Biomedical subjects

Min He

Publications and source records attributed to Min He.

At least 19 recordsLinked to original sources

PubMed2026

Deep learning-based multimodal pathogenomics integration for precision cancer prognosis.

BACKGROUND: Recent studies have revealed valuable prognostic insights in haematoxylin and eosin (H&E)-stained histological sections and transcriptomic profiles, suggesting potential applications in machine learning. However, existing methods lack sufficient intra- and inter-modal interactions, and face challenges in clinical validation due to incomplete multimodal data. METHODS: We proposed PathoGems (PathoGenomics-based integrative survival prediction), a weakly-supervised, interpretable multimodal learning framework that integrates histology and genomic profiles for precise cancer prognosis prediction. To evaluate the robustness of PathoGems, we initially curated a dataset of 1965 cases across four cohorts from The Cancer Genome Atlas (TCGA), including breast, colorectal, glioblastoma, and esophageal cancers. For external validation, PathoGems was further evaluated on four independent cohorts, consisting of 76 breast cancer and 41 esophageal squamous cell carcinoma cases from Zhejiang Cancer Hospital, as well as 102 colorectal cancer and 58 glioblastoma cases from the Clinical Proteomic Tumor Analysis Consortium (CPTAC). RESULTS: PathoGems effectively stratified patients into favorable and unfavorable risk groups, revealing significant differences in histological patterns, genomic features, and overall survival (log-rank test, p < 0.05). Moreover, the model’s predictions are further supported by visualization and transcriptomic analysis, enhancing interpretability and reliability. CONCLUSIONS: By fusing histological and clinicogenomic multimodal models, PathoGems will provide a solid foundation for developing an innovative tool that aids clinicians in making informed decisions and selection personalized treatment strategies for cancer patients.

Humans↗

PubMed2025

Rice transcription factor bHLH25 confers resistance to multiple diseases by sensing H2O2.

Hydrogen peroxide (H2O2) is a ubiquitous signal regulating many biological processes, including innate immunity, in all eukaryotes. However, it remains largely unknown that how transcription factors directly sense H2O2 in eukaryotes. Here, we report that rice basic/helix-loop-helix transcription factor bHLH25 directly senses H2O2 to confer resistance to multiple diseases caused by fungi or bacteria. Upon pathogen attack, rice plants increase the production of H2O2, which directly oxidizes bHLH25 at methionine 256 in the nucleus. Oxidized bHLH25 represses miR397b expression to activate lignin biosynthesis for plant cell wall reinforcement, preventing pathogens from penetrating plant cells. Lignin biosynthesis consumes H2O2 causing accumulation of non-oxidized bHLH25. Non-oxidized bHLH25 switches to promote the expression of Copalyl Diphosphate Synthase 2 (CPS2), which increases phytoalexin biosynthesis to inhibit expansion of pathogens that escape into plants. This oxidization/non-oxidation status change of bHLH25 allows plants to maintain H2O2, lignin and phytoalexin at optimized levels to effectively fight against pathogens and prevents these three molecules from over-accumulation that harms plants. Thus, our discovery reveals a novel mechanism by which a single protein promotes two independent defense pathways against pathogens. Importantly, the bHLH25 orthologues from available plant genomes all contain a conserved M256-like methionine suggesting the broad existence of this mechanism in the plant kingdom. Moreover, this Met-oxidation mechanism may also be employed by other eukaryotic transcription factors to sense H2O2 to change functions.

Hydrogen Peroxide↗

PubMed2024

A novel splice-altering TNC variant (c.5247A > T, p.Gly1749Gly) in an Chinese family with autosomal dominant non-syndromic hearing loss.

BACKGROUND: This study aims to analyze the pathogenic gene in a Chinese family with non-syndromic hearing loss and identify a novel mutation site in the TNC gene. METHODS: A five-generation Chinese family from Anhui Province, presenting with autosomal dominant non-syndromic hearing loss, was recruited for this study. By analyzing the family history, conducting clinical examinations, and performing genetic analysis, we have thoroughly investigated potential pathogenic factors in this family. The peripheral blood samples were obtained from 20 family members, and the pathogenic genes were identified through whole exome sequencing. Subsequently, the mutation of gene locus was confirmed using Sanger sequencing. The conservation of TNC mutation sites was assessed using Clustal Omega software. We utilized functional prediction software including dbscSNV_AdaBoost, dbscSNV_RandomForest, NNSplice, NetGene2, and Mutation Taster to accurately predict the pathogenicity of these mutations. Furthermore, exon deletions were validated through RT-PCR analysis. RESULTS: The family exhibited autosomal dominant, progressive, post-lingual, non-syndromic hearing loss. A novel synonymous variant (c.5247A > T, p.Gly1749Gly) in TNC was identified in affected members. This variant is situated at the exon-intron junction boundary towards the end of exon 18. Notably, glycine residue at position 1749 is highly conserved across various species. Bioinformatics analysis indicates that this synonymous mutation leads to the disruption of the 5' end donor splicing site in the 18th intron of the TNC gene. Meanwhile, verification experiments have demonstrated that this synonymous mutation disrupts the splicing process of exon 18, leading to complete exon 18 skipping and direct splicing between exons 17 and 19. CONCLUSION: This novel splice-altering variant (c.5247A > T, p.Gly1749Gly) in exon 18 of the TNC gene disrupts normal gene splicing and causes hearing loss among HBD families.

Adult↗

PubMed2006

Isolation and characterization of meridamycin biosynthetic gene cluster from Streptomyces sp. NRRL 30748.

Meridamycin is a non-immunosuppressive, FKBP12-binding natural macrolide with potential therapeutic applications in a variety of medical conditions. To set the stage for structural modification of meridamycin by genetic engineering, we have cloned and completely sequenced approximately 117 kb of DNA encompassing the meridamycin biosynthetic gene cluster from the producing strain, Streptomyces sp. NRRL 30748. Clustered in the center of the cloned DNA stretch are six genes responsible for the construction of the core structure of meridamycin, including merP encoding a non-ribosomal peptide synthase for pipecolate-incorporation, four PKS genes (merA-D) together encoding 1 loading module and 14 extension modules, and merE encoding a cytochrome P450 monooxygenase. A number of genes with potential pathway-specific regulatory or resistance functions have also been identified. The absence of the gene encoding lysine cyclodeaminase in the sequenced gene cluster and the rest of the genome of NRRL 30748 indicated the synthesis of pipecolate in this strain is not through the common lysine cyclodeamination route previously described for rapamycin and FK506/FK520 biosynthesis. An efficient conjugation method has been developed for Streptomyces sp. NRRL 30748 to facilitate the genetic manipulation of meridamycin biosynthetic gene cluster. Disruption of merP resulted in the complete abolition of meridamycin production, proving the identity of the gene cluster. A novel meridamycin analogue, C36-keto-meridamycin, has been successfully generated through deletion of a DNA fragment encoding KR1 domain of MerA from the chromosomal DNA.

Base Sequence↗

PubMed2006

Pipecolic acid in microbes: biosynthetic routes and enzymes.

Pipecolic acid is an important precursor of many useful microbial secondary metabolites. Pipecolic acid-derived moieties are often crucial for the biological activities of some microbial natural products with pharmaceutical applications. Understanding the biogenesis of pipecolic acid in microorganisms would be a significant step toward the mutasynthesis of novel analogs of choice. This review focuses on various microbial pathways and enzymes for pipecolic acid synthesis, especially those related to the origination of pipecolic acid moieties in secondary metabolites.

2-Aminoadipic Acid↗

PubMed2006

Vitamin C inactivates the proteasome inhibitor PS-341 in human cancer cells.

PURPOSE: PS-341 (bortezomib, Velcade), the first proteasome inhibitor approved by the Food and Drug Administration for the treatment of patients with relapsed multiple myeloma, induces apoptosis in human cancer cell lines. Vitamin C (ascorbic acid) is an essential water-soluble vitamin required for many normal physiologic functions and has to be obtained through diet or supplemental tablets in humans. Here we studied the potential effect of vitamin C on the anticancer activity of PS-341 in human cancer cell lines. EXPERIMENTAL DESIGN: The effects of vitamin C on apoptosis induction by PS-341 alone and by PS-341 combined with tumor necrosis factor-related apoptosis-inducing ligand were studied. In addition, the effects of vitamin C and other antioxidants on PS-341-mediated proteasome inhibition were also examined. Finally, the direct chemical interaction between vitamin C and PS-341 was determined. RESULTS: Vitamin C abrogated the ability of PS-341 to induce apoptosis in various human cancer cell lines, to induce G(2)-M arrest, and to augment apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand. Moreover, vitamin C suppressed PS-341-mediated inhibition of proteasome activity. PS-341 itself did not induce generation of intracellular reactive oxygen species whereas other antioxidants failed to abrogate its biological activity. Importantly, we detected a direct chemical interaction between vitamin C and PS-341. CONCLUSION: Vitamin C directly binds to PS-431, thus inactivating PS-341 independent of its antioxidant activity. Our findings suggest that vitamin C may have a negative effect on PS-341-mediated anticancer activity.

Antineoplastic Agents↗

PubMed2006

Mutational data integration in gene-oriented files of the Hermansky-Pudlak Syndrome database.

Hermansky-Pudlak Syndrome (HPS) is a genetically heterogeneous disorder characterized by oculocutaneous albinism and prolonged bleeding due to abnormal vesicle trafficking to lysosomes and related organelles such as melanosomes and platelet dense granules. This HPS database (HPSD; http://liweilab.genetics.ac.cn/HPSD/) provides integrated, annotatory, and curative data that is distributed in a variety of public databases or predicted by bioinformatics servers for the recently cloned human and mouse HPS genes, as well as for the genes responsible for HPSrelated syndromes, such as ChediakHigashi Syndrome (CHS), Griscelli syndrome (GS), oculocutaneous albinism (OCA), Usher syndrome type 1B (USH1B), and ocular albinism (OA). The HPSD is designed by using a unique GeneOriented File (GOF) format. Seven blocks (genomic, transcript, protein, function, mutation, phenotype, and reference) are carefully annotated in each userfriendly GOF entry. The HPSD emphasizes paired human and mouse GOF entries. The genes included in this database (currently 58 in total) are arbitrarily divided into four categories: 1) Human and Mouse HPS, 2) Mouse HPS Only, 3) Putative Mouse or Human HPS, and 4) HPS Related Syndromes. All the mutations in these genes are integrated in the GOFs. We expect that these very informative and peerreviewed GOFs will be shortcuts to utilize the webbased information for the emerging interdisciplinary studies of HPS.

Animals↗

PubMed2006

Longitudinal analysis of T-cell receptor variable beta chain repertoire in patients with acute graft-versus-host disease after allogeneic stem cell transplantation.

T-cell receptor variable beta chain (TCRBV) repertoire spectratyping involves the estimation of CDR3 length distributions for monitoring T-cell receptor diversity and has proven useful for analyses of immune reconstitution and T-cell clonal expansions in graft-versus-host disease (GVHD) and graft-versus-leukemia after allogeneic stem cell transplantation. We performed a longitudinal spectratype analysis of 23 TCRBV families in 28 patients who underwent allogeneic T cell-depleted peripheral blood stem cell transplantation. Sixteen patients subsequently developed acute GVHD. We recently developed statistical methods that bring increased power and flexibility to spectratype analysis and allow us to analyze TCRBV repertoire development under appropriately complex statistical models. Applying these methods, we found that patients with acute GVHD demonstrated TCRBV repertoire development statistically distinct from that repertoire development in patients without GVHD. Specifically, GVHD patients showed spectratypes indicative of lower diversity and greater deviation from the spectratypes expected in healthy individuals at intermediate times. Most individual TCRBV subfamilies had spectratypes statistically distinguishable between GVHD and non-GVHD patients at 6 months after transplantation. These results suggest that the T-cell receptor repertoire perturbations associated with acute GVHD are widely spread throughout the TCRBV families.

Acute Disease↗

PubMed2006

Intramedullary spinal tuberculoma: report of three cases.

BACKGROUND: Intramedullary spinal tuberculoma is a rare form of central nervous system tuberculosis. This article describes the successful management of intramedullary spinal tuberculoma in 3 patients who received treatment between 2000 and 2003. CASE DESCRIPTION: The character of 3 cases was analyzed retrospectively, including clinical manifestation and magnetic resonance imaging findings. All masses were excised totally under microscope. Histopathologic examination revealed tuberculoma. Postoperatively, all patients received a 6 to 9 month course of ATT. The outcome was favorable. CONCLUSIONS: The intramedullary spinal tuberculoma must be considered in the differential diagnosis of the spinal cord compression in patients with a history of tuberculosis. When confronted with a progressing neurologic deficit and poor response to ATT, surgical intervention should be considered. The optimal treatment is a combination of microsurgical resection and ATT.

Adult↗

PubMed2006

Thoracic spine extradural arteriovenous fistula: case report and review of the literature.

BACKGROUND: Spinal extradural arteriovenous fistula is a rare, disabling, but potentially treatable disease. Only 27 cases have been reported so far in the past 40 years. CASE DESCRIPTION: An 18-year-old adolescent girl developed repeated back pain and mild paraplegia after a training course. Magnetic resonance imaging revealed a vessel-like lesion at the spinal extradural space, compressing the spinal medulla at the T5 level. Angiography disclosed a focal fistula fed by branches of the intercostal artery. The vascular mass was surgically removed and confirmed pathologically. CONCLUSION: Spinal extradural arteriovenous fistulas have an arterial supply that originates outside the spinal dura, with venous draining into the spinal extradural venous plexus. They may lead to myelopathy, radiculopathy, or spontaneous extradural hematoma, due to dilated vein compression, blood stealing, or spinal venous hypertension. Extradural hematoma needs emergency laminectomy and clot evacuation. And extradural arteriovenous fistulas should be treated actively by embolization, surgical resection, or both. Appropriate treatment will stabilize the patient or result in neurological improvement.

Adolescent↗

PubMed2006

Ethanol inhibits L1 cell adhesion molecule activation of mitogen-activated protein kinases.

Inhibition of the functions of L1 cell adhesion molecule (L1) by ethanol has been implicated in the pathogenesis of the neurodevelopmental aspects of the fetal alcohol syndrome (FAS). Ethanol at pharmacological concentrations has been shown to inhibit L1-mediated neurite outgrowth of rat post-natal day 6 cerebellar granule cells (CGN). Extracellular signal-related kinases (ERK) 1/2 activation occurs following L1 clustering. Reduction in phosphoERK1/2 by inhibition of mitogen-activated protein kinase kinase (MEK) reduces neurite outgrowth of cerebellar neurons. Here, we examine the effects of ethanol on L1 activation of ERK1/2, and whether this activation occurs via activation of fibroblast growth factor receptor 1 (FGFR1). Ethanol at 25 mm markedly inhibited ERK1/2 activation by both clustering L1 with cross-linked monoclonal antibodies, or by L1-Fc chimeric proteins. Clustering L1 with subsequent ERK1/2 activation did not result in tyrosine phosphorylation of the FGFR1. In addition, inhibition of FGFR1 tyrosine kinase blocked basic fibroblast growth factor (bFGF) activation of ERK1/2, but did not affect activation of ERK1/2 by clustered L1. We conclude that ethanol disrupts the signaling pathway between L1 clustering and ERK1/2 activation, and that this occurs independently of the FGFR1 pathway in cerebellar granule cells.

Animals↗

PubMed2006

Biosynthetic pathway for mannopeptimycins, lipoglycopeptide antibiotics active against drug-resistant gram-positive pathogens.

The mannopeptimycins are a novel class of lipoglycopeptide antibiotics active against multidrug-resistant pathogens with potential as clinically useful antibacterials. This report is the first to describe the biosynthesis of this novel class of mannosylated lipoglycopeptides. Included here are the cloning, sequencing, annotation, and manipulation of the mannopeptimycin biosynthetic gene cluster from Streptomyces hygroscopicus NRRL 30439. Encoded by genes within the mannopeptimycin biosynthetic gene cluster are enzymes responsible for the generation of the hexapeptide core (nonribosomal peptide synthetases [NRPS]) and tailoring reactions (mannosylation, isovalerylation, hydroxylation, and methylation). The NRPS system is noncanonical in that it has six modules utilizing only five amino acid-specific adenylation domains and it lacks a prototypical NRPS macrocyclizing thioesterase domain. Analysis of the mannopeptimycin gene cluster and its engineering has elucidated the mannopeptimycin biosynthetic pathway and provides the framework to make new and improved mannopeptimycins biosynthetically.

Anti-Bacterial Agents↗

PubMed2006

[Changes in P-selectin expression after brain injury in rats].

OBJECTIVE: To explore the relationship between expression thange of P-selectin after brain injury and secondary brain damage. METHODS: Sixty SD rats were randomized into 3 equal groups, namely the control group, mild injury group and severe injury group and animal models of brain injury were established in SD rats according to the method of Feeney. P-selectin expression in the brain tissues were determined at 6 h and l, 3, and 7 days following brain injury (n=5 for each time point). Imaging analysis was performed using computerized imaging technique. RESULTS: P-selectin expression and neutrophil infiltration in the brain tissues increased significantly 6 h after brain injury (P<0.05), reaching the peak level at postoperative 24 h and then gradually decreased. CONCLUSION: P-selectin expression and neutrophil infiltration increase significantly following brain injury, and the time course and distribution of P-selectin expression are consistent with the secondary damage of the brain, strongly suggesting the involvement of P-selectin upregulation in the secondary insult after brain injury.

Animals↗

PubMed2006

[Effects of 3'-azido-deoxythymidine on telomerase activity and protein expression of hepatocarcinoma cell line SMMC-7721].

BACKGROUND & OBJECTIVE: The mechanism of inhibiting telomerase activity by telomerase inhibitors is very complex, and involves common actions of many proteins. This study was to investigate the effects of 3'-azido-deoxythymidine (AZT) on telomerase activity and protein expression of hepatocarcinoma cell line SMMC-7721, and explore possible mechanism of inhibiting telomerase activity in SMMC-7721 cells by AZT. METHODS: Optimized concentration and treatment time of AZT were detected by MTT assay. After treatment with AZT, the telomerase activity in SMMC-7721 cells was detected by real-time fluorescent quantitative TRAP (FQ-TRAP) assay; the apoptosis of SMMC-7721 cells was detected by TUNEL assay and flow cytometry (FCM); the changes of specific proteins were monitored by raman spectra assay and surface-enhanced laser desorption time of flight-mass spectrum (SELDI-TOF-MS) with protein chip assay. RESULTS: The optimized treatment time of AZT was 48 h, and the optimized concentration of AZT was 20 mmol/L. When treated with 20 mmol/L AZT for 48 h, the telomerase activity in SMMC-7721 cells was inhibited by 53.85% of control (P<0.001); apoptotic morphologic changes of SMMC-7721 cells were observed; the apoptosis rate of SMMC-7721 cells was 13.5%; 7 spectral peak of proteins were changed; 24 proteins were up-regulated and 8 were down-regulated in SMMC-7721 cells. All of the 32 distinct proteins were small molecular proteins. CONCLUSION: AZT can inhibit the telomerase activity and induce apoptosis of SMMC-7721 cells, which is related to specific small molecular proteins.

Apoptosis↗

PubMed2006

[Influences of perioperative metoprolol on hemodynamics and myocardial ischaemia in elderly patients undergoing noncardiac surgery].

OBJECTIVE: To observe the influences of metoprolol on hemodynamics and myocardial ischaemia in elderly patients undergoing noncardiac surgery. METHODS: Thrity patients (60 approximately 75 years) undergoing elective noncardiac surgery were randomly divided into a metoprolol group (n = 15) and a control group (n = 15). In the metoprolol group, metoprolol (0. 5 mg and 1.5 mg) was slowly injected into the vein of patients before the induction of intravenous anesthesia and after the tracheal intubation. The hemodynamic indice (invasive BP, HR and rate pressure product-RPP), the myocardial ischaemia indice (reversible ST segment depression of ECG II, V5 leads more than 0.1 mv or reversible ST segment elevation more than 0.2 mv from the baseline, ST segment depression or elevation over 1 min), the myocardial damage indice (serum cardiac troponin I, cTn I), and the indice of metoprolol cardiac and the respiratory adverse effects (incidence of HR below 50 beats/min, average doses of atropine, airway peak pressure) were observed intraoperatively. RESULTS: The HR and RPP were lower before the tracheal induction than the baseline (before anesthesia) in all patients, but there is no significant difference between the two groups (P > 0.05). During the tracheal intubation, the HR and RPP of the control group significantly increased, compared with the baseline (P < 0.05) and those of metoprolol group (P < 0.05). The incidence of perioperative hypertension was higher in the control group than that in the metoprolol group. The incidence of myocardical ischaemia episode was 30% in the control group, and 13% in the metoprolol group (P < 0.01). The release of cTn I was detected in 5 patients in the control group, and 2 patients in the metoprolol group (P < 0.05). The incidence of HR < 50 beats/min, and the average doses of atropine had no statistic difference between the two groups, but a tendency of high incidence of bradycardia in the metoprolol group occurred when abdominal viscera was tracted by surgical manupilation. There was no significant difference in airway peak pressure, SpO2 and PET CO2 between the two groups (P > 0.05). CONCLUSION: Intravenous administration of 0.5 mg and 1. 5 mg metoprolol before the induction of anesthesia and after the tracheal intubation has several advantages, including the decrease of myocardial oxygen consumption, the improvement of hemodynamic stability, and the lowering perioperative incidence of myocardial ischeamia and damage, but the tendency of high bradycardia incidence caused by peritoneal traction should be noticed.

Adrenergic beta-Antagonists↗

PubMed2005

Syntaxins 3 and 4 are concentrated in separate clusters on the plasma membrane before the establishment of cell polarity.

Syntaxins 3 and 4 localize to the apical and basolateral plasma membrane, respectively, of epithelial cells where they mediate vesicle fusion. Here, we report that before establishment of cell polarity, syntaxins 3 and 4 are confined to mutually exclusive, submicron-sized clusters. Syntaxin clusters are remarkably uniform in size, independent of expression levels, and are distinct from caveolae and clathrin-coated pits. SNAP-23 partially colocalizes with both syntaxin 3 and 4 clusters. Deletion of the apical targeting signal of syntaxin 3 does not prevent sorting into clusters away from syntaxin 4. Syntaxin 3 and 4 cluster formation depends on different mechanisms because the integrity of syntaxin 3 clusters depends on intact microtubules, whereas syntaxin 4 clusters depend on intact actin filaments. Cholesterol depletion causes dispersion of syntaxin 3 but not syntaxin 4 clusters. In migrating cells, syntaxin clusters polarize to the leading edge, suggesting a role in polarized exocytosis. These results suggest that exocytosis occurs at small fusion sites exhibiting high local concentrations of SNARE proteins that may be required for efficient membrane fusion. The establishment of separate clusters for each syntaxin suggests that the plasma membrane is inherently polarized on an ultrastructural level even before the establishment of true cell polarity.

Actins↗

PubMed2005

Twenty-year secular changes in sex specific lung cancer incidence rates in an urban Chinese population.

The objective of this study was to describe trends in the incidence rates of primary lung cancer in a geographically defined Chinese population. Primary lung cancer cases (N=40,022) diagnosed between 1981 and 2000 were identified by the Tianjin Cancer Registry. Age-specific and age-adjusted incidence rates to the world standard population were examined in both males and females. Age-period-cohort (APC) model and Poisson regression were used to assess the cohort effects and incidence trends. Crude and age-adjusted incidence rates in the study period were: 66.2/100,000 and 45.2/100,000 in males; and 47.7/100,000 and 28.2/100,000 in females, respectively. The major birth cohort effect can be described as for those born before 1940, in every age group lung cancer incidence rate increased as the birth years advanced. For those born after 1940, age specific incidence rates decreased as the birth years advanced. Results from the Poisson regression analyses suggested a statistically significant increasing trend of incidence rates of lung cancer from 1981 to 1990 and changed little afterwards. Through first 10 years of the study period between 1981 and 2000, lung cancer incidence rates increased in both males and females. While the study results suggest that the age-adjusted incidence rates may have reached their peak and may even decline, as the Chinese population ages, and smoking prevalence remains high, the number of new lung cancer cases will continue to increase and overall burden of lung cancer will remain high.

Adult↗

PubMed2005

Electron transfer versus proton transfer in gas-phase ion/ion reactions of polyprotonated peptides.

The ion/ion reactions of several dozen reagent anions with triply protonated cations of the model peptide KGAILKGAILR have been examined to evaluate predictions of a Landau-Zener-based model for the likelihood for electron transfer. Evidence for electron transfer was provided by the appearance of fragment ions unique to electron transfer or electron capture dissociation. Proton transfer and electron transfer are competitive processes for any combination of anionic and cationic reactants. For reagent anions in reactions with protonated peptides, proton transfer is usually significantly more exothermic than electron transfer. If charge transfer occurs at relatively long distances, electron transfer should, therefore, be favored on kinetic grounds because the reactant and product channels cross at greater distances, provided conditions are favorable for electron transfer at the crossing point. The results are consistent with a model based on Landau-Zener theory that indicates both thermodynamic and geometric criteria apply for electron transfer involving polyatomic anions. Both the model and the data suggest that electron affinities associated with the anionic reagents greater than about 60-70 kcal/mol minimize the likelihood that electron transfer will be observed. Provided the electron affinity is not too high, the Franck-Condon factors associated with the anion and its corresponding neutral must not be too low. When one or the other of these criteria is not met, proton transfer tends to occur essentially exclusively. Experiments involving ion/ion attachment products also suggest that a significant barrier exists to the isomerization between chemical complexes that, if formed, lead to either proton transfer or electron transfer.

Electrons↗