Lin Ma
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Lin Ma has a total of 29 co-authors. Here are the top co-authors by number of shared publications:
Yongmin Chen
Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570102, P.R. China
5 shared publications- Qifu Li
Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, China
4 shared publications Shuang Chen
The First Affiliated Hospital of Hainan Medical University
3 shared publicationsSongrong Li
Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570102, P.R. China
3 shared publicationsXi Kuang
Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570102, P.R. China
3 shared publicationsHongzhan Liao
Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570102, P.R. China
2 shared publications
Latest Publications
- Open Access
- 5 March 2025
- Published by Spandidos Publications in Oncology Letters
- Vol. 29 (5) , 1-2
[Corrigendum] miR‑181a‑5p inhibits the proliferation and invasion of drug‑resistant glioblastoma cells by targeting F‑box protein 11 expression
[This corrects the article DOI: 10.3892/ol.2020.12098.].
- 5 March 2025
- Published by Spandidos Publications in Oncology Letters
- Vol. 29 (5) , 1-2
Open Access[Corrigendum] miR‑181a‑5p inhibits the proliferation and invasion of drug‑resistant glioblastoma cells by targeting F‑box protein 11 expression
[This corrects the article DOI: 10.3892/ol.2020.12098.].
- Open Access
- 12 July 2021
- Published by Taylor & Francis in Neurological Research
- Vol. 43 (12) , 1031-1039
Safety and efficacy of intravascular therapy in patients with progressive stroke caused by intracranial large vascular occlusion exceeding the time window of 24 hours
To compare endovascular and drug therapies for efficacy and safety in patients with a progressive stroke caused by intracranial large vascular occlusion exceeding the time window of 24 hours.A tota...
- 12 July 2021
- Published by Taylor & Francis in Neurological Research
- Vol. 43 (12) , 1031-1039
Open AccessSafety and efficacy of intravascular therapy in patients with progressive stroke caused by intracranial large vascular occlusion exceeding the time window of 24 hours
To compare endovascular and drug therapies for efficacy and safety in patients with a progressive stroke caused by intracranial large vascular occlusion exceeding the time window of 24 hours.A tota...
- Open Access
- 11 February 2021
- Published by Wiley in Epilepsia Open
- Vol. 6 (2) , 323-330
An epidemiological survey of epilepsy in tropical rural areas of China
Objective: Epilepsy is a chronic neurological disease that is characterized by seizures. Seizure episodes, stigma, and high medical costs associated with this condition caused significant psychological distress. This study aimed to evaluate epidemiological characteristics and treatment status of epilepsy in individuals existing in the tropical rural areas of Hainan Province of China.Methods: A household survey on epilepsy was conducted among the rural population of Chengmai County, Danzhou City, Baoting Autonomous County (Li and Miao nationalities), and Dingan County in Hainan Province, China. A screening questionnaire based on the standard screening questionnaires of the World Health Organization (WHO) was designed and a screening instrument of International Community‐based Epilepsy Research Group was used. Individuals suspected or previously diagnosed with epilepsy were reexamined by an experienced neurologist. Further clinical data were collected from subjects with confirmed diagnosis of epilepsy.Results: This study included 16 676 subjects with 8827 men (52.93%) and 7849 women (47.07%). Majority of the study subjects included were of Han Chinese (N = 13 145, 78.83%), and the remaining were of Li minority ethnicity. The incidence of epilepsy was 0.24 per 1000, and the total prevalence of active epilepsy was 2.33 per 1000. The prevalence of epilepsy in the Han and Li nationalities was 3.27 and 2.27 per 1000, respectively, which was shown to be higher in people aged ≥ 60. The initial onset of epilepsy tended to trigger among children aged between 0 and 9 years old. Initial assessment revealed that the treatment gap for active epilepsy was 58.97%, and stroke is shown as the most common cause of symptomatic epilepsy.Significance: The prevalence and incidence of epilepsy in tropical rural areas of Hainan Province were close to those of the earlier findings that are reported in other regions of China and lower than those remaining in the tropical areas around the world. There exists a huge treatment gap for active epilepsy, which indicates an urgent need for a rational intervention strategy.
- 11 February 2021
- Published by Wiley in Epilepsia Open
- Vol. 6 (2) , 323-330
Open AccessAn epidemiological survey of epilepsy in tropical rural areas of China
Objective: Epilepsy is a chronic neurological disease that is characterized by seizures. Seizure episodes, stigma, and high medical costs associated with this condition caused significant psychological distress. This study aimed to evaluate epidemiological characteristics and treatment status of epilepsy in individuals existing in the tropical rural areas of Hainan Province of China.Methods: A household survey on epilepsy was conducted among the rural population of Chengmai County, Danzhou City, Baoting Autonomous County (Li and Miao nationalities), and Dingan County in Hainan Province, China. A screening questionnaire based on the standard screening questionnaires of the World Health Organization (WHO) was designed and a screening instrument of International Community‐based Epilepsy Research Group was used. Individuals suspected or previously diagnosed with epilepsy were reexamined by an experienced neurologist. Further clinical data were collected from subjects with confirmed diagnosis of epilepsy.Results: This study included 16 676 subjects with 8827 men (52.93%) and 7849 women (47.07%). Majority of the study subjects included were of Han Chinese (N = 13 145, 78.83%), and the remaining were of Li minority ethnicity. The incidence of epilepsy was 0.24 per 1000, and the total prevalence of active epilepsy was 2.33 per 1000. The prevalence of epilepsy in the Han and Li nationalities was 3.27 and 2.27 per 1000, respectively, which was shown to be higher in people aged ≥ 60. The initial onset of epilepsy tended to trigger among children aged between 0 and 9 years old. Initial assessment revealed that the treatment gap for active epilepsy was 58.97%, and stroke is shown as the most common cause of symptomatic epilepsy.Significance: The prevalence and incidence of epilepsy in tropical rural areas of Hainan Province were close to those of the earlier findings that are reported in other regions of China and lower than those remaining in the tropical areas around the world. There exists a huge treatment gap for active epilepsy, which indicates an urgent need for a rational intervention strategy.
- Open Access
- 26 January 2021
- Published by Frontiers Media SA in Frontiers in Neuroscience
- Vol. 14
SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy
Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein involved in the extracellular matrix and interactions between cells during neural development of the central nervous system (CNS). Oxidative glutamate toxicity is involved in CNS diseases, including epilepsy, Alzheimer’s disease, and ischemic stroke. However, the molecular mechanism of nerve injury is not fully understood in CNS diseases. Herein, the glutamate-induced nerve damage model was used to explore the molecular mechanisms affecting nerve damage. The levels of SPARC and autophagy were increased in glutamate-induced HT22 hippocampal nerve injury. In summary, the current study confirmed that SPARC regulates autophagy in HT22 hippocampal nerve cells, and its knockdown reduces the glutamate-induced HT22 hippocampal nerve injury by inhibiting autophagy. These findings suggested that SPARC plays a crucial role in nerve injury of CNS diseases.
- 26 January 2021
- Published by Frontiers Media SA in Frontiers in Neuroscience
- Vol. 14
Open AccessSPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy
Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein involved in the extracellular matrix and interactions between cells during neural development of the central nervous system (CNS). Oxidative glutamate toxicity is involved in CNS diseases, including epilepsy, Alzheimer’s disease, and ischemic stroke. However, the molecular mechanism of nerve injury is not fully understood in CNS diseases. Herein, the glutamate-induced nerve damage model was used to explore the molecular mechanisms affecting nerve damage. The levels of SPARC and autophagy were increased in glutamate-induced HT22 hippocampal nerve injury. In summary, the current study confirmed that SPARC regulates autophagy in HT22 hippocampal nerve cells, and its knockdown reduces the glutamate-induced HT22 hippocampal nerve injury by inhibiting autophagy. These findings suggested that SPARC plays a crucial role in nerve injury of CNS diseases.
- Open Access
- 14 September 2020
- Published by Spandidos Publications in Oncology Letters
- Vol. 20 (5) , 1
miR‑181a‑5p inhibits the proliferation and invasion of drug‑resistant glioblastoma cells by targeting F‑box protein 11 expression
Glioblastoma (GBM) is the most common malignant primary tumor in the human central nervous system. The present study aimed to explore the molecular mechanism by which microRNA (miR)‑181a‑5p targets the F‑box protein 11 (FBXO11) in glioma cells to inhibit cell proliferation and invasion. Reverse transcription‑quantitative (RT‑q)PCR was performed to detect the expression levels of miR‑181a‑5p in U251TR cells, U251 cells, primary GBM tissues and relapsed GBM tissues in order to determine the association between miR‑181a‑5p and the chemoresistance of GBM cells. The expression levels of miR‑181a‑5p in GBM cells were modulated via transfecting miR‑181a‑5p mimics and inhibitors. Cell Counting Kit‑8 assays were undertaken to assess the effects of miR‑181a‑5p on drug sensitivity and proliferation of GBM cells. Wound healing assays were performed to examine the effects of miR‑181a‑5p on the migratory ability of GBM cells. Furthermore, the effects of miR‑181a‑5p on the invasive ability of GBM cells were analyzed using an in vitro invasion assay. Flow cytometry analysis was carried out to determine whether overexpression of miR‑181a‑5p can promote the apoptotic rate of GBM cells. RT‑qPCR and western blotting were employed to detect the effects of miR‑181a‑5p on mRNA and protein expression of FBX011. miR‑181a‑5p exhibited low expression in resistant GBM cell lines and recurrent tumor tissues. Dual‑luciferase reporter assays were utilized to detect luciferase activity to verify the targeted regulatory association between miR‑181a‑5p and FBXO11. Upregulation of miR‑181a‑5p promoted the sensitivity of GBM cells to temozolomide (TMZ), increased the apoptotic rate of GBM cells and significantly inhibited the invasive and migratory capacities of GBM cells. In drug‑resistant glioma cells, compared with the miR‑negative control group and the blank group, the expression of miR‑181a‑5p was significantly upregulated (PFBXO11 gene expression, or may be associated with apoptosis.
- 14 September 2020
- Published by Spandidos Publications in Oncology Letters
- Vol. 20 (5) , 1
Open AccessmiR‑181a‑5p inhibits the proliferation and invasion of drug‑resistant glioblastoma cells by targeting F‑box protein 11 expression
Glioblastoma (GBM) is the most common malignant primary tumor in the human central nervous system. The present study aimed to explore the molecular mechanism by which microRNA (miR)‑181a‑5p targets the F‑box protein 11 (FBXO11) in glioma cells to inhibit cell proliferation and invasion. Reverse transcription‑quantitative (RT‑q)PCR was performed to detect the expression levels of miR‑181a‑5p in U251TR cells, U251 cells, primary GBM tissues and relapsed GBM tissues in order to determine the association between miR‑181a‑5p and the chemoresistance of GBM cells. The expression levels of miR‑181a‑5p in GBM cells were modulated via transfecting miR‑181a‑5p mimics and inhibitors. Cell Counting Kit‑8 assays were undertaken to assess the effects of miR‑181a‑5p on drug sensitivity and proliferation of GBM cells. Wound healing assays were performed to examine the effects of miR‑181a‑5p on the migratory ability of GBM cells. Furthermore, the effects of miR‑181a‑5p on the invasive ability of GBM cells were analyzed using an in vitro invasion assay. Flow cytometry analysis was carried out to determine whether overexpression of miR‑181a‑5p can promote the apoptotic rate of GBM cells. RT‑qPCR and western blotting were employed to detect the effects of miR‑181a‑5p on mRNA and protein expression of FBX011. miR‑181a‑5p exhibited low expression in resistant GBM cell lines and recurrent tumor tissues. Dual‑luciferase reporter assays were utilized to detect luciferase activity to verify the targeted regulatory association between miR‑181a‑5p and FBXO11. Upregulation of miR‑181a‑5p promoted the sensitivity of GBM cells to temozolomide (TMZ), increased the apoptotic rate of GBM cells and significantly inhibited the invasive and migratory capacities of GBM cells. In drug‑resistant glioma cells, compared with the miR‑negative control group and the blank group, the expression of miR‑181a‑5p was significantly upregulated (PFBXO11 gene expression, or may be associated with apoptosis.