BACKGROUND: Total hip arthroplasty with femoral neck prosthesis is being accepted by more and more doctors, but the effect of femoral neck prosthesis preservation or not on total hip arthroplasty is still uncertain. OBJECTIVE: To systematically evaluate the efficacy and safety of collum femoris preserving prosthesis in total hip arthroplasty. METHODS: CBM, CNKI, VIP, WanFang, PubMed, Embase and The Cochrane Library databases were searched systematically. The deadline was March 1,2018. All clinical controlled trials collum femoris preserving prosthesis in total hip arthroplasty were collected and methodological quality was evaluated one by one. RevMan 4.2 software was used for systematic evaluation. RESULTS AND CONCLUSION: (1) Four studies were included, involoing 302 patients. Because there were few studies and patients involved, and the outcome evaluation indicators were quite different, meta-analysis cannot be conducted, only descriptive systematic evaluation was performed. (2) Three studies compared the efficacy of two surgical methods in improving Harris score. Two of them considered that total hip arthroplasty with collum femoris preserving prosthesis was significantly better than total hip arthroplasty with non-collum femoris preserving prosthesis (P < 0.05). The other one considered that there was no significant difference between two surgical methods in improving Harris score (P > 0.05). (3) Two studies compared the efficacy of two surgical methods in improving the range of motion of the joint. One study showed that total hip arthroplasty with collum femoris preserving prosthesis was significantly better than total hip arthroplasty with non-prosthesis (P < 0.05). The other showed that there was no significant difference between the two surgical methods in improving the range of motion of the joint (P > 0.05). (4) One study showed that bone loss around the prosthesis in the total hip arthroplasty group with prosthesis was significantly less than that in the total hip arthroplasty group without collum femoris preserving prosthesis at 1 year postoperatively (P < 0.05). (5) One study found that the collum femoris preserving prosthesis in total hip arthroplasty group was superior to the non-collum femoris preserving prosthesis in total hip arthroplasty group in improving the Visual Analogue Scale at 1 year postoperatively (P < 0.05). (6) Two studies showed that no adverse prosthetic events such as loosening or sinking occurred at 1 year after total hip arthroplasty. (7) Two studies compared the differences in operation time and intraoperative bleeding volume, which showed no significant difference between two groups (P > 0.05). (8) One study found that the total amount of bleeding in total hip arthroplasty group with collum femoris preserving prosthesis was higher than that in total hip arthroplasty group without collum femoris preserving prosthesis (P < 0.05). (9) In summary, total hip arthroplasty with collum femoris preserving prosthesis has advantages in improving Harris score, decreasing the Visual Analogue Scale score and that bone loss around the prosthesis. More rigorous research is needed to increase the intensity of evidence.

Objective To analyze the drug resistance profile and risk factors for extensively drug resistant tuberculosis (XDR-TB) patients. Methods XDR-TB cases were identified by sixteen anti-TB drug susceptibility kits among inpatients with a diagnosis of laboratory-confirmed mycobacterium tuberculosis. Single-factor and Logistic analysis were used to analyze the risk factors for drug resistant of the first and second-line anti-TB drugs in XDR-TB patients. Results Resistant rate of rifampin, isoniazid and rifampicin were 100%, Resistant rate of streptomycin, rifampicin and dean, b sulfur isoniazid, levofloxacin and capreomycin were from 90% to 100%, resistant rate of kanamycin and amino salicylic acid were from 70% to 80%, resistant rate of amikacin from 60% to 70%, resistant rate of sulfur isoniazid was from 50% to 60%, resistant rate of ethambutol and moxifloxacin were from 40% to 50%, resistant rate of clarithromycin was from 10% to 20%, resistant rate of clofazimine 5.2%. 92.1% of XDR-TB patients were resistant to more than 10 anti-TB drugs, and the least of the patients were resistant to 6 anti-TB drugs.Logistic regression analysis showed the risk factors for XDR-TB first-and second-line anti-tb drugs included age ［20-40 year (OR=6.318, 95% CI:1.204-33.15, P=0.029;40-60 year (OR=4.772, 95% CI:0.973-23.392, P=0.054); 60 year (OR=41.366, 95% CI:2.909-588.265, P=0.006)］and anti-TB treatment history was retreatment(OR=28.013, 95% CI:3.357-233.766, P=0.002). Conclusions XDR-TB patients have serious drug resistance, but there were some drug treatable drug resistance types, and the risk factors mainly come from age and anti-TB treatment history.

Objective To investigate the role of neurotrophin-3 (NT-3) gene modified bone marrow mesenchymal stem cells (BMSCs) in treatment of acute cerebral infarction and its underlying mechanism.Methods Seventy-two SD male rats were randomly divided into model group,BMSCs group,and BMSCs+NT-3 group (n=24).Focal cerebral ischemia rat models were established by middle cerebral artery occlusion (MCAO);24 h after MCAO,rats in the BMSCs group and BMSCs+NT-3 group were given BMSCs and NT-3 gene modified BMSCs via tail intravenous injection,respectively.Modified neurological severity scale (mNSS) was performed one,6,12 and 24 d after MCAO;infarct sizes were measured by TTC staining one,12 and 24 d after MCAO;expressions of neuronspecific enolase (NSE) and nestin in the surrounding areas of infarction were detected by Western blotting 6 d after MCAO.Results As compared with those in the BMSCs group,significantly decreased mNSS scores in BMSCs+NT-3 group were noted 6,12 and 24 d after MCAO (P＜0.05).Rats in the BMSCs+NT-3 group had significantly smaller brain infarct sizes than the BMSCs group 12 and 24 d after MCAO (P＜0.05).Expressions of NSE and nestin in the BMSCs+NT-3 group were significantly higher than those in the BMSCs group 6 d after MCAO (P＜0.05).Conclusion Transplantation of NT-3 gene modified BMSCs can further improve neurological functions and reduce brain infarct sizes as compared with BMSCs transplantation,whose mechanism might be related to promote the differentiation of BMSCs into neurons.

Objective To investigate the therapeutic effect of hyperbaric oxygen on hemorrhage transformation and its possible mechanism in rats after cerebral infarction.Methods Seventy-two SD male rats were randomly divided into sham-operated group,model group,and hyperbaric oxygen group (n=24).Focal cerebral ischemia rat models were established by occluding the middle cerebral artery in model group and hyperbaric oxygen group,and the hemorrhage transformation models after cerebral infarction were prepared by intraperitoneal injection of hyperglycemia before ischemia reperfusion.Rats in the hyperbaric oxygen group were treated with hyperbaric oxygen 3 h after operation.Twenty-four h after operation,Neurological Function Scale was performed;infarct sizes were measured by TTC staining;amount of hemoglobin detected by spectrophotometric assay was used to evaluate the amount of blood loss in the brain tissues;nuclear transcription factor-κB (NF-κB) protein expression was detected by Western blotting;and the concentrations of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) in the penumbra of cerebral infarction were determined by ELISA.Results As compared with those in the model group,the Neurological Function Scale scores of hyperbaric oxygen group were significantly higher (11.50± 1.64 vs.16.04±2.09,P＜0.05).The brain infarct sizes,hemorrhagic volumes,NF-κB protein expression,and IL-1β and TNF-α concentrations in the hyperbaric oxygen group were significantly decreased as compared with those in the model group (33.7％±3.8％ vs.21.6％±4.1％,[11.94±2.26] μL vs.[8.21±1.96] μL,3.05±0.19 vs.2.26±0.25,[49.78±5.65] pg/mL vs.[31.88±2.96] pg/mL,and [31.11± 4.55] pg/mL vs.[19.39±3.19] pg/mL,P＜0.05).Conclusion Hyperbaric oxygen has therapeutic effect on hemorrhage transformation after cerebral infarction by reducing brain infarct sizes and hemorrhagic volumes,whose mechanism might be related to inhibition of NF-κB,IL-1β,and TNF-α expressions and reduce of inflammatory response.

BACKGROUND:Currently,there have been a variety of conservative and surgical treatment plans for spontaneous osteonecrosis of the knee,achieving excellent results.However,a broad consensus on indication and guide of surgical treatment has not been announced.In clinical practice,there is still a misunderstanding that unicondylar replacement or total knee arthroplasty should be performed upon the discovery of spontaneous osteonecrosis of the knee,while an urgent need for universal access to the concept of stepwise therapy. OBJECTIVE:To summarize and find the factors leading to the poor effect of conservative treatment in spontaneous osteonecrosis of the knee,which occurred on the medial femoral condyle,from the literature and clinical cases,at the same time,combined with the Koshino stage,to propose the strategy of stepwise spontaneous osteonecrosis of the knee treatment on the medial femoral condyle. METHODS:A systematic search of the literature database was conducted to summarize the factors leading to poor outcomes of conservative treatment in spontaneous osteonecrosis of the medial femoral condyle.Meanwhile,according to the Clinical&Health Records for analytics&Sharing system,the cases receiving conservative and surgical treatment in spontaneous osteonecrosis of the medial femoral condyle in the Department of Orthopedics of Guangdong Provincial Hospital of Chinese Medicine from January 2017 to January 2023 were analyzed retrospectively,then the causes of success and failure in typical cases were summarized and analyzed. RESULTS AND CONCLUSION:(1)Early diagnosis and treatment of spontaneous osteonecrosis of the knee were very important for prognosis.For sudden knee pain in some patients,if no obvious abnormality was found in the X-ray examination,and the symptoms persisted and could not be relieved for more than 1 week,an MRI examination was recommended to detect early spontaneous osteonecrosis of the knee.(2)The X-ray images of Koshino stage 1 and stage 2 of spontaneous osteonecrosis of the medial femoral condyle were difficult to be distinguished,which needed to be probed by MRI.MRI images of Koshino stage 1 were mainly characterized by bone marrow edema,and an osteonecrosis area with a clear boundary was not formed,while MR images of Koshino stage 2 showed a necrotic area with a clear boundary.(3)Five factors leading to the poor effect of conservative treatment on spontaneous osteonecrosis of the medial femoral condyle were summarized:a.The necrotic area was＞5 cm2;b.The necrotic area accounted for more than 40%of the condyle;c.relative compression percentage of medial meniscus≥33%(with or without medial meniscus injury and subchondral bone marrow edema);d.MRI depth of necrotic area(anterior-posterior diameter of sagittal necrotic area)＞20 mm;e.varus deformity of lower limb＞6°.(4)Conservative treatment of spontaneous osteonecrosis of the knee in Koshino stage 1 was good.For spontaneous osteonecrosis of the knee in Koshino stage 2,conservative treatment was preferred or combined with drilling decompression.If there was no relief or improvement of symptoms or in MRI after 3 months,while the patient had any of the previous five factors,then knee preservation surgery should be considered.For spontaneous osteonecrosis of the knee in Koshino stage 3 and stage 4,knee preservation surgery should be selected based on the previous five factors,including age,gender and activity level of the patient.Total knee arthroplasty was used for spontaneous osteonecrosis in Koshino stage 4,which was associated with symptomatic patellofemoral arthritis,valgus alignment,or necrotic area,which greatly affected the stability of unicondyle prosthesis.

OBJECTIVE： To study the effects of ligustrazine on miR-20b/VEGF and BMP2/Smad1 pathways in subchondral bone of knee osteoarthritis （KOA） model rats， and to investigate the mechanism of ligustrazine for KOA prevention and treatment. METHODS： Totally 18 healthy male SD rats were randomly divided into normal control group， model group and ligustrazine group， with 6 rats in each group. The rats in the latter two groups were used to establish KOA model by intra-articular injection of 4％ papain solution. From the 2nd day after the last injection， ligustrazine group was given intragastrical administration of Ligustrazine suspension （100 mg/kg） 2 mL； normal control group and model group were given intragastrical administration of isometrical normal saline， once a day， for consecutive 6 weeks. After the last after medication， the situation of bilateral knee articular cartilage of rats were observed after exposure. The knee joints of rats were sectioned and stained with HE. The pathological change of articular cartilage were observed by microscope and scored by modified Mankin’s score. mRNA expression of VEGF， BMP2 and Smad1， and the expression of miR-20b were detected by RT-PCR； the protein expression of VEGF， BMP2 and Smad1 were detected by Western blot assay. RESULTS： Model group and ligustrazine group suffered from cartilage injury of knee joint at varying degrees. Compared with normal control group， Mankin’s scores of knee joint and cartilage tissue were increased significantly in model group （P＜0.01）； mRNA and protein expression of BMP and Smad1， the expression of miR-20b in subchondral bone of model group were decreased significantly， while mRNA and protein expression of VEGF were increased significantly （P＜0.01）. Compared with model group， Mankin’s score of cartilage tissue were decreased significantly in ligustrazine group （P＜0.01）； mRNA and protein expression of BMP and Smad1， the expression of miR-20b in subchondral bone were increased significantly， while mRNA and protein expression of VEGF were decreased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： Ligustrazine can repair damaged articular cartilage in KOA model rats， the mechanism of which may be associated with inhibiting the protein expression of VEGF and activating BMP-2/Smad1 signaling pathway via up-regulating the expression of miR-20b， and promoting the degradation of VEGF mRNA in subchondral bone.

OBJECTIVE：To ex plore the protective effects of Longbie capsule contained serum （called“LBJN”for short ）on the apoptosis of chondrocytes induced by YAP inhibitor verteporfin and its mechanism. METHODS ：Primary human knee osteoarthritis（OA）chondrocytes were extracted by two-step enzymatic digestion ，and then identif ied by toluidine blue staining and type Ⅱ collagen immunofluorescence staining. The effects of 2，5 μmol/L verteporfin alone or combined with 5％LBJN on cell apoptosis were detected by flow cytometry. Solvent control （0.1％ DMSO）and 5％ LBJN were set. Western blot assay was adopted to detect the expression of apoptosis related proteins （YAP，Bcl-2，cleaved-caspase-3） after treated with 0.1％DMSO（solvent control ），2 μmol/L verteporfin，2 μmol/L verteporfin+5％LBJN 和 0（blank control ），2.5％ LBJN and 5％ LBJN for 48 h. The expression of autophagy related proteins （mTOR，Beclin-1，LC3A/B） after treated with 0 （blank control ），2.5％，5％ LBJN for 48 h were det ected by Western blot assay. RESULTS ：The isolated cells accorded with the characteristics of chondrocytes. Compared with 0.1％DMSO， the apoptosis rates of cells were increased significantly after treated with 2，5 μmol/L verteporfin（P＜0.05），and the effects of the two concentrations were similar （P＞0.05）. Compared with verteporfin alone ，2，5 μmol/L verteporfin combined with 5％LBJN could significantly decrease the apoptotic rate of cells （P＜0.05）. Compared with 0.1％DMSO，the protein expression of YAP and Bcl-2 were decreased significantly after treated with 2 μ mol/L verteporfin （P＜0.05）， while the protein expression of cleaved-caspase-3 were increased significantly （P＜0.05）. Compared with 2 μmol/L verteporfin，protein expression of YAP and Bcl-2 were increased significantly after treated with 2 μmol/L verteporfin+5％LBJN（P＜0.05），while the protein expression of cleaved-caspase-3 were decreased significantly （P＜0.05）. Compared with blank control ，the protein expression of YAP ，Bcl-2 and Beclin-1 were increased significantly after treated with 2.5％，5％LBJN（P＜0.05），while protein expression of cleaved-caspase- 3 and mTOR were decreased significantly （P＜0.05）. CONCLUSIONS ：LBJN can block the apoptosis of chondrocytes induced by YAP inhibitor verteporfin ，and its mechanism may be related to regulating the expression of apoptosis related proteins and enhancing autophagy of chondrocytes.