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S Y Lam

Publications and source records attributed to S Y Lam.

At least 19 recordsLinked to original sources
PubMed2006

Comparative analytical sensitivities of six rapid influenza A antigen detection test kits for detection of influenza A subtypes H1N1, H3N2 and H5N1.

BACKGROUND: Rapid and simple methods for diagnosing human influenza A (H5N1) disease urgently needed. The limited data so far suggest that the currently available rapid antigen detection kits have poor clinical sensitivity for diagnosis of human H5N1 disease. OBJECTIVES: To compare the analytical sensitivity of six commercially available rapid antigen detection kits for the detection of "human" (subtypes H1N1, H3N2) and "avian" (subtype H5N1) influenza A viruses. STUDY DESIGN: Six commercially available test kits for the detection of influenza A were investigated. Analytic sensitivity for the detection of two contemporary H1N1, two H3N2 and three H5N1 viruses was determined using virus culture as a reference method. RESULTS AND CONCLUSIONS: Each test kit detected the H5N1 virus subtypes as efficiently as they detected conventional human viruses of subtypes H1N1 or H3N2. However, limits of detection of influenza viruses of all subtypes by antigen detection kits were >1000-fold lower than virus isolation. Thus, the reportedly poor clinical sensitivity of these antigen detection kits for diagnosis of patients with H5N1 disease is not due to a difference of sensitivity for detecting avian influenza H5N1 compared to human influenza viruses.

Animals↗
PubMed2004

HAb18G/CD147-mediated calcium mobilization and hepatoma metastasis require both C-terminal and N-terminal domains.

HAb18G/CD147 is a heavily glycosylated protein containing two immunoglobulin superfamily domains. Our previous studies have indicated that overexpression of HAb18G/CD147 enhances metastatic potentials in human hepatoma cells by disrupting the regulation of store-operated Ca2+ entry by nitric oxide (NO)/cGMP. In the present study, we investigated the structure-function of HAb18G/CD147 by transfecting truncated HAb18G/CD147 fragments into human 7721 hepatoma cells. The inhibitory effect of HAb18G/CD147 on 8-bromo-cGMP-regulated thapsigargin-induced Ca2+ entry was reversed by the expression of either C or N terminus truncated HAb18G/CD147 in T7721deltaC and T7721deltaN cells, respectively. The potential effect of HAb18G/CD147 on metastatic potentials, both adhesion and invasion capacities, of hepatoma cells was abolished in T7721deltaC cells, but not affected in T7721deltaN cells. Release and activation of matrix metalloproteinases (MMPs), MMP-2 and MMP-9, were found to be enhanced by the expression of HAb18G/CD147, and this effect was abolished by both truncations. Thapsigargin significantly enhanced release and activation of MMPs (MMP-2 and MMP-9) in non-transfected 7721 cells, and this effect was negatively regulated by SNAP. However, no effects of thapsigargin or SNAP were observed in T7721 cells, and expression of HAb18G/CD147 enhanced secretion and activation of MMPs at a stable and high level. Taken together, these results suggest that both ectodomain and intracellular domains of HAb18G/CD147 are required to mediate the effect of HAb18G/CD147 on the secretion and activation of MMPs and metastasis-related processes in human hepatoma cells by disrupting the regulation of NO/cGMP-sensitive intracellular Ca2+ mobilization although each domain may play different roles.

Antigens, CD↗
PubMed2004

Features predicting adverse outcomes of status epilepticus in childhood.

OBJECTIVE: To examine variables that might predict abnormal outcome of status epilepticus among children. DESIGN: Retrospective study. SETTING: Regional hospital, Hong Kong. PATIENTS: All children younger than 15 years who were admitted to the paediatric intensive care unit with status epilepticus between 1997 and 2002. MAIN OUTCOME MEASURES: Neurodevelopmental outcomes. RESULTS: Two of the 25 patients died, resulting in a mortality rate of 8%. No deaths were due to status epilepticus itself. No patient with febrile or idiopathic status epilepticus developed epilepsy. Neurological deterioration was observed in a quarter (six of 23) of the survivors. Symptomatic aetiology (acute or remote) and refractory status epilepticus were associated with adverse outcomes (P<0.05). Young age at status epilepticus (<12 months) and duration of status epilepticus (>60 minutes) tended to be more frequent among those who developed adverse outcome. Rectal diazepam was given before hospital arrival in only four patients. CONCLUSIONS: Paediatric patients with status epilepticus who had normal neurodevelopmental status before the onset of an attack and who did not sustain an acute insult to the central nervous system or have progressive encephalopathy, had favourable outcomes. Prompt use of rectal diazepam or buccal midazolam administered by caretakers or paramedics should be encouraged.

Age Factors↗
PubMed2004

Merosin-deficient congenital muscular dystrophy in two siblings.

Congenital muscular dystrophies are a group of heterogeneous inherited autosomal recessive disorders. The so-called 'pure' or 'occidental' form is further divided into merosin-positive and merosin-negative subgroups. Merosin is also expressed in the nervous system and its deficiency could affect development of the nervous system. The authors report two siblings with merosin-negative congenital muscular dystrophy. The clinical picture, biopsy findings, and abnormalities as detected by the magnetic resonance imaging of the two patients are presented.

Child↗
PubMed2003

Expression, immunolocalization, and functional activity of Na+/H+ exchanger isoforms in mouse endometrial epithelium.

The luminal fluid microenvironment of the uterus is important for sperm capacitation and embryo development. In an attempt to understand the possible role of Na(+)/H(+) exchangers (NHEs) in uterine function, the mRNAs of different NHE isoforms as well as their subcellular localization (apical versus basolateral) and functional activity were investigated in mouse endometrial epithelial cells using reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and intracellular pH (pH(i)) measurement techniques. The presence of NHE1, NHE2, and NHE4, but not NHE3 mRNAs were revealed by RT-PCR. Immunostaining showed that NHE1, NHE2, and NHE4 were present in both apical and basolateral membranes. The pH(i) recovery from intracellular acidification was Na(+)-dependent; however, the rate of pH(i) recovery depending on basolateral Na(+) was 12.4 times faster than that depending on apical Na(+). The Na(+)-dependent rate of pH(i) recovery was also inhibited by amiloride, indicating H(+) extrusion through NHEs; however, the amiloride sensitivity of the apical membrane was less than that of the basolateral membrane, suggesting the involvement of different types of NHEs in the two membranes. The results indicate that the basolaterally located NHE1, NHE2, and NHE4, in addition to participating in the homeostatic control of intracellular pH, may play a role in H(+) extrusion in order to achieve transepithelial HCO(3)(-) secretion. The apically located NHEs may be involved in mediating Na(+) absorption as alternatives of or complementary to epithelial Na(+) channels.

Animals↗
PubMed2002

Non-accidental carbon monoxide poisoning from burning charcoal in attempted combined homicide-suicide.

OBJECTIVE: To describe an emerging form of serious child abuse in combined homicide-suicide in Hong Kong. METHOD: This is a retrospective hospital chart review in a regional hospital in Hong Kong from January to December 2000. RESULTS: Eight children, with a mean age of 7.8 years (range 0.5-11 years), from four families were admitted to hospital because of non-accidental exposure to carbon monoxide when their parents attempted suicide by burning charcoal. A 7-year-old boy died on arrival. His 5.6-year-old sister and another 6-month-old boy had cerebral hypoxia on admission. Hyperbaric oxygen therapy was used in both cases, with rapid improvement, although there were persistent neurological deficits in the girl. The other children in the present study were asymptomatic and none had delayed neurological sequelae. Concomitant use of sedatives was also detected in three of the surviving patients. CONCLUSIONS: Non-accidental poisoning with carbon monoxide appears to be a new means of child abuse with potentially serious consequences. Concomitant intoxication with psychotropic drugs is common in such cases. The reason for parents killing their own children under such circumstances was unclear, but a desire to exact revenge on an estranged partner was suggested.

Adult↗
PubMed2002

Life threatening acute epiglottitis in acute leukemia.

We report an 8-year-old boy who developed a life-threatening acute epiglottitis during induction chemotherapy for acute promyelocytic leukemia. He survived the infection with emergency tracheostomy, treatment with broad spectrum antibiotics and amphotericin, and the use of granulocyte-macrophage colony stimulating factor. No organism was identified. A literature review identified 18 cases of acute epiglottitis in cancer patients. Sixteen of them were suffering from hematologic malignancies and three patients had received bone marrow transplantation. Unlike the usual case of epiglottitis, the majority (15 out of 18) of affected patients were adults and none of the infections was associated with Haemophilus influenzae. Streptococcus pneumoniae and Candida albicans were the most frequently identified pathogens. Early recognition and aggressive supportive care are required for successful management.

Acute Disease↗
PubMed2002

Postnatal hypoxemia increases angiotensin II sensitivity and up-regulates AT1a angiotensin receptors in rat carotid body chemoreceptors.

In the present study, the effects of postnatal hypoxemia on the AT1 angiotensin receptor-mediated activities in the rat carotid body were studied. Angiotensin II (Ang II) concentration-dependently increased the chemoreceptor afferent activity in the isolated carotid body. Single- or pauci-fiber recording of the sinus nerve revealed that the afferent response to Ang II was enhanced in the postnatally hypoxic carotid body. To determine whether the increased sensitivity to Ang II is mediated by changes in the functional expression of Ang II receptors in the carotid body chemoreceptors, cytosolic calcium ([Ca2+]i) was measured by spectrofluorimetry in fura-2 acetoxymethyl ester-loaded type I cells dissociated from carotid bodies. Ang II (25-100 nM) concentration-dependently increased [Ca2+]i in the type I cells. The proportion of clusters of type I cells responsive to Ang II was higher in the postnatally hypoxic group than in the normoxic control (89 vs 66%). In addition, the peak [Ca2+]i response to Ang II was enhanced 2- to 3-fold in the postnatally hypoxic group. The [Ca2+]i response to Ang II was abolished by pretreatment with losartan (1 microM), an AT1 receptor antagonist, but not by PD-123177 (1 microM), an AT(2) antagonist. Double-labeling immunohistochemistry confirmed that an enhanced immunoreactivity for AT1 receptor was co-localized to the lobules of type I cells in the hypoxic group. In addition, RT-PCR analysis of subtypes of AT1 receptors showed an up-regulation of AT1a but a down-regulation of AT1b receptors, indicating a differential regulation of the expression of AT1 receptor subtypes by postnatal hypoxia in the carotid body. These data suggest that postnatal hypoxemia is associated with an increased sensitivity of peripheral chemoreceptors in response to Ang II and an up-regulation of AT1a receptor-mediated [Ca2+]i activity of the chemoreceptors. This modulation may be important for adaptation of carotid body functions in the hypoxic ventilatory response and in electrolyte and water homeostasis during perinatal and postnatal hypoxia.

Angiotensin II↗
PubMed2001

Local regulation of anion secretion by pituitary adenylate cyclase-activating polypeptide in human colonic T84 cells.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a novel hypothalamic peptide, which has been shown to exert various functions in a number of tissues, including exocrine and endocrine tissues. The present study investigated the role of local PACAP in the control of anion secretion by the human colonic T84 cell. Both bioactive forms of PACAP-27 and PACAP-38 gave rise to a dose-dependent increase in the short-circuit current (I(SC)). However, there was a reversal in the order of potency observed at different concentration ranges for the two bioactive forms. PACAP-27 was greater than PACAP-38 when the peptide concentrations were below 10 n m; PACAP-38 was greater than PACAP-27 in the range of 10-80 n m. The effects of both PACAP forms were restricted to the apical aspect of the T84 cell. The I(SC)responses to both PACAP-27 and PACAP-38 were suppressed respectively by the non-selective Cl(-)channel blocker, diphenylamine-dicarboxylic acid (DPC), by the Ca(2+)dependent Cl(-)channel blocker, diisothiocyanatostilbene-disulfonic acid (DIDS) and by the Ca(2+)chelator, BAPTA-AM, indicating the involvement of Ca(2+). The expression of PACAP was demonstrated and localized specifically to the perinuclear cytoplasm of the T84 cell using immunocytochemistry, indicating its epithelial origin. Thus, the present data suggest that, in addition to the well-known cAMP-dependent pathway, PACAP may play a role in regulating colonic Cl(-)secretion via a Ca(2+)-dependent pathway, perhaps through two distinct PACAP receptor subtypes. Moreover, the regulation of anion secretion by T84 cells may be mediated by locally formed PACAP in an autocrine or paracrine fashion.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2001

Functional expression of angiotensin II receptors in type-I cells of the rat carotid body.

Angiotensin II increases afferent discharge from the carotid body in vitro. We hypothesized that angiotensin II receptors (AT receptors) are expressed functionally in the type-I cell of the carotid body. Cytosolic free [Ca2+] ([Ca2+]i) in type-I cells freshly dissociated from rat carotid bodies was measured spectrofluorimetrically. Angiotensin II (10-100 nM) concentration-dependently increased [Ca2+]i in type-I cells. The [Ca2+]i response was blocked by pretreatment with losartan (1 microM), an AT1 receptor antagonist, but not by blockade of AT2 receptors with PD- 123319 (1 microM). Moreover, the gene expression of AT1 receptors was assessed by the reverse transcriptase polymerase chain reaction and gene transcripts of both AT1a and AT1b receptors were detected in the carotid body. In addition, immunohistochemical study revealed that AT1 immunoreactivity was localized in lobules of type-I cells in the carotid body. Taken together, these results suggest that type-I cells in the rat carotid body express functional angiotensin II receptors. The binding of angiotensin II to the AT1 receptors increases [Ca2+]i, a key step of the intracellular signalling cascade following the activation of the receptors. It is concluded that angiotensin II modulates carotid body chemoreceptor function directly via AT1 receptors in the type-I cell.

Angiotensin II↗
PubMed2000

Testicular hormonal regulation of the renin-angiotensin system in the rat epididymis.

Evidence for the existence of an intrinsic angiotensin system based on locally formed angiotensinogen as a precursor for angiotensin production has been demonstrated in the rat epididymis. The data strongly support the presence of an epididymal renin-angiotensin system (RAS) which may be important for epididymal and sperm functions. In the present study, the effects of castration and testicular hormonal replacement on the expression of RAS components from the rat epididymis are investigated at the gene and protein levels. Results from northern blot and western blot analyses consistently showed that the expression of angiotensinogen mRNA and protein was apparently abolished by castration whereas their expression was completely restored to control levels when the castrated rats were hormonally replaced with either testosterone alone or with combined testosterone and estradiol. Northern blot did not detect any signal for angiotensinogen mRNA while western blot could detect a weak signal for angiotensinogen protein when the castrated rats were replaced with estradiol alone. Renin could be detected neither in control, castrated nor hormonally replaced rats. Moreover, the expression of angiotensin II receptor, type I (AT1) was almost abolished by castration as demonstrated by northern blot and reverse transcription-polymerase chain reaction. These data indicate that the expression of RAS by the rat epididymis at the levels of its precursor angiotensinogen and its receptor AT1, is subject to the regulation of testicular hormones and its expression appears to be predominantly testosterone-dependent.

Angiotensinogen↗
PubMed2000

Chronic hypoxia upregulates the expression and function of AT(1) receptor in rat carotid body.

In the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and by immunohistochemistry. The effect of chronic hypoxia on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Results from RT-PCR revealed that chronic hypoxia exhibited differential effects on the gene expression of Ang II receptors, namely AT(1) and AT(2), in the carotid body. The mRNA expression for subtypes of the AT(1) receptor, AT(1a) and AT(1b), was significantly increased in the carotid body with chronic hypoxia. To further investigate the localization of the AT(1) receptor, an immunohistochemical study was performed. The results showed that AT(1) receptor immunoreactivity was found in lobules of glomus cells in the carotid body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demonstrated that chronic hypoxia enhanced the AT(1) receptor-mediated excitation of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT(1) receptors in the rat carotid body. The upregulation of the expression also enhances AT(1) receptor-mediated excitation of the carotid body afferent activity. This might be important in the modulation of cardiorespiratory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.

Angiotensin II↗
PubMed1998

Concurrent and independent HCO3- and Cl- secretion in a human pancreatic duct cell line (CAPAN-1).

The present study investigated both HCO-3 and Cl- secretions in a human pancreatic duct cell line, CAPAN-1, using the short-circuit current (Isc) technique. In Cl-/HCO-3-containing solution, secretin (1 microM) or forskolin (10 microM) stimulated a biphasic rise in the Isc which initially reached a peak level at about 3 min and then decayed to a plateau level after 7 min. Removal of external Cl- abolished the initial transient phase in the forskolin-induced Isc while the plateau remained. In HCO-3/CO2-free solution, on the contrary, only the initial transient increase in Isc was prominent. Summation of the current magnitudes observed in Cl--free and HCO-3-free solutions over a time course of 10 min gave rise to a curve which was similar, both in magnitude and kinetics, to the current observed in Cl-/HCO-3-containing solution. Removal of external Na+ greatly reduced the initial transient rise in the forskolin-induced Isc response, and the plateau level observed under this condition was similar to that obtained in Cl--free solution, suggesting that Cl--dependent Isc was also Na+-dependent. Bumetanide (50 microM), an inhibitor of the Na+-K+-2Cl- cotransporter, and Ba2+ (1 mm), a K+ channel blocker, could reduce the forskolin-induced Isc obtained in Cl-/HCO-3-containing or HCO-3-free solution. However, they were found to be ineffective when external Cl- was removed, indicating the involvement of these mechanisms in Cl- secretion. On the contrary, the HCO-3-dependent (in the absence of external Cl-) forskolin-induced Isc could be significantly reduced by carbonic anhydrase inhibitor, acetazolamide (45 microM). Basolateral application of amiloride (100 microM) inhibited the Isc; however, a specific Na+-H+ exchanger blocker, 5-N-methyl-N-isobutylamiloride (MIA, 5-10 microM) was found to be ineffective, excluding the involvement of the Na+-H+ exchanger. However, an inhibitor of H+-ATPase, N-ethylmaleimide did suppress the Isc (IC50 = 22 microM). Immunohistochemical studies also confirmed the presence of a vacuolar type of H+-ATPase in these cells. H2DIDS (100 microM), an inhibitor of Na+-HCO-3 cotransporter, was without effect. Apical addition of Cl- channel blocker, diphenylamine-2,2'-dicarboxylic acid (DPC, 1 mm), but not disulfonic acids, DIDS (100 microM) or SITS (100 microM), exerted an inhibitory effect on both Cl- and HCO-3-dependent forskolin-induced Isc responses. Histochemical studies showed discrete stainings of carbonic anhydrase in the monolayer of CAPAN-1 cells, suggesting that HCO-3 secretion may be specialized to a certain population of cells. The present results suggest that both HCO-3 and Cl- secretion by the human pancreatic duct cells may occur concurrently and independently.

Antiporters↗
PubMed1998

Ammonia clearance by peritoneal dialysis and continuous arteriovenous hemodiafiltration.

We report the use of continuous arteriovenous hemodiafiltration (CAVHD) in a neonate with severe hyperammonemia due to a urea cycle disorder. We compared the ammonia clearance (C(NH3)) for peritoneal dialysis (PD) and CAVHD. C(NH3) for CAVHD was 7.45 ml/min per m2 at a dialysate flow of 300 ml/h and was 10.55 ml/min per m2 at a dialysate flow rate of 600 ml/h. The mean PD clearance was 2.15 ml/min per m2. Our data suggest that CAVHD is superior to PD for the removal of plasma ammonia. We conclude that CAVHD should be considered a reasonable alternative in the treatment of neonatal hyperammonemia in urea cycle disorders when medical treatment fails.

Ammonia↗
PubMed1997

Nodular histiocytic/mesothelial hyperplasia: a lesion potentially mistaken for a neoplasm in transbronchial biopsy.

This report describes two examples of nodular histiocytic/ mesothelial hyperplasia as seen in transbronchial biopsy that initially led to serious consideration of neuroendocrine neoplasm or meningioma. The biopsies showed nodular collections of cohesive polygonal or round cells with ovoid or deeply grooved nuclei and a moderate amount of finely granular cytoplasm. Nuclear pleomorphism was mild. Immunohistochemical studies showed few cells staining for cytokeratin and the mesothelial marker HBME-1, whereas most cells were decorated by the histiocytic marker PG-M1 (CD68). This lesion appears to be identical to nodular mesothelial hyperplasia as described in hernia sacs and mesothelial/monocytic incidental cardiac excrescences, and we propose modifying the designation to "nodular histiocytic/mesothelial hyperplasia" to take into account the marked predominance of histiocytes over mesothelial cells. The clues to recognition of the true nature of the lesion are clinicopathologic correlation and identification of strips of low cuboidal (mesothelial) cells in the vicinity, and the diagnosis can be further confirmed by immunohistochemical staining. Nodular histiocytic/mesothelial hyperplasia probably results from irritation to the mesothelial lining by various causes leading to focal aggregation of histiocytes within retraction pockets or crevices of the serosal cavity.

Biopsy↗