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Biomedical subjects

Ann Chen

Publications and source records attributed to Ann Chen.

28 records · Page 2Linked to original sources
PubMed2004

Dual biological functions of an interleukin-1 receptor antagonist-interleukin-10 fusion protein and its suppressive effects on joint inflammation.

The aim of this study was to construct and purify a novel interleukin-1 receptor antagonist (IL-1ra)-interleukin-10 (IL-10) fusion protein and determine its biological function and anti-inflammatory effects. The isolated cDNAs of two inhibitory cytokines (IL-1ra, IL-10) were used to construct a cDNA for the IL-1ra-IL-10 fusion protein. The expressed recombinant cytokines and fusion product were purified and their biological properties analysed. The anti-IL-1 effect was evaluated by using a thymocyte-proliferation assay, and the IL-10 effect was investigated by the inhibition of interferon-gamma (IFN-gamma) production from splenocytes. The clinical response and histological analyses were studied in an adjuvant arthritic rat model. The fusion protein was 38 000 molecular weight in size. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting demonstrated that the purified protein was recognized by both IL-1ra and IL-10 antibodies. The fusion protein significantly inhibited IL-1-mediated thymocyte proliferation and concanavalin A (ConA)-primed IFN-gamma production from splenocytes. The fusion protein also suppressed joint swelling (paw circumference reduced from 5.0 +/- 0.2 to 4.1 +/- 0.1 cm; paw thickness approximately 2 mm in difference) and synovial inflammation in adjuvant arthritis of rats. Our investigations indicate that this fusion protein effectively suppresses inflammatory arthritis and may initiate a trend for future clinical application to target multiple molecules at the same time.

Animals↗
PubMed2004

Disappearing calvarium in Gorham disease: MR imaging characteristics with pathologic correlation.

Gorham disease is a rare condition characterized by intraosseous neoplastic proliferation of hemangiomatous tissue with progressive, massive osteolysis. We present a pathologically proved case of Gorham disease that involved the left parietal bone in a 23-year-old man. Imaging studies including conventional radiography of the skull, CT, MR imaging, and Technetium-99 m (Tc-99 m) scintigraphy demonstrated a large skull defect without associated soft tissue mass over the left parietal skull. Contrast enhancement and increased isotope uptake along the margin of the defect were shown at gadolinium-enhanced T1-weighted MR imaging and Tc-99 m methylene diphosphate (Tc-99 m MDP) bone scintigraphy. Pathologic study revealed intraosseous angiomatosis at the periphery of the osteolytic skull lesion.

Adult↗
PubMed2003

Propofol ameliorates liver dysfunction and inhibits aortic superoxide level in conscious rats with endotoxic shock.

Propofol, widely used as a sedative agent, is known to exert antioxidant and anti-inflammatory effects in vitro. We studied the effects of propofol on hemodynamics and the function of several organs in conscious rats with endotoxemia. Intravenous injection of rats with endotoxin (lipopolysaccharide) caused hypotension, vascular hyporeactivity and tachycardia as well as significant lung, liver and kidney damage. Hepatocellular damage caused by lipopolysaccharide for 6 h was significantly attenuated in the lipopolysaccharide+propofol group. Aortic superoxide anion (O(2)(radical)(-)) production, but not plasma nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) level, was also suppressed by propofol in lipopolysaccharide-injected rats. Light microscopy showed that propofol attenuated the marked infiltration of neutrophils in liver tissues from lipopolysaccharide-injected rats. Moreover, the survival rate of the lipopolysaccharide+propofol group at 16 h was significantly increased when compared with that of the lipopolysaccharide group (53% vs. 12%). These results suggest that inhibition of aortic O(2)(radical)(-) production and amelioration of liver dysfunction contribute to the beneficial effect of propofol in conscious rats with endotoxic shock.

Animals↗
PubMed2003

Necrotizing enterocolitis and gastrointestinal complications after indomethacin therapy and surgical ligation in premature infants with patent ductus arteriosus.

BACKGROUND: Indomethacin is the most frequently used pharmacological agent for closure of a patent ductus arteriosus (PDA) in premature infants. However, reports of complications, particularly, necrotizing enterocolitis (NEC) and isolated gastrointestinal perforation have generated concerns about the use of this medication. OBJECTIVES: A retrospective study to compare the incidence of NEC, NEC-related gastrointestinal complications and isolated gastrointestinal perforation among premature infants treated for a PDA with either, indomethacin alone (I), surgical ligation alone (L), or indomethacin followed by surgical ligation (I-L). METHODS: The medical records of 224 infants that underwent treatment, either pharmacological or surgical, for a PDA, confirmed by echocardiography, over a 4-year period (1995 to 1998) were analyzed. Treatment history and gastrointestinal complications were reviewed. RESULTS: Of the 224 infants, 108 (48.2%) were treated with I, 50 (22.3%) by L, 66 (29.5%) with I-L. The clinical characteristics of the three treatment groups were similar and no differences in the incidence of NEC were observed between groups. NEC occurred in 14 (13%) of the I group, seven (14%) of the L group, and eight (12%) of the I-L group. The rate of NEC related gastrointestinal complications and isolated gastrointestinal perforation were also similar among groups. CONCLUSION: In this large retrospective study, indomethacin treatment for a significant PDA in premature infants was not associated with a greater risk for NEC or NEC-related gastrointestinal complications than surgical ligation.

Birth Weight↗
PubMed2002

Biphasic effects of exogenous phospholipase D on vessel tone.

There exists functional significance for agonists stimulated phospholipase D (PLD) and exogenous PLD in different systems, but the functional importance of PLD on vessel tone is not clear. We studied the functional importance of PLD in whole animals and in isolated vessel preparation. In in vivo study, we demonstrated that intravenous injection of PLD at 10, 30, and 100 units to male Sprague-Dawley rats did not significantly alter the mean arterial blood pressure and heart rate in 30 minutes. However, in a denuded vessel preparation, PLD from 10(-3) units/ml to 10 units/ml induced vasoconstriction from 2.8 +/- 1.7 % to 30.5 +/- 1.7 % of maximal KCI contraction in calcium enriched physiological salt solution (PSS). This vasoconstrictive effects of PLD were significantly inhibited by omission of extracellular calcium from PSS or by pretreatment the vessels with nifedipine (10(-6) M). Pretreated the denuded vessels with a protein kinase C inhibitor, chelerythrine (10(-6) M), did not significantly alter the vasoconstrictive effects of PLD. These results indicate that calcium channel rather than protein kinase C activation is involved in PLD-induced vasoconstriction. In endothelium-intact vessels, application of PLD from 10(-4) units/ml to 10 units/ml induced endothelium dependent relaxation in vessels precontracted with phenylephrine (10(-6) M). This relaxation effects of PLD were inhibited by pretreatment of vessels with indomethacin (10(-5) M) or with N-nitro-L-arginine (L-NAME, 10(-4) M), suggesting prostaglandin and nitric oxide released by PLD stimulation. The biphasic effects of PLD on vessel tone are mediated by extracellular calcium and by endothelium-derived nitric oxide and prostaglandin.

Animals↗
PubMed2002

Evidence for the early involvement of interleukin 17 in human and experimental renal allograft rejection.

Inflammatory processes can stimulate renal epithelial cells to release cytokines, chemoattractants and matrix proteins into the interstitium, thus contributing to interstitial injury during acute allograft rejection. To test the role of interleukin 17 (IL-17) in this process, cultured human renal epithelial cells (hRECs) were first established and treated with or without human IL-17 (hIL-17) for 2, 4, 8 and 10 h in vitro. Significant elevations of IL-6 and IL-8 levels were noted in the supernatants in a dose-dependent and time-dependent manner, as also for IL-6 mRNA expression. Secondly, using a rat acute allograft rejection model, the correlation between IL-17 expression and histopathological changes was serially studied. The results demonstrated that increased expression of IL-17 protein on infiltrating mononuclear cells (MNCs) was detectable on day 2. This corresponds to the borderline change of acute rejection according to the Banff classification, and it increased progressively to day 5. Serial study of IL-6, IL-8 and IL-17 mRNA expression of the renal allograft confirmed IL-17 mRNA expression in the allograft early on post-transplant day 2, whereas IL-6 and IL-8 expression started on day 3. Thirdly, IL-17 expression was observed in human renal allograft and urinary sediment. IL-17 protein expression was found in human subclinical (borderline) rejection renal allograft biopsy tissue and none in biopsy tissue not showing any evidence of rejection. There was also a 100% detectable rate of IL-17 mRNA expression in the MNCs of urinary sediment of patients with subclinical borderline rejection. These results demonstrate that hRECs exposed to IL-17 can produce inflammatory mediators with the potential to stimulate early alloimmune responses, which may also serve to give warning of acute renal allograft rejection.

Analysis of Variance↗
PubMed2002

Pulmonary function changes and immunomodulation of Th 2 cytokine expression induced by aminophylline after sensitization and allergen challenge in brown Norway rats.

BACKGROUND AND OBJECTIVE: Evidence has shown that aminophylline has bronchoprotective, anti-inflammatory, and immunomodulatory effects. Our purpose was to evaluate the effect of different doses of aminophylline on the late-phase reaction, bronchial hyperresponsiveness (BHR) and T cell-related cytokine mRNA expression in brown Norway rats induced by ovalbumin (OA) sensitization. METHODS: Forty rats were equally divided into four groups. Groups I, II, and III animals were sensitized and subsequently provoked with OA. Aminophylline 25 mg/kg was given intraperitoneally to the group I animals and 5 mg/kg to group II animals. Group III animals received intraperitoneal normal saline. Group IV breathed aerosolized saline as a control. After OA provocation, the animals were anesthetized. Pulmonary function tests were performed at baseline and after varying doses of acetylcholine. Thereafter, bronchoalveolar lavage was performed and the lungs were examined histologically. Total RNA was extracted from lung tissue and reverse transcriptase-polymerase chain reaction was performed using primers for interleukin (IL)-2, IL-4, IL-5, IL-6, IL-10, interferon-gamma, inducible nitric oxide synthase, and beta-actin. RESULTS: Group III had worse pulmonary function tests, more severe BHR, and more severe lung inflammation, higher IL-4 and IL-10 cytokine levels in bronchoalveolar lavage fluid, and higher IL-4, IL-5, IL-6, IL-10, tumor necrosis factor-alpha and inducible nitric oxide synthase mRNA expression than the other three groups. Expression of IL-2 and interferon-gamma was significantly reduced in group III. CONCLUSIONS: Both low and high dose aminophylline are effective in preventing late-phase bronchoconstriction, BHR, and an inflammatory response. Aminopylline decreases T helper cell 2-related cytokine mRNA expression but increases T helper cell 1-related cytokines mRNA expression.

Allergens↗
PubMed2002

Oxidized cellulose (Surgicel) granuloma mimicking a primary ovarian tumor.

A 37-year-old woman presented with left lower quadrant pain and vaginal spotting 1 month after hysterectomy and right salpingo-oophorectomy, which were performed for hemoperitoneum related to a ruptured corpus luteum. An 8-cm left ovarian mass was removed that had a microcystic, mucoid sectioned surface. Histological examination revealed that the mass consisted of a massive foreign-body granulomatous reaction to oxidized cellulose (Surgicel). To our knowledge, this is only the second report of an ovarian Surgicel granuloma.

Adult↗
PubMedDate not supplied

Attenuation of mouse mesangial cell contractility by high glucose and mannitol: involvement of protein kinase C and focal adhesion kinase.

Hyperglycemia and mannitol activate protein kinase C (PKC) and induce mesangial cell hypocontractility that subsequently may modulate renal function. Since focal adhesion kinase (FAK) activation is known to be linked with PKC activity, FAK may also be involved in mesangial cell contraction. To facilitate our understanding of the PKC- and FAK-modulating mechanism, we developed an in vitro model of mouse mesangial cell hypocontractility induced by hyperglycemia or mannitol. Mouse mesangial cells (CRL-1927) were exposed to: normal D-glucose (group N), high D-glucose (group H), and control groups at the same osmolality as H plus L-glucose (group L) and mannitol (group M). Changes in the planar surface area of cells in response to 1 microM phorbol 12-myristate 13-acetate (PMA) were determined. Western blot analyses for PKC, phosphorylated (p)-PKC, tyrosine phosphorylation, FAK, and p-FAK were done on each of these four groups. The effects of mannitol in various doses on cell contraction and activation of PKC and FAK were also assayed. The planar surface areas of groups H and M both showed an attenuated change in response to PMA stimulation. Before PMA stimulation, the baseline PKC expression of groups H and M showed a higher expression of p-PKC alpha and delta than that seen in group N (p < 0.05). Results of tyrosine phosphorylation and immunoprecipitation showed that FAK may be involved in this contraction process. The total amount of FAK showed no significant difference among the four experimental groups; however, p-FAK was found to have significantly increased in group M (p < 0.05). The use of PKC and tyrosine kinase inhibitors reduced PMA-induced mesangial cell contraction in all four groups. Activation of PKC alpha, delta, and FAK with the resultant inhibition of mesangial cell contraction by mannitol was found to be dose-dependent. These results may provide a correlation between increased expression of several PKC isoforms and, in particular, increased phosphorylation levels of PKC alpha and delta and hypocontractility induced by high glucose and mannitol treatment. Furthermore, the mannitol-induced hypocontractility involving PKC and FAK occurred in a dose-dependent manner.

Animals↗