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Biomedical subjects

B Qiu

Publications and source records attributed to B Qiu.

35 records · Page 2Linked to original sources
PubMed1999

[Amplification of phytoplasma 16S rDNA from banana bunchy top disease, RFLP and sequence analysis of 16S rDNA fragment].

Extract DNA from banana plants with banana bunchy top disease and amplify the phytoplasma 16S rDNA fragment by nested PCR. The classification of the phytoplasma established on the basis of 16S rDNA restriction patterns was examined by performing a sequence analysis of 16S rDNA fragment. The RFLP pattern, sequence data and phylogenic tree showed that this phytoplasma should belong to Group I(Phytoplasma asteri).

Base Sequence↗
PubMed1998

CGRP upregulation in dorsal root ganglia and ileal mucosa during Clostridium difficile toxin A-induced enteritis.

We have previously reported that pretreatment of rats with capsaicin (an agent that ablates sensory neurons) or CP-96345 (a substance P receptor antagonist) dramatically inhibits fluid secretion and intestinal inflammation in ileal loops exposed to Clostridium difficile toxin A. The aim of this study was to determine whether calcitonin gene-related peptide (CGRP), a neuropeptide also found in sensory afferent neurons, participates in the enterotoxic effects of toxin A. Administration of toxin A was also found to increase CGRP content in dorsal root ganglia and ileal mucosa 60 min after toxin exposure. Furthermore, immunohistochemical studies demonstrated increased neuronal staining for CGRP 2 h after toxin A treatment. Pretreatment of rats with CGRP-(8-37), a specific CGRP antagonist, before instillation of toxin A into ileal loops significantly inhibited toxin-mediated fluid secretion (by 48%), mannitol permeability (by 83%), and histological damage. We conclude that CGRP, like substance P, contributes to the secretory and inflammatory effects of toxin A via increased production of this peptide from intestinal nerves, including primary sensory afferent neurons.

Animals↗
PubMed1998

[Gamma knife treatment of meningiomas].

From October 1995 to July 1997, 52 cases of meningioma were treated with gamma knife radiosurgery. Twenty-eight cases were followed up by CT or MR. The follow-up period was from 2 to 22 months. Follow-up imaging evaluation showed tumor size shrinkage in 8 cases, central density decrease in 10 cases, no change in 8 cases and tumor volume increase in 2 cases. The actual 1-year tumor growth control rate was 92%. Radiation-induced edema was noted in 9 cases, including 7 cases of the nonbasal tumor and 2 cases of basal one. The indications and efficacy of gamma knife treatment of the meningioma were discussed. Our preliminary experience suggests that gamma knife is an effective and safe technique for carefully selected patients with meningiomas.

Adult↗
PubMed1998

[MRI observation on Arnold-Chiari I malformation].

Craniocerical junction of 42 patients with Arnold-Chiari I malformation (ACM-1) and 41 normal controls were studied. In addition to the decendent tonsil, all the components in the posterior cranial fossa including the 4th ventricle, oblongata medulla and the sinus confluence of patients with ACM- 1 were decended. Although the spinal foramen magnum anterior -posterior diameter was smaller but not statistically different from the control. The results suggest that the main pathology of ACM- 1 is the shallow and small posterior cranial fossa and the resulted organ decendent as a whole.

Adolescent↗
PubMed1997

Increased substance P responses in dorsal root ganglia and intestinal macrophages during Clostridium difficile toxin A enteritis in rats.

Previously we reported that pretreatment of rats with the substance P (SP) antagonist CP-96,345 inhibits the enterotoxic responses following administration of toxin A from Clostridium difficile into ileal loops, indicating that SP participates in the intestinal responses to this toxin. We now report that injection of toxin A into rat ileum causes a rapid increase in SP content in lumbar dorsal root ganglia (DRG) and mucosal scrapings 30-60 min after toxin A administration. Toxin A-mediated fluid secretion, mannitol permeability, and ileal histologic damage is significantly increased only after 2 hr. Toxin A also causes an increase in the abundance of SP mRNA in lumbar DRG and ileal mucosa as measured by reverse transcription-PCR. Lamina propria macrophages (LPMs) obtained from toxin A-injected loops release greater amounts of tumor necrosis factor alpha (TNFalpha) and SP as compared with LPMs isolated from buffer-injected loops (P < 0.01). Pretreatment of rats with the SP antagonist CP-96,345 inhibits toxin A-mediated TNFalpha release from isolated LPMs, whereas an inactive enantiomer (CP-96,344) of the SP antagonist has no effect. LPMs obtained from toxin A-injected ileal loops incubated in vitro with SP (10(-8) to 10(-9) M) show enhanced TNFalpha secretion, whereas LPMs isolated from buffer-injected loops do not respond to SP. In addition, LPMs obtained from toxin A-injected ileal loops incubated in vitro with CP-96,345 showed a diminished TNFalpha release. Our results indicate that activated LPMs secrete SP during toxin A enteritis that can lead to secretion of cytokines, suggesting an autocrine/paracrine regulation of cytokine secretion by SP from LPMs during intestinal inflammation.

Animals↗
PubMed1997

Effects of chronic nicotine ingestion on pressor response to Nomega-Nitro-L-arginine methyl ester and ex vivo concentration and relaxation response of aorta to L-arginine.

Effects of nitric oxide synthase inhibition on blood vessels were studied in nicotine-treated rats. Male Sprague-Dawley rats drank a nicotine solution with a concentration of 25 or 50 microg/ml for 15 days. The blood pressure and heart rate of chloralose-anaesthetized rats and isolated aortic strip contractions were measured. NomegaNitro-L-arginine methyl ester (L-NAME)-induced hypertension was significantly reduced after chronic nicotine treatment. The Emax of contractions of isolated aortic strips to noradrenaline were dose-dependently enhanced by nicotine and the potentiation was abolished by L-arginine. The relaxation of aortic strips to acetylcholine was significantly decreased in nicotine-treated rats, whereas L-arginine, but not D-arginine, reversed this action. Neither nicotine nor L-NAME affected the heart rate. The results show that chronic nicotine treatment reduced the pressor response of L-NAME.

Acetylcholine↗
PubMed1997

Electron microscopic perspectives of gill pathology induced by 1-naphthyl-N-methylcarbamate in the goldfish (Carassius auratus Linnaeus).

This experiment has clarified the ultrastructural pathology, by scanning (SEM) and transmission electron microscopy (TEM), induced by 1-naphthyl-N- methylcarbamate (carbaryl) in the gills of juvenile goldfish (Carassius auratus Linneaus). Carbaryl is a low toxicity pesticide commonly used in forestry and agriculture and for controlling aquatic weeds and crustacean predators of shellfish, and has been known to cause gill damage in fish and clams. A variety of cellular changes were observed after exposure of goldfish for 96 h to a sublethal dose of 10 mg carbaryl/l of water. SEM revealed secondary lamellar fusion, distortion, thinning, and mucus release. TEM responses included enlargement of subepithelial lymphatic spaces and mitochondrial disruption and distortion of the lamellar covering epithelium. Pillar cells became detached and chloride cells were vacuolated. Fish were able to withstand these changes in subacute experiments due to redundancy in gill surface area.

Animals↗
PubMed1997

[Therapy for intracranial lesions by gamma knife].

The authors summarized 281 patients with intracranial lesions treated by gamma knife (GK) during Sept. 1995-Sept. 1996. The patients included 170 males and 111 females with age ranging from 5 to 85 years (average of 49.9 years). Seventy-seven patients received a follow-up 3.3-12.5 months. The average of Karnofsky Performance Status was 70.8 in pre-operation and 83.9 in post-operation; the average of tumor volume was 17.1 cm3 in pre-operation and 13.6 cm3 in post-operation; the average of lesion diameter was 2.8 cm and 2.4 cm in pre- and post-operation. respectively. GK radiosurgery has achieved the goal to improve the quality of life and to prolong the life of those patients with malignant intracranial tumors.

Adolescent↗
PubMed1996

A neurotensin antagonist, SR 48692, inhibits colonic responses to immobilization stress in rats.

We previously reported that short-term immobilization stress of rats causes increased colonic mucin release, goblet cell depletion, prostaglandin E2 secretion, and colonic mast cell activation, as well as increased colonic motility. The purpose of this study was to investigate whether neurotensin (NT), a peptide expressed in both brain and digestive tract, participates in these responses. Rats were pretreated with SR 48692 (1 mg/kg, i.p.), an NT antagonist, 15 min before immobilization (30 min). The administration of the antagonist significantly inhibited stress-mediated secretion of colonic mucin, prostaglandin E2, and a product of rat mast cells, rat mast cell protease II (P < 0.05), but did not alter the increase in fecal pellet output caused by immobilization stress. Immobilization stress also resulted in a quantifiable decrease in the abundance of NT receptor mRNA in rat colon compared with that in colonic tissues from nonimmobilized rats as measured by densitometric analysis of in situ hybridization studies (P < 0.03). We conclude that the peptide NT is involved in colonic goblet cell release and mucosal mast cell activation after immobilization stress.

Animals↗
PubMed1996

Nitric oxide inhibits rat intestinal secretion by Clostridium difficile toxin A but not Vibrio cholerae enterotoxin.

BACKGROUND & AIMS: Intestinal inflammation is associated with increased synthesis of nitric oxide, whereas inhibition of NO synthase (NOS) reduces experimental chronic intestinal inflammation. The aim of this study was to test the effects of NO blockers and donors on acute intestinal inflammation induced by Clostridium difficile toxin A in rat ileum. METHODS: Rats received NOS inhibitors or NO donors before measurement of toxin-mediated ileal secretion and permeability changes. Mucosal mast cell and neutrophil activity were measured by release of rat mast cell protease II and myeloperoxidase activity, respectively. RESULTS: NOS inhibitors augmented but an NO donor inhibited toxin A-mediated ileal secretion and permeability when given before but not after toxin administration. Neither an NOS inhibitor nor an NO donor had any effect on cholera toxin-mediated secretion. Mast cell degranulation and neutrophil infiltration occurred after injection of toxin A or an NOS inhibitor, whereas the NO donor blocked both toxin A effects. CONCLUSIONS: NOS inhibitors augmented and an NO donor blocked the intestinal effects of toxin A but not of cholera toxin. NO protects against toxin A by inhibition of intestinal mast cells and neutrophils, which are activated by toxin A, but not by cholera toxin.

Acetylcysteine↗
PubMed1996

A receptor decoy inhibits the enterotoxic effects of Clostridium difficile toxin A in rat ileum.

BACKGROUND & AIMS: Clostridium difficile toxin A causes secretion and intestinal inflammation in rodents by binding to a specific trisaccharide Gal alpha 1-3Gal beta 1-4 GlcNAc on enterocyte receptors. The purpose of this study was to explore the ability of Synsorb 90 (Synsorb Biotech Inc., Calgary, Alberta, Canada), and inert support carrying this trisaccharide, to bind toxin A in vitro and to inhibit its enterotoxic effects in vivo. METHODS: Binding of [3H]toxin A to Synsorb 90, Synsorb 83 (beta-mannose attached), and Chromosorb P (inert support with no sugar attached) (Synsorb Biotech Inc.) was measured. The inhibitory effects of these compounds on toxin A-mediated fluid secretion, mannitol permeability, and histological damage were measured in ileal loops in vivo. RESULTS: Toxin A showed specific binding to Synsorb 90, bearing the specific trisaccharide that binds toxin A, but not to Synsorb 83 or to Chromosorb P. Pretreatment of rats with Synsorb 90 by gavage (200 mg/kg body wt), but no Synsorb 83 or Chromosorb P at the same doses, dramatically reduced toxin A-associated fluid secretion and permeability. CONCLUSIONS: An immobilized toxin A receptor sequesters toxin A in the intestinal lumen and inhibits its effects of ileal mucosa. These results suggest a potential use for this agent in treating patients with C. difficile colitis.

Animals↗
PubMed1996

Acute stress causes mucin release from rat colon: role of corticotropin releasing factor and mast cells.

We determined the effects of immobilization stress on rat colonic mucus release and mast cell degranulation and examined whether corticotropin releasing factor (CRF) was involved in these responses. After 30-min immobilization, rats were killed, colonic mucosal explants were cultured, and levels of rat mast cell protease II (RMCP II) and prostaglandin E2 (PGE2) were measured. Mucin release from explants was assayed by incorporation of [3H]glucosamine into colonic mucin and by histological evaluation of goblet cell depletion. Stress caused significant increases of colonic RMCP II, PGE2, and mucin release and fecal pellet output and caused an approximately 10-fold increase in colonic mucosal levels of cyclooxygenase-2 (COX-2) mRNA. These stress-associated changes were reproduced by intravenous or intracerebral injection of CRF in conscious, nonstressed rats. Pretreatment of rats with the CRF antagonist alpha-helical-CRF9-41, hexamethonium, atropine, or bretylium, or the mast cell stabilizer lodoxamide inhibited stress-induced release of RMCP II, PGE2, and mucin, whereas indomethacin prevented mucin release but not mast cell degranulation. Hexamethonium and CP-96,345, a substance P antagonist, inhibited fecal pellet output caused by stress. We conclude that CRF released during immobilization stress increases colonic transit via a neuronal pathway and stimulates colonic mucin secretion via activation of neurons and mast cells.

Animals↗
PubMed1996

Treatment of cutaneous T cell lymphoma with low doses of interferon alpha-2b.

OBJECTIVE: To evaluate the optimal dose and route of interferon-alpha-2b (INF-alpha-2b) given to the Chinese patients with cutaneous T-cell lymphomas (CTCL). PATIENTS AND METHODS: Sixteen Chinese patients with CTCL treated with INF-alpha-2b were evaluated. They were divided into groups according to the TNM Classification: I B (8 patients), II A (2), II B (5) and IV B (1). During induction INF-alpha-2b was given intramuscularly every other day or two times a week, beginning with a dose of 1-3 x 10(6) IU. Depending on tolerance, the dosage could be increased weekly to a maximum tolerated dose of 18 x 10(6) IU (mean, 6 x 10(6) IU/week) with administration two or three times a week. Patients with clinical response were given maintenance dosage from the start. Thereafter the dosage was gradually decreased after disappearance of skin lesions. Three patients were treated by combining intramuscular and intralesional injection of INF. RESULTS: Six patients (I B, 2 patients: II A, 2, II B, 2) achieved complete response (CR). Seven patients (I B, 5 patients) showed partial response. The overall response rate in this group was 81.25%. The prominent initial clinical response in three patients was manifested early at one week after intramuscular treatment with INF and then the skin lesions were resistant to the therapy but disappeared rapidly by combining intralesional injection of INF. The conditions of those patients obtaining CR within 3 to 6 weeks were stable for 1-36 weeks. CONCLUSIONS: This study had demonstrated that the overall response rate in treatment of patients with CTCL was 81.25% and higher (85.7%-87.5%) in the subgroups at early stages I and II of the disease. The dosage (mean dose of 6 x 10(6) IU/week) adopted by us is optimal for the Chinese patients with CTCL. Intralesional injection of INF could be recommended.

Adult↗
PubMedDate not supplied

Reduction of colonic mucus by repeated short-term stress enhances experimental colitis in rats.

The role of stress in inflammatory bowel disease remains debated and few studies have tested the role of stress in conjunction with experimental animal models of colitis. In this investigation we tested the hypothesis that cold-restraint stress would adversely effect the severity of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats, and examined mechanisms for the response. Results indicated that increasing intermittent prior exposures to stress significantly enhanced TNBS-induced colitis severity. An associated stress-induced decrease in colonic mucin glycoprotein content, reduction in goblet cells, and histochemical mucin suggested reduced mucin was a pathogenetic factor. Myeloperoxidase content increased and mast cell counts in the colon decreased but colonic permeability only temporarily increased with increasing stress exposure. Prior adrenalectomy or administration of an adrenergic blocking agent did not prevent the colonic changes to stress, but mast cell stabilization or inhibition of cholinergic pathways reduced the stress-induced colonic changes.

Adrenalectomy↗
PubMedDate not supplied

Percutaneous optical imaging system to track reporter gene expression from vasculatures in vivo.

This study develops a percutaneous optical imaging system for tracking fluorescent reporter gene expression in vasculatures. We build a percutaneous optical imaging system that primarily comprised a 1.5-mm, semi-rigid, two-port optical probe. The performance of the optical probe is first tested in vitro with cell phantoms, and then the feasibility of the percutaneous optical imaging system is validated in vivo in eight femoral artery segments of two pigs. The green fluorescent protein (GFP) gene is locally delivered into four arterial segments, while saline is delivered to the four contralateral arterial segments as controls. The targeted arteries are localized using color Doppler, and thereafter the optical probe is positioned to the target arterial segments under ultrasound guidance. Optical imaging captures are obtained using different exposure times from 10 to 60 s. Subsequently, the GFP- and saline-targeted arteries are harvested for fluorescent microscopy confirmation. The percutaneous optical probe is successfully positioned at a distance approximately 2 mm from the targets in all eight arteries. The in-vivo imaging shows higher average signal intensity in GFP-treated arteries than in saline-treated arteries. This study demonstrates the potential using the percutaneous optical imaging system to monitor, in vivo, reporter gene expression from vasculatures.

Animals↗