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the knowledge economy, providing solutions to the significant local. preference to steroid injections. Further research should be performed. The propositus was a healthy 34-year old male native of Isparta, a city situated in Western Turkey. Informed consent was obtained from the patient. He had no symptoms attributable to a hemolytic process. Hematological data were as follows: Hb 16.9 g/dl, RBC 5.8x1012/L; PCV 0.49 L/L, MCV 84 fL, MCH 29 pg; MCHC 34.4 g/dL, reticulocytes 1 %. An abnormal hemoglobin with a mobility similar to that of Hb J was detected by cellulose acetate electrophoresis at pH 8.6, and had same electrophoretic mobility with Hb A by citrate agar electrophoresis at pH 6.2 [6]. Modified chromatographic analysis of red cell lysate was done by HPLC using a cation exchange column. The column was an Ion-Exchange Cartridge column, 0.59x3.6 cm manufactured by BioRad and obtained from MedTex Company, Istanbul, Turkey. The chromatogram was developed with sodium phosphate and sodium azide buffers. Abnormal Hb was 20.0 % of the total Hb; HbA2; 2.0% and Hb A ;77.3% [6]. HbF value was determined by alkali denaturation method and found as 0.7 % [7]. The p50 values obtained (using the Radiometer ABL 700; Radiometer ABL, Copenhagen, Denmark) at pH 7.4 and at 37 °C, were 24.96 mmHg for a whole arterial blood sample from propositus and 28.67 mmHg for that of the normal control [6]. The result of an Isopropanol stability test was negative [6,8]. Ten ml of peripheral blood, collected with EDTA as the anticoagulant, were sent for structural DNA analysis by overnight express courier to the Titus H.J. Huisman Hemoglobinopathy Laboratory, Medical College of Georgia, Augusta, GA, USA. DNA was extracted from peripheral blood leukocytes as previously described by Poncz et al [9]. The α1 - and α2- globin genes were separately amplified as described before [10]. Polymerase chain reaction (PCR) products were then purified with the Prep-A Gene DNA purification Kit (Bio-Rad Laboratories, Hercules, CA, USA) and subjected to cycle sequencing with the BDT (Big Dye Terminator) method on an ABI PRISMTM 377 Cycle Sequencer, according to manufacturer's instructions (Applied BioSystems Inc., Foster City, CA, USA) at the Molecular Biology Core Facility, Medical College of Georgia, Augusta, GA, USA. Sequencing of the α2-globin gene did not reveal any abnormality, shown in Figure 2. However, nucleotide sequencing of the α1-globin gene showed a C ->A mutation at codon 120 in exon–3, thus identifying the variant as Hb J-Meerut [ α120 (H3) Ala -> Glu], as illustrated in Figure 1.

The propositus was a healthy 34-year old male native of Isparta, a city situated in Western Turkey. Informed consent was obtained from the patient. He had no symptoms attributable to a hemolytic process. Hematological data were as follows: Hb 16.9 g/dl, RBC 5.8x1012/L; PCV 0.49 L/L, MCV 84 fL, MCH 29 pg; MCHC 34.4 g/dL, reticulocytes 1 %. An abnormal hemoglobin with a mobility similar to that of Hb J was detected by cellulose acetate electrophoresis at pH 8.6, and had same electrophoretic mobility with Hb A by citrate agar electrophoresis at pH 6.2 [6]. Modified chromatographic analysis of red cell lysate was done by HPLC using a cation exchange column. The column was an Ion-Exchange Cartridge column, 0.59x3.6 cm manufactured by BioRad and obtained from MedTex Company, Istanbul, Turkey. The chromatogram was developed with sodium phosphate and sodium azide buffers. Abnormal Hb was 20.0 % of the total Hb; HbA2; 2.0% and Hb A ;77.3% [6]. HbF value was determined by alkali denaturation method and found as 0.7 % [7]. The p50 values obtained (using the Radiometer ABL 700; Radiometer ABL, Copenhagen, Denmark) at pH 7.4 and at 37 °C, were 24.96 mmHg for a whole arterial blood sample from propositus and 28.67 mmHg for that of the normal control [6]. The result of an Isopropanol stability test was negative [6,8]. Ten ml of peripheral blood, collected with EDTA as the anticoagulant, were sent for structural DNA analysis by overnight express courier to the Titus H.J. Huisman Hemoglobinopathy Laboratory, Medical College of Georgia, Augusta, GA, USA. DNA was extracted from peripheral blood leukocytes as previously described by Poncz et al [9]. The α1 - and α2- globin genes were separately amplified as described before [10]. Polymerase chain reaction (PCR) products were then purified with the Prep-A Gene DNA purification Kit (Bio-Rad Laboratories, Hercules, CA, USA) and subjected to cycle sequencing with the BDT (Big Dye Terminator) method on an ABI PRISMTM 377 Cycle Sequencer, according to manufacturer's instructions (Applied BioSystems Inc., Foster City, CA, USA) at the Molecular Biology Core Facility, Medical College of Georgia, Augusta, GA, USA. Sequencing of the α2-globin gene did not reveal any abnormality, shown in Figure 2. However, nucleotide sequencing of the α1-globin gene showed a C ->A mutation at codon 120 in exon–3, thus identifying the variant as Hb J-Meerut [ α120 (H3) Ala -> Glu], as illustrated in Figure 1..

This was a single-center prospective cohort study with historical that included ED patients ≥21 years old presenting with a primary complaint of chest pain in two time periods. The primary outcome was patient disposition. Secondary outcomes focused on 30-day ED bounce back and major adverse cardiac events (MACE). We used multivariate logistic regression to estimate the odds ratio (OR) and its 95% confidence interval (CI)..