BACKGROUND:Microtubule-associated protein-2 is a kind of important regulatory factor in regulating tubulin assembly. As one of the main members of microtubule-associated proteins, microtubule-associated protein-2 plays an important role in the repairing and development of the nervous system function. It has been found that microtubule-associated protein-2 can promote the repair and rebuilding of injured nerves. OBJECTIVE:To summarize the relationship between microtubule-associated protein-2 and nerve injury as wel as the mechanism of action. METHODS:The PubMed database and CNKI database were retrieved by the fist author for the articles related to microtubule-associated protein-2 published from January 1976 to January 2015. The key words were“microtubule-associated protein-2 (MAP-2), nerve injury, progress”in English and Chinese, respectively. In the same field, articles published recently or in authorized journals were preferred. Repetitive or old articles were excluded, and final y 82 articles were included in result analysis. RESULTS AND CONCLUSION:Microtubule-associated protein-2 is involved in nerve repair, and plays a promoting role in neuronal morphology and plasticity. To increase the concentration of microtubule-associated protein-2 contributes to the recovery of neurologic function in the early stage after nerve injury.

Objective:To investigate the expression of TIP30 in gastric cancer tissues and analyze its impact with angiogenesis. Methods: The expression of TIP30 and CD34-labeled mi-crovessel density (MVD)were measured by immunohistochemical staining in 52 cases of gastric carcinomas and 47cases of Para-cancer tissues. Results: the positive rate of TIP30 was 53.8% and 85.1% in cancerous tissues and para- cancer tissues, there were significant differences between them(?2=11.22,P

Objective To explore the appliacation value of FPSAR between the serum f-PSA and t-PSA in hyperplasia of prostate by YAG Laser.Methods 150 cases with benign prostate hyperplasia(BPH)and 24 cases with prostate pcaancer were selected.The value of f-PSA、t-PSA、FPSAR was determined by TRFIA.Results The tPSA,f-PSA after treatment were significantly lower than before treatment in the two groups(t =2.984,2.701,P ＜0.05).The FPSAR after treatment was significantly higher than before treatment in the two groups(t =2.335,P ＜0.05);The patients of FPSAR≤0.05 in the overlapped field(t-PSA 4～45.5μg/L),the sensitivity of diagnosing PCa is 91.7％(22/24)[t-PSA ＞ 45.5 μg/L(17/24)+(t-PSA 4～45.5 μg/L,FPSAR ≤ 0.15)(5/24)].To examine the PCa with high sensitiveity,it provided the reliable basis for selecting BPH correctly.The patients of BPH group after TUEP was followed up for 6～12 months.The t-PSA is(2.13 ± 0.45)μg/L、f-PSA is(0.85 ± 0.26)μg/L、FPSAR is (0.39 ± 0.06)μg/L.There is no significant difference compared with that after treatment for a month.The international prostate symptom score,(I-PSS)is from(28.3 ± 5.8)points dropped to(12.5 ± 2.1)points.The quality of life,(QOL)is from(4.1 ± 0.6)points dropped to(1.3 ± 0.1)points.The residual urine volume(RUV)is form(93 ±61)ml reduced to(15 ±9)ml.The urination after operation have improvedsignificantly.The Qmax is from average 6.3(2.6～9.5)ml/s before operation raise to 18.4(14.6～22.3)ml/s after operation.Campared with the pre-operation,there is significant difference.Conclusion The application of serum PSA was impoetantin case selection hyperplasia of prostate,comparison of the level changing before and after operation and following up the patients after operation by YAG Laser.

Acute Disease ; Humans ; Nervous System Diseases ; diagnosis ; therapy ; Organophosphate Poisoning ; diagnosis ; therapy

Objective To investigate the effects of hydrogen sulfide on autophagy and the apoptosis after acute spinal cord injury in rats. Methods Thirty-six adult male SD rats (250-300 g) were randomly divided into three groups (n=12 for each group):sham operation group (Sham group), spinal cord injury group (Model group) and hydrogen sulfide pre-treatment group (H2S group). Allen’s method was used to establish the rat model of spinal cord injury. Rats of sham operation group re?ceived only laminectomy. Rats of H2S group received sodium hydrosulphide injection intraperitoneally (50μmol/kg) 1h after spinal cord injury, and Model group was given the same amount of saline solution. Rats in the three groups were sacrificed 24 h after spinal cord injury, then the spinal cord was removed. The expressions of LC3, p70S6K and Cleaved caspase-3 were detected by Western blot assay. The expression of LC3 was also detected by immunofluorescence. The cell apoptosis was as?sessed by TUNEL stain. Results Compared with Sham group, the expression levels of LC3Ⅱ/LC3Ⅰand Cleaved caspase-3 were increased in Model group, but the expression of p70S6K decreased and cell apoptosis increased in Model group (P<0.01). Compared with Model group, the expression levels of LC3Ⅱ/LC3Ⅰand Cleaved caspase-3 were decreased significant?ly, while the expression of p70S6K increased and cell apoptosis decreased significantly in H2S group (P < 0.01). Conclu?sion Hydrogen sulfide can inhibit autophagy and reduce cell apoptosis after acute spinal cord injury in rats.

Objective To study the effect of Exendin-4 on oxidative stress and neural apoptosis following spinal cord injury (SCI). Methods Adult male SD rats, with weight between 200-250 g, were randomly divided into three groups (12 in each group):Sham group, SCI group and Exendin-4 group (Ex-4 group). Rats in Sham group achieved spinal cord exposure. SCI group and Ex-4 group were induced according to Allen′s test (using a weight-drop device). Rats in Ex-4 group were ad?ministrated with Exendin-4 (10 μg/rat) through intraperitoneal injection immediately after establishment of SCI models. Rats in Sham group and SCI group were given the same volume of normal saline solution instead. Level of malondialdehyde (MDA) and the activity of catalase (CAT) were assessed in spinal cord tissues 24 hour after drug administrations. Neural apoptosis was detected by TUNEL staining and the expression levels of caspase-9 and AIF were determined using Western blot. Results Compared with Sham group, the levels of MDA, caspase-9 and AIF as well as neuronal apoptosis rate in?creased obviously, while activity of CAT decreased markedly in SCI group(P<0.01). Compared with SCI group, the levels of MDA, caspase-9 and AIF as well as the neuronal apoptosis rate decreased obviously, while activity of CAT increased re?markably in Exendin-4 group(P < 0.01). Conclusion Exendin-4 restrain neural apoptosis following spinal cord injury through relieving oxidative damage.

Objective To investigate the effects of edaravone (EDA) on cell apoptosis induced by endoplasmic reticu?lum stress (ESR) after spinal cord injury (SCI) in rats. Methods Thirty-six healthy adult SD rats were randomly divided in?to three groups (12 rats for each group):Sham group, SCI group and EDA group. The rat model of SCI was made by Allen’s method and the sham group was only received laminectomy and kept the spinal cord intact. Rats in sham group and SCI group accepted the same volume and frequency of saline injection as EDA group. The EDA group was given 10 mg/kg EDA once every 12 h intraperitoneally. Three days after injuring, the spinal cords were harvested, and the protein levels of C/EBP homologous protein (CHOP), Cleaved caspase-12 and Cleaved caspase-3 were detected by Western blot assay. Immunofluo?rescence staining was used to analyze the positive ratio of caspase-12 and CHOP in spinal cord of three groups. Meanwhile, TUNEL staining was used to identify cell apoptosis of spinal cord. Results Compared with sham group, the protein levels of CHOP, Cleaved caspase-12 and Cleaved caspase-3 were obviously higher in SCI group (P<0.01);the proportion of Cas?pase-12 and CHOP positive cells was significantly increased (P<0.01), and the apoptotic rates were also significantly in?creased in spinal cord (P<0.01). However, compared with SCI group, the protein levels of CHOP , Cleaved caspase-12 and Cleaved caspase-3 were significantly decreased in EDA group (P<0.01);the proportion of Caspase-12 and CHOP positive cells was significantly reduced (P<0.01), and the apoptotic rates were also significantly decreased in spinal cord (P<0.01). Conclusion EDA has neuroprotective potential to spinal cord injury. The mechanism of its neuroprotective effect may asso?ciate with its inhibitory effect to the cell apoptosis induced by endoplasmic reticulum stress after SCI.

Objective To explore the treatment experience of acute paraquat poisoning,thus to explore the prognostic factors and treatment measures.Methods The clinical data of 87 patients with paraquat poisoning who were treated with combined therapy in our hospital emergency department 2014-2015 were retrospectively analyzed.Results 49 cases survived and 38 cases were died in 87 paraquat poisoning patients,the survival rate was 56.32％.The average paraquat of the death group was 65.3mL,which was significantly higher than 41.2mL of the survival group(t =16.65,P ＜ 0.01).Conclusion Amount of poisoning is the key to the prognosis,white blood cells were significantly increased,early or large areas of lung disease is an important factor in poor prognosis;early gastric lavage,cathartic and timely blood purification,application of adrenal cortex hormones,antioxidant and other comprehensive treatment can reduce mortality.

Objective:To explore the clinical and imaging characteristics of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) caused by mitochondrial DNA 14453G>A (m.14453G>A) mutation.Methods:A case of MELAS caused by m.14453G>A mutation in the First Affiliated Hospital of Harbin Medical University on October 12, 2021 was reported. At the same time, the reported cases of MELAS and Leigh syndrome (LS) caused by the m.14453G>A mutation were reviewed. This enabled a comprehensive summarization, analysis, and comparison of these cases.Results:The patient was a female. She has suffered from the disease since 13-year old with seizures, accompanied by the disturbance of mood and the loss of memory. Brain magnetic resonance imaging findings consisted of lesions in frontal, parietal, occipital, temporal lobe and cerebellar. The patient was initially considered with autoimmune encephalitis and posterior reversible encephalopathy syndrome. Since direct sequencing of the complete mitochondrial genome from blood of the patient revealed m.14453G>A mutation in ND6 gene, and the mutation rate was 17.0%, the patient eventually diagnosed with MELAS based on clinical manifestations, imaging examinations, and genetic testing results. Using "m.14453G>A" as the search term, the relevant literature in China and abroad was retrieved and those with complete clinical data were identified. A total of 11 cases of m.14453G>A mutation including this case were reported, of whom 5 patients were diagnosed as MELAS, and 6 patients were diagnosed as LS. Among the 11 patients, those being adolescent or adult and with lesions in the cortex and subcortical white matter were probably be MELAS; those being infant or young child and with lesions in basal ganglia, thalamus and brainstem could be LS. Conclusions:Mitochondrial disease caused by m.14453G>A gene mutation shows a great heterogeneity, which can cause MELAS and LS. The clinical phenotype of the m.14453G>A mutation may be related to the age of onset and lesion′ s location.

Muscle atrophy caused by nerve injury is a common and difficult clinical problem. The development of stem cell researches has opened up a new way for the treatment of nerve injury-induced muscle atrophy. The induced pluripotent stem cells(iPSCs)can differentiate into various types of cells and have more advantages than embryonic stem cells (ESCs). After being transplanted into the damaged area, iPSCs are guided by neurogenic signals to the lesion sites, to repair the damaged nerve, promote generation of axon myelination, rebuild neural circuits and restore physiological function. Meanwhile, iPSCs can also differentiate into muscle cells and promote muscle tissue regeneration. Therefore, it would be possible to attenuate muscle atrophy caused by nerve injury with iPSCs treatment.
Animals ; Disease Models, Animal ; Embryonic Stem Cells ; Humans ; Induced Pluripotent Stem Cells ; cytology ; transplantation ; Muscular Atrophy ; therapy