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Zhong Wen

Publications and source records attributed to Zhong Wen.

6 recordsLinked to original sources
PubMed2005

[Cat-scratch disease].

OBJECTIVE: To study the etiology, epidemiology, clinical and pathological features, diagnose and treatment of cat-scratch disease(CSD). METHOD: The clinical information of 1 case was reported and the literatures were also reviewed. RESULT: Bartonella henselae was the primary pathogen of CSD. Almost all patients with CSD were in contact with animals, especially cat or dog before the occurrence of the disease. All the patients had the self-limited swelling of local lymph nodes and commonly a fever. The pathological feature was necrotic granulation-like micro abscessation, and a pleomorphous argyrophil G- bacillus could be showed by Warthin-Starry or Brown-Hopp stainings in the swelling lymph nodes. CONCLUSION: CSD is a self-limited bacterial infectious disease. And its clinical features,biopsy and special stainings of swelling lymph nodes are helpful to the final diagnosis. Gentamicin, rifadin, ciprofloxacin, clarithromycin, bactrim, mitramycin, or resection of swelling lymph nodes had good effects on treating CSD.

Bartonella henselae↗
PubMed2002

Evidence for S-nitrosothiol-dependent changes in fibrinogen that do not involve transnitrosation or thiolation.

S-nitrosoglutathione (GSNO, 50 microM) inhibited the initial rate of thrombin-catalyzed human and bovine fibrinogen polymerization by approximately 50% to 68% respectively. Inhibition was also observed with other structurally varied S-nitrosothiols (RSNOs) including sugar derivatives of S-nitroso-N-acetylpenicillamine (SNAP). The fact that the same concentration of GSNO had no effect on thrombin-dependent hydrolysis of tosylglycylprolylarginine-4-nitroanilide acetate suggested that this inhibition was due to GSNO-induced changes in fibrinogen structure. This result was confirmed by CD spectroscopy where GSNO or S-nitrosohomocysteine increased the alpha-helical content of fibrinogen by approximately 15% and 11%, respectively. S-carboxymethylamido derivatives of glutathione or homocysteine had no effect on the fibrinogen secondary structure. The GSNO-dependent secondary structural effects were reversed on gel filtration chromatography, suggesting that the effects were allosteric. Further evidence for fibrinogen-GSNO interactions was obtained from GSNO-dependent quenching of the intrinsic fibrinogen Trp fluorescence and the perturbation of the GSNO circular dichroic absorbance as a function of [fibrinogen]. The K(d)s of 3 to 10 microM for fibrinogen-GSNO interactions with a stoichiometry of 2:1 (GSNO:fibrinogen) were estimated from isothermal titration calorimetry and fluorescence quenching, respectively. These results suggest that RSNOs induce changes to fibrinogen structure by interacting at specific aromatic rich domains. Three such putative RSNO-binding domains have been identified in the unordered, aromatic residue-rich C-termini of the alpha-chains of fibrinogen.

Amino Acid Sequence↗
PubMed2002

Novel substrates for nitric oxide synthases.

Enzymatic generation of nitric oxide (NO) by nitric oxide synthase (NOS) consists of two oxidation steps. The first step converts L-arginine to N(G)-hydroxy-L-arginine (NOHA), a key intermediate, and the second step converts NOHA to NO and L-citrulline. To fully probe the substrate specificity of the second enzymatic step, an extensive structural screening was carried out using a series of N-alkyl (and N-aryl) substituted-N'-hydroxyguanidines (1-14). Among the eleven N-alkyl-N'-hydroxyguanidines evaluated, N-n-propyl (2), N-iso-propyl (3), N-n-butyl (4), N-s-butyl (5), N-iso-butyl (6), N-pentyl (8) and N-iso-pentyl (9) derivatives were efficiently oxidized by the three isoenzymes of NOS (nNOS, iNOS and eNOS) to generate NO. N-Butyl-N'-hydroxyguanidine (4) was the best substrate for iNOS (K(m)=33 microM) and N-iso-propyl-N'-hydroxyguanidine (3) was the best substrate for nNOS (K(m)=56 microM). When the alkyl substituents were too small (such as ethyl 1) or too large (such as hexyl 10 and cyclohexyl 11), the activity decreased significantly. This suggests that the van der Waals interaction between the alkyl group and the hydrophobic cavity in the NOS active site contributes significantly to the relative reactivity of compounds 3-11. Moreover, five N-aryl-N'-hydroxyguanidines were found to be good substrates for iNOS, but not substrates for eNOS and nNOS. N-phenyl-N'-hydroxyguanidine was the best substrate among them (K(m)=243 microM). This work demonstrates that N-alkyl substituted hydroxyguanidine compounds are novel NOS substrates which 'short-circuit' the first oxidation step of NOS, and N-aryl substituted hydroxyguanidine compounds are isoform selective NOS substrate.

Animals↗
PubMed2002

[Telomere shortening in the pathogenesis of nasopharyngeal carcinoma].

OBJECTIVE: To explore the role of telomere shortening in the pathogenesis of nasopharyngeal carcinoma (NPC). METHODS: Southern blotting was employed to determine the mean telomere length (MTL) in 42 tumor samples and 15 samples of the tissues adjacent to the tumors obtained from 42 NPC patients, along with the tissue specimens from 17 patients with chronic nasopharyngitis. RESULTS: In NPC tissues, the length of the MTL was 4.5+/-2.3 kb, obviously shorter than those of the MTL in tissues adjacent to the tumor 14.6+/-2.8 kb and in chronic nasopharyngitis 15.8+/-3.1 kb. CONCLUSION: Telomere shortening may play an important role in the pathogenesis of nasopharyngeal epithelium cell malignancies.

Adult↗
PubMed2002

[Down-regulation of telomerase and its RNA and apoptosis in the HNE1 cell line of nasopharyngeal carcinoma induced by retinoid].

OBJECTIVE: To explore the down-regulation of telomerase as well as its RNA and apoptosis induced by retinoid acid. METHOD: After HNE1 cell lines of NPC were incubated with 10(-5) mol of retinoid in 6 days, the expression of telomerase and its RNA and the apoptosis of HNE1 cell lines were detected respectively with TRAP PCR ELISA, RT-nested PCR, apoptosis indexes and trans-electron microscope. RESULT: After 6 days when RA was added to the HNE1 cell line, the morphological change and suspending of HNE1 cells were found and the HNE1 cells reduced. Meanwhile, the expression of telomerase and hTR was obviously inhibited and the telomerase activity was only the 1/2 of the control with the use of ELISA indirect quantitative assay. Apoptosis indexes and apoptosis cells in RA groups were higher than those in control (P < 0.05). CONCLUSION: The expression of telomerase and hTR are obviously inhibited and the apoptosis of HNE1 cell lines is also induced by retinoid.

Apoptosis↗