Biomedical subjects

J F Wang

Publications and source records attributed to J F Wang.

At least 145 records · Page 8Linked to original sources

PubMed1994

Basic fibroblast growth factor (basic FGF) in isolated ovine thyroid follicles: thyrotropin stimulation and effects of basic FGF on DNA synthesis, iodine uptake and organification, and the release of insulin-like growth factors (IGFs) and IGF-binding proteins.

We examined the effects of thyroid-stimulating hormone (TSH) on basic fibroblast growth factor (basic FGF) expression in isolated ovine thyroid follicles in vitro, and the effects of exogenous basic FGF on thyroid growth and function, to elucidate the significance of increased basic FGF expression during TSH-induced rat thyroid hyperplasia in vivo. Primary cultures of ovine thyroid follicles were maintained in serum-free Ham's modified F-12M medium containing transferrin, somatostatin, and glycyl-histidyl-lysine (designated 3H) with or without basic FGF alone, or in combination with TSH (100 microU/mL) and cortisol (10 nM). Following 48 h incubation, cells were harvested and total RNA prepared for the detection of basic FGF mRNA using Northern blot analysis and ribonuclease protection assay. Basic FGF in the cytoplasm and extracellular matrix fractions was quantified by radioimmunoassay. Basic FGF mRNA transcripts of 3.7, 3.0, and 2.2 kb, respectively, were found in thyroid follicles cultured in 3H medium, and the abundance of each increased between 2- and 3-fold following incubation with 10-50 microU/mL TSH, although higher concentrations of TSH were less effective. Similar results were seen using a more sensitive ribonuclease protection assay. Cells cultured in control, 3H medium contained 2.4 +/- 0.5 fmol immunoreactive basic FGF/micrograms cell DNA within the cytoplasm and 21.1 +/- 1.5 fmol/micrograms DNA within the extracellular matrix (mean +/- SD, n = 6). A significant increase (p < 0.05) in basic FGF content was seen in both cell compartments following incubation with 50 or 100 microU/mL TSH, while 250 microU/mL was less effective.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

The roles of nitric oxide and hydrogen peroxide production in lipopolysaccharide-induced intestinal damage.

The importance of gastrointestinal injury in endotoxin-induced shock and multiple organ failure is of great interest. In this paper we describe a method to assess the degree of intravascular congestion and bleeding into the wall of the intestine by determining the hemoglobin content of the tissue. After validating this method, we used it to study the mechanism of jejunal injury induced by intravenous injection of Escherichia coli lipopolysaccharide (LPS, 50 mg/kg bw), the role of nitric oxide release in maintaining the integrity of endothelial cells, and the participation of H2O2 production in the LPS-induced intestinal damage in rats. Our results show that after the administration of LPS at the dose of 50 mg/kg intravenously, the hemoglobin content of the jejunum (17.8 mg/100 mg tissue) increased 7.7-fold over that of control animals (2.3 mg/100 mg), reflecting a serious degree of congestion, bleeding, and damage in the gastrointestinal tract. Administration of nitro-L-arginine methyl ester (L-NAME) not only enhanced this injury, but also markedly decreased the dose of LPS necessary to induce intestinal damage. Infusion of L-arginine (300 mg/kg bolus plus infusion 600 mg/kg.h intravenously) protected the intestine against LPS or LPS plus L-NAME. Inhibition of basal nitric oxide release by L-NAME produced significant changes in cardiovascular variables, but failed to induce a significant bleeding damage. However, when inhibition of NO release was combined with enhanced H2O2 production by a small dose of LPS, a serious bleeding damage was observed. This was accompanied by a marked decrease in mesenteric blood flow and cardiac output. High dose of LPS induced the above effects, and thus could be responsible for the bleeding damage, while low dose of LPS that fails to inhibit nitric oxide, did not induce any intestinal bleeding. It seems that inhibition of NO release and stimulation of H2O2 production are both involved in the LPS-induced bleeding damage.

Animals↗

PubMed1994

The porA gene in serogroup A meningococci: evolutionary stability and mechanism of genetic variation.

Molecular analyses were applied to the genes encoding variants of the serosubtyping antigen, the class 1 outer membrane protein (PorA), from 55 serogroup A Neisseria meningitidis strains. These genes were evolutionarily stable and exhibited a limited range of genetic variation, primarily generated by recombination. Translation of the gene sequences revealed a total of 19 distinct amino acid sequences in the variable regions of the protein, 6 of which were not recognized by currently available serosubtyping monoclonal antibodies. Knowledge of these amino acid sequences permitted a rational re-assignment of serosubtype names. Comparison of the complete genes with porA gene sequences from serogroup B and C meningococci showed that serogroup A possessed a limited number of the possible porA genes from a globally distributed gene pool. Each serogroup A subgroup was characterized by one of four porA gene types, probably acquired upon subgroup divergence, which was stable over periods of decades and during epidemiological spread. Comparison with other variable genes (pil and iga) indicated that the three alleles were independently assorted within the subgroup, suggesting that their gene types were older than the subgroups in which they occurred.

Alleles↗

PubMed1994

Hormonal regulation and biological actions of insulin-like growth factor binding proteins in isolated ovine thyroid follicles.

The ability of TSH to stimulate synthesis and release of thyroid hormones in ovine thyroid follicles in vitro depends partially on a synergy with insulin-like growth factors (IGFs). The cellular availability of IGFs may be influenced by the release of several IGF binding proteins (IGFBPs). The purposes of these studies was to 1) further characterize the species of IGFBPs synthesized by thyroid follicles, 2) examine the ability of TSH and cortisol to alter IGFBP gene expression and protein release, and 3) investigate the actions of exogenous IGFBPs on thyroid cell function. Adult sheep thyroid follicles were isolated after collagenase digestion, grown to confluence in Coon's modified Ham's F12M medium (OH) with the addition of transferrin, glycylhistidyl-lysine, somatostatin (3H), cortisol and insulin, and maintained in serum-free test media with or without further supplements for up to 48 h. Conditioned media were analyzed for IGFBP presence by Western ligand blotting, and by immunoblotting using specific antisera against bovine IGFBP-2 and human IGFBP-5. IGFBP mRNAs from follicles were identified by Northern blot hybridization using [32P]labeled complementary DNAs encoding ovine IGFBP-1 or -2, and rat IGFBP-4, -5, or -6. Uptake and organification of Na[125I] were measured by incorporation into trichloroacetic acid-precipitable material. Isolated thyroid follicles synthesized four species of IGFBPs in either 0H or 3H medium as detected by ligand blotting, of sizes 40-46, 34, 28, and 18 kilodaltons (kDa), respectively. The 32 kDa IGFBP was identified immunologically as IGFBP-2, whereas the 28 kDa and 18 kDa species were identified as IGFBP-5. Northern blot hybridization of total RNA from cells in 3H medium demonstrated an IGFBP-2 messenger RNA (mRNA) [1.4 kilobase (kb)], an IGFBP-4 mRNA (2.6 kb), and two IGFBP-5 mRNAs (6 kb and 1.8 kb). No IGFBP-1 or -6 mRNAs were detected. Incubation of cultured follicles with TSH (30-500 microU/ml) caused a dose-dependent decrease in the abundance of all IGFBP mRNAs and released proteins, which were reduced further by TSH together with cortisol (10 nM). When the inhibitory effect of TSH and cortisol was removed, IGFBP-2 mRNA increased within 3 h and was 7-fold greater within 12 h. IGFBP-2 did not appear in the conditioned medium until 12 h after TSH removal, along with the other IGFBP species.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Role of 3', 5' cyclic adenosine monophosphate and protein kinase C in the regulation of insulin-like growth factor-binding protein secretion by thyroid-stimulating hormone in isolated ovine thyroid cells.

Isolated sheep thyroid follicles release insulin-like growth factors (IGF)-I and -II together with IGF-binding proteins (IGFBPs). We previously showed that TSH suppresses the biosynthesis and release of IGFBPs in vitro which may increase the tissue availability of IGFs, allowing a synergy with TSH which potentiates both thyroid growth and function. Many of the actions of TSH on thyroid cell function are dependent upon activation of adenylate cyclase, although increased synthesis of inositol trisphosphate and activation of protein kinase C (PKC) have also been implicated. We have now examined whether probable changes in intracellular cyclic adenosine monophosphate (cAMP) or PKC are involved in TSH-mediated suppression of IGFBP release. Confluent primary cultures of ovine thyroid cells were maintained in serum-free Ham's modified F-12M medium containing transferrin, somatostatin and glycyl-histidyl-lysine (designated 3H), and further supplemented with sodium iodide (10(-8)-10(-3) mol/l), dibutyryl cAMP (0.25-1 mmol/l), forskolin (5-20 mumol/l) or 12-O-tetradecanoylphorbol-13-acetate (TPA; 10(-11)-10(-6) mol/l), with or without exposure to TSH (200 microU/ml). The uptake and organification of Na [125I] by cells was examined after test incubations of up to 48 h, and IGFBPs in conditioned media were analysed by ligand blot using 125I-labelled IGF-II. The PKC activity in the cytosol and plasma membrane fractions of cells was measured by phosphorylation of histone using [gamma-32P]ATP, and PKC immunoreactivity was visualized by Western immunoblot analysis. While dibutyryl cAMP or forskolin largely reproduced the stimulatory effect of TSH on iodine organification, they did not mimic the inhibitory effect of TSH on the secretion of IGFBPs of 43, 34, 28 and 19 kDa. Incubation with physiological or pharmacological concentrations of iodide (10(-6)-10(-3) mol/l) for up to 48 h significantly decreased TSH action on iodide uptake and organification but did not alter the inhibitory action of TSH on IGFBP release. Incubation of cells with 10(-11)-10(-6) mol TPA/l for 24 h inhibited the subsequent ability of TSH both to potentiate iodine organification and to suppress IGFBP release. In 3H medium, PKC activity was predominantly recovered from the membrane fraction but, following incubation for 48 h with TSH, the enzyme was no longer translocated to the membrane and was recovered predominantly from the cytosol.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Increase of basic fibroblast growth factor (FGF) and FGF receptor messenger RNA during rat thyroid hyperplasia: temporal changes and cellular distribution.

Goitre was induced in adult rats by acute (1 or 2 weeks) or chronic (4 or 10 weeks) administration of methimazole together with a low iodine diet. Involution of thyroid growth was then observed at 16 weeks, 4 weeks after withdrawal of goitrogens and reversion to a normal diet. Experimental animals quickly became hypothyroid compared with controls and exhibited thyroid hyperplasia (control (n = 10): total serum thyroxine (T4) 66 +/- 4 nmol/l, thyroid weight 5 +/- 1 mg/100 g body weight, means +/- S.D.; experimental (n = 10): T4 undetectable, thyroid weight 27 +/- 4 mg/100 g body weight after 2 weeks of treatment). Thyroid growth rate subsequently slowed between 2 and 10 weeks. Messenger RNA for basic fibroblast growth factor (basic FGF) and for the high-affinity FGF receptor, was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for basic FGF and its receptor were detectable in thyroids from control rats at all times, while none was detected in the livers from any animal. Basic FGF and receptor mRNAs increased, and were detected at greatest abundance in hyperplastic thyroids at 1 and 2 weeks respectively, during goitre formation, but subsequently declined in parallel with thyroid growth rate at 4 and 10 weeks. When quantified by radioimmunoassay, basic FGF extracted from thyroids was fivefold greater than in controls after 1 week of goitrogen treatment (control (n = 4): 24 +/- 9 pmol/micrograms DNA; goitre (n = 4): 100 +/- 16 pmol/micrograms DNA; P < 0.05). Basic FGF and FGF receptor mRNAs localized by in situ hybridization predominantly to the epithelial cell population within follicles. Localization by immunohistochemistry demonstrated that basic FGF was present in the thyroids of control rats, and was largely associated with the basement membrane of follicles. During thyroid hyperplasia, increased basic FGF immunoreactivity appeared over the cytoplasm of follicular epithelial cells and was lost from the extracellular matrix. Thyroid involution following removal of goitrogen/low iodine treatment was associated with a decrease in mRNA for basic FGF or its receptor, and a loss of immunoreactive basic FGF from the cytoplasm of follicular cells. These results suggest that autocrine expression of basic FGF and FGF receptor could contribute to thyroid hyperplasia in rats.

Animals↗

PubMed1994

Altered expression of insulin-like growth factor-I (IGF-I) and IGF binding proteins during rat thyroid hyperplasia and involution.

We have investigated changes in the synthesis and localization of insulin-like growth factor (IGF)-I and IGF binding proteins (IGFBPs) in thyroid tissues during the induction of goitre in iodine-deficient rats, and during the subsequent involution of the gland following goitrogen withdrawal. Goitre was induced in adult rats by acute (1 or 2 weeks) or chronic (4 or 10 weeks) administration of methimazole together with a low iodine diet. After twelve weeks the goitrogenic stimuli were removed and thyroids examined 4 weeks later. Circulating T4 levels became undetectable within two weeks of goitrogen administration while thyroid weight had increased five-fold. The thyroids continued to increase in size up to 10 weeks, but at a slower growth rate. IGF-I mRNA, detected by ribonuclease protection assay, was present in the control rat thyroid and increased in abundance after both 1 and 2 weeks of goitrogen administration. Levels of IGF-I mRNA showed a relative decline with prolonged goitrogen administration, and following thyroid involution the hybridization signal was similar to that seen in control glands. Northern blot hybridization showed that IGFBP-2, -3 and -5 mRNAs were all present in growth-quiescent, control thyroids and those encoding IGFBP-2 and -3 were elevated in the goitrous glands and remained so as long as goitrogen was administered, thereafter declining during thyroid involution. IGF-I and IGFBP-2 and -3 mRNAs and synthesized peptides, detected by in situ hybridization and immunohistochemistry respectively, were found to co-localize predominantly in follicular epithelial cells. IGFBP-5 mRNA abundance was unaltered during goitre formation, but was increased in the involuting thyroid. Both IGFBP-5 mRNA and peptide were localized to the parafollicular cells (C-cells) which were increased in number during involution. The results suggest that an increased expression of IGF-1 may contribute to early goitre formation, but that a relative increase in the abundance of IGFBP-2 and -3 may limit IGF availability at later times, and facilitate a slowing of thyroid growth rate. The discrete expression of IGFBP-5 by C-cells suggests that it could contribute indirectly to goitre formation or involution by acting in a paracrine fashion.

Animals↗

PubMed1994

[The study of repairing ability of freeze-dried bone allograft].

There were many methods to preserve allogeneic bone allograft, however, a lot of studies have shown that the freeze-dried bone allograft banking is the best one. But it is not clear what temperature to lyophilize the allograft is better. In this experiment, we used method, in which the temperature of lyophilization was raising naturally and regularly, to lyophilize the allograft. The repairing ability of the freeze-dried allograft was studied in rabbits and comparison was made with that of autograft and fresh allograft. The results indicated that the repairing ability of bone defects was not significantly different between autograft and freeze-dried allograft. There was no significant difference between autograft and fresh allograft 3 weeks after transplantation, but significant difference was noted 8 weeks after grafting. It is suggested that this might be associated with the latent period before immunological rejection and the method itself, in which the temperature of lyophilization raising naturally is beneficial.

Animals↗

PubMed1994

Serum neuron-specific enolase levels in patients with small cell carcinoma of the uterine cervix.

Serum neuron-specific enolase (NSE) is a tumor marker for neuroendocrine tumors or tumors of neuroepithelial origin. While the clinical application of NSE in small cell lung cancer has been established, its role in small cell carcinoma of the uterine cervix is unknown. We examined serum NSE in six patients with cervical small cell carcinoma and 13 patients with cervical squamous cell carcinoma. Elevated serum NSE was noted in four of six patients (67%) with small cell carcinoma, but none of the 13 patients with squamous cell carcinoma. An extremely high NSE serum level (154.7 ng/mL) was found in one patient with recurrence of small cell carcinoma, suggesting its correlation with disease extension. Although further studies to evaluate its relevance to prognosis, treatment effect, and early detection of recurrence are in progress, this preliminary result seems promising.

Adult↗

PubMed1994

[A case control study on risk factors of endometrial carcinoma in Tianjin].

A case-control study was conducted on risk factors of endometrial carcinoma in Tianjin. The data was analysed with chi 2 test an linear logistic regression. The risk factors of endometrial carcinoma including age of marriage, menopause, body mass index, exposure to X-ray, hypertension, pregnancies, and lactation were investigated. The results showed that body mass index, and exposure to X-ray were predominant risk factors; while pregnancies and lactation were protective factors.

Adult↗

PubMed1994

Expression of human hepatitis B virus surface antigen gene in transgenic tobacco.

Expression of Human hepatitis B virus surface antigen (HBsAg) gene in plant was reported for the first time. The recombinant plasmid pRoKII-HBsAg was constructed by inserting HBsAg gene into the downstream of CaMV 35S promoter of binary vector pRoKII and then introduced into Agrobacterium tumefaciens LBA4404. The kanamycin-resistant plants were obtained by Agrobacterium-mediated transformation system. It was shown that HBsAg gene was expressed in transgenic tobacco plants and their progenies by ELISA. The spherical particles of psi 22 nm is the leaf extract of transgenic tobacco were observed by immunosorbent electron microscopy.

Gene Expression↗

PubMed1994

Integration and expression of human growth hormone gene in Caladium bicolor.

Human growth hormone (hGH) gene has been inserted into the plasmid pLGV1103 to give the recombinant plasmid pLB-9. It has been introduced into the agrobacterium containing plasmid pGV3850. The recombinant Ti plasmid pGL198(hGH) has been obtained by homologous recombination. The monocotyledon Caladium bicolor has been transferred with pGL198 (hGH) with the leaf-disk co-cultivation method, and transgenic plants have been regenerated. The results of nopaline analysis, NPT II detection Southern blot and Western blot show that the hGH gene was integrated into the genome of Caladium bicolor, and a 22-kD protein was synthesized in the transgenic plants.

Gene Transfer Techniques↗

PubMed1993

Alcohol administration attenuates LPS-induced expression of inducible nitric oxide synthase in Kupffer and hepatic endothelial cells.

This study investigates the effects of in vivo ethanol (primed infusion, causing 170-190 mg% plasma alcohol for 12 hours) and/or LPS (12 hours after injection of E. coli LPS 1 mg/kg bw.) on the mRNA expression of inducible nitric oxide synthase (NOS II) in hepatic cells measured by competitive PCR technique, and on hepatic release of reactive nitrogen intermediates (RNI, NO2- + NO3-). Perfused livers from alcohol- or saline-infused animals did not release measurable amounts of RNI. Under these conditions small amounts of NOS II mRNA were expressed in Kupffer and endothelial cells, while it was not detectable in parenchymal cells. LPS treatment along with markedly elevating hepatic RNI release increased NOS II mRNA levels by 35- and 200-fold, in endothelial and Kupffer cells, respectively. LPS injection and alcohol infusion to the same animal decreased hepatic RNI release by about 70% and almost completely inhibited the LPS-induced, elevated NOS II mRNA in Kupffer or endothelial cells. No similar changes were observed in the parenchymal cells. These data suggest that the primary target of in vivo LPS in upregulating hepatic NO release are the nonparenchymal cells. Furthermore, alcohol inhibits the LPS-induced response which may influence immune-related hepatic function.

Amino Acid Oxidoreductases↗

PubMed1993

Movement of the guide sequence during RNA catalysis by a group I ribozyme.

Ribozymes derived from the self-splicing pre-ribosomal RNA of Tetrahymena act as sequence-specific endonucleases. The reaction involves binding an RNA or DNA substrate by base pairing to the internal guide sequence (IGS) to form helix P1. Site-specific photo-crosslinking localized the 5' end of the IGS in helix P1 to the vicinity of conserved bases between helices P4 and P5, supporting a major feature of the Michel-Westhof three-dimensional structure model. The crosslinked ribozyme retained catalytic activity. When not base-paired, the IGS was still specifically crosslinked, but the major site was 37 A distant from the reactive site in the experimentally supported three-dimensional model. The data indicate that a substantial induced-fit conformational change accompanies P1 formation, and they provide a physical basis for understanding the transport of oligonucleotides to the catalytic core of the ribozyme. The ability of RNA to orchestrate large-scale conformational changes may help explain why the ribosome and the spliceosome are RNA-based machines.

Animals↗

PubMed1993

Luminol chemiluminescence in rat macrophages and granulocytes: the role of NO, O2-/H2O2, and HOCl.

Luminol chemiluminescence was increased up to five-fold by L-arginine and markedly inhibited by NG-nitro-L-arginine (L-NNA) in phorbol ester (PMA) or opsonized zymosan-activated rat Kupffer cells, and in PMA-activated rat peritoneal and alveolar macrophages. While in Kupffer cells these effects did occur without pretreatment with lipopolysaccharides (LPS), LPS pretreatment was a requirement in peritoneal and alveolar macrophages. Azide (0.05 mM) had no effect on luminol chemiluminescence in the macrophages. The changes in luminol chemiluminescence were accompanied by parallel changes in nitric oxide (NO) formation. Macrophage superoxide anion radical (O2-) production was not significantly changed by addition of L-arginine and L-NNA nor by pretreatment with LPS. No hypochlorous acid (HOCl) formation was detectable in the macrophages. In contrast, in rat granulocytes activated by a variety of stimuli including PMA, zymosan, the chemotactic peptide formyl-methionyl-leucyl-phenylalanine and the calcium ionophore A23187 with or without pretreatment with LPS, L-arginine and L-NNA had no effect on luminol chemiluminescence. Luminol chemiluminescence, however, was largely inhibited by 0.05 mM azide. The activated granulocytes released significant amounts of HOCl but did not generate NO. These results demonstrate that NO may largely contribute to luminol chemiluminescence in rat macrophages, in which HOCl formation does not occur. On the other hand, HOCl is the reactive oxygen species responsible for luminol chemiluminescence in rat granulocytes, where NO is formed only in minor quantities, if at all.

Animals↗

PubMed1993

Suppression by [D-Pen2, D-Pen5]enkephalin on cyclic AMP dependent protein kinase-induced, but not protein kinase C-induced increment of intracellular free calcium in NG108-15 cells.

In neuroblastoma X glioma NG108-15 cell lines, KCl 50 mM produced a significant increase in [Ca2+]i which was blocked completely by voltage-dependent Ca2+ channel antagonist verapamil. High K(+)-induced increase in [Ca2+]i can be suppressed by selective delta opioid agonist [D-Pen2, D-Pen5]enkephalin (DPDPE) (an effect completely reversed by opioid antagonist naloxone), but not by the mu agonist ohmefentanyl (OMF) or kappa agonist 66A-078. Aside from high K+ stimulation, a number of chemicals can produce an increase in [Ca2+]i, i.e., selective adenylate cyclase activator forskolin, the membrane permeable cyclic AMP (cAMP) analogue dibutyryl-cAMP (Bt2cAMP) and the activator of protein kinase C (PKC) 12-O-tetradecanoylphorbol 13-acetate (TPA). All these effects can be readily blocked by verapamil. DPDPE blocks the increase in [Ca2+]i induced by forskolin and Bt2cAMP, but not that by TPA. The results suggest that cAMP dependent protein kinase-, but not PKC-induced Ca2+ influx mechanism seems to be involved in the delta receptor mediated opioid effect.

Analgesics↗

PubMed1993

Cyclic AMP mediates mu and delta, but not kappa opioid analgesia in the spinal cord of the rat.

Intrathecal (i.t.) injection of the membrane-permeable cyclic AMP (cAMP) analogue dibutyryl-cyclic AMP (Bt2cAMP) in 3 successive doses of 12.5, 12.5 and 25 ug in rats was very effective in reversing the antinociceptive effects produced by mu agonist morphine or delta agonist DPDPE, but not that by kappa agonist dynorphin A-(1-13). cAMP content of the spinal cord was significantly decreased by morphine, but not by dynorphin A-(1-13). The results imply that a decrease in spinal cAMP content may be important for the antinociceptive effect elicited by mu and delta, but not kappa opioid receptor agonists.

Analgesia↗

PubMed1993

Antigenic and epidemiologic properties of the ET-37 complex of Neisseria meningitidis.

A special collection of 336 Neisseria meningitidis strains was established that spanned the genetic variability, as defined by multilocus enzyme electrophoresis, of the ET-37 complex (228 strains isolated in different continents between the 1960s and the 1980s) and of other serogroup C meningococci (108 strains). Of the strains in the ET-37 complex, 90% were serogroup C and 10% were serogroup B. Most ET-37 complex strains were serotype 2a and serosubtype P1.5,2 or P1.5,y; most expressed class IIb pilin. Twenty-six Opa proteins differing in electrophoretic mobility or reactivity with monoclonal antibodies were variably expressed by different members of the ET-37 complex, although only four opa genes were detected in individual strains. Despite this overall diversity, most isolates from any one outbreak were fairly homogeneous.

Antigenic Variation↗