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At least 19 recordsLinked to original sources
PubMed1977

Adsorption protein of bacteriophage fl: solubilization in deoxycholate and localization in the fl virion.

A complex containing the minor coat protein or adsorptionprotein (A protein) of bacteriophage fl has been solubilized from the fl virion, using the detergent deoxycholate. This complex was resolved from the fl DNA and from the fl major coat protein, or B protein, by gel filtration in the presence of deoxycholate. The A protein complex migrated as a single band on sodium dodecyl sulfate-urea-polyacrylamide gels corresponding to a molecular weight of 60 000. Analysis of the amino acid composition and amino terminal residues of this preparation indicates that the preparation contains a 20% contamination of additional protein species. Antibody against purified fd A protein is cross-reactive with deoxycholate-purified fl A protein and with fl phage. Electron microscopic observation of negatively stained complexes of fl phage with this anti-fd A protein antibody and ferritin conjugated goat anti-rabbit IgG antibody revealed phages with ferritin particles at their termini or complexes of two or more phages joined together at one end by ferritin, indicating that the complex of A protein molecules is located at one end of the filamentous fl virion.

Adsorption↗
PubMed1987

Lymphoma cell line (FL-18) and Epstein-Barr virus-carrying cell line (FL-18-EB) obtained from a patient with follicular lymphoma: monoclonal derivation and different properties.

A novel cell line, FL-18, was established from the pleural effusion of a patient with follicular small cleaved cell lymphoma. At the same time, an Epstein-Barr virus (EBV) nuclear antigen (EBNA)-positive cell line, FL-18-EB, was established from the EBV-infected culture of the same pleural effusion cells. Both cell lines had the same monoclonal surface immunoglobulin (IgG kappa), and they had the same karyotype as that of the fresh pleural effusion cells in which a reciprocal translocation between the long arm of chromosomes 14 and 18 [t(14;18)(q32;q21)] was detected. Gene rearrangement analysis of immunoglobulin heavy-chain gene (JH) and kappa light-chain gene (J kappa) showed the same rearranged configuration in the two cell lines; however, some morphological and phenotypic differences were found. The FL-18-EB cells, which were morphologically similar to common EBNA-positive lymphoblastoid cell lines of normal B cell origin at the initial phase of culture, were larger than the FL-18 cells and contained multinucleated giant cells. The FL-18 cells lacked cytoplasmic immunoglobulin and were positive for common acute lymphoblastic leukemia antigen (CALLA), whereas the FL-18-EB cells had cytoplasmic immunoglobulin and were negative for CALLA. Thus, the phenotype of FL-18-EB seems to be a result of a shift by EBV infection to a more mature stage in the B cell differentiation pathway than that of FL-18. The paired availability of EBV-free and EBV-infected cell lines of a neoplastic clone is unique and valuable in considering EBV infectibility of neoplastic B cells and resultant phenotypic changes.

Aged↗
PubMed1990

Amplified and rearranged bcl-2 gene in two lymphoma cell lines, FL-218 and FL-318, carrying a 14;18 translocation.

Two human B-cell lines carrying a 14;18 chromosome translocation [t(14;18)(q32;q21)], designated FL-218 and FL-318, were established from effusion cells of two Japanese patients manifesting the transformed histology of follicular lymphoma. The FL-218 and FL-318 cell lines were composed of cells in the hyperdiploid range, which had two and three or four 18q- chromosomes, respectively. These 18q- chromosomes were not distinguishable from an 18q- chromosome derived from t(14;18) since they exhibited the same banding pattern. Southern blot analysis revealed that in both cell lines, breakage of the bcl-2 gene occurred within the major breakpoint cluster region and the truncated gene juxtaposed to an immunoglobulin heavy chain gene locus. The autoradiographic intensity of the retained fragment each on 18q- chromosome was more enhanced than that of the translocated fragment on 14q+ chromosome. These findings suggest that the extra 18q- chromosome found in t(14;18)-positive cancer does not arise from de novo independent t(14;18) but from duplication of a preexisting 18q- chromosome.

Aged↗
PubMed1992

Evidence of a dual function in fl(2)d, a gene needed for Sex-lethal expression in Drosophila melanogaster.

In Drosophila melanogaster, the female sexual development of the soma and the germline requires the activity of the gene Sxl. The somatic cells need the function of the gene fl(2)d to follow the female developmental pathway, due to its involvement in the female-specific splicing of Sxl RNA. Here we report the analysis of both fl(2)d1 and fl(2)d2 mutations: (1) fl(2)d1 is a temperature-sensitive mutation lethal in females and semilethal in males; (2) fl(2)d2 is lethal in both sexes; (3) the fl(2)d1/fl(2)d2 constitution is temperature-sensitive and lethal in females, while semilethal in males. The temperature-sensitive period of fl(2)d1 in females expands the whole development. SxlM1 partially suppresses the lethality of fl(2)d1 homozygous females and that of fl(2)d1/fl(2)d2 constitution, whereas it does not suppress the lethality of fl(2)d2 homozygous females. The addition of extra Sxl+ copies does not increase the suppression effect of SxlM1. The fl(2)d1 mutation in homozygosis and the fl(2)d1/fl(2)d2 constitution, but not the fl(2)d2 in homozygosis, partially suppress the lethality of SxlM1 males. This suppression is not prevented by the addition of extra Sxl+ copies. The semilethality of both fl(2)d1 and fl(2)d1/fl(2)d2 males, and the lethality of fl(2)d2 males, is independent of Sxl function. There is no female synergistic lethality between mutations at fl(2)d and neither at sc or da. However, the female synergistic lethality between mutations at Sxl and either sc or da is increased by fl(2)d mutations. We have analyzed the effect of the fl(2)d mutations on the germline development of both females and males. For that purpose, we carried out the clonal analysis of fl(2)d1 in the germline. In addition, pole cells homozygous for fl(2)d2 were transplanted into wild-type host embryos, and we checked whether the mutant pole cells were capable of forming functional gametes. The results indicated that fl(2)d mutant germ cells cannot give rise to functional oocytes, while they can form functional sperm. Moreover, SxlM1 suppresses the sterility of the fl(2)d1 homozygous females developing at the permissive temperature. Thus, with respect to the development of the germline the fl(2)d mutations mimic the behavior of loss-of-function mutations at the gene Sxl. Females double heterozygous for fl(2)d and snf1621 are fully viable and fertile. fl(2)d2 in heterozygosis partially suppresses the phenotype of female germ cells homozygous for snf1621; however, this is not the case with the fl(2)d1 mutation. The fl(2)d mutations partially suppress the phenotype of the female germ cells homozygous for ovoDIrSI.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

The Drosophila melanogaster fl(2)d gene is needed for the female-specific splicing of Sex-lethal RNA.

In Drosophila melanogaster, sex determination and dosage compensation are under the control of the Sex-lethal (Sxl) gene. We have identified a gene, female-lethal-2-d (fl(2)d), located in the second chromosome, that interacts with Sxl. fl(2)d homozygous clones, induced during the larval stage of fl(2)d/+ females, develop male structures instead of female ones. fl(2)d homozygous females hypertranscribe their two X chromosomes, as measured by comparing the level of the X-linked sgs-4 transcript, which is dosage compensated, with that of the autosomal sgs-3 transcript. Thus, with respect to the processes of sex determination and dosage compensation, loss-of-function mutations at the fl(2)d and at the Sxl genes are equivalent. Moreover, fl(2)d homozygous female larvae express the Sxl transcripts characteristic of males. These results indicate that the fl(2)d gene is needed for the sex-specific splicing pattern of the Sxl RNA that occurs in females, thus suggesting the involvement of the fl(2)d gene in the positive autoregulatory pathway of Sxl.

Animals↗
PubMed1990

Purification and some properties of the fast migrating alkaline phosphatase in FL-amnion cells (the Kasahara isoenzyme) and its cDNA cloning.

One of two main FL-amnion cell alkaline phosphatase (AP), the fast migrating one (FL-APF) has been reported to be identical to Kasahara isoenzyme (K.I.), which occurs preferentially in sera of patients with primary hepatoma. We purified FL-APF of which the apparent molecular weight was 135,000 by gel filtration, and that of the subunit was 62,000 on SDS/PAGE, indicating homodimeric structure of FL-AL-APF. FL-APF was found to react with monoclonal antibody against adult intestinal AP, but not with monoclonal antibody to placental AP. We isolated FL-APF cDNA clone from FL-amnion cells, of which cDNA was 2525 base pairs in length. Nucleotide sequence of the coding region and the 3' untranslated region was identical to the sequence of human adult intestinal AP cDNA. But the untranslated region of the 5' end of the isolated clone was slightly longer than that of intestinal AP. Hence, FL-APF (K.I.) may occur by altered glycosylation of intestinal AP.

Alkaline Phosphatase↗
PubMed1975

[Anti-inflammatory activity of a new quinoid polyradical (FL-70)].

The anti-inflammatory activity of FL 70, a derivative of 2,5-dihydroxy-benzoic acid, was examined in a number of conventional experimental models. In addition, FL-70 was tested for its inhibitory action on enzymes. The results were as follows: 1. The induction of a local inflammatory reaction and the subsequent i.v. injection of trypan blue showed that FL 70 reduces the capillary permeability. 2, FL-70 significantly suppresses exudation in the formalin-induced peritonitis of the rat. 3. A slight inhibition of an edema in the footpad of the rat induced by formalin-dextran was not shown to be statistically significant. 4. Local swelling could be markedly inhibited in the turpentine-oil induced inflammatory reaction of the rabbit. 5. Exudation and formation of granulomatous tissue was inhibited in Selye's granuloma. 6. FL-70 markedly inhibited the local inflammatory reaction accompanying the cutaneous reaction in experimental vaccinia infection of the rabbit skin. The size of the infiltration after intracutaneous infection of the virus was not reduced. 7. FL-70 could not prevent the onset of clinical signs, if administered in experimental allergic encephalitis. 8. The activity of acid phosphatase was inhibited by FL-70. Alcaline phosphatase, cholinesterase, leucin aminopeptidase, glucose-6- phosphatase-dehydrogenase (G-6-PDH), trypsin and chymotrypsin were unaffe-ted. FL-70 inhibits the following, G-6-PDH activated reduction process: glucose-6-phosphate (see article).

Animals↗
PubMed2026

PLayer-FL: A Principled Approach to Personalized Layer-wise Cross-Silo Federated Learning.

Non-identically distributed data is a major challenge in Federated Learning (FL). Personalized FL tackles this by balancing local model adaptation with global model consistency. One variant, partial FL, leverages the observation that early layers learn more transferable features by federating only early layers. However, current partial FL approaches use predetermined, architecture-specific rules to select layers, limiting their applicability. We introduce Principled Layer-wise-FL (PLayer-FL), which uses a novel federation sensitivity metric to identify layers that benefit from federation. This metric, inspired by model pruning, quantifies each layer's contribution to cross-client generalization after the first training epoch, identifying a transition point in the network where the benefits of federation diminish. We first demonstrate that our federation sensitivity metric shows strong correlation with established generalization measures across diverse architectures. Next, we show that PLayer-FL outperforms existing FL algorithms on a range of tasks, also achieving more uniform performance improvements across clients.

Journal Article↗
PubMed1987

Intercellular contacts and the organization of actin filaments in cultured epithelial FL cells are altered by growth on type I collagen and treatment with 12-O-tetradecanoylphorbol-13-acetate through the modulation of interactions between cells and the substratum.

We have investigated the effects of various types of collagen and a tumor-promoting phorbol ester on intercellular contacts and the organization of actin in human amnion epithelial FL cells and mouse fibroblast 3T3-A31 cells. Our purpose was to investigate how modulation of interactions between cells and the substratum leads to alterations in intercellular contacts and organization of actin filaments. When cells were cultured on dishes coated with a solution containing type I collagen, but not type IV, changes were induced in the morphology of FL cells and their intercellular contacts. Type I collagen also caused changes in the organization of their actin filaments, although no such effects were observed with 3T3-A31 cells. In contrast, 12-O-tetradecanoylphorbol-13-acetate (TPA) caused morphological changes, dissociation of groups of cells, and reorganization of actin filaments in cultures of FL and 3T3-A31 cells. It also disrupted the sites of adhesion of FL cells to the substratum. Both type I collagen and TPA rapidly induced spreading of FL cells in the absence of serum. However, cis-hydroxyproline, known to inhibit secretion of collagen, did not suppress the TPA-induced dissociation of groups of FL cells. These results suggest that the interactions with type I collagen of epithelial FL cells, but not of fibroblastic 3T3-A31 cells, tend to disorganize cellular morphology, intercellular contacts, and actin filaments in ways similar to, but not directly related to, the effects of TPA.

Actins↗
PubMed1979

Isolation of UV-sensitive variants of human FL cells by a viral suicide method.

A new method (viral suicide method) for the isolation of UV-sensitive mutants is described. Colonies of mutagenized human FL cells were infected with UV-irradiated Herpes simplex viruses and surviving ones which seemed to be deficient in host cell reactivation (HCR) were examined for their UV sensitivity. Nineteen of 238 clones examined were sensitive to UV irradiation at the time of the isolation. After recloning, four of these clones have been studied and two (UVS-1 and UVS-2) of them are stable in their UV sensitivity for 4 months in culture. UV sensitivity of UVS-1, UVS-2, and the parental FL cells are as follows: the extrapolation numbers (n) are 2.2, 2.1, and 1.8 and mean lethal doses (D0) are 2.9, 3.7, and 7.8 J/m2 for UVS-1, UVS-2, and the parental FL cells, respectively- They are no more sensitive than FL cells to X-irradiation. The ability of HCR in UVS-2 cells is apparently lower than that in FL cells, whereas UVS-1 cells are the same as FL cells in the ability.

Amnion↗
PubMed1991

A hybrid form of alkaline phosphatase produced in FL-amnion cells.

FL-amnion cells have mainly two alkaline phosphatase (AP) isozymes, of which the faster migrating one (FL-APF) on 5% polyacrylamide gel electrophoresis has proved to be identical to the Kasahara isozyme, a tumor-associated AP of intestinal type. But the other slower migrating one (FL-APs) remains to be characterized. Immunological and enzymic examination of purified FL-APs revealed that it is a hybrid form of AP consisting of one subunit with a molecular weight of 66,200 coming from the same subunit as that of FL-APF and another one with a molecular weight of 58,000 from placental AP subunit with modified glycosylation.

Alkaline Phosphatase↗
PubMed1987

Serological relationship between mouse adenovirus strains FL and K87.

Three-week-old outbred mice were inoculated intraperitoneally or orally and intranasally with the FL or K87 strains of mouse adenovirus and bled at intervals after infection. Serum was tested by both the complement fixation and indirect immunofluorescence tests for reactivity with either virus antigen. A unilateral relationship was detected between FL and K87 strains. Serum from mice given the FL strain of virus reacted in both tests with FL and K87 antigens. Serum from mice given the K87 strain reacted only with the homologous antigen. Serum antibody titers were generally higher in the immunofluorescence test than in the complement fixation test. These observations stress the need to use both FL and K87 antigens for specific serologic diagnosis of adenovirus infection in mouse colonies.

Adenoviridae↗
PubMed1992

Studies of composite grafts of fetal pancreas (FP) and fetal liver (FL) in the streptozotocin-induced diabetic rat.

A hepatotrophic effect of pancreatic islets on co-transplanted hepatocytes has been described recently by Ricordi et al. We investigated a possible reciprocal effect of co-transplanted fetal liver (FL) on fetal pancreas (FP) isografted into streptozotocin diabetic rats. FL was co-transplanted with FP in three sites: the new intramural small bowel (ISB) site, the conventional renal subcapsular (RSC) site, and the historically inhospitable intramuscular (IM) site. Overall, as compared to grafts of FP alone, composite FP/FL grafts consistently provided earlier restoration of normoglycemia in streptozotocin diabetic recipients (24 +/- 8 vs. 67 +/- 43 days P = 0.001). The proportion of recipients rendered normoglycemic and the clearance of glucose was site-dependent. For FP and FP/FL recipients respectively, the ISB site resulted in 100% normoglycemia in both groups (19/19 and 6/6), the RSC site resulted in 71% (5/7) and 40% (2/5) and the IM site resulted in 14% (1/7) and 67% (6/9). In normoglycemic recipients, glucose clearance was normal or supraphysiologic except for the RSC site. Composite isografts brought about normoglycemia in 75% (6/8) of recipients treated with beta-cell toxic doses of cyclosporine that prevented reversal of diabetes in recipients of FP alone. Co-transplantation of FL benefits FP through paracrine mechanisms mediated by unknown factor(s). Thus, as compared to grafts of FP alone, composite FP/FL grafts established normoglycemia more rapidly, mitigated cyclosporine toxicity and corrected diabetes when transplanted in the small bowel site. There are several mediators that may be responsible for these paracrine effects between the liver cells and the pancreas. IGF-1 elaborated by FL is the most likely trophic factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Comparative biological characterization of mouse adenovirus strains FL and K 87 and seroprevalence in laboratory rodents.

The growth, stability and seroprevalence in laboratory rodents of the two known strains of mouse adenovirus were compared. The FL strain of mouse adenovirus grew in both L 929 murine fibroblasts and in CMT-93 murine rectal carcinoma cells, whereas the K 87 strain grew only in CMT-93 cells. The bulk of the FL progeny virus was released from the host cells. K 87 virus was largely cell-associated. Both virus strains were stable at 37 degrees C in liquid medium. The K 87 strain was completely inactivated after 5-15 minutes at 56 degrees C, whereas FL infectivity was still detected after two hours at this temperature. Both virus strains were stable in the dessicated state for 14 days, although FL viability was more dependent on the presence of protein in the virus diluent. Seroepidemiologic data suggest that viruses antigenically related to mouse adenovirus are more prevalent among laboratory rats than among laboratory mice and that the virus(es) infecting rats differ from those infecting mice. Results of retrospective serologic testing suggest an association between mouse adenovirus and an outbreak of disease in a mouse breeding colony.

Adenoviridae↗
PubMed1986

Binding of cardiotoxin analogue III from Formosan cobra venom to FL cells.

The binding equilibrium at 37 or 0 degrees C of 125I-cardiotoxin analogue III (CT III) to fetal lung (FL) cells (cultured human amnion cells) was achieved within 1 h, and the binding at 37 degrees C was irreversible. The Scatchard analysis at 37 degrees C on the binding of 125I-CT III indicated that FL cells had two types of binding sites with different association constants. The association constant and the number of high-affinity sites was 1.1 X 10(10) mol-1 or 2.8 X 10(6) per FL cell, respectively. At 37 or 0 degrees C, the cytotoxicity of CT III paralleled the amount of bound CT III to FL cells, and at 37 degrees C was inhibited by the presence of acidic phospholipids.

Binding Sites↗
PubMed1975

Attachment of lipoprotein to murein (peptidoglycan) of Escherichia coli in the presence and absence of penicillin FL 1060.

In vivo studies on the attachment of lipoprotein to the murein (peptidoglycan) of Escherichia coli showed that it takes several generations of growth until the amount of lipoprotein on newly made murein is equilibrated. The technique used involves degradation of the sodium dodecyl sulfate-insoluble murein-lipoprotein complex (sacculus, rigid layer) with lysozyme and separation of the labeled products on paper. No lipoprotein was found on murein subunits incorporated during a pulse of [3H]diaminopimelate for 1 min in logarithmically growing cells at 37 C. Even after one doubling of the cell mass, only 4 to 8% of the labeled murein was isolated as bound to lipoprotein. With uniformly labeled murein, 30% remains bound to lipoprotein after lysozyme treatment, corresponding to three murein subunits. Therefore it can be concluded that during pulse labeling either no lipoprotein is incorporated into the newly synthesized murein or no murein subunits are inserted into existing murein around lipoprotein attachment sites. Longer pulse and pulse-chase experiments argue for the latter interpretation. It is therefore concluded that incorporation of murein subunits into the growing murein polymer is not at all a random process. Instead, quite large areas of murein, on which lipoprotein is situated, seem to be preserved. Under the influence of penicillin FL 1060 murein synthesis is 50% inhibited. The rate of lipoprotein attachment is less affected so that increasing amounts of lipoprotein become attached during spheroplast formation. By the time the stationary growth phase has been reached, the lipoprotein content of the murein has doubled. Diaminopimelate auxotrophic mutants require, in the presence of penicillin FL 1060, more diaminopimelate for full growth than in the absence of penicillin FL 1060. This finding and the fact that murein synthesis is always inhibited by 50% over a wide range of penicillin concentration (1 to 1,000 mug/ml) point to the inhibition of an enzymatic step of murein synthesis which can be partially bypassed by a second enzyme, less efficient but resistant to penicillin FL 1060.

Binding Sites↗
PubMed1974

Activity of FL 1060, a new beta-lactam antibiotic, against urinary tract pathogens.

The effect of the new beta-lactam antibiotic FL 1060 on urinary tract pathogens, of which 71 were sensitive to and 100 resistant to ampicillin, is presented here. When tested by conventional methods FL 1060 was found to be highly active against ampicillin-sensitive strains of E. coli but phenotypically resistant variants readily emerged, particularly when a large inoculum was used. Thirty-one per cent of ampicillin-resistant strains were found to be sensitive to less than 500 mug FL 1060 per ml, and in general this antibiotic was more active than ampicillin against resistant strains. In a system simulating the mechanical features of the urinary bladder the activity of FL 1060 against three sensitive strains of E. coli was found to be greater than ampicillin in conditions of low, but not high, osmolality.

Ampicillin↗