Biochemistry (Moscow)最新文献

{"title":"Association of Neutrophil Elastase Activity, Oxidative Stress, Energy and Glutamate Metabolism Parameters with Behavior and Learning in Wistar Rats in a Postnatal Valproate Model of Autism Spectrum Disorder","authors":"Anna A. Stakhanova,&nbsp;Olga G. Voskresenskaya,&nbsp;Olga K. Savushkina,&nbsp;Tatyana A. Prokhorova,&nbsp;Elena B. Tereshkina,&nbsp;Ekaterina V. Semina,&nbsp;Svetlana A. Zozulya,&nbsp;Natalia V. Kost,&nbsp;Yulia A. Chaika","doi":"10.1134/S0006297926600158","DOIUrl":"10.1134/S0006297926600158","url":null,"abstract":"<p>To study biochemical mechanisms underlying the development of autism spectrum disorders (ASD), an experimental model based on early postnatal administration of valproic acid (VPA) to Wistar rats was used. Social behavior impairments characteristic of ASD was accompanied by cognitive impairments and were associated with the increased neutrophil elastase (NE) activity in the serum and cerebellum of the rats treated with VPA. Increased NE activity in the cerebellum may indicate development of neuroinflammation. Impaired antioxidant defense under the influence of VPA was manifested by the increased glutathione S-transferase (GST) activity in the serum and cerebellum of rats. Correlation analysis revealed a link between the NE activity and formation of social behavior in animals. Enzymes of glutamate metabolism (glutamate dehydrogenase and glutamine synthetase) and antioxidant defense enzymes that regulate oxidative stress (OS) levels correlated with formation and maintenance of the acquired skills in both control and experimental animals.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"956 - 966"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMGB1 Protein in Alcohol-Related Psychopathological Disorders at Various Stages of Alcohol Dependence","authors":"Tamara P. Vetlugina,&nbsp;Elena V. Epimakhova,&nbsp;Ivan V. Voevodin,&nbsp;Valentina D. Prokopieva,&nbsp;Nikolay A. Bokhan","doi":"10.1134/S0006297926600237","DOIUrl":"10.1134/S0006297926600237","url":null,"abstract":"<p>Background. Chronic alcohol consumption in alcohol dependence (AD) is associated with various molecular and cellular dysfunctions. One of the key mechanisms involved is the extracellular release of HMGB1 (high-mobility group box 1), a nuclear protein that acts as a proinflammatory signaling molecule. However, the dynamics of peripheral HMGB1 levels across different stages of AD and its association with psychopathological symptoms remain insufficiently understood. Objective. To investigate peripheral HMGB1 concentrations in patients with AD during different disease stages – alcohol withdrawal syndrome (AWS), post-abstinence state (PAS), and remission – and to assess their associations with clinical characteristics of the disease. Patients and Methods. The study included 53 men aged 30-60 years diagnosed with AD and 19 conditionally healthy men who served as controls for biological analyses. Clinical and biological assessments were performed at three time points: (1) during AWS; (2) after completion of standard therapy (PAS); and (3) during remission following hospital discharge. The severity of psychopathological symptoms was evaluated using validated clinical rating scales. Serum HMGB1 concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Results. Patients with AD demonstrated significantly elevated serum HMGB1 levels during AWS and PAS compared with controls, whereas HMGB1 concentrations decreased to control values during remission. Correlation and ROC analyses revealed that higher HMGB1 levels were associated with a less pronounced reduction in psychopathological symptoms following treatment. Conclusion. Peripheral HMGB1 may represent a promising biomarker for monitoring treatment response and predicting relapse risk in AD.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"967 - 978"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1134/S0006297926600237.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Status and Morphological Changes of Astrocytes under Reductive Stress in vitro: Neural Network Analysis","authors":"Svetlana V. Novikova,&nbsp;Nataliya A. Kolotyeva,&nbsp;Arseniy K. Berdnikov,&nbsp;Taisia E. Shcheveleva,&nbsp;Ivan V. Simkin,&nbsp;Yulia K. Komleva,&nbsp;Egor V. Yakovlev,&nbsp;Nikita P. Kryuchkov,&nbsp;Stanislav O. Yurchenko,&nbsp;Alla B. Salmina","doi":"10.1134/S0006297926600274","DOIUrl":"10.1134/S0006297926600274","url":null,"abstract":"<p>Reductive stress caused by excessive accumulation of reducing equivalents (NADH, NADPH, glutathione), is increasingly recognized as a pathogenetic factor at the early stages of neurodegenerative diseases. However, its impact on the morphofunctional properties of astrocytes remains poorly understood. We performed the first comprehensive quantitative assessment of biochemical and morphological changes in cultured primary rat astrocytes under chronic reductive stress modeled using dithiothreitol (DTT, 500 μM, 24 h). To enable morphometric analysis of live, unstained cells, we developed and trained a semantic segmentation model based on the YOLOv11 architecture, which enables objective assessment of complex branched cell morphology in phase-contrast images while avoiding fixation-related artifacts. DTT-induced reductive stress caused a significant increase in the total pool of nicotinamide coenzymes (<i>p</i> &lt; 0.01) and elevated mitochondrial superoxide production without compromising mitochondrial membrane potential. Morphometric analysis revealed a sustained enlargement of astrocyte soma area and increase in the number of astrocyte processes, along with a reduced branching complexity. These findings provide new insights into the role of redox imbalance in regulating glial function and may expand our understanding of the early mechanisms of neurodegenerative diseases.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"979 - 991"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to: BDNF as a Mediator between Body Metabolism and Brain Function in Health and Disease: The Case of Alcohol Dependence","authors":"Danil I. Peregud,&nbsp;Nataliya V. Gulyaeva","doi":"10.1134/S0006297926060015","DOIUrl":"10.1134/S0006297926060015","url":null,"abstract":"","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"1050 - 1050"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Metabolites of Lactic Acid Bacteria on Nerve Cells of the Microbiota–Gut–Brain Axis","authors":"Konstantin V. Sobol","doi":"10.1134/S0006297926600377","DOIUrl":"10.1134/S0006297926600377","url":null,"abstract":"<p>This review examines the key pathways of bidirectional communication between the gut and brain along the microbiota–gut–brain axis, with particular emphasis on the effects of metabolites of lactic acid bacteria (metLABs) on neurons of the enteric and central nervous systems. Special attention is given to the role of metLABs in intracellular signaling. The review further explores the direct effects of metLABs on mitochondrial function in nervous tissue, neuronal plasticity, and neuritogenesis. Potential mechanisms for the release of neurotrophic factors in both cells and host organism following exposure to metLABs or probiotic products are analyzed. Although clinical evidence remains limited, existing studies suggest that regular consumption of metLAB-containing fermented foods may positively influence brain functions through modulation of the microbiota–gut–brain axis. At least two ongoing clinical trials currently investigate whether normalization of the gut microbiota through probiotic interventions can slow the progression of Alzheimer’s disease. As this field continues to advance rapidly, further studies are expected to provide important insights into the therapeutic potential of microbiota-targeted strategies for neurological health.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"867 - 892"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of Metabolic Stress in Vascular Organoids under Normal Conditions and with AD/PD-Associated Genetic Backgrounds","authors":"Anna V. Blagova,&nbsp;Elizaveta S. Perepelitsa,&nbsp;Anakha Satish,&nbsp;Dmitry A. Lifanov,&nbsp;Victoria I. Zhdankina,&nbsp;Anna A. Kopylova,&nbsp;Polina V. Guk,&nbsp;Alla B. Salmina,&nbsp;Sergey N. Illarioshkin","doi":"10.1134/S0006297926600286","DOIUrl":"10.1134/S0006297926600286","url":null,"abstract":"<p>Vascular organoids derived from human induced pluripotent stem cells (iPSCs) are promising models for studying vascular pathology, including neurodegenerative diseases. In this study, we investigated signs of mitochondrial dysfunction in the vascular organoids derived from the iPSCs of a healthy donor, as well as patients with Alzheimer’s disease (AD) and Parkinson’s disease (PD). In the conditioned medium of vascular organoids from the PD patient-derived cells, but not from the AD patient-derived cells, a trend toward a disrupted NAD⁺/NADH balance was observed, accompanied by the reduced expression of the connexin 43 (Cx43) protein. A sign of metabolic vulnerability of endothelial cells in the vascular organoids from the PD patient-derived cells, but not from normal or AD patient-derived organoids, manifested as reduced expression of c-Myc was observed. Changes in the membrane potential were detected in the vascular organoids from the AD and PD patient-derived, as well as increase in the mitochondrial superoxide anion production were observed, which may indicate development of oxidative stress in the microvessel cells during neurodegeneration.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"992 - 1005"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Relationships between Cerebral Cortex Metabolism, Behavior, and ECG Parameters in Rats under Physiological Conditions and after Pyruvate Dehydrogenase Inhibition","authors":"Anastasia V. Graf,&nbsp;Alexey V. Kazantsev,&nbsp;Victoria I. Bunik","doi":"10.1134/S0006297926600444","DOIUrl":"10.1134/S0006297926600444","url":null,"abstract":"&lt;p&gt;Sex-specific interactions between neurosignaling systems, which generate, propagate, and terminate signals in nervous tissue, and metabolic pathways that support these processes may underlie sex differences in adaptation and therapeutic efficacy. This study aimed to characterize these interactions as systemic indicators of sex-specific adaptive responses in a rat model of metabolic stress induced by the inhibition of pyruvate dehydrogenase complex (PDC), which catalyzes the key reaction linking anaerobic glycolysis to aerobic glucose oxidation. To inhibit brain PDC, we used a single intranasal administration of methyl acetylphosphinate (MeAcP), a phosphinate analog of pyruvate, or dimethyl acetylphosphonate (AcPMe&lt;sub&gt;2&lt;/sub&gt;), a membrane-permeable precursor of phosphonate pyruvate analogs. Effects were assessed 24 h post-administration by measuring biochemical and physiological parameters in the cerebral cortex, including glutamate levels, glutamine synthetase (GS) activity, and activities of enzymes in the tricarboxylic acid (TCA) cycle and affiliated pathways. Neurosignaling was evaluated using surrogate indicators: ECG (electrocardiogram) parameters and spontaneous behavior in the open field test. Relationships between measured parameters were analyzed using Spearman’s rank correlation coefficients, with the correlation strength classified according to the Chaddock’s scale. In control animals, no sex differences were observed in the mean values of biochemical or ECG parameters. However, behavioral parameters (e.g., grooming and locomotion) and the overall structure of correlations between the studied parameters exhibited marked sex dependence. In control females, strong correlations were detected between ECG parameters and GS activity, whereas in males, ECG parameters were strongly associated with malic enzyme (ME) activity. Male controls also showed strong correlations between locomotor/exploratory behavior and activities of ME, PDC, and 2-oxoglutarate dehydrogenase complex (OGDC). Administration of PDC inhibitors induced a sex-specific reorganization of relationships between neurosignaling indicators and glutamate metabolism, which eliminated pronounced sex differences in locomotor activity observed in controls, while revealing new sex-related differences in glutamate levels, glutamate dehydrogenase (GDH) and ME activities, grooming bout duration, and freezing time. The reduction in glutamate levels observed in females following PDC inhibition was consistent with the established decrease in &lt;i&gt;de novo&lt;/i&gt; glutamate synthesis from glucose under conditions of impaired substrate flux through the TCA cycle. Overall, these findings demonstrate that the relationships among metabolic, behavioral, and ECG parameters are inherently sex-specific. Moreover, the homeostatic response of the cerebral cortex to PDC inhibition reshapes these relationships, thereby modifying sex-dependent biochemical and behavioral characteristics observed under control ","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"1006 - 1022"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoinflammatory Markers in Patients with Affective Disorders: Genetic Polymorphisms, Peripheral Cytokine Levels, and Expression of IL-1β, IL-13, TNF-β, and TGF-α in Peripheral Blood Mononuclear Cells","authors":"Ekaterina V. Mikhalitskaya,&nbsp;Lyudmila A. Levchuk,&nbsp;Anastasia S. Boiko,&nbsp;Natalya M. Vyalova,&nbsp;Elena V. Epimakhova,&nbsp;Diana Z. Paderina,&nbsp;Olga V. Roschina,&nbsp;German G. Simutkin,&nbsp;Nikolay A. Bokhan,&nbsp;Svetlana A. Ivanova","doi":"10.1134/S0006297926600304","DOIUrl":"10.1134/S0006297926600304","url":null,"abstract":"<p>Cytokines play a critical role in brain functioning by modulating neurotransmitter and energy metabolism, neuroplasticity, and neuronal activity. Dysregulated or excessive cytokine production can disrupt neuronal metabolic processes and contribute to brain dysfunction. Among the proposed mechanisms underlying the development and progression of affective disorders (ADs), the cytokine hypothesis emphasizes the role of inflammatory markers as key factors in the development of depressive pathologies. The aim of this study was to investigate molecular characteristics of selected immunoinflammatory markers in patients with AD. The study included 239 patients diagnosed with AD and 205 healthy controls. Polymorphic variants of the immunoinflammatory genes <i>IL1B</i> (<i>rs16944</i>, <i>rs1143627</i>), <i>IL13</i> (<i>rs1295686</i>), <i>TNFB</i> (<i>rs2229094</i>), and <i>TGFA</i> (<i>rs2166975</i>) were analyzed, and cytokine levels in the blood serum and peripheral blood mononuclear cells were measured. As association was identified between the <i>rs2229094</i> polymorphism of the <i>TNFB</i> gene and AD: the carriage of the <i>A</i> allele and the <i>AA</i> genotype of this variant was associated with an increased risk of AD. Furthermore, the levels of TGF-α and IL-13 in peripheral blood mononuclear cells and the serum content of TNF-β were significantly elevated in patients with AD compared with healthy controls. These pilot findings suggest that the studied cytokines may contribute to the pathogenetic mechanisms underlying development of ADs.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"780 - 788"},"PeriodicalIF":2.2,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1134/S0006297926600304.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148020957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Conjugate of Aminoadamantane and Tetrahydro-γ-Carboline Inhibits Accumulation of Mutant α-Synuclein A53T in the Cellular Model of Proteinopathy","authors":"Marina V. Burak,&nbsp;Nadezhda E. Pukaeva,&nbsp;Victoria S. Kryshkova,&nbsp;Olga A. Kukharskaya,&nbsp;Maya R. Nazdracheva,&nbsp;Sergey A. Pukhov,&nbsp;Kirill A. Rachenkov,&nbsp;Alla V. Stavrovskaya,&nbsp;Vladimir P. Fisenko,&nbsp;Michail S. Kukharsky,&nbsp;Sergei O. Bachurin","doi":"10.1134/S0006297926600079","DOIUrl":"10.1134/S0006297926600079","url":null,"abstract":"<p>Pathological aggregation of α-synuclein is a key event in the development of synucleinopathies, such as Parkinson’s disease and Lewy body dementia. Currently, no effective disease-modifying therapy is available, necessitating the search for new therapeutic agents. One promising strategy involves the use of low-molecular-weight compounds capable of inhibiting the formation of toxic protein aggregates. This study evaluates the anti-aggregation properties of EC3222x, a conjugate of pharmacophoric fragments of amantadine and a fluorinated derivative of tetrahydro-γ-carboline. α-<b>S</b>ynucleinopathy was modeled <b>i</b>n the SH-SY5Y neuroblastoma cell line by transfection with a plasmid vector encoding the mutant human α-synuclein A53T protein. EC3222x at a concentration of 1 µM reduced the number of cells with α-synuclein A53T aggregates. Its efficacy was comparable to that of SynuClean-D and Buntanetap, known inhibitors of α-synuclein aggregation. Treatment with EC3222x reduced both the level of diffusely distributed intracellular α-synuclein and the formation of mature fibrillar aggregates and large aggresomes. Importantly, EC3222x did not affect the accumulation of another aggregation-prone protein, TDP-43, in a similar cellular model, indicating its specificity for α-synuclein. These findings suggest that EC3222x may represent a promising candidate for the development of therapeutic agents targeting synucleinopathies.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"789 - 799"},"PeriodicalIF":2.2,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148021017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multidirectional Effects of SARS-CoV-2 Coronavirus Proteins on Amyloid Transformation of Alpha-Synuclein","authors":"Yulia Y. Stroylova,&nbsp;Anastasiya V. Konstantinova,&nbsp;Denis V. Pozdyshev,&nbsp;Ivan A. Katrukha,&nbsp;Reza Yousefi,&nbsp;Vladimir I. Muronetz","doi":"10.1134/S0006297926600559","DOIUrl":"10.1134/S0006297926600559","url":null,"abstract":"<p>Parkinson’s disease is associated with amyloid aggregation of alpha-synuclein, which could be affected by the proteins of the SARS-CoV-2 coronavirus, possibly accelerating and provoking neurodegeneration. The purpose of this work was to compare the effects of the N-protein and the receptor binding domain (RBD) of the S protein on fibrillization of the alpha-synuclein preparation produced using an original technique that excludes presence of non-native forms of alpha-synuclein that alter kinetics of the process. Presence of an elongated form of alpha-synuclein in the previously studied protein preparations is associated with the erroneous reading of the rare for <i>E. coli</i> TGA stop codon in the pET33b(+) expression plasmid as tryptophan, which led to the continued translation to the next stop codon. To prevent this effect, a new plasmid design was suggested with replacement of the original stop codon with a double stop codon TAA, which made it possible to obtain a homogeneous protein preparation without the admixture of alpha-synuclein with increased molecular weight. It has been shown that the N-protein is able to accelerate alpha-synuclein fibrillization, while the RBD of the S protein inhibits aggregation. According to the electron microscopy data, structure of the fibrils formed in the presence of viral proteins is also different. The obtained data are important for understanding the mechanisms of development of post-covid synucleinopathies, as well as consequences of vaccination with the viral proteins.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"836 - 846"},"PeriodicalIF":2.2,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148020970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}