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Biomedical subjects

X Qin

Publications and source records attributed to X Qin.

At least 73 records · Page 4Linked to original sources
PubMed1999

Intestinal synthesis and lymphatic secretion of apolipoprotein A-IV after cessation of duodenal fat infusion: mediation by bile.

We tested whether secretion of apolipoprotein (apo) A-IV depends upon intestinal triglyceride (TG) transport by comparing output kinetics of TG and apo A-IV during and after duodenal lipid infusion in lymph-fistula rats. Lipid infusion (triolein, 40 mumol/h, 8 h) produced increases in lymphatic TG and apo A-IV output. After 8 h, triolein infusate was replaced with glucose-saline; TG output returned to basal levels 4-5 h later. However, apo A-IV output continued at significantly elevated levels until 20 h after the start of the experiment. Bile diversion blocked this continued output of A-IV during the post-lipid period, and resulted in basal TG output that was 75% lower than in bile-intact rats. Return of bile or low-dose triolein infusion (5 mumol/h) into the intestine reversed these effects. There were no differences in hepatic synthesis or filtration of plasma A-IV into lymph between bile-intact and bile-diverted groups. Intestinal A-IV synthesis was elevated in both groups even during the post-lipid period. The results support the hypothesis that intestinal triglyceride transport drives apo A-IV secretion, and suggest the existence of a bile-dependent, post-translational mechanism for the control of lymphatic apo A-IV output.

Animals↗
PubMed1999

Large motor neuron involvement in Stiff-man syndrome: a qualitative and quantitative study.

Stiff-man syndrome (SMS) is characterized by fluctuating muscular rigidity and spasm. Recently, antibodies against glutamic acid decarboxylase (GAD), the enzyme catalyzing the synthesis of y-amino butyric acid (GABA), have been detected in SMS patients. An autoimmune mechanism against GAD was thus proposed for the suppression of GABAergic inhibitory interneurons, resulting in rigidity and spasm. We conducted quantitative investigations on the ventral horn of the spinal cord and its GAD immunoreactivity, post mortem, in a SMS patient and four controls. In the spinal cord of the SMS patient, we found a 70%, 33% and 27% reduction (P < 0.05) in the density of neurons with somal areas of 1000-1500 microm2, 500-1000 microm2, and 0-500 microm2, respectively. The density of neurons with a somal area greater than 1500 microm2 was not reduced, although some neurons in this class showed central chromatolytic changes. The affected muscles exhibited neurogenic atrophy. GAD-like immunoreactivity in the spinal gray matter was not significantly decreased. The density of Purkinje cells, known to contain high amounts of GAD, was not significantly reduced. While the co-occurrence of elevation of anti-GAD antibody in the serum and reduction in the density of small spinal neurons was confirmed, that of smaller alpha-motor neurons and gamma-motor neurons, the qualitative changes in larger alpha-motor neurons, and the preservation of spinal GAD-like immunoreactivity and non-spinal GAD-containing neurons suggest the involvement of factors other than autoimmune mechanisms through anti-GAD antibodies. More diverse mechanisms may be associated in the pathogenesis of SMS.

Cell Count↗
PubMed1999

Effect of lidocaine on improving cerebral protection provided by retrograde cerebral perfusion: a neuropathologic study.

OBJECTIVE: To determine whether lidocaine can improve the neuropathologic results in canine brains after retrograde cerebral perfusion (RCP). DESIGN: Randomized, blinded, experimental study. SETTING: University animal laboratory. PARTICIPANTS: Mongrel dogs. INTERVENTIONS: Fourteen mongrel dogs were placed on 120 minutes of hypothermic (20 degrees C) RCP. Following the RPC, they then resumed cardiopulmonary bypass and rewarming for 60 minutes. In the lidocaine group (n = 8), lidocaine was administered continuously; in the control group (n = 6), normal saline was administered. Cerebral perfusion fixation was performed at the end of the experiment. MEASUREMENTS AND MAIN RESULTS: The number of ischemic cells in 200 neurons was counted in the parietal cortex, CA1 sector of the hippocampus, CA3 sector of the hippocampus, ventral posterolateral nucleus of the thalamus, and Purkinje cells of the cerebellar cortex. Those in the parietal cortex, CA1 sector of the hippocampus, and ventral posterolateral nucleus of the thalamus were significantly less in the lidocaine group than in the control group (25.8+/-17.3 v 53.7+/-12.0; p < 0.01; 17.0+/-8.5 v 54.7+/-22.1; p < 0.01; and 16.9+/-17.8 v 49.7+/-28.4; p < 0.05, respectively). The total number of ischemic cells in the five examined regions was also significantly less in the lidocaine group than in the control group (89.5+/-19.4 v 219.5+/-45.5; p < 0.01). CONCLUSION: Continuous lidocaine significantly alleviated the ischemic neuropathologic injury after RCP and thus possibly improved cerebral protection.

Anesthetics, Local↗
PubMed1999

Reduced lung tumorigenesis in human methylguanine DNA--methyltransferase transgenic mice achieved by expression of transgene within the target cell.

Human methylguanine-DNA methyltransferase (MGMT) transgenic mice expressing high levels of O6-alkylguanine-DNA alkyltransferase (AGT) in lung were crossbred to A/J mice that are susceptible to pulmonary adenoma to study the impact of O6-methylguanine (O6mG)-DNA adduct repair on NNK-induced lung tumorigenesis. Expression of the chimeric human MGMT transgene in lung was identified by northern and western blot analysis, immunohistochemistry assay and enzymatic assay. AGT activity was 17.6 +/- 3.2 versus 1.2 +/- 0.4 fmol/microg DNA in lung of MGMT transgenic mice compared with non-transgenic mice. Immunohistochemical staining with anti-human AGT antibody showed that human AGT was expressed throughout the lung. However, some epithelial cells of bronchi and alveoli did not stain for human AGT, suggesting that the human MGMT transgene expression was heterogeneous. After 100 mg/kg NNK i.p. injection in MGMT transgenic mice, lung AGT activity remained much higher and levels of lung O6mG-DNA adducts in MGMT transgenic mice were lower than those of non-transgenic mice. In the tumorigenesis study, mice received 100 mg/kg NNK at 6 weeks of age and were killed 44 weeks later. Ten of 17 MGMT transgenic mice compared with 16 of 17 non-transgenic mice had lung tumors, P < 0.05. MGMT transgenic mice had lower multiplicity and smaller sized lung tumors than non-transgenic mice. Moreover, a reduction in the frequency of K-ras mutations in lung tumors was found in MGMT transgenic mice (6.7 versus 50% in non-transgenic mice). These results indicate that high levels of AGT expressed in mouse lung reduce lung tissue susceptibility to NNK-induced tumorigenesis due to increased repair capacity for O6mG, subsequently, decreased mutational activation of K-ras oncogene. Heterogeneity in the level of AGT expressed in different lung cell populations or other forms of carcinogenic DNA damage caused by NNK may explain the residual incidence of lung tumors in MGMT transgenic mice.

Adenoma↗
PubMed1999

Transgenic expression of human MGMT blocks the hypersensitivity of PMS2-deficient mice to low dose MNU thymic lymphomagenesis.

Mice deficient in the DNA mismatch repair (MMR) gene, PMS2, develop spontaneous thymic lymphomas and sarcomas. We have previously shown that PMS2(-/-) mice were hypersensitive to a single i.p. injection of 50 mg/kg of N-methyl-N-nitrosourea (MNU) for thymic lymphoma induction. We postulated that MNU sensitivity was due to formation of O(6)-methylguanine (O(6)-mG), which, if unrepaired by O(6)-alkylguanine DNA alkyltransferase (AGT), leads to apoptosis in MMR competent cells and O(6)-mG:T mismatches in MMR deficient cells. Tumor induction is less in MMR(+/+) mice because cells with residual DNA adducts die, whereas mutagenized cells survive in MMR(-/-) mice. Overexpression of AGT (encoded by the methylguanine DNA methyltransferase-MGMT-gene) is known to block MNU induced tumorigenesis in mice with functional MMR. To further determine the sensitivity of PMS2(-/-) mice to MNU and the protective effect of hAGT overexpression, a low dose of MNU (25 mg/kg) was studied in PMS2(-/-) mice and PMS2(-/-)/hMGMT(+) mice. No thymic lymphomas were found in MNU-treated PMS2(+/+) and PMS2(+/-) mice. At 1 year, 46% of the MNU-treated PMS2(-/-) mice developed thymic lymphoma, compared with an incidence of 25% in both untreated PMS2(-/-) mice and MNU treated PMS2(-/-)/hMGMT(+) mice. In addition, a significantly shorter latency in the onset of thymic lymphomas was seen in MNU-treated PMS2(-/-) mice. K-ras mutations were detected almost equally in the thymic lymphomas induced by MNU in both PMS2(-/-) and PMS2(-/-)/hMGMT(+) mice, but not in the spontaneous lymphomas. These data suggest that PMS(-/-) mice are hypersensitive to MNU, that there are different pathways responsible for spontaneous and MNU induced thymic lymphomas in PMS2(-/-) mice, and that overexpression of hMGMT protects the mice by blocking non-K-ras pathways.

Adenosine Triphosphatases↗
PubMed1999

Effects of recombinant insulin-like growth factor-binding protein-4 on bone formation parameters in mice.

Insulin-like growth factor (IGF)-binding protein-4 (IGFBP-4), one of the most abundant IGFBPs produced by bone cells, is a potent inhibitor of IGF actions in vitro. To evaluate the modulation of IGF actions on bone formation in vivo by IGFBP-4, we produced intact and fragment (50- to 100-fold reduced IGF affinity) forms of BP-4 and examined their local and systemic effects using biochemical markers. Local administration of IGF-I over the right parietal bone significantly increased bone extract alkaline phosphatase activity; this was completely blocked by an equimolar dose of intact IGFBP-4, but not IGFBP-4 fragment. A single sc administration of IGF-I (2 microg/g BW) significantly increased bone formation markers in both serum and skeletal extracts; surprisingly, so did intact IGFBP-4, but not fragment IGFBP-4. Subcutaneous administration of an equimolar dose of IGFBP-4 along with IGF-I did not significantly block the IGF-I effect. Administration of intact IGFBP-4 significantly increased the serum 50-kDa IGF pool and decreased the 150-kDa IGF pool without significantly changing total IGF-I. We postulate that the increase in the 50-kDa IGF pool might enhance IGFs bioavailability via a mechanism involving IGFBP-4-specific protease. This study demonstrates for the first time that a single local administration of IGFBP-4 inhibits IGF-I-induced increases in bone formation, whereas systemic administration of IGFBP-4 alone increases serum levels of bone formation markers.

Alkaline Phosphatase↗
PubMed1999

Studies on the role of human insulin-like growth factor-II (IGF-II)-dependent IGF binding protein (hIGFBP)-4 protease in human osteoblasts using protease-resistant IGFBP-4 analogs.

To characterize the insulin-like growth factor binding protein-4 (IGFBP-4) protease produced by human osteoblasts (hOBs), we localized and determined the role of the proteolytic domains in human IGFBP-4 (hIGFBP-4) in modulating IGF-II actions. N-terminal amino acid sequence and mass spectrometric analyses of the 6xHis-tagged IGFBP-4 proteolytic fragments revealed that Met135-Lys136 was the only cleavage site recognized by the IGF-II-dependent IGFBP-4 protease produced by hOBs. This cleavage site was confirmed by the finding that deletion of His121 to Pro141 blocked proteolysis. However, unexpectedly, deletion of Pro94 to Gln119 containing no cleavage site had no effect on IGF-II binding activity but blocked proteolysis. Addition of the synthetic peptide corresponding to this region at concentrations of 250 or 1000 molar excess failed to block IGFBP-4 proteolysis. These data suggest that residues 94-119 may be involved in maintaining the IGFBP-4 conformation required to expose the cleavage site rather than being involved in direct protease-substrate binding. To determine the physiological significance of the IGF-II-dependent IGFBP-4 protease, we compared the effect of the wild-type IGFBP-4 and the protease-resistant IGFBP-4 analogs in blocking IGF-II-induced cell proliferation in normal hOBs, which produce IGFBP-4 protease, and MG63 cells, which do not produce IGFBP-4 protease. It was found that protease-resistant IGFBP-4 analogs were more potent than the wild-type protein in inhibiting IGF-II-induced cell proliferation in hOBs but not in MG63 cells. These data suggest that IGFBP-4 proteolytic fragments are not biologically active and that IGFBP-4 protease plays an important role in regulating IGFBP-4 bioavailability and consequently the mitogenic activity of IGFs in hOBs.

Amino Acid Sequence↗
PubMed1999

[The clinical features of myocardial infarction in patients younger than 35 years and over 45 years of age].

OBJECTIVE: To investigate the clinical features and the characteristics of coronary angiography in young patients with myocardial infarction. METHODS: 27 patients younger than 35 years with myocardial infarction were studied with respect to their history, habit of smoking and drinking and body weight index. Comparison was made between the left ventricular ejection fraction with ultrasound method and X-ray heart/chest ratio in patients with or without thrombolytic therapy. Selective coronary angiography was performed in 23 of the 27 patients. RESULTS: All of the 27 patients were male. 81.5% of them had smoking index more than 100, 55.5% drinking index more than 150, 51.9% family history of hypertension and 72.2% low blood level of HDL cholesterol. Most of the cardiac accidents took place in the night and morning. 17.4% of the patients had angiographically normal coronary arteries and 30.0% mild stenosis (no significant stenosis). 39.1%, 8.7% and 4.4% of the patients had one-vessel, two-vessel and three- vessel disease respectively. The frequency of patients with left ventricular ejection fraction less than 0.5 was 6.0% in patients with thrombolytic therapy and 33.3% without. CONCLUSION: 47.8% of the patients younger than 35 years with myocardial infarction has no or no significant stenosis of the coronary arteries. Heavy smoking is the most important one of relative factors for young patients with myocardial infarction. Other factors include low blood level of HDL cholesterol, drinking index of more than 150 and family history of hypertension in order. Thrombolysis treatment helps to maintain ventricular performance.

Adult↗
PubMed1999

[Anaerobic infection and its rapid detection in surgical patients].

OBJECTIVE: To investigate anaerobic infection and its rapid detection in surgical patients. METHODS: 372 specimens were collected from surgical patients for anaerobe detection. To find a rapid detectable method, 110 specimens were collected for comparative studies by using indirect immunofluorescent antibody technique (IFA), enzyme labeled antibody technique (ELAT) and general cultural method (CM). RESULTS: The isolation rate of anaerobes was rather high in pyothorax (88.9%), abdominal abscess (86.7%), appendicitis (83.9%) and cerebral abscess (all five cases were positive). In burn wounds, the rate was about 23.6% especially in deep burn wounds. Among 212 strains detected, the predominant anaerobes were as follows B. melaninogenicus (28.8%), B. fragilis (25%), F. nucleatum (7.5%), C. perfringens (7.5%), and peptostreptococcus (5.7%); most of them (87.8%) were non-sporing anaerobes. Mixed infection with aerobes accounted for 64%. The survey of rapid detection was conducted in B. fragilis, B. melaninogenicus, C. perfringens, F. nucleatum and peptostreptococcus. The detectable rate was higher in IFA (79.1%) and ELAT (80.9%) than in CM (37.3%). CONCLUSION: IFA and ELAT might be rapid, specific, sensitive, and simple for detecting anaerobes.

Abdominal Abscess↗
PubMed1999

[Technique of enzyme digestion adding brushing for isolating bronchial epithelial cells].

This study improved the previous techniques of harvesting rabbit bronchial epithelial cells. With 0.05% of trypsin on the epithelial side of trachea and bronchus, a mild digestion was used before a brushing protocol. The cells were identified with immunocytochemistry and electron microscope, both the cell viability and the membrane integrity of cells were evaluated. A comparison analysis of this method with the simple mechanic brushing and the simple digestion method were done. The results showed that, with this method, cells in a high purity and high viability could be obtained and the recovered cell number could be enough for experiments. It can be concluded that the method is useful and effective for isolating bronchial epithelial cells especially for small animals.

Animals↗
PubMed1999

[Affection of epidermal growth factor on VIP secretion and VIPR expression in airway epithelial cells].

In order to confirm the essential role of vasoactive intestinal peptide(VIP) on protection of local airway epithelium and investigate the modulation of the protective effect of VIP, secretion of VIP and expression of VIP receptor(VIPR) were studied in bronchial epithelial cells(BEC), and alveolar macrophages (AM). The radioimmunoassay was used for determining VIP secretion and the radio-ligand affinity analysis for VIPR expression. The effect of epidermal growth factor(EGF) was observed. The results showed that: 1. Both BEC and AM secreted VIP basically without remarkable stimulus, and some vesicles with electron-dense core which usually exist specifically in neuropeptide secreting cells were found in plasma of BEC; 2. In a dose-dependent manner, EGF promoted BEC to secrete VIP(r = 0.84, P < 0.05), and it was found that VIP secretion from AM was also elevated in EGF pretreated group(P < 0.05); 3. EGF exhibited a dose-dependent up-regulatory effect on the expression of VIPR in BEC(r = 0.95, P < 0.01). These results indicate that VIP may play an essential role in the protection at local airway by autocrine or paracrine, and the protective effect can be modulated by growth factors.

Animals↗
PubMed1999

[The relationship between nasopharynx surface-active agents and otitis media effusion].

This experiment was done with a view to exploring the etiologic mechanism and new therapy of otitis media effusion (OME). The amount of lecithin, which is representative of the surfactants in the nasopharynx irrigation wash liquid, was determined by photometry in 40 cases OME and 40 normal controls. The results showed the surfactant of otitis media effusion (8.637 +/- 2.730 mg/L) was significantly lower than that of normal (39.212 +/- 2.437 mg/L) in the nasopharynx irrigation wash liquid (P < 0.01). The surfactant of child group of OME (8.062 +/- 2.925 mg/L) significantly lower than that of normal control(39.787 +/- 2.557 mg/L, P < 0.01). The surfactant of otitis media effusion in the nasopharynx irrigation wash liquid was not associated with the course of OME. These data suggest that the surfactant reduction in the nasopharynx could indirectly reflect the level of the surfactant in the eustachian tube and the middle ear and influence the eustachian tube function. Surfactant reduction may be one of the etiologic mechanisms of OME. Increasing the surfactant in the nasopharynx and eustachian tube could be beneficial to reducing the persistent otitis media effusion.

Adolescent↗
PubMed1999

[Measurement of surfactant in-irrigating fluid from the nasopharynx of patients with secretory otitis media].

OBJECTIVE: Dysfunction of the eustachian tube is believed to play a role in the pathogenesis of secretory otitis media (SOM). In the animal model, previous investigators have found that surfactant in the eustachian tube could decrease the eustachian tube opening pressure and improve eustachian tube functions. Because the nasopharynx is anatomically adjacent to the eustachian tube and the membrane of the nasopharynx continues to the middle ear via the eustachian tube, we hypothesized that the surfactant could also present in the nasopharynx and then designed the following experiment to confirm this hypothesis. METHODS: The concentrations of surfactants in the nasopharyngeal irrigating fluid were measured in normal control and SOM patients. RESULTS: (1) The surfactant from the SOM patients were significantly lower than that from the normal control (8.637 +/- 2.730) mg/L vs. (39.212 +/- 2.437) mg/L. (2) The concentration of surfactant from child SOM was also significantly lower than that of the normal control (8.062 +/- 2.925) mg/L vs. (39.787 +/- 2.557) mg/L. (3) The concentration of surfactant of SOM was not associated with the course of SOM. CONCLUSION: Surfactant reduction in the nasopharynx could indirectly reflect the level of the surfactant in the eustachian tube and the middle ear and influence the eustachian tube function. So surfactant reduction is one of the causative factors in SOM. The strategy of increasing surfactant in the nasopharynx and eustachian tube should be beneficial to reducing persistent secretory otitis media.

Adolescent↗
PubMed1998

Structure-function analysis of the human insulin-like growth factor binding protein-4.

To identify the molecular mechanism by which insulin-like growth factor binding protein-4 (IGFBP-4) exerts its inhibitory effects on insulin-like growth factor (IGF) actions, we localized and determined the role of the IGF binding domain in modulating IGF actions in human osteoblasts. Deletion analysis using IGFBP-4 expressed in bacteria revealed that the N-terminal sequence Leu72-Ser91 was essential for IGF binding. The C-terminal fragments (His121-Glu237 or Arg142-Glu237) did not bind to IGF but loss of these regions decreased IGF binding activity. Detailed deletion analysis identified the residues Cys205-Val214 as the motif to facilitate IGF binding. Mitogenic studies revealed that an IGFBP-4 mutant (His74 replaced by Pro74) and an N-terminal peptide (N terminus to Thr71) with little IGF binding activity failed to inhibit IGF-II-induced human osteoblast proliferation. An N-terminal peptide (N terminus to Asn182) with reduced IGF binding activity inhibited IGF action but with lower potency. In contrast, an IGFBP-4 mutant (His74 replaced with Ala74) exhibited similar IGF binding activity and potency in inhibiting the activity of IGF-II compared with the wild type. Therefore, the N-terminal sequence (Leu72-Ser91) and the C-terminal sequence (Cys205-Val214) are necessary to form the high affinity IGF binding domain, which is the major structural determinant of the IGFBP-4 function.

Amino Acid Sequence↗
PubMed1998

In rice, Oryzalin and abscisic acid differentially affect tubulin mRNA and protein levels.

The effect of the anti-microtubular drug Oryzalin (3,5-dinitro-N4,N4-dipropylsulfanilamide) on growth and elongation of rice (Oryza sativa L. cv. Arborio) roots and coleoptiles was investigated. At 100 nM, Oryzalin strongly reduced primary root elongation, caused loss of cell anisotropy and the disappearance of the cortical microtubule array. Under these conditions the amounts of alpha- and beta-tubulin protein, but not mRNA, were heavily reduced. Similar data were also obtained in coleoptile segments treated with different concentrations of Oryzalin. However, when coleoptile elongation was inhibited by cis-abscisic acid, remarkable decreases in alpha- and beta-tubulin accumulation were observed to occur at the mRNA level but not at the protein level. The transcriptional decreases could be reversed by re-addition of 3-indole acetic acid. Altogether, these data indicate that rice tubulin accumulation can be controlled at different levels, mRNA or protein, in response to Oryzalin or abscisic acid treatments.

Abscisic Acid↗
PubMed1998

Generation and testing of mutants of Enterococcus faecalis in a mouse peritonitis model.

A previously described mouse peritonitis model was used to study derivatives of Enterococcus faecalis strain OG1RF. The addition of sterile rat fecal extracts (SRFE) lowered the LD50 of OG1RF >10-fold. Hemolysin production caused a 35-fold lower LD50 and a much shorter survival, similar to previous results using a peritonitis model without SRFE. A purine (but not a pyrimidine) auxotroph was considerably less lethal than wild type; gelatinase mutants were also attenuated. A suicide vector was generated with an enterococcal selectable marker in order to disrupt a gene encoding an E. faecalis antigen; the resulting mutant was not attenuated despite a slower growth rate. In conclusion, this model allows attenuated mutants to be detected, corroborates prior reports that hemolysin is a virulence factor, and suggests a role for gelatinase in virulence of E. faecalis in mice; the attenuated purine auxotroph may provide a system for developing vectors for in vivo expression systems.

Animals↗
PubMed1998

Effect of disruption of a gene encoding an autolysin of Enterococcus faecalis OG1RF.

A mutant (TX5127) of Enterococcus faecalis OG1RF was generated by disruption mutagenesis of a previously described autolysin gene. TX5127 formed longer chains (2 to 10 cells per chain) than wild-type OG1RF (mainly single cells) during growth in broth even though it had a growth rate similar to that of the parental strain as measured by turbidity and cell count. Autolysin activity, as defined by the ability to lyse heat-killed Micrococcus lysodeikticus cells, was absent in TX5127, while this activity was easily detectable in OG1RF. However, disruption of this autolysin gene did not block the ability of TX5127 to hydrolyze E. faecalis cell walls compared to that of OG1RF. The autolysis rate of cells of TX5127 in 10 mM sodium phosphate buffer (pH 6.8) was slower than that of wild-type OG1RF. TX5127 also showed a decreased rate of lysis in the presence of penicillin, as measured by changes in the turbidity of the culture during 24 h of incubation at 37 degrees C and a slightly decreased effect of penicillin as measured by time-kill curves. The virulence of TX5127 was similar to that of OG1RF in the mouse peritonitis model, indicating that the autolysin of E. faecalis is not important for infection in this model.

Animals↗