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Biomedical subjects

S Wong

Publications and source records attributed to S Wong.

At least 19 recordsLinked to original sources

Establishment of a Chinese hamster ovary cell line that expresses grp78 antisense transcripts and suppresses A23187 induction of both GRP78 and GRP94.

GRP78, a 78,000 dalton protein residing in the endoplasmic reticulum, is postulated to play important roles in protein folding and cell survival during calcium and other physiological stress. Here we describe the construction of an eukaryotic expression vector for the constitutive expression of grp78 antisense RNA and the creation of a CHO cell line, 78WO, which expresses high levels of the grp78 antisense RNA through amplification of the stably transfected antisense vector. We observed that whereas 78WO maintains a basal level of GRP78 similar to that of control cells, GRP78 is no longer inducible by A23187. The 78WO cells have undergone a compensatory increase in grp78 transcription such that the effects of antisense are cancelled out at the protein level under nonstressed conditions. In these same cells, GRP94, a 94,00 dalton ER protein, is also rendered noninducible by A23187. This provides the first evidence that the regulation of two ER proteins might be coupled such that the failure to induce GRP78 results in the down-regulation of GRP94. The 78WO cell line grows with a doubling time of about 26 hr and exhibits decreased tolerance to A23187, suggesting the GRPs contribute to cell viability under calcium stress. The establishment of this cell line, which can be stably maintained, will provide a useful tool for testing whether the induction of the GRPs is important for protein folding or transport and whether their enhanced synthesis is the cause or consequence of a variety of physiological adaptations.

Animals

Identification of a new EF-hand superfamily member from Trypanosoma brucei.

We identified several open reading frames between the regions encoding calmodulin and ubiquitin-EP52/1 in the genome of Trypanosoma brucei. One of these, EFH5, encodes a protein 192 amino acids long. The EFH5 transcript is present in poly(A)+ mRNA and is present at similar levels in the mammalian bloodstream form and the insect procyclic form. EFH5 contains four EF-hand homolog domains, two of which are inferred to bind Ca2+ ions. We expressed EFH5 as a fusion protein in Escherichia coli and demonstrated calcium-binding activity of the fusion protein using the 45Ca-overlay technique. The function of EFH5 remains unknown; however, as the fourth EF-hand homolog identified in trypanosomes, it attests to the broad range of functions assumed by calcium functioning as a second messenger. EFH5, which is most closely related to LAV1-2 from Physarum, represents a distinct subfamily among the EF-hand-containing proteins.

Amino Acid Sequence

Antiarthritic profile of BF-389--a novel anti-inflammatory agent with low ulcerogenic liability.

BF-389, dihydro-4-(3,5-di-tert-butyl-4-hydroxybenzylidene)-2-methyl-2H-1,2- oxazin-3(4H)-one, is a potent, orally active, antiarthritic and analgesic agent with low ulcerogenic potential. A comparison of the activity profiles of BF-389 and naproxen showed similarities in: (1) suppression of developing and chronic adjuvant arthritis (AA); (2) maximal inhibitory response, as shown by the E(max) values in the developing and established AA models; (3) inhibition of bone degenerative changes associated with chronic adjuvant arthritis; and (4) analgesic activity in the acetic acid and phenylquinone writhing assays. Though BF-389 has been shown to be a potent inhibitor of cyclooxygenase, IC50 = 0.84 +/- 0.25 microM against the production of PGE2 in vitro, there is a great difference from most cyclooxygenase inhibitors; it also inhibits the 5-lipoxygenase enzyme. For BF-389, the IC50 for in vitro LTB4 formation was found to be 3.65 +/- 1.19 microM. The ulcerogenic potential of BF-389 was compared to that of naproxen using a five-day in vivo ulcerogenic rat assay. The UD50 for naproxen was found to be approximately 30 mg/kg/day, p.o. Based upon efficacy in the DEV AA and EST AA models, UD50/ED50 values for naproxen were estimated to be 0.7 and 1.9, respectively. For BF-389 the UD50 was shown to be 520 (389-695) mg/kg/day, p.o., and the corresponding UD50/ED50 values were calculated to be 84 and 28, respectively, thus demonstrating the wide margin of safety between efficacy and ulcerogenicity in rats.

Animals

Should the JT rather than the QT interval be used to detect prolongation of ventricular repolarization? An assessment in normal conduction and in ventricular conduction defects.

It has been suggested that the JT rather than QT interval properly reflects repolarization duration in ventricular conduction defects (VCD). The authors examined the influence of QRS duration on the JT and QT intervals in 20,687 normal adult subjects and 2,865 subjects with various categories of VCD. Estimates for coefficients for multiple regression of QRS duration on QT and JT intervals combined with a correction term for heart rate (HR) were determined for each VCD category. QRS duration accounted for about 16% of total QT variation, but had a practically negligible effect on JT interval in complete bundle branch blocks. A single-parameter formula was derived for the JT prolongation index of the form JTI = JT(HR + 100)/518, with a JTI > or = 112 identifying repolarization prolongation in all VCD categories. It is concluded that it is preferable to predict JT rather than QT as a more appropriate index of duration of repolarization in VCD.

Adult

Protein kinase C impairs the coupling of the GTP-binding protein to LTB4 receptor in neutrophil.

In the present study, the mechanism of LTB4 receptor down regulation by protein kinase C (PKC) has been investigated using porcine neutrophil membranes. Pretreatment of intact porcine neutrophils with 12-O-tetradecanoylphorbol-13-acetate (TPA) for 2 min prior to the preparation of plasma membrane, demonstrated a reduced binding sites (Bmax) for LTB4 without altering the receptor affinity (Kd). This effect of TPA on LTB4 receptor binding was found to be due to the activation of PKC as membrane treated with purified PKC (type III) produced the same effect. When membranes from neutrophils pretreated with TPA were exposed to non-hydrolyzable GTP analog, GTP-gamma S, or GMP-PNP, no further decrease in receptor Kd was observed, while the Bmax was reduced to the level observed in TPA treated samples. Treatment of isolated neutrophil membranes with purified PKC reduced the Bmax and blocked the effect of GTP analogs on the receptor affinity. These results suggest that, PKC interrupts the receptor binding to G-protein.

Animals

Allelic polymorphism of the Trypanosoma brucei polyubiquitin gene.

We have characterized a second T. brucei polyubiquitin gene (UbB) that is highly similar in the coding and flanking regions to a previously described T. brucei polyubiquitin gene (UbA). However, UbB differs from UbA in 2 respects: (1) the predicted carboxy-terminal amino acid of UbB is methionine, as opposed to leucine in UbA, and (2) UbB contains approximately 13 ubiquitin repeats, as opposed to approximately 30 repeats in UbA. In Southern blots of intact T. brucei DNA separated by pulsed field gel electrophoresis, the polyubiquitin sequences have been shown to reside on band 19, which may contain 3 chromosomes. Three experiments that target a neomycin-resistance gene to the polyubiquitin locus demonstrate a one-to-one ratio of polyubiquitin 3-flanking sequences, which suggests that UbA and UbB are alleles rather than duplications. Four additional strains of T. brucei and one strain of T. equiperdum show variation in their polyubiquitin gene size, suggesting that this is a common polymorphism.

Alleles

Difficult diagnosis of the fragile X syndrome made possible by direct detection of DNA mutations.

Genetic recombination near the fragile X locus (Xq27.3) has frequently been a problem in linkage studies of families in which the fragile X is segregating. This case report illustrates the resolution of a difficult situation in a fragile X family for whom cytogenetic studies were inconclusive and where recombination had twice confounded attempts at prenatal DNA diagnosis by RFLP analysis. Using a newly developed DNA probe, StB12.3, for direct detection of DNA instability in the fragile X locus, the presence of the fragile X was ascertained definitively in a prenatal DNA sample.

Blotting, Southern

Thyroxine sulfate is a major thyroid hormone metabolite and a potential intermediate in the monodeiodination pathways in fetal sheep.

T3 and rT3 production rates in the fetus account for roughly only a third of the total T4 production rate; thus, the fate of the majority of T4 produced in the fetus is unknown (the "T4 disposal gap"). We developed sensitive and specific T4 sulfate (T4S) and T3 sulfate (T3S) RIAs to investigate the roles of these compounds in fetal T4 metabolism. T3, T4, T3S, and T4S were determined in a variety of tissue fluid and/or serum samples obtained from fetal, newborn (n = 6), and adult (n = 6) sheep. Four groups of fetal animals, with gestational ages of 94 days (n = 5), 110-111 days (n = 6), 130-131 days (n = 6), and 145 days (n = 6; term = 150 days), were studied. In addition, type I 5'-monodeiodinase (5'-MDI) activity was quantified in liver and kidney tissues. 5'-MDI activities were lower in 94- to 131-day-old fetuses than in fetuses near term or in newborn animals. Mean serum T3 concentrations increased progressively from 94 days (19 ng/dl) to term (371 ng/dl), while mean T3S and T4S serum concentrations were highest at 130 days gestation (237 and 989 ng/dl), decreasing to term. Serum T3S and T4S concentrations decreased further in newborns and adult sheep. T4S and T3S levels in allantoic fluid were significantly higher than those in urine and amniotic fluid in all fetal age groups studied. T4S levels in bile were high from 94-130 days gestation (873-1006 ng/dl), decreasing by 50% at term (529 ng/dl). T4S concentrations in meconium were 46- to 83-fold higher than those in bile from 94 days gestation to term. In contrast, bile T3S levels increased progressively from 94-145 days gestation (191-605 ng/dl), while meconium T3S levels decreased during the same period (33-14 micrograms/100 g). These data demonstrate that 1) sulfated iodothyronines, particularly T4S, are major thyroid hormone metabolites in the fetus; 2) both T4S and T3S are excreted into bile and urine and concentrated in meconium and allantoic fluid; and 3) the high levels of T4S and T3S in serum and other fluids may reflect lower tissue type I 5'-MDI activities. We speculate that T4S and T3S may be further metabolized to other sulfated metabolites and may account in part for the T4 disposal gap in fetal sheep.

Allantois

Dietary aluminum and Alzheimer's disease.

Aluminum accumulation has been implicated in the development of Alzheimer's Disease, a hallmark of which is decreased brain glucose metabolism. Dietary sources of aluminum include that which comes from the contact of food with aluminum cook ware, containers, foil, and utensils. Normal aluminum intake from all sources is estimated as 12-14 mg per day. We have evaluated brain glucose metabolism in the presence of physiologically achievable levels of aluminum, in the range 10(-15) to 10(-5) M. Our results indicate no effect of aluminum in the range tested. Thus the contact of food with aluminum cooking utensils cannot alone raise plasma aluminum concentrations to the millimolar levels required to decrease brain glucose metabolism. Non dietary pathophysiological mechanisms are operating which lead to the accumulation of tissue aluminum, since most of dietary aluminum is excreted by the kidney.

Aged

Platelet activation leads to increased c-src kinase activity and association of c-src with an 85-kDa tyrosine phosphoprotein.

We have used platelets as a model system to study the function of c-src in signal transduction and cell adhesion. Numerous proteins were found to be phosphorylated on tyrosine in response to thrombin-induced platelet activation and aggregation. Two phases of phosphorylation were observed, with the second phase, but not the first, being inhibited by blocking platelet aggregation with an Arg-Gly-Asp-Ser tetrapeptide. As a first step towards identifying those proteins phosphorylated on tyrosine and to determine the specific role of p60src during platelet activation, we looked for changes in p60src kinase activity and for associations of p60src with other tyrosine phosphoproteins. The data presented here demonstrate an increase in p60src kinase activity within 1 min of thrombin-induced activation. Furthermore, p60src transiently associates with a tyrosine phosphoprotein during platelet activation and aggregation. This tyrosine phosphoprotein, p80/85, is a previously characterized cytoskeletal substrate for v-src in transformed cells. The data presented here suggest a model in which p60src functions in platelets to link upstream events, such as cell-surface adhesive interactions, with changes in platelet shape and cytoskeletal organization.

Amino Acid Sequence

Sex differences in the evolution of the electrocardiographic QT interval with age.

OBJECTIVE: To investigate sex differences in the evolution of the QT interval with age. SUBJECTS AND METHODS: A community-based representative North American population sample of 14,379 children and adults aged from birth to 75 years. The measured QT intervals (QTm) were determined by a computer algorithm and QTm, corrected for heart rate (HR), was expressed as QT index: QTI = (QTm/Tp) x 100, where QTp is the predicted QT from the formula QTp (ms) = 656/(1 + HR/100). MAIN RESULTS: The QTI values of females were significantly longer than of males in all age groups from 15 to 50 years tested at yearly intervals. This difference was due to a 20 ms drop in rate-corrected QT values in adolescent males after puberty, whereas QT values of females remained unchanged throughout the growth, maturation and reproductive years. The new QT prediction formula explained 83% of total QT variance in females and 82% in males after adjustment for heart rate and for the observed significant influence of ventricular excitation time (QRS duration) on QT interval in both sexes and a correction for QT age trend in males. CONCLUSIONS: The sex difference in the QT interval is due to QT shortening in males after puberty rather than QT prolongation in women during reproductive years. The fact that QRS duration is a significant determinant of the QT interval has important theoretical implications for attempts to model the ventricular repolarization process and it indicates that the traditional concept of reverse sequence of ventricular repolarization is not universally valid in all myocardial regions.

Adolescent

Glucose regulated protein induction and cellular resistance to oxidative stress mediated by porphyrin photosensitization.

Photodynamic therapy (PDT) utilizes a tumor localizing porphyrin photosensitizer in the clinical treatment of cancer. At a mechanistic level, porphyrin photosensitization generates reactive oxygen species which initiate oxidative damage to a wide spectrum of biomolecules. Cellular stress proteins are also increased following oxidative stress treatments. In the current study, we examined porphyrin photosensitizing parameters associated with induction of the glucose regulated family of stress proteins. Elevated levels of mRNA encoding glucose regulated proteins (GRPs) as well as increases in GRP protein synthesis were observed for mouse radiation induced fibrosarcoma cells exposed to an extended (16-h) porphyrin incubation prior to light exposure. However, a short (1-h) porphyrin incubation prior to light treatment (designed to produce comparable phototoxicity as PDT using the 16-h porphyrin incubation protocol) was associated with only minimal increases in GRP mRNA levels or GRP protein synthesis. The relationship between GRP levels and PDT sensitivity was examined in radiation induced fibrosarcoma cells pretreated with the calcium ionophore A-23187 in order to overexpress GRPs prior to photosensitization. Resistance to PDT was observed in cells overexpressing GRPs only under photosensitizing conditions associated with the extended porphyrin incubation protocol, and this response was not due to changes in cellular porphyrin uptake. In separate experiments, a transient elevation of GRP mRNA levels was observed in transplanted mouse mammary carcinomas following in vivo PDT treatments. Our results indicate that specific targets of oxidative damage (modulated by porphyrin incubation conditions) instead of generalized cellular exposure to reactive oxygen species are correlated with PDT mediated GRP induction. In this regard, GRP induction may be a useful in vivo biochemical marker of PDT mediated injury. These results also support the hypothesis that GRPs may play a role in modulating sensitivity to cellular stresses including certain types of oxidative injury.

Animals

Molecular heterogeneity of the fragile X syndrome.

The fragile X syndrome is an X-linked disorder which has been shown to be associated with the length variation of a DNA fragment containing a CGG trinucleotide repeat element at or close to the fragile site. Phenotypically normal carriers of the disorder generally have a smaller length variation than affected individuals. We have cloned the region in cosmids and defined the area containing the amplified sequence. We have used probes from the region to analyse the mutation in families. We show that the mutation evolves in different ways in different individuals of the same family. In addition we show that not all fragile X positive individuals show this amplification of DNA sequence even though they show expression of the fragile site at levels greater than 25%. One patient has alterations in the region adjacent to the CGG repeat elements. Three patients in fragile X families have the normal fragment with amplification in a small population of their cells. These observations indicate that there is molecular heterogeneity in the fragile X syndrome and that the DNA fragment length variation is not the only sequence responsible for the expression of the fragile site or the disease phenotype.

Base Sequence

Ly-49 multigene family. New members of a superfamily of type II membrane proteins with lectin-like domains.

Ly-49 (YE1/48, A1) is a dimer protein expressed on subpopulations of murine NK cells. It is a member of a superfamily of type II transmembrane proteins containing carbohydrate recognition domains (CRD). In the mouse genome, the detection of multiple restriction fragments that cross-hybridize with Ly-49 cDNA probes suggests the presence of related genes. In this study, we have isolated several genomic clones encoding portions of CRD sequences highly homologous to the CRD of Ly-49. By using primers based on the consensus sequences of the genomic clones, expression of Ly-49-related genes was detected by the polymerase chain reaction in various organs, including lung, kidney, liver, spleen, and thymus. Two full-length cDNA clones that are highly homologous to the Ly-49 gene were subsequently isolated from a lung cDNA library. At the nucleotide level, the two clones are 72% and 80% identical to Ly-49 in their translated regions, but their sequences are different from those of the genomic clones characterized to date. The two cDNA clones potentially encode type II transmembrane proteins containing CRD that are very similar to Ly-49. These amino acid sequences are also homologous to other members of the superfamily of CRD-containing type II transmembrane proteins, including hepatic lectins and the low affinity IgER (CD23). The homology is most evident in the CRD but is also significant in other domains. These results demonstrate the existence of several functional genes that are highly related to Ly-49. These genes comprise a subfamily within the superfamily of type II transmembrane proteins containing CRD.

Amino Acid Sequence

Outcome of prophylactic therapy for idiopathic anaphylaxis.

OBJECTIVE: To determine the efficacy of a prophylactic regimen (prednisone, H1 blockade, and sympathomimetic amine therapy) in patients with idiopathic anaphylaxis. DESIGN: Clinical trial before and after treatment. SETTING: Referral-based allergy clinic at a major medical center. PATIENTS: Fifty-three patients with a history compatible with idiopathic anaphylaxis for at least 6 months before presentation to the allergy service and with subsequent management by the service for at least 6 months. INTERVENTIONS: Patients with frequent life-threatening symptoms were treated with a prophylactic regimen. Patients with infrequent episodes of idiopathic anaphylaxis were only treated acutely for each episode of anaphylaxis. MEASUREMENTS AND MAIN RESULTS: The results favored prophylactic treatment with prednisone for patients who were classified as generalized-frequent in the clinical outcome measures of frequency (per patient per year) of episodes (mean before treatment, 7.31 +/- 6.46; after treatment, 3.61 +/- 4.73; P less than 0.02) and emergency room visits (mean before treatment, 1.94 +/- 3.42; after treatment, 0.21 +/- 0.44; P less than 0.005) and for patients classified as angioedema-frequent in the frequency of episodes (mean before treatment, 14.93 +/- 15.89; after treatment, 2.58 +/- 2.18; P less than 0.003) and emergency room visits (mean before treatment, 0.76 +/- 1.01; after treatment, 0.07 +/- 0.11; P less than 0.025). No statistically significant difference was found for patients classified as generalized-infrequent in the frequency of episodes (mean before treatment, 2.01 +/- 1.30; after treatment, 1.36 +/- 1.79) or of the emergency room visits (mean before treatment, 0.56 +/- 0.71; after treatment, 0.32 +/- 0.75) or for patients classified as angioedema-infrequent in the frequency of episodes (mean before treatment, 1.94 +/- 1.55; after treatment, 2.03 +/- 2.16) or of emergency room visits (mean before treatment, 0.27 +/- 0.44; after treatment, 0.37 +/- 0.59). CONCLUSIONS: Prophylactic treatment with prednisone and H1 antihistamines with or without sympathomimetic amines improves clinical outcome in patients who are classified as idiopathic anaphylaxis-angioedema frequent and idiopathic anaphylaxis-generalized frequent.

Adolescent