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Biomedical subjects

F F Becker

Publications and source records attributed to F F Becker.

At least 109 records · Page 6Linked to original sources
PubMed1982

Lateral tarsal strip procedure for the correction of paralytic ectropion.

Otolaryngologists are frequently confronted with patients suffering from permanent facial paralysis. This condition often results in a severe cosmetic and functional deformity of the lower eyelid called paralytic ectropion. Conservative measures are often unsatisfactory and surgical correction is needed. Tarsorrhaphy and cautery have been advocated in the past, but are usually unsatisfactory. The most standard surgical procedure in use at the present time is a modification of the Kuhnt-Szymanowski procedure which is useful in repositioning the lax eyelid and allowing for lid shortening. This procedure involves removal of a portion of the midtarsal plate, but does not correct the lax lateral canthal tendon which is the cause of the pathology in paralytic ectropion. In 1979, in the ophthalmologic literature, Anderson and Gordy reported the tarsal strip procedure for the correction of paralytic and senile ectropion. This paper describes the lateral tarsal strip procedure which involves a lateral canthotomy, division of the lateral portion of the lower eyelid into musculocutaneous and tarsoconjunctival layers, removal of a portion of the conjunctiva and suturing the resulting tarsal strip to the periosteum of the inner aspect of the orbital rim laterally to shorten and elevate the lower eyelid. The procedure is presented in diagrams and close-up operative photographs. Before and after photographic documentations of two clinical cases are also presented. Since this procedure has been employed for only about two years, long-term results are not yet available; however, the author feels that this procedure will offer a significant improvement in the surgical treatment of paralytic ectropion.

Aged↗
PubMed1982

The characterization of trypan blue-induced tumors in Wistar rats.

Trypan blue is an azo dye widely used for testing cell viability. The dye has been identified as a mutagen and a carcinogen. In some strains of rats, particular Wistar rats, chronic exposure induces a reticuloendothelial neoplasm, predominantly in the liver. These tumors were studied with the use of immunologic cell membrane markers, electron microscopy, and histochemistry to characterize tumor cell type. The authors have studied this tumor in two inbred lines of Wistar rats to compare the efficacy of two previously described dye regimens on tumor incidence and to ascertain whether a short, intense exposure was as effective as chronic protracted exposure. No significant difference in tumor incidence was observed between the two regimens. These studies suggest that the tumor is composed of a macrophage-like cell that retains some characteristics of normal macrophages and that is a reproducible model for carcinogen-induced lymphoreticular human lymphomas.

Animals↗
PubMed1982

Alterations of bioelectric potential in primary hepatocellular carcinomas induced by N-2-fluorenylacetamide or diethylnitrosamine.

Primary hepatocellular carcinoma(s) (PHC) induced in rats by N-2-fluorenylacetamide (AAF) or diethylnitrosamine (DEN) were examined for their bioelectric potential (EP). N-2-Fluorenylacetamide-induced PHC differed from age-matched normal livers by a mean of -12.9, which is significant at p less than 0.001. They also differed from non-PHC-bearing surrounding liver by -4.75 mV, significant at p less than 0.05. Diethylnitrosamine-induced PHC differed from normal liver by -13.5 mV and from background liver by -9.95 mV, both significant at p less than 0.001. To determine the contribution of cell division to these differences, regenerating livers were examined. The levels of mixed function oxidases in PHC and in regenerating livers reported in the literature appeared to correlate with the measured EP. We, therefore, studied the effects of chemical inhibitors and an inducer of this enzyme system. The alterations of mixed function oxidase were demonstrated to parallel those of EP.

2-Acetylaminofluorene↗
PubMed1982

Morphological classification of mouse liver tumors based on biological characteristics.

Examination of three strains of inbred mice suggested that specific morphological types of hepatic tumors are the result of genetic predisposition while other types of tumors are associated with exposure to chemical carcinogens. A simple classification system is proposed. Additional studies indicated that a putative promoting agent, such as phenobarbital, increased the incidence of those tumor types usually associated with spontaneous appearance and only in strains with a genetic predisposition to spontaneous tumorigenesis. Carcinogens induce an increase in all types of tumors.

2-Acetylaminofluorene↗
PubMed1981

Alterations in polyadenylated messenger ribonucleic acid from free and total polysomes of a rat hepatoma.

We examined the homology between polysomal polyadenylated ribonucleic acid (mRNA) populations of hepatoma 252, a tumor which is deficient in the synthesis of plasma proteins, and those of normal and regenerating rat liver. Hybridization of polyadenylated mRNA populations with homologous or heterologous complementary deoxyribonucleic acids showed that mRNA from total and free polysomes from hepatoma 252 lack sequences which are present in normal or regenerating liver. Although there are obvious differences in the abundance of sequences between tumor and normal or regenerating liver polysomal mRNA, we did not detect, with the techniques used in this work, tumor-specific sequences. Analysis of hybridization curves using derivative plots did not reveal the presence in tumor mRNA of a high complexity class not present in normal liver. We conclude that alterations in mRNA populations of free and total polysomes of this tumor primarily reflect processes of genetic restriction rather than the derepression of previously unexpressed genes.

Animals↗
PubMed1981

Differential inhibition of rat liver DNA polymerases in vitro by direct-acting carcinogens and the protective effect of a thiol reducing agent.

The direct-acting carcinogens acetoxyacetylaminofluorene, methylnitrosourea, and N-methyl-N'-nitro-N-nitrosoguanidine were tested for their ability to inhibit rat liver DNA polymerase-alpha, -beta, and -gamma activity in vitro. DNA polymerase-alpha was the most sensitive, polymerase-beta was the most resistant, and polymerase-gamma exhibited an intermediate response. When the reactions were reassayed in the presence and absence of dithiothreitol, a thiol reducing agent, it was shown that the inhibition by carcinogens was generally reversible with increasing dithiothreitol, except that polymerase-beta recovered only 80-90% of control values. These and binding data suggest that DNA polymerase-beta, the putative repair enzyme, is highly resistant to carcinogen damage. This resistance may contribute to the retention of normal function and fidelity of the repair enzyme during carcinogen exposure in vivo and to a normal cellular repair.

Acetoxyacetylaminofluorene↗
PubMed1981

Chromatin conformation modulates repair of single strand interruptions by polynucleotide ligase-[3H] AMP.

Conformationally distinct chromatin populations were utilized as substrates to quantitate the relative amount of and accessibility of internal 5'-phosphomonoester breaks in DNA-chromatin. In these studies, a constant amount of chromatin as well as deproteinized DNA derived from the respective chromatin sample was titrated with increasing quantities of adenylated polynucleotide ligase intermediate. This enzyme intermediate releases its AMP moiety while repairing a DNA single strand interruption, release of AMP being directly proportional to the number of internal 5'-phosphomonoester breaks repaired. Results of this study indicate that the ability of polynucleotide ligase to repair DNA breaks within chromatin was affected by the conformational state of the chromatin. The degree of conformational constraint present in a given chromatin, therefore, determined the capacity of the enzyme to repair internal DNA 5'-phosphomonoester breaks.

Adenosine Monophosphate↗
PubMed1981

DNA methylation and methylase levels in normal and malignant mouse hepatic tissues.

The status of DNA methylation, as measured by the 5-methylcytosine content of nuclear DNA, was examined in normal livers and in chemically induced or spontaneous primary hepatocellular carcinoma (PHC) arising in three strains of mice. The DNA from spontaneous tumors of genetic origin in C3H mice and also from acetylaminofluorene, chlordane, or 3'-methyl-4-dimethylaminoazobenzene-induced tumors in C57Bl and B6C3 mice was undermethylated compared to the levels in background and normal liver samples. The DNA methylase activities from normal liver, background liver, and PHC were assayed in C3H mice to determine whether the observed genomic undermethylation is related to a dysfunction of this enzyme and were compared to the rates of DNA synthesis in these tissues. Since DNA methylase levels from tumor nuclei were elevated compared to background, it is concluded that the undermethylation found in the tumor genomes of this system is not due to inactivation nor a significant deficiency of the activity of this enzyme relative to the demand in tumors for methylation of de novo synthesized DNA.

Animals↗
PubMed1981

Reconstructive surgery of the mental canthal region.

The complexity of the medial canthal area is discussed and the importance of complete tumor removal with microscopically controlled excision emphasized.. Immediate reconstruction is recommended in most instances. Defects to be reconstructed are divided into nasal and eyelid sides of the medial canthal region and subdivided into superficial and deep defects. The reconstructive modalities used in the various defects are illustrated and the advantages and disadvantages of each explored.

Basal Cell Carcinoma↗
PubMed1981

Inhibition of spontaneous hepatocarcinogenesis in C3H/HeN mice by transplanted hepatocellular carcinomas.

Cell suspensions of tumor fragments derived from spontaneous or chemically induced primary hepatocellular carcinomas obtained from inbred C3H/HeN mice were transplanted into young male mice of the same strain. Transplantable hepatocellular carcinomas were excised as soon as they were detected, and all recipient mice were killed at one year of age. In control C3H/HeN mice, the incidence of primary hepatocellular carcinomas was 41% (41 of 100). In mice in which there was no growth of transplantable carcinomas, whether originally given injections of tumor cell suspensions or fragments, the overall incidence of primary hepatocellular carcinomas was 49% (35 of 72) with one to six tumors per liver at time of sacrifice. Transplantable hepatocellular carcinomas were established only in mice that had received tumor fragments. In these mice, from which established transplantable hepatocellular carcinomas had been excised, the overall incidence of primary hepatocellular carcinomas was 12% (3 of 25) with one tumor being found in each of three livers. The time of appearance of excision of transplantable hepatocellular carcinoma did not affect this decrease in primary hepatocellular carcinoma incidence.

Animals↗
PubMed1981

Fibronectin production by human mammary cells.

Human mammary cells were examined for the presence of the high-molecular-weight surface glycoprotein fibronectin. Early passage mammary epithelial cell and fibroblast cultures from both carcinomas and normal tissues were tested for the presence of cell-associated fibronectin by immunofluorescence microscopy and for the synthesis and secretion of fibronectin by specific immunoprecipitation of metabolically labeled protein. In vivo frozen sections of primary carcinomas and normal tissues were tested for the localization of fibronectin by immunofluorescence microscopy. In contrast to the extensive fibrillar networks of fibronectin found in the fibroblast cultures, the epithelial cell cultures from both tissue sources displayed a pattern of cell-associated fibronectin characterized by powdery, punctate staining. However, the cultured epithelial cells, as well as the fibroblasts, secreted large quantities of fibronectin into the medium. Putative myoepithelial cells also displayed extensive fibrillar networks of fibronectin. The difference in cell-associated fibronectin distribution between the epithelial cells and the fibroblasts and putative myoepithelial cells provided a simple means of quantitating stromal and myoepithelial cell contamination of the mammary epithelial cells in culture. In vivo, normal tissues showed fibronectin primarily localized in the basement membrane surrounding the epithelial cells and in the stroma. Most primary carcinomas displayed powdery, punctate staining on the epithelial cells in addition to the fibronectin present in the surrounding stroma.

Basement Membrane↗
PubMed1981

DNA methylase activity of normal liver, regenerating liver, and a transplantable hepatocellular carcinoma.

DNA from transplantable hepatocellular carcinoma (THC) 252 has recently been found to have a lower 5-methylcytosine content than DNA from normal or regenerating rat liver. We have determined that DNA methylase, purified 200-fold from nuclei of regenerating rat liver, can add more methyl groups to THC 252 DNA than to DNA from normal or regenerating rat liver. Furthermore, a similarly purified DNA methylase from THC 252 was found to methylate THC 252 DNA at a higher rate than it methylated DNA from normal or regenerating liver. The larger number of unmethylated sites in THC 252 DNA was not due to a deficiency of DNA methylase since the level of methylase activity of nuclear extracts from THC 252 was 2.7 times that of normal liver and 1.5 times that of regenerating liver. Methylases from these three sources had similar rats of reaction with different DNA substrates. These findings suggest that the hypomethylation of THC 252 DNA is not due to decreased methylase activity or to altered enzyme specificity.

Animals↗
PubMed1980

Decreased fidelity in one subspecies of DNA polymerase-alpha that appears during N-2-acetylaminofluorene hepatocarcinogenesis.

During the exposure of rat livers to the hepatocarcinogen 2-acetylaminofluorene (N-2-fluorenylacetamide), it was demonstrated that the cytoplasmic DNA polymerase-alpha (E.C. 2.7.7.7) was strikingly error-prone when compared to that of normal liver (Chan, J.Y.H. and Becker, F.F. (1979) Proc. Natl. Acad. Sci. U.S.A. 76, 814-818). The fidelity of polymerization of these enzymes was assayed by determining the incorporation of noncomplementary deoxyribonucleotide triphosphates (misincorporation) on a poly(dA-dT) template. To identify the mechanism of infidelity, we modified and extended our purificaton scheme. As a result, a subspecies of polymerase-alpha 1 was identified and separated from the normal component, polymerase-alpha 2. Polymerase-alpha 1 activity eluted from a phosphocellulose column at 0.07-0.12 M NaCl, while polymerase-alpha 2 eluted at 0.15-0.2 M NaCl. Polymerase-alpha 2 demonstrated normal fidelity throughout the various steps of purification while polymerase-alpha 1, despite being purified some 10 250-fold, continued to demonstrate a severe degree of infidelity.

2-Acetylaminofluorene↗