To quantitatively evaluate the upper-limb spasticity of stroke patients in recovery stage, the relationship between surface electromyography (sEMG) characteristic indexes from biceps brachii and triceps brachii and the spasticity were explored, which provides the electrophysiological basis for clinical rehabilitation. Ten patients with spasticity after stroke were selected to be estimated by modified Ashworth (MAS) assessment and a passive elbow sinusoidal motion experiment was carried out. At the same time, the sEMG of biceps and triceps were recorded. The results shows that the reflex electromyographic threshold could reflect the physiological mechanism of spasticity and had significant correlation with MAS scale which showed that sEMG could be prosperous for the clinical quantitative evaluation of spasticity of stroke patients.
Electromyography ; Humans ; Muscle Spasticity ; physiopathology ; Muscle, Skeletal ; physiopathology ; Stroke ; physiopathology

Objective To evaluate and analyze the characteristics of cognitive and memory disorders in patients suffering cerebral infarction. Methods The scores of overall cognitive function including orientation to time and place, immediate memory, calculation, delayed memory, naming, repeat, understanding, reading, writing, visuospatial function were evaluated by mini-mental state estimate (MMSE) and the scores of memory function including immediate learning and memory , short time delayed recall , long time delay memories were evaluated by WHO/UCLA Auditory Verbal Learning Test. Statistical analysis were done in patients with cerebral infarction and healthy controls. Results The scores of overall cognitive function, memory scores as well as immediate recall , short-delayed recall , long-delayed recall in cerebral infarction patients were much lower than those of healthy controls (P < 0.001). Conclusion The overall cognitive function and memory function declined significantly , also immediate memory and short term memory were remarkable impaired in patients with cerebral infarction, resulting their memory characteristics were similar to patients with Alzheimer′s disease.

Objective To investigate the changes and prognostic significance of bone marrow(BM) oil drop and megakaryocyte counts after chemotherapy in acute myeloid leukemia (AML) patients (non-M3).Methods Ninty-nine adult patients with denovo AML (non-M3) were retrospectively analyzed to evaluate the change of BM oil drop and megakaryocyte counts and their influences on overall survival(OS) and disease free survival (DFS) during all stages of standardized therapy.Results The median DFS and OS were 21 (2-88);months and 70 (4-89) months,respectively; and 3-year predicted DFS and OS were 47.3 ％ and 55.8 ％,respectively.After AML patients (non-M3) achieving complete remission (CR) by induction therapy,BM oil drop tended to increase along with postremission chemotherapy cycle accumulation, while megakaryocyte counts tended to decrease.The univariate analysis indicated that megakaryocyte counts decreased after the second course of postremission therapy. BM oil drop increased after the first to the third course of postremission therapy.Grade of myelofibrosis in BM biopsy,serum lactate dehydrogenase (LDH) level at diagnosis,flow cytometric immunophenotyping, the percentage of BM blast cells at diagnosis and the percentage of residual leukemic cells (RLC) during aplasia (7-10 days after the end of induction therapy) had prognostic significance.Multivariable COX analysis indicated the percentage of BM blast cells at diagnosis and change of BM oil drop after the third postremission therapy were independent prognostic factors for DFS (P =0.010,0.018 respectively),and RLCs during aplasia and change rate of the megakaryocyte counts after the second postremission therapy were independent prognostic factors for OS (P =0.009, 0.038respectively).Conclusion After AML patients (non-M3) achieving CR by induction therapy,BM oil drop tends to increase along with postremission chemotherapy cycles accumulation,while the megakaryocyte counts tend to decrease.Dynamic observations of bone marrow oil drop and megakaryocyte counts are helpful for assessing the prognosis of acute myeloid leukemia (non-M3).

Background:Deoxyhypusine synthase(DHPS)is a key factor in post-translational modification of the precursor of eukaryotic initiation factor 5A(eIF-5A),and eIF-5A is closely related to the regulation of proliferation and invasion of tumor cells. Aims:To investigate the expression of DHPS in gastric cancer and its clinical significance,and to explore the possible mechanism of its effect on metastasis of gastric cancer. Methods:Tissue microarray containing 92 gastric cancer tissues and paired adjacent cancerous tissues was employed to detect the DHPS expression by using immunohistochemical staining,and the correlation of DHPS expression with the clinicopathological characteristics of gastric cancer was analyzed. DHPS-siRNA and GC7,an inhibitor of DHPS were used,respectively to intervene human gastric cancer cell line MGC803. The invasive ability of MGC803 cells was assessed by cell invasion assay,and the expressions of metastasis-related proteins including vascular endothelial growth factor(VEGF),matrix metalloproteinase 2(MMP2)and MMP9 were detected by ELISA. Results:In 62(67.4%)cases of gastric cancer,DHPS was highly expressed,and its expression was closely related to tumor diameter,TNM stage and depth of invasion(P <0.05),but not related to gender,age,lymph node metastasis and distant metastasis(P >0. 05). Both DHPS-siRNA and GC7 could down-regulate the invasiveness of MGC803 cells,while the former could also reduce the expressions of VEGF,MMP2 and MMP9 proteins(P <0.05). Conclusions:DHPS is highly expressed in gastric cancer and associated with tumor invasion and progression. DHPS is expected to be a new target for diagnosis and treatment of gastric cancer because of its regulatory effect on invasion and metastasis of tumor cells.

Osteosarcoma needs to continuously induce angiogenesis to satisfy its own nutritional supply in the process of development. Therefore, the inhibition of osteosarcoma cell-induced angiogenesis as a target has become a research hot in recent years. Currently, vascular inhibitors targeting mRNA-encoded protein have been applied in clinic, but the efficacy is poor. Non-coding RNA (ncRNA) is a type of RNA molecules that do not participate in protein coding. ncRNA can regulate the angiogenesis of osteosarcoma by regulating the secretion of vascular factors such as vascular endothelial growth factor, angiogenin-2 and hypoxia-inducible factor 1 or the interaction between ncRNAs. This article reviews the role of ncRNA in the angiogenesis of osteosarcoma to provide references for clinical targeted therapy strategies for osteosarcoma.

Immobilization of enzymes is important and widely applied in biocatalysis. Streptomyces platensis gene gox, encoding an extracellular L-glutamate oxidase (Gox), was fused to cellulose binding domain (CBDcex) from Cellulomonas fimi and the recombinant protein Gox-CBD was expressed in Escherichia coli. The fusion protein (Gox-CBD) was immobilized onto microcrystalline cellulose. The preparation conditions, binding capacity, properties and stability of the immobilized enzyme were studied. Under the condition of 4 ℃, for 1 hour, the fusion protein Gox-CBD was able to bind microcrystalline cellulose at a ratio of 9.0 mg of protein per gram of microcrystalline cellulose. Enzymatic properties of free and immobilized L-glutamic oxidase (Gox-CBD) were compared. The specific activity of the immobilized enzyme decreased, but its thermal stability increased a lot compared with that of the free Gox-CBD. After incubation at 60 ℃ for 30 min, 70% of the total activity remained whereas the free recombinant Gox completely lost its activity. The immobilized protein was tightly bound to microcrystalline cellulose at pH below 10 or more than 5 mmol/L NaCl. The fusion protein of Gox-CBD can be specifically immobilized on the microcrystalline cellulose on a single step. Therefore, our findings can provide a novel strategy for protein purification and enzyme immobilization.

Objective: To investigate PLOD2 expression in esophageal squamous cell carcinoma, and to explore the potential mechanism by which PLOD2 promotes tumor metastasis. Methods: The expression of PLOD2 in 60 cases of esophageal squamous cell carcinoma (the patients were collected at the first Affiliated Hospital of Xinxiang Medical University, from January 2016 to December 2017) was investigated by immunohistochemistry. Fibrillar collagen formation and collagen deposition were detected by picrosirius red staining. Correlation of PLOD2 expression with clinical pathologic features of the patients was performed using χ² test and Kaplan-Meier analysis. After EC-109 cells were transfected with LV-vector and LV-over/PLOD2, the expression of PLOD2 was detected by real time PCR and the impact of POLD2 on invasion in EC-109 cells was determined by transwell migration and invasion assays. The expression of PLOD2/AKT epithelial-to-mesenchymal transition signal pathway related proteins was detected by Western blot. Results: The expression level of PLOD2 in esophageal squamous cell carcinoma was 81.7% (49/60 cases),higher than their paired noncancerous tissues(8.3%, 5/60; P<0.01), and correlated significantly with tumor depth of invasion and nodal metastasis (P<0.01). Picrosirius red staining showed that collagen deposition was increased and the degree of fibrillar organization was enhanced in carcinoma tissues that had higher PLOD2 expression. Transwell migration and invasion assays showed that PLOD2 significantly promoted the migration and invasion ability of EC-109 cells. Western blot showed that PLOD2 significantly increased the expression levels of p-FAK, p-AKT and vimentin in EC-109 cells. Conclusions Esophageal squamous cell carcinoma has a high expression of PLOD2 that correlates with tumor invasion and lymph node metastasis. PLOD2 promotes invasion and metastasis of esophageal squamous cell carcinoma through epithelial-to-mesenchymal transition via FAK/AKT signal pathway.

Objective To investigate the changing trend and epidemiological characteristics of the incidence and mortality of chronic kidney disease (CKD) with age, period and birth cohort in Chinese population. Methods Based on the data of incidence and mortality of CKD in Chinese population aged 20-80 years from 1990 to 2019 in GHDx database, joinpoint regression model was used to analyze the incidence and mortality trend of CKD. An age-period-cohort model was constructed to analyze the effects of age, period, and birth cohort on the trend of CKD incidence and mortality. Results Joinpoint regression analysis showed that the standardized incidence rate of chronic kidney disease in Chinese population increased from 146.37/100 000 in 1990 to 161.52/100 000 in 2019, while the standardized mortality rate decreased from 12.98/100 000 in 1990 to 11.23/100 000 in 2019. The APC model analysis showed that the risk of CKD incidence and death in the Chinese population increased with age, while the risk of CKD incidence increased with the increase of period. The risk of death did not change significantly with the increase of period. The cohort born later had a lower risk of CKD incidence and death compared to the cohort born earlier. Conclusion At present, the age effect and period effect of the incidence and death risk of chronic kidney disease in China are dominant. It is important to take effective measures and intervene in a timely manner, especially to strengthen the protection of older high-risk groups born earlier.

Objective　To explore the mediating role of cognitive function in the association between literacy level and depressive symptoms in middle-aged and elderly people in China. Methods　 Using the fourth national follow-up data of the China Health and Elderly Care Tracking Survey 2018, 8 124 middle-aged and elderly people aged 45 years and above were included as the study subjects. The PROCESS 4.0 program was used to test the mediating effect of cognitive function between literacy level and depressive symptoms, and the Bootstrap method was used for the mediator variable validation. Results The detection rate of depressive symptoms among middle-aged and elderly people in China was 38.10%. After controlling for gender, place of residence, marital status, smoking, alcohol consumption, and exercise, literacy level was a negative predictor of depressive symptoms in middle-aged and elderly people (β =－0.480, t =－11.248, P<0.001). Cognitive function accounted for 58.75% of the amount of mediating effect between literacy level and depressive symptoms. Conclusion 　Literacy level and cognitive function are associated with depressive symptoms in middle-aged and elderly people. Literacy level can influence depressive symptoms directly or indirectly through the mediation of cognitive dysfunction.

RBM46 is a germ cell-specific RNA-binding protein required for gametogenesis, but the targets and molecular functions of RBM46 remain unknown. Here, we demonstrate that RBM46 binds at specific motifs in the 3'UTRs of mRNAs encoding multiple meiotic cohesin subunits and show that RBM46 is required for normal synaptonemal complex formation during meiosis initiation. Using a recently reported, high-resolution technique known as LACE-seq and working with low-input cells, we profiled the targets of RBM46 at single-nucleotide resolution in leptotene and zygotene stage gametes. We found that RBM46 preferentially binds target mRNAs containing GCCUAU/GUUCGA motifs in their 3'UTRs regions. In Rbm46 knockout mice, the RBM46-target cohesin subunits displayed unaltered mRNA levels but had reduced translation, resulting in the failed assembly of axial elements, synapsis disruption, and meiotic arrest. Our study thus provides mechanistic insights into the molecular functions of RBM46 in gametogenesis and illustrates the power of LACE-seq for investigations of RNA-binding protein functions when working with low-abundance input materials.
Animals ; Mice ; 3' Untranslated Regions/genetics* ; Cell Cycle Proteins/metabolism* ; Gametogenesis/genetics* ; Meiosis/genetics* ; Nuclear Proteins/genetics* ; RNA-Binding Proteins/genetics*