Author: Avsic-Zupanc, Tatjana ; Sall, Amadou A. ; Dedushaj, Isuf ; Ozkul, Aykut ; Korukluoglu, Gülay ; Schmaljohn, Connie S. ; El-Sanousi, Ahmed ; Chinikar, Sadegh ; Bouloy, Michelle ; Bino, Silvia ; Neyts, Johan ; Christova, Iva ; Koçak Tufan, Zeliha ; Humolli, Isme ; Weidmann, Manfred ; Paweska, Janusz ; Jansen van Vuren, Petrus ; Uyar, Yavuz ; Elaldi, Nazif ; Niedrig, Matthias ; Zeller, Herve ; Hufert, Frank T. ; Hewson, Roger ; Lyssen, Pieter ; Swanepoel, Robert ; Papa, Anna ; Mirazimi, Ali ; Weber, Friedemann ; Burt, Felicity

In countries from which Crimean-Congo haemorrhagic fever (CCHF) is absent, the causative virus, CCHF virus (CCHFV), is classified as a hazard group 4 agent and handled in containment level (CL)-4. In contrast, most endemic countries out of necessity have had to perform diagnostic tests under biosafety level (BSL)-2 or -3 conditions. In particular, Turkey and several of the Balkan countries have safely processed more than 100 000 samples over many years in BSL-2 laboratories. It is therefore advocated that biosafety requirements for CCHF diagnostic procedures should be revised, to allow the tests required to be performed under enhanced BSL-2 conditions with appropriate biosafety laboratory equipment and personal protective equipment used according to standardized protocols in the countries affected. Downgrading of CCHFV research work from CL-4, BSL-4 to CL-3, BSL-3 should also be considered.

01 Oct 1991·Journal of Clinical InvestigationQ1 · MEDICINE

Role of endothelial-leukocyte adhesion molecule 1 (ELAM-1) in neutrophil-mediated lung injury in rats.

Q1 · MEDICINE

Article

Author: Dame, Michael K. ; Smith, C. Wayne ; Lane, Caryl L. ; Ward, Peter A. ; Anderson, Donald C. ; Varani, James ; Mulligan, Michael S.

Two murine monoclonal antibodies (CL-3 and CL-37, both F(ab')2) to human endothelial-leukocyte adhesion molecule-1 (ELAM-1) were found to react immunohistochemically with rat pulmonary artery endothelial cells that had been pretreated with tumor necrosis factor (TNF alpha). CL-3, but not CL-37, blocked in vitro adherence of neutrophils to TNF alpha-treated endothelial cells and the killing of TNF alpha-treated rat endothelial cells by phorbol ester activated neutrophils. In rats treated systemically with CL-3, there was a 70% reduction in accumulation of neutrophils in glycogen-induced peritoneal exudates. Treatment of animals with CL-37 anti-ELAM-1 did not reduce neutrophil accumulation under the same conditions. When IgG immune complex deposition was induced in dermis and in lungs of rats, treatment with CL-3 anti-ELAM-1 markedly reduced vascular injury as measured by changes in vascular permeability (leakage of 125I-albumin) and hemorrhage (extravasation of 51Cr-red blood cells). The protective effects of CL-3 anti-ELAM-1 were related to greatly diminished recruitment of neutrophils (as assessed morphologically, by tissue extraction of myeloperoxidase, and by retrieval, via bronchoalveolar lavage, of neutrophils from lung). CL-37 had no protective effects in vivo after deposition of immune complexes in lung. Using either CL-3 or CL-37 anti-ELAM-1, immunohistochemical analysis of lungs undergoing IgG immune complex-induced injury revealed a striking upregulation of ELAM-1 in the lung vasculature (venules and interstitial capillaries), with a peak intensity developing between 3 and 4 h after deposition of immune complexes in lung. Vascular beds of spleen, liver, and kidney failed to show upregulation of ELAM-1 under these same conditions. The immunohistochemical reactivity of rat lung was abolished if the anti-ELAM-1 preparation was first absorbed with monolayers of human umbilical vein endothelial cells that had been pretreated with TNF alpha. Untreated human endothelial cells failed to cause loss of lung reactivity of the anti-ELAM-1 preparation. These data indicate that ELAM-1 is upregulated in the pulmonary vasculature of rats during deposition of immune complexes and that ELAM-1 appears to play an obligate role in the recruitment of neutrophils.

01 Aug 1990·Zhonghua wai ke za zhi [Chinese journal of surgery]

[Value of fecal detection of cancer-associated antigens using monoclonal antibodies in the diagnosis of colorectal cancer].

Article

Author: Yuan, M

Detection of cancer-associated antigens in feces by the method of binding inhibition ELISA using monoclonal antibodies were performed in sixty patients with colorectal cancer; seventy with non-malignant gastrointestinal diseases: and one hundred healthy individuals. Monoclonal antibodies used were: anti-colonic cancer CL-2, CL-3, and anti-pancreatic cancer PS-9, PS-10. The level of cancer-associated antigens detected in feces were significantly higher in patients with colorectal cancer than that of non-malignant GI diseases or healthy individuals. The positive rate of the antigens in colorectal cancer patients and normal individuals were: 61.1% vs. 7% as detected by CL-2; 53.4% vs. 9% by CL-3; 55% vs. 8% by PS-9; and 53.3% vs. 8% by PS-10. When a "cocktail" of CL-2, PS-9, and PS-10 was used, the positive rate was 92.5% in cancer patients, and 14% in control group. Cancer-associated antigens were found to be positive in all seven early staged (Duke's A) colorectal cancer patients. These results indicate the value of assaying cancer-associated antigen in feces as an aid to the diagnosis of colorectal cancer, especially in the early stage.

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