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Aim: This study examined the relationship between continuity of social participation and progression of frailty among community‐dwelling older adults, by baseline frailty level. Methods: This study was part of a 3‐year community‐based cohort study among adults aged ≥65 years, living independently in a rural municipality in Japan. Mail surveys were carried out in 2016, 2018 and 2019. This study involved 2799 participants who responded to the question about social participation in every survey. Frailty was evaluated by Kihon Checklist total scores. Social participation was categorized into consistent non‐participation, interrupted recent non‐participation, interrupted recent participation and consistent participation. We assessed the relationship between social participation and change in frailty scores using general linear regression analysis, stratifying the participants into groups by their frailty level at baseline. Results: There was a smaller frailty score increase in the robust (β −0.61, 95% CI −0.99 to −0.22) and prefrail groups (β −0.73, 95% CI −1.18 to −0.27) for consistent participation than consistent non‐participation. Interrupted recent participation showed significant suppression in the prefrail group (β −0.96, 95% CI −1.60 to −0.32). Social participation had no clear effect on progression in the frail group. Conclusions: Consistent social participation might reduce the progression of frailty in robust and prefrail people. Inconsistent participation might also help to reduce progression in prefrail older adults. It is important for prefrail older adults to return to their social activities and continue to engage as long as possible, even if their participation was intermittent in the past. Geriatr Gerontol Int 2023; 23: 25–31. [ABSTRACT FROM AUTHOR]

Background: After experiencing several cases of transfusion‐transmitted hepatitis E (TT‐HE) in Hokkaido, Northern Japan, hepatitis E virus (HEV) screening in blood donors, using a nucleic acid amplification test (NAT), was introduced in 2005. Study Design and Methods: The frequency of HEV RNA‐positive donations (2005–2019) was investigated, and the HEV RNA‐positive specimens were phylogenetically analyzed. In August 2014, the 20‐pooled NAT (20P‐NAT) was replaced with an individual‐NAT (ID‐NAT) system. Results: Until 2019, the frequency of HEV RNA‐positive donors was 0.011% (289/2,638,685) with 20P‐NAT and 0.043% (597/1,379,750) with ID‐NAT, and no TT‐HE cases were observed in Hokkaido. The prevalence among male, but not female donors, increased significantly between 2015 and 2019. Eighty‐nine percent of HEV isolates from donors were genotype 3 and the remainder were genotype 4, and many clusters existed in each genotype. ALT levels at the time of donation were significantly higher in donors with genotype 4. Four subgenotypes, namely 3a (37%), 3b (41%), 3e (6%), and 4c (10%), comprised 94% of the total. During this period, the most identified subgenotype, 3a, transitioned to 3b. Majority of the HEV strains within the same clusters were detected in the same geographical region around the same period. Many of the human HEV isolates were shown to coexist closely with animal HEV isolates phylogenetically. Conclusion: In Hokkaido, multiple divergent HEV strains have been circulating, and small outbreaks of hepatitis E have occurred in the last 15 years. The results suggested that HEV NAT can contribute significantly in ensuring safety during blood transfusions. [ABSTRACT FROM AUTHOR]

Background To reduce the risk of human parvovirus B19 ( B19 V) transmission through contaminated blood for transfusion and plasma-derived products, the Japanese Red Cross ( JRC) Blood Centers introduced B19V antigen screening by chemiluminescent enzyme immunoassay ( CLEIA- B19V) in 2008. Study Design and Methods Donor samples that were positive by CLEIA- B19V screening were tested for B19V DNA. The sensitivity of CLEIA- B19V was tested using samples of all three genotypes and B19V DNA-positive donations. B19V DNA-positive donations and pooled plasma were quantitatively assayed for B19V DNA. B19V DNA-positive donations were phylogenetically analyzed by polymerase chain reaction direct sequencing. Results The sensitivity of CLEIA- B19V was inferred to be approximately 6.3 log IU/ mL with the genotype samples and 6.4 log IU/ mL with B19V DNA-positive donor samples. Of 417 CLEIA- B19V-positive samples from 1,035,560 donations in Hokkaido, Japan, 101 were positive for B19V DNA. The 198 strains of B19V DNA-positive donations in Hokkaido over the past 15 years clustered exclusively with Genotype 1. After introduction of CLEIA-B19V, the viral load for B19V DNA in all 772 pooled plasma for fractionation from donors in nationwide Japan did not exceed 4 log IU/ mL. Conclusion CLEIA- B19V can detect all three genotypes of B19V (viral load >6.3 log IU/ mL) and limit the viral load (<4 log IU/ mL) in pooled plasma, and thus such screening has further reduced the risk of transfusion-transmitted B19V infection. These results show that CLEIA- B19V screening at the JRC Blood Centers can be an alternative approach to comply with recommendations regarding B19V in the United States and Europe. [ABSTRACT FROM AUTHOR]

HLA Class II antibody-initiated activation of monocytes possessing the corresponding antigen is thought to participate in the pathogenesis of transfusion-related acute lung injury (TRALI). Pulmonary edema, a hallmark of TRALI, is caused by increasing vascular permeability. To investigate the contribution of HLA Class II antibody and monocytes to the development of pulmonary edema in TRALI, we studied whether the permeability of human lung microvascular endothelial cells (HMVECs) could be enhanced by coculturing HMVECs with peripheral blood mononuclear cells (PBMNCs) in the presence of HLA Class II antibody-containing plasma, which was implicated in TRALI (anti-HLA-DR plasma). In addition, similar experiments were performed with human umbilical vein endothelial cells (HUVECs). The endothelial permeability to fluoresceinated dextran, which was added from the start of coculture, was measured. The coculture of HMVECs or HUVECs with PBMNCs in the presence of anti-HLA-DR plasma resulted in the increase of endothelial permeability in the corresponding antigen-antibody-dependent manner. CV-3988, a platelet-activating factor (PAF) receptor antagonist, almost completely suppressed the increase in endothelial permeability. Neutralizing antibodies to tumor necrosis factor (TNF)-α alone and simultaneous addition of the antibodies to TNF-α and interleukin (IL)-1β to the coculture partially suppressed the permeability increase of HMVECs and HUVECs, respectively. HLA Class II antibody and monocytes in the corresponding antigen-antibody combination caused the enhancement of endothelial permeability. PAF, TNF-α, and/or IL-1β might be involved in the endothelial permeability increase. HLA Class II antibody-initiated monocyte activation could lead to the development of pulmonary edema in TRALI. [ABSTRACT FROM AUTHOR]

BACKGROUND: Type I allergic reactions such as urticaria-like manifestations constitute a large percentage of transfusion-related adverse events. Along with donor factors, patient factors might be involved in these reactions. Sera from some patients with chronic idiopathic urticaria show histamine-releasing activity (HRA). Sera from patients who develop Type I allergic reaction might possess HRA. STUDY DESIGN AND METHODS: Pretransfusion serum samples were collected. Mast cells were cultured from peripheral blood CD34+ cells and mixed with the serum samples. Cells with elevated intracytoplasmic Ca2+ concentrations were monitored using flow cytometry to evaluate Ca2+ influx–inducing activity (CaIA) in serum. The amount of histamine released into the supernatant was measured using an enzyme immunoassay kit to evaluate HRA. In some assays, cells were incubated with pertussis toxin (Ptx). RESULTS: CaIA values were higher (p < 0.05) in sera from patients with reactions (27.68 ± 20.38 [n = 145]; range, 0.49-84.90) than in sera of patients without reactions (10.70 ± 6.50 [n = 54]; range, 2.67-36.97) and control sera (9.67 ± 5.88 [n = 107]; range, 1.11-25.68). No difference in CaIA was found between patients with (27.38 ± 20.46 [n = 88]) and without (28.38 ± 20.59 [n = 57]) skin manifestations. However, CaIA was higher (p < 0.05) in patients with pure urticaria (mean, 30.58 ± 21.3 [n = 30]; range, 70.43-4.1) than in patients with fever alone (mean, 18.61 ± 14.71 [n = 18]; range, 45.94-3.19). Levels of HRA were higher (p < 0.001) in CaIA-positive sera than in CaIA-negative sera. Both CaIA and HRA were blocked by Ptx. CONCLUSION: Elevated CaIA and HRA in pretransfusion sera might be attributable to adverse reactions, especially to urticaria-like manifestation. The Gi protein–coupled receptor complexes on mast cells and its ligand must be involved. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although we reported two cases of transfusion-transmitted hepatitis E in Japan, the prevalence of hepatitis E virus (HEV) in Japanese blood donors is not very clear. STUDY DESIGN AND METHODS: Blood samples of donors who were deferred from donation because of elevated alanine aminotransferase (ALT) levels were collected from all Japanese Red Cross Blood Centers and subjected to HEV tests. RESULTS: Among the 41 donors with elevated ALT levels higher than 500 IU per L in Hokkaido, HEV RNA was detected in 8 (19.5%) samples. In 1389 donor samples with ALT levels of higher than 200 IU per L in nationwide Japan, the numbers of positive HEV RNA, immunoglobulin M (IgM) anti-HEV, and immunoglobulin G (IgG) anti-HEV samples were 15 (1.1%), 14 (1.0%), and 45 (3.2%), respectively. Although RNA-positive donors were predominantly male and found in any geographic area of Japan, they tended to be higher in number in eastern Japan including Hokkaido and lower in number in western Japan. Of the 23 HEV-positive samples, 19 were Genotype 3 and 4 were Genotype 4. DNA sequences of the 9 isolates showed more than 98.5 percent homology with the known swine HEV isolates. In 1062 donor samples with ALT levels of 61 to 199 IU per L, the percentages of IgM and IgG anti-HEV–positive samples were 0.1 and 2.7 percent, respectively, although there was no HEV RNA–positive sample. CONCLUSION: HEV markers (HEV RNA and anti-HEV) were detected in donors with elevated ALT levels who were widely distributed over Japan. The prevalence and incidence were higher in eastern Japan than in western Japan. [ABSTRACT FROM AUTHOR]

Abstract: Cyanobacterial genomes generally contain two groEL genes, referred to as groEL1 and groEL2. The purpose of this study is to elucidate a role of groEL2 in the adaptation of the thermophilic cyanobacterium Thermosynechococcus elongatus to hot environments. Both groEL genes were found to be heat-induced, while only groEL2 was greatly cold-induced. Primer extension and gel mobility shift analyses indicated that transcriptional regulation of groEL2 is different from that of groESL1. The groEL2 gene was dispensable under normal growth conditions at 50°C as a groEL2 disruptant was viable. This groEL2 mutant was highly sensitive to both high and low temperatures. [Copyright &y& Elsevier]

BACKGROUND: The generation of inflammatory mediators from monocytes activated by HLA Class II antibodies is thought to play important roles in the etiology of nonhemolytic transfusion reactions. Increased permeability of endothelial cells contributes to the pathogenesis of rash, urticaria, angioedema, and pulmonary edema, which are symptoms of transfusion reactions. STUDY DESIGN AND METHODS: We investigated whether inflammatory mediators released from monocytes upon stimulation by HLA Class II antibodies could increase endothelial permeability. Human endothelial cell monolayers were incubated with cell-free supernatants of peripheral blood mononuclear cells (PBMNCs) stimulated with HLA Class II antibody–containing plasma (anti-HLA-DR plasma), which has been implicated in severe nonhemolytic transfusion reactions. The permeability of endothelial cells to dextran was measured. RESULTS: The supernatants of PBMNCs stimulated with the anti-HLA-DR plasma in corresponding antigen-antibody combinations were able to increase endothelial permeability. At least 3 hours of exposure of PBMNCs to anti-HLA-DR plasma was required to produce a supernatant that could induce a significant increase in permeability. Simultaneous addition of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) neutralizing antibodies to the activated PBMNC supernatant significantly reduced the increase in permeability. Treatment of the endothelial cells with an inhibitor of nuclear factor κB (NF-κB), but not inhibitors of apoptosis, significantly prevented the increase in permeability. CONCLUSION: Both TNF-α and IL-1β, generated from PBMNCs by anti-HLA-DR plasma in a corresponding antigen-antibody–dependent manner, led to an increase in endothelial permeability. The activation of monocytes by the HLA-DR antibodies and the resultant inflammatory mediators could contribute to the pathogenesis of rash, urticaria, angioedema, and pulmonary edema after transfusion. [ABSTRACT FROM AUTHOR]

BACKGROUND: Five cases of transfusion transmission of hepatitis E virus (HEV) have been reported so far. The infection routes of the causative donors remain unclear, however. Also, the progress of virus markers in the entire course of HEV infection has not been well documented. STUDY DESIGN AND METHODS: Nucleic acid testing was performed by real-time reverse transcription–polymerase chain reaction targeting the open reading frame 2 region of HEV. Full-length nucleotide sequences of HEV RNA were detected by direct sequencing. RESULTS: Lookback study of a HEV-positive donor revealed that the platelets (PLTs) donated from him 2 weeks previously contained HEV RNA and were transfused to a patient. Thirteen relatives including the donor were ascertained to enjoy grilled pork meats together in a barbecue restaurant 23 days before the donation. Thereafter, his father died of fulminant hepatitis E and the other 6 members showed serum markers of HEV infection. In the recipient, HEV was detected in serum on Day 22 and reached the peak of 7.2 log copies per mL on Day 44 followed by the steep increase of alanine aminotransferase. Immunoglobulin G anti-HEV emerged on Day 67; subsequently, hepatitis was resolved. HEV RNA sequences from the donor and recipient were an identical, Japan-indigenous strain of genotype 4. HEV RNA was detectable up to Day 97 in serum, Day 85 in feces, and Day 71 in saliva. CONCLUSION: A transfusion-transmitted hepatitis E case by blood from a donor infected via the zoonotic food-borne route and the progress of HEV markers in the entire course are demonstrated. Further studies are needed to clarify the epidemiology and the transfusion-related risks for HEV even in industrialized countries. [ABSTRACT FROM AUTHOR]

BACKGROUND: There has been controversy over whether HLA alloimmunization is a risk factor for platelet (PLT) transfusion refractoriness (PTR) in hematopoietic peripheral blood progenitor cell transplantation (HPBPCT). STUDY DESIGN AND METHODS: Reported here is a boy with relapsed leukemia who developed fatal PTR after a peripheral blood progenitor cell transplantation (PBPCT) as a second HPBPCT from his mother. To elucidate the cause of PTR, a single-antigen assay (FlowPRA, One Lambda), a magnetic particles mixed passive hemagglutination test, and anti-human immunoglobulin-lymphocyte cytotoxicity test were performed on serum samples of the patient and his mother. RESULTS: Although HLA Class I antibodies were absent in his serum sample before HPBPCT, the serum sample after the first bone marrow transplantation (BMT) reacted weakly with beads coated with multiple HLA Class I molecules. After PBPCT, the positive reaction markedly increased. Although HLA-B44 antibody emerged transiently after BMT, the apparent generation of antibodies against HLA-A2 and -A24 as well as HLA-B44 occurred after PBPCT. The continuous appearance of HLA Class I antibodies coincided with the duration of marked PTR after PBPCT. The patient, however, had no antibodies against PLT-specific glycoproteins. Unidentified HLA Class I–reactive antibodies were detected in maternal serum sample. CONCLUSION: Although the patient appeared to be immunized to allogeneic HLA Class I molecules after BMT, profound HLA alloimmunization might have occurred after PBPCT in this case. It is possible that the administration of large numbers of immunocompetent cells sensitive to alloantigens at PBPCT causes the aberrant and persistent production of the HLA Class I antibodies. [ABSTRACT FROM AUTHOR]

BACKGROUND: HLA Class II antibodies are thought to be involved in severe transfusion reactions including transfusion-related acute lung injury (TRALI). The activation of monocytes by HLA Class II antibody may play an important role in the etiology of TRALI. CASE REPORT: An 81-year-old man with non-Hodgkin's lymphoma (Clinical Stage IIIA) received a plateletpheresis unit containing at least 4 × 1011 platelets because of thrombocytopenia and a bleeding tendency. Approximately 30 minutes after the start of transfusion, he developed chills, tachycardia, dyspnea, lumber, and abdominal pain and then a fever (40.3°C). His SaO2 dropped to 70 percent. The transfusion was discontinued immediately. His symptoms disappeared after treatment with oxygen and the administration of corticosteroid and aminophyrine. A chest X-ray showed no sign of pulmonary edema. RESULTS: The donor serum sample had HLA-DR antibodies against multiple DR antigens including DR13, the recipient's HLA-DR type. The cross-match between the patient's lymphocytes and the donor serum was positive. The treatment of peripheral blood mononuclear cells from healthy subjects bearing DR13 antigen with the donor plasma caused the secretion of inflammatory cytokines (i.e., interleukin [IL]-1β, IL-6, and tumor necrosis factor-α) and neutrophil-activating chemokines (i.e., IL-8 and CXCL1/GRO-α) in a cognate antigen-antibody relationship. In addition, the secretion of inflammatory cytokines appeared to require the involvement of CD32 and/or CD16. CONCLUSION: HLA-DR antibodies, detected in this case, had biologic functions to induce production of not only inflammatory cytokines but also neutrophil-attractant chemokines in vitro, which could contribute to the etiology of severe nonhemolytic transfusion reactions. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor regarding the donor reactions among African-American and Caucasian first-time whole-blood donors, published in the August 2005 issue of "Transfusion."

Anti-CD36 isoantibody in blood recipients is reported to cause refractoriness to platelet (PLT) transfusions and posttransfusion purpura–like syndrome. There are few reports, however, about the effects of passively transfused blood products containing this isoantibody on recipients. A 67-year-old Japanese woman underwent brain surgery. On the 6th postoperative day, the patient experienced tightness of the chest and nausea after receiving a transfusion of fresh frozen plasma (FFP). When she manifested hypotension, the transfusion was discontinued. No cutaneous manifestation was observed. The patient's condition gradually improved soon after the administration of steroids. Her pretransfusion PLT count was 17.1 × 104 perµL. It decreased to 1.9 × 104 perµL 12 hours after transfusion and recovered to 15.4 × 104 perµL 8 days after transfusion. The donor of the FFP had a Type I CD36 deficiency. Flow cytometric analysis identified anti-CD36 isoantibody in the FFP. The cross-match between the patient's PLTs and the FFP was positive. The FFP induced the aggregation of PLTs derived from healthy adults. This is the first reported case of life-threatening adverse effects and thrombocytopenia caused by passively transfused anti-CD36 isoantibody. The possibility of passive infusion of this antibody should be considered in the evaluation of life-threatening transfusion reactions followed by thrombocytopenia. [ABSTRACT FROM AUTHOR]

Backgrounds and Aim: Intrasinusoidal microthrombosis is considered to be a cause of massive hepatocyte death in fulminant hepatic failure. Generally, apoptotic cells express phosphatidyl serine (PS) outside the plasma membrane, which is also expressed on the surface of activated platelets and accelerates fibrin–thrombus formation. Therefore, the acceleration of blood coagulation on the surface of apoptotic hepatocytes may occur because hepatocytes are in direct contact with plasma that passes through fenestrations of the sinusoidal endothelium. To test this hypothesis, we investigated the coagulation activity of apoptotic hepatocytes. Methods: (1) The apoptosis of Hep G2 cells was induced by staurosporin (STS). PS expression was determined by confocal microscopy with FITC-annexin V, a specific inhibitor of PS activity. (2) One million HepG2 cells treated with STS with or without pretreatment with annexin V were exposed to activated factor X, CaCl2 and prothrombin. Thrombin generation was determined using a thrombin-specific chromogenic substrate. Results: (1) The percentage of apoptotic cells and PS-expressing cells markedly increased following the STS-treatment. (2) The thrombin generation significantly increased with STS-treatment in a dose dependent manner. (3) The increase in thrombin generation by STS-treatment was abolished following pretreatment with annexin V. Conclusion: Apoptotic hepatocytes accelerate blood coagulation through the expression of a PS-dependent pro-coagulant surface. [Copyright &y& Elsevier]

In industrialized countries, sporadic cases of hepatitis E have been reported in individuals who have never been in an endemic area. Hepatitis E virus (HEV) infection commonly occurs via the fecal-oral route but a potential risk of transfusion transmission route has been suggested. A 67-year-old Japanese male patient who had never been abroad received a transfusion of blood from 23 voluntary donors and developed acute hepatitis with unknown etiology after transfusion. His blood samples were tested for viral markers of hepatitis viruses. HAV, HBV, HCV, CMV, and EBV were ruled out as causative agents in this case. The patient's blood sample in the acute phase contained HEV RNA as well as IgM and IgG anti-HEV. HEV RNA was also detected in one of the FFP units transfused. The donor had no history of traveling abroad and had a normal ALT level at the time of donation. The PCR products from the patient and the donor showed complete identity for two distinct regions of HEV within open reading frame 1. The patient was infected with HEV via transfused blood from a volunteer donor. A potential risk of posttransfusion hepatitis E should be considered even in nonendemic countries. [ABSTRACT FROM AUTHOR]

Background: RANTES, one of the PLT-derived biologic response modifiers, accumulates in PLT concentrates (PCs) during storage and may play a causative role in nonhemolytic transfusion reactions (NHTRs) after PC transfusion.Study Design and Methods: To investigate the association of RANTES with NHTRs, the biologic activity of RANTES in the supernatant of stored PC at the intravascular concentration expected after PC transfusion was assessed by examining chemotaxis and histamine release in human basophils. In addition, the levels of RANTES in PCs involved in NHTRs were compared with those in PCs causing no transfusion reactions.Results: The supernatant of PC diluted to contain 1 nM RANTES significantly increased the migration of and release of histamine from basophils. Neutralizing antibody to RANTES suppressed the PC-triggered migration, but not histamine release. The levels of RANTES in PCs involved in NHTRs after PC transfusion were comparable to those in PCs that did not cause any transfusion reactions.Conclusion: RANTES that accumulated in PCs during storage was biologically active in a basophil chemotaxis assay at the intravascular concentration expected after PC transfusion. However, the NHTRs after PC transfusion were not simply related to the RANTES level in PCs. [ABSTRACT FROM AUTHOR]

BACKGROUND: Nonenveloped and thermostable viruses such as parvovirus B19 (B19) can be transmitted to patients who are receiving plasma-derived coagulation factor concentrates treated by the S/D method for inactivating enveloped viruses. Therefore, it is important to develop and validate new methods for the inactivation of nonenveloped viruses. STUDY DESIGN AND METHODS: Suspensions of B19 in coagulation factor concentrates (FVIII) were irradiated with UVC light. B19 infectivity was determined by an indirect immunofluorescence assay using CFU-E, as a host cell, derived from peripheral blood CD34+ cells. The effects of catechins on B19 infectivity and on FVIII activity after UVC illumination were also examined. RESULTS: The indirect immunofluorescence assay estimated the B19 infectivity of samples containing virus copies of 10[sup 5] to 10[sup 11] per 10 µL to be a median tissue culture-infectious dose of 10[sup 0.3] to 10[sup 5.4] per 10 µL. B19 was inactivated by 3 log at 750 J per m² of UVC radiation and was undetectable after 1000 or 2000 J per m² of irradiation. However, FVIII activity decreased to 55 to 60 percent of pretreatment activity after 2000 J per m² of UVC radiation. This was inhibited in the presence of rutin or catechins. Epigallocatechin gallate could maintain FVIII activity at almost 100 percent of pretreatment activity after 2000 J per m² of UVC radiation, while B19 infectivity was decreased to undetectable levels, which resulted in >3.9 log inactivation. CONCLUSION: UVC radiation in the presence of catechins, especially epigallocatechin gallate, appears to be an effective method of increasing the viral safety of FVIII concentrates without the loss of coagulation activity. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor in response to the article about the efficacy of hepatitis B virus of pooled donor samples.