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Biomedical subjects

W Cai

Publications and source records attributed to W Cai.

At least 109 records · Page 6Linked to original sources

[Comparitive study of three images examination in preoperative localization of parathyroid adenoma].

The ability to localize parathyroid adenoma with B ultrasound, CT scan and thal-lium-technetium scanning (TTS) was eraluated in 41 randomly selected patients with parathyroid adenoma proved pathologically from May, 1985 to May, 1993. The results indicated that the sensitivity was 92.86%, 73.91% and 33.3%; the specificity, 95.65%, 94.2% and 100%; and the accuracy, 95%, 89.1%, 83.3% in above three images examinations. Therefore, the predictable positive rates were 86.6%, 80.95 and 100%; the predictable nagative rates were 97.78%, 91.55%, 0%. There was no significant difference between B ultrasound and CT scan (P > 0.05) in the detection of the location of adenomas. We suggest that B ultrasound could be the first choice in the detection of the location of parathyroid adenoma before surgery, and the CT scan be applied for the unascertained patents who had B ultrasound exam, or surgical exploration, and those with suspected mediastinal adenoma.

Adenoma↗

[Relationship between the structure--modified N- and C- termini and the biological activity of TNF alpha molecule].

In order to elucidate the relationship between N-, C-termini of TNF alpha and it's biological activity, a TNF alpha derivative 10 (TNF alpha D10) was prepared by changing amino acid at the N-terminus positions Ser(4), Ser(5), Asp(10) and C-terminus position Leu(157) to N-terminus Cys(4), Thr(5), Arg(10) and C-terminus Phe(157) with PCR site-directed mutagenesis. The results showed that the expression level of this mutein has not altered but its cytotoxic activity increased. This might result from trimer formation of TNF alpha D10 by changing N-terminal Ser(4) residue to Cys. HPLC showed that the molecular weight of TNF alpha D10 was 17kD, 35kD, 55kD respectively. In addition, we also found that the stability of TNF alpha D10 was less than that of TNF alpha when to be stored at -20 degrees C for two months. It might be caused by changing Leu(157) to Phe(157).

Base Sequence↗

Effect of 3'-untranslated region on expression of TNF alpha cDNA in Escherichia coli.

A construct pRL-rhTNF alpha 2, in which the 110 bp 3'-untranslated region of rhTNF alpha cDNA was deleted, was transformed in E.coli. The expression level of several positive transformants was determined. The results showed that the expression of pRL-TNF alpha 2 was stable and the biological characteristics of the protein product were the same as that of pRL-rhTNF alpha. Furthermore, the expression level of pRL-rhTNF alpha 2 was increased. It is suggested that the 3'-untranslated region may have some effects on gene expression. A TA-rich sequence, TTTATTA, contained in the 3'-untranslated region of pRL-rhTNF alpha may be involved in the inhibitory effect on gene expression.

Base Sequence↗

A novel single-base mutation in the glucose 6-phosphate dehydrogenase gene is associated with chronic non-spherocytic haemolytic anaemia.

More than 80 variants of glucose-6-phosphate dehydrogenase (G6PD) are associated with chronic nonspherocytic haemolytic anaemia (CNSHA); however, the molecular basis of this association is not fully understood. We have used the polymerase chain reaction and nucleotide sequence analysis to characterize a new G6PD variant, which we designate as G6PD Bari, in a G6PD-deficient boy affected by CNSHA. A single mutation leading to an amino-acid substitution was detected in the G6PD coding region, viz. a C->T transition at position 1187 predicting leucine at residue 396 in the enzyme; proline is invariably present in evolutionary distant G6PD molecules at this position. Inheritance in the patient's family was demonstrated by the polymerase chain reaction followed by diagnostic restriction enzyme analysis. The C->T transition responsible for G6PD Bari maps close to several other mutations previously identified in G6PD variants associated with CNSHA.

Adolescent↗

The measurement of DNA content in Wilms' tumor and its clinical significance.

DNA content analysis with paraffin-embedded tissue was performed by flow cytometry on extracted nuclei from 42 Wilms' tumors. DNA histograms showed diploid in 13, tetraploid in 12, and aneuploid in 17. The frequency of DNA aneuploid was 40.48%. The 2- and 5-year survival rates were 84% and 75.16%, respectively, for patients with the DNA diploid pattern; the 2- and 5-year DNA aneuploid survival rates were 47.06% and 41.18% (P < .03 and P < .05), respectively. The 2- and 5-year survival rates for DNA tetraploid were in between, both 55.90%. For patients with stage I and II, the difference in the 2- and 5-year survival rates between DNA diploid plus tetraploid and DNA aneuploid was even more significant (P < .004 and P < .002, respectively). Thus, DNA aneuploid is an important indicator of poor prognosis in Wilms' tumor, especially for stages I and II.

Child↗

Cooperativity among herpes simplex virus type 1 immediate-early regulatory proteins: ICP4 and ICP27 affect the intracellular localization of ICP0.

The results of transient expression assays and studies of viral mutants have shown that three of the five immediate-early proteins of herpes simplex virus type 1 (HSV-1) perform regulatory functions, individually and cooperatively. As part of efforts designed to explore the molecular basis for the functional cooperativity among ICP0, ICP4, and ICP27 in the regulation of HSV gene expression, we have examined the intracellular localization of ICP0 in cells infected with ICP4 and ICP27 null mutant viruses by indirect immunofluorescence. Although ICP0 was localized predominantly to the nuclei of wild-type virus-infected cells, it was found exclusively in the nuclei of ICP27 mutant-infected cells and in both the cytoplasm and nuclei of ICP4 mutant-infected cells, the cytoplasmic component being especially strong. These observations indicate that both ICP4 and ICP27 can affect the intracellular localization of ICP0. Transient expression assays with plasmids that express wild-type and mutant forms of ICP0, ICP4, and ICP27 confirmed that ICP4 promotes and that ICP27 inhibits the nuclear localization of ICP0. These results confirm the observations made for mutant virus-infected cells and indicate that the localization pattern seen in infected cells can be established by these three immediate-early proteins exclusive of other viral proteins. The C-terminal half of ICP27 was shown to be required to achieve its inhibitory effect on the nuclear localization of ICP0. The region of ICP0 responsive to ICP27 was mapped to the C terminus of the molecule between amino acid residues 720 and 769. In addition, the concentration of ICP27 was shown to have a significant effect on the intracellular localization of ICP0. Because the major regulatory activities of ICP0, ICP4, and ICP27 are expressed in the nucleus, the ability of these three proteins collectively to determine their own localization patterns within cells adds a new dimension to the complex process of viral gene regulation in HSV.

Animals↗

[Studies on Clonorchiasis sinensis control in Sanshui City, Guangdong province].

During 1986 to 1988 and 1990 to 1992, Dongyong Township and Guanyuan Township in Sanshui City, Guangdong Province were selected as demonstration areas for clonorchiasis sinensis control by using measures of repeated examination and treatment respectively. After two years' examination and treatment, the population infection rates were from 43.6% to 13.2% in Dongyong Township and from 78.5% to 36.3% in Guanyuan Township. The first intermediate host was Alocimma longicornis, and the second intermediate hosts were Parabramis bransula and Ctenopharyngodon idellus. The adult worms of Clonorchis sinensis were found in the bile ducts of cats, dogs and pigs which may be the reservoir hosts.

China↗

Herpes simplex virus (HSV) glycoproteins B and K inhibit cell fusion induced by HSV syncytial mutants.

Herpes simplex virus type 1 (HSV-1) glycoproteins K and B (gK and gB) are intimately involved in virus-induced fusion of cells. Certain mutations in the UL27 (gB) and UL53 (gK) genes confer a syncytial (syn) phenotype characterized by extensive fusion of infected cells and giving rise to multinucleated cells. We have used HSV-1 syn mutants in conjunction with transfected cells or adenovirus vectors to overexpress wild-type gK or gB, in order to study the role of these proteins in virus-induced membrane fusion. Transient expression of wild-type gK inhibited fusion induced by HSV-1 encoding a mutant form of gK (syn gK) but not by viruses encoding a mutant form of gB (syn gB). Stably transformed cells expressing relatively high levels of gK suppressed cell fusion induced by HSV-1 mutants with lesions in the gK gene but not an HSV-1 with a syn mutation in the gB gene. In addition, there were marked reductions in the plaquing efficiencies and yields of HSV-1 on these cell lines. Cell fusion caused by HSV-1 syn20, a mutant encoding syn gK, was suppressed when cells were coinfected with an Ad vector, AdgK, which expresses wild-type gK. AdgK did not suppress fusion induced by HSV-1 KTTS.1, which expresses syn gB. Conversely, cells coinfected with AdgB, an Ad vector expressing a wild-type form of gB and HSV-1 KTTS.1 (syn gB) were not fused, whereas cells coinfected with AdgB and HSV-1 syn20 (syn gK) were fused. Expression of a number of other HSV-1 glycoproteins using Ad vectors did not reduce membrane fusion induced by syn gK or syn gB. Together, these results support models in which gK and gB participate directly in the fusion of HSV-infected cells. Mutant forms of gB and gK apparently disregulate the fusion process, whereas wild-type forms of gB and gK can act to suppress membrane fusion induced by their mutant counterparts.

Adenoviridae↗

The herpes simplex virus type 1 regulatory protein ICP0 enhances virus replication during acute infection and reactivation from latency.

ICP0 is a potent activator of herpes simplex virus type 1 gene expression in transient assays and in productive infection. A role for ICP0 in reactivation from latency in vivo has also been suggested on the basis of the observation that viruses with mutations in both copies of the diploid gene for ICP0 reactivate less efficiently than wild-type virus. Because the ICP0 gene is contained entirely within the coding sequences for the latency-associated transcripts (LATs), ICP0 mutants also contain mutations in LAT coding sequences. This overlap raises the question of whether mutations in ICP0 or the LATs, which have also been implicated in reactivation, are responsible for the reduced reactivation frequencies characteristic of ICP0 mutants. Two approaches were taken to examine more definitively the role of ICP0 in the establishment and reactivation of latency. First, a series of ICP0 nonsense, insertion, and deletion mutant viruses that exhibit graded levels of ICP0-specific transactivating activity were tested for parameters of the establishment and reactivation of latency in a mouse ocular model. Although these mutants are ICP0 LAT double mutants, all nonsense mutants induced the synthesis of near-wild-type levels of the 2-kb LAT, demonstrating that the nonsense linker did not disrupt the synthesis of this LAT species. All mutants replicated less efficiently than the wild-type virus in mouse eyes and ganglia during the acute phase of infection. The replication efficiencies of the mutants at these sites corresponded well with the ICP0 transactivating activities of individual mutant peptides in transient expression assays. All mutants exhibited reduced reactivation frequencies relative to those of wild-type virus, and reactivation frequencies, like replication efficiencies in eyes and ganglia, correlated well with the level of ICP0 transactivating activity exhibited by individual mutant peptides. The amount of DNA of the different mutants varied in latently infected ganglia, as demonstrated by polymerase chain reaction analysis. No correlation was evident between reactivation frequencies and the levels of viral DNA in latently infected ganglia. Thus, replication and reactivation efficiencies of ICP0 mutant viruses correlated well with the transactivating efficiency of the corresponding mutant peptides. In a second approach to examining the role of ICP0 in latency, a single copy of the wild-type gene for ICP0 was inserted into the genome of an ICP0- LAT- double mutant, 7134, which exhibits a marked impairment in its ability to replicate in the mouse eye and reactivate from latency.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗

Influence of medicinal herbs on phagocytosis by bovine neutrophils.

Twenty-six herbal preparations made from 24 medicinal herbs, categorized as antipyretics in Chinese materia medica, were tested in vitro to determine their effects upon phagocytosis of 32P-labelled Staphylococcus aureus by neutrophils isolated from bovine blood and milk. The percentage of phagocytosis was determined after incubating (1 hour at 37 degrees C) 1.25 x 10(7) neutrophils, 1 x 10(8) 32P-labelled S. aureus and 10% skimmed milk with herbal solutions. Concentrations of herbal preparations tested were 100%, 10% and 1% (v/v). When compared with PBSS (0.01 M phosphate buffered saline solution) controls, most of the herbs at high concentrations inhibited phagocytosis while at lower concentrations phagocytosis was increased. All 26 herbal preparations significantly increased blood neutrophil activity at their proper concentrations. The most active herbs in promoting blood neutrophil phagocytosis were observed for Herba verbenae, Flos chrysanthemi, Flos lonicerae, Radix sophorae flavescentis, Herba houttuyniae, Radix isatidis, Herba patriniae, Berberini sulfatis at the lowest concentration and for Folium hibisci at the high concentration with the increased percentage of more than 40.0% in comparison with PBSS control. Of the 19 herbal preparations tested with milk neutrophils, 18 herbs greatly increased phagocytosis at suitable concentrations. The most active preparations in stimulating milk neutrophil functions included Folium hibisci, Flos chrysanthemi, Radix bupleuri, Radix stellariae, Herba houttuyniae, Herba senecionis scandentis, Caulis lonicerae and Flos lonicerae which increased phagocytosis by over 35.0%.

Animals↗

Herpes simplex virus type 1 ICP0 regulates expression of immediate-early, early, and late genes in productively infected cells.

The herpes simplex virus type 1 protein, ICP0, can activate expression of all kinetic classes of viral promoters in transient expression assays. To examine the role of ICP0 in the regulation of viral gene expression during productive infection, we characterized the wild-type virus, an ICP0 null mutant (7134), and several ICP0 nonsense mutant viruses with regard to virus replication and protein synthesis in Vero cells. Relative to wild-type virus, 7134 was severely deficient in viral growth and protein synthesis at low multiplicities of infection but exhibited a nearly wild-type phenotype at high multiplicities. The phenotypes of the ICP0 nonsense mutants were intermediate between those of the wild-type virus and 7134 in that the more ICP0-coding sequence expressed by a given nonsense mutant, the more wild type-like was its phenotype. The location of the ICP0 domain responsible for transactivation during productive infection was confirmed to be within the N-terminal portion of the protein, as previously shown in transient expression assays. Immunoprecipitation and immunofluorescence tests were used to detect low-level expression of selected immediate-early (IE), early (E), and late (L) proteins by mutant and wild-type viruses following low-multiplicity infection. The 7134 deletion mutant and several nonsense mutants expressed markedly reduced levels of E and L proteins but wild-type levels of the IE protein, ICP4. Because the latency-associated transcripts (LATs) are specified by the strand opposite that which encodes ICP0, the ICP0 deletion and nonsense mutants are by definition ICP0-LAT double mutants. The ability of a LAT- ICP0+ mutant to replicate as efficiently as wild-type virus at low multiplicities and the ability of ICP0-expressing 0-28 cells to complement the defects of the mutants in E and L protein synthesis indicates that the phenotypes of the mutants are caused by mutations in ICP0 and not the LATs. Thus, we conclude that ICP0 up-regulates E and L but not necessarily IE gene expression during productive infection. The activation of IE gene expression by ICP0 during productive infection is likely overshadowed by the activity of the virion-associated protein, VP16. This hypothesis was tested by transfection of Vero cells with infectious mutant and wild-type viral DNAs. In such tests, no VP16 is present at early times posttransfection. Significantly fewer cells transfected with infectious 7134 DNA expressed ICP4 than cells transfected with KOS DNA. This reduction was fully reversed by cotransfection with an ICP0-expressing plasmid.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Acupuncture and the nervous system.

Acupuncture is based on neuroanatomy and neurophysiology. At each acupuncture point, there are peripheral nerves and terminals. Acupuncture will be useful for further understanding of the nervous system. A conceptual view of acupuncture's physiology is presented.

Acupuncture Analgesia↗