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Precise orientation of symmetry-mismatched epilayers on van der Waals (vdW) substrates via heteroepitaxy has commonly been achieved through surface treatment processes to accommodate weak interlayer registry and bonding strength, thereby limiting the range of material combinations for heterostructure design. In this study, we investigate the influence of lattice instabilities in a structurally modulated vdW TaCo2Te2 substrate on the growth and alignment of a symmetry-mismatched bulk CoxTey epilayer using in situ heating in a transmission electron microscope (TEM). We show that a Peierls-like lattice instability occurs in TaCo2Te2 at a transition temperature of ∼523 K, which was corroborated by phonon calculations. Postheat-treated samples reveal a thermally induced surface diffusion process and the dominant lateral growth of the CoxTey epilayer on the TaCo2Te2 vdW layers, as observed in cross-sectional TEM images. Temperature-dependent selected area electron diffraction (SAED) patterns reveal that the quasi-vdW CoxTey/TaCo2Te2 heterointerface acquires directional locking by aligning larger interlayer lattice mismatch along the lattice instability axis of TaCo2Te2, while preserving a strong lattice matching along the orthogonal direction. This heterostructure exhibits precise interlayer registry with one-dimensional lattice incommensuration along the lattice instability axis, resulting from structural distortion to accommodate lattice-mismatch strain. Moreover, the interfacial reconstruction of TaCo2Te2 back to the distorted phase stabilizes the lattice-locking of the quasi-vdW heterointerface at elevated temperatures. These findings encourage the expansion of material diversity for designing and predicting multidimensional heterostructures by leveraging lattice instabilities to guide epitaxy.

The antigens in the MNS blood group system, presented on glycophorin (GP), are regulated by the GYPA, GYPB, and GYPE genes. Some hybrid GP can express Mia antigen, the most common being GP.Mur. Of potential clinical significance in transfusion practice, GYP*Mur homozygotes can produce anti-JENU because they lack expression of the high-frequency JENU antigen. Although serological typing using anti-Mia is very likely to identify GP.Mur, this method cannot reliably distinguish the underlying GP or confirm the zygosity of GP.Mur, which is relevant for transfusion safety. We, therefore, developed and validated a polymerase chain reaction with high-resolution melting (PCR-HRM) assay for distinguishing homozygous GYP*Mur from heterozygous GYP*Mur/GYPB and homozygous GYPB genotypes. An HRM assay targeting exon 3 of GYP(B-A-B) hybrid genes was designed and validated using 186 Mi(a+) samples with known sequencing data. This assay was subsequently applied to 211 DNA samples from Thai blood donors, including Mi(a+) and Mi(a-) samples. HRM analysis showed high concordance with sequencing data in 184 of 186 validated samples. Discrepant cases were attributable to rare sequence variations that altered melting profiles. Among Mi(a+) samples not previously sequenced, 81.45% were classified as GYP*Mur/GYPB, 3.97% as GYP*Mur/GYP*Mur, 12.58% as GYP*Thai/GYPB, and 2% as other clusters, which were identified as rare variants by sequencing. All Mi(a-) samples were consistently classified as homozygous GYPB. Our PCR-HRM assay can rapidly and reliably discriminate homozygous GYP*Mur from heterozygous GYP*Mur/GYPB and homozygous GYPB genotypes. Rare or unexpected variants can be identified when DNA quality is well controlled, and appropriate quality controls are applied. Accordingly, this method may serve as a practical first-line screening tool to support transfusion safety, particularly in populations with a high prevalence of hybrid GP.

This case study examines a 22-year-old unmarried woman who experienced shock resulting from rupture of a corpus luteum cyst. During the perioperative period, the patient received multiple transfusions of red blood cells and fresh frozen plasma. Subsequently, the patient developed transfusion-related acute lung injury 6 h following the final blood transfusion. The findings indicated that the inflammatory characteristics of antiphospholipid syndrome and deep vein thrombosis were closely associated with the onset of transfusion-related acute lung injury. Surgical procedures and multiple perioperative blood transfusions, particularly those involving fresh frozen plasma, were identified as significant contributors to the acute onset of transfusion-related acute lung injury. It is crucial for healthcare professionals to improve blood transfusion management and increase awareness of transfusion-related acute lung injury, especially in African countries with limited medical resources.

Interpretation of antibody identification panels remains a manual, expertise-intensive step in transfusion testing; interpretive errors and long turnaround times persist even in well-equipped hospitals. Existing commercial software is closed source and often omits enzyme-phase, cold-phase, and dosage-sensitive exclusion rules, limiting third-party verification and local adaptation. We developed IrregulAB, an open-source (LGPL) web application that encodes serologic decision rules in two stages. First, a rule-based screening stage applies LISS, enzyme, and cold rule-out logic with safeguards for antigen dosage in heterozygotes to discard antibodies incompatible with the observed reaction pattern. Second, a minimal-set solver exhaustively searches for the smallest antibody combination(s) that reproduce all assessable reactions and reports all equally plausible solutions. The system was evaluated on 108 development antibody-identification panels and 35 held-out temporal validation panels. The screening stage retained the complete reference antibody set in 93% of development panels and 91% of held-out temporal validation panels. The minimal-set stage produced at least one valid explanatory antibody combination in 87% of development panels and 89% of held-out temporal validation panels. IrregulAB is a transparent, rule-based decision-support tool for trained immunohematology personnel; it is not an autonomous antibody-identification or reporting system. By exposing every encoded decision rule, it enables independent verification, local tuning, and more standardized review of routine antibody workups under expert supervision. Its current performance was evaluated retrospectively in a single-center Bio-Rad gel-card dataset; multicenter and multi-platform validation is required before wide clinical implementation.

IntroductionSickle cell disease (SCD) confers a three-to fivefold increase in the prevalence of intracranial aneurysms (IA). Flow diversion (FD) requires mandatory dual antiplatelet therapy (DAPT), yet perioperative transfusion to reduce hemoglobin S (HbS) risks delayed hemolytic transfusion reaction (DHTR). No guidelines address this conflict between DHTR-associated coagulopathy and mandatory DAPT. We report the largest FD series in SCD.MethodsRetrospective single-center case series of SCD patients undergoing FD for IA (2017 to 2026). Of 12 SCD patients treated for aneurysms, seven received FD and comprised the analytic cohort.ResultsSeven patients (5 HbSS, 2 HbS/&#x3b2;0-thalassemia; median age 38; 71% female) harbored 29 aneurysms; 12 were treated with FD across 8 procedures using 15 devices. HbS <30% was achieved in 3 of 7 (43%); one patient underwent FD at HbS 78.5% due to alloimmunization. Clopidogrel hyporesponsiveness was identified in 2 of 4 TEG-tested patients (50%). Procedure-related mortality was 14% (1/7): fatal DHTR with DIC on postoperative day 8, the first reported DHTR-DAPT collision. Procedure-related morbidity included one intraoperative thrombus and one vasospasm episode, both resolved without sequelae (2/8 procedures, 25%). Additional events included asymptomatic in-stent stenosis and delayed stroke from SCD vasculopathy. At last follow-up, 5 of 6 survivors maintained mRS 0 to 1.Discussion and ConclusionFD is technically feasible in SCD, but the 14% procedure-related mortality from a fatal DHTR exposes the unresolved conflict between transfusion-associated hyperhemolysis and mandatory DAPT. CYP2C19-mediated clopidogrel resistance and alloimmunization pose additional challenges that require predefined protocols and prospective multicenter registries.

Amniotic fluid embolism (AFE) and placental abruption represent two of the most catastrophic obstetric emergencies, sharing a common pathway of severe coagulopathy while differing fundamentally in their underlying pathophysiology. AFE is characterized by sudden cardiovascular collapse, respiratory distress, and disseminated intravascular coagulation (DIC), likely triggered by an anaphylactoid-like reaction to fetal antigens entering maternal circulation. The condition manifests with both consumptive coagulopathy and hyperfibrinolysis, with platelet counts frequently falling below 50,000/&#x3bc;L and precipitous drops in fibrinogen levels. Management requires immediate advanced cardiac life support and aggressive hemodynamic support, mechanical ventilation, and massive transfusion protocols guided by viscoelastic testing. Emerging therapies include extracorporeal membrane oxygenation for refractory cardiopulmonary collapse and recombinant factor VIIa for intractable hemorrhage. Placental abruption results from premature placental separation and presents vaginal bleeding, abdominal pain, and fetal compromise. The condition arises from chronic uteroplacental ischemia and decidual arteriopathy, with retroplacental hematomas serving as massive sources of tissue factors that trigger the coagulation cascade. Abruption-related DIC primarily manifests consumption coagulopathy. Unlike AFE, urgent delivery of the fetus and placenta can eliminate the source of thromboplastic material, often resolving the coagulopathy. Both conditions demand, among others, institutional preparedness with established massive transfusion protocols and multidisciplinary teams trained in obstetric critical care. While advances in viscoelastic testing, targeted factor concentrates, and life support technologies have improved outcomes, AFE and placental abruption continue to challenge even experienced obstetric teams.

Confirmation of HLA-C*07:262 by third-generation sequencing, differing from C*07:02:01:01 by a single nucleotide substitution in exon 2.

The HLA-C*01:02:100 allele differs from HLA-C*01:02:01:01 by a single synonymous nucleotide change in Exon 7.

Massive transfusion protocols are essential in trauma resuscitation but may inadvertently increase the risk of acute hemolytic transfusion reactions (AHTRs), which are typically caused by ABO incompatibility. Recognition is difficult because signs of hemolysis can mimic trauma-related hemorrhage or coagulopathy. Cognitive biases in emergency decision-making may further delay diagnosis. Although ABO-incompatible AHTR remains exceptionally rare in trauma, it is easily overlooked in the context of polytrauma. We describe three cases of ABO-incompatible AHTR admitted to a tertiary trauma center. First, a 52-year-old man with multiple injuries received three mis-issued AB+ units instead of group O blood. He developed hemoglobinuria, coagulopathy, and fatal multiorgan failure. The second case involved an 81-year-old man with multiple comorbidities who underwent hip fracture fixation; due to a mislabeled admission sample, he received A+ instead of B+ blood, resulting in persistent anemia, renal failure, and death. The third case was a 30-year-old woman with severe head and thoracic trauma who received incompatible blood under an emergency release protocol. She developed hemolysis, neurologic decline, and sepsis, and ultimately died of multiorgan failure. In all three patients, early post-transfusion anemia and hemodynamic instability were attributed to trauma, delaying recognition of hemolysis. AHTR may therefore be overlooked in trauma settings, where its manifestations overlap with injury-related complications and cognitive biases such as anchoring and premature closure may impair diagnostic reasoning. Strict transfusion safety protocols, heightened vigilance when hemoglobin levels fail to rise, and awareness of cognitive errors may improve early recognition and patient outcomes.

In 2012, the International Society of Blood Transfusion (ISBT) formalized the JR blood group system (ISBT 032), with Jra (ISBT 032001) as its only antigen. Jra is located on a multipass membrane glycoprotein named ABCG2. ABCG2, or ATP-binding cassette subfamily G member 2, is also known as breast cancer resistance protein (BCRP) or CD338. This glycoprotein participates in various physiological, biochemical and metabolic processes in the human body. It is encoded by the ABCG2 gene, located on chromosome 4. In recent years, the ABCG2 gene variants have been gradually unraveled through the deeper study of the JR blood group system. Meanwhile, the JR blood group system is clinically important, being associated with fetal and neonatal anemia, hydrops fetalis, neonatal jaundice, hemolytic disease of the fetus and newborn (HDFN), and hemolytic transfusion reaction (HTR). Furthermore, its carrier molecule, ABCG2, is associated with hyperuricemia/gout and mirror syndrome. In addition, ABCG2 plays an important regulatory role in a variety of physiological and pathological processes, such as the regulation of uric acid metabolism, the maintenance of folate and porphyrin homeostasis, the regulation of blood-brain barrier substance exchange, and the regulation of anti-tumor drug transport and drug resistance. This study reviews the distributional characteristics, molecular biological features, immunological features and clinical significance of the JR blood group system and ABCG2.

Hydrogen peroxide (H&#x2082;O&#x2082;) plays a crucial role in both biological and industrial systems. Excessive H&#x2082;O&#x2082; can lead to oxidative stress, cellular damage, and process-related issues in manufacturing. For this reason, fast and sensitive detection methods are needed. In this study, Ni-CoWO&#x2084; nanoparticles, belonging to the bimetallic nanozymes family, were used as catalysts to promote the oxidation of ortho-phenylenediamine (OPD) by H&#x2082;O&#x2082;. Polyoxometalates are renowned for their structural diversity, large surface area, and robust redox activity, making them exceptional candidates for catalytic applications. Ni-CoWO&#x2084; was prepared using a hydrothermal method and characterized using SEM-EDX, XRD, and FT-IR techniques. The nanoparticles exhibited an even distribution of nickel and cobalt within a multi-metallic framework, resulting in numerous active sites and a high surface-to-volume ratio. Compared to the system without the catalyst, Ni-CoWO&#x2084; significantly improved the reaction rate, produced a stronger yellow color, and reduced the oxidation time. The reaction was monitored by visible spectrophotometry, spectrofluorimetry, and smartphone-based colorimetry. A linear range of 0.5-150 &#xb5;M and a limit of detection of 485 nM for H2O2, and a linear range of 1-125 &#xb5;M for glucose were obtained by the spectrophotometry. In spectrofluorimetry, it showed a linear range of 0.1-50 &#xb5;M, and LOD was 64 nM. In the smartphone-based method, RGB (Red, Green, Blue) and CMYK (Cyan, Magenta, Yellow, Key (Black)) were used for colorimetric and fluorimetric determination. Overall, the results demonstrate that Ni-CoWO&#x2084; is a low-cost and effective nanocatalyst for H&#x2082;O&#x2082; and glucose sensing, with significant potential for both biological and industrial applications.

The HLA-A*68:343N, HLA-C*12:455N and HLA-DRB1*04:409N alleles detected by next-generation sequencing during routine typing.

Identification of five new HLA alleles by next-generation sequencing.

Babesia microti is a transfusion-transmitted pathogen. The US Food and Drug Administration (FDA) recommends blood donor screening only in endemic states, whereas the Military Health System performs universal Babesia screening regardless of geographic location. However, the epidemiology of Babesia positivity and clinical follow-up among blood donors in non-endemic regions remains poorly characterized. We conducted a retrospective study evaluating Babesia screening results from three military blood donation centers in non-endemic states: Naval Base San Diego, Wright-Patterson Air Force Base, and Joint Base San Antonio-Lackland. All donations collected between January 1, 2021 and December 31, 2025 underwent nucleic acid testing using the Procleix Babesia Assay. Positive donors underwent retrospective chart review to assess demographics, confirmatory testing, clinical follow-up, and treatment outcomes. Among 97,861 donations screened, eight donors tested positive for Babesia (8.17 per 100,000 donations). San Diego demonstrated the highest positivity rate (11.53 per 100,000), followed by Wright-Patterson (8.55 per 100,000) and San Antonio (5.82 per 100,000). Five donors were active-duty military personnel with medical records available for review, and three underwent follow-up clinical evaluation. Follow-up approaches varied considerably and include empiric treatment without confirmatory testing, antibody testing, peripheral blood smear evaluation, and polymerase chain reaction (PCR) testing. All clinically evaluated donors were asymptomatic, and there were no documented complications related to babesiosis. Babesia positivity among military blood donors in non-endemic regions was rare. Variation in diagnostic evaluation and clinical management highlights the need for standardized follow-up protocols for military donors with positive screening results.

This case report describes a suspected coagulation disorder induced by cefoperazone/sulbactam administered for anti-infective therapy. The coagulopathy may be associated with the inhibition of vitamin K synthesis and utilization caused by cefoperazone/sulbactam. The patient was admitted with severe right thalamic intracerebral hemorrhage complicated by Klebsiella pneumoniae infection and remained on total parenteral nutrition (TPN) due to concomitant gastrointestinal dysfunction. We initiated anti-infective therapy with cefoperazone/sulbactam at a dose of 2&#xa0;g administered intravenously every 12&#xa0;h for seven consecutive days. On the eighth day of treatment, the patient developed severe coagulation dysfunction, with prothrombin time (PT) markedly prolonged to 262.9&#xa0;s. Cefoperazone/sulbactam was immediately discontinued, and vitamin K1 along with plasma transfusion was administered. By the third day after intervention, the patient's coagulation function significantly improved, and PT returned to normal levels. Causality assessment using the Naranjo Adverse Drug Reaction Probability Scale yielded a score of 7, indicating a probable association between the adverse event and cefoperazone/sulbactam use. This case report emphasizes that cefoperazone/sulbactam may cause extremely severe coagulation dysfunction, manifested as markedly prolonged PT in this patient. Clinicians should remain vigilant for this potential adverse reaction and closely monitor coagulation parameters during treatment.

The HLA-A*24:677 allele differs from HLA-A*24:02:01:01 by a single non-synonymous nucleotide change in exon 2.

Viral hepatitis A&#xa0;(VHA) is primarily transmitted via the faecal-oral route. Transmission through blood transfusion products is rare. In 2025, during an ongoing VHA epidemic in the Czech Republic, cases of hepatitis A&#xa0;virus (HAV) transmission through transfusion blood products from an asymptomatic donor were detected. The donor was only found to be HAV positive after developing clinical symptoms. Infected blood transfusion products (leukocyte-depleted erythrocytes and thrombocytes) were administered to two recipients, who subsequently developed infection. One of them, a&#xa0;paediatric patient, presented with anicteric VHA without complications, while the other immunocompromised patient had prolonged viremia. These cases highlight the risk of HAV transmission through blood transfusions, particularly during epidemics. Asymptomatic viremia in donors makes it impossible to detect infection without targeted testing. The introduction of direct nucleic acid testing (NAT) for HAV during a&#xa0;period of increased incidence of infection would improve the safety of blood transfusions.

To conduct blood group identification and genetic analysis on a pregnant woman suspected for having ABO blood group chimerism, and to explore the blood group identification methods and formation mechanisms of her chimerism. A pregnant woman with mixed-field (MF) agglutination reactions in ABO forward typing detected at the Department of Transfusion, Zhongshan Hospital, Xiamen University on May 10, 2025 was selected as study subject. Blood grouping was carried out using a microcolumn gel method and saline method. The two populations of red blood cells (RBCs) from the proband, including those agglutinated and non-agglutinated with anti-A reagent, were separated for repeated blood grouping. Flow cytometry was used to quantitatively analyze the proportion of the two RBC populations. ABO genotyping was conducted via direct sequencing and PacBio long-read single-molecule real-time (SMRT) sequencing. Short tandem repeat (STR) analysis was performed on the proband's blood, buccal swabs, hair follicle samples, and the blood samples of her parents. Genetic analysis was carried out using multiplex PCR testing for Y-chromosome microdeletions, chromosomal karyotyping, and fluorescence in situ hybridization (FISH). This study was approved by the Medical Ethics Committee of the hospital (Ethics No.: xmzsyyky 2025-070). The proband's RBCs showed 4+ MF agglutination with anti-A, anti-A1, and anti-AB antibodies. After separation, agglutinated RBCs presented the A1 phenotype and non-agglutinated RBCs presented the O phenotype. Phenotyping for 14 additional RBC antigens showed no MF reaction. Flow cytometry showed that A-phenotype RBCs have accounted for 31.6%, and O-phenotype RBCs have accounted for 69.4%. Direct sequencing of the ABO gene revealed that the proband had an A1.02/O.01.01 genotype. SMRT sequencing results confirmed the presence of three distinct ABO allelic haplotypes: O.01.01 (containing the IVS4+102C>A variant), O.01.01, and A1.02. STR analysis showed that the TH01 and Penta E loci in the proband's multiple tissue samples all exhibited dual paternal and maternal DNA contributions, and a characteristic Y-chromosome peak was detected at the AMEL locus. Multiplex PCR for Y-chromosome microdeletions confirmed that the proband carried the AZFa/b/c, SRY and ZFY genes. G-banded karyotype analysis showed that the proband has a karyotype of 46,XY[1]/46,XX[99]. FISH revealed that the proportion of XY-karyotype cells in cultured peripheral blood was significantly lower than uncultured specimens. The proband is an ABO blood group chimera and a tetragametic chimera with a 46,XY/46,XX karyotype distributed throughout the body. This chimerism has originated from the fusion of male and female dizygotic twin embryos during early development.

Although adverse reactions and injuries associated with blood donation are typically self-sustaining, they may defer donors from making future blood donations. This study aimed to determine the prevalence and predictors of adverse reactions in whole blood donors, thereby identifying potential targets for interventions to reduce such events. A total of 5,003 whole blood donations were analyzed over a two-year period. Donor demographic, medical, and biometric parameters were recorded and examined for associations with adverse donor reactions. The overall prevalence of vasovagal reactions was 1.7% and 287 donors (5.74%) experienced adverse events (AEs). Strong predictors of adverse reactions included younger age, first-time donation, low body weight, donation around noon, and a pre-donation waiting period exceeding 30 minutes. Vasovagal reaction rates reported in the literature vary widely, ranging from 0.09% to 2.24%. Most studies, including the present one, found no significant gender differences in reaction rates; in this study, males and females experienced almost similar rates (1.7% vs. 1.8%). These findings are instrumental in identifying donors at greater danger of developing undesirable reactions. Enhanced monitoring during and after donation, along with timely intervention, may facilitate to prevent many of these adverse and unpleasant events and improve donor retention.