Search PubMed⌕ Search

Biomedical subjects

S C Lo

Publications and source records attributed to S C Lo.

At least 91 records · Page 5Linked to original sources

Comparison of laboratory tests used for identification of the lupus anticoagulant.

A comparison of the sensitivities of the ten most commonly used tests for the identification of the lupus anticoagulant (LA) and the lupus cofactor phenomenon was undertaken on 18 patients. All investigations, except the cardiolipin-antibody ELISA assay, were carried out using patient's plasma alone followed by a 1:1 mix with control plasma. Dilution studies (1:3, 1:6, 1:9--patient:control) were also carried out. The kaolin clotting time (KCT) was the only test positive in all patients at all dilutions, while the dilute activated partial thromboplastin time with kaolin (Dil-APTT) registered 17 of 18 positive at all dilutions. Both the dilute Russell viper venom time (Dil-RVVT) and the tissue thromboplastin inhibition time (TTI) (1/500 thromboplastin) identified the LA in 17 of 18 patients on initial testing but were less sensitive in the dilution studies. The KCT is not a suitable test for routine laboratory use, as it requires an individual filtration step. Therefore a combination of either the Dil-APTT or Dil-RVVT together with the TTI (1/500 dilution thromboplastin) is recommended for routine LA screening, as all patients with LA in this study were identified using these easily automated tests. The lupus cofactor phenomenon was most frequently demonstrated using the Dil-APTT.

Antibodies↗

A novel virus-like infectious agent in patients with AIDS.

A novel virus-like infectious agent (VLIA), obtained by direct transfection of DNA from Kaposi's sarcoma of a patient with acquired immune deficiency syndrome (AIDS), was transmissible from culture to culture by cell-free filtrate. VLIA contained an outer limiting membrane and had a buoyant density of 1.17-1.20 g/ml in a sucrose gradient. The DNA genome of VLIA was estimated to be greater than 150 kilobase (kb) pairs and carried repetitive sequences. An 8.6 kb pair cloned probe (psb-8.6) and a 2.2 kb pair cloned probe (psb-2.2) of VLIA detected specific sequences in DNA of VLIA infected cells, but not in DNA of uninfected NIH/3T3 cells. By Southern blot hybridization analysis, VLIA was distinct from all known members of human herpes virus, from vaccinia virus, monkey herpes virus saimiri (HVS), and mouse cytomegalovirus (MCMV). Using synthetic primers with the VLIA specific DNA sequences and the polymerase chain reaction (PCR) method, we detected VLIA sequences in DNA isolated from 7 out of 10 patients with AIDS. VLIA infection was identified in spleen, liver, brain, lymph node, Kaposi's sarcoma tissues, or peripheral blood mononuclear cells from these patients, but not in 5 different organs and a tumor from 5 subjects without AIDS. Antiserum raised against VLIA in rabbit positively immunostained brain and lymph node tissues from these AIDS patients.

Acquired Immunodeficiency Syndrome↗

Fatal infection of silvered leaf monkeys with a virus-like infectious agent (VLIA) derived from a patient with AIDS.

Four silvered leaf monkeys, inoculated with a virus-like infectious agent (VLIA) derived from transformed NIH/3T3 cells (sb51) transfected with Kaposi's sarcoma DNA of an AIDS patient, showed wasting syndromes and died in 7-9 months. Two monkeys had a transient lymphadenopathy in earlier stages. Two moribund animals showed lymphopenia. Although 3 of the VLIA inoculated monkeys had persistent low grade fever early in the infection, the animals became afebrile in the later stages. One VLIA inoculated animal had a prominent antibody response, which occurred 7 months after VLIA inoculation. The other 3 monkeys had a transient or poor antibody response in the later stages. These 3 animals revealed periodic VLIA antigenemia during the course of the experiment. A control monkey was killed 8 months after the last VLIA inoculated monkey succumbed and showed neither an antibody response nor evidence of antigenemia. VLIA-specific DNA could be directly detected in necropsy tissues of all 4 monkeys inoculated with VLIA using the polymerase chain reaction method. VLIA infection was identified in all 4 spleens, 2 of 4 livers, 1 of 2 kidneys, and all 3 brains tested from these 4 animals, but not in the tissues from the control monkey. The necropsy examination of the 4 VLIA inoculated animals revealed no opportunistic infections, acute inflammatory lesions, malignancy or cause of death other than VLIA infection. We believe that the VLIA caused a fatal systemic infection in these monkeys.

Acquired Immunodeficiency Syndrome↗

Virus-like infectious agent (VLIA) is a novel pathogenic mycoplasma: Mycoplasma incognitus.

The newly recognized pathogenic virus-like infectious agent (VLIA), originally reported in patients with AIDS but also known to be pathogenic in previously healthy non-AIDS patients and in non-human primates, was cultured in cell-free conditions using a modified SP-4 medium and classified as a member of the order Mycoplasmatales, class Mollicutes. The infectious microorganism is tentatively referred to as Mycoplasma incognitus. M. incognitus has the unique biochemical properties of utilizing glucose both aerobically and anaerobically, as well as having the ability to metabolize arginine. Among all known human mycoplasmas, these specific biochemical characteristics were found previously only in a rarely isolated species, M. fermentans. In comparison with M. fermentans, M. incognitus appears to be even more fastidious in cultivation requirements and fails to grow in all tested mycoplasma media other than modified SP-4 medium. In addition, M. incognitus grows much more slowly, has a smaller spherical particle size and occasional filamentous morphology, and forms only irregular and very small colonies with diffuse edges on agar plates. Antigenic analysis using polyclonal and monoclonal antibodies and DNA analysis of sequence homology and restriction enzyme mappings in M. incognitus, M. orale, M. hyorhinis, M. hominis, M. pneumoniae, M. fermentans, M. arginini, M. genitalium, M. salivarium, Ureaplasma urealyticum, and Acholeplasma laidlawii revealed that M. incognitus is distinct from other mycoplasmas, but is most closely related to M. fermentans.

Animals↗

Identification of Mycoplasma incognitus infection in patients with AIDS: an immunohistochemical, in situ hybridization and ultrastructural study.

Monoclonal antibodies (Mabs) were developed against antigens from a pure culture of Mycoplasma incognitus grown in modified SP-4 medium. All the Mabs obtained were shown to react only with M. incognitus, and not with other species of human mycoplasma. The Mabs identified M. incognitus immunohistologically in thymus, liver, spleen, lymph node, or brain from 22 patients with AIDS, as well as in 2 placentas delivered by patients with AIDS. Using an 35S-labeled DNA probe specific for M. incognitus and in situ hybridization technique, we also identified M. incognitus-specific genetic material in these tissues. Furthermore, ultrastructural studies of the specific areas of tissues which were highly positive for M. incognitus antigens revealed characteristic structures of mycoplasma organisms. These mycoplasma-like particles could be identified intracellularly and extracellularly. Histopathology of the tissues infected by M. incognitus varied from no pathological changes to fulminant necrosis with or without an associated inflammatory reaction. M. incognitus, a novel pathogenic mycoplasma, was cytopathic and cytocidal.

Acquired Immunodeficiency Syndrome↗

Association of the virus-like infectious agent originally reported in patients with AIDS with acute fatal disease in previously healthy non-AIDS patients.

We studied 6 patients from 6 different geographic areas who presented with acute flu-like illnesses. The patients developed persistent fevers, lymphadenopathy or diarrhea, pneumonia, and/or heart, liver, or adrenal failure. They died in 1-7 weeks. These patients had no serological evidence of HIV infection and could not be classified as AIDS patients according to CDC criteria. The clinical signs as well as laboratory and pathological studies of these patients suggested an active infectious process, although no etiological agent was found despite extensive infectious disease work-ups during their hospitalization. Post-mortem examinations showed histopathological lesions of fulminant necrosis involving the lymph nodes, spleen, lungs, liver, adrenal glands, heart, and/or brain. No viral inclusion cells, bacteria, fungi, or parasites could be identified in these tissues using special tissue stains. We report that immunohistochemistry using rabbit antiserum raised against VLIA, the virus-like infectious agent previously identified in patients with AIDS and shown to cause fatal systemic infection in primates, revealed VLIA antigens in these necrotizing lesions. In situ hybridization using an 35S labeled VLIA-specific DNA probe also detected VLIA genetic material in the areas of necrosis. Furthermore, virus-like particles closely resembling VLIA were identified ultrastructurally in these histopathological lesions. VLIA was associated with the systemic necrotizing lesions in these previously healthy non-AIDS patients with an acute fatal disease.

Acquired Immunodeficiency Syndrome↗

A trans-acting gene is required for the phenotypic expression of a tyrosinase gene in Streptomyces.

The melanin locus (melC) from Streptomyces antibioticus was previously shown to be composed of two open reading frames (ORFs), melC1 and melC2. The melC2 ORF codes for the polypeptide chain of tyrosinase (apotyrosinase). The function of melC1 is not known except that insertional mutation within it abolishes the tyrosinase activity. Here, we show that in Streptomyces lividans TK64 harboring melC1 mutated and melC2 intact (melC1- melC2+) plasmids, while there was no tyrosinase activity, melC transcript was synthesized and apotyrosinase could be detected. The apotyrosinase could be activated to a limited degree by incubation with copper ions, or by mixing the mycelial extract from a culture harboring a melC1- melC2+ (pPF950) plasmid with that from a culture containing a melC1+ melC2- (pSA1) plasmid. Complementation analysis showed that melC1 acted in trans on the tyrosinase gene expression. Together, these results suggest that melC1 encodes or regulates a copper-transfer protein serving an in vivo copper-donor function in the biosynthesis of active tyrosinase.

Catechol Oxidase↗

Radiological image compression using error-free irreversible two-dimensional direct-cosine-transform coding techniques.

Some error-free and irreversible two-dimensional direct-cosine-transform (2D-DCT) coding, image-compression techniques applied to radiological images are discussed in this paper. Run-length coding and Huffman coding are described, and examples are given for error-free image compression. In the case of irreversible 2D-DCT coding, the block-quantization technique and the full-frame bit-allocation (FFBA) technique are described. Error-free image compression can achieve a compression ratio from 2:1 to 3:1, whereas the irreversible 2D-DCT coding compression technique can, in general, achieve a much higher acceptable compression ratio. The currently available block-quantization hardware may lead to visible block artifacts at certain compression ratios, but FFBA may be employed with the same or higher compression ratios without generating such artifacts. An even higher compression ratio can be achieved if the image is compressed by using first FFBA and then Huffman coding. The disadvantages of FFBA are that it is sensitive to sharp edges and no hardware is available. This paper also describes the design of the FFBA technique.

Angiography↗

NADH-methemoglobin reductase activity in the erythrocytes of newborn and adult mammals.

NADH-MR activity was measured in the erythrocytes of newborn and adult horses, pigs, cattle, sheep, goats, red kangaroos, fruit bats, rats, mice, rabbits and humans. Our results fail to support an earlier hypothesis that higher NADH-MR activity may be an adaptation to increased ruminal nitrite production leading to accelerated oxidation of fetal hemoglobin.

Aging↗

Compression of radiological images with 512, 1,024, and 2,048 matrices.

A comprehensive study was performed using the full-frame bit-allocation compression technique on 78 radiological images, including digitized radiographs, computed radiographs, and computed tomography images. Each radiograph was digitized to 2,048 X 2,048 X 10, 1,024 X 1,024 X 10, and 512 X 512 X 10 matrices, respectively, with a laser scanner. Five compression ratios were used to compress each image, and reconstructed images from each compressed data set were obtained. Altogether, the authors studied 842 images, including the original and compressed-reconstructed images and the images obtained from the difference between the original and the reconstructed images. The results indicate that acceptable compression ratios for 2,048, 1,024, and 512 matrices are 25:1, 20:1, and 10:1, respectively, based on a mean-square error of 0.02%.

Angiography↗

Characteristics of hepatitis B surface antigen produced in yeast.

We have constructed an expression plasmid for regulated expression of the hepatitis B surface antigen gene in yeast using promoter of the yeast Pho5 gene. In the yeast transformants, the monomeric HBsAg (22K dalton) was estimated to constitute approximately 3% of the total proteins. On extraction, the HBsAg was found to have a buoyant density of 1.18 g/ml and an Sw.20 value of 54. Electron microscopy revealed particles of heterogeneous size ranging from 18-28 nm. When the yeast HBsAg was used to immunize guinea pigs, the anti-HBsAg antibodies produced could react with human serum HBsAg.

Animals↗

Radiological image compression: full-frame bit-allocation technique.

A full-frame bit-allocation technique has been developed for radiological image compression based on encoding the cosine transform of the image. Six different types of diagnostic images were used to examine this technique, and the results have been encouraging. Reconstructed images from compressed-image data with compression ratios of 4:1, 8:1, 12:1, and 16:1 did not have excessive visual degradation. It is concluded that this technique is suitable for diagnostic image compression.

Computers↗

Vascular tumors produced by NIH/3T3 cells transfected with human AIDS Kaposi's sarcoma DNA.

Patients with the acquired immunodeficiency syndrome (AIDS) have a high incidence of Kaposi's sarcoma. The etiology, histogenesis, and neoplastic nature of this neoplasm have been controversial. We have therefore searched for transforming gene(s) associated with AIDS Kaposi's sarcoma. DNA from an AIDS patient's Kaposi's sarcoma was transfected into NIH 3T3 cells. Control DNA was derived from human fibroblasts or salmon sperm. Kaposi's sarcoma DNA, but not the control DNA, transforms NIH/3T3 cells with a frequency of approximately 0.02 foci per 5 X 10(5) cells/micrograms DNA. The primary and secondary transfectants contain human repetitive DNA sequences. The transfected clones produced hemorrhagic angiosarcomatous neoplasms when implanted in nude mice. The histology of the nude mouse tumors is very similar to human Kaposi's sarcoma. The tumor produced by some transfectants is highly invasive and metastatic in nude mice. No significant homologues of rasN, rasH, rasK, v-sis, v-src and v-fes oncogenes (known to transform NIH/3T3 cells) were identified in the Kaposi's sarcoma DNA-transformed cells. Thus, AIDS Kaposi's sarcoma DNA may contain a distinct transforming gene(s).

Acquired Immunodeficiency Syndrome↗

Role of nonhemoglobin heme accumulation in the terminal differentiation of Friend erythroleukemia cells.

The differentiation of murine erythroleukemia cells (T3C12 Friend cells) on treatment with dimethyl sulfoxide (DMSO) has been correlated with an early and extended overproduction of heme. The cessation of cell replication and the development of nuclear condensation, changes which are associated with the terminal differentiation of these cells, occur when the level of heme rises 0.1 nmol/10(6) cells over that amount which can be complexed by globin protein. A significant fraction of the excess heme is localized in the nuclei of the DMSO-treated cells. The addition of exogenous hemin facilitates the onset of terminal differentiation in the DMSO-treated T3C12 cells, whereas only the induction of globin gene expression is observed in the absence of DMSO. To study the role of heme in erythroid differentiation, a Friend cell variant (R10) has been isolated whose synthesis and accumulation of heme in response to DMSO is deficient. This variant grows logarithmically in the presence of DMSO and fails to terminally differentiate. When exogenous hemin is added, the DMSO-treated R10 cells stop replicating. In the absence of DMSO, however, hemin-treated R10 cells continue to grow and express their globin genes without exhibiting other signs of terminal differentiation. The combined results support the conclusion that both the DMSO treatment and the accumulation of excess heme are required to bring about the terminal differentiation of Friend erythroleukemia cells. Preliminary evidence is presented which suggests that in addition to the induction of heme and globin synthesis, DMSO also induces a heme activation process which is required for differentiation. The possible relationship of this process to the terminal differentiation of erythroid cells is discussed.

Animals↗

Localization of globin gene replication in Friend Leukemia cells to a specific interval of the S phase.

Murine erythroblastic leukemia cells, infected with Friend leukemia virus, were grown and synchronized in suspension culture by a double-block procedure involving medium depletion and treatment with excess thymidine. Replicating cultures were then caused to synthesize DNA during the early, middle, or late third of the S period with bromodeoxyuridine as a precursor. The bromodeoxyuridine density-labeled DNA and normal DNA were isolated by sedimentation in a cesium chloride density gradient and analyzed for the level of globin-specific DNA by hybridization with radioactive cDNA of the globin messenger RNA. Globin genes were found to be replicated near the end of the middle third of the S phase. The incorporation of bromodeoxyuridine into DNA also resulted in a lowered induction of hemoglobin synthesis in dimethyl sulfoxide-treated cells. In this case, the sensitivity was correlated with the introduction of bromodeoxyuridine into DNA replicated in early S phase. The possibility that this fraction of DNA, which is low in globin gene content, carries genes regulating the erythroid differentiation or the expression of globin genes is discussed.

Animals↗

Control of globin gene expression by steroid hormones in differentiating Friend leukemia cells.

Low levels of dexamethasone and related glucocorticoid hormones suppress the expression of globin genes during the DMSO-induced differentiation of Friend leukemia cells. In this response, the glucocorticoids appear to act at both the transcriptional and post-transcriptional levels in that 10(-8) M dexamethasone prevents the accumulation of both globin mRNA and globin protein, whereas 10(-9) M dexamethasone allows the accumulation of normal levels of hybridizable globin mRNA but prevents the accumulation of globin protein. This suppressive action of dexamethasone is more effective with DMSO as the inducer of globin gene expression than with hemin as the inducer. In contrast to the situation with glucocorticoids, certain sex steroids (etiocholanolone, testosterone and estradiol) facilitate the expression of globin genes in DMSO-treated Friend leukemia cells. The modulation of globin gene expression by steroid hormones is achieved in DMSO-treated cells without altering the growth and morphological changes which characteristically attend the differentiation of these cells.

Cell Differentiation↗