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Biomedical subjects

C Jansson

Publications and source records attributed to C Jansson.

At least 37 records · Page 2Linked to original sources
PubMed1997

Hormonal status of short children born small for gestational age.

The present study was undertaken to evaluate the hormonal status in a subgroup of prepubertal children born small for gestational age (SGA) who lacked postnatal catch-up growth. In this subgroup, a reduced rate of growth hormone (GH) secretion was found, compared with reference groups of healthy children born appropriate for gestational age, of either normal or short stature at the time of investigation. In addition, an abnormal pattern of GH secretion was observed in short children born SGA, which was most pronounced in the younger children, and involved an increased frequency of GH peaks of low amplitude, combined with increased baseline secretion. Levels of insulin-like growth factor I (IGF-I) and IGF-binding protein-3 were also reduced in short children born SGA, compared with the reference groups. These findings may explain, in part, the lack of postnatal catch-up growth in short children born SGA.

Adolescent↗
PubMed1997

Influence of gender on the correlation between plasma growth hormone profiles and urinary growth hormone excretion.

A lot of interest has been directed towards the measurement of urinary growth hormone (GH) excretion instead of plasma GH profiles or provocation tests. We investigated the factors influencing the relationship between 24- and 3-hour plasma GH profiles and urinary GH excretion in a cohort of 113 pediatric patients with growth disorders and healthy volunteers. Plasma and urinary GH were measured by polyclonal immunoassays differing in cross-reactivity with 20 kD GH (100 versus 46%), but not with 22-kD, dimer, deamidated and pituitary GH. In the 24-hour urine samples, only urinary GH excretion expressed as nanograms per 24 h correlated with plasma GH parameters, whereas the correlations for short-term samples were strongest if urinary GH excretion was expressed as nanograms per gram creatinine (r = 0.70-79, p < 0.00005-0.0001). In short-term samples urinary GH excretion depends on urinary volume and should thus be expressed in nanograms per gram creatinine, whereas 24-hour samples correlate best when urinary GH is expressed as nanograms per period. We found a significant sex difference (p < 0.02) in the correlation between 24-hour plasma GH profiles and urinary GH excretion with strong correlations in the female group (r = 0.63-0.78, p < 0.00005-0.0002) and a lack of correlation in the male group. The sex difference in the correlations between serum and urinary GH may reflect sex differences in GH profiles and metabolism, with urinary GH better reflecting the basal and slowly clearing portion of plasma GH than spontaneous GH peaks. The difference in cross-reactivities of molecular GH forms in polyclonal assays may have an impact on the correlation between plasma and urinary GH. Thus, the diagnostic value of urinary GH measurement as compared to serum GH profiles needs to be further evaluated.

Adolescent↗
PubMed1997

Increased proportion of circulating non-22-kilodalton growth hormone isoforms in short children: a possible mechanism for growth failure.

Current knowledge about the interaction between GH and its receptor suggests that the molecular heterogeneity of circulating GH may have important implications for growth. The aim of this study was to investigate the proportion of circulating non-22-kDa GH isoforms in prepubertal children with short stature (height less than -2 SD score) of different etiologies. We have also evaluated the relationships among the ratio of non-22-kDa GH isoforms, auxology, and spontaneous GH secretion. The study groups consisted of 17 girls with Turner's syndrome (TS), aged 3-13 yr, 25 children born small for gestational age (SGA) without postnatal catch-up growth, aged 3-13 yr; and 24 children with idiopathic short stature (ISS), aged 4-15 yr. The results were compared with those from 23 prepubertal healthy children of normal stature (height +/- 2 SD score), aged 4-13 yr. Serum non-22-kDa GH levels, expressed as a percentage of the total GH concentration, were determined by the 22-kDa GH exclusion assay, which is based on immunomagnetic extraction of monomeric and dimeric 22-kDa GH from serum and quantitation of non-22-kDa GH using a polyclonal antibody-based GH assay. All samples were selected from spontaneous GH peaks in 24-h GH profiles. The median proportion of non-22-kDa GH isoforms was increased in children born SGA (9.8%; P = 0.05) and girls with TS (9.9%; P = 0.01), but not in the group of children with ISS (8.9%), compared with that in normal children (8.1%). Individually, increased proportions of non-22-kDa GH isoforms, with values more than 2 SD above the mean for the normal group, were observed in 5 girls with TS, 5 children born SGA, and 4 children with ISS. In children born SGA, the proportion of non-22-kDa GH isoforms was directly correlated with different estimates of spontaneous GH secretion [mean 24-h GH concentration (r = 0.41; P = 0.04), area under the curve over baseline (r = 0.41; P = 0.04), and GH peak area (r = 0.61; P = 0.003)], whereas it was inversely correlated with height SD score (r = -0.42; P = 0.04). In conclusion, an increased proportion of circulating non-22-kDa GH isoforms was observed at spontaneous GH peaks in some non-GH-deficient short children. Our results suggest that the ratio of non-22-kDa GH isoforms in the circulation may have important implications for normal and abnormal growth.

Adolescent↗
PubMed1997

Growth response to growth hormone (GH) treatment relates to serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 in short children with various GH secretion capacities. Swedish Study Group for Growth Hormone Treatment.

The purpose of the study was to evaluate the relationship between the 1-yr (n = 193) and 2-yr (n = 128) growth response and the individual serum concentrations of insulin-like growth factor I (IGF-I) and IGF-binding protein 3 (IGFBP-3) before and during GH treatment. Our study group of prepubertal short children had from very low to high GH secretory capacity, estimated during an arginine-insulin tolerance test, and the ages ranged from 3-15 yr at the start of treatment. Their serum levels of IGF-I and IGFBP-3 were low before treatment compared to those in an age-related reference group of prepubertal children and increased significantly from the start to 1 month of GH treatment. The mean increase in height SD score was 0.80 SD score after 1 yr of GH treatment and 1.26 SD score after 2 yr, with a wide range. In univariate analyses the highest correlation coefficients to the 2-yr growth response were found to be vs. the following variables from the start of treatment: IGF-I SD score (r = -0.49), log maximum GH concentration (log GHmax) during the arginine-insulin tolerance test (r = -0.47), difference between the height SD score of the individual child and the midparental height SD score (diffSD score; r = -0.45), IGFBP-3 SD score (r = -0.39), age (r = -0.30), short term change in IGFBP-3 SD score (r = 0.37), and IGF-I SD score (r = 0.34). In multivariate stepwise regression analysis, 41% of the variation in the 2-yr growth response could be explained by IGF-I SD score or log GHmax together with age at the start of treatment, weight SD score at 1 yr of age, and diffSD score. When both IGF-I SD score and GHmax were included and when the short term changes in IGF-I SD score were added, 46% and 58% of the variation, respectively, could be explained. The regression algorithms using different combinations of variables and their corresponding prediction intervals are also presented.

Adolescent↗
PubMed1997

Circulating non-22 kDa growth hormone isoforms in healthy children of normal stature: relation to height, body mass and pubertal development.

The proportion of non-22 kDa GH isoforms was evaluated in 93 healthy children (48 boys aged 6.8-18.4 years and 45 girls aged 3.9-18.4 years) of normal stature (height +/- 2 s.d. score) at different stages of puberty. In addition, correlations among the proportion of non-22 kDa GH isoforms, auxology, spontaneous GH secretion and biochemical measurements were investigated. Serum non-22 kDa GH levels, expressed as percentage of total GH concentration in the samples, were determined by the 22 kDa GH exclusion assay, in which monomeric and dimeric 22 kDa GH are removed from serum and the non-22 kDa GH isoforms are quantitated using a polyclonal antibody GH assay. Samples were selected from spontaneous GH peaks in 24-h GH profiles. For boys, the median proportion of non-22 kDa GH isoforms was 8.5% (range 3.2-26.6%) and for girls it was 9.6% (1.8-17.4%), with no influence of age and no sex-related difference in prepubertal (boys, 7.2%; girls, 8.8%) or pubertal children (boys, 9.1%; girls, 9.9%). However, the median proportion of non-22 kDa GH isoforms was significantly higher in pubertal boys (9.1%) than in prepubertal boys (7.2%; P = 0.03). In pubertal boys, height S.D. scores (SDS) were inversely correlated to the proportion of non-22 kDa GH isoforms (r = -0.38; P = 0.02), especially at mid-puberty (r = -0.7; P = 0.01), indicating that the presence of increased amounts of circulating non-22 kDa GH isoforms was associated with less growth. In prepubertal children, positive correlations between non-22 kDa GH and weight SDS (r = 0.46; P = 0.03), weight-for-height SDS (r = 0.51; P = 0.01) and body mass index (r = 0.42; P = 0.04) were observed. No significant correlations were seen with spontaneous GH secretion or measurements of IGF-1, IGF-binding protein-3, insulin and leptin. These findings in normal children indicate that the proportion of circulating non-22 kDa GH isoforms may have physiologic significance for growth and metabolism in different stages of development, and emphasize the importance of evaluating the circulating ratio of 22 kDa and non-22 kDa GH in children with growth disorders.

Adolescent↗
PubMed1997

Growth hormone (GH) assays: influence of standard preparations, GH isoforms, assay characteristics, and GH-binding protein.

The impact of the adoption of the new biosynthetic growth hormone (GH) WHO International Reference Preparation (IRP 88/624), and the recommendation to report results in microgram/L instead of mU/L, is described. Conversion factors were determined by comparing both the linear and nonlinear relations of the GH values. The Pharmacia polyclonal IRMA (p-IRMA) and the DELFIA monoclonal time-resolved immunofluorometric assay (trIFMA) with kit calibrators calibrated either against the pituitary-derived WHO IRP 80/505 or the new 88/624 were evaluated. Conversion factors of 4.17 mU/L = 1 microgram/L for the p-IRMA and 4.31 mU/L = 1 microgram/L for the trIFMA were necessary. Different cross-reactivity patterns for the deaminated and dimer 22-kDa, 20-kDa, and 17-kDa GH isoforms were found. Expected GH recovery was similar when the measured values were adjusted according to the results of the cross-reactivity study.

Adolescent↗
PubMed1996

Growth hormone status in six children with fetal alcohol syndrome.

OBJECTIVE: Prenatal alcohol exposure may cause fetal alcohol syndrome (FAS), which is associated with pre- and postnatal retardation. MATERIALS AND METHODS: Spontaneous 24-h growth hormone (GH) secretion was measured in six prepubertal short children with FAS (two boys and four girls) aged 4-14 years. The response to a GH stimulation test, and levels of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) were also measured. Comparisons were made between the children with FAS and healthy children of both normal and short stature, as well as children born small for gestational age (SGA). RESULTS: There were no differences in the mean area under the curve above the baseline or the maximum level of GH during a 24-h period (GHmax) between the children with FAS and the reference groups. However, the estimated rate of spontaneous 24-h GH secretion in children with FAS was similar to that of children born SGA, but lower than in children of normal stature (p = 0.02). The plasma concentrations of IGF-I and IGFBP-3 were in the lower parts of the normal range. CONCLUSION: We conclude that GH secretion in short children with FAS is similar to that in short children born SGA; that is, in the lower range of normal children.

Adolescent↗
PubMed1996

Changes in serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 levels during growth hormone treatment in prepubertal short children born small for gestational age.

The aims of this study were to describe the basal serum levels of insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) and to evaluate their changes during daily GH treatment (0.1 IU/kg; 33 micrograms/kg) for up to 2 yr in prepubertal short children born small for gestational age (SGA) and to correlate these changes with the growth response to GH therapy. Seventy-two prepubertal short children (height SD score, -5.4 to -2.0; age, 2.0-12.9 yr) born SGA (54 boys and 18 girls), eight of whom (six boys and two girls) had signs of Silver-Russell syndrome, participated in the study. The serum concentrations of IGF-I and IGFBP-3 were converted into SDS using our reference values for prepubertal healthy children. The mean (+/-SD) change in height SDS during the year before the start of GH treatment was 0.1 (0.2) and increased to 0.8 (0.4) during the first year (P < 0.001) and to 0.6 (0.3) during the second year of therapy (P < 0.001). Basal levels of both IGF-I and IGFBP-3 were significantly reduced compared with the reference values. The mean (+/-SD) basal serum concentration of IGF-I was -0.6 (1.1) SD score, and 80% of the SGA children had IGF-I levels below the 50th percentile of the reference group. The corresponding values for IGFBP-3 were -0.4 (1.0) SD score and 63%. The mean IGF-I level increased significantly by 55% from baseline to day 10 of treatment, by 76% on day 90, by 90% after 1 yr, and by 123% after 2 yr of GH treatment. The mean increases in IGFBP-3 were not as great: 25%, 27%, 35%, and 43%, respectively. The 1-yr growth response, expressed as the change in height SD score, correlated negatively with both the basal serum concentration of IGF-I (r = -0.37; P < 0.001) and IGFBP-3 (r = -0.35; P < 0.01), whereas a positive correlation was found to the 10-day percent increase in IGF-I (r = 0.32; P < 0.05). No correlations were found with the initial changes in IGFBP-3. Using a multiple stepwise linear regression analysis, the model using chronological age at the start of GH therapy, the mother's height expressed as a SD score, and the short term percent increase in IGF-I accounted for 42% of the variance in the 1-yr growth response. With the inclusion of 24-h GH profiles, 59% of the variability of the growth response could be explained. It is concluded that short prepubertal children born SGA show an increased growth rate in response to GH therapy. Their mean IGF-I and IGFBP-3 levels before treatment were low and correlated negatively with the growth response to treatment, indicating GH insufficiency. Finally, up to 59% of the variability in the 1-yr growth response to GH treatment could be explained by models using auxological and biochemical variables.

Abnormalities, Multiple↗
PubMed1995

A new dhfrVIII trimethoprim-resistance gene, flanked by IS26, whose product is remote from other dihydrofolate reductases in parsimony analysis.

A new plasmid-borne gene, dhfrVIII, encoding high-level trimethoprim resistance (TpR) was found in an intestinal Escherichia coli. It seems to be a widely occurring mediator of TpR. Among 973 examined TpR E. coli, the new resistance gene was found in 13 (1.3%) isolates from Sweden, Finland and Nigeria. The new gene was sequenced and found to code for a dihydrofolate reductase (DHFR) of 169 amino acids (M(r) 19005). The dhfrVIII gene on the studied plasmid pLMO226 was observed to be flanked by IS26 elements. The dhfrVIII gene and a 3' unidentified open reading frame (ORF) seem to be borne on a compound transposon with IS26 at its ends, since the configuration of two IS26 flanking dhfrVIII and the unidentified ORF was conserved among the isolates that were probe-positive for the gene. Phylogeny parsimony analysis showed the dhfrVIII-encoded enzyme to be only remotely related to other known plasmid-mediated, drug-resistant DHFR. Only a few of the latter form well-supported monophyletic groups.

Amino Acid Sequence↗
PubMed1994

Changes of amino acid sequence in PEST-like area and QEEET motif affect degradation rate of D1 polypeptide in photosystem II.

The degradation rate of the D1 polypeptide was measured in three Synechocystis PCC 6803 mutants in vivo. Mutations were introduced into a putative cleavage area of the D1 polypeptide (QEEET motif) and into the PEST-like area. PEST sequences are often found in proteins with a high turnover rate. The QEEET-motif mutants are CA1 [delta (E242-E244);Q241H] and E243K, and the third mutation, E229D, was directed to the PEST-like area. During high-light illumination (1500 mumol photons m-2 s-1) that induced photoinhibition of photosystem II (PSII), the half-life time of the D1 polypeptide in mutant E229D (t 1/2 = 35 min) was about twice as long as in AR (control strain) cells (t 1/2 = 19 min). In growth light (40 mumol photons m-2 s-1), the degradation rate of the D1 polypeptide in E229D and AR strains was the same (t 1/2 approximately 5 h). In growth light the D1 polypeptide was degraded faster in both QEEET-motif mutants than in the AR strain, but in photoinhibitory light the degradation rates were similar. According to these results, the highly conservative QEEET motif as such is not required for the proteolytic cut of the D1 polypeptide, but it does affect the rate of degradation. No simple correlation existed between the degradation rate of the D1 polypeptide and the susceptibility of PSII to photoinhibition in mutant and AR cells under our experimental conditions.

Amino Acid Sequence↗
PubMed1993

Functional analysis of the human alpha 2C-C4 adrenergic receptor in insect cells expressed by a luciferase-based baculovirus vector.

A click beetle luciferase-based baculovirus expression vector is described for functional analysis and high level expression of a human alpha 2-adrenergic receptor (alpha 2AR) in Sf9 insect cells. The resultant recombinant baculovirus construct, AcLucGR-alpha 2(C4), was isolated by utilizing the light emitting properties of luciferase and used for abundant expression of the alpha 2C-C4 receptor protein in this lepidopteran insect cell line. A maximal expression of alpha 2-receptors at a level of 1.370 pmol/mg protein was obtained at 48 h after infection as determined by ligand-binding experiments using the alpha 2-receptor antagonist, [3H]rauwolscine. The receptor agonists, noradrenaline and clonidine, displaced the [3H]rauwolscine binding with Ki values 12.3 +/- 1.54 microM and 1.23 +/- 0.11 microM, respectively. The recombinant receptors were functionally intact since the agonists inhibited forskolin-stimulated cAMP production. Here, however, the maximal inhibition was obtained at 36 h after the infection. The results presented here, suggest that the baculovirus expression vector system (BEVS) provides a simple method for abundant expression of functional alpha 2-receptor subtypes. In addition, co-expression of luciferase proved to be useful for screening and isolation of the recombinant baculovirus.

Adrenergic alpha-Antagonists↗
PubMed1993

Effects of the phospholipid environment in the plasma membrane on receptor interaction with the adenylyl cyclase complex of intact cells.

In this study we have examined the effects of variations of the plasma membrane phospholipid and cholesterol content on the metabolic functions of the adenylyl cyclase complex in intact cells. Exposure of cells to 0.1 U/ml of sphingomyelinase led to the degradation of 75, 55 and 40% of the cellular total sphingomyelin mass in human skin fibroblasts (HSF), Chinese hamster lung fibroblasts (CHLF) and rat liver hepatocytes (RLH), respectively. Degradation of sphingomyelin in native cells led in turn to a reduction (within 60 min) of the plasma membrane cholesterol content (by 25, 15 and 10%, respectively). This manipulation of the plasma membrane lipid content did not affect the forskolin or prostaglandin E1-induced activation of adenylyl cyclase (as measured from the conversion of [3H]adenine via [3H]ATP to [3H]cAMP). These manipulations did, however, increase the basal rate of [3H]cAMP formation in rat liver hepatocytes (but not in the fibroblast cell types). With Chinese hamster lung fibroblasts, transfected to express an alpha 2-adrenergic receptor, it was observed that the alpha 2-adrenergic receptor-induced inhibition of adenylyl cyclase activity was slightly (but significantly) diminished in sphingomyelin and cholesterol-depleted cells. With isolated rat liver hepatocytes it was observed that the glucagon (receptor) mediated activation of adenylyl cyclase was also reduced in sphingomyelinase-treated cells. In another set of experiments, CHLF and RLH cells were exposed for 2 h to vesicles prepared from dilauroylphosphatidylcholine, to increase the lateral packing density in the outer leaflet of the plasma membrane. In such treated cells, the receptor-coupling to adenylyl cyclase was markedly reduced both in CHLF (the alpha 2-adrenergic receptor) and RLH (the glucagon-receptor) cells. We conclude that the direct activation of adenylyl cyclase (i.e., by forskolin) is not markedly affected by manipulations outer leaflet phospholipid composition (either reduction of sphingomyelin or increase of phosphatidylcholine), whereas receptor-coupled events clearly are.

Adenylyl Cyclase Inhibitors↗
PubMed1993

Site-specific mutations in the D1 polypeptide affect the susceptibility of Synechocystis 6803 cells to photoinhibition.

Photoinhibition of photosystem II in the cyanobacterium Synechocystis 6803 was followed after site-specific mutagenesis of the D1 polypeptide. Mutations were created in the stromal/cytosolic loop connecting helices D and E. Two mutations E243K and CA1, a deletion of the three glutamates 242-244 and a substitution Q241H, were made in the putative cleavage area of the D1 polypeptide. A third mutation E229D was made in the PEST-like sequence. Mutants and control cells were illuminated and FV/FM was recorded. Compared to the control, the mutants were less photoinhibited. Fluorescence relaxation after a single flash was delayed in CA1. Restoration of FV/FM after photoinhibition in the mutants was totally dependent on protein synthesis while control cells were able to recover partially also when protein synthesis was inhibited. In addition, the protein synthesis-dependent recovery of CA1 was slowed down. Our results indicate a correlation between the mutated amino acids and photoinhibition of photosystem II.

Amino Acid Sequence↗
PubMed1993

Differential expression of the psbA genes in the cyanobacterium Synechocystis 6803.

The 5' region and transcription initiation sites of the psbA-2 and psbA-3 genes of Synechocystis 6803 were determined. The otherwise highly homologous genes were shown to diverge significantly in the 5' noncoding regions. The transcription start site for the psbA-2 gene was mapped to position -49 upstream of the coding region and for the psbA-3 gene to position -88, i.e. 38 bp upstream of the psbA-2 transcription start point. Both genes exhibit promoter elements, which conform in sequence and position to Escherichia coli consensus motifs. The two genes share identical -35 sequences but differ in their -10 sequences. Primer extension analysis demonstrated that the psbA-2 and psbA-3 genes are differentially expressed, with > 90% of the total psbA transcripts being produced by the psbA-2 gene and the rest by the psbA-3 gene. Inactivation of the psbA-2 gene resulted in an eightfold up-regulation of the psbA-3 gene. The strikingly higher stability of the psbA transcripts in darkness compared to light, and the accumulation of a specific decay intermediate under dark conditions was reported previously. We show here that this dark-stability applies to both the psbA-2 and psbA-3 transcripts. The psbA-3 transcript did not appear to produce the processed intermediate, arguing for the involvement of the 5' non-coding region as a determinant in psbA transcript degradation.

Bacterial Proteins↗
PubMed1993

Axillary biopsy compared with dissection in the staging of lymph nodes in operable breast cancer. A randomised trial.

OBJECTIVE: To compare the accuracy of axillary dissection with that of axillary node biopsy for staging of lymph nodes in operable breast cancer. DESIGN: Randomised study. SETTING: District hospital, Oestersund, Sweden. SUBJECTS: 200 women with operable breast cancer who presented between 1985-87 and 1989-91. INTERVENTIONS: Women were randomised (n = 100 in each group) to have either axillary dissection (in which all fat tissue was removed from the axilla) or biopsy (in which the lower half of the axillary fat, together with obviously malignant nodes were removed for histopathological examination). MAIN OUTCOME MEASURES: Number of nodes harvested by each method, and number that contained metastases. RESULTS: Nodes that contained metastases were found in 43 of the patients in the dissection group and 46 of those who had undergone biopsy alone. The median (range) yield of nodes in the dissection group was 8.5 (0-16) and in the biopsy group 6 (0-14), p < 0.001. In only two patients (one in each group) were no nodes identified. Patients without histologically confirmed node metastases were followed up for a median of 30 months; one in the biopsy group had a metastatic node detected three months after operation. During the last 100 operations the surgeon was asked to assess clinically whether the patients had involved nodes or not; this had a sensitivity of 59% and a specificity of 89%. CONCLUSION: Axillary node dissection and biopsy give similar results in the staging of breast cancer. Perioperative clinical judgement is unsatisfactory.

Adult↗
PubMed1993

Time-resolved immunofluorometric assay of human growth hormone.

We describe a time-resolved immunofluorometric assay (trIFMA) for human growth hormone (hGH), in which monoclonal antibody (mAb)-coated microtiter strip wells and a europium (Eu) chelate-labeled mAb are used. We compare the new trIFMA, in which two mAbs are used, with an immunoradiometric assay (IRMA) in which polyclonal antibodies are used. Serum samples (n = 185) from 36 children with various diagnoses were analyzed. In addition, 24-h profile samples (72 per child) from 39 children were analyzed. The trIFMA was more sensitive (detection limit, 0.03 mIU/L) than existing IRMAs. Both the intra- and interassay CVs were < or = 10.6% for hGH concentrations between 1 and 100 mIU/L. The trIFMA is technically simple and rapid, requires no centrifugation or separation reagent, and has a counting time of only 1 s per sample. In addition, the Eu label is nontoxic, presents no waste-disposal problems, and has a long shelf-life. Finally, the assay requires only small volumes of serum (25 muL), which is of considerable importance in pediatric use. The mAbs used for the trIFMA selectively bind the 22-kDa form of hGH, with the result that the assay detects about 80% of the amount detected by the polyclonal IRMA.

Antibodies, Monoclonal↗