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SAMHD1 Research Digest — 2026-06-21

Generated by samhd1_monitor | Model: claude-sonnet-4-6

Summary: 27 papers evaluated | 12 high-relevance (≥7) | 9 medium (5–6) | 6 low (3–4) | 0 scored <3

🔴 High Relevance (Score 7–10)

Added to Zotero automatically

Nucleotide metabolism reprogramming in obesity-associated cardiovascular inflammation: a new perspective (from Cardiology/Immunometabolism)
Taoming Qian; Mei Zhang; Yuhan Liu; Donghao Guo; Juan Jin — Frontiers in Immunology 2026
Score: 9/10 | Pathways: dNTPase, NLRP3, POLG-mtDNA, VDAC1, urate-NLRP3, treatment-target, clinical-phenotype, other

This paper directly models the SAMHD1→dNTP accumulation→mitochondrial dNTP import (SLC25/PNC transporters)→mtDNA oxidation→NLRP3 hyperactivation axis that is the core PURPLE and GOLD mechanism of the disease profile, demonstrating it in a cardiovascular/macrophage context with therapeutic node identification, making it highly mechanistically relevant even without the specific A565T variant.
DOI: 10.3389/fimmu.2026.1829718

The leaked mitochondrial DNA activated the cGAS-STING signaling pathway and exacerbated the motor dysfunction in mice caused by MPTP. (from Neurology/movement disorders)
Zhu Guangyao; Yu Xuanjie; Guo Yi; Yang Liting; Yang Qianhui — 2026
Score: 8/10 | Pathways: cGAS-STING, VDAC1, POLG-mtDNA, treatment-target, other

This paper directly demonstrates the BLUE stream mechanism central to the disease model: mitochondrial stress → mtDNA leakage into cytosol → cGAS-STING activation → neuroinflammation, and validates STING inhibition as a therapeutic target, with direct relevance to the SAMHD1/VDAC1-mtDNA escape axis even though SAMHD1 is not mentioned.
DOI: 10.1016/j.expneurol.2026.115876

STING-OPTN signaling confers cytoprotection through TBK1-dependent mitophagy. (from Cell biology / mitochondrial quality control)
Zebo Huang; Jin-Yi Lin; Ling-Jun Cheng; Yong Wu; Xiangzheng Gao — Cell reports 2026
Score: 8/10 | Pathways: cGAS-STING, ISG15-mitophagy, VDAC1, POLG-mtDNA, mTOR-lysosomal, treatment-target

This paper directly implicates the cGAS-STING pathway as an upstream regulator of mitophagy via TBK1-OPTN signaling, which is mechanistically central to the BLUE and RED streams of the disease model—where constitutive STING activation from VDAC1/mtDNA escape not only drives IFN-I but also perturbs mitochondrial quality control, and the STING-OPTN mitophagy axis disruption switches cells toward apoptosis, directly mirroring the double mitophagy block (ISGylation of MFN1/2 and BECN1) and the apoptosis-autophagy switch (BIK/BH3) predicted in the family's pathomechanism.
DOI: 10.1016/j.celrep.2026.117515

STING1 senses mitochondrial damage to promote mitophagy. (from Cell biology / autophagy)
Zebo Huang; Jin-Yi Lin; Ling-Jun Cheng; H. Tan; Hanming Shen — Autophagy 2026
Score: 8/10 | Pathways: cGAS-STING, ISG15-mitophagy, POLG-mtDNA, ME-CFS, treatment-target

This paper directly demonstrates that STING1 acts as a non-canonical upstream regulator of PINK1/Parkin-dependent mitophagy via TBK1-OPTN phosphorylation, revealing a critical mechanistic intersection with the RED and BLUE streams of the disease model: in SAMHD1 haploinsufficiency, chronic cGAS-STING activation would simultaneously drive IFN-I (canonical) and dysregulate mitophagy quality control (non-canonical), and disruption of the STING1-TBK1-OPTN axis shifts cell fate toward apoptosis rather than pro-survival mitophagy, directly explaining the double mitophagy block and accumulation of damaged mitochondria central to the family's interferon-mitochondrial syndrome.
DOI: 10.1080/15548627.2026.2689463

cGAS-STING signaling pathway: a central pathological mechanism and emerging therapeutic target for postoperative cognitive dysfunction. (from Anesthesiology/Perioperative Neuroscience)
Wu Xiaoqin; Zhong Baolin; Xu Yongxing; Lai Yinsiqing; Wen Xinming — 2026
Score: 7/10 | Pathways: cGAS-STING, NLRP3, VDAC1, POLG-mtDNA, ISG15-mitophagy, treatment-target

This review directly describes the mtDNA-cGAS-STING-neuroinflammation axis with pyroptosis and mitophagy failure as central mechanisms, which maps precisely onto the BLUE and RED streams of the SAMHD1 haploinsufficiency model, and identifies cGAS-STING inhibition and mitophagy promotion as therapeutic targets directly applicable to this disease mechanism.
DOI: 10.1016/j.brainres.2026.150432

Runx1-Snx9 axis drives the pathological secretion of mitochondrial-derived vesicles to activate cGAS-STING signaling in acute pancreatitis. (from Gastroenterology/Pancreatology)
Gao Mengqi; Xiao Guohui; Chen Kunhao; Li Shiyu; Chen Cong — 2026
Score: 7/10 | Pathways: cGAS-STING, VDAC1, POLG-mtDNA, NLRP3, other

This paper directly characterizes a novel upstream mechanism (Runx1-Snx9 axis) driving mitochondrial-derived vesicle secretion and mtDNA release that activates macrophage cGAS-STING signaling — the same BLUE stream pathway central to SAMHD1 haploinsufficiency — providing a mechanistic parallel for how cytosolic/extracellular mtDNA fragments trigger chronic interferon activation, even though the context is acute pancreatitis rather than SAMHD1 dysfunction.
DOI: 10.1186/s12951-026-04687-6

Environmental enrichment mitigates sevoflurane-induced neurodevelopmental injury via cGAS-STING-dependent microglial modulation. (from Pediatric anesthesiology/neurodevelopment)
Li Feixiang; Gong Bingqing; Wu Haiyan; Yang Yongyan; Luo Ying — 2026
Score: 7/10 | Pathways: cGAS-STING, VDAC1, POLG-mtDNA, ME-CFS, other

This paper directly demonstrates the mitochondrial dysfunction → mtDNA release → cGAS-STING activation → microglial neuroinflammation → synaptic/cognitive impairment axis, which is mechanistically identical to the BLUE stream in the SAMHD1 haploinsufficiency model, and validates mtDNA-driven cGAS-STING as a tractable intervention target in a neurodevelopmental context relevant to the AuDHD phenotype in the proband.
DOI: 10.1186/s13578-026-01610-2

Beyond proteostasis: LONP1 as an immunometabolic checkpoint in health and disease. (from Mitochondrial biology / proteostasis)
Xie Lin; Wu Li-Hong; Ni Xin-Cheng; Zhang Jiang-Nan — 2026
Score: 7/10 | Pathways: cGAS-STING, POLG-mtDNA, NLRP3, VDAC1, mTOR-lysosomal, ME-CFS, treatment-target, other

LONP1 directly regulates mtDNA maintenance and its deficiency triggers mtDNA release activating cGAS-STING—the BLUE stream core mechanism in this disease—while also modulating metabolic enzymes relevant to the mitochondrial-inflammatory convergence and SARS-CoV-2 pathogenesis relevant to ME/CFS post-viral trigger, making this a high-value adjacent mechanism with novel treatment implications.
DOI: 10.1016/j.bcp.2026.118170

Mitophagy in Macrophages: A Metabolic Checkpoint in Inflammation-to-Repair Transition in Atherosclerosis. (from Cardiology/atherosclerosis)
Jie Zhou; Hanxiu Liu; Sen Ma; Haoyang Wang; Ni He — Journal of the American Heart Association 2026
Score: 7/10 | Pathways: cGAS-STING, NLRP3, VDAC1, ISG15-mitophagy, treatment-target, POLG-mtDNA

This review directly covers the RED and BLUE stream mechanisms—PINK1/Parkin mitophagy block, mtDNA release activating cGAS-STING and NLRP3 inflammasome in macrophages—with therapeutic targets (metformin, resveratrol, MCC950-analogous NLRP3 inhibition) that map precisely onto the ISG15-mitophagy double-block and VDAC1-cGAS-STING axes central to the SAMHD1 haploinsufficiency syndrome, though SAMHD1 itself is not mentioned.
DOI: 10.1161/jaha.125.048103

The COX2-PGE2-PKA Axis Suppresses Antiviral Immunity by Inhibiting mtDNA-Dependent STING Activation (from Virology/innate immunity (HSV-1 infection model))
P. Vo; Julien Cicero; Zichen Wang; Hiroyuki Hakozaki; Thomas S. Hoang — bioRxiv 2026
Score: 7/10 | Pathways: cGAS-STING, POLG-mtDNA, ISG15-mitophagy, ME-CFS, treatment-target

This paper directly addresses the mtDNA-cytosol-cGAS-STING-IFN-I axis (BLUE stream) and mitophagy regulation thereof, revealing that COX2/PGE2/PKA/STOML2 suppresses STING activation by clearing immunostimulatory cytosolic mtDNA via mitophagy—a regulatory circuit highly relevant because in SAMHD1 haploinsufficiency the mtDNA-cGAS-STING pathway is constitutively overactivated and the ISG15/MFN1/MFN2 mitophagy block prevents this clearance, making COX2/PGE2/PKA axis modulation a potential therapeutic lever.
DOI: 10.64898/2026.04.03.716411

Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis (from Cardiology/Vascular biology)
Hao Liu; Shuai Zhao; Huiqin Gao; Yue Wang; Junyan Gao — Precision Clinical Medicine 2026
Score: 7/10 | Pathways: cGAS-STING, NLRP3, VDAC1, ISG15-mitophagy, JAK-STAT, POLG-mtDNA, treatment-target

This review directly covers the core convergent mechanism of the disease profile—mt-DAMPs (including mtDNA escape via mitochondrial membrane permeability changes analogous to VDAC1 macropore opening) activating cGAS-STING to drive type I interferon production and NLRP3-mediated IL-1β release—while also detailing the PINK1-Parkin mitophagy pathway that is blocked by ISGylation of MFN1/MFN2 in the RED stream, providing mechanistic depth and atherosclerosis-relevant treatment targets applicable to the interferonopathy-mitochondrial syndrome.
DOI: 10.1093/pcmedi/pbag010

Cytosolic Immunostimulatory DNA Ligands and DNA Damage Activate the Integrated Stress Response, Stress Granule Formation, and Cytokine Production (from Cancer immunotherapy / DNA damage biology)
Trupti Devale; Lekhana Katuri; Gauri Mishra; Aditya Acharya; Praveen Manivannan — Cells 2026
Score: 7/10 | Pathways: cGAS-STING, JAK-STAT, ME-CFS, treatment-target, other

This paper directly characterizes the STING-PERK-G3BP1 signaling axis linking cytosolic dsDNA sensing (including mtDNA escape, the core BLUE pathway) to the integrated stress response, stress granule formation, and IFN-I/cytokine production — mechanisms directly downstream of SAMHD1 haploinsufficiency-driven dNTP pool expansion and VDAC1-mediated mtDNA release, and identifies PERK as a novel druggable node that could modulate the chronic interferonopathy in this family.
DOI: 10.3390/cells15020139

🟡 Medium Relevance (Score 5–6)

Review and add to Zotero manually if warranted

Restoring BECN1-Mediated Autophagy Mitigates Acute Lung Injury Caused by Zinc Oxide Nanoparticles. (from Pulmonary toxicology/nanotoxicology)
Lejiao Mao; Meiling Tan; Xuejun Jiang; Jun Zhang; Ge Xu — Free radical biology & medicine 2026
Score: 6/10 | Pathways: ISG15-mitophagy, NLRP3, mTOR-lysosomal, treatment-target

This paper directly demonstrates that BECN1 haploinsufficiency (heterozygous knockout) impairs mitophagy flux causing accumulation of dysfunctional mitochondria, ROS, and inflammatory cascades—mechanistically parallel to the RED stream where ISGylation of BECN1 blocks autophagy flux in the SAMHD1 disease model, and validates Tat-Beclin1 as a pharmacological rescue strategy for BECN1-dependent mitophagy failure.
DOI: 10.1016/j.freeradbiomed.2026.05.317

Immunoglobulin G complexes from post-infectious ME/CFS, including post-COVID ME/CFS disrupt cellular energetics and alter inflammatory marker secretion (from Neuroimmunology/autoimmunity)
Zheng Liu; Claudia Hollmann; S. Kalanidhi; S. Lamer; Andreas Schlosser — Brain, Behavior, & Immunity - Health 2026
Score: 6/10 | Pathways: ME-CFS, VDAC1, ISG15-mitophagy, JAK-STAT, clinical-phenotype, other

This paper directly characterizes ME/CFS (including post-COVID ME/CFS) IgG-mediated mitochondrial fragmentation and energetic disruption in endothelial cells, providing mechanistic autoimmune context for the proband's post-viral ME/CFS phenotype, with mitochondrial fragmentation highly relevant to the ISG15-MFN1/2 mitophagy block and VDAC1 macropore streams in the disease model.
DOI: 10.1016/j.bbih.2026.101187

Interferon stimulatory DNA activates the DNA damage signaling through ATM and DNA-PK sensing (from DNA damage response / genome stability)
Samira Kemiha; Lorena Rejón-Franco; Estelle Ghibaudo; R. Eloiflin; Morgane Chema — The Journal of Biological Chemistry 2026
Score: 6/10 | Pathways: cGAS-STING, POLG-mtDNA, ME-CFS, other

This paper demonstrates that cytoplasmic ISD (the same stimulus generated by VDAC1-mediated mtDNA escape in the BLUE stream) co-activates ATM and DNA-PK damage response kinases independently of cGAS-STING, revealing a parallel DDR arm that could amplify genomic instability and checkpoint activation in SAMHD1 haploinsufficiency where chronic cytosolic dsDNA (from ox-mtDNA fragments) is present.
DOI: 10.1016/j.jbc.2026.111362

African swine fever virus pE199L, as a mitophagy receptor, suppresses antiviral innate immunity to promote viral replication. (from Veterinary virology / ASFV vaccinology)
Xiaoxuan Li; Binbin Ren; Danyang Zhang; Miao Dan; Dongying Liu — Autophagy 2026
Score: 6/10 | Pathways: cGAS-STING, ISG15-mitophagy, ME-CFS, other

This paper directly addresses the cGAS-STING pathway and PINK1/Parkin-dependent mitophagy as targets of viral immune evasion—mechanisms central to the SAMHD1 A565T syndrome—demonstrating that mitophagic clearance of TBK1 suppresses type I interferon production, which is the inverse of the constitutive IFN-I overactivation and mitophagy block seen in this family, providing mechanistic insight into how mitophagy flux regulation gates cGAS-STING-IFN-I signaling amplitude.
DOI: 10.1080/15548627.2026.2654982

B33-01 Cisd1 Regulates the Sting Pathway Through the Ubiquitin-proteasome System to Ameliorate COPD Progression (from Pulmonology/COPD)
J. Gao; Y. Song — American Journal of Respiratory and Critical Care Medicine 2026
Score: 6/10 | Pathways: cGAS-STING, JAK-STAT, other

This paper describes a mitochondria-to-STING innate immunity axis where CISD1 (a mitochondrial iron-sulfur protein) regulates STING degradation via K48-ubiquitination through Ubr5, directly engaging the cGAS-STING-TBK1-IRF3 pathway that is a core loop (BLUE) in the SAMHD1 haploinsufficiency mechanism, offering a novel STING regulatory checkpoint (ubiquitin-proteasome degradation) relevant to modulating the chronic interferon signature seen in the family, though SAMHD1 and dNTP biology are not addressed.
DOI: 10.1093/ajrccm/aamag162.1786

Toward a Molecular Reclassification of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Integrating Multi-Omics, Machine Learning, and Precision Medicine (from Computational biology / precision medicine / multi-omics)
Joshua Frank; Nicole Nesterovitch; Chetana Movva; N. Klimas; L. Nathanson — International Journal of Molecular Sciences 2026
Score: 6/10 | Pathways: ME-CFS, JAK-STAT, POLG-mtDNA, cGAS-STING, NLRP3, ISG15-mitophagy, treatment-target, other

This review directly addresses ME/CFS molecular reclassification and identifies chronic innate immune activation, mitochondrial dysfunction, and genetic risk variants as core pathophysiology—all of which map onto the SAMHD1 A565T interferon-mitochondrial syndrome mechanism—but does not specifically implicate SAMHD1, cGAS-STING, or the dNTPase axis, making it a high-quality contextual reference for the proband's ME/CFS phenotype rather than a mechanistic confirmation.
DOI: 10.3390/ijms27104436

Ca2+-driven self-amplified nanoplatform targeting ER-mitochondrial calcium crosstalk for synergistic apoptosis induction and tumor immune microenvironment remodeling (from Oncology/nanomedicine)
Yucui Ding; Xinyu Liu; Jianlong Fu; Jianyue Xue; Xueni Fan — Materials Today Bio 2026
Score: 5/10 | Pathways: cGAS-STING, VDAC1, NLRP3, other

The paper directly engages the IP3R-GRP75-VDAC complex, mitochondrial permeability transition, and Mn2+-driven cGAS-STING activation—all mechanistically overlapping with the BLUE and PURPLE streams of the SAMHD1 interferonopathy model—but in an oncology/nanomedicine context with no connection to SAMHD1 haploinsufficiency, dNTP pool dysregulation, or the family's clinical phenotypes.
DOI: 10.1016/j.mtbio.2026.103339

Human Endogenous Retroviruses in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Emerging Roles in Pathogenesis, Immunity, Biomarkers and Therapeutics (from Virology/Retrovirology)
K. D. Perera; E. Oltra; S. Carding — International Journal of Molecular Sciences 2026
Score: 5/10 | Pathways: ME-CFS, cGAS-STING, JAK-STAT, AGS-spectrum, other

The paper addresses ME/CFS pathogenesis through HERV-driven innate immune activation (including cGAS-STING sensing, LTR-driven interferon amplification, and JAK-STAT signaling) which overlaps mechanistically with the IFN-I loop central to SAMHD1 haploinsufficiency syndrome, and HERV reactivation is plausibly potentiated by the dNTP pool expansion that SAMHD1 normally suppresses (since SAMHD1 restricts retrotransposon/HERV reverse transcription), but the paper does not address SAMHD1, VDAC1, NLRP3, mitochondrial pathways, or ISG15-mitophagy directly.
DOI: 10.3390/ijms27104309

Dual-targeting macrophage membrane nanosystem enhances radiotherapy-induced antitumor immunity via synergistic nuclear and mitochondrial DNA damage. (from Oncology/Nanomedicine)
Guangyu Ju; Qi Ding; Hongcang Gu; Rao Liu; Xiao Liu — Biomaterials science 2026
Score: 5/10 | Pathways: cGAS-STING, VDAC1, POLG-mtDNA, JAK-STAT, other

This paper demonstrates that mitochondrial membrane permeabilization (analogous to VDAC1 macropore opening in the BLUE stream) causes cytosolic accumulation of mitochondrial nucleic acids activating innate immune signaling and type I interferon, which mechanistically parallels the SAMHD1/VDAC1-mtDNA-cGAS-STING axis, but the context is engineered radiotherapy enhancement in glioma with no SAMHD1 involvement.
DOI: 10.1039/d6bm00279j

🟢 Low Relevance (Score 3–4)

Potential specialty bridges — skim titles

TFEB-mediated autophagy dysregulation links with PRPF31 deficiency-induced photoreceptor death via PLK4 downregulation. (from Ophthalmology/retinal genetics)
Lujia Zhang; Yuntao Qu; S. Yao; Luying Han; Guangming Liu — Experimental eye research 2026
Score: 4/10 | Pathways: mTOR-lysosomal, other

This paper describes a haploinsufficiency-driven autophagic hyperactivation and mitochondrial dysfunction cascade (PLK4-TFEB axis) that shares conceptual overlap with the lysosomal/autophagy failure and mitochondrial damage themes in the SAMHD1 syndrome, but involves entirely different genes (PRPF31, PLK4, TFEB) in a retinal degeneration context with no connection to interferon signaling, dNTP metabolism, cGAS-STING, or any other core SAMHD1 pathway.
DOI: 10.1016/j.exer.2026.111000

C-terminal tail of MAVS dictates organelle targeting and innate immune response (from Cell biology / virology)
Terence Lee; Kiki Cham; Dong-Yan Jin — Cell Communication and Signaling : CCS 2026
Score: 4/10 | Pathways: cGAS-STING, other

MAVS organelle-specific signaling is upstream of IRF3/IFN-β activation (a convergent endpoint in the BLUE stream), but this paper addresses RNA sensing via RIG-I-like receptors rather than the cGAS-STING/VDAC1-mtDNA axis central to SAMHD1 haploinsufficiency, making the connection tangential despite sharing IRF3 and type I interferon as readouts.
DOI: 10.1186/s12964-026-02753-y

Perturbation of RNA homeostasis impairs mitochondrial respiration during poxvirus infection through excess RNA accumulation. (from Virology/RNA biology)
Djamal Brahim Belhaouari; Anil Pant; Santiago Navarro-Forero; Fernando Cantu; Zh — Proceedings of the National Academy of Sciences of the United States of America 2026
Score: 4/10 | Pathways: POLG-mtDNA, ME-CFS, other

This paper reveals an interferon-independent mechanism by which RNA accumulation directly impairs mitochondrial membrane potential and respiration, which is tangentially relevant as the SAMHD1 haploinsufficiency model involves mitochondrial dysfunction, but the paper's core mechanism (excess RNA perturbing mitochondria during poxvirus infection) is not a primary pathway in the SAMHD1 A565T disease model and involves no direct overlap with cGAS-STING, VDAC1, ISG15, NLRP3, or dNTPase axes.
DOI: 10.1073/pnas.2605194123

Genetic and transcriptomic signatures of host control in HIV-1 infection. (from Infectious disease / virology)
Oreshkov Sergey; Thorball Christian W; Meylan Jenny; Muriset Maude; Calmy Alexan — 2026
Score: 3/10 | Pathways: dNTPase, other

This paper identifies SAMHD1 as an HIV-1 restriction factor counteracted by Vpx in passing, but focuses on transcriptomic correlates of HIV load control rather than SAMHD1 dNTPase function, haploinsufficiency, or the cGAS-STING/interferonopathy/mitochondrial pathways central to the disease profile.
DOI: 10.1186/s12977-026-00679-4

Degradable STING nanomodulators orchestrate the innate-to-adaptive immune response for NIR-II photothermal-immunotherapy via a cancer-immunity cycle (from Nanomedicine/oncology)
Qiaolin Wei; Zirui Zhu; Yue Li; Siying Sun; Ge Gao — Materials Today Bio 2026
Score: 3/10 | Pathways: cGAS-STING, other

While this paper involves cGAS-STING pathway activation, it does so in the context of engineered cancer nanoparticle immunotherapy using exogenous Zn2+/ROS/photothermal stimulation in solid tumors, with no mechanistic relevance to SAMHD1 haploinsufficiency, endogenous dNTP pool dysregulation, interferonopathy, or any of the family's clinical phenotypes.
DOI: 10.1016/j.mtbio.2026.103028

Bispecific Macrophage Nano-Engager Couples Dual Checkpoint Blockade with Stimulator of Interferon Genes Activation to Potentiate Antitumor Immunity. (from Oncology/Nanomedicine)
Bao-Toan Dang; Khang-Yen Pham; Huyen T. Le; Thoa Thi Kim Nguyen; A. T. Vu — ACS nano 2026
Score: 3/10 | Pathways: cGAS-STING, JAK-STAT, other

This paper activates STING pharmacologically (SR717 agonist) in a tumor immunotherapy context, which is mechanistically opposite to the disease profile where cGAS-STING is pathologically overactivated by cytosolic mtDNA fragments; the paper's engagement with STING/IFN pathways is incidental to its oncology focus and offers no direct mechanistic insight into SAMHD1 haploinsufficiency or the interferonopathy cascade.
DOI: 10.1021/acsnano.6c01144

Pathway Coverage This Week

  • cGAS-STING: 21 papers
  • other: 20 papers
  • POLG-mtDNA: 15 papers
  • VDAC1: 12 papers
  • treatment-target: 12 papers
  • ME-CFS: 11 papers
  • ISG15-mitophagy: 10 papers
  • NLRP3: 9 papers
  • JAK-STAT: 8 papers
  • mTOR-lysosomal: 4 papers
  • dNTPase: 2 papers
  • clinical-phenotype: 2 papers
  • urate-NLRP3: 1 papers
  • AGS-spectrum: 1 papers