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Biomedical subjects

M Poon

Publications and source records attributed to M Poon.

At least 19 recordsLinked to original sources
PubMed2004

Best evidence topic reports. Oral corticosteroids in acute urticaria.

A short cut review was carried out to establish whether the addition of oral corticosteroids to antihistamines leads to a more rapid resolution of urticaria. Thirty nine papers were found using the reported search, of which two presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these best papers are tabulated. A clinical bottom line is stated.

Acute Disease↗
PubMed2003

Hereditary diffuse leucoencephalopathy with spheroids.

Hereditary diffuse leucoencephalopathy with spheroids (HDLS) is a rare inherited progressive leucoencephalopathy characterised by giant neuroaxonal swellings (spheroids) within the CNS white matter. The case is reported of a 45 year old woman with a rapidly progressive fulminant illness course characterised by progressive cognitive decline with depressive features. A presumed dominant inheritance pattern was elicited. This report reviews the literature on HDLS and the relation of this disorder to other conditions with giant neuroaxonal swellings.

Atrophy↗
PubMed2001

Role for p27(Kip1) in Vascular Smooth Muscle Cell Migration.

BACKGROUND: Rapamycin is a potent inhibitor of smooth muscle cell (SMC) proliferation and migration. Rapamycin-mediated inhibition of SMC proliferation is associated with upregulation of the cyclin-dependent kinase inhibitor p27(Kip1). Previously, we showed that mixed embryonic fibroblasts obtained from p27(Kip1)(-/-) mice were relatively rapamycin-resistant, suggesting that p27(Kip1) plays an integral role in modulating the antiproliferative effects of rapamycin. We hypothesized that the antimigratory effect of rapamycin may also be mediated by p27(Kip1). METHODS AND RESULTS: Rapamycin (1 to 10 nmol/L) inhibited basic fibroblast growth factor-induced migration of wild-type (WT) but not p27(Kip1)(-/-) SMCs in a dose-dependent manner (P<0.05) in a modified Boyden chamber. The effects of rapamycin on aortic SMC explant migration were also studied with WT, p27(+/-), and p27(-/-) mice. Rapamycin 4 mg. kg(-1). d(-1) IP for 5 days inhibited SMC migration by 90% in the WT and p27(Kip1)(+/-) (P<0.05) but not p27(Kip1)(-/-) animals. CONCLUSIONS: Lack of p27(Kip1) reduces rapamycin-mediated inhibition of SMC migration. These novel findings suggest a role for p27(Kip1) in the signaling pathway(s) that regulates SMC migration.

ADP Ribose Transferases↗
PubMed2001

Dexamethasone inhibits macrophage accumulation after balloon arterial injury in cholesterol fed rabbits.

Macrophages play a critical role in the development and progression of atherosclerosis. This study was designed to examine the effect of the glucocorticoid, dexamethasone, (Dex), on macrophage accumulation after acute arterial injury. Twenty New Zealand white rabbits were fed a 2% cholesterol, 6% peanut oil, rabbit chow diet for one month prior to bilateral balloon dilatation of the femoral arteries. Ten rabbits received Dex (1 mg/kg, im.) the day before and then daily for 7 days after arterial injury; control rabbits received vehicle only. Seven days after injury, Dex treatment resulted in a 96% and 77% reduction (P < 0.002) in the mean number of macrophages accumulating in the intima and media, respectively. This effect was apparently not due to a reduction in the number of circulating monocytes or to the ability of monocytes from Dex treated animals to adhere to endothelium or migrate in response to a chemotactic signal, determined in vitro under static conditions. It was associated with a 61% reduction in monocyte chemoattractant protein-1 (MCP-1) antigen (P < 0.004) in the injured arterial wall (media+intima). Glucocorticoids may be useful in attenuating the inflammatory response and subsequent foam-cell accumulation after arterial injury.

Animals↗
PubMed2000

CC chemokine I-309 is the principal monocyte chemoattractant induced by apolipoprotein(a) in human vascular endothelial cells.

BACKGROUND: Lipoprotein(a) [Lp(a)] is a risk factor for atherosclerosis; however, the mechanisms are unclear. We previously reported that Lp(a) stimulated human vascular endothelial cells to produce monocyte chemotactic activity. The apolipoprotein(a) [apo(a)] portion of Lp(a) was the active moiety. METHODS AND RESULTS: We now describe the identification of the chemotactic activity as being due to the CC chemokine I-309. The carboxy-terminal domain of apo(a) containing 6 type-4 kringles (types 5 to 10), kringle V, and the protease domain was demonstrated to contain the I-309-inducing portion. Polyclonal and monoclonal anti-I-309 antibodies as well as an antibody against a portion of the extracellular domain of CCR8, the I-309 receptor, inhibited the increase in monocyte chemotactic activity induced by apo(a). I-309 antisense oligonucleotides also inhibited the induction of endothelial monocyte chemotactic activity by apo(a). I-309 mRNA was identified in human umbilical vein endothelial cells. Apo(a) induced an increase in I-309 protein in the endothelial cytoplasm and in the conditioned medium. Immunohistochemical studies have identified I-309 in endothelium, macrophages, and extracellular areas of human atherosclerotic plaques and have found that I-309 colocalized with apo(a). CONCLUSIONS: These data establish that I-309 is responsible for the monocyte chemotactic activity induced in human umbilical vein endothelial cells by Lp(a). The identification of the endothelial cell as a source for I-309 suggests that this chemokine may participate in vessel wall biology. Our data also suggest that I-309 may play a role in mediating the effects of Lp(a) in atherosclerosis.

Antibodies↗
PubMed2000

Radical retropubic prostatectomy: bladder neck preservation versus reconstruction.

PURPOSE: We compare bladder neck contracture, urinary continence and positive surgical margin rates after bladder neck preservation and excision with radical retropubic prostatectomy. MATERIALS AND METHODS: A retrospective analysis of clinical and pathological findings, and followup of 220 patients who underwent radical retropubic prostatectomy was performed. Patients were divided into 3 groups of bladder neck preservation (101), "tennis racket" reconstruction (63) and anterior bladder tube reconstruction (56). RESULTS: Mean followup was 19.7, 36.7 and 16.2 months, respectively, for bladder neck preservation, tennis racket reconstruction and anterior bladder tube reconstruction. Overall, bladder neck contracture occurred in 22 of 220 cases (10%), including 5 of 101 (5%) with bladder neck preservation, 7 of 63 (11%) with tennis racket reconstruction and 10 of 56 (18%) with anterior bladder tube reconstruction, which approached statistical significance (p = 0.061). Urinary continence was assessed by a third party telephone interview of 165 patients. Continence rates at 1 year were 93% for bladder neck preservation, 96% for tennis racket reconstruction and 97% for anterior bladder tube reconstruction, which was not statistically significant (p = 0.68). Positive margin rates were 27.4% with bladder neck preservation versus 30.5% with excision, which was not significantly different. CONCLUSIONS: There are no statistically significant differences in return of urinary continence, bladder neck contracture rates or positive margins between bladder neck preservation and excision.

Adult↗
PubMed1999

Testicular volume of boys after inguinal herniotomy: combined clinical and radiological follow-up.

A total of 173 boys aged 10 to 179 months with previous unilateral inguinal herniotomy were called back for follow-up. Clinical and ultrasound examinations of the scrotum were performed. The interval between operation and follow-up was 6 to 123 months (mean 31.68 months). One boy (0.58%) had a more than 50% and 10 (5.8%) had a more than 25% decrease in testicular volume on the operated side when compared with the non-operated side.

Adolescent↗
PubMed1999

Identification of a novel dexamethasone-sensitive RNA-destabilizing region on rat monocyte chemoattractant protein 1 mRNA.

Glucocorticoids are potent anti-inflammatory agents widely used in the treatment of human disease. We have previously shown that the inflammatory cytokine monocyte chemoattractant protein 1 (MCP-1) is regulated posttranscriptionally by glucocorticoids in arterial smooth muscle cells (SMC). To elucidate the mechanism mediating this effect, in vitro-transcribed radiolabeled MCP-1 mRNA was incubated with cytoplasmic extracts from SMC and analyzed by gel electrophoresis. Extracts from SMC treated with platelet-derived growth factor (PDGF) did not degrade the transcripts for up to 3 h. In contrast, extracts from cells treated with 1 microM dexamethasone (Dex) alone or in combination with PDGF degraded the probe with a half-life of approximately 15 min. Dex had maximal effect at concentrations above 0.01 microM and was effective on both rat and human MCP-1 transcripts. By deletion analysis, the Dex-sensitive region of the MCP-1 mRNA was localized to the initial 224 nucleotides (nt) at the 5' end and did not involve an AU-rich sequence in the 3' untranslated end. The 224-nt region conferred Dex sensitivity to heterologous mRNA. These studies provide new insights into the molecular mechanisms underlying the effect of glucocorticoids on gene expression.

Animals↗
PubMed1999

Trapidil inhibits monocyte chemoattractant protein-1 and macrophage accumulation after balloon arterial injury in rabbits.

Trapidil (triazolopyrimidine) is an antiplatelet agent that acts in part as a phosphodiesterase inhibitor and as a competitive inhibitor of the platelet-derived growth factor (PDGF) receptor. Trapidil has been shown to attenuate intimal hyperplasia in rat and hamster models of balloon arterial injury and to inhibit restenosis after percutaneous transluminal coronary angioplasty in several small clinical trials. Monocyte chemoattractant protein-1 (MCP-1) is a PDGF-inducible monocyte chemoattractant that is thought to play a particularly important role in recruiting monocyte/macrophages to sites of atherosclerosis and vessel injury. We hypothesized that, because of its ability to antagonize PDGF-mediated events, trapidil would inhibit the synthesis of MCP-1 and decrease macrophage accumulation in the injured arterial wall. Hypercholesterolemic rabbits were treated with trapidil (60 mg/kg/day subcutaneously) the day before and then daily for 6 days after balloon injury of the femoral artery; control rabbits received vehicle only. Trapidil resulted in a 75% reduction in MCP-1 expression and macrophage accumulation in the arterial wall 7 days after injury. This study suggests that trapidil has potent anti-inflammatory properties and that its activity in attenuating intimal hyperplasia may be in part attributed to its effects on macrophage accumulation.

Animals↗
PubMed1998

Noninvasive In vivo high-resolution magnetic resonance imaging of atherosclerotic lesions in genetically engineered mice.

BACKGROUND: The pathogenesis of atherosclerosis is currently being investigated in genetically engineered small animals. Methods to follow the time course of the developing pathology and/or the responses to therapy in vivo are limited. METHODS AND RESULTS: To address this problem, we developed a noninvasive MR microscopy technique to study in vivo atherosclerotic lesions (without a priori knowledge of the lesion location or lesion type) in live apolipoprotein E knockout (apoE-KO) mice. The spatial resolution was 0.0012 to 0.005 mm3. The lumen and wall of the abdominal aorta and iliac arteries were identified on all images in apoE-KO (n=8) and wild-type (n=5) mice on chow diet. Images obtained with MR were compared with corresponding cross-sectional histopathology (n=58). MR accurately determined wall area in comparison to histopathology (slope=1.0, r=0.86). In addition, atherosclerotic lesions were characterized in terms of lesion shape and type. Lesion type was graded by MR according to morphological appearance/severity and by histopathology according to the AHA classification. There was excellent agreement between MR and histopathology in grading of lesion shape and type (slope=0.97, r=0.91 for lesion shape; slope=0. 64, r=0.90 for lesion type). CONCLUSIONS: The combination of high-resolution MR microscopy and genetically engineered animals is a powerful tool to investigate serially and noninvasively the progression and regression of atherosclerotic lesions in an intact animal model and should greatly enhance basic studies of atherosclerotic disease.

Animals↗
PubMed1998

Platelet-derived growth factor-specific regulation of the JE promoter in rat aortic smooth muscle cells.

JE is a member of the family of "immediate early" genes induced by growth factors and cytokines. JE encodes a low molecular weight secretory glycoprotein analogous to the human monocyte chemoattractant protein, MCP-1. JE and MCP-1 proteins are thought to play an important role in inflammation and in the recruitment of monocyte/macrophages to the vessel wall during the development of atherosclerosis. We have previously reported that the induction of JE in rat aortic smooth muscle cells (SMC) was specific to platelet-derived growth factor (PDGF) and was not seen with other growth agonists. Using a luciferase reporter system and transient transfection assays of rat aortic SMC, we now report the identification of a region in the proximal rat JE promoter that is responsive to PDGF but not to other growth factors (angiotensin II and alpha-thrombin) or cytokines (interleukin 1-beta and tumor necrosis factor-alpha). The full response to PDGF (approximately 6-fold) requires the cooperative activity of two potentially novel cis-acting elements, at positions -146 to -128 and -84 to -59. While each element produces a different pattern in electrophoretic mobility shift assays, they appear to bind the same PDGF-responsive species. Further analysis of these regions should provide important insights into PDGF-specific responses in vascular SMC.

Angiotensin II↗
PubMed1998

Haemophilia B: database of point mutations and short additions and deletions--eighth edition.

The eighth edition of the haemophilia B database (http://www.umds.ac. uk/molgen/haemBdatabase.htm ) lists in an easily accessible form all known factor IX mutations due to small changes (base substitutions and short additions and/or deletions of <30 bp) identified in haemophilia B patients. The 1713 patient entries are ordered by the nucleotide number of their mutation. Where known, details are given on: factor IX activity, factor IX antigen in circulation, presence of inhibitor and origin of mutation. References to published mutations are given and the laboratories generating the data are indicated.

Computer Communication Networks↗
PubMed1998

Complications employing the holmium:YAG laser.

We report the operative and early postoperative complications and limitations in 133 patients treated with the holmium laser. Complications included urinary tract infection (N = 3), postoperative bradycardia (1), inverted T-waves (1), intractable flank pain (1), urinary retention (1), inability to access a lower-pole calix with a 365-microm fiber (9), stone migration (5), and termination of procedure because of poor visibility (2). No ureteral perforations or strictures occurred, and no complications were directly attributable to the laser. The holmium laser was capable of fragmenting all urinary calculi in this study. In our initial experience, the holmium laser is safe and effective in the treatment of urinary pathology. Use of laser fibers larger than 200 microm occasionally limits deflection of the endoscope into a lower-pole or dependent calix.

Adolescent↗
PubMed1997

Apolipoprotein(a) induces monocyte chemotactic activity in human vascular endothelial cells.

BACKGROUND: Elevated levels of lipoprotein(a) [Lp(a)] are associated with premature atherosclerosis; however, the mechanisms are not known. Recruitment of monocytes to the blood vessel wall is an early event in atherogenesis. METHODS AND RESULTS: This study has found that unoxidized Lp(a) induced human umbilical vein endothelial cells (HUVECs) to secrete monocyte chemotactic activity (MCA), whereas LDL under the same conditions did not. In the absence of HUVECs, Lp(a) had no direct MCA. Endotoxin was shown not to be responsible for the induction of MCA. Actinomycin D and cycloheximide inhibited the HUVEC response to Lp(a), indicating that protein and RNA synthesis were required. The apolipoprotein(a) [apo(a)] portion of Lp(a) was identified as the structural component of Lp(a) responsible for inducing MCA. Lp(a) and apo(a) also stimulated human coronary artery endothelial cells to produce MCA. Granulocyte-monocyte colony-stimulating factor (GM-CSF) antigen was not detected in the Lp(a)-conditioned medium, nor was monocyte chemoattractant protein-1 mRNA induced in HUVECs by Lp(a). CONCLUSIONS: These findings suggest that Lp(a) may be involved in the recruitment of monocytes to the vessel wall and provide a novel mechanism for the participation of Lp(a) in the atherogenic process.

Apolipoproteins↗
PubMed1997

Flexible endoscope deflectability: changes using a variety of working instruments and laser fibers.

To measure the effects of different working instruments and holmium laser fibers on the deflectability in a variety of actively deflectable flexible endoscopes, a benchtop study was performed. The endoscopes studied were the Storz 7.5 flexible ureteroscope, the AUR-7 and AUR-9 flexible ureteroscopes (Circon-ACMI), a prototype Mitsubishi flexible ureteroscope (Mitsubishi Optics, Inc.), the ACN flexible cystoscope (Circon-ACMI), and the Storz flexible cystoscope. Working instruments included 1.6F (Wolf) and 1.9F (Microvasive) electrohydraulic lithotripsy (EHL) probes, 1.9F two-prong graspers and Bagley baskets, 2.4F Segura and helical baskets (Microvasive), 3.0F Segura basket, and 200- and 365-micron holmium laser fibers (Xintec). In ureteroscopes, the effect of 1.6F and 1.9F EHL probes ranged from having no effect in the Xintec 6,000, to decreasing deflection by 30 degrees in the AUR-7. Working instruments that were 2.4F or greater reduced deflection from 33 degrees to 93 degrees. Better deflectability was noted with the 200-micron holmium laser fiber than with the 365-micron fiber. The diameter of the working instrument did not affect deflectability as severely in cystoscopes. No significant differences in deflection existed between the 365-micron and 200-micron fibers in the flexible nephroscopes tested. In general, working instruments less than 2.4F and the 200-micron laser fiber have little effect on deflectability compared with working instruments 2.4F or larger and the 365-micron fiber. Flexible cystoscopes, with their larger working channels and stronger deflection cables, are affected less by working instrument diameter than are flexible ureteroscopes.

Cystoscopes↗
PubMed1997

Apolipoprotein(a) is a human vascular endothelial cell agonist: studies on the induction in endothelial cells of monocyte chemotactic factor activity.

Elevated levels of lipoprotein(a), Lp(a), are associated with premature atherosclerosis; however, the mechanisms of its atherogenicity are not known. Recruitment of monocytes to the blood vessel wall is an early event in atherogenesis. Since Lp(a) is associated with macrophages in the plaque, we have examined the effect of Lp(a) on inducing monocyte chemotactic activity (MCA) in vascular endothelial cells. We report that Lp(a) and apo(a) induced human umbilical vein (HUVEC) and coronary artery endothelial cells to secrete monocyte chemotactic activity as early as 30 min of incubation. In the absence of cells, Lp(a) had no direct monocyte chemotactic activity. Actinomycin D and cycloheximide inhibited the HUVEC response, indicating that protein and RNA synthesis were required. Endotoxin was shown not to be responsible for the induction of monocyte chemotactic activity. Granulocyte monocyte-colony stimulating factor antigen was not detected in the Lp(a)-conditioned medium, nor was monocyte chemoattractant protein-1 mRNA induced by Lp(a). These results suggest that Lp(a) may be involved in the recruitment of monocytes to the vessel wall, thus providing a novel mechanism for the participation of Lp(a) in the atherogenic process.

Apolipoproteins A↗