Shuanglin Hao

2.2k total citations
61 papers, 1.8k citations indexed

About

Shuanglin Hao is a scholar working on Physiology, Cellular and Molecular Neuroscience and Neurology. According to data from OpenAlex, Shuanglin Hao has authored 61 papers receiving a total of 1.8k indexed citations (citations by other indexed papers that have themselves been cited), including 49 papers in Physiology, 39 papers in Cellular and Molecular Neuroscience and 17 papers in Neurology. Recurrent topics in Shuanglin Hao's work include Pain Mechanisms and Treatments (49 papers), Nerve injury and regeneration (22 papers) and Botulinum Toxin and Related Neurological Disorders (17 papers). Shuanglin Hao is often cited by papers focused on Pain Mechanisms and Treatments (49 papers), Nerve injury and regeneration (22 papers) and Botulinum Toxin and Related Neurological Disorders (17 papers). Shuanglin Hao collaborates with scholars based in United States, Japan and China. Shuanglin Hao's co-authors include Marina Mata, David J. Fink, Joseph C. Glorioso, Shue Liu, Darren Wolfe, Hiroshi Iwasaki, Osamu Takahata, D J Fink, Wenwen Zheng and Xuexing Zheng and has published in prestigious journals such as Journal of Neuroscience, PLoS ONE and Annals of Neurology.

In The Last Decade

Shuanglin Hao

59 papers receiving 1.7k citations

Peers

Shuanglin Hao
Ohannes K. Melemedjian United States
Julie Wieseler‐Frank United States
Annemarie Ledeboer United States
Burkhard Schütz Germany
De‐Yong Liang United States
Gudarz Davar United States
Pradipta Ray United States
Darrell R. Smith Canada
Kelley F. Kitto United States
Ohannes K. Melemedjian United States
Shuanglin Hao
Citations per year, relative to Shuanglin Hao Shuanglin Hao (= 1×) peers Ohannes K. Melemedjian

Countries citing papers authored by Shuanglin Hao

Since Specialization
Citations

This map shows the geographic impact of Shuanglin Hao's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Shuanglin Hao with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Shuanglin Hao more than expected).

Fields of papers citing papers by Shuanglin Hao

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Shuanglin Hao. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Shuanglin Hao. The network helps show where Shuanglin Hao may publish in the future.

Co-authorship network of co-authors of Shuanglin Hao

This figure shows the co-authorship network connecting the top 25 collaborators of Shuanglin Hao. A scholar is included among the top collaborators of Shuanglin Hao based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Shuanglin Hao. Shuanglin Hao is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Feng, Zhouyan, Jiang‐Nan Wu, Guicheng Wang, et al.. (2025). Postoperative loss of perineuronal nets in the hippocampal CA1 region results in memory consolidation deficits. Brain Research Bulletin. 229. 111433–111433. 1 indexed citations
2.
Kanda, Hirotsugu, et al.. (2025). Viral vector-mediated interleukin 10 for gene therapy on chronic pain. Molecular Pain. 21. 834591546–834591546. 1 indexed citations
3.
4.
Sakai, K, et al.. (2020). Low-Threshold Mechanosensitive VGLUT3-Lineage Sensory Neurons Mediate Spinal Inhibition of Itch by Touch. Journal of Neuroscience. 40(40). 7688–7701. 14 indexed citations
5.
Kanda, Hirotsugu, et al.. (2020). Viral Vector–Mediated Gene Transfer of Glutamic Acid Decarboxylase for Chronic Pain Treatment: A Literature Review. Human Gene Therapy. 31(7-8). 405–414. 16 indexed citations
6.
Yi, Hyun, Jun Gu, Daigo Ikegami, et al.. (2019). The mitochondrial calcium uniporter contributes to morphine tolerance through pCREB and CPEB1 in rat spinal cord dorsal horn. British Journal of Anaesthesia. 123(2). e226–e238. 13 indexed citations
7.
8.
Yi, Hyun, Shue Liu, Daigo Ikegami, et al.. (2017). Phosphorylated CCAAT/Enhancer Binding Protein β Contributes to Rat HIV-Related Neuropathic Pain:In VitroandIn VivoStudies. Journal of Neuroscience. 38(3). 555–574. 19 indexed citations
9.
Kanda, Hirotsugu, Shue Liu, Takafumi Iida, et al.. (2015). Inhibition of Mitochondrial Fission Protein Reduced Mechanical Allodynia and Suppressed Spinal Mitochondrial Superoxide Induced by Perineural Human Immunodeficiency Virus gp120 in Rats. Anesthesia & Analgesia. 122(1). 264–272. 34 indexed citations
10.
Kanda, Hirotsugu, Wan Huang, Shue Liu, et al.. (2015). Gene Transfer of Glutamic Acid Decarboxylase 67 by Herpes Simplex Virus Vectors Suppresses Neuropathic Pain Induced by Human Immunodeficiency Virus gp120 Combined with ddC in Rats. Anesthesia & Analgesia. 120(6). 1394–1404. 21 indexed citations
11.
Huang, Wan, Wenwen Zheng, Handong Ouyang, et al.. (2014). Mechanical Allodynia Induced by Nucleoside Reverse Transcriptase Inhibitor Is Suppressed by p55TNFSR Mediated by Herpes Simplex Virus Vector Through the SDF1 alpha/CXCR4 System in Rats. Anesthesia & Analgesia. 118(3). 671–680. 20 indexed citations
12.
Zheng, Wenwen, Wan Huang, Shue Liu, et al.. (2014). Interleukin 10 Mediated by Herpes Simplex Virus Vectors Suppresses Neuropathic Pain Induced by Human Immunodeficiency Virus gp120 in Rats. Anesthesia & Analgesia. 119(3). 693–701. 18 indexed citations
13.
Zheng, Xuexing, Wenwen Zheng, Shue Liu, et al.. (2012). Crosstalk Between JNK and NF-κB in the KDO2-Mediated Production of TNFα in HAPI Cells. Cellular and Molecular Neurobiology. 32(8). 1375–1383. 4 indexed citations
14.
Zheng, Xuexing, Handong Ouyang, Shue Liu, et al.. (2011). TNFα is involved in neuropathic pain induced by nucleoside reverse transcriptase inhibitor in rats. Brain Behavior and Immunity. 25(8). 1668–1676. 31 indexed citations
15.
Hao, Shuanglin, Shue Liu, Xuexing Zheng, et al.. (2010). The Role of TNFα in the Periaqueductal Gray During Naloxone-Precipitated Morphine Withdrawal in Rats. Neuropsychopharmacology. 36(3). 664–676. 62 indexed citations
16.
Hao, Shuanglin, Darren Wolfe, Joseph C. Glorioso, Marina Mata, & David J. Fink. (2008). Effects of transgene‐mediated endomorphin‐2 in inflammatory pain. European Journal of Pain. 13(4). 380–386. 43 indexed citations
17.
Mata, Marina, et al.. (2004). Central sprouting of uninjured small fiber afferents in the adult rat spinal cord following spinal nerve ligation. European Journal of Neuroscience. 20(7). 1705–1712. 20 indexed citations
18.
Hao, Shuanglin, Marina Mata, Darren Wolfe, et al.. (2003). HSV-mediated gene transfer of the glial cell-derived neurotrophic factor provides an antiallodynic effect on neuropathic pain. Molecular Therapy. 8(3). 367–375. 69 indexed citations
19.
Hao, Shuanglin, Osamu Takahata, & Hiroshi Iwasaki. (2000). Intrathecal endomorphin-1 produces antinociceptive activities modulated by alpha 2-adrenoceptors in the rat tail flick, tail pressure and formalin tests. Life Sciences. 66(15). 195–204. 39 indexed citations
20.
Hao, Shuanglin & Hidemichi Ogawa. (1998). Naltrexone, but not atropine or yohimbine, antagonizes suppression of formalin-induced spinal sensitization by intrathecal nociceptin. Life Sciences. 63(11). A167–A173. 11 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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