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Objective:To evaluate the clinical effect of direct anterior total hip arthroplasty in the treatment of hip osteoarthritis.Methods:From December 2017 to December 2020, 82 patients with hip osteoarthritis who received total hip arthroplasty in the department of orthopedics, 541 General Hospital, including 41 patients with direct anterior total hip arthroplasty as the observation group, and 41 patients with lateral total hip arthroplasty as the control group. The general indicators of the two groups of patients during the perioperative period (time of ambulatory activity, hospitalization, amount of intraoperative bleeding, and operation time) and the clinical efficacy evaluation indicators [visual analogue score (VAS), Harris hip joint function score, Western Ontario and McMaster Universities Arthritis Index (WOMAC) score] were compared.Results:The time of ambulatory activity was (15.54 ± 2.67) and (19.32 ± 3.18) h, after operation, respectively, and the time of hospitalization was (6.87 ± 0.87) and (8.03 ± 1.04) d, respectively, in the observation group and the control group. The differences between the two groups were statistically significant ( t = 5.83, 5.48, P < 0.001); there was no statistically significant difference between the two groups in the amount of intraoperative bleeding and operation time ( t = 0.81, 0.13, P > 0.05). There were statistically significant differences between the observation group and the control group in VAS (3 d, 1 month, 6 month after operation), Harris hip joint function score (1, 6 month after operation) and WOMAC score (1, 6 month after operation, t = 7.50, 11.03, 10.70, 6.20, 7.34, 7.10, 8.34, P < 0.001). The Harris hip joint function score and WOMAC score of patients in the same group between 1, 6 month after operation and pre-operation were significantly different ( P < 0.05). Conclusion:Direct anterior total hip arthroplasty is effective in the treatment of hip osteoarthritis, and can significantly improve the function of the hip joint and relieve the pain of the hip joint compared with lateral total hip arthroplasty.
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Aim To explore the protective effect of Zishen Huoxue Prescription on OGD/R-induced primary hippocampal neuron damage in rats and the possible mechanism. Methods After the isolated primary hippocampal neurons were identified by immunofluorescence, OGD/R induced neuronal damage, and the changes of autophagic flux at different re-oxygenation time were observed by confocal laser scanning microscopy. After OGD/R-induced primary hippocampal neurons were intervened with serum containing Zishen Huoxue Prescription, cell viability was detected by CCK-8, cell apoptosis was detected by flow cytometry, autophagosomes were detected by transmission electron microscopy, and autophagy-related protein expressions were detected by Western blot. Results 10% Zishen Huoxue Prescription-containing serum could significantly improve cell viability and reduce the proportion of cell apoptosis, increase the number of autophagosomes in neurons, and up-regulate the expression of autophagy-related protein PINK1, Parkin, and pATG16L1. Conclusions Zishen Huoxue Prescription can effectively resist OGD/R-induced apoptosis of primary hippocampal neurons in rats, and its effect may be related to the regulation of PINK1-Parkin pathway to promote mitophagy.
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Objective:To observe the clinical effect of total hip arthroplasty via Watson-Jone approach in treatment of hip osteoarthritis caused by advanced Kashin-Beck disease.Methods:Forty six patients with hip osteoarthritis caused by advanced Kashin-Beck disease who were admitted to Department of Orthopedics of 541 General Hospital from January 2018 to June 2019 were selected as observation subjects, of which 23 patients received the conventional posterolateral approach as the control group, and the other 23 patients received the Watson-Jone approach as the study group. The Harris scores of the hip joints, the degree of pain (visual analogue scale), and complication rate of postoperative follow-up were compared between the patients of two groups before and after operation at different time periods (3, 6, 12, 24 months).Results:The preoperative Harris scores of the study group and the control group were (36.28 ± 6.57) and (37.51 ± 6.29) points, respectively, and the difference was not statistically significant ( t = 0.65, P = 0.520); at 3, 6, 12 and 24 months after operation, the scores were (86.65 ± 5.26), (80.91 ± 5.39), (88.59 ± 5.08), (83.33 ± 5.26), (90.37 ± 4.55), (85.05 ± 4.61), (92.06 ± 4.37), and (88.72 ± 4.56) points, the differences were statistically significant ( P < 0.05). The preoperative hip pain scores of the study group and the control group were (8.08 ± 0.45) and (7.96 ± 0.49) points, respectively, and the difference was not statistically significant ( t = 0.87, P = 0.392) ; at 3, 6, 12 and 24 months after operation, the scores were (2.08 ± 0.51), (2.55 ± 0.55), (1.68 ± 0.46), (2.07 ± 0.41), (1.32 ± 0.38), (1.71 ± 0.41), (1.01 ± 0.22), and (1.18 ± 0.28) points, the differences were statistically significant ( P < 0.05). The complication rate of postoperative in the study group was 0 (0/23), which was significantly lower than that [17.39% (4/23)] of the control group (χ 2 = 4.38, P = 0.036). Conclusion:Watson-Jone approach is adopted in total hip arthroplasty for patients with hip osteoarthritis caused by advanced Kashin-Beck disease, which can significantly reduce the pain of the hip joint and improve the function of the hip joint, with fewer postoperative complications, and is conducive to postoperative rehabilitation.
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Objective: To investigate the clinical value of left ventricular function assessment in patients with cardiovascular disease by fully automatic quantified three-dimensional transthoracic echocardiography. Methods: One hundred and ninety-seven patients with cardiac diseases were examined by three-dimensional transthoracic echocardiography from September 2017 to May 2019. Data from 61 patients with grade 1 echocardiographic image quality were used to determine the default boundary values of endocardial end-diastolic and end-systolic phases. Clinical features were analyzed based on electronic medical records. The accuracy and repeatability of this strategy was evaluated by comparing left ventricular end-diastolic volume (LVEDV), end-systolic volume (LVESV) and left ventricular ejection fraction (LVEF) measured by automated quantitative three-dimensional echocardiography and those measured by conventional manual transthoracic echocardiography, the latter served as gold standard. Results: The levels of LVEDV, LVESV and LVEF measured by automatic three-dimensional echocardiography were positively correlated with values obtained by manual measurement(r=0.97,0.97, 0.98, 0.97, 0.97, 0.96;P<0.05). The levels of LVEDV and LVESV measured by full-automatic three-dimensional echocardiography were significantly higher than those obtained by manual three-dimensional echocardiography(all P<0.05). The classification and correlation of systolic dysfunction in patients with abnormal ventricular wall motion by automatic three-dimensional echocardiography were significantly improved after manual calibration (κ=0.74, P=0.00) as compared to without manual calibration (κ=0.63, P=0.00). The inter-observer and intra-observer variability of fully automated three-dimensional echocardiography were significantly smaller than manual three-dimensional echocardiography(both P<0.05). Conclusion: Fully automatic quantified three-dimensional transthoracic echocardiography possesses excellent accuracy and repeatability in measuring left ventricular volume and function, and it is feasible for clinical application.
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Humans , Cardiovascular Diseases , Echocardiography , Echocardiography, Three-Dimensional , Feasibility Studies , Stroke Volume , Ventricular Function, LeftРеферат
In the original publication, the label of Fig. 2C should be read as "GFAP/lectin/DAPI" not "DMP1/GFAP/lectin/DAPI".
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The mammalian central nervous system (CNS) is considered an immune privileged system as it is separated from the periphery by the blood brain barrier (BBB). Yet, immune functions have been postulated to heavily influence the functional state of the CNS, especially after injury or during neurodegeneration. There is controversy regarding whether adaptive immune responses are beneficial or detrimental to CNS injury repair. In this study, we utilized immunocompromised SCID mice and subjected them to spinal cord injury (SCI). We analyzed motor function, electrophysiology, histochemistry, and performed unbiased RNA-sequencing. SCID mice displayed improved CNS functional recovery compared to WT mice after SCI. Weighted gene-coexpression network analysis (WGCNA) of spinal cord transcriptomes revealed that SCID mice had reduced expression of immune function-related genes and heightened expression of neural transmission-related genes after SCI, which was confirmed by immunohistochemical analysis and was consistent with better functional recovery. Transcriptomic analyses also indicated heightened expression of neurotransmission-related genes before injury in SCID mice, suggesting that a steady state of immune-deficiency potentially led to CNS hyper-connectivity. Consequently, SCID mice without injury demonstrated worse performance in Morris water maze test. Taken together, not only reduced inflammation after injury but also dampened steady-state immune function without injury heightened the neurotransmission program, resulting in better or worse behavioral outcomes respectively. This study revealed the intricate relationship between immune and nervous systems, raising the possibility for therapeutic manipulation of neural function via immune modulation.
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Recent studies have shown that the chemokine receptor CXCR3 and its ligand CXCL10 in the dorsal root ganglion mediate itch in experimental allergic contact dermatitis (ACD). CXCR3 in the spinal cord also contributes to the maintenance of neuropathic pain. However, whether spinal CXCR3 is involved in acute or chronic itch remains unclear. Here, we report that Cxcr3 mice showed normal scratching in acute itch models but reduced scratching in chronic itch models of dry skin and ACD. In contrast, both formalin-induced acute pain and complete Freund's adjuvant-induced chronic inflammatory pain were reduced in Cxcr3 mice. In addition, the expression of CXCR3 and CXCL10 was increased in the spinal cord in the dry skin model induced by acetone and diethyl ether followed by water (AEW). Intrathecal injection of a CXCR3 antagonist alleviated AEW-induced itch. Furthermore, touch-elicited itch (alloknesis) after compound 48/80 or AEW treatment was suppressed in Cxcr3 mice. Finally, AEW-induced astrocyte activation was inhibited in Cxcr3 mice. Taken together, these data suggest that spinal CXCR3 mediates chronic itch and alloknesis, and targeting CXCR3 may provide effective treatment for chronic pruritus.
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Animals , Mice , Acetamides , Therapeutic Uses , Chemokine CXCL10 , Metabolism , Chloroquine , Toxicity , Chronic Disease , Cyclopropanes , Dehydration , Dinitrofluorobenzene , Disease Models, Animal , Formaldehyde , Toxicity , Freund's Adjuvant , Toxicity , Mice, Inbred C57BL , Mice, Knockout , Motor Activity , Pain , Pruritus , Pathology , Pyrimidines , Therapeutic Uses , Receptors, CXCR3 , Genetics , Metabolism , Skin , Pathology , Spinal Cord , Metabolism , Pathology , Time Factors , p-Methoxy-N-methylphenethylamine , ToxicityРеферат
The blood-brain barrier (BBB) is a tight boundary formed between endothelial cells and astrocytes, which separates and protects brain from most pathogens as well as neural toxins in circulation. However, detailed molecular players involved in formation of BBB are not completely known. Dentin matrix protein 1 (DMP1)-proteoglycan (PG), which is known to be involved in mineralization of bones and dentin, is also expressed in soft tissues including brain with unknown functions. In the present study, we reported that DMP1-PG was expressed in brain astrocytes and enriched in BBB units. The only glycosylation site of DMP1 is serine89 (S89) in the N-terminal domain of the protein in mouse. Mutant mice with DMP1 point mutations changing S89 to glycine (S89G), which completely eradicated glycosylation of the protein, demonstrated severe BBB disruption. Another breed of DMP1 mutant mice, which lacked the C-terminal domain of DMP1, manifested normal BBB function. The polarity of S89G-DMP1 astrocytes was disrupted and cell-cell adhesion was loosened. Through a battery of analyses, we found that DMP1 glycosylation was critically required for astrocyte maturation both in vitro and in vivo. S89G-DMP1 mutant astrocytes failed to express aquaporin 4 and had reduced laminin and ZO1 expression, which resulted in disruption of BBB. Interestingly, overexpression of wild-type DMP1-PG in mouse brain driven by the nestin promoter elevated laminin and ZO1 expression beyond wild type levels and could effectively resisted intravenous mannitol-induced BBB reversible opening. Taken together, our study not only revealed a novel element, i.e., DMP1-PG, that regulated BBB formation, but also assigned a new function to DMP1-PG.
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Animals , Female , Male , Mice , Astrocytes , Cell Biology , Metabolism , Blood-Brain Barrier , Cell Biology , Metabolism , Cells, Cultured , Extracellular Matrix Proteins , Genetics , Metabolism , Glycosylation , Proteoglycans , Metabolism , Reverse Transcriptase Polymerase Chain ReactionРеферат
OBJECTIVE@#To explore the relationship between HLA-A, -B, -C, -DRB1, -DQB1 gene polymorphism and aplastic anemia (AA)of 65 cases in Northern China.@*METHODS@#The high resolution genotyping of HLA-A, -B, -C, -DRB1, -DQB1 alleles in 65 AA patients and 772 healthy controls was performed with polymerase chain reaction-sequence specific oligonucleotide (PCR-SSO), the relationship between HLA-A, -B, -C, -DRB1, -DQB1 gene polymorphism and aplastic anemia was analyzed by Pearson Chi-square,Continuity Correction, Two-sided Fisher's Exact Test and Odds Ratio.@*RESULTS@#The HLA-B*1302(10% vs 4.21%), B*3501(7.69% vs 3.89%), DRB1* 0701(10% vs 4.73%), DRB1*0901(19.23% vs 7.58%), DQB1*0202(9.23% vs 3.76%) gene frequency in AA patients was higher than those in health controls, the difference was statistically significant (P<0.05), the χ were 9.049, 4.336, 6.838, 20.974 and 8.968, OR ratio was 2.528, 2.061, 2.239, 2.904 and 2.605. However, the HLA-A*3303(1.54% vs 6.93%), DQB1*0302(1.54% vs 6.02%) gene frequency in AA patients was lower than those in healthy controls, the difference was statistically significant (P<0.05), the χ was 5.726 and 4.505, the OR ratio were 0.210 and 0.244.@*CONCLUSION@#The polymorphism of HLA-A, -B, -DRB1, -DQB1 alleles is associate with AA in these patient cases, the HLA-B*1302, HLA-B*3501, HLA-DRB1*0701, HLA-DRB1*0901 and HLA-DQB1*0202 may be sensitive genes to AA, while the HLA-A*3303 and HLA-DQB1*0302 may be protective genes on AA.
Тема - темы
Humans , Alleles , Anemia, Aplastic , Genetics , China , Gene Frequency , Genetic Predisposition to Disease , HLA Antigens , Genetics , Polymorphism, GeneticРеферат
@#Objective To explore the possible mechanism of quercetin on apoptosis of hippocampal neurons cultured in high glucose. Methods Hippocampus was obtained from newborn 24 hours Sprague-Dawley rats and then primarily cultured.Then hippocampal neurons were divided into normal control group,high glucose group,quercetin group,quercetin+Akt inhibitor group and Akt agonist group.After each group was cultured in different conditioned medium for 72 hours,they were detected the apoptosis of neurons with flow cytometry,and the expression of Akt,p-Akt,Bcl-2 and Bax with Western blotting.Results Compared with the normal control group,the apoptosis rate of hippocampal neurons increased significantly(P<0.01),and p-Akt/Akt and Bcl-2/Bax decreased significantly(P<0.01)in the high glucose group.Compared with the high glucose group,the apoptosis rates of hippocampal neurons decreased significantly(P<0.01),and p-Akt/Akt and Bcl-2/Bax increased significantly(P<0.01)in the quercetin group and the Akt agonist group.Compared with the quercetin+Akt inhibi-tor group,the apoptosis rate of hippocampal neurons decreased significantly(P<0.01),and p-Akt/Akt and Bcl-2/Bax increased significantly (P<0.01)in the quercetin group.Conclusion Quercetin could reduce the apoptosis of hippocampal neurons cultured in high glucose,which may be achieved by increasing the phosphorylation of Akt protein in Akt signal pathway,and then increasing the expression of Bcl-2 and in-hibiting the expression of Bax.
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Objective·To establish a cell-based screening system for identification of compounds with activity in regulating retinoic acid receptor (RARα) stability. Methods·The modified pMSCV plasmid constructs, named as RARα-EGFP-IRES-DsRed, consists of enhanced green fluorescent protein (EGFP) fusing to RARα and red fluorescent protein (DsRed) as internal references incorporating the internal ribosome entry site (IRES) as interval sequence. The RARα-EGFP-IRES-DsRed plasmid was stably transfected into NB4 cells which were named as NB4-pMGIR-RARα. Fluorescence signals of EGFP and DsRed indirectly reflecting the expression of RARα, were detected by flow cytometry in cells that were treated with all-trans retinoic acid, sodium valproate, cytarabine, lenalidomide, etoposide, montelukast and gambogic acid, respectively. Effects of these compounds on the expression of RARα protein were further examined by Western blotting. Results·A double fluorescence reporter system for screening compounds that can increase the stability of RARα protein was successfully established, and sodium valproate was identified as a potent compound to promote the stability of RARα. Conclusion·The double fluorescence reporter system can be used to screen compounds regulating the stability of RARα protein, which can be further used to identify compounds regulating the stability of other proteins.
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Some patients have symptoms and signs of angina pectoris and relevant evidence of ischemia,but coronary angiography suggested no obvious coronary stenosis.Part of them is caused by coronary microcirculation dysfunction (CMD),which cannot be clinically identified early due to current techniques.Microcirculation dysfunction is corre-lated with occurrence of major clinical events,which can be used as strong predictor for prognosis.Therefore,un-derstanding of its pathological mechanism is help to guide the diagnosis and treatment.The present article made a re-view on pathological mechanism and typing of CMD.
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Some patients have symptoms and signs of angina pectoris and relevant evidence of ischemia,but coronary angiography suggested no obvious coronary stenosis.Part of them is caused by coronary microcirculation dysfunction (CMD),which cannot be clinically identified early due to current techniques.Microcirculation dysfunction is corre-lated with occurrence of major clinical events,which can be used as strong predictor for prognosis.Therefore,un-derstanding of its pathological mechanism is help to guide the diagnosis and treatment.The present article made a re-view on pathological mechanism and typing of CMD.
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Objective To investigate how human umbilical cord mesenchymal stem cells (MSCs) in vitro regulate the miRNA profile of activated peripheral blood CD4+T cells from patient with primary Sj?gren's syndrome (pSS). Methods Peripheral blood CD4+T cells from patient with pSS were sorted and divided into healthy naive group, pSS naive group, pSS activated group, MSC treatment group and MSC (pre-stimulated by IFN-γ) treatment group. CD4+ T cells were counted. MiRNA microarray technology was used to detect the expression profile of CD4+T cells, and the expression of miRNA125b and miRNA155 was verified by real time quantification-polymerase chain reaction (RT-PCR). Mean in groups were compared using ANOVA, and multiple comparisons were used with LSD method. Results Both MSCs and IFN-γ-MSCs could inhibit the proliferation of activated CD4+ T cells in a MSC-dependent manner, but there was no significant difference between two groups. Microarray analysis found that the differentially enriched miRNAs in pSS na?ve (vs healthy na?ve), pSS activation (vs pSS na?ve), MSC treatment (vs pSS activation) and pre-IFN-γ MSC treatment (vs pSS activation) were 42 miRNAs, 56 miRNAs, 21 miRNAs and 24 miRNAs, respectively. Furthermore, the expressions of miRNA125b and miRNA155 were verified by RT-PCR and found that miRNA125b relative level in 5 groups was 1.02 ±0.13, 0.80 ±0.11, 0.44 ±0.17, 0.76 ±0.17 and 0.81 ±0.15 (F=18.32, P<0.01), and miRNA155 was 1.5 ±0.8, 3.9 ±1.3, 8.4 ±2.6, 10.1 ±4.2 and 11.2 ±5.0 (F=26.65, P<0.01). Conclusion MSCs can regulate miRNA profile of activated CD4+ T cells in peripheral blood of patient with pSS, and partially reverse down-regulated miR-125b in activated CD4+T cells, which may play a regulatory role in inhibiting the activation of CD4+T cells by MSCs.
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Aim To investigate the effect of flavonoids from Prinsepia utilis Royle( FPR) on the histomorphol-ogy of kidney in diabetic mice, and to investigate its protective mechanism. Methods Diabetic mice in-duced by alloxan were given FPR orally each day for four weeks. After the administration for two and four weeks, ten mice in each group were randomly sacri-ficed. The kidneys were removed and weighed. The extracted renal tissue was embedded with paraffin and sectioned, the sections were stained with Hematoxylin and Eosin(HE)、Periodic acid Schiff(PAS) and Go-mori, and then observed under the microscopy. 1mm3 of renal cortex fixed with glutaral in four centi-degree , and then the ultrastructure of each group was observed under the electron microscope respectively after four weeks′ treatment. Results Compared with the model control group, in the treatment group, observation un-der the microscopy showed that glomerular volume and mesangial cells reduced, FPR could relieve thickening of the glomerular basement membrane ( GBM ) , little inflammatory cells infiltrated in the interstitium,tubular epithelial cells almost became normal, renal tubule had little glucogen, fiber decreased in the interstitium of renal tubule. Observation under the electron micro-scope indicated that foot process in podocytes lined up in order, mitochondria of the renal tubule’ s epithelial cell almost recovered. Conclusion FPR can relieve the changes of renal pathology,improve renal function, and delay the progression of pathologic changes of kid-ney in diabetic mice partly through reducing the blood glucose and the blood lipid.
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<p><b>OBJECTIVE</b>To investigate the correlation between genotypes and biochemical phenotypes of phenylalanine hydroxylase (PAH) in patients with phenylketonuria (PKU).</p><p><b>METHODS</b>Thirteen exons and flanking introns of PAH gene in 102 patients with high blood phenylalanine levels (Phe > 120 umol/L) at initial diagnosis were amplified with polymerase chain reaction and analyzed with single strand conformation polymorphism (SSCP), denaturing high performance liquid chromatography (DHPLC) and DNA sequencing. Correlation between genotypes and biochemical phenotypes was analyzed.</p><p><b>RESULTS</b>Biochemical assaying has indicated that 69 patients had classical PKU (Phe> 1200 umol/L), 31 were moderate (Phe 600-1200 umol/L), and 2 were mild (Phe 400-600 umol/L). More than 41 mutations and 75 genotypes have been identified. There were 9 (8.8%) homozygous mutations, which included 3 cases with R111X/R111X, 1 case with IVS4-1G>A/IVS4-1G>A, 3 cases with R243Q/R243Q and 2 cases with V399V/V399V. Among these 8 belonged to classic PKU phenotypes, except for a R243Q/R243Q genotype which has led to a moderate phenotype. In 91 patients carrying compound PAH mutations, 61 were classic, 29 were moderate, and 1 was mild. Patients who were heterozygous for R111X/R243Q and EX6-96A>G(Y204C)/R243Q were found with both classic and moderate PKU phenotypes. Certain individuals who have carried 2 null mutant alleles such as R111X/V399V, EX6-96A>G/Y356X and EX6-96A>G/V399V only showed a moderate phenotype. Individuals with R111X/A165D and R176X/A165D genotypes, on the other hand, respectively presented moderate and classic PKU phenotypes.</p><p><b>CONCLUSION</b>Ninety percent of our patients are compound heterozygotes. Independent assortment of mutant alleles has resulted in a complex genotype-phenotype correlation. Although in most cases a correlation may be found, caution should still be taken upon genetic counseling. The phenomena where similar or even identical genotype may give rise to different biochemical phenotypes have implied that other factors may also influence the phenylalanine metabolism.</p>