Detection of HCV core antigen in HCV RNA positive, anti-HCV negative blood donations from Polish blood donors.
Explore the source record for details and available documents.
Blood Donors↗
Biomedical subjects
S R Lee
Publications and source records attributed to S R Lee.
Studies of the central neural pathways to the stomach and Zusanli (ST36).
The purpose of this morphological study was to investigate the relation between the meridian, meridian points and viscera using neuroanatomical tracers. The common locations of the spinal cord and brain projecting to the stomach and Zusanli were observed following injection of CTB (cholera toxin B subunit) and pseudorabies viruses (PRV-Ba, Bartha strain and PRV-Ba-Gal, galactosidase insertion) into the stomach and Zusanli (ST36). After 4-5 days of survival following injection into twelve rats, they were perfused, and their spinal cords and brains were frozen sectioned (30 microm). These sections were stained by X-gal histochemical, CTB and PRV-Ba immunohistochemical staining methods, and examined with the light microscope. The results were as follows: Commonly labeled medulla oblongata regions were dorsal motor nucleus of vagus nerve (DMV), nucleus tractus solitarius (NTS) and area postrema (AP) following injection of CTB and PRV-Ba-Gal into stomach and Zusanli, respectively. In the spinal cord, commonly labeled neurons were found in thoracic, lumbar and sacral spinal segments. Densely labeled areas were found in lamina IV, V, VII (intermediolateral nucleus) and X of the spinal cord. In the brain, commonly labeled neurons were found in the Al noradrenalin cells/Cl adrenalin cells/caudoventrolateral reticular nucleus, dorsal motor nucleus of vagus nerve, nucleus tractus solitarius, area postrema, raphe obscurus nucleus, raphe pallidus nucleus, raphe magnus nucleus, gigantocellular nucleus, locus coeruleus, parabrachial nucleus, Kolliker-Fuse nucleus, A5 cell group, central gray matter, paraventricular hypothalamic nucleus, lateral hypothalamic nucleus, retrochiasmatic hypothalamic nucleus, bed nucleus of stria terminalis and amygdaloid nucleus. Thus central autonomic center project both to the stomach and Zusanli. These morphological results suggest that there is a commonality of CNS cell groups in brain controlling stomach (viscera) and Zusanli (limb).
Acupuncture Points↗
Overexpression of Akt inhibits NGF-induced growth arrest and neuronal differentiation of PC12 cells.
To investigate the role of Akt in nerve growth factor (NGF)-induced neuronal differentiation, PC12 cells ectopically expressing wild-type or dominant-inhibitory forms of Akt were analyzed. NGF-induced neurite outgrowth was greatly accelerated in cells expressing dominant-inhibitory Akt, compared to parental PC12 cells, but was almost completely blocked in cells expressing wild-type Akt. Since neuronal differentiation requires an arrest of cell growth, several aspects of cell growth of the different cell lines were compared. Cells expressing wild-type Akt were not susceptible to the growth-arresting effect of NGF, whereas parental PC12 cells and notably cells expressing mutant Akt were so affected. Accompanying this, the expressions of CDKs and p21(WAF1) were down- and up-regulated, respectively, in both parental PC12 cells and cells expressing mutant Akt. When treated with some growth arrest-inducing agents such as sodium nitroprusside, forskolin and butyrolactone I, cells expressing wild-type Akt regained their responsiveness to the effects of NGF on differentiation. In summary, our results indicate that Akt overrides the growth-arresting effect of NGF and thereby, negatively regulates neuronal differentiation.
4-Butyrolactone↗
Clinical characteristics of unexplained sudden cardiac death in Korea.
In Western countries, sudden cardiac death (SCD) is closely related to coronary artery disease, but in Korea the clinical characteristics of SCD are not well determined. Over a 4-year period (June 1995 to May 1999), 186 cases of SCD, ranging in age from 16 to 75 years, were admitted to the Chonnam National University Hospital. In 82 (44.1%) of these, neither symptoms nor evidence of structural heart disease was found and so their clinical characteristics were investigated. There were 66 (80.5%) men and 16 (19.5%) women (male/female ratio = 4.1:1). The mean age was 50 +/- 14 years: 19 (23.2%) were in their 40s, 21 (25.6%) in their 50s, and 17 (20.7%) in their 60s. The time of circulatory collapse witnessed in 68 cases of SCD showed 2 peaks: between midnight and 03.00h (n=16, 23.5%) and between 09.00h and midday (n=15, 22.1%). Unexplained SCD occurred at home in 48 (64.9%) cases and on the street in 12 (16.2%); it occurred during normal daily routine activity in 23 (39.6%) and during sleep in 15 (25.9%). Thirty-three patients (40.2%) experienced various prodromal symptoms, including chest discomfort (n=13, 15.9%) and dyspnea (n=8, 9.8%). The electrocardiogram taken on arrival recorded asystole in 65 (79.3%) and ventricular fibrillation in 17 (20.7%). Idiopathic ventricular fibrillation was diagnosed in 14 (10 men, 4 women; 45 +/- 11 years) of 21 patients who recovered spontaneous circulation. Five (6.1%) patients were discharged alive, and an implantable cardioverter-defibrillator was implanted in 2. Unexplained SCD is common in Korea and develops predominantly in middle-aged males around midnight or in the late morning usually with no prodromal symptoms (59.8%). Idiopathic ventricular fibrillation is thought to be one of the important causes.
Adolescent↗
Idiopathic multilocular thymic cyst: CT features with clinical and histopathologic correlation.
OBJECTIVE: We performed this study to describe the CT features of idiopathic multilocular thymic cysts with clinical and histopathologic correlation. CONCLUSION: Multilocular thymic cysts typically manifest on CT as unilocular or multilocular cystic thymic masses, often with soft-tissue attenuation components. CT cannot be used to distinguish neoplastic from nonneoplastic soft-tissue components.
Adolescent↗
Association of focal adhesion kinase with fibronectin and paxillin is required for precartilage condensation of chick mesenchymal cells.
We show that tyrosine phosphorylation of FAK was increased as precartilage condensation occurred, followed by a subsequent decrease in proliferation of in vitro micromass culture of wing bud mesenchymal cells. FAK was associated with fibronectin and paxillin, which were maximal at day 3 of culture. FAK was also associated with signaling molecules such as PLC-gamma and PI3-kinase through c-Src. The beta1 integrin antibody and several inhibitors of signaling molecules such as herbimycin A, U73122, LY294002, as well as cytochalasin D, an actin depolymerizing agent, remarkably decreased tyrosine phosphorylation of FAK and its association with fibronectin and paxillin during condensation. resulting in a marked inhibition of condensation and chondrogenesis. Taken together, our findings suggest that beta1 integrin-mediated interaction of mesenchymal cells and fibronectin signals to accelerate the precartilage condensation through tyrosine phosphorylation of FAK and its association with paxillin. This signaling pathway is required for precartilage condensation and subsequent cartilage nodule formation in chondrogenesis.
Animals↗
Hydrogen peroxide: a key messenger that modulates protein phosphorylation through cysteine oxidation.
Ligand-receptor interactions can generate the production of hydrogen peroxide (H(2)O(2)) in cells, the implications of which are becoming appreciated. Fluctuations in H(2)O(2) levels can affect the intracellular activity of key signaling components including protein kinases and protein phosphatases. Rhee et al. discuss recent findings on the role of H(2)O(2) in signal transduction. Specifically, H(2)O(2) appears to oxidize active site cysteines in phosphatases, thereby inactivating them. H(2)O(2) also can activate protein kinases; however, although the mechanism of activation for some kinases appears to be similar to that of phosphatase inactivation (cysteine oxidation), it is unclear how H(2)O(2) promotes increased activation of other kinases. Thus, the higher levels of intracellular phosphoproteins observed in cells most likely occur because of the concomitant inhibition of protein phosphatases and activation of protein kinases.
Animals↗
Melatonin attenuates the changes in polyamine levels induced by systemic kainate administration in rat brains.
Systemically administered kainate has been demonstrated to induce neuronal damage and changes of the levels of biochemical substances related to neurotoxicity. Polyamines are thought to be important in the generation of edema and neuronal cell loss associated with various type of excitotoxicity. Melatonin exerts potent free radical scavenging, antioxidant, and neuroprotective properties. This study was designed to estimate the effect of exogenous melatonin administration on the changes of polyamine levels in rat brains after systemic administration of kainate. Kainate [10 mg/kg, intraperitoneally (i.p.)] was injected into the rats to produce excitotoxicity. Melatonin (15 mg/kg, i.p.) was administered 1 h before, immediately after, and 1 h after kainate treatment. We examined the polyamine [putrescine (PU), spermidine (SD) and spermine (SM)] levels in the cerebral cortex and hippocampus and neuronal density in the hippocampal CA1 and CA3 subsectors in brain sections. PU levels were increased 8 and 24 h after kainate treatment and the administration of melatonin attenuated these changes. Only minor changes were noted in the levels of the polyamine SD and SM after the kainate treatment. In histology, neuronal injuries in the hippocampal CA1 and CA3 subsectors were examined 3 days after kainate treatment and melatonin reduced the kainate-induced neuronal injuries. Our results show that melatonin inhibits the polyamine responses in the cerebral cortex and hippocampus following kainate-induced excitotoxicity and PU may be responsible for the protective effect of melatonin against kainate-induced excitotoxicity.
Animals↗
Identification of proteins containing cysteine residues that are sensitive to oxidation by hydrogen peroxide at neutral pH.
A procedure for detecting proteins that contain H(2)O(2)-sensitive cysteine (or selenocysteine) residues was developed as a means with which to study protein oxidation by H(2)O(2) in cells. The procedure is based on the facts that H(2)O(2) and biotin-conjugated iodoacetamide (BIAM) selectively and competitively react with cysteine residues that exhibit a low pK(a), and that the decrease in the labeling of cell lysate proteins with BIAM caused by prior exposure of cells to H(2)O(2) or to an agent that induces H(2)O(2) production can be monitored by streptavidin blot analysis. This procedure was applied to rat pheochromocytoma PC12 cells directly treated with H(2)O(2), mouse hippocampal HT22 cells in which H(2)O(2) production was induced by glutamate, and human erythroleukemia K562 cells in which H(2)O(2) production was induced by phorbol myristate acetate. It revealed that several cell proteins contain cysteine or selenocysteine residues that are selectively oxidized by H(2)O(2). Three of these H(2)O(2)-sensitive proteins were identified as a member of the protein disulfide isomerase family, thioredoxin reductase, and creatine kinase, all of which were previously known to contain at least one reactive cysteine or selenocysteine at their catalytic sites. This procedure should thus prove useful for the identification of proteins that are oxidized by H(2)O(2) generated in response to a variety of extracellular agents.
Alkylation↗
Mammalian thioredoxin reductase: oxidation of the C-terminal cysteine/selenocysteine active site forms a thioselenide, and replacement of selenium with sulfur markedly reduces catalytic activity.
Mammalian cytosolic thioredoxin reductase (TrxR) has a redox center, consisting of Cys(59)/Cys(64) adjacent to the flavin ring of FAD and another center consisting of Cys(497)/selenocysteine (SeCys)(498) near the C terminus. We now show that the C-terminal Cys(497)-SH/SeCys(498)-Se(-) of NADPH-reduced enzyme, after anaerobic dialysis, was converted to a thioselenide on incubation with excess oxidized Trx (TrxS(2)) or H(2)O(2). The Cys(59)-SH/Cys(64)-SH pair also was oxidized to a disulfide. At lower concentrations of TrxS(2), the Cys(59)-SH/Cys(64)-SH center was still converted to a disulfide, presumably by reduction of the thioselenide to Cys(497)-SH/SeCys(498)-Se(-). Specific alkylation of SeCys(498) completely blocked the TrxS(2)-induced oxidation of Cys(59)-SH/Cys(64)-SH, and the alkylated enzyme had negligible NADPH-disulfide oxidoreductase activity. The effect of replacing SeCys(498) with Cys was determined by using a mutant form of human placental TrxR1 expressed in Escherichia coli. The NADPH-disulfide oxidoreductase activity of the purified Cys(497)/Cys(498) mutant enzyme was 6% or 11% of that of wild-type rat liver TrxR1 with 5, 5'-dithiobis(2-nitrobenzoic acid) or TrxS(2), respectively, as substrate. Disulfide formation induced by excess TrxS(2) in the mutant form was 12% of that of the wild type. Thus, SeCys has a critical redox function during the catalytic cycle, which is performed poorly by Cys.
Animals↗
Protective effect of topiramate against hippocampal neuronal damage after global ischemia in the gerbils.
The purpose of this study was to examine whether topiramate would reduce neuronal damage after transient global ischemia in the gerbils because topiramate blocks voltage sensitive sodium channels and non-N-methyl-D-aspartate receptors and enhances gamma-aminobutyric acid-mediated inhibitory transmission. Both common carotid arteries were occluded for 3 min with microaneurysmal clips. The gerbils were treated with topiramate (50, 100, or 200 mg/kg, i.p.) immediately after ischemia. Neuronal cell damage in the hippocampal CA1 region was evaluated quantitatively 7 days after ischemia. Topiramate at the dose of 50 mg/kg failed to reduce hippocampal neuronal damage. However, topiramate when administered at the dose of 100 or 200 mg/kg significantly reduced hippocampal neuronal damage in dose-dependent manner (P<0.001 and P<0.0005, respectively). These results suggest that topiramate has a neuroprotective effect against neuronal damage following global ischemia in the gerbils.
Animals↗
45-year follow-up of hepatitis C virus infection in healthy young adults.
BACKGROUND: The sequelae during the first two decades after acute hepatitis C virus (HCV) infection have been well studied, but the outcome thereafter is unknown. OBJECTIVE: To conduct an extended study of the natural history of HCV infection by using archived serum specimens originally collected between 1948 and 1954. DESIGN: Retrospective cohort study. SETTING: A university, a Veterans Affairs medical center, and a medical follow-up agency that had access to the serum specimens and accompanying demographic and medical records. PARTICIPANTS: 8568 military recruits who were evaluated for group A streptococcal infection and acute rheumatic fever between 1948 and 1954. Blood samples were taken from the recruits and, after testing, were stored frozen for almost 45 years. MEASUREMENTS: The presence of antibodies to HCV was determined by enzyme-linked immunoassay, supplementary recombinant immunoblot assay, and polymerase chain reaction for HCV RNA. Morbidity and mortality were also assessed. RESULTS: Of 8568 persons, 17 (0.2%) had positive results on enzyme-linked immunosorbent assay and recombinant immunoblot assay. The rate was 1.8% among the African-American persons and 0.1% among the white persons in the total sample (relative risk, 25.9 [95% CI, 8.4 to 80.0]). During the 45-year follow-up, liver disease occurred in 2 of the 17 HCV-positive persons (11.8%) and 205 of the 8551 HCV-negative persons (2.4%) (ethnicity-adjusted relative risk, 3.56 [CI, 0.94 to 13.52]). Seven of the 17 HCV-positive persons (41 %) and 2226 of the 8551 HCV-negative persons (26%) had died by December 1996 (ethnicity-adjusted relative risk, 1.48 [CI, 0.8 to 2.6]). Of persons who were HCV-positive, 1 (5.9%) died of liver disease 42 years after the original phlebotomy, 5 (29%) died of non-liver-related disease a median of 37 years after the original phlebotomy, and 1 (5.9%) died of unknown causes. One hundred nineteen HCV-negative persons (1.4%) died of liver disease. CONCLUSIONS: The rate of HCV infection from 1948 to 1954 among a sample of military recruits parallels that among present-day military recruits and volunteer blood donors. During 45 years of follow-up, HCV-positive persons had low liver-related morbidity and mortality rates. This suggests that healthy HCV-positive persons may be at less risk for progressive liver disease than is currently thought.
Aged↗
Hairless mouse epidermal antioxidants and lipid peroxidation assessed by He-Ne laser.
BACKGROUND AND OBJECTIVE: To evaluate the possibility of oxygen radical damage in the skin after He-Ne laser irradiation according to dose intensity and time. STUDY DESIGN/MATERIALS AND METHODS: The He-Ne laser (lambda = 632.8, 10 mW) was used on the skin of mice with 1, 3, and 5 joule (J/cm2) dose rates for 1, 5, and 7 days in each case, and the results were compared with normal and anesthetic nonirradiated skins. The efficacy was determined by the formation of thiobarbituric acid-reactive substances (TBARS) in a 10-minute period and expressed as a concentration of malondialdehyde (MDA) from the lipid peroxidation of epidermal tissue, and total superoxide dismutases (SODs) and catalase activities, correlated with histologic biopsies. RESULTS: Data from epidermal SODs, catalase activity and the degree of lipid peroxidation at low-power radiation showed that repeated exposure had led to the induction of free radical damage and of epidermal changes as confirmed by microscopic study. The application of the He-Ne laser at 1, 3, and 5 J intensity for 5 days caused a gradual increase in the SODs and catalase activities, while the levels of TBARS were slightly decreased in the mouse epidermis. However, these patterns were reversed after 3 and 5 J irradiations for 5 and 7 days laser treatment. Furthermore, microscopic examinations revealed that the laser-irradiated skin changed the release of stratum granule from epidermis to hair follicle, and produced blood vessel thrombosis of the dermal capillary plexus. CONCLUSION: The presence of lipid peroxidation in the hairless mouse skin after exposure to He-Ne laser energy intensity of over 3 J for over 5 days was demonstrated. This lipid peroxidation could have been generated from oxygen free radicals. The histologic and oxidative enzymatic correlations on lipid peroxidation in the skin have provided a better understanding of He-Ne laser therapy-tissue interactions. It is possible to take advantage of these findings to evaluate pathologic skin conditions and effective laser dosage more efficiently.
Animals↗
Performance of second- and third-generation RIBAs for confirmation of third-generation HCV EIA-reactive blood donations. Retrovirus Epidemiology Donor Study.
BACKGROUND: Licensure of an enhanced HCV screening assay (HCV 3.0 EIA) without concurrent licensure of a complementary supplemental assay (i.e., RIBA HCV 3.0 strip immunoblot assay [RIBA-3]) decoupled screening and supplemental testing. In March 1998, the FDA Center for Biologics Evaluation and Research (CBER) recommended the use of RIBA-3 on RIBA HCV 2.0 strip immunoblot assay (RIBA-2)-indeterminate units screened with HCV EIA 3.0. STUDY DESIGN AND METHODS: The sensitivity of RIBA-2 and RIBA-3 was compared in tests on HCV 3.0 EIA-repeatably reactive (RR) units identified immediately after the implementation of HCV 3.0 EIA screening. Two protocols were evaluated: parallel testing of HCV 3.0 EIA-RR units by RIBA-2 and RIBA-3 and reflex testing of HCV 3.0 EIA-RR and RIBA-3-confirmed-positive units by RIBA-2. All specimens with discordant RIBA-2 and RIBA-3 results and a representative sampling with concordant RIBA results were tested by PCR. RESULTS: In the parallel testing protocol, 99,777 donations were screened, with 245 HCV 3.0 EIA-RR specimens included in the study. Of 166 RIBA-2-positive samples, 165 tested positive in RIBA-3 (1 sample reacted to the control superoxide dismutase antigen in RIBA-3). Thirty-two (74%) of 43 RIBA-2-indeterminate specimens and 4 (11%) of 36 RIBA-2-negative specimens tested positive in RIBA-3. HCV RNA was identified in 5 (16%) of 32 RIBA-2-indeterminate/RIBA-3-positive donations, as well as in 26 (70%) of 37 concordant RIBA-2/RIBA-3-positive donations. In the reflex testing protocol, 292,459 donations were screened, with 709 HCV 3.0 EIA-RR specimens included in the study. RIBA-3 testing yielded 517 (73%) positive specimens, of which 50 (9.7%) tested indeterminate and 15 (2.9%) tested negative in RIBA-2. Among the RIBA-discordant specimens, 10 (20%) RIBA-2-indeterminate specimens and 1 (7%) RIBA-2-negative specimens tested positive in PCR; in comparison, 60 (77%) of 78 concordant RIBA-2/RIBA-3-positive units tested positive in PCR. CONCLUSIONS: RIBA-3 is significantly more sensitive than RIBA-2 in testing of HCV 3.0 EIA-screened donations. During the review process of this manuscript, the FDA licensed the RIBA-3 test.
Blood Donors↗
Detection of hepatitis C core antigen in the antibody negative 'window' phase of hepatitis C infection.
BACKGROUND AND OBJECTIVES: Despite improvements in assays for anti-HCV, there remains a significant delay before the appearance of antibodies following infection, during which, circulating viral RNA is present. We have evaluated a prototype assay for the serological detection of hepatitis C virus (HCV) core antigen with specimens derived from the early phase of HCV infection. MATERIALS AND METHODS: Serial specimens from 24 individuals undergoing HCV seroconversion were tested for the presence of anti-HCV, HCV RNA and HCV core antigen. RESULTS: HCV antigen was detected at the same time as HCV RNA in 83% (20/24) cases. The mean time to the first detection of HCV antigen was approximately 1 day later than HCV RNA. Overall, 87% of HCV-RNA-positive specimens contained detectable HCV core antigen. CONCLUSION: These results indicate that HCV core antigen can be identified by routine serological ELISA in specimens from the early antibody-negative phase of HCV infection. A test for HCV core antigen may be a useful test for identifying window phase blood donations from antibody negative donors infected with HCV.
Enzyme-Linked Immunosorbent Assay↗
Molecular cloning and characterization of a mitochondrial selenocysteine-containing thioredoxin reductase from rat liver.
A thioredoxin reductase (TrxR), named here TrxR2, that did not react with antibodies to the previously identified TrxR (now named TrxR1) was purified from rat liver. Like TrxR1, TrxR2 was a dimeric enzyme containing selenocysteine (Secys) as the COOH-terminal penultimate residue. A cDNA encoding TrxR2 was cloned from rat liver; the open reading frame predicts a polypeptide of 526 amino acids with a COOH-terminal Gly-Cys-Secys-Gly motif provided that an in-frame TGA codon encodes Secys. The 3'-untranslated region of the cDNA contains a canonical Secys insertion sequence element. The deduced amino acid sequence of TrxR2 shows 54% identity to that of TrxR1 and contained 36 additional residues upstream of the experimentally determined NH2-terminal sequence. The sequence of this 36-residue region is typical of that of a mitochondrial leader peptide. Immunoblot analysis confirmed that TrxR2 is localized almost exclusively in mitochondria, whereas TrxR1 is a cytosolic protein. Unlike TrxR1, which was expressed at a level of 0.6 to 1.6 microgram/milligram of total soluble protein in all rat tissues examined, TrxR2 was relatively abundant (0.3 to 0.6 microgram/mg) only in liver, kidney, adrenal gland, and heart. The specific localization of TrxR2 in mitochondria, together with the previous identification of mitochondria-specific thioredoxin and thioredoxin-dependent peroxidase, suggest that these three proteins provide a primary line of defense against H2O2 produced by the mitochondrial respiratory chain.
Amino Acid Sequence↗
Propofol administration reduces hippocampal neuronal damage induced by kainic acid in rats.
The goal of this study was to determine whether propofol has protective effect against kainic acid (KA)-induced excitotoxicity. Administration of propofol (25 mg kg-1 i.p.) was done 2 h before KA (10 mg kg-1 i.p.), immediately after, and 2 h, 4 h, 6 h, and 12 h after the KA, and twice daily for an additional three days. Neuronal cell death in CA1 and CA3 subsector of hippocampus was evaluated quantitatively four days after KA. The KA and propofol-injected rats had a greater number of surviving neuronal cells than did KA (and vehicle)-injected rats. Our results suggest that propofol holds potential for the protection of neuronal cells against KA induced excitotoxicity.
Anesthetics, Intravenous↗
Comparison of basophil histamine releasability between atopic and nonatopic asthmatics.
To compare the mediator releasability between atopic and nonatopic asthmatics, we measured basophil histamine releasability (BaHR) using a calcium-ionophore A23187 and anti-IgE in 137 subjects who were treated at Seoul National University Hospital. Subjects were categorized into atopic (group AA, n=77) or nonatopic asthmatics (group NA, n=32), or normal controls (group NC, n=28). Serum total IgE levels were determined and correlation with BaHR was assessed. Anti-IgE-induced maximal BaHR in groups AA, NA, and NC was 41.0+/-3.2, 23.1+/-4.5, and 16.8+/-3.8, respectively (mean+/-SE, %). Anti-IgE-induced BaHR in group AA was significantly higher than that in groups NA and NC (p<0.05). Calcium ionophore A23187-induced maximal BaHR was 43.1+/-2.8, 40.8+/-4.4, and 50.5+/-5.2, respectively (mean+/-SE, %), and there was no significant difference among the groups. Serum total IgE level correlated significantly with anti-IgE-induced maximal BaHR (r=0.281, p<0.01) but not with that induced by calcium ionophore A23187. In conclusion, IgE receptor-related BaHR is higher in atopic asthmatics than in nonatopic asthmatics, and this increased BaHR in atopics is significantly associated with increased serum total IgE level.
Asthma↗