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Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.
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Abstract: Monoclonal antibodies (mAb) against toxic shock syndrome toxin-1 (TSST-1) were generated that block two of the most important biologic activities of TSST-1, nonspecific T lymphocyte mitogenicity and the suppression of immunoglobulin synthesis. Fourteen hybridomas producing antibody against TSST-1 were isolated independently. The culture supernatant and ascitic fluids from each were analyzed to determine the mAb isotypes. Seven of the mAb were IgG1, and the remaining seven were IgM; all the mAb had kappa light chains. Immunoglobulin was partially purified from hybridoma-generated ascitic fluid by ammonium sulfate precipitation and tested for the ability to block TSST-1-induced mitogenicity and immunosuppression. Three mAb (all IgG1) were shown to block both the toxin-induced mitogenicity and the suppression. None of the mAb tested inhibited just one of the two toxin activities. The neutralizing mAb were then used in Western analysis with previously mapped cyanogen bromide (CNBr)-generated toxin fragments to localize the aforementioned biologic functions. The Western blot analysis showed that the mitogenic and the suppressive functions of TSST-1 were located on a 14,000 dalton internal CNBr fragment.
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Localization of biologic functions of toxic shock syndrome toxin-1 by use of monoclonal antibodies and cyanogen bromide-generated toxin fragments.

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Abstract: Several investigators have reported an association between low serum cholesterol levels and an increased frequency of colorectal cancer. Because low cholesterol levels may be a result of an established cancer, we have investigated the relation between serum cholesterol levels and the frequency of colorectal adenomas, which are thought to be precursors of colon cancer. We prospectively studied 1083 consecutive patients who underwent colonoscopy (241 of whom were excluded because of malignant disease, chronic inflammatory bowel disease, familial polyposis, or partial colectomy). In the remaining 842 patients, analysis of covariance was performed to evaluate the contribution of serum cholesterol to the risk of colorectal adenoma. Serum cholesterol levels were significantly and positively associated with the frequency of colorectal adenoma in subjects of both sexes. After adjustment for age and body-mass index, this positive association remained significant between the top quintile and the lowest quintile for serum cholesterol, with regard to the total study group (odds ratio, 2.0; 95 percent confidence limits, 1.1 and 3.6) and men only (odds ratio, 2.2; 95 percent confidence limits, 1.0 and 4.8). We conclude that there is not an inverse correlation between serum cholesterol levels and the risk of colorectal adenomas; on the contrary, there appears to be a small positive association.
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Relation between the frequency of colorectal adenoma and the serum cholesterol level.

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Abstract: The McDonough strain of feline sarcoma virus (SM-FeSV) transforms fibroblast cell lines in culture and produces fibrosarcomas in domestic cats. SM-FeSV does not induce haematopoietic malignancies in spite of the fact that its viral oncogene, v-fms, codes for a glycoprotein related to the receptor for the mononuclear phagocyte colony stimulating factor, CSF-1. The v-fms-coded polypeptide includes the complete extracellular domain of the c-fms proto-oncogene product and retains the ability to bind CSF-1 specifically. The two molecules have very similar sequences except at their extreme carboxyl terminal ends where 40 amino acids of the c-fms-coded glycoprotein are replaced by 11 unrelated residues in the v-fms product. Autophosphorylation of the c-fms gene product on tyrosine is enhanced by CSF-1 addition, whereas phosphorylation of the v-fms-coded glycoprotein appears to be constitutive. We now show that introduction of the v-fms gene into simian virus-40 (SV40)-immortalized, CSF-1 dependent macrophages renders them independent of CSF-1 for growth and tumourigenic in nude mice. These factor-independent cell lines express unaltered levels of the c-fms product which is down-modulated in response to either CSF-1 or the tumour promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). The induction of factor independence by a non-autocrine mechanism suggests that the v-fms product is an unregulated kinase that provides growth stimulatory signals in the absence of ligand.
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The v-fms oncogene induces factor independence and tumorigenicity in CSF-1 dependent macrophage cell line.