Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human leukocyte interferon, HuIFN-alpha (LE), has been tested in combination with radiotherapy and chemotherapy for previously untreated small cell lung cancer. Nine patients with limited disease received high-dose IFN followed by a low-dose regimen; and six patients had a low-dose regimen from the beginning. The high dosage of IFN consisted of 800 X 10(6) IU given as a continuous intravenous infusion for 5 days, followed by 6 X 10(6) IU i.m. three times weekly. If the first site of disease progression was local or in a central nervous system location, radiotherapy (55 Gy/20 F/7 weeks locally and/or 30 Gy/10 F/2 weeks whole brain) was applied and IFN was continued. Chemotherapy was administered only if there was disease dissemination outside the chest. Three patients achieved minor response for as long as 20, 25, and 42 weeks, respectively, with IFN alone. Three of five complete responders to IFN-radiotherapy died 18, 33, and 41 weeks from the start of IFN treatment without chemotherapy. Autopsy did not reveal macroscopic or microscopic tumor at any site, but there was severe radiation pneumonitis. Four of nine patients were administered chemotherapy subsequent to IFN-radiotherapy because of disease dissemination. The median length of survival of the entire group was 41 weeks. On the low-dose regimen, one patient achieved partial response with IFN alone (duration, 12 weeks); of five evaluable patients three achieved complete remission and two partial remission to IFN-radiotherapy, and one of the three complete responders to IFN-radiotherapy died of severe radiation pneumonitis at 21 weeks from the start of IFN treatment. No tumor was detected at autopsy. The study is in progress. Average survival at present is 33 weeks. The results derived from both our studies suggest a growth-delaying effect of HuIFN-alpha (Le) on small cell lung cancer. They also suggest potentiation of radiation by HuIFN-alpha (Le). Memory and psychomotor dysfunction, fatigue, and anorexia were dose limiting with both short-duration, high-dose and long-duration, low-dose IFN therapy. We feel that IFN, as part of a combined multimodality treatment of small cell lung cancer, may play a role by delaying metastatic dissemination.
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PMID:Human leukocyte interferon as part of a combined treatment for previously untreated small cell lung cancer. 298 40

Cryptococcus neoformans and Cryptococcus gattii are closely related pathogenic fungi that cause pneumonia and meningitis in both immunocompromised and immunocompetent hosts and are a significant global infectious disease risk. Both species are found in the environment and are acquired via inhalation, leading to an initial pulmonary infection. The infectious propagule is unknown but is hypothesized to be small desiccated yeast cells or spores produced by sexual reproduction (opposite- or same-sex mating). Here we characterize the morphology, germination properties, and virulence of spores. A comparative morphological analysis of hyphae and spores produced by opposite-sex mating, same-sex mating, and self-fertile diploid strains was conducted by scanning electron microscopy, yielding insight into hyphal/basidial morphology and spore size, structure, and surface properties. Spores isolated by microdissection were found to readily germinate even on water agarose medium. Thus, nutritional signals do not appear to be required to stimulate spore germination, and as-yet-unknown environmental factors may normally constrain germination in nature. As few as 500 CFU of a spore-enriched infectious inoculum (approximately 95% spores) of serotype A C. neoformans var. grubii were fully virulent (100% lethal infection) in both a murine inhalation virulence model and the invertebrate model host Galleria mellonella. In contrast to a previous report on C. neoformans var. neoformans, spores of C. neoformans var. grubii were not more infectious than yeast cells. Molecular analysis of isolates recovered from tissues of infected mice (lung, spleen, and brain) provides evidence for infection and dissemination by recombinant spore products. These studies provide a detailed morphological and physiological analysis of the spore and document that spores can serve as infectious propagules.
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PMID:Spores as infectious propagules of Cryptococcus neoformans. 1962 Mar 39

Most patients infected with highly pathogenic avian influenza A/H5N1 virus develop severe pneumonia resulting in acute respiratory distress syndrome, with extrarespiratory disease as an uncommon complication. Intranasal inoculation of ferrets with influenza A/H5N1 virus causes lesions in both the respiratory tract and extrarespiratory organs (primarily brain). However, the route of spread to extrarespiratory organs and the relative contribution of extrarespiratory disease to pathogenicity are largely unknown. In the present study, we characterized lesions in the respiratory tract and central nervous system (CNS) of ferrets (n = 8) inoculated intranasally with influenza virus A/Indonesia/5/2005 (H5N1). By 7 days after inoculation, only 3 of 8 ferrets had a mild or moderate bronchointerstitial pneumonia. In contrast, all 8 ferrets had moderate or severe CNS lesions, characterized by meningoencephalitis, choroiditis, and ependymitis, and centered on tissues adjoining the cerebrospinal fluid. These findings indicate that influenza A/H5N1 virus spread directly from nasal cavity to brain, and that CNS lesions contributed more than pulmonary lesions to the pathogenicity of influenza A/H5N1 virus infection in ferrets. In comparison, intratracheal inoculation of ferrets with the same virus reproducibly caused severe bronchointerstitial pneumonia. The method of virus inoculation requires careful consideration in the design of ferret experiments as a model for influenza A/H5N1 in humans.
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PMID:Pathogenesis of Influenza A/H5N1 virus infection in ferrets differs between intranasal and intratracheal routes of inoculation. 2164 Sep 72

The aim of this study was to assess the role of the acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) as biomarkers of inflammation and tissue injury on rats experimentally infected by Cryptococcus neoformans. For this purpose, 20 male rats were divided into two groups: 10 animals representing the uninfected control group (Group A) and 10 C. neoformans var. grubii infected animals (Group B). Blood and brain samples were collected on days 10 (A10 and B10), and 30 (A30 and B30) post-infection (PI) for hematological analyses; AChE (in lymphocytes and brain) and seric BChE activity; interleukins (IL-1, IL-6, and IL-10); nitrite/nitrate (NOx) levels; and markers of protein oxidation (AOPP) and lipid peroxidation (TBARS). As a result, when animals of Group A were compared to animals of Group B, it was observed leukocytosis (P<0.05) on day 10 PI; AChE activity increase (P<0.05) in lymphocytes (day 30 PI) and in brain (days 10 and 30 PI); BChE activity decrease (P<0.05) on day 10 PI; IL-1 and IL-6 increase (P<0.01) in both periods, while IL-10 had reduced levels (P<0.01) in the same periods; NOx levels increased (P<0.05) significantly on days 10 and 30 PI, while AOPP and TBARS levels increased significantly on day 30 PI; as well as pneumonia on infected rats. Therefore, based on the results obtained, it was possible to conclude that AChE and BChE behavior lead to a proinflammatory reaction evidenced by the enhancement of IL-1, IL-6, and NOx throughout the experiment associated with reduction on IL-10 levels, and cellular damage.
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PMID:Cholinesterase of rats experimentally infected by Cryptococcus neoformans: Relationship between inflammatory response and pathological findings. 2637 50