PubMed Health⌕ Search

Biomedical subjects

H Fan

Publications and source records attributed to H Fan.

At least 127 records · Page 7Linked to original sources
PubMed1997

[A study on location of poles of terminal leads of ventricular fractionated potentials].

To eliminate the electromyogram-noise-signal from recording ventricular fractionated potentials (VFP) of the terminal leads(TLs), the multi-locations of leads were used to record ECG and VFP in 36 cases of controls and 68 cases of coronary heart disease. It was shown that the electromyogram-noise-signal could be minimized when TLs located separately at the point of infraclavicular cross lines axillaries media and the point of upperinguen cross lines axillaries media, and the essential formation of the ECG and VFP signals could not be changed except the QRS potentials becoming higher.

Arm↗
PubMed1997

[Effect of different Anti-G suits on lower limb blood flow].

To study effects of different Anti-G suits (AGS) and different inflation pressure on human cardiac system, changes in lower limb arterial blood flow (BF), heart rate and blood pressure in 5 male subjects with three bladder coverage AGS and a capstain AGS were observed and recorded until inflation pressure reached to its maximum. The percent of bladder coverage was about 30%, 65% and 90% of lower body for three bladder AGS. All AGS were inflated to maximum pressure in +1Gz seating position. The results showed that calf BF, could be blocked by bladder AGS, and the relationship between the mean pressure for BF block and the percentage of bladder coverage was y = 29.66 - 16.35x. (P < 0.0001, r = -0.9229). While the thigh and calf BF was not blocked in subjects with the capsule AGS. The results indicate that the effect of "the higher bladder coverage AGS + lower IP" is probably equal to that of "the lower bladder coverage AGS + higher IP" in holding calf BF.

Aerospace Medicine↗
PubMed1997

[The development of a microcomputerized fetal electrocardiograph].

A new microcomputerized Fetal Electrocardiograph (FECG) is presented in this paper. A two-grade configuration (front-end & back-end) is designed for the instrument. The front-end processor is based on a Digital Signal Processor (DSP) TMS32010 and the Adaptive Noise Cancelling (ANC) algorithm to extract FECG with non-invasive method. The processed results are sent to the back-end personal computer for real time display, analysis and record. Clinical tests show the instrument is designed smartly and operated easily, and can be applied widely to many medical situations.

Electrocardiography↗
PubMed1996

Ribonucleotide reductase R2 component is a novel malignancy determinant that cooperates with activated oncogenes to determine transformation and malignant potential.

Ribonucleotide reductase is a highly regulated cell cycle-controlled activity that is essential for DNA synthesis and repair. A retroviral vector for the R2 component of mammalian ribonucleotide reductase, the rate-limiting protein for enzyme activity and DNA synthesis in proliferating cells, was constructed and introduced into mammalian cells. Expression of Myc epitope-tagged R2 protein in benign BALB/c 3T3 and NIH 3T3 cells leads to a greatly increased frequency of focus formation in cooperation with H-ras transformation. Four lines of H-ras-transformed mouse 10T1/2 fibroblasts showed increased growth efficiency in soft agar after infection with the recombinant R2 expression virus vector. Furthermore, cells with altered R2 expression also exhibited significantly reduced subcutaneous tumor latency and increased tumor growth rates in syngeneic mice, and showed markedly elevated metastatic potential in lung metastasis assays. The results indicate that altered R2 gene expression cooperates with ras in mechanisms of malignant progression. A major Ras pathway involves the Raf-1 protein, which is recruited to the plasma membrane for activation. We show that recombinant R2 expression leads to significant increases in membrane-associated Raf-1 protein and mitogenactivating protein kinase-2 activity suggesting a mechanism for the observed Ras/R2 synergism. In support of this finding, we observed that activated Rac-1, which operates parallel to Raf-1 and cooperates with Raf-1 in Ras activated pathways, also cooperates with R2 in cellular transformation. These studies demonstrate that the R2 protein can participate in other critical cellular functions in addition to ribonucleotide reduction, and that deregulated R2 is a novel tumor progressor determinant that cooperates in oncogene-mediated mechanisms, which control malignant potential.

3T3 Cells↗
PubMed1996

Suppression of malignancy by the 3' untranslated regions of ribonucleotide reductase R1 and R2 messenger RNAs.

Mammalian ribonucleotide reductase is rate limiting for the synthesis of DNA. The active enzyme is composed of two dissimilar components called R1 and R2, encoded by different genes. The 3' untranslated regions (3' UTRs) of R1 and R2 messages contain sequences that are important in regulating gene expression through changes in message stability. We have constructed expression plasmids containing the R1 or R2 mRNA 3' UTRs, and we show that transfection of these plasmids into highly malignant mouse 10 T1/2 cells significantly suppresses the tumorigenic properties of these cells in syngeneic mice when compared with cells transfected with the same plasmid lacking R1 or R2 3' UTR sequences or when compared with cells transfected with the same plasmid expressing a heterologous sequence as a control. Furthermore, cells expressing the R2 3' UTR exhibit significantly reduced potential to disseminate to the lungs of syngeneic animals in experimental metastasis assays. The tumor-suppressive effects of the mouse R1 and R2 3' UTRs were not confined to mouse cells, because human HeLa cells transfected with expression plasmids containing either RI or R2 3' UTRs were also significantly less tumorigenic in assays using BALB/c nu/nu mice. These studies demonstrate that the untranslated regions of ribonucleotide reductase mRNAs can function as modifiers of tumor cell development and for the more complex process of tumor dissemination. We propose that these malignancy-suppressive effects are mediated through RNA interactions with cellular components involved in growth regulation through mechanisms of posttranscriptional control of gene expression. In addition, these observations emphasize the enormous potential of untranslated RNA to act directly as modifiers of biological characteristics relevant to mechanisms of malignancy.

Animals↗
PubMed1996

Attachment of bacteria to model solid surfaces: oligo(ethylene glycol) surfaces inhibit bacterial attachment.

Bacterial cell attachment to the surfaces of self-assembled monolayers formed by the adsorption of omega-substituted alkanethiols on transparent gold films has been studied under defined bacterial culture and flow conditions. Phase contrast microscopy was used to quantify the attachment of two organisms, one of medical (Staphylococcus epidermidis) and one of marine (Deleya marina) importance. Self-assembled monolayers terminated with hexa(ethylene glycol), methyl, carboxylic acid and fluorocarbon groups were investigated. Over the range of experimental conditions, self-assembled monolayers formed from HS(CH2)11(OCH2CH2)6OH were found to be uniformly resistant to bacterial attachment, with a 99.7% reduction of attachment for both organisms when compared to the most fouled surface for each organism. On other surfaces, S. epidermidis and D. marina were shown to exhibit very different attachment responses to the wettability of the substratum. While the attachment of S. epidermidis correlated positively with surface hydrophilicity, D. marina showed a preference for hydrophobic surfaces. This study suggests that surfaces incorporating high densities of oligo(ethylene glycol) are good candidates for surfaces that interact minimally with bacteria.

Bacterial Adhesion↗
PubMed1996

Rapid isolation of endosomes from BHK cells: identification of DPP IV (CD26) in endosomes.

In plasma membrane glycoproteins the peripheral monosaccharides of the N-glycan side chains are degraded faster than the core oligosaccharides and the protein backbone. This intramolecular heterogeneous turnover is a typical characteristic of membrane glycoproteins and is termed remodeling or reprocessing. The mechanism of the reprocessing has been shown first for dipeptidyl peptidase IV (DPP IV, CD26). However, it is still a question in which subcellular compartment the enzyme machinery for the reprocessing is located. Since lysosomes could be excluded, it has been proposed that the responsible glycosidases are located at the plasma membrane, in endosomes, or in the trans-Golgi network. The present study is concerned with the possible role of endosomes in this process of reprocessing. We transfected nonpolarized BHK cells with rat DPP IV cDNA. By establishing a fast and efficient method to purify endosomes, we could identify for the first time significant amounts of DPP IV in endosomes and we suggest therefore that endosomes are closely related with the regulation of reprocessing of plasma membrane glycoproteins.

Animals↗
PubMed1996

A link between ferritin gene expression and ribonucleotide reductase R2 protein, as demonstrated by retroviral vector mediated stable expression of R2 cDNA.

We have constructed a retroviral expression vector for the mammalian ribonucleotide reductase R2 component. Stable infectants, which express a myc epitope tagged R2 protein from the vector cDNA were obtained and described for the first time. Cells containing the recombinant protein exhibited increased ribonucleotide reductase activity, and were resistant to the antitumour agent hydroxyurea, which targets the R2 component of ribonucleotide reductase. Furthermore, a direct link between ferritin gene expression and R2 protein was observed, since cells containing vector expressed recombinant R2 protein exhibited increased H-chain and L-chain ferritin gene expression.

3T3 Cells↗
PubMed1996

Differential spontaneous transformation in vitro of newly established mouse fibroblast lines carrying or lacking the viable yellow mutation (Avy) of the mouse agouti locus.

The pleiotropic effects of the viable yellow mutation (Avy), an allele of the mouse agouti coat-color locus, include increased susceptibility to spontaneous and chemically induced tumors that affect a wide variety of tissues. As a first step toward understanding the molecular basis of this phenomenon, we established permanent fibroblast-like cell lines from newborn Avy/a and control congenic a/a mice and compared their growth characteristics in vitro. From the VY/WffC3Hf/Nctr and YS/WffCH3f/Nctr-Avy inbre strains, each of which carries the Avy allele on a congenic background, 38 clonal Avy/a and 16 clonal a/a lines were established. Regardless of inbred strain, all Avy/a cell lines exhibited a significant degree of spontaneous transformation, as assessed by focus formation in monolayer culture, whereas none of the a/a cell lines formed foci in prolonged cultures. To test whether changes in dosage of the Avy- or a-bearing chromosomes were related to these events, we analyzed each cell line with a closely linked molecular probe from the Emv-15 locus, which in the VY strain detects a restriction fragment length variant (RFLV) informative for the Avy- and a-bearing chromosomes. Most of the transformed foci maintained heterozygosity for RFLVs detected by the probe, but two of the transformants lost the a-associated RFLV, and at least one of the transformants exhibited amplification of the Avy-associated RFLV. When the transformants were analyzed with 5' sequences derived from the recently cloned agouti gene, three of eight transformants lost the a-associated RFLV, and two of the transformants showed amplification of the Avy-associated RFLV. Reverse transcriptase-polymerase chain reaction assays indicated that agouti RNA was detected in Avy/a, not a/a cell lines. Surprisingly, some of the Avy/a transformants lacked agouti RNA. These results suggest that deregulated expression of the Avy allele is required for the initiation but not for the maintenance of transformation of the Avy/a cell cultures. These cell lines may provide an in vitro culture system for studying the effect of the agouti gene on tumorigenicity as well as to potentially study other pleiotropic phenotypes.

Agouti Signaling Protein↗
PubMed1996

Occurrence of silent RNA editing in chloroplasts: its species specificity and the influence of environmental and developmental conditions.

We have identified three new C-to-U RNA editing sites, one in atpF and two in atpA transcripts from tobacco chloroplasts. Two of them lead to amino acid substitutions to restore the conserved amino acid found in the corresponding genes of other plants. However, one editing site in the atpA transcript was found to take place partially at the third base of a serine codon (CUC_ to CUU_), thus not leading to an amino acid substitution. This is the first report of silent editing in chloroplasts. The extent of silent editing depends on plastid stage and light conditions, while editing as another site (found 4 nt upstream from the silent editing site) takes place constitutively even in non-photosynthetic cultured cells and bleached white seedlings grown in the presence of spectinomycin and streptomycin. In pea and spinach, despite a conservation in sequence, no editing at the site corresponding to the silent site in tobacco was found. This observation suggests that the silent editing detected in this study is species-specific.

Amino Acid Sequence↗
PubMed1996

Comparison of transformation by manganese sulfate and 5-azacytidine in Rat 6 cells overexpressing the c-myc oncogene.

Rat 6 cells are not transformed by treatment with the well-known carcinogens benzo[a]pyrene (BP) or N-methyl-N-nitro-N'-nitrosoguanidine (MNNG). Upon retroviral transduction of the mouse c-myc gene, Rat 6 cells showed mildly altered morphology and formed microcolonies in soft agar; furthermore, they could be transformed by BP and MNNG to form large colonies in agar (Hsiao et al. (1992) Mol. Carcinogenesis, 5, 140-154). In the current report, we tested the sensitivity of the c-myc-overexpressing cells (Rat 6/c-myc) to two additional chemicals: 5-azacytidine and MnSO4. These chemicals differ from the direct-acting mutagens tested previously. 5-Azacytidine, a potent DNA methylation inhibitor, induced growth of large colonies in soft agar cultures of Rat 6 or Rat 6/c-myc cells. On the other hand, MnSO4 only induced transformation in Rat 6/c-myc cells, but not the parental Rat 6 cells. Transformants induced by 5-azacytidine lost c-myc-induced apoptotic cell death, whereas MnSO4-induced transformants showed a higher degree of apoptosis than the parental Rat 6/c-myc cells. These results suggest that MnSO4 co-operates with overexpressed c-myc in inducing transformation, while 5-azacytidine transformation is independent of c-myc overexpression and may involve alterations in the regulation of apoptosis.

Animals↗
PubMed1996

Nonadherent cultures of human monocytes kill Mycobacterium smegmatis, but adherent cultures do not.

Human peripheral blood monocytes are permissive for the growth of Mycobacterium tuberculosis, but the fate of nonpathogenic Mycobacterium smegmatis in these cells is not known. Since M. smegmatis may be used as a host with which to express and screen for M. tuberculosis genes needed for survival in monocytes, we determined whether human peripheral blood monocytes could restrict the growth of Mycobacterium smegmatis. Adherent human peripheral blood monocytes were permissive for the growth of M. smegmatis, as measured by ex vivo [3H]uracil uptake. However, human peripheral blood monocytes which were cultured nonadherently in Teflon wells were able to restrict the growth of M. smegmatis while remaining permissive for the growth of M. tuberculosis H37Ra. The loss of viability of M. smegmatis in nonadherent cells was correlated with an increase in nonspacious phagocytic vacuoles. The killing of M. smegmatis was not blocked by NG-monomethyl-L-arginine, suggesting that it was not due to the production of reactive nitrogen intermediates. Incubation of the monocytes for 1 to 7 days before infection had no effect on the fate of M. smegmatis, suggesting that adherence versus nonadherence, and not differentiation, was the key determinant for the difference in functional ability. Nonadherent human peripheral blood monocytes may be a more appropriate model than adherent cells for the study of factors employed by bacterial to survive within monocytes and for selection screening of bacterial genes needed for intracellular survival.

Blood Bactericidal Activity↗
PubMed1996

[Pathological observation and immunohistochemistry study of Type I, III, IV collagen in mitral valve and cardiac interstitium of rheumatic disease].

OBJECTIVES: To examine the pathological base of mitral valve and cardiac interstitium of rheumatic disease, and to explore the relationship between Type I, and III, IV collagen in mitral and cardiac interstitium of rheumatic heart disease. METHODS: HE and ABC method special staining were used to observe the mitral valve and cardiac interstitium pathology in 26 case. RESULTS: Diffused collagen fibroplasia, hyaline and amyloid degeneration were noted and sometimes associated local necrosis and calcification in myocardial interstitium and in mitral valve. It was a significant pathologic characteristic of rheumatic heart disease. The localization of Type I, III and IV collagen in the valve and myocardiac tissues was studied by ABC method of immunohistochemistry. Significant fibroplasia of collagen Type I and III was found in the valve, cordae tendon and myocardial interstitium of rheumatic heart disease. The composition and secretion of collagen Type I and III were expressed not only in fibroblasts but also in myocardial cells. CONCLUSIONS: The pathologic foundation of valve and myocardial fibrosis is collagen fibroplasia. The degree of fibroplasia is related to the repeated reaction of chronic rheumatic inflammation.

Adult↗
PubMed1996

[Vaginal bleeding patterns and the regularity in use of Norplant].

OBJECTIVES: To understand vaginal bleeding patterns and the regularity in use of Norplant, and find out the main cause of termination that Norplant users can not bear. METHODS: A total of 306 menstrual diaries of Norplant users for 5 years were analyzed. The analysis of bleeding patterns was carried out by using the reference period approach and followed the guidelings published by WHO. RESULTS: The total number of vaginal bleeding days and the number of spotting days in the first reference periods were 36.6 days and 21.5 days, respectively. They were decreased obviously in the third reference period. The number of bleeding days was not obviously changed. The percentage of irregular bleeding was predominent in all of the bleeding patterns, 43.1%-57.6% usually. The percentage of prolonged bleeding was 13.4%-31.0%, secondly. The percentage of "normal" was only 33%. The number of bleeding days and the percentage of prolonged bleeding were more in bleeding termination group than in continuation group. The percentage of irregular bleeding was lower. CONCLUSIONS: During the initial stage of use of Norplant the total number of vaginal bleeding days was increased, but decreased obviously after 6 months. This change was influenced by the number of spotting days. Irregular bleeding and prolonged bleeding were main types of the disturbance of menstrual cycles after use of Norplant, The main cause of termination was prolonged bleeding.

Adult↗
PubMed1995

Binding sites of monoclonal antibodies and dihydropyridine receptor alpha 1 subunit cytoplasmic II-III loop on skeletal muscle triadin fusion peptides.

Triadin binds to the dihydropyridine receptor (DHPr) and the junction foot protein (JFP) in Western blot protein overlay experiments. Fusion peptides were synthesized using an expression system, pGSTag, which includes a protein kinase A phosphorylation site. Expressed peptides are DHPr664-799 encoding rabbit skeletal DHPr alpha1 subunit amino acids 664-799, triadin 1 (1-49), triadin 2 (68-389), triadin 2' (110-389), triadin 2a (68-278), triadin 2a1 (67-163), triadin 2a2 (165-240), triadin 2b (242-389), triadin 2b1 (242-299), triadin 3 (370-706), triadin 3a (370-562), triadin 3b (551-706), triadin 3b1 (551-672), and triadin 3b2 (673-706) (the numbers in parentheses correspond to the amino acid sequence of triadin). The triadin monoclonal antibodies, GE4.90 and AE8.91, bind to intact triadic vesicles as well as to vesicle fragments prepared after treatment with Triton X-100, indicating that they have cytoplasmic epitopes. MAb AE8.91 binds to triadin 2, 2', 2a, and 2a1, while mAb GE4.90 binds to triadin 3, 3b, and 3b2 indicating that residues 110-163 and the C-terminal 34 amino acids contain cytoplasmic domains. Radiolabeled DHPr664-799 binds to triadin in intact vesicles under nonreducing and reducing conditions. It binds to triadin fusion peptides, triadin 2, 2a, 3, 3b, and 3b1, but no to triadin 1 or triadin 3b2. The binding to triadin 2a is the most prominent. Direct binding between DHPr-644-799 and JFP was not seen. These experimental findings indicate that triadin contains an extensive cytoplasmic domain that binds to the domain of DHPr which is considered critical for signal transmission during skeletal muscle excitation-contraction sampling.

Amino Acid Sequence↗