Along with the rapid development of genetic engineering technology and antibody engineering technology, the humanized monoclonal antibody has been rapidly developed and gradually replaces the rat sourced monoclonal antibody. In this paper, we establish two new logarithmically completely monotonic functions involving the real-valued special functions according to two preferred interaction geometries, necessary and sufficient conditions are presented for one of them to be logarithmically completely monotonic. As a consequence, a sharp inequality involving the real-valued special functions is deduced to solve the problems of genetically engineered antibody.
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Adrenocortical carcinoma is a rare endocrine tumour with poor prognosis. Herein we report a case of adrenocortical carcinoma which was non-functioning, and non-metastasizing. A female patient presented with vague abdominal pain and palpable lump on examination. A large sized adrenal mass on Ultrasonography (USG) and computed tomography was revealed. USG guided fine needle aspiration cytology was performed, the smears were highly suspicious of malignancy.
Twenty Five Years of Drug Discovery at the University of California Targeting Kinetoplastid Parasites
This review summarizes 25 years of screening compounds against three major kinetoplastid parasites, Trypanosoma brucei, Trypanosoma cruzi, and Leishmania spp. The work was carried out at two University of California campuses by a consortium of scientists. The history of this effort is summarized beginning with DARPA and NIAID TDRU projects. The compound collections that were screened came from both academic and industry sources.
Porphyromonas gingivalis (P. gingivalis) is a primary etiologic agent of generalized aggressive and chronic forms of periodontitis. It releases toxins called ‘gingipains’.Gingipains, (Arginine-and Lysine-specific cysteine proteinases) are proteases that are critical virulence factors in progression of periodontitis and degradation of cytokines expressed during inflammation. HRgpA and RgpB (products of two distinct but related genes) induce vascular permeability by activation of the kallikrein/kinin pathway and activating the blood coagulation system which in turn induces gingival crevicular fluid production and progression of inflammation leading to alveolar bone loss.