent necroinflammation in the liver, pro-inflammatory cytokines secreted in response to cell injury have a central role in the pathogenesis of liver fibrosis. We aimed to investigate the association of cytokine gene polymorphism and liver fibrosis among Chinese patients with chronic hepatitis B.Polymorphisms at interleukin-10 (IL-10-627, -1117), interleukin-1-beta (IL-1beta-511, -31, -3964), interleukin-1 receptor antagonist (IL-1RN), and tumor necrosis factor-alpha (TNF-alpha-308, -238) among Chinese chronic hepatitis B patients were determined. Severe liver fibrosis was defined as Ishak fibrosis score = 4 (of 6).Fifty-nine of 273 (22%) patients had severe fibrosis. The distribution of genotypes for IL-10-627 was CC (11%), CA (41%), and AA (48%). The CC genotype at IL-10-627 was protective against severe fibrosis (odds ratio (OR) 0.11; 95% CI 0.014-0.82; P = 0.032). After adjusted for baseline variables, the adjusted OR of CC genotypes at IL-10-627 for severe fibrosis was 0.063 (95% CI 0.06-0.64; P = 0.063). Other gene polymorphisms at IL-1beta, IL-1RN, TNF-alpha, and IL-10 had no significant association with severe fibrosis. Weak linkage disequilibrium was observed between IL-10-627 and IL-10-1117 with linkage disequilibrium coefficient of 0.12 (P < 0.001). The distribution of haplotypes of IL-10-1117 and IL-10-627 was A-A (69%), A-C (26%), and G-C (5%). High and intermediate IL-10 production (A-C and G-C) haplotypes were protective against severe fibrosis (OR 0.62; 95% CI 0.39-0.99; P = 0.046).High production genotype and haplotypes of IL-10 were associated with less severe liver fibrosis in chronic hepatitis B in Chinese

Short-wavelength ablation of molecular solids: pulse duration and wavelength effects

As liver fibrosis is the result of persistent necroinflammation in the liver, pro-inflammatory cytokines secreted in response to cell injury have a central role in the pathogenesis of liver fibrosis. We aimed to investigate the association of cytokine gene polymorphism and liver fibrosis among Chinese patients with chronic hepatitis B.Polymorphisms at interleukin-10 (IL-10-627, -1117), interleukin-1-beta (IL-1beta-511, -31, -3964), interleukin-1 receptor antagonist (IL-1RN), and tumor necrosis factor-alpha (TNF-alpha-308, -238) among Chinese chronic hepatitis B patients were determined. Severe liver fibrosis was defined as Ishak fibrosis score = 4 (of 6).Fifty-nine of 273 (22%) patients had severe fibrosis. The distribution of genotypes for IL-10-627 was CC (11%), CA (41%), and AA (48%). The CC genotype at IL-10-627 was protective against severe fibrosis (odds ratio (OR) 0.11; 95% CI 0.014-0.82; P = 0.032). After adjusted for baseline variables, the adjusted OR of CC genotypes at IL-10-627 for severe fibrosis was 0.063 (95% CI 0.06-0.64; P = 0.063). Other gene polymorphisms at IL-1beta, IL-1RN, TNF-alpha, and IL-10 had no significant association with severe fibrosis. Weak linkage disequilibrium was observed between IL-10-627 and IL-10-1117 with linkage disequilibrium coefficient of 0.12 (P < 0.001). The distribution of haplotypes of IL-10-1117 and IL-10-627 was A-A (69%), A-C (26%), and G-C (5%). High and intermediate IL-10 production (A-C and G-C) haplotypes were protective against severe fibrosis (OR 0.62; 95% CI 0.39-0.99; P = 0.046).High production genotype and haplotypes of IL-10 were associated with less severe liver fibrosis in chronic hepatitis B in Chinese