Biomedical subjects

Hua Xie

Publications and source records attributed to Hua Xie.

At least 37 records · Page 2Linked to original sources

PubMed2004

Modulation of tryptase secretion from human colon mast cells by histamine.

AIM: To investigate the ability of histamine to modulate tryptase release from human colon mast cells and the potential mechanisms. METHODS: Enzymatically dispersed cells from human colons were challenged with histamine, anti-IgE or calcium ionophore A23187 (CI), and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure. RESULTS: Histamine at concentrations from 1 ng/mL was able to induce a "bell" shape dose related release of tryptase from colon mast cells. The maximum release of tryptase was approximately 3.5 fold more than spontaneous release. As little as 10 ng/mL histamine showed a similar potency to 10 microg/mL anti-IgE in induction of tryptase release. Histamine induced release of tryptase initiated at 10 s when histamine (100 ng/mL) was added to cells, gradually increased thereafter, and completed at 5 min. Both pertussis toxin or metabolic inhibitors were able to inhibit histamine induced tryptase release. When histamine and anti-IgE were added to colon mast cells at the same time, the quantity of tryptase released was similar to that induced by anti-IgE alone. The similar results were observed with CI. However, when various concentrations of histamine were incubated with cells for 20 min before adding anti-IgE or CI, the quantity of tryptase released was similar to that was induced by histamine alone. CONCLUSION: Histamine is a potent activator of human colon mast cells, which represents a novel and pivotal self-amplification mechanism of mast cell degranulation.

Colectomy↗

PubMed2004

Activation of human colon mast cells through proteinase activated receptor-2.

AIM: To investigate the ability of agonists of PAR-2 to stimulate release of tryptase and histamine from human colon mast cells and the potential mechanisms. METHODS: Enzymatically dispersed cells from human colons were challenged with tc-LIGRLO, tc-OLRGIL, SLIGKV, VKGILS, trypsin, anti-IgE or calcium ionophore A23187, and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibre-based fluorometric assay. RESULTS: Both PAR-2 agonists tc-LIGRLO-NH2 and SLIGKV-NH2 were able to induce dose dependent release of tryptase and histamine from colon mast cells. More than 2.5 fold increase in both tryptase and histamine release was provoked by 100 micromol/mL tc-LIGRLO-NH2, in comparison with only 2.0 fold increase being stimulated by SLIGKV-NH2. The reverse peptides tc-OLRGIL-NH2 and VKGILS -NH2 at the concentrations tested had no effect on the release of these two mediators. The maximum tryptase release elicited by tc-LIGRLO-NH2 was similar to that induced by anti-IgE (10 microg/mL) or calcium ionophore (1 microg/mL), though the latter was a more potent stimulus for histamine release. Both histamine and tryptase release in response to tc-LIGRLO-NH2 were completed within 3 min. Trypsin at concentrations from 1.0 to 100 microg/mL was capable of provoking a dose dependent release of tryptase as well as histamine with a maximum of 16 ng/mL tryptase and 14 ng/mL histamine release being achieved. An approximately 80% and 70% inhibition of trypsin induced release of tryptase and histamine were observed with SBTI, respectively. Pretreatment of cells with metabolic inhibitors or pertussis toxin abolished the actions of tc-LIGRLO-NH2, SLIGKV-NH2 and trypsin. CONCLUSION: The agonists of PAR-2 and trypsin are potent secretagogues of human colon mast cells, which are likely to contribute to the development of inflammatory disorders in human gut.

Colectomy↗

PubMed2004

Inhibition of tryptase release from human colon mast cells by protease inhibitors.

AIM: To investigate the ability of protease inhibitors to modulate tryptase release from human colon mast cells. METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors, and tryptase release was determined. RESULTS: IgE dependent tryptase release from colon mast cells was inhibited by up to approximately 37%, 40% and 36.6% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2Me (ZIGPFM), N-tosyl-L-phenylalanyl-chloromethyl ketone (TPCK), and alpha1-antitrypsin, respectively. Similarly, the inhibitors of tryptase leupeptin, N-tosyl-L-lysine chloromethyl ketone (TLCK) and lactoferrin were also able to inhibit anti-IgE induced tryptase release by a maximum of 39.4%, 47.6% and 36.6%, respectively. The inhibitory actions of chymase inhibitors, but not tryptase inhibitors on colon mast cells were enhanced by preincubation of them with cells for 20 min before challenged with anti-IgE. At a concentration of 10 microg/mL, protamine was able to inhibit anti-IgE and calcium ionophore induced tryptase release. However, at 100 microg/mL, protamine elevated tryptase levels in supernatants. A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced tryptase release. The significant inhibition of calcium ionophore induced tryptase release was also observed with the inhibitors of tryptase and chymase examined. The inhibitors tested by themselves did not stimulate tryptase release from colon mast cells. CONCLUSION: It was demonstrated for the first time that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced tryptase release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man.

Colectomy↗

PubMed2004

Modulation of histamine release from human colon mast cells by protease inhibitors.

AIM: To investigate the ability of protease inhibitors to modulate histamine release from human colon mast cells. METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors, and histamine release was determined. RESULTS: IgE dependent histamine release from colon mast cells was inhibited by up to approximately 37%, 26% and 36.8% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2Me (ZIGPFM), N-Tosyl-L-phenylalanyl-chloromethyl ketone (TPCK), and alpha1-antitrypsin, respectively. Similarly, inhibitors of tryptase leupeptin, N-tosyl-L-lysine chloromethyl ketone (TLCK), lactoferrin and protamine were also able to inhibit anti-IgE induced histamine release by a maximum of some 48%, 37%, 40% and 34%, respectively. Preincubation of these inhibitors with cells for 20 min before challenged with anti-IgE had small effect on the inhibitory actions of these inhibitors on colon mast cells. A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced histamine release. The significant inhibition of calcium ionophore induced histamine release was also observed with the inhibitors of tryptase and chymase examined. Apart from leupeptin and protamine, the inhibitors tested by themselves did not stimulate colon mast cells. CONCLUSION: It was demonstrated that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced histamine release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man.

Colectomy↗

PubMed2004

Laser-assisted vascular end to end anastomosis of elastin heterograft to carotid artery with an albumin stent: a preliminary in vivo study.

BACKGROUND AND OBJECTIVES: Laser-assisted end to end vascular anastomosis of an elastin heterograft to native artery may prevent problems associated with currently available vascular synthetic grafts and conventional suture anastomosis. STUDY DESIGN/MATERIALS AND METHODS: A total of 21 anastomoses in the carotid arteries of 7 domestic swine were performed with an 800 nm laser and an albumin stent plus solder. There were 5 artery to artery and 16 elastin heterograft to native artery anastomoses. Operative parameters, vascular patency, and histology of the anastomoses were evaluated. RESULTS: Out of 21 anastomoses, 16 were patent for 3 hours. One artery to artery anastomosis was thrombosed and four elastin heterograft to artery anastomoses were excluded from the study due to heterograft burst. The average amount of applied energy was 212 J for artery to artery anastomosis and 273 J for elastin heterograft to native artery. Histology shows coagulative necrosis of the adventitia, hypereosinophilic contraction band in the media of native arteries and no changes in elastin heterografts. CONCLUSIONS: Laser-assisted vascular anastomosis (LAVA) of elastin heterograft to medium size vessel using an albumin stent is feasible. Chronic studies are warranted to determine long-term patency and histology of the LAVA.

Albumins↗

PubMed2004

Vascular intramural strain imaging using arterial pressure equalization.

Peripheral vascular strain imaging has limited strain dynamic range because arterial wall deformations only exhibit small strains under physiologic pressures. A noninvasive freehand ultrasound (US) scanning procedure was performed to apply external force, comparable to the force generated in measuring a subject's blood pressure, to achieve higher strains by equalizing the internal arterial baseline pressure. When the applied pressure matched the internal baseline diastolic pressure, intramural strain and strain rate increased by a factor of 10 over a cardiac cycle. Radial arterial strain was assessed within the vessel wall over the entire deformation procedure using a phase-sensitive 2-D speckle-tracking algorithm. The feasibility of this technique to assess vascular nonlinear elastic properties is demonstrated in an ex vivo experiment and further supported by in vivo measurements. With some uncertainty associated with the elastic properties of surrounding tissue, an elastic modulus reconstruction procedure was developed to estimate the nonlinear elastic properties of the vascular wall.

Adult↗

PubMed2004

Staging deep venous thrombosis using ultrasound elasticity imaging: animal model.

Deep venous thrombi undergo progressive hardening with age. However, the evolution rate remains poorly characterized by both invasive and noninvasive techniques. In a previous study (Emelianov et al. 2002), we demonstrated the potential of ultrasound elasticity imaging to noninvasively detect and age thrombus using a rat-based model. Knowing that thrombi harden over time is useful, but the value of the technique relies on whether the age of a thrombus can be predicted from strain estimates, and how accurate these predictions are. The objective of the present study is to answer these two questions. In the previous study, thrombus elasticity changes were monitored only on day 3, 6 and 9 after surgically induced formation of thrombosis in rat inferior vena cavas. In this study, ultrasound elasticity imaging was performed on two independent groups of rats (16 in total) starting from day 3 through day 10 with more temporal samples through the thrombus maturation process. For each rat, thrombus hardness was quantified at each scan interval by measures of normalized strains and reconstructed relative Young's moduli. In both groups, strain magnitudes exhibit progressive decrease as clots age. The relationship between the normalized strain and the clot age was developed from the first group and evaluated by the second group. Statistical analysis showed that the age estimation accuracy is within 0.8 day. If further research can successfully transfer the animal clot-hardening model to human patients, we believe that elasticity imaging will become a key component of venous compression ultrasound for effective diagnosis and treatment of deep venous thrombosis.

Animals↗

PubMed2004

Optimal dye concentration and irradiance for laser-assisted vascular anastomosis.

OBJECTIVE: This investigation was done in order to find optimal indocyanine green (ICG) concentration and energy irradiance in laser vascular welding. BACKGROUND DATA: Many studies have shown that laser tissue welding with albumin solder/ICG may be an effective technique in surgical reconstruction. However, there are few reports regarding optimal laser settings and concentrations of ICG within the albumin solder in laser-assisted vascular anastomosis. MATERIALS AND METHODS: Porcine carotid artery strips (n = 120) were welded in end-to-end by diode laser with 50% albumin solder of 0.01, 0.1, and 1.0 mM ICG at irradiance of 27.7, 56.7, and 76.9 W/cm(2), respectively. Temperature was measured by inserting thermocouples outside and inside the vessel. Tensile strength and histology were studied. RESULTS: Temperature and strength of the anastomosis significantly decreased (all p < 0.05) with increasing ICG concentration at 56.7 W/cm(2). Histological study showed minimal thermal injury limited to adventitia and no appreciable difference between all groups. CONCLUSIONS: ICG concentration within solder is the most important factor affecting both vascular temperature and tensile strength. The optimal balance between strength and minimal thermal injury may be achieved primarily at 56.7 W/cm(2) and 0.01 mM ICG.

Anastomosis, Surgical↗

PubMed2004

Laser-assisted end-to-end vascular anastomosis of elastin heterograft to carotid artery with an albumin stent in vivo.

BACKGROUND DATA: Laser-assisted end-to-end vascular anastomosis of an elastin heterograft to native artery may avoid the problems associated with currently available vascular synthetic grafts and conventional suture anastomosis. METHODS: A total of 21 anastomoses in the carotid arteries of seven domestic pigs were performed with an 800-nm laser and an albumin stent plus solder. There were five artery to artery and 16 elastin heterograft to native artery anastomoses. Operative parameters, vascular patency, and histology of the anastomoses were evaluated. RESULTS: Out of 21 anastomoses, 20 were patent at 3 h. The average amount of total energy used was 212 Joules in artery to artery anastomosis and 273 Joules in elastin heterograft to native artery. Histology shows coagulative necrosis of the adventitia, hypereosinophilic contraction band in the media in native artery, and no change in elastin heterografts. CONCLUSIONS: Laser-assisted vascular anastomosis of elastin heterograft to medium size vessel is possible. Albumin stent played an important role in strength of the anastomosis. Chronic studies are warranted to determine long-term patency and histology of the laser-assisted vascular anastomosis.

Albumins↗

PubMed2004

Feasibility of applying ultrasound strain imaging to detect renal transplant chronic allograft nephropathy.

Chronic renal transplantation fibrosis, often termed Chronic Allograft Nephropathy, may progress undetected. Since renal fibrosis may be accompanied by a change in measurable elastic tissue properties, ultrasound strain management may be useful in it detection. Ultrasound strain imaging was performed for two subjects with renal transplants; one with normal renal function and one with mild renal insufficiency and biopsy demonstrated fibrosis. Subjects underwent ultrasound examination with application of a controlled deformation using phase-sensitive, two-dimensional speckle tracking to evaluate internal tissue motion to measure tissue displacement and strain. Measurements over multiple beams for an equivalent deformational stress showed there was a threefold difference in renal cortical strain between the two subjects. These data suggest that ultrasound elasticity imaging may prove useful in measuring mechanical changes related to fibrosis with the transplant kidney.

Adult↗

PubMed2004

Porphyromonas gingivalis genes involved in fimA regulation.

Porphyromonas gingivalis is an important component of the complex plaque biofilm that is a direct precursor of periodontal disease. The major fimbriae are required for attachment to oral surfaces and are an important virulence factor. Fimbrillin (FimA) expression in P. gingivalis is inhibited by surface molecule of Streptococcus cristatus, an early colonizer of dental plaque. In this study, differential display PCR was used to identify P. gingivalis genes that are regulated in response to S. cristatus. Of several differentially expressed genes, pg2131 and pg2167 were upregulated by S. cristatus signaling molecules. A null mutant of pg2167 did not transcriptionally regulate fimA following exposure to S. cristatus. In fact, fimA transcription was enhanced in the pg2167 mutant, suggesting that pg2167 may act to repress fimA expression. In contrast, a mutation in pg2131 did not affect transcription of fimA in the presence of S. cristatus. However, production of fimbrillin was significantly diminished in the pg2131 mutant, implicating involvement in posttranscriptional regulation in fimbriation. These data suggest that P. gingivalis fimbriation is controlled by more than one regulation mechanism, involving both transcriptional and posttranscriptional processes.

Bacterial Proteins↗

PubMed2004

Development of SSR markers for the phylogenetic analysis of almond trees from China and the Mediterranean region.

Expressed sequence tag (EST) derived simple sequence repeats (SSRs, microsatellites) were screened and identified from 3863 almond and 10 185 peach EST sequences, and the spectra of SSRs in the non-redundant EST sequences were investigated after sequence assembly. One hundred seventy-eight (12.07%) almond SSRs and 497 (9.97%) peach SSRs were detected. The EST-SSR occurs every 4.97 kb in almond ESTs and 6.57 kb in peach, and SSRs with di- and trinucleotide repeat motifs are the most abundant in both almond and peach ESTs. Twenty one EST-SSRs were thereafter, developed and used together with 7 genomic SSRs, to study the genetic relationship among 36 almond (P. communis Fritsch.) cultivars from China and the Mediterranean area, as well as 8 accessions of other related species from the genus Prunus. Both EST-derived and genomic SSR markers showed high cross-species transferability in the genus. Out of the 112 polymorphic alleles detected in the 36 cultivated almonds, 28 are specific to Chinese cultivars and 25 to the others. The 44 accessions were clustered into 4 groups in the phylogenetic tree and the 36 almond cultivars formed two distinct subgroups, one containing only Chinese cultivars and one of unknown origin and the other only those originating from the Mediterranean area, indicating that Chinese almond cultivars have a distinct evolutionary history from the Mediterranean almond. Our preliminary results indicated that common almond was more closely related to peach (P. persica (L.) Batsch.) than to the four wild species of almond, (P. mongolica Maxim., P. ledebouriana Schleche, P. tangutica Batal., and P. triloba Lindl.). The implications of these SSR markers for evolutionary analysis and molecular mapping of Prunus species are discussed.

Alleles↗

PubMed2004

Inhibition of histamine release from human mast cells by natural chymase inhibitors.

AIM: To investigate the ability of natural chymase inhibitors to modulate histamine release from human mast cells. METHODS: Enzymatically dispersed cells from human lung, tonsil, and skin were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of the natural chymase inhibitors secretory leukocyte protease inhibitor (SLPI) and alpha(1)-antitrypsin, then histamine release was determined. RESULTS: IgE-dependent histamine release from lung, tonsil, and skin mast cells were inhibited by up to 70 %, 61 %, and 62 %, respectively following incubation with alpha(1)-antitrypsin (5000 nmol/L). SLPI 5000 nmol/L was also able to inhibit anti-IgE-dependent histamine released from lung, tonsil and skin mast cells by up to approximately 72 %, 67 %, and 58 %, respectively. While neither alpha(1)-antitrypsin nor SLPI by themselves altered histamine release from lung, tonsil and skin mast cells, they were able to inhibit calcium ionophore-induced histamine release from lung and tonsil mast cells. CONCLUSION: Both micro(1)-antitrypsin and SLPI could potently inhibit IgE-dependent and calcium ionophore- induced histamine release from dispersed human lung, tonsil, and skin mast cells in a concentration-dependent manner, which suggested that they were likely to play a protective role in mast cell associated diseases including allergy.

Antibodies, Anti-Idiotypic↗

PubMed2004

[Effect of tryptase inhibitors on histamine release from human colon mast cells].

AIM: To investigate the effect of tryptase inhibitors (TPIs) on histamine release from human colon mast cells. METHODS: Human mast cells were prepared by digestion of colon tissue and with collagenase and hyaluronidase, cultured with four kinds of TPIs, leupeptin, protamine, TLCK, and lactoferrin for 15 min at 37 degrees Celsius respectively. A glass fibre-based fluorometry assay was used to detect histamine in mast cell suspension. RESULTS: 200 mmol/L leupeptin and 100 mmol/L protamine were able to stimulate histamine release from colon mast cells, while TLCK and lactoferrin did not. All TPIs inhibited anti-IgE-induced histamine release in a concentration dependent manner, and the inhibitory rates were 48.7%, 36.7%, 40.2% and 34.1%, respectively. However preincubation of TPIs with mast cells for 20 min at 37 degrees Celsius before adding anti-IgE had little effect on anti-IgE induced histamine release. All TPIs were able to inhibit calcium ionophore (CI)-induced histamine release, and the maximum inhibition rate was between 25%-32%. Inhibition on histamine release by leupeptin and TLCK obviously enhanced when colon mast cells were preincubated with them for 20 min before adding CI. However, under the same condition, protamine failed to inhibit histamine release. CONCLUSION: We prove for the first time that TPIs inhibit anti-IgE-and CI-induced histamine release from human colon mast cells, suggesting that it is possible to treat inflammatory bowel disease or other mast cell-related diseases by using TPIs.

Cells, Cultured↗

PubMed2004

Modulation of tryptase and histamine release from human lung mast cells by protease inhibitors.

Inhibition of IgE dependent histamine release from human mast cells by protease inhibitors has been observed in skin, tonsil and synovial tissues. However, little is known about the actions of protease inhibitors on tryptase release from human lung mast cells. We therefore examined the ability of protease inhibitors to modulate tryptase and histamine release from human lung mast cells. IgE dependent tryptase release from dispersed lung mast cells was inhibited to a maximum of approximately 53.8% and 44.5% by N-a-tosyl-L-lysine chloromethyl ketone (TLCK) and N-p-Tosyl-L-phenylalanine chloromethyl ketone (TPCK), respectively. A similar degree of inhibition of calcium ionophore A23187 (CI) induced tryptase release was also observed with these two inhibitors. Preincubation of TLCK or TPCK with the mast cells at 37 degrees C for 20 minutes before addition of anti-IgE or CI did not improve their ability to inhibit anti-IgE and CI induced tryptase release. At a concentration of 10 microg/ml, protamine inhibited anti-IgE or CI induced tryptase release; but at 100 microg/ml, it increased anti-IgE and CI induced release of tryptase from lung mast cells. A concentration dependent inhibition of anti-IgE and CI induced release of histamine from lung mast cells was also observed with TLCK, TPCK and protamine. The maximum inhibition of anti-IgE induced histamine release was approximately 40.7%, 40.2% and 33.4% with TLCK, TPCK and protamine, respectively. At the concentrations tested, TLCK and TPCK by themselves did not stimulate tryptase and histamine release from lung mast cells. A specific inhibitor of aminopeptidase, amastatin, had no effect on anti-IgE induced tryptase and histamine release and was used as control. In conclusion, it was demonstrated that protease inhibitors are able to inhibit IgE dependent tryptase and histamine release from human lung mast cells, which suggested that they could be developed to a novel class of anti-inflammatory drugs to treat allergic conditions in man.

Female↗

PubMed2004

[Correlations between chymase activity, levels of tryptase, and eotaxin in the sputum of patients with chronic obstructive pulmonary disease and their clinical implications].

OBJECTIVE: To investigate the correlations between chymase activity, levels of tryptase, interleukin-8 (IL-8), eotaxin, neutrophil and eosinophil numbers in the sputum of elderly patients with chronic obstructive pulmonary disease (COPD) and their clinical implications. METHODS: A total of 73 elderly patients with COPD (21 severe, 21 moderate and 31 mild) were recruited into the study. IL-8 and eotaxin levels were detected with Sandwich enzyme-linked immunosorbent assay (ELISA) procedures and tryptase levels were measured with antibody against tryptase with Uni CAP system. Chymase activity was determined spectrophotometrically (410 nm) by the rate of hydrolysis of 0.7 mmol/L N-succinyl-L-Ala-L-Ala-L-Pro-L-Phe-p-nitroanilide (SAAPP) in NaCl 1.5 mol/L and Tris 0.3 mol/L The specific activity of chymase was expressed as mU/ml. Actions of protease inhibitors on chymase activities were also examined with enzyme assay. RESULTS: (1) At acute attack stage, the sputum levels of tryptase of patients with severe, moderate and mild COPD were 284.0, 215.0 and 59.5 ng/L, respectively. The sputum levels of tryptase in the severe and moderate patients were greater than that in mild patients (P <0.01). The tryptase levels in the sputum of all patients were significantly decreased following treatment( 151.0, 92.0, 3.3 ng/L respectively; P <0. 01). At acute attack stage, the sputum levels of IL-8 and eotaxin were 1 299. 8,454. 9,78.7 ng/L; 22.7, 15.1, 7.4 ng/L, respectively. Severe and moderate-patients were greater than that of patients at mild stages. At convalescent stage,the sputum levels of IL-8 and eotaxin were 1 037. 5,326.6, 67.9 ng/L; 7.9, 6.3, 6.8 ng/L, respectively. The IL-8 and eotaxin levels in the sputum of severe and moderate patients were significantly decreased following treatment (P < 0.01). (2) The specific chymase activities of severe and moderate patients were higher than mild patients. Native protease inhibitors alpha1-antitrypsin (alpha1-AT) and soy bean trypsin inhibitor (SBTI) inhibited 83% and 89% enzymatic chymase activity, respectively. (3) The numbers of neutrophils and eosinophils in sputum were increased in patients with COPD at the acute stage compared with the mild convalescent stage. At all remission stages, the elevated numbers of cells were significantly reduced. (4) At acute attack stage of patients with COPD, there were correlations between the sputum levels of tryptase, IL-8, eotaxin, neutrophils and eosinophils; and there were correlations between the sputum levels of tryptase, chymase and neutrophils. CONCLUSION: COPD is not merely a neutrophil associated disease, but mast cells, eosinophils and their released mediators also actively contribute to the pathogenesis of the disease.

Aged↗

PubMed2003

Liquid chromatography determination of 10-hydroxycamptothecin in human serum by a column-switching system containing a pre-column with restricted access media and its application to a clinical pharmacokinetic study.

A simple, rapid, sensitive column-switching HPLC method is described for the analysis of the 10-hydroxycamptothecin (HCPT) in human serum. A pre-column containing restricted access media (RAM) is used for the sample clean-up and trace enrichment and is combined with a C18 column for the final separation. The analytical time is 8 min. The HCPT is monitored with fluorescence detector, excitation and emission wavelengths being 385 and 539 nm, respectively. There is a linear response range of 1-1000 ng/ml with correlation coefficient of 0.998 while the limit of quantification is 0.1 ng/ml. The intra-day and inter-day variations are less than 5%. This analytic procedure has been applied to a pharmacokinetic study of HCPT in clinical patients and the pharmacokinetic parameters of one-compartment model are calculated.

Antineoplastic Agents, Phytogenic↗

PubMed2003

[Eosinophilic cystitis in children:a report of six cases and review of literature].

OBJECTIVE: Eosinophilic cystitis is a very rare tumor-like inflammatory disease especially in children. It can involve any portion of the bladder and interfere with its function. Here we present 6 pediatric cases and review the literature. METHODS: Six children, with mean age of 8.3 years, were referred to our clinic. Their major complaints included voiding urgency, frequency, dysuria, enuresis, intermittent hematuria and abdominal pain. Ultrasound, CT scan and voiding cystourethrogram (VCUG) showed diffuse thickening of bladder wall and a filling-defect lesion. They all suggested the possibility of bladder tumor. The final diagnosis of eosinophilic cystitis was made by cystoscopic tissue biopsy or open surgery. Patients underwent bladder autoaugmentation, mass resection or mere oral administration of corticosteroid and antibiotics respectively. RESULTS: 5 among 6 patients were followed up for 5 - 28 months. Their voiding complaints and image changes gradually disappeared. Up to now, there is no relapse. CONCLUSIONS: The clinical presentation of eosinophilic cystitis includes irritative voiding symptoms, hematuria and abdominal pain. Tumor-like changes could be found in the imagination examinations. A biopsy is mandatory to establish the diagnosis. Treatment in general varies from the removal of the antigenic stimulus, if identifiable, to administration of corticosteroid and antibiotics. When patients fail to respond to the medication treatment, the opening operation could be required.

Adolescent↗