Publications by authors named "Guanglu Yang"

7 Publications

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Case Report: A Case Report and Literature Review of 3p Deletion Syndrome.

Front Pediatr 2021 10;9:618059. Epub 2021 Feb 10.

Department of Pediatric, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.

The aim of the present study is to explore the clinical and genetic characteristics of 3p deletion syndrome to improve clinicians' understanding of the disease. The clinical manifestations, process of diagnosis and treatment, and genetic characteristics of an individual case of 3p deletion syndrome were analyzed. CNKI, Wanfang Data, and the Biomedical Literature Database (PubMed) were searched. The search time limit, using "3p deletion syndrome" and "" as keywords, was from the creation of the database up to June 2020. Related data were reviewed. The proband was a male child with general developmental and intellectual disabilities, special facial features and congenital heart disease. The child was the parents' first pregnancy and first born. Gene microarray analysis showed a 10.095 Mb deletion in the 3p26.3-p25.3 region, resulting in a heterozygous mutation of the gene; thus, the patient was diagnosed with 3p deletion syndrome. At the time of diagnosis, the child was 1 year of age and was responding to comprehensive rehabilitation training. A total of 29 well-documented cases were found in the literature, of which 19 cases had an onset within 1 year of birth, and mainly manifested with mental and motor development disabilities and abnormal facial features, with different gene deletions, depending on the size and location of the 3p deletion. The genetic test results of the child in this study indicated a heterozygous deletion of the gene on the short arm of chromosome 3, which was a unique feature of this study, since it was rarely mentioned in other reports of 3p deletion syndrome. The clinical phenotype of this syndrome is complex as it can include intellectual and motor development backwardness, low muscle tone, certain abnormal facial features (low hairline, bilateral ptosis, widely spaced eyes, a forward nose, left ear auricle deformity, a high-arched palate, a small jaw), and the deformation of systems such as the gastrointestinal tract and the urinary tract malformation or symptoms of epilepsy. As clinical manifestations can be relatively mild, the syndrome is easy to miss or misdiagnose. Clinical workers need to be aware of this disease when they find that children have special features, such as stunted growth, low muscle tone or ptosis, and it needs to be diagnosed through genetic testing. Most children are able to develop certain social skills after rehabilitation treatment.
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http://dx.doi.org/10.3389/fped.2021.618059DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7902511PMC
February 2021

Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress.

BMC Complement Med Ther 2021 Feb 19;21(1):69. Epub 2021 Feb 19.

Department of Traumatology and Orthopedics, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, People's Republic of China.

Background: Endoplasmic reticulum stress (ERS) is one of the main mechanisms of spinal cord injury (SCI) pathology and can affect the physiological state of neurons. Icariin (ICA), the main pharmacological component of Epimedium, can relieve the symptoms of patients with SCI and has obvious protective effects on neurons through ERS.

Methods: PC12 cells were induced to differentiate into neurons by nerve growth factor and identified by flow cytometry. Cell proliferation was detected by CCK8 method, cell viability was detected by SRB assay, apoptosis was detected by flow cytometry and microstructure of ER was observed by transmission electron microscope. Western blot was used to detect the protein expression of CHOP and Grp78, and qPCR was used to detect the mRNA expression of CHOP and Grp78.

Results: The results of CCK8, SRB and flow cytometry showed that ICA could relieve ERS and reduce apoptosis of PC12 cells. The results of transmission microscope showed that ICA could reduce apoptosis of PC12 cells caused by ERS. The results of Western blot and q-PCR showed that ICA could inhibit ERS by down-regulating the expression of CHOP and Grp78.

Conclusions: ICA can inhibit ERS and promote the repair of PC12 cells by down-regulating the expression of CHOP and Grp78. ICA has the potential to promote the recovery of spinal cord injury.
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http://dx.doi.org/10.1186/s12906-021-03233-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7896365PMC
February 2021

[Research progress of different mechanical stimulation regulating chondrocytes metabolism].

Sheng Wu Yi Xue Gong Cheng Xue Za Zhi 2020 Dec;37(6):1101-1108

Department of Traumatology & Orthopedics, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, P.R.China;Laboratory of New Techniques of Restoration & Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine, Nanjing 210023, P.R.China;School of Chinese Medicine, School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, P.R.China.

As a kind of mechanical effector cells, chondrocytes can produce a variety of physical and chemical signals under the stimulation of multiaxial load , which affect their own growth, development and apoptosis. Therefore, simulating the mechanical environment has become a research hotspot in the culture of chondrocytes . Although a large number of reports have fully proved that different mechanical stimulation can regulate the metabolism of chondrocytes, the loading scheme has not been agreed. Starting from different mechanical forms, this review will explore the differences in the regulation of chondrocyte metabolism by different mechanical stimuli, so as to find an advantage scheme to promote the growth and proliferation of chondrocytes and to develop a more stable, effective and reliable experimental strategy.
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http://dx.doi.org/10.7507/1001-5515.202001044DOI Listing
December 2020

Jisuikang Promotes the Repair of Spinal Cord Injury in Rats by Regulating NgR/RhoA/ROCK Signal Pathway.

Evid Based Complement Alternat Med 2020 28;2020:9542359. Epub 2020 Nov 28.

Department of Traumatology and Orthopedics, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.

Jisuikang (JSK) is an herbal formula composed of many kinds of traditional Chinese medicine, which has been proved to be effective in promoting the rehabilitation of patients with spinal cord injury (SCI) after more than ten years of clinical application. However, the mechanisms of JSK promoting nerve regeneration are yet to be clarified. The aim of this study was to investigate the effects of JSK protecting neurons, specifically the regulation of NgR/RhoA/ROCK signal pathway. The motor function of rats was evaluated by the BBB score and inclined plate test, Golgi staining and transmission electron microscope were used to observe the microstructure of nerve tissue, and fluorescence double-labeling method was used to detect neuronal apoptosis. In this study, we found that JSK could improve the motor function of rats with SCI, protect the microstructure (mitochondria, endoplasmic reticulum, and dendritic spine) of neurons, and reduce the apoptosis rate of neurons in rats with SCI. In addition, JSK could inhibit the expression of Nogo receptor (NgR) in neurons and the NgR/RhoA/ROCK signal pathway in rats with SCI. These results indicated JSK could improve the motor function of rats with SCI by inhibiting the NgR/RhoA/ROCK signal pathway, which suggests the potential applicability of JSK as a nerve regeneration agent.
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http://dx.doi.org/10.1155/2020/9542359DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7735860PMC
November 2020

A novel mutation of SGSH and clinical features analysis of mucopolysaccharidosis type IIIA.

Medicine (Baltimore) 2018 Dec;97(52):e13758

Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, P.R. China.

Rationale: The aim of this study was to analyze the clinical and imaging features of a pediatric patient with mucopolysaccharidosis type IIIA (MPS IIIA) and a novel mutation of the N-sulfoglucosamine sulfohydrolase (SGSH) in 1 pedigree.

Patient Concerns: An 8-year-old female patient presented with developmental regression, seizures, cerebral atrophy, thickened calvarial diploe, apathy, esotropia, slender build, thick hair, prominent eyebrows, hepatomegaly, ankle clonus, muscle and joint contractures, and funnel chest.

Diagnoses: The patient was diagnosed as autosomal recessive (AR) MPS IIIA with a novel mutation in the SGSH gene.

Interventions: Genomic DNA was extracted from the peripheral blood and next-generation sequencing (NGS) technology was used to detect pathogenic genes, and the Sanger method was applied to perform pedigree verification for the detected suspicious pathogenic mutations.

Outcomes: The NGS done for the girl and her family showed 2 variations that were both missense mutations in SGSH. The c.1298G > A (p.Arg433Gln) was a known mutation, and the c.630 G > T (p.Trp210Cys) was a novel variation.

Lessons: The common clinical manifestations of MPS IIIA were rapid developmental regression, seizures, cerebral atrophy, and thickened calvarial diploe. The results showed that the c.630 G > T was likely pathogenic according to bioinformatics analysis, which probably was a novel mutation. This study reports 1 case of MPS IIIA with some clinical features as determined via clinical and genetic analysis, and found a new mutation in the SGSH gene.
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http://dx.doi.org/10.1097/MD.0000000000013758DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314651PMC
December 2018

Acylated ghrelin protects hippocampal neurons in pilocarpine-induced seizures of immature rats by inhibiting cell apoptosis.

Mol Biol Rep 2013 Jan 6;40(1):51-8. Epub 2012 Nov 6.

Department of Pediatrics, Shengjing Hospital, China Medical University, Shenyang 110004, China.

Ghrelin has two major molecular forms, acylated ghrelin (AG) and unacylated ghrelin (UAG). Only AG to bind growth hormone secretagogue receptor 1a (GHSR-1a) has central endocrine activities. An antiapoptotic effect of AG in cortical neuronal cells has recently been reported. However, whether there is a neuroprotective effect of AG in hippocampal neurons of pilocarpine-induced seizures in rats, is still unknown. Therefore, in the present study, the underlying mechanism of AG on lithium-pilocarpine-induced excitotoxicity was examined in the hippocampus of rat. The results showed that AG inhibited pilocarpine-induced apoptosis. Exposure of rats to the receptor-specific antagonist D-Lys-3-GHRH-6 abolished the protective effects of AG against epilepsy. Administration of AG resulted in increased expression of phosphor-Akt in status epilepticus model in rats, which was accompanied with the attenuation of hippocampal cell death. Furthermore, administration of AG resulted in decreased expression of phosphor-JNK in pyramidal neurons of hippocampus after status epilepsy, which was also accompanied with the attenuation of hippocampal cell death, too. In addition, AG increased the Bcl-2/Bax ratio and inhibited caspase-3 activation. The data indicate that AG can function as a neuroprotective agent that inhibits apoptotic pathways. These effects may be mediated via activation of the PI3K/Akt pathway.
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http://dx.doi.org/10.1007/s11033-012-1993-1DOI Listing
January 2013

Sema3F downregulates p53 expression leading to axonal growth cone collapse in primary hippocampal neurons.

Int J Clin Exp Pathol 2012 5;5(7):634-41. Epub 2012 Sep 5.

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang 110004, China.

Hippocampal nerve growth is regulated by the coordinated action of numerous external stimuli, including positively acting neurotrophin-derived growth cues and restrictive semaphorin cues, however the underlying cellular mechanisms remain largely unclear. We examined the potential cellular mechanism of Semaphorin3F (Sema3F) in cultured primary hippocampal neurons. We show that Sema3F can down-regulate p53 expression in primary hippocampal neurons, thereby contributing to growth cone collapse. Sema3F suppressed p53-induced pathways, which we show to be required to maintain growth cone structure. Sema3F-induced growth cone collapse was partially reversed by overexpression of p53, which promoted growth cone extension. Inhibition of p53 function by inhibitor, siRNAs, induced axonal growth cone collapse, whereas p53 over-expression led to larger growth cones in cultured primary hippocampal neurons.These data reveal a novel mechanism by which Sema3F can induce hippocampal neuron growth cone collapse and provide evidence for an intracellular mechanism for cross talk between positive and negative axon growth cues.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438774PMC
February 2013