Factor X + Factor IX (Factor X P Behring)

Factor V is an anticoagulant of the extrinsic pathway of coagulation and modifier of thrombin generation in hemophilia A.

Jewell Megan M, Baird Christine H CH, Thornhill Dianne D, Ashour Zaina Z et al.

Factor V (FV) links procoagulant amplification to anticoagulant feedback, but how FV limits tissue factor-initiated coagulation are not fully defined. We hypothesized that procofactor FV downregulates factor X (FX) activation by tissue factor:factor VIIa (TF:FVIIa), independently of tissue factor pathway inhibitor α (TFPIα), and that this mechanism is especially important in hemophilia. Thrombin generation was measured in FV/FVIII‑immunodepleted plasma and synthetic plasma while titrating FV, with TFPIα removed, blocked, or re-added. TF:FVIIa activation of FX was measured on phosphatidylserine‑containing or phosphatidylserine‑free liposomes with antibodies against the FV light chain and C2 domain. FV and TFPIα levels modulated thrombin generation in plasma from people with hemophilia A. In TF‑initiated coagulation lacking TFPIα, thrombin generation peaked at 2 nM FV and decreased as FV increased; at 20 nM FV (normal concentration), peak thrombin and thrombin generation rate were reduced by up to 50-80%, with larger effects at low FVIII. In purified TF:FVIIa assays, FV reduced FX activation by ~80% at physiologic concentration and inhibited FX activation on TF-expressing fibroblasts. Increasing PS content enhanced FX activation and increased the FV-sensitive component, while blocking the FV light chain or C2 domain partially relieved inhibition. In hemophilia A plasma, higher FV was associated with longer lag time and time-to-peak, and lower peak thrombin independent of TFPIα. Thus, FV is an endogenous anticoagulant that inhibits TF-initiated coagulation by limiting FX activation by TF:FVIIa through a membrane-dependent mechanism. This mechanism refines models of coagulation initiation and may help explain how FV variation contributes to bleeding and thrombosis.

Spray-induced gene silencing targeting ZmHSF20 enhances maize thermotolerance.

Zhang Jie J, Zhang Zichen Z, Lin Mingzhou M, Dai Mingqiu M et al.

Spray-induced gene silencing (SIGS) is an emerging, time-efficient, and eco-friendly strategy for crop trait manipulation. Heat stress severely threatens global maize production; however, whether SIGS can be effectively applied to improve maize heat tolerance remains largely unexplored. The transcription factor ZmHSF20, a class B2a heat shock factor, has been identified as a negative regulator of maize thermotolerance that represses the ZmHSF4-ZmCESA2 module (Li et al. 2024), yet whether its silencing via a non-transgenic RNA-based approach can confer heat protection is unknown. Here, we designed a specific artificial small RNA atsRNA-ZmHSF20 targeting ZmHSF20 and evaluated its potential in improving maize thermotolerance via the SIGS approach. Compared with untreated plants, foliar application of atsRNA-ZmHSF20 significantly enhanced maize heat tolerance, leading to a remarkable increase in survival rate from 7.94% to 41.37% (~ 5.2-fold improvement). Physiological analyses revealed that exogenous application of atsRNA-ZmHSF20 mitigated heat-induced oxidative damage, as evidenced by reduced ROS accumulation, ion leakage (IL), and malondialdehyde (MDA) content. At the molecular level, downregulating ZmHSF20 prior to heat stress pro-conditioned the plants for thermal tolerance by activating the previously characterized ZmHSF4-ZmCESA2 module, transcriptionally upregulating cell wall organization and cellulose biosynthesis pathways. This study provides an initial proof-of-concept for harnessing SIGS to enhance maize abiotic stress tolerance and offers a promising non-transgenic strategy for future applications in enhancing crop thermotolerance. The online version contains supplementary material available at 10.1007/s11032-026-01698-x.

DIEP reconstruction in a patient with Factor V Leiden deficiency: A case report and literature review.

Quinn Olivia O, Bhatti Sumbal S, Rosich-Medina Anais A

We report a 63-year-old female with Factor V Leiden deficiency who underwent a left delayed DIEP flap reconstruction with contralateral symmetrising breast reduction following mastectomy. Hypercoagulable disorders are theorised to increase flap failure risk. Current evidence and operative guidance are limited. A focused review of the literature is provided.

Comment on "Stump Ischemia Is a Possible Risk Factor for Late-Onset Pancreatic Fistula After Distal Pancreatectomy".

Xu Shitang S