Objective To review the research progress of ultrasound in the diagnosis and treatment of shoulder diseases, in order to provide a theoretical basis for the further development of ultrasound in shoulder surgery. Methods The recent literature on the application of ultrasound in the shoulder joint was extensively reviewed. The application of ultrasound in the diagnosis and treatment of shoulder joint diseases, and the advantages and disadvantages of ultrasound were analysed, and the development trend of ultrasound technology in the shoulder joint area was prospected. Results At present, the diagnosis of shoulder joint diseases mainly relies on MRI, however, with the development of ultrasound technology, ultrasound with the characteristics of convenient, reliable, and real-time dynamic evaluation is more and more recognized in the diagnosis process of shoulder joint diseases, combined with three-dimensional ultrasound, ultrasound intervention, and elastography can improve the accuracy, sensitivity, and specificity of the diagnosis, and is suitable for the diagnosis and treatment of various shoulder joint diseases, which is expected to carry out early prevention of shoulder joint diseases in the future and achieve more refined and minimally invasive treatment. ConclusionUltrasound technology has wide application prospect in shoulder joint diseases, but it is still in the developing stage, and the subjective dependence needs to be solved further.
Objective To review the progress of a disintegrin and metalloproteinase with thrombospondin motif 4 (ADAMTS-4) and ADAMTS-5 in osteoarthritis. Methods Recent literature about the ADAMTS-4 and -5 in osteoarthritis was analyzed; the structure, function, inhibitors of the ADAMTS-4 and -5, and the relationship between the proteases and osteoarthritis were analyzed and summarized. Results ADAMTS-4 and -5 can reduce chondrocyte and extracellular matrix by degrading aggrecan and cartilage oligomeric matrix protein, which induced the pathogenesis of osteoarthritis. Conclusion ADAMTS-4 and -5 have been demonstrated to play important roles in osteoarthritis. It can better guide treatment and prevention of osteoarthritis to further study related mechanism of ADAMTS-4 and -5, and to promote the establishment of a clinical drug targets.
Objective To investigate the effect of adenovirus vector mediated transfer of human herpes simplex virus thymidine kinase (HSVtk) gene inhibits intimal hyperplasia of vein grafts. Methods Auto vein graft models of Wistar rats were established. Adenovirus vector dwelled in cervical veins which were transplanted into inferior renal abdominal aorta. The combination of HSVtk (4×109 plaque forming units) and ganciclovir (GCV) was applied to test the inhibition effect. GCV was infused 〔60 mg/(kg·d), IP, Bid〕 from day 3 to day 21 after transplantation. Vein samples were harvested and the existence of HSVtk DNA was measured by PCR and the mRNA of it was studied by in situ hybridization. Van gieson (VG) and proliferating cell nuclear antigen (PCNA) stains were carried out in paraffin sections to study the thickness of neointima and smooth muscle cells (SMCs) proliferation with a computer-assisted analysis system. The apoptosis of SMCs also was detected by TUNEL. Results The existence of HSVtk gene in veins and its transcription were demonstrated. Morphometric analysis demonstrated a reduced intima thickness in the group receiving combination therapy (HSVtk/GCV) compared with HSVtk alone 〔(17.2±3.2) μm versus (31.1±2.5) μm, P＜0.05〕. GCV per se had no effect on intimal hyperplasia after vein transplantation. The apoptosis of SMCs increased significantly and expression of PCNA decreased in HSVtk/GCV gene therapy group versus blank control group 〔(9.1±2.3)% vs (28.7±3.6)%, P＜0.05; (38.7±5.6)%vs (18.5±2.6)%, P＜0.05〕. Conclusion GCV conditions reduction of intimal hyperplasia after intraluminal delivery of HSVtk in transplanting vena veins involving SMCs apoptosis.
Objective To observe the changes of retinal nerve fiber layer (RNFL) thickness in patients with Alzheimer's disease (AD). Methods Twenty eyes of 40 patients with mild and (or) moderate AD confirmed by clinical examination (AD group) were included in the study. There were 11 males and 9 females with an average age of (72.75±8.25) years. Age and gender-matched normal 20 objectives were in the normal control group. Among them, there were 11 males and 9 females with a mean age of (71.05±7.08) years. There was no significant difference in gender composition, age and intraocular pressure between the two groups (P＞0.05). There were significant differences in visual acuity, cup disc ratio and mini-mental state examination score (P＜0.05). All eyes underwent high-resolution optical coherence tomography (OCT) examination. With a diameter of 3.4 mm and a center on the center of the optic disc, circular fast scans on optic disc were performed to obtain an average disc RNFL thickness, signal threshold ＞6. Computer image analysis system was used to measure the RNFL thickness from superior, inferior, temporal and nasal quadrants, and the average RNFL thickness. The changes of RNFL thickness between the two groups and between different eyes of the same group were compared. Results Compared with the normal control group, the average (t=5.591), superior (t=8.169, 8.053) and inferior (t=12.596, 11.377) thickness of RNFL in both eyes in AD group were thinner, the differences were significant (P＜0.05); the temporal (t=1.966, 0.838）and nasal (t=2.071, 0.916) thickness of RNFL in both eyes of AD group were thinner, but the difference was not statistically significant (P＞0.05). There was no significant difference of the mean and different quadrant RNFL thickness between different eyes in AD group and normal control group (AD group: t=0.097, 0.821, 0.059, 0.020, 0.116; normal control group: t=0.791, 1.938, 1.806, 2.058, 1.005; P＞0.05). Conclusion The RNFL thickness around the optic disc in AD patients is thinner; This occurs first in superior and inferior quadrants of the optic disc.
Objective To investigate the influence of RNA interference targeting c-Jun gene on the proliferation of rat vascular smooth muscle cells (VSMCs). Methods The experiment was performed with c-Jun siRNA （c-Jun siRNA group）, control reverse sequence siRNA (control siRNA group) or no siRNA (control group). VSMCs were transfected with siRNA targeting c-Jun gene by liposome. Effects of c-Jun siRNA on mRNA and protein expressions of c-Jun were examined by RT-PCR analysis and Western blot respectively. MTT test and 3H-TdR incorporation were used to detect VSMCs proliferation. Cell cycle analysis of VSMCs in vitro was determined by flow cytometer. Results The expression levels of mRNA and protein of c-Jun in c-Jun siRNA group were significantly lower than those in control group （P＜0.05， P＜0.01). There was no significant difference between control group and control siRNA group （Pgt;0.05）. Proliferation activity of VSMCs decreased significantly in c-Jun siRNA group compared with that in control group （P＜0.05） and VSMCs was blocked in the G0/G1 phase of cell cycle significantly （P＜0.05）. There was no significant difference between control group and control siRNA group （Pgt;0.05）. Conclusion c-Jun gene silenced by RNA interference can inhibit VSMCs proliferation effectively in vitro.
Diabetes mellitus patients have the characteristics of higher morbidity of ischemic stroke, severe symptoms, more recurrent stroke and higher mortality. Current studies have shown that stroke patients with or without diabetes mellitus have different pathophysiological mechanisms during stroke progress. Accordingly, treatment that is beneficial to non-diabetes mellitus patients may not be beneficial to diabetes mellitus stroke patients. This article reviews the current research status of pathophysiological mechanism of diabetes mellitus complicated with ischemic stroke, and provides reference for the relevant research of drug intervention in diabetes mellitus patients complicated with stroke.
Objective To explore the potential mechanism of Shuganning injection for non-alcoholic fatty liver disease (NAFLD) through network pharmacology and molecular docking techniques. Methods Information on the active compounds of Shuganning injection and their target proteins, as well as disease-related targets of NAFLD, were collected from multiple public databases from May 23rd to 28th, 2024, for protein interaction network analysis and pathway enrichment analysis. A multi-level network of “herb-compound-target-disease” of Shuganning injection for NAFLD was constructed. Molecular docking was performed on the top 5 key active compounds ranked in the degree centrality of the “core target-active compound” network and the core action targets. Results Finally, 140 active compounds of Shuganning injection and 486 potential targets, 1058 NAFLD-related targets, 154 common targets for NAFLD and Shuganning injection were obtained. Topological analysis of the common target protein interaction network identified 16 key target proteins of protein kinase B1, peroxisome proliferator-activated receptor alpha, peroxisome proliferator-activated receptor gamma, sterol regulatory element-binding protein 1, interleukin-6, and matrix metalloproteinase-9, etc. The gene ontology enrichment analysis showed that their genes were involved in 179 biological processes, 13 cellular components, and 48 molecular functions. The Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that their genes were involved in 99 pathways of cancer, lipid and atherosclerosis, NAFLD and insulin resistance, etc. The constructed multi-level network of “herb-compound-target-disease” consisted of 102 nodes and 208 edges. The molecular docking results showed that the 5 key active compounds of baicalin, acacetin, sitosterol, β-sitosterol, and ganoderic acid A had high affinity for the core target proteins. Conclusion Shuganning injection may exert therapeutic effects on NAFLD through active compounds like baicalin, acacetin, sitosterol, β-sitosterol and ganoderic acid A, acting on key target proteins such as protein kinase B1, peroxisome proliferator-activated receptor alpha, peroxisome proliferator-activated receptor gamma, sterol regulatory element-binding protein 1, interleukin-6, and matrix metalloproteinase-9, regulating pathways related to lipids and atherosclerosis, NAFLD, and insulin resistance.
ObjectiveTo evaluate the most efficient method for transfection of human umbilical cord mesenchymal stem cells (HUMCSs) in vivo. MethodsHUCMSCs were isolated from human umbilical cord and cultured, which were labelled by PKH26 and lentivirus-GFP, then were observed by using a fluorescence microscope. Sixty SD rats were randomly divided into PKH26 transfection group and lentivirus-GFP transfection group. The right hepatic lobe of rat was resected, then the transfected stem cells were injected into portal vein. The rats were sacrificed on day 3, 8, and 13 after transfection. The liver specimens were observed by using a fluorescence microscope. Flow cytometry was used to evaluate the percentage of transfected stem cells and the apoptotic stem cells. ResultsThe third generation of HUCMSCs labelled by PKH26 and lentivirus-GFP were spindle shaped. PKH26 red dye was evenly distributed in the cell membrane of HUCMSCs and could be clearly labelled. The HUCMSCs labelled by lentivirus-GFP were green fluorescence under the fluorescence microscope, and it was clear and stable. The HUCMSCs were clear and could be clearly distinguished on day 3 after transfection by two methods in vivo. As the time went by, red was faded and blurred, then was gradually disappeared on day 13 after transfection in the HUCMSCs stansfected by PKH26; but the color in the HUCMSCs stansfected by lentivirus-GFP were clear at all the time points. The transfection rate of the lentivirus-GFP was significantly higher that that of the PKH26 (P < 0.05), the rate of apoptotic stem cells had no significant differences at all the time points between these two groups (P > 0.05). ConclusionLentivirus-GFP transfection is a higher efficient method for stem cell labelling in vivo, it could be used to observe transplantation cells for a long time in future.
ObjectiveTo investigate the expression of extracellular signalregulated kinase (ERK) and p38 mitogenactivated protein kinase （p38 MAPK） in autogenous vein grafts during vascular remodeling.MethodsAn autogenous vein graft model was established by transplanting the right jugular vein to infrarenal abdominal aorta in 80 Wistar rats. Vein graft samples were harvested 6 hours, 24 hours, 3 days, 7 days, 2 weeks, 4 weeks, 6 weeks and 8 weeks after surgery. Gene expression of ERK and p38 MAPK was measured by reverse transcriptionPCR. Western blot was used to detect the expression of protein products and phosphorylation protein products of ERK and p38 MAPK. Apoptosis of vascular smooth muscle cells (VSMCs) was determined by TUNEL. Proliferating cell nuclear antigen(PCNA) of VSMCs also was studied.ResultsThe expression of ERK1 mRNA and p38 MAPK mRNA increased considerably after surgery. ERK1 mRNA reached the peak on the 7th day 〔（33.2±14.2）%, P＜0.01〕, but p38 MAPK mRNA reached the peak on the second week after surgery 〔(58.8±26.2）%, P＜0.01〕. The expression of ERK1/2 detected by western blot reached the peak during 1 to 2 weeks and decreased gradually to normal level 6 weeks after surgery. The expression of p38 MAPK reached the peak during 2 to 4 weeks and decreased to 1/4 to 1/2fold 8 weeks after surgery. There was a positive relationship between ERK1 and PCNA(r=0.759 6，P＜0.01) and a positive relationship between p38 MAPK and apoptosis(r=0.892 2，P＜0.01). ConclusionActivation of MAPK system exists in autogenous vein grafts and it may become a new target for the therapy of stenosis after vein grafts.