Analysis of ABO grouping discrepancies among patients from a tertiary hospital in Korea.

BACKGROUND: Accurate ABO typing is essential for preventing ABO incompatibility reactions. However, the causes of ABO grouping discrepancy has not been sufficiently studied, and it may vary among different ethnic populations. Thus, the aim of this retrospective study was to investigate the causes of ABO discrepancy in the East Asian population. MATERIALS AND METHODS: A retrospective observational study on ABO typing discrepancy among patients in a tertiary hospital was carried out using the electronic medical record database of Samsung Medical Center (Seoul, Korea) between July 2016 and May 2019. RESULTS: ABO grouping was performed on 551,959 blood samples during the study period; 1468 events of serologic ABO discrepancy were determined from 1334 (0.24 %) samples. A total of 134 samples (0.02 %) presented multiple causes of ABO discrepancy. Weak/missing serum reactivity (594, 40.5 %) was the most frequent reason for ABO discrepancy, followed by extra serum reactivity (370, 25.2 %), weak/missing red cell reactivity (267, 18.2 %), mixed-field red cell reactivity (176, 12.0 %), and extra red cell reactivity (61, 4.2 %). In the category of weak/missing red cell reactivity, ABO subgroup was the most common reason, and using ABO genotyping, 26.2 % of the cases genotyped were found to be related to the cis-AB allele. CONCLUSIONS: Our results suggest that the incidence and cause of ABO typing discrepancies vary among institutes and ethnic groups. Our data helps to better understand and facilitate the resolution of ABO typing discrepancies in patients.

Molecular basis of serological weak D phenotypes and RhD typing discrepancies identified in the Korean population.

BACKGROUND: The molecular basis of RhD blood groups differs with race/ethnicity. This study aimed to investigate the molecular basis of serological weak D phenotypes and RhD typing discrepancies in the Korean population. MATERIALS AND METHODS: The RhD status of 188,852 Korean patients was initially determined using the automated microplate method and manual tile method. In case of no agglutination, weak D testing was further performed using the tube and gel methods. Serologically D-negative samples with C+ and/or E+ were tested using polymerase chain reaction-sequence specific primers for four RHD targets and/or exon 9 sequencing. Samples showing a serological weak D phenotype or an RhD typing discrepancy were subjected to full RHD gene sequencing. RESULTS: Of the 32 samples showing a serological weak D phenotype and 191 samples showing a serologically D-negative phenotype with C+ and/or E+, 23 and 50 were genotyped, respectively. Among the weak D samples, the most common alleles were RHD*15 (n=6), RHD*13.01 (n=4), and RHD*01W.25 (n=4), and no variant was found in two samples. RHD*01EL.01 (n=26) accounted for more than half of the D-negative samples. Of the seven samples that were typed as D-positive using the automated microplate method but showed weak reactivity using the tile method, four were genotyped, and the results were as follows: RHD*01W.33 (n=2), RHD*01W.43 (n=1), and no variant found (n=1). DISCUSSION: In our cohort, various D variant alleles including RHD*15 were identified; however, RHD*01W.1, RHD*01W.2, RHD*01W.3, RHD*09.03.01, and RHD*09.04, accounting for more than 95% of Caucasians with a serological weak D phenotype, were not found. Our study reaffirms that the distribution of D variant alleles differs between East Asians and Caucasians. Our findings also indicate that some D variants including RHD*01W.33 and RHD*01W.43 are at risk of being mistyped as D-positive by a highly sensitive RhD typing method such as an automated microplate method.

Absence of association between codon 129 and 219 polymorphisms of the prion protein gene and vascular dementia.

BACKGROUND: Polymorphisms of the prion protein gene (PRNP) are known to cause a strong susceptibility to the occurrence of prion diseases, such as Creutzfeldt-Jakob disease, and might be associated with other neurodegenerative disorders. However, an association between PRNP polymorphisms and vascular dementia (VaD) has not been reported thus far. OBJECTIVE: To investigate whether the PRNP polymorphisms are associated with an increased risk for developing VaD in the Korean population. METHODS: We compared the genotype, allele and haplotype frequencies of PRNP polymorphisms in 160 VaD patients with those in 236 healthy Koreans. RESULTS AND CONCLUSION: Codon 129 (M129V) and 219 (Q219K) polymorphisms in Korean VaD patients were found in the open reading frame of PRNP. Our study shows that there is no significant difference in the genotype, allele and haplotype frequencies of PRNP codon 129 and 219 polymorphisms between Korean VaD patients and normal controls. This was the first genetic association study of the polymorphisms of PRNP with VaD.

The evidence for GABAB receptor-mediated regulation of acid-base balance: involvement of Na+/H+ exchanger and Na+/HCO3- cotransporter.

A comparative analysis of the effects of gamma-aminobutyric acid (GABA) on the expressions of Na+/H+ exchanger 1 (NHE1) and Na+/HCO3- cotransporter (NBC) was investigated in order to extend our understanding of the mechanism of GABA receptor-mediated acid-base balance using a gerbil model. In vigabatrin (VGB, GABA degradation inhibitor) treated gerbils, both NHE1 and NBC immunoreactivities in the hippocampus were significantly elevated, as compared with the controls. Analogous to VGB treatment, baclofen (GABAB receptor agonist) treatment also evoked elevations of both NHE1 and NBC expressions in the hippocampus, whilst their expressions were unaffected by muscimol (GABAA receptor agonist) treatment. Therefore, our findings suggest that GABAB receptor-mediated regulation of NHE1 and NBC expressions may participate in acid-base balance in the gerbil hippocampus.

Altered corticotropin-releasing factor (CRF) receptor immunoreactivity in the gerbil hippocampal complex following spontaneous seizure.

Considerable attention has been focused on the role of corticotropin-releasing factor (CRF) in neuropsychiatric disorders and neurodegenerative diseases including epilepsy. Therefore, in the present study, we investigated the temporal and spatial alteration of CRF receptor in the gerbil hippocampal complex in order to characterize the possible changes and associations with different sequelae of spontaneous seizure in these animals. Thirty minutes postictal, a decline in CRF receptor immunoreactivity was observed in the granule cells and hilar neurons. In the subiculum, CRF receptor immunoreactivity was also significantly decreased at this time point. Twenty-four hours after seizure onset, the immunoreactivity in these regions recovered to the pre-seizure level. Moreover, 30 min after seizure in the entorhinal cortex, the density of CRF receptor immunoreactivity began to decrease, particularly in the layers II and III, compared to pre-seizure group. Nevertheless, 24h after seizure onset, CRF receptor immunodensity had recovered to its seizure-sensitive (SS) level. These results suggest that altered CRF receptor expression in the hippocampal complex may affect tissue excitability and seizure activity in SS gerbils.

Changed vesicular GABA transporter immunoreactivity in the gerbil hippocampus following spontaneous seizure and vigabatrin administration.

To identify the roles of vesicular gamma-aminobutyric acid (GABA) transporter (VGAT) in epileptogenesis and the recovery mechanisms in spontaneous seizure, we conducted a chronological and comparative analysis of VGAT expression. VGAT immunoreactivity was stronger in the seizure resistant group than that in the pre-seizure group of seizure sensitive (SS) gerbils. In 3 h postictal group, the density of VGAT immunoreactivity was significantly increased in the hippocampus, as compared to pre-seizure group. In 24 h postictal group, VGAT immunodensity had recovered to its pre-seizure level. In addition, VGAT immunoreactivity in the hippocampus was also increased by vigabatrin (GVG) administration. These results suggest that decreased VGAT expression in the SS gerbil hippocampus may affect epileptogenesis in this animal, and that the subsequent alteration in its expression induced by seizure and the administration of GVG may reflect a modulation of GABA release to alleviate seizure activity.

Activation of p38 MAP kinase in the rat dorsal root ganglia and spinal cord following peripheral inflammation and nerve injury.

The intrathecal administration of p38 MAP kinase (p38) inhibitor has been shown to reduce hyperalgesia. In the present study, we investigated the activation of p38 in the rat dorsal root ganglion (DRG) and spinal cord following peripheral tissue inflammation and nerve injury immunohistochemically. Peripheral inflammation and chronic constriction injury (CCI) of the sciatic nerve induced a significant increase in the percentage of phosphorylated (P-) p38-immunoreactive (IR) neurons, primarily small sized ones in bilateral DRGs. In contrast, following axotomy, a significant decrease in the percentage of IR neurons was observed in ipsilateral DRGs. In addition, a marked increase was observed in the number of P-p38-IR microglia in the ipsilateral laminae I-IV and IX of the spinal cord following peripheral inflammation, CCI or axotomy. These findings suggest that p38 may play an important role in hyperalgesia and the activation of the spinal microglia.

Changes in Na(+)-K(+)-Cl(-) cotransporter immunoreactivity in the gerbil hippocampus following spontaneous seizure.

The immunoreactivity of Na(+)-K(+)-Cl(-) cotransporter (NKCC) in the gerbil hippocampus associated with various sequelae of spontaneous seizures were investigated in order to identify the roles of NKCC in the epileptogenesis and the recovery mechanisms in these animals. The NKCC immunoreactivities in the CA2-3 regions, the subiculum and the entorhinal cortex, were significantly more intensified in the pre-seizure group of seizure sensitive (SS) gerbils than in the seizure resistant (SR) gerbils. Following the on-set of seizure, the immunoreactivity of NKCC was significantly changed. In the hippocampal complex except the CA1 region, NKCC immunoreactivity in GABAergic neurons was significantly decreased 30 min after seizure on-set, versus the pre-seizure group. On the other hand, NKCC immunoreactivity was dramatically elevated in the CA1 regions, and 3 h postictal NKCC immunoreactivity increased significantly in the dentate gyrus and the dendrites of the pyramidal cells in the CA2-3 regions. These findings suggest that altered NKCC expression may be associated with seizure activity, and have an important role in the postictal recovery by regulating GABA-mediated inhibitory circuit in the hippocampal complex of the gerbil.

Alterations in Na+/H+ exchanger and Na+/HCO3- cotransporter immunoreactivities within the gerbil hippocampus following seizure.

In this study, a chronological and comparative analysis of the immunoreactivities of Na(+)/H(+) exchanger 1 (NHE1), Na(+)/HCO(3)(-) cotransporter (NBC) and Na(+)/Ca(2+) exchanger (NCE) was conducted in order to identify the effects of spontaneous seizure on their protein expression levels using the gerbil model. The distribution of NHE1 and NBC immunoreactivity in the hippocampus of seizure-resistant (SR) gerbils was similar to that observed in the pre-seizure group of seizure-sensitive (SS) gerbils. From 30 min to 3 h after the onset of the seizure, both NHE1 and NBC immunoreactivities were elevated in the hippocampus, as compared to the pre-seizure group of SS gerbils. At 6 h postictal, these immunoreactivities in the hippocampus had reduced to the pre-seizure level. However, NCE immunoreactivity within the hippocampus was unaltered. These findings suggest that the changes in both NHE1 and NBC immunoreactivity within the hippocampus following seizure may affect tissue excitability and play a role in the reduction of the seizure activity in the gerbil.