Heat-killed pathogenic Leptospira interrogans serovar rachmati induced the production of gamma interferon (IFN-γ) and the IFN-γ-inducing cytokines interleukin-12p40 (IL-12p40) and tumor necrosis factor alpha in human whole blood in vitro. The production of IFN-γ was largely dependent on IL-12. These data establish that pathogenic leptospires can stimulate the production of type I cytokines involved in cellular immunity
In a study on the dose-response relationship for longwave UVA (UVA1; 340-400 nm) carcinogenesis in hairless mice scratch marks appeared after months of daily exposure as an unwanted side effect. Tumor induction in the highest of the 4 tested dose groups (receiving a daily dose of 430 kJ/m2 of 365-nm radiation) could not be determined because extensive scarification occurred prior to the development of any tumors. The induction of scratch marks could be scored and quantified in all 4 dose groups tested. The UVA1 dose-dependencies for the induction of tumors and scratch marks were compared. We found that the induction of scratch marks depended mainly on the cumulative UVA1 exposure, whereas tumor induction showed a lesser dose-dependency. An attempt was made to prevent the apparent pruritogenic effect of UVA1 irradiation and to understand its mechanism. The influence of ketanserin, a serotonin/histamine antagonist, on the UVA1 induction of scratch marks was tested in groups of 8 mice daily irradiated with 430 kJ/m2. No difference was found between treated and untreated animals. Histological examination of skin biopsies from irradiated mice from the 430-kJ/m2 dose group from the UVA1 carcinogenic experiment, showed no changes in numbers of mast cells or other inflammatory features when compared to skin biopsies from unirradiated control mice. This indicated that UVA1-induced scratching is not mediated through mast cell release of serotonin and/or histamine. An adequate therapeutic treatment which can prevent UVA1-induced scratching would enable us to test tumor induction with UVA1 over a larger dose range, and may provide additional insight in how this radiation damages the skin. It remains conjectural whether there exists an analogous UVA-induced pruritus in human skin.
An 82-year-old woman presented with a palpable mass in the right supraclavicular fossa. Her medical history included coronary artery disease, for which she underwent percutaneous transluminal coronary angioplasty; mild aortic valve stenosis, and a pacemaker to treat a third-degree atrioventricular block. Nine years before this clinical presentation, she was diagnosed with a pT4NoMo (limited disease) stage small-cell lung cancer (SCLC) of the left upper lobe. She was treated with five cycles of cyclophosphamide, doxorubicin, and etoposide containing chemotherapy every 3 weeks, which resulted in a complete response followed by prophylactic cranial irradiation. She had a smoking history of 30 pack years but had stopped smoking 9 years earlier. She had an Eastern Cooperative Oncology Group performance score of 1 with normal vital signs and, apart from the palpable mass, no abnormalities on physical examination. Laboratory investigations revealed normal blood cell counts, renal, and liver function. A computed tomography scan of the thorax showed a solid lobulated leasion in the right upper lobe extending in the right supraclavicular fossa and mediastinal lymph node enlargement. Both this mass and the right upper lobelesion were fluorodeoxyglucose avid on positron emission tomography-computed tomography scanning as was a small mass adjacent to the right adrenal gland. A biopsy was taken from
High energy trauma may cause injury to tracheobronchial structures. This is sometimes difficult to diagnose immediately. Pneumomediastinum and (bilateral) pneumothorax seen on a CT-scan of the thorax may suggest possible damage to central airways. Emergency bronchoscopy should be performed to detect and locate a possible tracheobronchial injury.
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