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Whether coronavirus disease 2019 (COVID-19) vaccination promotes viral clearance in older patients has not been reported. We performed a retrospective review of patients hospitalized with COVID-19. This study included 24 patients with COVID-19 admitted to Hiroshima City Funairi Citizens Hospital between June 1 and July 10, 2021. Nine patients who were vaccinated (median age: 72 years) were compared with 15 patients who were not vaccinated (median age: 70 years). Viral clearance was confirmed by SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR). Antibody titers were measured to assess vaccination efficacy. The vaccinated group had a higher negative conversion rate than that in the non-vaccinated group on RT-PCR testing before discharge (83% vs. 36%, P = 0.064). Antibody titers on admission and 10 ± 2 days after onset were significantly higher in the vaccinated group than those in the non-vaccinated group (35 vs. 0 binding antibody units (BAU)/mL, P = 0.012; and 114 vs. 7 BAU/mL, P = 0.032, respectively). Stimulating antibody production by vaccination may promote faster viral clearance in older patients who develop COVID-19., This research was funded by “Advanced study aim to contribute creating new evidence in COVID-19 based on the local government-academia collaboration research system in Hiroshima”: AMED Research Program on Emerging and Re-emerging Infectious Diseases, Grant Number JP20fk0108453.

Direct sequencing is a popular method to discover mutations in candidate genes responsible for hereditary diseases. A certain type of mutation, however, can be missed by the method. Here, we report a comprehensive genomic quantitative polymerase chain reaction (qPCR) to complement the weakness of direct sequencing. Upshaw-Schulman syndrome (USS) is a recessively inherited disease associated with severe deficiency of plasma ADAMTS13 activity. We previously analyzed ADAMTS13 in 47 USS patients using direct sequencing, and 44 of them had either homozygous or compound heterozygous mutations. Then, we sought to reveal more extensive defects of ADAMTS13 in the remaining three patients. We quantified copy numbers of each ADAMTS13 exon in the patients by using genomic qPCR. Each primer pair was designed to contain at least one of the two primers used in direct sequencing, to avoid missing any exonic deletions. The qPCR demonstrated heterozygous loss of exons 7 and 8 in one patient and exon 27 in the other, and further analysis revealed c.746_987+373del1782 and c.3751_3892+587del729, respectively. Genomic qPCR provides an effective method for identifying extensive defects of the target genes.

Primary pyomyositis is a bacterial infection of the skeletal muscle commonly affecting children with Staphylococcus aureus most often isolated as a pathogen. However, pyomyositis caused by anaerobic bacteria is rare in adults. Here, we report a case of solitary Pyomyositis of the left rhomboideus muscle in an immunocompetent person. A 70-year-old Japanese male presented with high fever and left shoulder pain. His muscle below the lower edge of the left scapula was tender and swollen. His laboratory examinations revealed severe inflammation. Computed tomography showed a solitary low-density area around a contrast enhancement in the left rhomboideus muscle. He was diagnosed as having solitary pyomyositis. Although his symptoms did not improve despite empiric intravenous administration of antibiotics, an incision was performed. Streptococcus anginosus and Streptococcus intermedius were isolated from the culture of drainage fluid. His symptoms gradually disappeared after the incisional drainage and continuous administration of antibiotics. Pyomyositis did not recur after his discharge. To the best of our knowledge, this is the first report on anaerobic pyomyositis of the shoulder muscle.

Actin-binding proteins filamin A (FLNA) and B (FLNB) are expressed in endothelial cells and play an essential role during vascular development. In order to investigate their role in adult endothelial cell function, we initially confirmed their expression pattern in different adult mouse tissues and cultured cell lines and found that FLNB expression is concentrated mainly in endothelial cells while FLNA is more ubiquitously expressed. Functionally, siRNA-knockdown of endogenous FLNB in HUVEC inhibited Vascular Endothelial Growth Factor (VEGF)-induced in vitro angiogenesis by decreasing endothelial cell migration capacity, whereas FLNA ablation did not alter these parameters. Moreover, FLNB-depleted cells increased their substrate adhesion with more focal adhesions. The molecular mechanism underlying this effect implicates modulation of small GTP binding protein Rac-1 localization and activity, with altered activation of its downstream effectors p21 protein Cdc42/Rac-activated kinase (PAK)-4/5/6 and its activating guanine nucleotide exchange factor Vav-2. Moreover, our results suggest the existence of a signaling complex including FLNB, Rac-1 and Vav-2 under basal conditions that would further interact with VEGFR2 and integrin αVβ5 after VEGF stimulation. In conclusion, our results reveal a crucial role for FLNB in endothelial cell migration and in the angiogenic process in adult endothelial cells.

Follicular lymphoma is a low grade malignant lymphoma. However, some follicular lymphomas undergo histological transformation into higher grade malignant lymphomas. We recently encountered a diffuse large cell lymphoma which seemed to have progressed from a follicular lymphoma and which finally transformed into a small non-cleaved lymphoma. Each stage of the histological transformation was accompanied by increasing clinical grades of malignancy. It was suspected that in our patient a follicular lymphoma initially developed due to rearrangement of the BCL2 gene, and then underwent histological transformation into a diffuse large cell lymphoma, which was associated with p53 mutation. Subsequent rearrangement of C-MYC promoted the histological transformation of this diffuse large cell lymphoma into a small non-cleaved lymphoma. Our findings indicate that p53 mutation and rearrangement of C-MYC are involved in the histological transformation of follicular lymphomas into more advanced lymphomas.