Pub Date : 2015-01-01DOI: 10.3724/SP.J.1206.2014.00023
Qiran Li, Yue Qi, Mq Tian, K. Zhang, Xian Liu
Internet addiction(IA) as a behavioral addiction is currently becoming a serious mental health issue around the globe. According to the neurobiological model of brain development, exploring the neural mechanisms of reward seeking behavior and cognitive control in internet addicts may help in developing treatments for individuals with IA. Behavioral research has indicated that IA is commonly associated with enhanced reward sensitivity and decreased inhibitory control. Additionally, research focused on the neural mechanisms of IA indicates that deficits in the reward or cognitive control systems might be a high risk factor for addictive behaviors.Compared with substance addictions, IA, as a kind of psychological addiction, has a specific reward mechanism.While previous research has deepened the understanding of the psychological and neural mechanisms in IA, there still exist many issues surrounding diagnosis and treatment of IA: the screening criteria are not scientific; the classification is ambiguous; the effect of intervention and treatment is controversial; causal research is scarce; and research paradigms are flawed. Substantial future research is needed to explore, fully understand, and treat IA.
{"title":"Neural Mechanisms of Reward Seeking Behavior and Cognitive Control in Individuals With Internet Addiction","authors":"Qiran Li, Yue Qi, Mq Tian, K. Zhang, Xian Liu","doi":"10.3724/SP.J.1206.2014.00023","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2014.00023","url":null,"abstract":"Internet addiction(IA) as a behavioral addiction is currently becoming a serious mental health issue around the globe. According to the neurobiological model of brain development, exploring the neural mechanisms of reward seeking behavior and cognitive control in internet addicts may help in developing treatments for individuals with IA. Behavioral research has indicated that IA is commonly associated with enhanced reward sensitivity and decreased inhibitory control. Additionally, research focused on the neural mechanisms of IA indicates that deficits in the reward or cognitive control systems might be a high risk factor for addictive behaviors.Compared with substance addictions, IA, as a kind of psychological addiction, has a specific reward mechanism.While previous research has deepened the understanding of the psychological and neural mechanisms in IA, there still exist many issues surrounding diagnosis and treatment of IA: the screening criteria are not scientific; the classification is ambiguous; the effect of intervention and treatment is controversial; causal research is scarce; and research paradigms are flawed. Substantial future research is needed to explore, fully understand, and treat IA.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"230 1","pages":""},"PeriodicalIF":0.3,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77474686","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}
Pub Date : 2015-01-01DOI: 10.16476/J.PIBB.2014.0230
Xiaoling Li, P. Xy, Zeng Zy, Strong, Li Gy, W. Xiong, Zhang Xy, M. Zhou, D. Xue, Li Yw, Jing Yz, Wang Ym, B. Kuang
Long noncoding RNA(lnc RNA) play important roles in cancer progression. HOX transcript antisense RNA(HOTAIR) was observed upregulated in a variety of tumors. Over-expression of HOTAIR is a poor prognostic factor. HOTAIR interacts with Polycomb Repressive complex 2(PRC2), resulting in histone H3tri-methylated atlysine27(H3K27me3), which silences the expression of some down-stream genes, such as WIF-1,PTEN and p21, then mediated Wnt, Akt and p53 signaling pathways transduction. As a result, the properties of tumor, including invasion and metastasis, evading growth suppressors, resisting apoptosis and inducing angiogenesis would be affected. Thoroughly elucidate mechanisms of HOTAIR in cancer development will have important theoretical significance in cancer etiology and pathogenesis. As an important biomarker and potential target, HOTAIR may also has important clinical application in cancer's early diagnosis, therapeutic evaluation,prognosis, and even potential gene therapy.
{"title":"Progress of Long Noncoding RNA HOTAIR in Human Cancer","authors":"Xiaoling Li, P. Xy, Zeng Zy, Strong, Li Gy, W. Xiong, Zhang Xy, M. Zhou, D. Xue, Li Yw, Jing Yz, Wang Ym, B. Kuang","doi":"10.16476/J.PIBB.2014.0230","DOIUrl":"https://doi.org/10.16476/J.PIBB.2014.0230","url":null,"abstract":"Long noncoding RNA(lnc RNA) play important roles in cancer progression. HOX transcript antisense RNA(HOTAIR) was observed upregulated in a variety of tumors. Over-expression of HOTAIR is a poor prognostic factor. HOTAIR interacts with Polycomb Repressive complex 2(PRC2), resulting in histone H3tri-methylated atlysine27(H3K27me3), which silences the expression of some down-stream genes, such as WIF-1,PTEN and p21, then mediated Wnt, Akt and p53 signaling pathways transduction. As a result, the properties of tumor, including invasion and metastasis, evading growth suppressors, resisting apoptosis and inducing angiogenesis would be affected. Thoroughly elucidate mechanisms of HOTAIR in cancer development will have important theoretical significance in cancer etiology and pathogenesis. As an important biomarker and potential target, HOTAIR may also has important clinical application in cancer's early diagnosis, therapeutic evaluation,prognosis, and even potential gene therapy.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"16 4","pages":""},"PeriodicalIF":0.3,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72618059","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}
Pub Date : 2014-10-01DOI: 10.3724/SP.J.1206.2014.00209
Wang Gu-yan
As a new independent subject, biophysics emerged in the early 1950's. The Institute of Biophysics, Chinese Academy of Sciences, was established in 1958. It was the milestone of the beginning of biophysics in China. This review introduces the foundation and the early development of biophysics in China, and the establishment of the interdisciplinary subjects, including radiation biology, bio-cybernetics, astrobiology, and bionics.
{"title":"Foundation of Biophysics and Establishment of Interdisciplinary Subjects in China","authors":"Wang Gu-yan","doi":"10.3724/SP.J.1206.2014.00209","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2014.00209","url":null,"abstract":"As a new independent subject, biophysics emerged in the early 1950's. The Institute of Biophysics, Chinese Academy of Sciences, was established in 1958. It was the milestone of the beginning of biophysics in China. This review introduces the foundation and the early development of biophysics in China, and the establishment of the interdisciplinary subjects, including radiation biology, bio-cybernetics, astrobiology, and bionics.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"23 1","pages":""},"PeriodicalIF":0.3,"publicationDate":"2014-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76128232","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}
Pub Date : 2014-08-01DOI: 10.3724/SP.J.1206.2013.00412
Chen Ping, L. Qing, Ma Xiao-Jie, Wang Shi-Jie, L. Qiong, Ni Jiazuan
{"title":"Screening and Verifying The Interactive Protein of Selenoprotien W in Human Brain","authors":"Chen Ping, L. Qing, Ma Xiao-Jie, Wang Shi-Jie, L. Qiong, Ni Jiazuan","doi":"10.3724/SP.J.1206.2013.00412","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00412","url":null,"abstract":"","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"57 1","pages":""},"PeriodicalIF":0.3,"publicationDate":"2014-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83987426","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}
Pub Date : 2014-03-01DOI: 10.3724/SP.J.1206.2014.00007
Jie-yu He, Feng Liu
Aging causes a general decline in physiological function that leads to various metabolic and cardiovascular diseases. The links between aging and aging-associated diseases remain to be fully established,but recent studies demonstrate that suppressing the mammalian/mechanistic target of rapamycin(mTOR) signaling pathway extends longevity and delays aging-associated metabolic and neurodegenerative diseases. As a key regulator of metabolism and aging,the mTOR signaling pathway has now become a hot spot for the development of effective therapeutic treatment for aging and aging-related diseases.
{"title":"MTOR signaling in aging and aging-associated diseases","authors":"Jie-yu He, Feng Liu","doi":"10.3724/SP.J.1206.2014.00007","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2014.00007","url":null,"abstract":"Aging causes a general decline in physiological function that leads to various metabolic and cardiovascular diseases. The links between aging and aging-associated diseases remain to be fully established,but recent studies demonstrate that suppressing the mammalian/mechanistic target of rapamycin(mTOR) signaling pathway extends longevity and delays aging-associated metabolic and neurodegenerative diseases. As a key regulator of metabolism and aging,the mTOR signaling pathway has now become a hot spot for the development of effective therapeutic treatment for aging and aging-related diseases.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"63 1","pages":"257-265"},"PeriodicalIF":0.3,"publicationDate":"2014-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84066058","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}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2014.00115
Yaoqian Pan, B. Pan, Xing-you Liu, Ruili Li, J. Yue
{"title":"Dicer and its miRNAs are necessary gene and regulatory factors for differentiation and proliferation of vascular smooth muscle cell","authors":"Yaoqian Pan, B. Pan, Xing-you Liu, Ruili Li, J. Yue","doi":"10.3724/SP.J.1206.2014.00115","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2014.00115","url":null,"abstract":"","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"55 1","pages":"1255-1264"},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90933438","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}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2013.00306
Z. Cai, Y. Xin
Inflammasomes activation is critical for both innate and adaptive immunity through their regulation of interleukin 1β(IL-1β) and IL-18.Prolonged inflammasomes activation can lead to exaggerated expression of signaling components as well as pro-inflammatory cytokines that can damage the host,resulting in chronic inflammatory diseases and autoimmune disorders.Therefore,pathways of deactivation are important to balance the immune responses.However,recent discoveries have uncovered a plethora of pathogenic strategies to inhibit the activation of inflammasome signal pathways and the production of pro-inflammatory cytokines to evade immune responses.Elucidation of these mechanisms might be helpful to the rational design of therapy against infectious diseases and other inflammasome-dependent inflammatory processes.
{"title":"Negative Regulation of Inflammasome Signaling","authors":"Z. Cai, Y. Xin","doi":"10.3724/SP.J.1206.2013.00306","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00306","url":null,"abstract":"Inflammasomes activation is critical for both innate and adaptive immunity through their regulation of interleukin 1β(IL-1β) and IL-18.Prolonged inflammasomes activation can lead to exaggerated expression of signaling components as well as pro-inflammatory cytokines that can damage the host,resulting in chronic inflammatory diseases and autoimmune disorders.Therefore,pathways of deactivation are important to balance the immune responses.However,recent discoveries have uncovered a plethora of pathogenic strategies to inhibit the activation of inflammasome signal pathways and the production of pro-inflammatory cytokines to evade immune responses.Elucidation of these mechanisms might be helpful to the rational design of therapy against infectious diseases and other inflammasome-dependent inflammatory processes.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"62 1","pages":""},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77582368","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}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2013.00320
Can Gao, Xing-yu Li
Extrasynaptic NMDA receptors, which locate in the extrasynaptic site rather than synaptic site have shown to mediate cell death pathway, while synaptic NMDA receptors play an important role in learning and memory and mediate cell survival pathway. This review discussed the reasons of their different distribution between synaptic and extrasynaptic sites, the different molecular mechanisms for signaling pathways of cell fate, as well as their roles in Alzheimer's disease(AD) based on the structure and function of NMDA receptors. Finally, we proposed a reasonable outlook on the treatment of AD from the view of extrasynaptic NMDA receptor.
{"title":"Progress in The Studies on Synaptic and Extrasynaptic NMDA Receptors and The Roles in Alzheimer′s Disease","authors":"Can Gao, Xing-yu Li","doi":"10.3724/SP.J.1206.2013.00320","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00320","url":null,"abstract":"Extrasynaptic NMDA receptors, which locate in the extrasynaptic site rather than synaptic site have shown to mediate cell death pathway, while synaptic NMDA receptors play an important role in learning and memory and mediate cell survival pathway. This review discussed the reasons of their different distribution between synaptic and extrasynaptic sites, the different molecular mechanisms for signaling pathways of cell fate, as well as their roles in Alzheimer's disease(AD) based on the structure and function of NMDA receptors. Finally, we proposed a reasonable outlook on the treatment of AD from the view of extrasynaptic NMDA receptor.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"126 1","pages":""},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76389648","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}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2013.00206
Yuan-yuan Fan, B. Long, Fang Liu, Luyu Zhou, Kun Wang, Peifeng Li
MicroRNAs(miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7,and also in a murine heart failure model,implying that miR-30b might play an important role in heart diseases.To study miR-30b in vivo function,we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain(α-MHC).qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice(P 0.05).miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure.At present,little is known about how miR-30b regulates myocardial infarction.We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls.Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion,these transgenic mice had lower releases of LDH,CK and cTn玉(P 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P 0.05).Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice.In conclusion,miR-30b has protective effect upon ischemic-reperfusion injury.And it may provide a new therapeutic approach for preventing and treating myocardial infarction.
{"title":"Establishment of Cardiomyocyte-specific miR-30b Transgenic Mice and Exploring The Function of miR-30b","authors":"Yuan-yuan Fan, B. Long, Fang Liu, Luyu Zhou, Kun Wang, Peifeng Li","doi":"10.3724/SP.J.1206.2013.00206","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00206","url":null,"abstract":"MicroRNAs(miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7,and also in a murine heart failure model,implying that miR-30b might play an important role in heart diseases.To study miR-30b in vivo function,we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain(α-MHC).qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice(P 0.05).miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure.At present,little is known about how miR-30b regulates myocardial infarction.We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls.Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion,these transgenic mice had lower releases of LDH,CK and cTn玉(P 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P 0.05).Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice.In conclusion,miR-30b has protective effect upon ischemic-reperfusion injury.And it may provide a new therapeutic approach for preventing and treating myocardial infarction.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"222 1","pages":"575-582"},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85901467","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}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2013.00396
Z. Yong, Zhou Ming, Xia-Yu Li, Zhang Wen-ling, Gong Zhao-Jian, Li Qian-jin, Xiao-Ling Li, Zeng Zhao-yang, Ma Jian, Shen Shou-rong, W. Fang, Xiong Wei
Secretion on the surface of human nasal mucosa contains many innate proteins,the key factors of which are SPLUNC1 and LPLUNC1,members of the palate,lung and nasal epithelium clone(PLUNC) family.These two proteins are highly expressed in nasopharyngeal epithelium with the relative specificity.Both of them have bacterial/permeability-increasing protein(BPI) domain which can bind to lipopolysaccharide(LPS) to inhibit or kill bacterial growth directly.They also have the immuno defense function to protect nasopharyngeal epithelium from Epstein-Barr virus(EBV) and some other pathogenic microorganism effectively.These proteins play a significant role in the process of chronic inflammation and carcinogenesis of nasopharyngeal epithelium by inhibiting the secretion of inflammatory factors,such as IL-6,through activating NF-κB and STAT3 signaling pathways.In addition,they also can suppress nasopharyngeal carcinoma(NPC) cell growth and induce cell apoptosis through MAPK and miR-141-PTEN-AKT signaling pathways when the PLUNC proteins are re-expressed in NPC cell lines.Further study about the mechanism of PLUNC protein family in pathogenesis of NPC has important significance for the prevention and treatment guidance of NPC.
{"title":"The Effect and Mechanism of PLUNC Protein Family Against Inflammation and Carcinogenesis of Nasopharyngeal Carcinoma","authors":"Z. Yong, Zhou Ming, Xia-Yu Li, Zhang Wen-ling, Gong Zhao-Jian, Li Qian-jin, Xiao-Ling Li, Zeng Zhao-yang, Ma Jian, Shen Shou-rong, W. Fang, Xiong Wei","doi":"10.3724/SP.J.1206.2013.00396","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00396","url":null,"abstract":"Secretion on the surface of human nasal mucosa contains many innate proteins,the key factors of which are SPLUNC1 and LPLUNC1,members of the palate,lung and nasal epithelium clone(PLUNC) family.These two proteins are highly expressed in nasopharyngeal epithelium with the relative specificity.Both of them have bacterial/permeability-increasing protein(BPI) domain which can bind to lipopolysaccharide(LPS) to inhibit or kill bacterial growth directly.They also have the immuno defense function to protect nasopharyngeal epithelium from Epstein-Barr virus(EBV) and some other pathogenic microorganism effectively.These proteins play a significant role in the process of chronic inflammation and carcinogenesis of nasopharyngeal epithelium by inhibiting the secretion of inflammatory factors,such as IL-6,through activating NF-κB and STAT3 signaling pathways.In addition,they also can suppress nasopharyngeal carcinoma(NPC) cell growth and induce cell apoptosis through MAPK and miR-141-PTEN-AKT signaling pathways when the PLUNC proteins are re-expressed in NPC cell lines.Further study about the mechanism of PLUNC protein family in pathogenesis of NPC has important significance for the prevention and treatment guidance of NPC.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":"26 1","pages":""},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88866783","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：