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Acupuncture is a typical example of Traditional Chinese Medicine and has been used in China for hundreds of years to treat a wide range of illnesses. However, in the clinic, issues and deficiencies were primarily seen in four areas: loss of accuracy in the operation process; difficulty understanding the depth of acupuncture; difficulty using reinforcing and reducing techniques; and lack of a clear dynamic effect of acupuncture points following acupuncture. Musculoskeletal ultrasonography may quantitatively evaluate the acupuncture location and display the distribution of small nerves near and within the fascia of the acupuncture point in real time. The subjects were asked how they felt about receiving Qi when the needle body reached different depths and different tissues. The Qi obtained from an acupuncture point and the connective tissue of the fascia can be further understood by combining the physiological response of the acupuncture point with the anatomical structure, which offers a new method for defining the nature of the acupuncture point and standardizing the acupuncture point.
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Pontos de Acupuntura , Terapia por Acupuntura , Ultrassonografia , Humanos , Terapia por Acupuntura/métodos , Ultrassonografia/métodos , Sistema Musculoesquelético/diagnóstico por imagemRESUMO
[This corrects the article DOI: 10.3389/fphar.2022.795613.].
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Ethnopharmacological relevance: Astragalus polysaccharide (APS), the most biologically active ingredient of Astragali Radix, is used to treat diabetes mellitus (DM)-related chronic wounds in traditional Chinese medicine for several decades. This herb possesses an anti-inflammatory effect. Our study proved that APS can reduce excessive inflammation at the late phase of wound-healing in diabetic ulcers. Aim of the study: To clarify the molecular mechanism of APS in promoting wound-healing via reducing excessive inflammation in diabetic ulcers during the late stages of wound-healing. Methods and materials: The rat model of the diabetic ulcers was established via intraperitoneal injection of streptozocin (60 mg/kg). We detected the regulation of APS on diabetic ulcers by measuring wound-healing rates. Bioinformatics was used to predict the target genes of APS, and autodocking was used to predict the combination of APS and target genes. Immunohistochemistry, Enzyme-linked immunosorbent assay, Western blot, immunofluorescence staining, flow cytometry, and flow cytometric sorting were investigated. Results: The results demonstrated that APS promoted wound-healing and inhibited excessive inflammation at the late phase of wound-healing in diabetic rats. Mechanistic findings showed that APS promoted the expression of ß-catenin and Rspo3 while inhibiting the expression of NF-KB and GSK-3ß, which leads to the transformation of M1-type macrophages into M2-type macrophages and thus reducing excessive inflammation at the late phase of wound-healing in diabetic ulcers. Conclusion: We found an interesting finding that APS promoted the polarization of macrophages towards M2-type through the ß-catenin/NF-κB axis to reduce excessive inflammation at the late phase of wound-healing. Therefore, APS may be a promising drug for treating diabetic ulcers in clinic.
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Algae, which are ubiquitous in ecosystems, have evolved a variety of light-harvesting complexes to better adapt to diverse habitats. Phycobilisomes/phycobiliproteins, unique to cyanobacteria, red algae, and certain cryptomonads, compensate for the lack of chlorophyll absorption, allowing algae to capture and efficiently transfer light energy in aquatic environments. With the advancement of microscopy and spectroscopy, the structure and energy transfer processes of increasingly complex phycobilisomes have been elucidated, providing us with a vivid portrait of the dynamic adaptation of their structures to the light environment in which algae thrive: 1) Cyanobacteria living on the surface of the water use short, small phycobilisomes to absorb red-orange light and reduce the damage from blue-violet light via multiple methods; 2) Large red algae inhabiting the depths of the ocean have evolved long and dense phycobilisomes containing phycoerythrin to capture the feeble blue-green light; 3) In far-red light environments such as caves, algae use special allophycocyanin cores to optimally utilize the far-red light; 4) When the environment shifts, algae can adjust the length, composition and density of their rods to better adapt; 5) By carefully designing the position of the pigments, phycobilisomes can transfer light energy to the reaction center with nearly 100% efficiency via three energy transfer processes.
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Cianobactérias , Ficobilissomas , Ficobilissomas/química , EcossistemaRESUMO
Objective Alpha-1-acid glycoprotein (ORM) was a new target for the development of weight loss drugs. To search for potential weight loss drugs that could target ORM from the compound library of already marketed drugs based on drug repurposing. Methods The pGL4.20-ORM1 promoter recombinant plasmid was contructed and validated, and then a lentiviral vector was utilized to establish stable AML12 cell lines expressing ORM1 promoter-LUC-PURO. This cell line was employed for high-throughput screening of compounds from the marketed drug library, and the luminescence value of the cells was characterized by enzyme marker. Results Primary screening and secondary screening of 1 470 compounds identified 42 compounds that increased ORM1 promoter expression and could be used for further weight loss effect assessment. Conclusion This study successfully constructed LV-AML12-ORM1 promoter-LUC-PURO stable expression cell lines using lentiviral vectors, laying a foundation for efficient and stable screening of weight loss drugs targeting ORM.
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Objective To calculate the absorbed doses and conversion coefficients of various organs in humans after oral administration of urea-14C, and to provide a convenient method for evaluating the internal radiation dose caused by ingestion of urea-14C in Chinese population. Methods The Chinese reference human voxel model was imported into the FLUKA software to simulate the absorbed doses to organs under internal exposure to 14C, and to obtain the dose conversion coefficients for oral administration of urea-14C. Results The absorbed dose conversion coefficients for the stomach, colon, bladder, heart, and muscles were 0.029, 0.029, 0.32 (0.24), 0.028, and 0.029 mGy/MBq in negative cases, and 0.079, 0.078, 0.18 (0.15), 0.076, and 0.080 mGy/MBq in positive cases. The committed effective dose coefficients were 0.041 (0.037) mSv/MBq in negative cases and 0.082 (0.081) mSv/MBq in positive cases. Conclusion The dose conversion coefficients obtained in this study can provide important parameters for evaluating the absorbed dose to Chinese population after oral administration of urea-14C.
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Objective:To investigate the protective effect of naringenin on acute lung injury related with sepsis; To discuss its possible mechanism.Methods:Totally 30 male SD rats were randomly divided into sham-operation group, model group, naringin low-, medium- and high-dosage groups, with 6 rats in each group. The sepsis-related acute lung injury model was established by cecal ligation and puncture in all groups except the sham-operation group. After modeling, naringin low-, medium- and high-dosage groups were given naringin 20 mg/kg, 40 mg/kg and 80 mg/kg, respectively for gavage, while the sham-operation group and the model group were given the same volume of distilled water by gavage, once a day, for 2 days. Pathological changes in lung tissue were observed using HE staining. The levels of 1L-1, IL-6 and IL-18 in bronchoalveolar lavage fluid (BALF) were measured by ELISA; the expression of TNF-α in lung tissue was detected by immunofluorescence histopathology; the expressions of TGF-β1, TGF-βR1 and Smad2 were detected by Western Blot. An agonist group and a naringin plus agonist group were set up, with 6 mice in each group, and the expressions of TGF-β1 and Smad2 protein in the lung tissue of each group were detected by immunohistochemical staining to verify the effect of naringin on the expressions of TGF-β1 and Smad2 protein.Results:Compared with the model group, the pathological injury of lung tissue in naringin groups were obviously alleviated, and the levels of IL-1β, IL-6 and IL-18 in BALF decreased ( P<0.01), the protein expressions of TNF-α, TGF-β1, TGF-βR1 and Smad2 in lung tissue decreased ( P<0.01 or P<0.05). Further verification found that the expressions of TGF-β1 and Smad2 in the agonist group increased ( P<0.01), while the expressions of TGF-β1 and Smad2 in the naringin agonist group decreased ( P<0.01). Conclusion:Naringin can reduce the inflammatory response in the lung of the rats to protect against sepsis-related acute lung injury, and its protective effect could be related to the inhibition of the TGF-β1/Smad2 signaling pathway.
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Fever of unknown origin(FUO)is a difficulty in clinical diagnosis and treatment.Patients with FUO come to seek medical consultation usually with fever as the main complaint,and the accompanying symptoms and signs are generally atypical.The pathogenesis of FUO remains conflicting in the field of modern western medicine,and its treatment is still focused on empirical anti-inflammatory management,which has the deficiency of delayed diagnosis,limited therapeutic options,poor therapeutic effects,and obvious adverse reactions.In the field of traditional Chinese medicine(TCM),FUO generally results from the dysfunction of zang-fu organs and the imbalance of yin and yang,and has the clinical features of long duration of illness,unknown etiology,complexity of illness,recurrent attacks,and difficult to be cured.Based on the six-meridian syndrome differentiation,Chief Physician LI Chuang-Peng pointed out that the pathogenesis of FUO is characterized by the combined disease of shaoyin and yangming,and put forward the therapeutic principle of warming shaoyin and unblocking yangming.He proposed the use of Dahuang Fuzi Decoction(mainly composed of Rhei Radix et Rhizoma and Aconiti Lateralis Radix Praeparata)plus Yiyi Fuzi Baijiang Powder(mainly composed of Coicis Semen,Aconiti Lateralis Radix Praeparata and Patriniae Herba)to subside fever and eliminate pathogen,together with Asari Radix et Rhizoma for guiding the medicine directly to the shaoyin.Moreover,therapies of strengthening and activating spleen and stomach,nourishing yin to produce fluid,and unblocking the blood vessels can be used for eliminating the pathogen and supporting the healthy qi.
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AIM To identify the endophytic fungus G-(JK)-2 from Orixa japonica Thunb.and to study its secondary metabolites and their α-glucosidase inhibitory activities.METHODS Through the ITS sequence,the evolutionary tree that identifies the endophytic fungus G-(JK)-2 was established.Then 45 days rice solid medium of endophytic fungus G-(JK)-2 was extracted by methanol,and then by ethyl acetate.The ethyl acetate extract was separated and purified by silica gel chromatography,Sephadex LH-20,and semi-preparative HPLC.The structures of obtained compounds were identified by physicochemical properties and spectral data.Their α-glucosidase inhibitory activities were evaluated by PNPG method.RESULTS The endophytic fungus G-(JK)-2 from O.japonica was identified as Fusarium nematophilum.Thirteen compounds were isolated and identified as p-hydroxybenzaldehyde(G1),4-hydroxyacetophenone(G2),anhydromevalonolactone(G3),flazine(G4),salicylic acid(G5),p-hydroxybenzoic acid(G6),di-(2-ethylhexyl)-phthalate(G7),terephthalic acid bis(2-ethyl-hexyl)ester(G8),thymine(G9),uridine(G10),adenosine(G11),2′-deoxyuridine(G12),nicotinic acid(G13).The inhibitory effect of each compound on α-glucosidase was in sequence of G4>G11>G10>G13>G12.CONCLUSION All compounds are first isolated from the endophytic fungi of the O.japonica,and G10,G11,G13 are first isolated from the endophytic fungi of Fusarium.G4 and G11 have mild inhibition to α-glucosidase.
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Tumor progression is closely related to tumor tissue metabolism and reshaping of the microenvironment. Oral squamous cell carcinoma (OSCC), a representative hypoxic tumor, has a heterogeneous internal metabolic environment. To clarify the relationship between different metabolic regions and the tumor immune microenvironment (TME) in OSCC, Single cell (SC) and spatial transcriptomics (ST) sequencing of OSCC tissues were performed. The proportion of TME in the ST data was obtained through SPOTlight deconvolution using SC and GSE103322 data. The metabolic activity of each spot was calculated using scMetabolism, and k-means clustering was used to classify all spots into hyper-, normal-, or hypometabolic regions. CD4T cell infiltration and TGF-β expression is higher in the hypermetabolic regions than in the others. Through CellPhoneDB and NicheNet cell-cell communication analysis, it was found that in the hypermetabolic region, fibroblasts can utilize the lactate produced by glycolysis of epithelial cells to transform into inflammatory cancer-associated fibroblasts (iCAFs), and the increased expression of HIF1A in iCAFs promotes the transcriptional expression of CXCL12. The secretion of CXCL12 recruits regulatory T cells (Tregs), leading to Treg infiltration and increased TGF-β secretion in the microenvironment and promotes the formation of a tumor immunosuppressive microenvironment. This study delineates the coordinate work axis of epithelial cells-iCAFs-Tregs in OSCC using SC, ST and TCGA bulk data, and highlights potential targets for therapy.
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Humanos , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas de Cabeça e Pescoço , Neoplasias Bucais/metabolismo , Terapia de Imunossupressão , Fator de Crescimento Transformador beta , Neoplasias de Cabeça e Pescoço , Perfilação da Expressão Gênica , Microambiente TumoralRESUMO
Objective To establish normal reference values for left ventricular trabecular and papillary muscle mass(TPMM)in Chinese adults using MRI and to explore its impact factors.Methods A total of 168 healthy Chinese adults were retrospectively included,and compacted and total left ventricular myocardial mass(LVM)were measured using traditional and dedicated methods,respectively.TPMM was calculated from the difference between total and compacted LVM.Independent sample t-tests and analysis of variance were used to explore the differences in TPMM among genders and age groups,while multiple linear regression was used to explore the independent correlation between TPMM and age,gender,heart rate,systolic blood pressure(SBP),fasting blood glucose(FBG),and body mass index(BMI).Results TPMM for men was significantly larger than that for female(P<0.001).TPMM in the elderly group was significantly larger in female(P<0.05),but not in men.Multiple linear regression showed that BMI and SBP were both independently positively correlated with TPMM,and female and heart rate were independently negatively correlated with TPMM(P<0.05).Conclusion This study provides age-and gender-specific normal reference values for TPMM in Chinese adults.Gender,heart rate,BMI,and SBP are all independently associated with TPMM.
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Objective To conduct an epidemiological survey of common congenital heart disease(CHD)among children in ethnic minority areas in southeastern Guizhou and to explore the influencing factors of delayed medical treatment.Methods From January 2019 to July 2022,18 850 children aged 3 months to 14 years in Qiandongnan Miao and Dong Autonomous Prefecture were selected;105 children with CHD were included in the training set,and they were divided into delayed group(80 cases)and non-delayed group(25 cases)according to whether or not to delay medical treatment.In addition,children with CHD(35 cases)from July 2022 to December 2022 were included in the validation set.The general data of the subjects in the two groups were compared and ana-lyzed.Multivariate logistic regression was performed and risk scoring model was constructed.Results The preva-lence of CHD in 18 850 children was 5.57‰(105/18 850),with the highest prevalence in Liping County,and the lowest in Huangping County.The proportion of children with secondary atrial septal defect was the highest,and that of the aortic valve malformation was the lowest.Among the complex cases of CHD,the proportion of children with single type was the highest,and that of children with three or more types were the lowest.Among children with CHD,the rate of delayed medical treatment was 76.19% (80/105).The median delay in medical treatment was 12 months,with an average of(18.78±4.77)months.Multifactor logistic regression analysis showed that heart murmur(level 2~3),less-educated(primary and secondary school)guardian,family per capita income<2 000 yuan,and frequent drinking of the guardian were independent risk factors for delayed medical treatment(P<0.05),and commercial settlement of medical expenses was independent protective factor(P<0.05).Risk scoring model divided the children into three groups:low risk(≤80 points),medium risk(>80 points and≤134 points)and high(>134 points)risk group.The evaluation of the model show that it was accurate,effective,safe,and reliable.Conclusion The highest prevalence is observed in Liping County.The proportion of children with secondary atrial septal defect and the proportion of children with single type are the highest.Delayed medical treat-ment is found in most of the children with CHD.Cardiac murmur,education background of the guardian,per capita family income,guardian alcohol consumption,and medical expense settlement method are all independent influencing factors for delayed medical treatment.
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Acute respimtory distress syndrome(ARDS)is an acute diffuse inflammatory lung injury caused by various internal and external lung injury factors.It has complex pathogenesis,rapid onset and high mortality,which seriously endangers human life and health.Pulmonary fibrosis is one of the important pathologic processes of ARDS occurrence and development,and it is also an important cause of death in ARDS patients.To a certain extent,the severity of pulmonary fibrosis in ARDS is determined by the dynamic balance of macrophage-fibroblast interactions.Therefore,this article aims to review the interaction mechanism of macrophage-fibroblasts in the pro-cess of ARDS pulmonary fibrosis,and provide new methods and ideas for the diagnosis and treatment of ARDS pul-monary fibrosis.
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ObjectiveTo understand the characteristics of PM2.5 pollution in the air of Pearl River Delta city in Guangdong Province under the COVID-19 epidemic and the health risks of inhaling elements in PM2.5. MethodsIn 2022, 10 PM2.5 monitoring points were set up in 10 districts in Guangzhou, Shenzhen, Foshan and Zhuhai, and air samples were collected for 7 consecutive days every month to analyze the concentration of PM2.5 and the 12 elements in PM2.5. The classic "four-step" method was used to evaluate the carcinogenic risk and chronic non-carcinogenic risk of the elements in air PM2.5 on health. The age-sensitive characteristics of metal elements were combined in the carcinogenic risk assessment, and age-sensitive factors were introduced to analyze the impact of air pollution on population health. ResultsA total of818 samples were collected. and the average annual PM2.5 concentration in the four cities of the Pearl River Delta was 30.17 (1.00-166.00, s=21.06) μg·m-3, which was lower than the concentration limit of the secondary standard of the Ambient Air Quality Standard (GB 3095-2012). The difference of PM2.5 concentration in the four cities was statistically significant. The PM2.5 concentrations in Zhuhai and Shenzhen, which were located near the sea, were lower than those in Guangzhou and Foshan. The monthly mean concentration of PM2.5 in the four cities was the lowest at 13.70 (4.00-34.00, s=5.93) μg·m-3 in July and the highest at 57.73 (14.00-146.00, s=27.96) μg·m-3 in January, showing a low concentration from May to October and a high concentration from November to April of the following year. The average daily PM2.5 concentration exceeded the secondary standard for 29 days, mainly distributed in January and November. The average annual mass concentration of elements in PM2.5 in the four cities was Al>Mn>Pb>As>Ni>Cr>Se>Sb>Cd>Tl>Be>Hg. AS and Mn have chronic non-carcinogenic risk in population, while Cr, AS, Cd, Be and Ni have carcinogenic risk in population. ConclusionThe PM2.5 pollution levels of the four cities in the Pearl River Delta are low and variable. Coastal cities are lower than non-coastal cities, which shows the characteristics of first decreasing and then increasing throughout the year. The order of mass concentration of metal elements of PM2.5 in four cities is basically the same except Be and Ni. As and Mn in PM2.5 show a certain degree of chronic non-carcinogenic risk, and As, Cr, Cd, Ni and Be have a certain degree of carcinogenic risk. The four cities need to take effective intervention measures to continue to strengthen the pollution control and health protection of Cr, As, Cd and Mn in the air, and control the health burden caused by air pollution.
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Objective To evaluate the pharmacodynamics of astragaloside Ⅳ derivatives for chronic heart failure, screen the candidate compounds and preliminarily explore the mechanism of the candidate compound HHQ16 against heart failure. Methods Chronic heart failure was induced by left anterior descending artery ligation in C57BL/6 mice for 4 weeks, and the mice were divided into 4 groups, including sham group, model group, positive control captopril group, and astragaloside Ⅳ derivatives group. After continuous intragastric administration for four weeks, the cardiac function was detected by echocardiography, and the optimal astragaloside Ⅳ derivative HHQ16 was selected for the treatment of heart failure. The preliminary mechanism for HHQ16 was further explored. The size of heart was observed by gross morphology; pathological changes were observed by HE staining; collagen deposition in the myocardium was observed by Masson staining; protein levels of myocardial fibrosis indexes COL1, COL3, and αSMA were detected by immunohistochemical staining, and mRNA levels of myocardial fibrosis indexes COL1, COL3, αSMA, and TGF-β1 were determined by qPCR technique. Results All astragaloside Ⅳ derivatives significantly improved cardiac function with increasing LVEF and LVFS, of which HHQ16 was the optimal compound. Compared with the model group, the heart volume of HHQ16 group was significantly reduced; myocardial hypertrophy was reduced; collagen deposition in myocardial tissues was reduced; and myocardial fibrosis indexes, COL1, COL3, αSMA and TGF-β1 mRNA levels, as well as the protein levels of COL1, COL3 and αSMA were significantly reduced. Conclusion HHQ16 is an optimal astragaloside Ⅳ derivatives for the treatment of chronic heart failure in mice, which could improve cardiac function by improving myocardial remodeling, and inhibit myocardial hypertrophy and myocardial fibrosis.
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Objective:To explore the feasibility of using self-made visual throat forceps to remove hypopharyngeal foreign bodies. Methods:The throat forceps were combined with the endoscope and connected to a monitor via a data cable resulting in a visual throat forceps apparatus. This device was utilized to examine and treat the hypopharyngeal foreign bodies. Results:Among 53 patients, foreign bodies were detected in 51,with 48 cases involving hypopharyngeal foreign bodies. All were successfully extracted using the visual throat forceps. Three cases, diagnosed as esophageal foreign bodies by electronic gastroscopy, were treated using the same method. Conclusion:Visual throat forceps can be used to examine the hypopharynx and remove foreign bodies. It has the advantages of simple operation, rapid operation, and high success rate of foreign body removal from the hypopharynx. It is worthy of clinical application.
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Humanos , Hipofaringe/cirurgia , Faringe/cirurgia , Endoscópios , Instrumentos Cirúrgicos , Corpos Estranhos/diagnósticoRESUMO
BACKGROUND:CXC motif chemokine 5(CXCL5)is a neutrophil activating peptide derived from epithelial cells,which may be involved in arterial diseases.However,there is yet no report on the effect of CXCL5 in vascular calcification. OBJECTIVE:To explore the role of CXCL5 in the vascular calcification of carotid atherosclerosis(CAS). METHODS:(1)Cytological experiment:Mouse vascular smooth muscle cells(VSMCs)were divided into five groups:osteogenic medium group,Vector group(vector,blank plasmid transfected into VSMCs),CXCL5 group(CXCL5 plasmid transfected into VSMCs),si-NC group(CXCL5 negative control siRNA transfected into VSMCs),si-CXCL5 group(CXCL5 siRNA transfected into VSMCs),Vector+LY2157299 group and CXCL5+LY2157299 group(LY2157299 transferred into the cells 24 hours after cell transfection).Alizarin red staining,alkaline phosphatase staining,and calcium content determination were performed to evaluate the osteogenic differentiation level of VSMCs.(2)Animal experiment:Forty-eight ApoE-/-mice were randomly divided into four groups(n=12 per group):Con+si-NC group,Con+si-CXCL5 group,CAS+si-NC group and CAS+si-CXCL5 group.Animal models were not prepared in the first two groups,in which si-NC or si-CXCL5 lentivirus was injected into the tail vein;carotid atherosclerosis models were made in the latter two groups,in which si-NC or si-CXCL5 lentivirus was injected into the tail vein.Von Kossa staining and immunohistochemical staining were used to evaluate carotid vascular calcification and the expression of CXCL5 and transforming growth factor-β receptor 1(TGFBR1)in mice. RESULTS AND CONCLUSION:In the CXCL5 group,the protein level of runt-related transcription factor 2(RUNX2)was up-regulated and the level of α-smooth muscle actin was down-regulated,in contrary to the findings in the si-CXCL5 group.In addition,CXCL5 overexpression upregulated the level of TGFBR1,while CXCL5 knockdown inhibited the level of TGFBR1.Compared with the Vector group,the intensity of alizarin red staining,alkaline phosphatase activity and calcium content in the CXCL5 group increased significantly(P<0.05).Compared with the si-NC group,the intensity of alizarin red staining,alkaline phosphatase activity and calcium content in the si-CXCL5 group decreased significantly(P<0.05).When LY2157299 inhibited TGFBR1 expression,the osteogenic differentiation of VSMCs induced by CXCL5 was reduced.Compared with the Con+si-NC group,the expression of CXCL5 protein in the carotid artery and calcification area in the CAS+si-NC group increased significantly(P<0.05).Compared with the CAS+si-NC group,the expression of CXCL5 protein in the carotid artery and vascular calcification area in the CAS+si-CXCL5 group decreased significantly(P<0.05).In addition,compared with the Con+si-NC group,the expression of RUNX2 protein in the carotid artery in the CAS+si-NC group increased significantly(P<0.05),while the expression of α-smooth muscle actin protein decreased significantly(P<0.05).Compared with the CAS+si-NC group,the expression of RUNX2 protein in the carotid artery in CAS+si-CXCL5 group decreased significantly(P<0.05),while the expression of α-smooth muscle actin protein increased significantly(P<0.05).In conclusion,CXCL5 can induce osteogenic transformation of VSMCs by activating the TGFBR1 pathway,and inhibition of CXCL5 expression is effective in improving carotid arterial calcification in CAS mice.
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BACKGROUND:Reactive oxygen species may be closely related to the occurrence and development of tendinopathy,but its exact role and related signal transduction mechanism have not been fully summarized. OBJECTIVE:To review current clinical or preclinical original studies,summarize the role of reactive oxygen species in tendinopathy and related signal transduction pathways and to explore its characteristics and whether there is a unified downstream pathway. METHODS:Relevant original studies in PubMed,Embase,Web of Science,as well as CNKI,WanFang,and VIP databases were searched by computer and the search results were screened and excluded according to the inclusion criteria.Ninety articles were finally included for review and analysis. RESULTS AND CONCLUSION:Reactive oxygen species affects the direction of tendon healing by simultaneously acting on tendon cells and the extracellular matrix,and it exhibits a bifacial effect in the treatment of tendinopathy.Concentration of reactive oxygen species may be the key to determining its direction of action.The possibility that low-dose reactive oxygen species can participate in the normal physiological healing of tendons or that tendon tissues are adaptive to stimulations may be the underlying mechanism that produces this characteristic effect.Reactive oxygen species affect the composition and structure of the extracellular matrix and normal tendon repair as well as maintain viability in response to external stimulations through matrix metalloproteinases,mitogen-activated protein kinases,mitochondrial apoptosis,the forkhead transcription factor O family,autophagy,inflammation,and antioxidant signaling pathways.Different reactive oxygen species stimulation intensities,durations,and external environments may cause different alterations in downstream molecular pathways and thus have different effects on the tendon.Due to the large gap in the number of literature included in the evaluation of the positive and negative effects of reactive oxygen species,it may cause some analytical error in the search for factors behind the characteristics of the action of reactive oxygen species in tendon.In addition,most experimental intervention conditions and results of interest are relatively homogeneous;therefore,the temporal and quantitative mechanisms of reactive oxygen species and the synergistic effects with other intervention factors have not been clarified,and the overall system of molecular actions of reactive oxygen species in tendinopathy has not been constructed.To conclude,reactive oxygen species might be involved in the treatment and prevention of tendinopathies as a beneficial factor in the future,and facilitate the exploration of oxidative stress signaling pathways and overall molecular action systems in tendinopathies thereafter,as well as lay the foundation for research on the therapeutic strategies of different antioxidants in tendinopathies to better prevent and treat tendon injury and degeneration.
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BACKGROUND:With social progress,the incidence rate of knee osteoarthritis is getting higher and higher in the face of the rapidly developing aging problem in the social population,and the number of total knee replacement operations is gradually increasing. OBJECTIVE:To study the relationship between prosthesis size and stress shielding by improving the tibial prosthesis base. METHODS:A female patient with severe knee osteoarthritis was selected.Based on Mimics,through extracting the bone structure of the knee joint and simulating the total knee replacement surgery,osteotomy,positioning,and implantation operations were carried out to establish the geometric modeling of the total knee replacement prosthesis(including the femoral prosthesis,tibial bracket,and tibial pad),and improve the design of the tibial prosthesis base,analyze the effect of different tibial prosthesis bases on stress shielding of surrounding bone tissue. RESULTS AND CONCLUSION:(1)Compared with single-stem tibial intramedullary stem prosthesis,the design of four-post tibial intramedullary stem prosthesis created a certain degree of stress shielding around the short stem.However,compared with a thicker single long stem,this stress shielding effect was significantly reduced,and the load was evenly distributed among the four short stems,so there was no stress concentration at the bottom of the pile.(2)The design with a rectangular hole in the middle not only provided relatively good stability,but also helped to reduce stress shielding of cancellous bone to a certain extent,with a reduction rate of 77.5%.(3)Compared with a single-stem tibial intramedullary stem prosthesis,both the four-post tibial intramedullary stem prosthesis and the four-post tibial intramedullary stem prosthesis with a hole in the middle have good stability,which can reduce stress shielding to a certain extent without causing stress concentration,providing theoretical guidance for the design of the tibial intramedullary stem.
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BACKGROUND:Increasing studies have found that estrogen has a certain correlation with tendinopathy,but for a long time,there are few experiments and summaries of estrogen in tendinopathy,which makes it difficult for specialists and scholars in related fields to fully understand the research status. OBJECTIVE:To summarize the current clinical or preclinical original research,so as to summarize the role of estrogen in tendinosis,and make a certain prospect for the evaluation and management of estrogen in tendinosis in the future. METHODS:Relevant literature in PubMed,Web of Science,CNKI,WanFang,and VIP databases were searched by computer.Search time was from January 2008 to September 2023.The search terms were"oestrogen,estrogen,estrogen receptor,tendinopathy,tendonopathy,sinew,tendon,tendons,myotenositis"in English and"estrogen,estrogen receptor,tendinosis,tendon,tendinitis"in Chinese.According to the selection criteria,the search results were screened and excluded,and finally 60 documents were included for review and analysis. RESULTS AND CONCLUSION:In vivo studies have shown that estrogen can promote tendon anabolism.In vitro experiments have also proved that various estrogens can promote the proliferation of tendon cells and reduce inflammation and apoptosis,but most of the experiments are limited to animal models.Estrogen receptor β acts more in tendon injury and repair processes,but estrogen receptor α has not been found to have a major impact on tendon injury.The expression of estrogen receptor β can repair the tendon by affecting the formation of fat,the deposition of type I collagen and reducing the apoptosis of tendon cells,while its over-expression may promote inflammation and angiogenesis,thus promoting the inflammatory process and playing a role in tendon injury.Animal studies have shown that estrogen deficiency may reduce the synthesis efficiency of collagen in the tendon,decrease the elasticity of tendon,inhibit the synthesis and metabolism of the tendon,which is not conducive to the repair of tendon injury,while normal level of estrogen may stimulate the synthesis of type I collagen in tendon and promote the proliferation and metabolism of tendon cells.At present,the molecular mechanism of estrogen in tendon injury has not been fully explained.More experiments focus on tendon collagen synthesis,cell proliferation and apoptosis.Only a few documents have studied the molecular mechanisms of estrogen receptor β deficiency regulating interferon regulatory factor 5-chemokine ligand 3 axis,E2 regulating estrogen receptor α and PI-3K-Akt signaling pathways,and high levels of estradiol reducing the level of free-circulating insulin-like growth factor.Various estrogens,including endogenous estrogens and phytoestrogens,are beneficial to the repair of tendinopathy at normal levels,and estrogen receptor β mainly affects the formation of fat,the deposition of type I collagen and the reduction of apoptosis of tendon cells through,which lays a foundation for the future treatment of tendinopathy with different subtypes of estrogens in vivo and the influence of estrogen membrane receptors on tendinopathy.