Search PubMed⌕ Search

Biomedical subjects

F L Chan

Publications and source records attributed to F L Chan.

At least 19 recordsLinked to original sources
PubMed2004

The relaxant effect of urocortin in rat pulmonary arteries.

Urocortin is a potent vasodilator, which plays physiological or pathophysiological roles in systemic circulation. However, little is known about its action on pulmonary circulation. The present study was aimed to characterize some cellular mechanisms underlying the relaxant effect of urocortin in isolated rat pulmonary arteries. Changes in isometric tension were measured on small vessel myographs. Urocortin inhibited U46619-induced contraction with reduction of the maximal response. Urocortin-induced relaxation was independent of the presence of endothelium. Inhibitors of nitric oxide (NO)-dependent dilator, NG-nitro-L-arginine methyl ester or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one, did not affect the relaxation. Astressin (100-500 nM), a corticotropin-releasing factor (CRF) receptor antagonist and KT5720, a protein kinase A (PKA) inhibitor reduced urocortin-induced relaxation. Urocortin produced less relaxant effect in 30 mM K+- than U46619-contracted arterial rings. Urocortin did not reduce CaCl2-induced contraction in 60 mM K+-containing solution. Ba2+ (100-500 microM) but not other K+ channel blockers reduced the relaxant responses to urocortin. Urocortin also relaxed the rings preconstricted by phorbol 12,13-diacetae in normal Krebs solution while this relaxation was less in a Ca2+-free solution. Our results show that urocortin relaxed rat pulmonary arteries via CRF receptor-mediated and PKA-dependent but endothelium/NO or voltage-gated Ca2+ channel-independent mechanisms. Stimulation of Ba2+-sensitive K+ channel may contribute to urocortin-induced relaxation. Finally, urocortin relaxed pulmonary arteries partly via inhibition of a PKC-dependent contractile mechanism.

Animals↗
PubMed2003

Persistent adrenal enhancement may be the earliest CT sign of significant hypovolaemic shock.

AIM: To report two cases of intense and persistent adrenal enhancement on computed tomography (CT) examinations of the abdomen. MATERIALS AND METHODS: Two patients presented with septic shock, one due to pyogenic liver abscess and the other strangulated obturator hernia with gangrenous bowel. Both patients were resuscitated with fluid before undergoing unenhanced and enhanced CT. RESULTS: In both patients intravascular volume was not reduced as evident by normal calibre of the aorta and inferior vena cava. One patient had abnormal enhancement pattern in the liver and kidneys, suggesting hypoperfusion. The other patient had normal enhancement pattern of the other abdominal viscera. Both patient subsequently died with multi-organ failure. CONCLUSION: We propose that adrenal enhancement may be a sign of hyperperfusion in early stage of shock due to the crucial role of the adrenal glands in this clinical situation. This may not persist with further circulatory compromise due to vasoconstriction. If confirmed, its recognition has potential value of identifying a therapeutic window before irreversible shock set in.

Adrenal Glands↗
PubMed2003

CT in acute mesenteric ischaemia.

Enhanced computed tomography (CT) is frequently performed for possible bowel ischaemia. It has the distinct advantage of possible detection of the causes of ischaemia. Radiologists therefore need to be familiar with the spectrum of diagnostic CT signs. We present the CT imaging findings in surgically proven cases of small bowel ischaemia. In addition to signs pertaining to the underlying aetiological pathology, bowel dilatation, bowel wall thickening, mural gas, occlusion of mesenteric vessels, ascites and infarct of other abdominal organs were observed.

Abdomen, Acute↗
PubMed2003

MRI of neonatal encephalopathy.

We present the magnetic resonance imaging (MRI) findings in neonatal encephalopathy, including hypoxic-ischaemic encephalopathy, perinatal/neonatal stroke, metabolic encephalopathy from inborn errors of metabolism, congenital central nervous system infections and birth trauma. The applications of advanced MRI techniques, such as diffusion-weighted imaging and magnetic resonance spectroscopy are emphasized.

Birth Injuries↗
PubMed2002

Prostate targeting: PSP94 gene promoter/enhancer region directed prostate tissue-specific expression in a transgenic mouse prostate cancer model.

To date, only a few prostate-specific vector genes have been tested for prostate targeting in gene therapy of prostate cancer (CaP). Current clinical trials of gene therapy of CaP utilize the only two available vector genes with a combination of a rat probasin promoter and a human PSA promoter sequence in an adenovirus vector to target CaP. There is an urgent need to establish additional vector gene systems to sustain and propagate the current research. Since PSP94 (prostate secretory protein of 94 amino acids) is one of the three most abundant proteins secreted from the human prostate and is generally considered to be prostate tissue-specific in both human and rodents, we performed a transgenic experiment to assess the promoter/enhancer region of PSP94 gene-directed prostate targeting. Firstly, a series of progressive deletion mutants of a 3.84 kb PSP94 gene promoter/enhancer region (including parts of the intron 1 sequence) linked with a reporter LacZ gene was constructed and assessed in vitro in cell culture. Next, transgenic mice were generated with two transgene constructs using the SV40 early region (Tag oncogene) as a selection marker. PSP94 gene promoter/enhancer region-directed SV40 Tag expression specifically in the mouse was demonstrated in three breeding lines (A, B, C, n = 374) by immunohistochemistry staining of Tag expression. Specific targeting to the prostate in the PSP94 gene-directed transgenic CaP model was characterized histologically by correlation of SV40 Tag-induced tumorigenesis (tumor grading) with puberty and age (10-32 weeks). Prostatic hyperplasia was observed as early as 10 weeks of age, with subsequent emergence of prostatic intraepithelial neoplasia (PIN) and eventually high grade carcinoma in the prostate. The PSP94 transgenic mouse CaP model was further characterized by its tumor progression and metastatic tendency at 20 weeks of age and also by its responsiveness and refractoriness to androgen manipulation. This study indicates that the PSP94 gene promoter/enhancer has the potential for prostate specific targeting and may ultimately be of use in gene therapy of CaP.

Animals↗
PubMed2002

Imaging of peripheral PNET: common and uncommon locations.

AIM: We present the imaging features of peripheral primitive neuroectodermal tumour (PNET) in eight children, highlighting the unusual locations of this tumour in three children. MATERIALS AND METHODS: At presentation, the tumours were studied with magnetic resonance imaging (MRI; n = 6), computed tomography (CT; n = 7) and ultrasound (US; n = 1). The diagnoses were confirmed histologically (n = 8), immunohistochemically (n = 8), by cytogenetics (n = 3) and electron microscopy (n = 1). Correlation with gross pathology, histology, treatment and outcome were obtained. RESULTS: The tumours were located in the chest wall (n = 2), shoulder, pelvis, small bowel mesentery, adrenal gland, dura mater and skin and subcutaneous tissue of the abdominal wall (n = 1 each). Peripheral PNET arising from the small bowel mesentery, adrenal gland and dura mater have not been previously reported in the English literature. The tumours were mainly large (mean size: 10.6 cm) and infiltrative. All tumours were heterogeneously hyperintense on T2-weighted MRI, heterogeneously iso/hypodense on CT and had variable contrast enhancement. Most tumours were heterogeneously hypointense to muscle on T1-weighted MRI. US showed a hypoechoic mass with a cystic component. CONCLUSION: Peripheral PNET can occur in unusual locations. The clinical and imaging features of peripheral PNET are non-specific, making tissue diagnosis essential. PNET should be included in the differential diagnosis of aggressive soft tissue tumours in children.

Adolescent↗
PubMed2001

Altered expression of extracellular matrix and proteinases in Noble rat prostate gland after long-term treatment with sex steroids.

BACKGROUND: Interactions between the epithelial cells and stromal tissues, which include the epithelial basement membrane, extracellular matrix, inducible factors, and various cell types, are believed to play a significant role in prostate gland carcinogenesis. Remodeling of extracellular matrix and degradation of basement membrane are the prerequisites for tumor cell invasion, and these changes are correlated with the expression of various proteinases. METHODS: The present study examined the alterations of epithelial basement membrane, extracellular matrix, and proteinase activities in the Noble rat prostate gland after long-term treatments with androgen and estrogen (T+DES or T+E(2) for 4-12 months) by histochemistry, immunohistochemistry, electron microscopy, and gelatin-gel zymography. RESULTS: After hormonal treatments, defects of epithelial basement membranes, such as focal disruption, diffuse staining and multilayering, were observed by histochemistry and immunohistochemistry in the dysplastic and neoplastic lesions induced in the lateral (LP) and ventral prostates (VP) but not in dorsal prostate (DP). An increase in the amount of extracellular matrix components, including hyaluronan (HA), chondroitin sulfate proteoglycan (CSPG) and tenascin, in the stroma of hormone-treated LP and VP was revealed by histochemistry and immunohistochemistry. Positive immunolabeling of matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) was detected in the fibromuscular layer surrounding the adenoma and adenocarcinoma induced in LP and VP after treatments with steroids for over 9-12 months. Zymography also detected an increase in activities of proteinases of apparent MW 120, 90, 86 and 68 kDa in the hormone-treated LP and VP, and these proteinases were characterized as metalloproteinases. In addition, two serine proteinases of MW 100 and 30 kDa were identified as being overexpressed in the hormone-treated LP and VP. Compared to LP and VP, there was no significant change in the proteinase activities in the hormone-treated DP. CONCLUSIONS: The present study demonstrated that the epithelial basement membrane and stromal extracellular matrix were altered in dysplastic and neoplastic Noble rat prostates. Since HA and CSPG (or their complexes) are highly anionic molecules, their increased accumulation in the altered prostatic stroma would tend to hydrate this tissue. This would create an environment more favorable for tumor growth and invasion. These morphological changes were also correlated with the concurrent increase in gelatinolytic proteinase activities induced in these prostates. The results suggest that the remodeling of the stromal tissue might play a role in the early stage of prostate carcinogenesis as shown in the Noble rat model.

Adenocarcinoma↗
PubMed2001

Different role of endothelium/nitric oxide in 17beta-estradiol- and progesterone-induced relaxation in rat arteries.

The present study was aimed to examine the different role of endothelium/nitric oxide in relaxation induced by two female sex hormones, 17beta-estradiol and progesterone in rat isolated aortas and mesenteric arteries. The isometric force of each ring was measured with Grass force-displacement transducers in the organ bathes. 17beta-Estradiol induced both endothelium-dependent and -independent relaxation in the rat aortas but only the endothelium-independent relaxation in the rat mesenteric arteries. In contrast. progesterone induced both endothelium-dependent and -independent relaxation in the rat mesenteric arteries but only endothelium-independent relaxation in rat aortas. N(G)-Nitro-L-arginine methyl ester and methylene blue attenuated the relaxant response to 17beta-estradiol in the aortic rings or to progesterone in the mesenteric arteries. Pretreatment with L-arginine antagonized the effect of N(G)-nitro-L-arginine methyl ester on sex hormone-induced relaxation. The endothelium contribution to relaxation seems to only relate to lower concentrations of 17beta-estradiol and progesterone. In summary, the present results clearly demonstrate a different role of the functional endothelium in the relaxant response to 17beta-estradiol or progesterone in the conduit vessel (aorta) and the resistance vessels (mesenteric artery). Nitric oxide contributes largely to the endothelium-dependent relaxation induced by 17beta-estradiol in the isolated aortas or by progesterone in the mesenteric arteries.

Animals↗
PubMed2001

Pulmonary sequelae of treatment for breast cancer: a prospective study.

PURPOSE: To prospectively study the effects of loco-regional radiotherapy in women with breast cancer. METHODS AND MATERIALS: Thirty consecutive patients with breast resection underwent clinical, lung function, radiographic, and thoracic high-resolution computed tomography evaluation before and at 1, 3, 6, and 12 months after adjuvant radiotherapy. Chemotherapy was also administered to 15 patients. RESULTS: Nineteen patients reported mild respiratory symptoms at 1 month, which resolved completely at 6 months after radiotherapy. Opacities were present on 80% of chest radiographs and in all patients on high-resolution computed tomography by 3 months. These opacities became compact and persisted on high-resolution computed tomography at 12 months. Lung function indices, including FEV1, FVC, TLC, and DLCO, progressively declined after radiotherapy, and was irreversible at 12 months (p < 0.05). Patients who received chemotherapy did not have significantly different lung function indices compared with their counterparts at all time points (p > 0.05). CONCLUSIONS: Our results have shown that adjuvant loco-regional radiotherapy, a common practice in breast cancer treatment, is associated with irreversible reduction in lung function parameters. These changes are accompanied by radiological evidence of persistent lung injury. Further studies should be performed to evaluate the incidence and long-term pulmonary sequelae of current treatment for breast cancer.

Adult↗
PubMed2001

Analysis of glycoconjugate patterns of normal and hormone-induced dysplastic Noble rat prostates, and an androgen-independent Noble rat prostate tumor, by lectin histochemistry and protein blotting.

BACKGROUND: Alteration of the expression of glycoconjugates is frequently observed in tumors. However, studies on the changes of cellular glycosylation in the early premalignant stage of prostate carcinogenesis are scarce. METHODS: The present study characterized and compared the glycoconjugates expressed in the dysplastic lateral prostate induced in Noble (Nb) rat by steroid hormones and a transplantable androgen-independent Nb rat prostatic carcinoma line (AIT) by lectin histochemistry and protein blotting. RESULTS: The results of lectin histochemistry show that the dysplastic prostatic epithelium elaborates altered patterns of glycosylation, which are distinct from the normal secretory epithelium. Some individual cells in the dysplastic epithelium were intensely labeled by the N-acetylgalactosamine (GalNAc)-specific (agglutins from Glycine max [SBA], Helix aspera [HAA], Helix pomatia [HPA], Vicia villosa [VVA], Erythrina cristigalli [ECA]) and complex-type oligosaccharide-specific (Phaseolus vulgaris agglutin [PHA-E]) lectins, indicating that these cells contained abundant GalNAc(alpha1,3)GalNAc/Gal and Gal(beta1,4)GlcNAc(alpha1,2)Man(alpha1,6) residues. These lectins also bound to some tumor cells in the AIT, suggesting that these sugar residues are common in some dysplastic and neoplastic prostatic cells. The study has also identified several lectins (agglutins from Griffonia simplicifolia [GS-I-B4], Arachis hypogaea [PNA], Ricinus communis [RCA-I], Maackia amurensis [MAA], Sambucus nigra [SNA]), which bound only to some AIT tumor cells but not to dysplastic epithelium, indicating that alpha/betaGal and sialic acid-containing glycoconjugates are expressed by neoplastic prostatic cells. The results of lectin blottings with Triticum vulgare agglutin [S-WGA] Ulex europaeus agglutin [UEA-I] and PHA-E have identified five major glycoprotein bands (of apparent molecular weights of 116, 79, 64, 61, and 57 kDa) in the microsomal fraction of testosterone plus 17beta-estradiol (T + E2)-treated lateral prostate. These lectin-reactive bands were not detected in the AIT extracts. In the AIT microsomal extract, two glycoprotein bands of molecular weights of 58 and 46 kDa were revealed by SBA and PNA. CONCLUSIONS: The present study shows that there is an increased expression of GalNAc(alpha1,3)GalNAc/Gal residues and triantennary complex-type oligosaccharides in the dysplastic epithelial cells as compared to normal secretory epithelial cells in rat lateral prostate. This altered expression of glycoconjugates revealed in the dysplastic epithelium indicates an aberrant glycosylation in the early premalignant stage of prostate carcinogenesis. The results also show that the AIT tumor cells are heterogeneous in their glycoconjugates and different from the dysplastic epithelial cells.

Animals↗
PubMed2001

H-type tracheo-oesophageal fistula: appearance on three-dimensional computed tomography and virtual bronchoscopy.

H-type tracheo-oesophageal fistula (TOF) is a rare type of fistula without oesophageal atresia. The symptoms are usually present at birth, but the diagnosis is often delayed. Traditionally, contrast oesophagography and/or fiberoptic bronchoscopy are used to confirm the diagnosis. We describe the imaging features of a case of H-type TOF seen on three-dimensional computed tomography and virtual bronchoscopy and the usefulness of these techniques in pre-operative evaluation.

Bronchoscopy↗
PubMed2001

Lace-like enhancement pattern of osteosarcoma of rib and liver metastasis in CT scans.

The rib is an uncommon site of osteosarcoma. With the use of adjuvant chemotherapy and aggressive surgical resection of the metastatic pulmonary lesions, extrapulmonary metastases are becoming more clinically evident. Primary rib osteosarcoma with extrapulmonary metastasis is exceedingly rare. A case is reported, showing that the pattern of metastasis of rib osteosarcoma is similar to that of primary bone osteosarcoma. The liver metastasis occurred after resection of the metastatic pulmonary lesions. A CT scan of the primary rib lesion and liver metastasis both showed a lace-like enhancement pattern, its histological appearance corresponding with neoplastic osteoid. With the increasing use of CT abdomen for localization of extrapulmonary metastases, lace-like enhancement may be seen more readily in the future.

Adult↗
PubMed2001

Vasorelaxant effects of cardamonin and alpinetin from Alpinia henryi K. Schum.

The vascular effects of cardamonin and alpinetin from Alpinia henryi K. Schum. were examined in the rat isolated mesenteric arteries. 1H and 13C nuclear magnetic resonance spectra showed that cardamonin is present in trans-form, and single-crystal radiographic structure revealed that alpinetin is present in S configuration. Both cardamonin and alpinetin produced a rightward shift in the concentration-response curve for phenylephrine in a noncompetitive manner, and they induced relaxation of phenylephrine-preconstricted arteries with respective mean inhibitory concentrations (IC50) of 9.3+/-0.6 microM and 27.5+/-2.8 microM. Both compounds also relaxed arteries preconstricted by endothelin I or U46619. Their relaxant effects were decreased in endothelium-removed rings. Pretreatment with N(G)-nitro-L-arginine methyl ester or methylene blue inhibited relaxation induced by both agents, and pretreatment with L-arginine reversed the effect of N(G)-nitro-L-arginine methyl ester on cardamonin-induced endothelium-dependent relaxation. The relaxant effects of cardamonin and alpinetin were unaffected by indomethacin (3 microM). Cardamonin and alpinetin inhibited 60 mM K+-induced contraction with respective IC50 of 11.5+/-0.3 microM and 37.9+/-3.6 microM. In addition, both agents inhibited the transient contraction induced by 3 microM phenylephrine or by 10 mM caffeine in Ca2+-free Krebs solution. Finally, these two agents also concentration dependently relax the arteries preconstricted by 1 microM phorbol 12,13-diacetate in Ca2+-free Krebs solution. These results indicate that purified cardamonin and alpinetin from A. henryi K. Schum. relaxed rat mesenteric arteries through multiple mechanisms. They induced both endothelium-dependent and -independent relaxation; the former is likely mediated by nitric oxide whereas the latter is probably mediated through nonselective inhibition of Ca2+ influx and intracellular Ca2+ release and inhibition of the protein kinase C-dependent contractile mechanism.

Animals↗
PubMed2001

Modulatory effect of protein kinase C activator on contractility of rat vas deferens.

The modulatory effect of the protein kinase C activator was examined on contraction of rat isolated vas deferens induced by constrictive agonists, noradrenaline (NA), ATP, BaCl2 and high K+. Phorbol 12,13-diacetate (PDA, 1 micromol/l) induced a transient extracellular Ca(2+)-dependent contraction while the inactive analogue, 4alpha-phorbol (1 micromol/l) had no effect. PDA significantly enhanced the peak amplitude of the contractile response to NA (0.1-10 micromol/l), ATP (100 micromol/l), Ba2+ (3 mmol/l) or high K+ (30 mmol/l). Staurosporine at 30 nmol/l reduced the enhancing effect of PDA on the agonist-induced contraction. NA (10 micromol/l) produced a phasic contraction followed by a sustained contraction, while ATP induced monophasic contraction. Pretreatment with nifedipine (10 nmol/l) had no effect on the phasic contraction induced by NA, but it significantly reduced ATP- or high K(+)-induced contraction. Staurosporine (30 nmol/l) alone attenuated the peak contractile response induced by NA or ATP but not by Ba2+. NA produced a transient contraction in Ca(2+)-free Krebs solution, and PDA (1 micromol/l) markedly enhanced this effect. These novel data indicate that activation of a protein kinase C-dependent mechanism not only affects contraction mediated by Ca2+ influx through voltage-sensitive Ca2+ channels, but also promotes intracellular Ca2+ release or intracellular Ca(2+)-mediated contractile mechanism in rat vas deferens.

Adenosine Triphosphate↗