Background: Recruiting of sufficient numbers of donors of blood products is vital worldwide. In this study we assessed the efficacy and cost-effectiveness of telephone calls and SMS reminders for re-recruitment of inactive blood donors.Methods: This single-centre, non-blinded, parallel randomised controlled trial in Guangzhou, China included 11,880 inactive blood donors whose last donation was between January 1 and June 30, 2014. The donors were randomly assigned to one of two intervention groups (telephone call or short message service [SMS] communications) or to a control group without intervention. SMS messages with altruistic appeal were adopted in the SMS group; in addition to altruistic appeal, reasons for deferral of blood donation were also asked in the telephone group. All participants were followed up for 1 year. The primary outcome was re-donation rate, and rates in different groups were compared by intention-to-treat (ITT) analysis and estimation of the average treatment effect on the treated (ATT). Secondary outcomes were the self-reported deterrents. Other outcomes included the re-donation interval, and the incremental cost-effectiveness ratio (ICER) of telephone calls and SMS reminders on re-recruitment.Results: ITT analysis revealed no significant differences in the re-donation rate among the three groups. ATT estimations indicated that among compliers, telephone calls significantly increased re-donation compared to both SMS reminders and no intervention. Donor return behaviour was positively associated with receiving reminders successfully, being male, older age, and previous donation history. The SMS reminder prompted donors to return sooner than no reminder within 6 months, and according to ICER calculations, SMS reminders were more cost-effective than telephone calls. Donors reported time constraints as the most main causes of self-deferral in the telephone group, and altruistic appeal had a positive effect on these donors.Conclusions: Interventions to reactivate inactive blood donors can be effective, with telephone calls prompting more donors to return but at a greater cost than SMS messages. SMS reminder with altruistic appeal can urge donors to re-donate sooner within 6 months than no reminder.Trial registration: NCT03366441(Reactivation of Inactive Blood Donors). Retrospectively registered 4 December 2017.

The proliferation of CAR‐T cells was hindered and cannot play its killing function well in solid tumors. And yet the regulatory mechanism of CAR‐T cell proliferation is not fully understood. Here, we showed that recombinant expression of CD19CAR in T cells significantly increased the basal activation level of CAR‐T cells and LCK activation. Both LCK and SMAD4 were essential for CAR‐T cells proliferation since over‐express LCK or SMAD4 significantly promotes CAR‐T cells proliferation, while knock‐down LCK or SMAD4 expression inhibited the proliferation of CAR‐T cells seriously. More cells go into apoptosis when knock‐down LCK or SMAD4 expression, and the cell cycle was arrested in G2/M or S phase, respectively. Over‐express LCK or SMAD4 significantly promotes phosphorylation of PI3K and Akt, while it was inhibited when cells were treated with PI3K and Akt inhibitors (LY294002 or MK2206). Further mechanism exploration experiments showed that SMAD4 bound on the promoter region of LCK regulating its expression. Taken together, we reported that the transcription factor SMAD4 regulated the expression of LCK and further involved in the PI3K/Akt signaling pathway to affect the proliferation of CAR‐T cells.

CD36, also known as glycoprotein IV, is classified into two distinct subgroups based on the presence or absence of its expression on monocytes. The CD36 gene spans approximately 50,000 base pairs. Historically, research has focused on identifying CD36 mutations through Sanger sequencing and next-generation sequencing (NGS), with limited exploration of haplotypes. In this study, we collected blood samples from donors with type I and type II CD36 deficiencies as well as from healthy controls, and employed single-molecule long-read sequencing (also known as Third-Generation Sequencing) of genomic DNA to analyze the genetic basis of CD36. The study identified 180 genetic variants, 12 of which were found to alter the amino acid sequence. Notably, four of these mutations (c.220 C > T; c.329_330delAC; c.430-1 G > C; c.1006 + 2 T > G) are premature termination mutations that lead to protein truncation. Using Fisher’s exact test, we statistically analyzed a specific haplotype, c.-132A > C and c.329_330delAC, along with their clinical phenotypes, revealing a strong association between these variants in the 5’ block and type I CD36 deficiency. We analyzed the CD36 gene sequences in platelet donors and patients with PTR (platelet transfusion refractoriness) and FNAIT (fetal and neonatal alloimmune thrombocytopenia), conducting a detailed haplotype analysis associated with type I CD36 deficiency and FNAIT.

S gene mutations may lead to undetectable HBsAg, contributing to occult HBV infection (OBI). Nucleic acid testing (NAT) has been widely implemented to reduce transfusion-transmitted OBI. However, distinguishing between false positives and true OBI among NAT+/HBsAg– donors remains challenging, as these individuals frequently exhibit inconsistent or fluctuating test results. This study aims to improve infection status confirmation and donor management by analyzing detection patterns and investigating S gene mutations. Blood donors were detected for HBV using individual-NAT and HBsAg enzyme-linked immunosorbent assays. Routine discriminatory test (dHBV), additional three repeated dHBV (3-repeated dHBV), and serological assays were conducted to confirm the infection status of NAT+/HBsAg– donors. Serial NAT results were analyzed to assess temporal fluctuations. S gene mutations related with OBI were identified through molecular characterization and sequencing analysis. A total of 336,537 blood donors were detected, and 556 (0.16%) NAT+/HBsAg– cases were identified. Among 297 donors undergoing confirmation, 112 (37.71%) were confirmed by routine dHBV, 152 (51.18%) by 3-repeated dHBV, and 43 (14.48%) by multiple serial NATs. In total, 187 donors (62.96%, 187/297) were confirmed HBV-infected, significantly higher than routine dHBV alone (P < 0.01). Among the 187 confirmed HBV-infected donors, only 59 (31.55%) were positive in all four dHBV tests, while 128 (68.45%) showed missed detections, suggesting extremely low viral loads. In serial NAT testing, 83 (73.45%, 83/113) of donors confirmed by dHBV showed no further NAT-positive results, and an average of 5.6 tests was needed to detect one extra positive case. Molecular analysis revealed that OBI samples had more mutations in both the major hydrophilic region (MHR) and non-MHR compared to HBsAg + donors (P < 0.05), with a significantly higher prevalence of the E2G mutation. OBI is a major contributor to inconsistent NAT results. Comprehensive measures, especially repeated testing, are recommended to improve confirmation rates and reduce the risk of re-entry of potentially infectious donors. Additionally, further molecular research on S gene mutations is essential for elucidating OBI mechanisms and enhancing assay sensitivity.