Early-stage antibody kinetics after the third dose of BNT162b2 mRNA COVID-19 vaccination measured by a point-of-care fingertip whole blood testing

Amid the Coronavirus Disease 2019 pandemic, we aimed to demonstrate the accuracy of the fingertip whole blood sampling test (FWT) in measuring the antibody titer and uncovering its dynamics shortly after booster vaccination. Mokobio SARS-CoV-2 IgM & IgG Quantum Dot immunoassay (Mokobio Biotechnology R&D Center Inc., MD, USA) was used as a point-of-care FWT in 226 health care workers (HCWs) who had received two doses of the BNT162b2 mRNA vaccine (Pfizer-BioNTech) at least 8 months prior. Each participant tested their antibody titers before and after the third-dose booster up to 14-days. The effect of the booster was observed as early as the fourth day after vaccination, which exceeded the detection limit (>30,000 U/mL) by 2.3% on the fifth day, 12.2% on the sixth day, and 22.5% after the seventh day. Significant positive correlations were observed between the pre- and post-vaccination (the seventh and eighth days) antibody titers (correlation coefficient, 0.405; p<0.001). FWT is useful for examining antibody titers as a point-of-care test. Rapid response of antibody titer started as early as the fourth day post-vaccination, while the presence of weak responders to BNT162b2 vaccine was indicated

Digenic inheritance of mutations in EPHA2 and SLC26A4 in Pendred syndrome

Enlarged vestibular aqueduct (EVA) is one of the most commonly identified inner ear malformations in hearing loss patients including Pendred syndrome. While biallelic mutations of the SLC26A4 gene, encoding pendrin, causes non-syndromic hearing loss with EVA or Pendred syndrome, a considerable number of patients appear to carry mono-allelic mutation. This suggests faulty pendrin regulatory machinery results in hearing loss. Here we identify EPHA2 as another causative gene of Pendred syndrome with SLC26A4. EphA2 forms a protein complex with pendrin controlling pendrin localization, which is disrupted in some pathogenic forms of pendrin. Moreover, point mutations leading to amino acid substitution in the EPHA2 gene are identified from patients bearing mono-allelic mutation of SLC26A4. Ephrin-B2 binds to EphA2 triggering internalization with pendrin inducing EphA2 autophosphorylation weakly. The identified EphA2 mutants attenuate ephrin-B2- but not ephrin-A1-induced EphA2 internalization with pendrin. Our results uncover an unexpected role of the Eph/ephrin system in epithelial function

Studies on hairy cell leukemia Part 2. Production of hairy cell leukemia-specific antiserum and its reactivities

Two B-cell lines, a hairy cell leukemia (HCL) line (ZK-H) and a normal lymphoblastoid line (ZK-N), were established in long-term culture from Peripheral blood of the same patient with HCL. An anti-HCL serum was prepared by immunizing a rabbit with ZK-H cells, rendered HCL-specific by absorption with ZK-N cells and tested in indirect membrane immunofluorescence. The absorbed antiserum reacted with 3 of 3 HCL lines but not with another 21 hemic cell lines, including 4 non-T, non-B cell lines, 6 T-cell lines, 9 B-cell lines and 2 myeloid cell lines. When tested against fresh normal and leukemic cells, positive reactions were observed in 5 of 5 HCL cases but not in 6 normal persons or in another 26 cases of various leukemias, except for a low percentage positive reaction in 2 of 6 cases of CLL. These results suggest that HCL cells possess a specific HCL-associated antigen which is shared by certain CLL cells but which is distinct from a B cell antigen. The method of production of hetero-antiserum used in the present experiment appears to obviate problems related to histocompatibility antigeris and would be useful for the immunodiagnosis of leukemias

Studies on hairy cell leukemia Part Ⅰ. Establishment of a hairy cell leukemia line and its characteristics

A hairy cell leukemia (HCL) line, ZK-H, and a normal lymphoblastoid cell line, ZK-N, were established from the peripheral blood of a 69-year-old male patient. The ZK-H cells and the patient's original hairy cells shared the same surface properties; both possessed membrane-bound IgG with kappa light chains and villous surface structures. The ZK-N cells were devoid of villous surface structures and polyclonal in that they consisted of cells having different membrane-bound heavy and light chains. Both the ZK-H and ZK-N lines carried Epstein Barr virus (EBV)-determined nuclear antigen, but the patient's fresh leukemic cells lacked this antigen. The ZK-H line had a hyperdiploid chromosome constitution of 47 and trisomy No. 2, but the ZK-N line had a normal chromosome constitution. The presence of membrane-bound immunoglobulin and B-cell tropic EBV in the ZK-H line provides evidence of the B-cell nature of HCL in this patient

Growth Factors Released from Gelatin Hydrogel Microspheres Increase New Neurons in the Adult Mouse Brain

Recent studies have shown that new neurons are continuously generated by endogenous neural stem cells in the subventricular zone (SVZ) of the adult mammalian brain. Some of these new neurons migrate to injured brain tissues and differentiate into mature neurons, suggesting that such new neurons may be able to replace neurons lost to degenerative disease or injury and improve or repair neurological deficits. Here, we tested whether delivering growth factors via gelatin hydrogel microspheres would support neurogenesis in the SVZ. Insulin-like growth factor-1 (IGF-1)-containing microspheres increased the number of new neurons in the SVZ. Hepatocyte growth factor (HGF)-containing microspheres increased the number of new neurons migrating from the SVZ towards the injured striatum in a stroke model in mouse. These results suggest that the strategy of using gelatin hydrogel microspheres to achieve the sustained release of growth factors holds promise for the clinical regeneration of damaged brain tissues from endogenous neural stem cells in the adult SVZ