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Biomedical subjects

S Fang

Publications and source records attributed to S Fang.

At least 73 records · Page 4Linked to original sources

Analysis of binding of monoclonal antibody to a malarial peptide by surface plasmon resonance biosensor and integrated rate equations.

Using biosensor technology and integrated rate equations, we have developed procedures to determine the kinetic parameters and equilibrium affinity constant of Ag-Ab interactions. The Ag used in these studies was a peptide that represents the major B cell epitope of the circumsporozoite protein of Plasmodium falciparum, a promising malaria vaccine candidate Ag. Measurements of association and dissociation rate constants of this peptide with the mAb 2A10 were determined by fitting integrated rate equations to binding data obtained with a BIAcore surface plasmon-resonance biosensor. We examined whether accurate estimates of initial velocity and final equilibrium levels of binding of Ab to peptides can be obtained using these methods, and whether kinetic rates and equilibrium constants obtained with systematic variation of the experimental parameters conform to a simple bimolecular model of binding. We found that initial velocity was approximately first order with respect to Ab concentration. When we used a series of four sensor cells with different peptides loads, however, we found that the initial velocity of binding appeared to be nearly independent of peptide concentration. Equilibrium analyses yielded dissociation constants of approximately 3 x 10(-7) M. Integrated rate treatment of biosensor data supports a critical examination of the assumptions on which the binding models are based and suggests a need to refine such models. Nevertheless, it provides a powerful quantitative tool for assessing the Ag-Ab binding reaction.

Amino Acid Sequence↗

Stoichiometry of recombinant cystic fibrosis transmembrane conductance regulator in epithelial cells and its functional reconstitution into cells in vitro.

We have generated several clones of Chinese hamster ovary, mouse epitheloid C127, and pig kidney epithelial LLCPK1 cells producing high levels of functional recombinant human cystic fibrosis transmembrane conductance regulator (CFTR). Processing of CFTR to the mature and fully glycosylated form in these cells is inefficient with only approximately 40% of all newly synthesized CFTR being converted to the mature form. Furthermore, expression of the most frequent mutant allele of the cystic fibrosis (CF) gene, the delta F508 mutant in these epithelial cells, indicated that it is biosynthetically arrested at the endoplasmic reticulum and fails to traffic to the plasma membrane. Using a combination of CFTR mutants and monoclonal antibodies, all the detectable recombinant CFTR in these cells was determined at least under the conditions used, to be present as a monomer. To demonstrate the feasibility of protein replacement therapy, we were able to effect the physical transfer of functional recombinant CFTR produced in Chinese hamster ovary cells to the plasma membranes of Ha3b fibroblasts, a cell line devoid of cAMP-stimulated chloride channels. Transfer of CFTR was mediated by the hemagglutinin viral fusion protein of influenza virus present on the Ha3b cells. Efficiency of transfer was up to 25% of the target cells, and CFTR chloride channel activity was detectable for up to 12 h post-fusion. Therefore, with the development of an appropriate formulation of fusogenic proteoliposome or virosome containing reconstituted purified CFTR, it should be feasible to introduce functional CFTR into CF-affected cells.

Adenosine Triphosphate↗

Colocalization of NADPH-diaphorase activity and certain neuropeptides in the esophagus of opossum (Didelphis virginiana).

Nitric oxide and various neuropeptides in the myenteric plexus regulate esophageal motility. We sought colocalization of nitric oxide synthase and neuropeptides in frozen sections of mid-portion of smooth-muscled opossum esophagus using NADPH-diaphorase activity to mark the synthase and immunoreactivity to detect peptides. The peptides, all with demonstrated physiological activity in this organ, were calcitonin gene-related peptide, galanin, neuropeptide Y, substance P, and vasoactive intestinal polypeptide. The ExtrAvidin Peroxidase immunostain for each peptide was carried up to the final peroxidase reaction with 3-amino-9-ethyl-carbazole. The NADPH-diaphorase reaction was applied with short incubation to provide light staining just before the peroxidase reaction was performed. We examined sections for the proportions of singly and dually labeled nerve cells in the myenteric plexus. NADPH-diaphorase activity was highly colocalized with calcitonin gene-related peptide (59%), galanin (54%), and vasoactive intestinal polypeptide (53%). It showed little colocalization with neuropeptide Y (10%) and substance P (8%). The proportions of all nerve cells containing each of the substances were: NADPH-diaphorase--33%, calcitonin gene-related peptide--30%, galanin--55%, neuropeptide Y--16%, substance P--35%, and vasoactive intestinal polypeptide--58%. We conclude that the nerves responsible for peristalsis in the esophagus may act by releasing nitric oxide along with other inhibitory substances, calcitonin gene-related peptide, galanin, and vasoactive intestinal polypeptide, but not excitatory substances, neuropeptide Y and substance P.

Animals↗

Vasoactive intestinal contractor: localization in the opossum esophagus and effects on motor functions.

BACKGROUND/AIMS: Vasoactive intestinal contractor (VIC), an endothelinlike peptide and a putative gastrointestinal hormone, contracts gastrointestinal smooth muscle. The aim was to study VIC in relation to esophageal function. METHODS: Intramural nerves in opossum esophageal smooth muscle strips were stimulated in the presence of various concentrations of VIC and were stained for VIC immunoreactivity. RESULTS: VIC caused an atropine-resistant increase in the amplitude of nerve-induced contractions of the circular muscle. VIC alone contracted longitudinal muscle, and this effect was nearly eliminated by 1 mmol/L atropine. VIC caused an atropine-resistant increase in the resting tone of the lower esophageal sphincter muscle, but it did not affect nerve-induced relaxation of that muscle. VIC-immunoreactive nerve fibers occurred in the longitudinal muscle layer, in the muscularis mucosae, and around the ducts of esophageal glands. A few such fibers were found in the circular muscle layer. Nerve fibers and cell bodies of the myenteric plexus showed VIC immunoreactivity. In the stomach, immunoreactive nerve fibers occurred in muscularis mucosae and circular muscle but not in longitudinal muscle. CONCLUSIONS: VIC is localized in neuronal elements of the opossum esophagus and excites contractions in esophageal smooth muscle.

Animals↗

Roles of Triton X-100 in NADPH-diaphorase histochemistry.

Triton X-100 is widely but not universally used in NADPH-diaphorase histochemical staining. We investigated its effect on the staining and examined nitroblue diformazan (NBF) production under the influence of Triton X-100. Exposure of opossum esophagus, intestine, and colon tissues to Triton X-100 before staining enhanced staining of nerve cells and fibers and suppressed staining of non-neural structures. Long exposures and high concentrations nearly abolished the staining of non-neural structures and decreased the staining of nerves. The use of an incubation medium containing Triton X-100 achieved the best staining of nerve cells and fibers. Addition of Triton X-100 to the incubation medium changed its color from yellow to purple; in the presence of tissues, this color change occurred much more quickly. Spectral analysis showed that Triton X-100 increases the rate of NBF formation in the presence of tissue supernatant. Triton X-100 increases it less in the absence of tissue supernatant. Therefore, Triton X-100 improves the histochemical staining, probably by catalyzing the activity of NADPH-diaphorase, by keeping the extracellular NBF in solution and thus suppressing the staining of non-neural structures, and by increasing the permeability of cell membranes.

Animals↗

Improvement in raw-starch-digesting glucoamylase production by electrofusion of Aspergillus niger.

By using the protoplasts of auxotrophic strains Aspergillus niger (lys- and arg-), the stable fusants were obtained. An optimal condition of hybrids to form colonies on MM/CM was found at A = 4.5kV/cm, Np = 32, Tp = 62.5 microseconds, T = 0.2s, Cy = 10, D = 3mm, and Ff = 60%. Through observation of the morphology, the size, the DNA content and the activity of glucoamylases, the differences between the fusants and segregants and their parental strains were shown. These results indicated the new possibility for strain improvement in A. niger.

Aspergillus niger↗

Inhibitory effect of cicletanine on vascular smooth muscle cell proliferation.

We investigated the effect of cicletanine on vascular smooth muscle cell proliferation. In cultured vascular smooth muscle cells from rat mesenteric artery, cicletanine (10(-5) to 10(-4) M) increased prostacyclin synthesis (measured as 6-keto-PGF1 alpha by radioimmunoassay) dose-dependently. When added to cells in which mitogenesis was activated by 10% fetal bovine serum, cicletanine (3.3 x 10(-5) to 10(-4) M) inhibited [3H] thymidine incorporation up to 31% of the control level. Inhibitory effect of cicletanine on mitogenesis was also confirmed at 48 h by cell counts (control: 18965 +/- 629, cicletanine 10(-4) M: 14840 +/- 430, n = 6). The effect of cicletanine on platelet-derived growth factor (PDGF)-stimulated [3H] thymidine incorporation was not abolished by prostaglandin synthesis inhibition with aspirin, but the prostacyclin analogue OP-41483 (125-1000 ng/ml) inhibited it dose-dependently. Calcium entry blockers, nifedipine (3.3 x 10(-6) M) and diltiazem (10(-4) M), inhibited both [3H] thymidine incorporation and cell proliferation, while furosemide did not affect it. Cicletanine also inhibited PDGF-stimulated [3H] thymidine incorporation in cultured glomerular mesangial cells. We conclude that cicletanine stimulates prostacyclin synthesis and inhibits cell proliferation in cultured vascular smooth muscle cells, which may possibly be related to the intracellular calcium mobilization. Such a property might be contributory to the antihypertensive activity of cicletanine.

Animals↗

Papillary collecting tubule responsiveness to vasoactive hormones in spontaneously hypertensive rats.

Renal papillary collecting tubule (RPCT) hormone responsiveness was compared between cultured RPCT cells from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Unstimulated cells from 4-week-old SHR produced less prostaglandin E2 (PGE2) and cyclic (c)AMP than comparable cells from WKY, while cells from both stains synthesized similar amounts of PGE2 after stimulation with arachidonate, A23187 or bradykinin and similar amounts of cAMP after stimulation with vasopressin or PGE2. There was no difference in basal or stimulated levels of cyclic (c)GMP between the strains. In RPCT cells from 16-week-old rats, basal levels of cAMP, cGMP and PGE2 were significantly lower than those from 4-week-old rats, but they did not differ between the strains. These results suggest that RPCT cells of SHR and WKY at the post-weaning period may differ in the metabolism of PGE2 and cAMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.

Age Factors↗

Inhibitory effect of sulindac on prostaglandin synthesis in cultured renal and vascular cells.

Sulindac, a non-steroidal anti-inflammatory drug (NSAID), is said to be less toxic to the kidney than the other NSAIDs. To examine this hypothesis we investigated the effects of sulindac and other NSAIDs on prostaglandin (PG) synthesis in cultured rat renal and vascular cells. In all cells examined, indomethacin, tiaprofenic acid, aspirin and ibuprofen (3.3 x 10(-5)-3.3 x 10(-4)M) inhibited both basal and arachidonic acid (AA)-stimulated PGE2 or PGI2 synthesis (measured as 6-keto-PGF1 alpha), while sulindac (3.3 x 10(-5)-3.3 x 10(-4)M) inhibited both basal and AA-stimulated PGE2 synthesis in renal papillary collecting tubule cells but not basal PGI2 synthesis in vascular smooth muscle cells or AA-stimulated PGE2 synthesis in glomerular mesangial cells. The order of potency for NSAIDs to inhibit PG synthesis in these cells was tiaprofenic acid, indomethacin greater than ibuprofen, aspirin greater than sulindac. It is suggested that the prodrug sulindac is biotransformed to the active sulfide in the intact kidney cells, which may be less prominent in glomerular mesangial or vascular smooth muscle cells.

Animals↗

Effect of in vitro aging on prostaglandin synthesis in cultured rat vascular smooth muscle cells.

Cultured rat vascular smooth muscle cells from mesenteric artery produced prostaglandin (PG)E2, PGF2 alpha, PGI2 and thromboxane (TX)A2 in response to arachidonic acid, calcium ionophore A23187, vasopressin and angiotensin II. PGI2 was the major product among these PGs. PG synthesis in these cells decreased with in vitro aging, but the distribution pattern of PG synthesis did not change up to the passage level 56. Therefore, it is suggested that imbalance among PGs may not be directly implicated in vascular diseases in aging.

Aging↗

Activities of morphinone and N-(cyclopropylmethyl)normorphinone at opioid receptors.

Morphinone (3) and N-(cyclopropylmethyl)normorphinone (4) were synthesized and tested on electrically stimulated smooth muscle preparations (guinea pig ileum and mouse vas deferens) and in mice. Compound 3 behaved as an agonist and 4 as an antagonist in vitro and in vivo. No pronounced nonequilibrium agonist or antagonist activity was observed with either compound.

Animals↗

Non-Hodgkin's lymphoma in children: results of treatment with LSA2-L2 protocol.

The results obtained with very intensive treatment in previously untreated patients early in the disease are encouraging, and we hope will change the philosophy of most investigators that even in far advanced disease such as those with marrow metastases or multiple primary sites, one can still obtain complete regression at all tumour sites within 1 to 1 1/2 months from onset of therapy by combined treatment with multiple chemotherapeutic agents and radiation therapy to one or more sites.

Adolescent↗