[Outcomes of total knee arthroplasty combined with the modified "overlap" technique in the treatment of knee osteoarthritis with permanent patellar dislocation].

Objective: To investigate the clinical outcomes of total knee arthroplasty (TKA) combined with the modified "overlap" technique in the treatment of end-stage knee osteoarthritis with fixed patellar dislocation. Methods: This is a retrospective case series study. Clinical data of 19 patients (22 knees) who underwent TKA combined with the modified "overlap" technique for the treatment of end-stage knee osteoarthritis with permanent patellar dislocation from January 2011 to January 2022 in the Department of Orthopaedics, the First Affiliated Hospital of Xinjiang Medical University were retrospectively analyzed. The cohort included 5 males (6 knees) and 14 females (16 knees), with an age of (60.6±12.2) years (range:33 to 77 years) and a body mass index of (25.4±4.1) kg/m² (range:20.0 to 33.0 kg/m²). Among them, 11 cases (12 knee) had valgus deformity, with Keblish classification showing mild in 2 cases (2 knees), moderate in 6 cases (6 knees), and severe in 4 cases (4 knees). All cases were treated using a medial parapatellar approach, with lateral retinaculum release combined with the "overlap" technique to restore the patellar trajectory. Knee function was evaluated using the American Knee Society (KSS) Score. Paired sample t tests were used for intergroup comparisons. Results: All patients successfully completed the surgery. Postoperatively, patellar dislocation, knee valgus deformity, flexion contracture deformity, and extensor lag were all corrected. All patients were followed up, with a follow-up duration of (63.8±35.2) months (range:24 to 136 months). One patient experienced periprosthetic infection 2 weeks postoperatively, 1 patient had recurrent patellar dislocation 2 months postoperatively, 1 patient developed knee stiffness 3 months postoperatively and underwent closed manipulation. No other patients exhibited signs of patellar dislocation or subluxation. At the last follow-up, the KSS clinical score improved from (36.4±12.7) points preoperatively to (83.4±6.3) points postoperatively (t=-15.15, P<0.01), and the KSS functional score improved from (30.7±11.1) points preoperatively to (77.6±8.3) points postoperatively (t=-14.37, P<0.01). The range of motion of the knee increased from 81.7°±19.6° preoperatively to 107.6°±12.5° postoperatively (t=-4.85, P<0.01). Conclusion: TKA combined with the modified "overlap" technique is an effective surgical option for the treatment of end-stage knee osteoarthritis with permanent patellar dislocation, demonstrating satisfactory clinical outcomes.

[A preliminary in vivo and in vitro study of endothelial cell pyroptosis in the periodontal inflammatory environment].

Objective: To observe whether endothelial cells undergo pyroptosis in the inflammatory periodontal environment by using a model in vivo and in vitro, providing an experimental basis for indepth understanding of the underlying pathogenesis of periodontitis. Methods: According to the classification of periodontal diseases of 2018, gingival tissues were collected from periodontally healthy subjects and patients with stage Ⅲ-Ⅳ, grade C periodontitis, who presented Department of Oral and Maxillofacial Surgery and Department of Periodontology, School of Stomatology, The Fourth Military Medical University from April to May 2022. Immunohistochemical staining was performed to detect the expression level and distribution of gasdermin D (GSDMD), a hallmark protein of cell pyroptosis, in gingival tissues. Periodontitis models were established in each group by ligating the maxillary second molar teeth of three mice for 2 weeks (ligation group). The alveolar bone resorption was determined by micro-CT (mice without ligation treatment were used as the control group), and the colocalization of GSDMD and CD31 were quantitatively analyzed by immunofluorescence staining in gingival tissues of healthy and inflammatory mice. Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and treated with lipopolysaccharide (LPS) of Porphyromonas gingivalis (Pg) combined with adenosine triphosphate (ATP) at various concentrations of 0.5, 1.0, 2.5, 5.0, and 10.0 mg/L, respectively, and the 0 mg/L group was set as the control group at the same time. Scanning electron microscopy was used to observe the morphology of HUVECs. Western blotting was used to detect the expression of gasdermin D-N terminal domains (GSDMD-N) protein and immunofluorescence cell staining was used to detect the expression and distribution of GSDMD. Cell counting kit-8 (CCK-8) was used to detect the proliferative ability of HUVECs, and propidium iodide (PI) staining was used to detect the integrity of cell membrane of HUVECs. Results: Immunohistochemistry showed that GSDMD in gingival tissues of periodontitis was mainly distributed around blood vessels and its expression level was higher than that in healthy tissues. Micro-CT showed that alveolar bone resorption around the maxillary second molar significantly increased in ligation group mice compared with control subjects (t=8.88, P<0.001). Immunofluorescence staining showed significant colocalization of GSDMD with CD31 in the gingival vascular endothelial cells in mice of ligation group. The results of scanning electron microscopy showed that there were pores of different sizes, the typical morphology of pyroptosis, on HUVECs cell membranes in the inflammatory environment simulated by ATP combined with different concentrations of LPS, and 2.5 mg/L group showed the most dilated and fused pores on cell membranes, with the cells tended to lyse and die. Western blotting showed that the expression of GSDMD-N, the hallmark protein of cell pyroptosis, was significantly higher in 2.5 and 5.0 mg/L groups than that in the control group (F=3.86, P<0.01). Immunofluorescence cell staining showed that the average fluorescence intensity of GSDMD in 2.5 mg/L group elevated the most significantly in comparison with that in the control group (F=35.25, P<0.001). The CCK-8 proliferation assay showed that compared to the control group (1.00±0.02), 0.5 mg/L (0.52±0.07), 1.0 mg/L (0.57±0.10), 2.5 mg/L (0.58±0.04), 5.0 mg/L (0.55±0.04), 10.0 mg/L (0.61±0.03) groups inhibited cell proliferation (F=39.95, P<0.001). PI staining showed that the proportion of positive stained cells was highest [(56.07±3.22)%] in 2.5 mg/L group (F=88.24, P<0.001). Conclusions: Endothelial cells undergo significant pyroptosis in both in vivo and in vitro periodontal inflammatory environments, suggesting that endothelial cell pyroptosis may be an important pathogenic factor contributing to the pathogenesis of periodontitis.

[One-stage revision using intra-articular vancomycin infusion effectively treats chronic prosthetic joint infection caused by Enterococcal].

Objective: To investigate the clinical effects of one-stage revision combined with intra-articular infusion of vancomycin in the treatment of chronic prosthetic joint infection (PJI) caused by Enterococcal. Methods: From May 2013 to June 2020,the clinical data of 9 patients (2 males and 7 females) with chronic Enterococcal PJI treated with one-stage revision using intra-articular infusion of vancomycin at Department of Orthopaedics,First Affiliated Hospital of Xinjiang Medical University were retrospectively analyzed,including 8 hips and 1 knee.A total of 9 patients with age of (63.9±11.7)years (range:43 to 76 years) were included, and the body mass index was (23.6±4.3)kg/m2 (range:18 to 30 kg/m2).There were 6 cases with antibiotic history and 5 cases with sinus tract.The joint fluid,infected tissue around the prosthesis and ultrasonic shock fluid of the prosthesis were collected during operation for microbial culture identification and drug sensitivity test.After thorough debridement of the infected site and removal of the infected prosthesis,a new prosthesis was implanted,then the drainage tube in the operation area was placed.After surgery,vancomycin(1.0 g,q12 h) was combined with intra-articular vancomycin(0.5 g,qd) in monomicrobial PJI,and vancomycin(1.0 g,q12 h) was combined with intra-articular vancomycin (0.5 g,qd) and imipenem/meropenem (0.5 g,qd),and the interval between the two drugs was 12 hours in polymicrobial PJI.Hip and knee functions were evaluated by Harris Hip Score or Knee Society Score(KSS),respectively.The comparison of hip function scores before and after operation was performed by paired t-test. Results: All patients were followed up for (60±39)months(range:24 to 110 months).Two cases were infected with Enterococcus faecium and 7 cases were infected with Enterococcus faecalis.There were 7 cases of monomicrobial infection and 2 cases of polymicrobial infection.Erythromycin(5/9),tetracycline(4/9),ciprofloxacin and ß-lactam antibiotics(3/9) were the top three antibiotics in Enterococci resistance rate.The sensitive antibiotics for Enterococcal were vancomycin,linezolid and tigecycline.The average duration of intravenous antibiotics was (14±1)days (range:13 to 17 days),and the average duration of antibiotics in articular cavity was (15±2)days(range:11 to 20 days).Mean duration of oral antibiotic use after discharge was (2±1)months(range:1 to 3 months).One case of polymicrobial PJI treatment failed,with a failure rate of 1/9.At last follow-up,the Harris score of patients with hip PJI increased from (43±6)points to (84±6)points(t=-11.899, P<0.01). KSS score of knee function was improved from 33 point pre-operatively to 85 point post-operatively;overall function score was improved from 35 point pre-operatively to 80 point post-operatively.During the treatment,no formation of sinus tract of the hip joint caused by a catheter,skin necrosis at the knee puncture site or leakage of joint fluid;no complications such as deep vein thrombosis and pulmonary embolism occurred. Conclusions: One-stage revision combined with intra-articular infusion of vancomycin can achieve acceptable infection control rate and joint function in patients with chronic Enterococcus PJI.However,the treatment of polymicrobial PJI still needs to be further verified.

[Correlation between professional quality of life and social support of Chinese nurses: a meta-analysis].

Objective: To systematically evaluate the correlation between professional quality of life and social support of Chinese nurses based on Pearson and Spearman correlation coefficients. Methods: In databases including PubMed, Cochrane Library, CINAHL, Medline, CBM, CNKI、Wanfang, and other databases were searched by computer for the literatures on correlation between Chinese nurses' professional quality of life and social support from January 2005 to July 2020. The Chinese and English search terms are "nurse" "professional quality of life" "empathy satisfaction" "empathy fatigue" "professional quality of life" "ProQOL" "comparison satisfaction" "comparison fatigue" "social support" "competent social support" "SSRS" "PSSS", etc. Literatures were screened according to the inclusion and exclusion criteria. After evaluating quality and extracting data, meta-analysis was conducted using RevMan 5.3 software. Results: A total of 12 studies were included. The meta analysis showed that nurses' compassion satisfaction, burnout, secondary traumatic stress were related to social support, summary r were 0.35, -0.26 and -0.23 respectively. The correlation between compassion satisfaction and social support were increased with sample, the south was higher than the north, and comprehensive departments were higher than other departments (P<0.05) . The correlation between burnout and social support were increased with time and sample, and the south was higher than the north, oncology was higher than others, non-random sampling was higher than random sampling, using ProQOL and Perceived Social Support Scale (PSSS) was higher than Professional Quality of Life Scale (ProQOL) and Social Support Racting Scale (SSRS) (P<0.05) . The correlation coefficient between secondary traumatic stress and social support in oncology was higher than others, random sampling was higher than non-random sampling, using ProQOL and PSSS was higher than ProQOL and SSRS (P<0.05) . Conclusion: There is a positive and weak correlation between compassion satisfaction and social support, and a negative and weak correlation between burnout and secondary traumatic stress and social support. There are differences in different time, research design, region and department.

Preparation and process optimization of microbial organic copper as a feed additive / Preparação e otimização do processo de cobre orgânico microbiano como aditivo alimentar

As an essential trace element for animals, copper significantly contributes to the growth and health of animals. Compared to inorganic trace elements, organic trace elements are better supplements; notably, they are acquired through microbial transformation. Therefore, we screened for copper-enriched microorganisms from high copper content soil to obtain organic copper. Sodium diethyldithio carbamate trihydrate was applied as a chromogenic agent for determining micro amounts of intracellular copper through spectrophotometry. In total, 50 fungi were isolated after the successful application of the screening platform for copper-rich microbes. Following morphological and molecular biology analyses, the N-2 strain, identified as Aspergillus niger sp. demonstrated showed better copper enrichment potential than others. Notably, the strain tolerance to copper was nearly thrice that of Saccharomyces cerevisiae, up to 1600mg/L. The content of the organic bound copper was 22.84mg Cu/g dry cell. Using the Central Composite Design (CCD) response surface method, we optimized the fermentation condition (inoculation amount, 13%; temperature, 28(C; pH, 5.0). Compared to the original strain results under the single factor fermentation condition, we reported an increase by 24.18% under the optimized conditions. Collectively, these findings provide a reference for uncovering new and low-cost organic copper additives.(AU)

Como elemento traço essencial para os animais, o cobre contribui significativamente para o crescimento e saúde dos animais. Comparado aos oligoelementos inorgânicos, os oligoelementos orgânicos são melhores suplementos; notavelmente, eles são adquiridos através de transformação microbiana. Portanto, nós selecionamos microorganismos enriquecidos com cobre de solos com alto teor de cobre para obter cobre orgânico. O carbamato de sódio diethyldithio trihidratado foi aplicado como agente cromogênico para a determinação de micro quantidades de cobre intracelular através da espectrofotometria. No total, 50 fungos foram isolados após a aplicação bem sucedida da plataforma de triagem para micróbios ricos em cobre. Após análises morfológicas e de biologia molecular, a cepa N-2, identificada como Aspergillus niger sp. demonstrou um melhor potencial de enriquecimento de cobre do que outras. Notavelmente, a tolerância da estirpe ao cobre foi quase três vezes maior que a da Saccharomyces cerevisiae, até 1600mg/L. O conteúdo de cobre ligado orgânico era de 22,84mg Cu/g de célula seca. Usando o método de superfície de resposta Central Composite Design (CCD), nós otimizamos a condição de fermentação (quantidade de inoculação, 13%; temperatura, 28C; pH, 5,0). Em comparação com os resultados da deformação original sob a condição de fermentação de fator único, relatamos um aumento de 24,18% sob as condições otimizadas. Coletivamente, estas descobertas fornecem uma referência para descobrir novos aditivos de cobre orgânico de baixo custo.(AU)

[Role and mechanism of low-dose lipopolysaccharide-treated human periodontal ligament stem cells on the expression of macrophage pro-inflammatory factors].

Objective: To investigate the effect of low dose lipopolysaccharide (LPS)-treated human periodontal ligament stem cells (HPDLSC) on the expression of macrophage pro-inflammatory factors and the mechanism involved. Methods: The primary HPDLSCs were obtained from healthy third molar periodontal ligament tissue. Phosphate buffer saline (PBS), 100 µg/L or 10 mg/L of LPS were used to treat HPDLSCs for 48 h, and their conditioned media were respectively co-cultured with THP-1-derived macrophages for 48 h. The corresponding experimental groups were PBS-treated HPDLSC-derived conditioned medium (CM-C) group, low dose LPS-treated HPDLSC-derived conditioned medium (CM-L) group, and high dose LPS-treated HPDLSC-derived conditioned medium (CM-H) group. Quantitative real-time PCR was performed to explore the mRNA expressions of macrophage interleukin (IL)-6, IL-8, IL-12, tumor necrosis factor-α (TNF-α) in the CM-C, CM-L and CM-H groups, and the expressions of nuclear factor (erythroid-derived 2)-like 2 (NRF2), glutamate-cysteine ligase catalytic subunit (GCLC), NAD(P)H quinone dehydrogenase 1 (NQO1) and heme oxygenase 1 (HO-1) in the CM-C and CM-L groups. Meanwhile, Western blotting was used to detect the change of nuclear and cytoplasmic NRF2 and the levels of GCLC and HO-1 in the CM-C and CM-L groups. The 2', 7'-dichlorofluorescein probe was adopted to detect the reactive oxygen species (ROS) levels of macrophages in the CM-C and CM-L groups and the data were characterized by the mean fluorescent intensity (MFI). Results: The mRNA expressions of macrophage pro-inflammatory factors IL-6, IL-8, IL-12 and TNF-α in the CM-H group (2.332±0.594, 3.601±0.639, 2.120±0.677 and 2.468±0.236) were significantly upregulated compared with those in the CM-C group (1.000±0.321, 1.000±0.151, 1.000±0.059 and 1.000±0.095) (P<0.05); while the relative mRNA levels of IL-6, IL-12 and TNF-α in the CM-L group (0.056±0.002, 0.215±0.024 and 0.567±0.071) were much lower than those in the CM-C group (1.000±0.209, 1.000±0.220 and 1.000±0.220) (P<0.05). At the mRNA level, the expression of NRF2 was significantly increased in the CM-L group (1.864±0.198) compared with that in the CM-C group (1.000±0.094) (P<0.05). At the protein level, the cytoplasmic NRF2 and nuclear NRF2 were increased in CM-L group (1.175±0.104 and 1.308±0.082) compared with those in the CM-C group (1.000±0.025 and 1.000±0.049) (P<0.05). Furthermore, the antioxidative genes, i.e. GCLC and NQO1, localized in NRF2 downstream, were significantly upregulated in the CM-L group (1.786±0.278 and 1.444±0.078) compared with the CM-C group (1.000±0.139 and 1.000±0.226) (P<0.05). The protein levels of GCLC and HO-1 were augmented in the CM-L group (1.159±0.036 and 1.412±0.075) in contrast with those in the CM-C group (1.000±0.050 and 1.000±0.013) (P<0.05). In addition, the MFI in the CM-L group (123 419±1 302) was significantly lower than that in the CM-C group (139 193±1 241) (P<0.05). Conclusions: Low-dose LPS-treated HPDLSCs could regulate oxidative stress response through activating the NRF2 signaling pathway of macrophages and further downregulating the expressions of macrophage pro-inflammatory factors.

[Analysis of pathogen distribution and drug resistance of acute,delayed and chronic periprosthetic joint infection].

Objective: To analyze the pathogen distribution and drug resistance in acute,delayed and chronic periprosthetic joint infection (PJI). Methods: The clinical data of 316 patients with periprosthetic infection after primary hip and knee arthroplasty admitted to the Department of Arthroplasty,the First Affiliated Hospital,Xinjiang Medical University from August 2010 to August 2020 were retrospectively analyzed.There were 146 males and 170 females,aged (62.3±14.2) years (range:22 to 89 years).One hundred and sixty one patients underwent total hip arthroplasty and 155 patients underwent total knee arthroplasty.According to the time of postoperative infection,the patients were divided into acute PJI group (65 cases),delayed PJI group (83 cases) and chronic PJI group (168 cases).The results of pathogen species,composition ratio and drug susceptibility tests were collected,and the independent sample t test,Chi-square test or Fisher's exact probability test were used for comparison. Results: Gram-positive bacteria were the main pathogens of PJI (49.7%,157/316),and the positive rates of culture in patients with acute PJI,delayed PJI and chronic PJI were 33.8% (22/65),55.4% (46/83) and 53.0% (89/168),and the difference was statistically significant(χ²=8.343,P=0.015).The common bacteria were coagulase-negative Staphylococcus (54.8%,86/157) and Staphylococcus aureus (30.6%,48/157),The drug-sensitivity to linezolid,vancomycin and tigacycline was 100%.The gram-negative bacteria were mainly Escherichia coli and Enterobacter cloacae,and the drug resistance rate to carbapenems was low,ranging from 0 to 9.09%.The drug resistance rates of acute PJI patients to rifampicin,ciprofloxacin and erythromycin were significantly higher than those of late onset and chronic PJI patients,the difference was statistically significant(rifampicin:χ²=14.332,P=0.001;ciprofloxacin:χ²=12.086,P=0.002;erythromycin:χ²=9.096,P=0.010);The drug resistance rate of acute PJI patients to levofloxacin,clindamycin and tetracycline was higher than that of chronic PJI patients,and the difference was statistically significant(levofloxacin:χ²=10.500,P=0.002; clindamycin: χ²=7.103,P=0.007; tetracycline: χ²=6.909,P =0.012).The resistance rate of ampicillin/sulbactam in acute PJI (60.0%) was significantly higher than that in chronic PJI (16.7%),and the difference was statistically significant(χ²= 5.853,P=0.040). Conclusion: Gram-positive bacteria are the main pathogens of PJI,and the resistance rate of pathogens of acute PJI is higher than that of late onset and chronic PJI.

Androgen receptor inhibition alleviated inflammation in experimental autoimmune myocarditis by increasing autophagy in macrophages.

OBJECTIVE: Experimental autoimmune myocarditis (EAM) is characterized by pronounced macrophage infiltration, cardiac necrosis, and cardiac fibrosis. Our previous studies have demonstrated that suppressed androgen receptor (AR) enables anti-inflammation to promote tissue repair by decreasing M1 macrophages and increasing M2 macrophages in an EAM model. Given that autophagy mediates inflammatory response in macrophages, we investigated whether AR inhibition executes its protective role in inflammation through the autophagy pathway in EAM. MATERIALS AND METHODS: To determine whether AR inhibition can perform its anti-inflammatory effects by upregulating autophagy, we pre-treated mice with 3-methyl adenine (3-MA), a pharmacological inhibitor of autophagy. Immunofluorescence assay and Western blot were used to detect autophagy levels and autophagy activity in five different groups. Immunofluorescence marked F4/80 and LC3 to illustrate the autophagy level in macrophages. TUNEL assays were used to detect the apoptosis level in heart tissue of five different groups. RESULTS: We demonstrated that AR inhibition resolves injury with sustained inhibition of inflammatory cytokines associated with enhanced autophagy, especially in macrophages. Increased LC3II/I expression corroborated complete autolysosome formation detected by electron microscopy and correlated with degradation of SQSTM1/p62 in the AR inhibition group by Western blot. These effects could be reversed within 3-MA, a pharmacological inhibitor of autophagy. Specifically, pharmacological inhibition of autophagy increased apoptosis and inflammation, which could be attenuated by AR inhibition. CONCLUSIONS: AR inhibition alleviates the inflammatory response and tissue apoptosis by enhancing autophagy, especially in macrophages.

[Inflammatory periodontal stem cells mediate interleukin-1ß secretion of macrophage by regulating macrophage endoplasmic reticulum stress].

Objective: To investigate the effect and mechanism of periodontal ligament stem cell (PDLSC) from inflammatory environment on the secretion of interleukin-1ß (IL-1ß) by macrophages. Methods: PDLSCs were pretreated with lipopolysaccharide (LPS) in order to simulate the inflammatory environment. Human monocyte cell line (THP-1) cells were treated with conditioned media collected from healthy and inflammatory PDLSCs respectively and divided into conditioned medium of health PDLSC (CM-H) group and conditioned medium of LPS-PDLSC (CM-LPS) group. After 24 h of co-culture, the condition media were abandoned and THP-1 cells were then cultured for another 24 h. The expression of IL-1ß in THP-1 cells supernatant was detected by enzyme-linked immunosorbent assay (ELISA). Quantitative real time-PCR (qRT-PCR) was used to detect the expression of glucose regulated protein 78 (GRP78), activating transcription factor-6 (ATF6), inositol requiring enzyme 1 (IRE1), protein kinase R-like endoplasmic reticulum kinase (PERK), CCAAT enhancer binding protein homologous protein (CHOP), activating transcription factor-4 (ATF4) and X box binding protein 1 spliced (XBP1s), which were all related with endoplasmic reticulum stress (ERS), in THP-1 cells. The expressions of proteins GRP78 and CHOP were detected by Western blotting. Furthermore, THP-1 cells, which pretreated with ER inhibitor 4-phenylbutyrate (4-PBA) for intervention experiments were grouped by various concentrations of 4-PBA including groups 0 (control group), 1, 10 and 20 mmol/L and treated with condition medium of inflammatory PDLSC. ELISA was used to detect IL-1ß expression and qRT-PCR to detect expression of ERS related genes. Results: ELISA results showed that the expression of IL-1ß in THP-1 cells of group CM-LPS [(31.35±2.11) ng/L] was significantly higher than group CM-H [(8.19±1.51) ng/L] (t=12.60, P<0.01). qRT-PCR results showed that the relative expressions of GRP78, ATF6, IRE1, PERK, CHOP, ATF4 and XBP1s genes in THP-1 cells of group CM-LPS (1.782±0.070, 1.387±0.204, 1.404±0.119, 1.777±0.187, 1.325±0.156, 1.295±0.066 and 1.137±0.149, respectively) were significantly higher than those in group CM-H (P<0.05). In the 4-PBA intervention experiment, compared with group 0 mmol/L, the expressions of GRP78, IRE-1, ATF-6, PERK and CHOP were significantly lower in group 1, 10 and 20 mmol/L (P<0.05). Moreover, compared with control group [(31.23±1.98) ng/L], the expression of IL-1ß in THP-1 cells were significantly lower in group 10 mmol/L [(21.20±0.37) ng/L] and group 20 mmol/L [(23.85±1.80) ng/L] (P<0.05) with ERS inhibited. Conclusions: PDLSC from inflammatory environment could promote IL-1ß secretion of macrophages through upregulating macrophages ERS.

[Clinicopathological features of autoimmune gastritis].

Objective: To study the clinicopathological characteristics and pathologic diagnosis of autoimmune gastritis. Methods: Fourteen biopsies of autoimmune gastritis were collected from January 2018 to March 2019 at Guangdong Provincial People's Hospital. Their clinical data, histological features and immunohistochemical (IHC) results were analyzed, with review of relevant literature. Results: All 14 patients' ages ranged from 41 to 79 years (mean 55 years). There were 12 females and 2 males. All patients had non-specific symptoms, but they all had positive serum anti-parietal cell antibody and/or anti-intrinsic factor antibody. Seven patients had variable degree of anemia. Two patients had concomitant H. pylori infection. Two patients presented with multiple protruding polyps in corpus/fundus, 0.2 to 0.9 cm in diameter, or multiple large lobulated and broad based polyps (0.8 to 3.5 cm in diameters). The former cases were diagnosed as type 1 neuroendocrine tumors, the latter were multiple hyperplastic polyps. Microscopically, autoimmune gastritis showed typical morphology, characterized by diffuse corpus-restricted atrophic gastritis with variable proportions of intestinal metaplasia, or pseudopyloric metaplasia, pancreatic, acinar metaplasia, foveolar hyperplasia and hyperplasia of the endocrine-like cells (ECL cells). Hyperplasia of ECL cells often needed IHC staining to confirm. CgA/Syn IHC stain highlighted linear and micronodular ECL cell hyperplasia. In the absence of concurrent or past H. pylori infection, the antrum was usually normal. Gastrin IHC stain showed hyperplasia of gastrin-producing cells (G cells) in the antrum. Two cases were in the early phase, six were in florid phase, and six were end phase. Conclusions: Most patients of autoimmune gastritis have non-specific symptoms or are asymptomatic and show various endoscopic findings. There are three histologic phases of autoimmune gastritis. Recognition of this entity would be beneficial for pathologists to avoid misdiagnosis. Pathologists can make preferred diagnosis of autoimmune gastritis depending on the histologic clues and prompt appropriate and timely management for the patients.

[Diagnostic value of D-dimer for chronic periprosthetic infection after hip and knee joint replacement].

Objective: To investigate the diagnose value of D-dimer for chronic periprosthetic infection (PJI) after hip and knee arthroplasty. Methods: A retrospective analyze was conducted on 168 patients underwent revision arthroplasty and primary arthroplasty at the First Affiliated Hospital of Xinjiang Medical University from November 2017 to December 2018.There were 58 males and 110 females, aged(58.6±14.5)years.There were 48 cases of chronic PJI (21 cases of knee joint, 27 cases of hip joint), 57 cases of aseptic loosening (16 cases of knee joint, 41 cases of hip joint), and 63 cases of normal follow-up patients after hip (35 cases) or knee (28 cases) arthroplasty.The levels of D-dimer, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were collected.The levels of D-dimer in patients with chronic PJI of hip and knee joints were compared by Mann-Whitney U test.The diagnostic efficacy of D-dimer, ESR and CRP in chronic PJI of hip and knee joints was analyzed by receiver operator curve (ROC). Results: The D-dimer level was significantly higher in knee chronic PJI patients than hip chronic PJI patients(M (Q(R)) ) (1 040 (1 140.5) µg/L vs.435 (605) µg/L, Z=3.169, P=0.002) . ROC analysis showed that the optimum cutoff value of D-dimer in the diagnosis of chronic PJI was 370.5 µg/L, the sensitivity was 90.5%, the specificity was 84.1%; the optimum cutoff value of CRP was 9.3 mg/L, the sensitivity was 95.2%, the specificity was 90.9%, the optimum cutoff value of ESR was 33 mm/h, the sensitivity was 90.5%, and the specificity was 88.6%.The optimum cutoff value of D-dimer in the diagnosis of chronic PJI of hip joint is 294 µg/L, the sensitivity of diagnosis is 66.7%, the specificity is 77.6%; the optimum cutoff value of ESR is 45 mm/h, the sensitivity of diagnosis is 55.6% , the specificity is 97.4%; the optimum cutoff value of CRP is 8.1 mg/L, the sensitivity of diagnosis is 74.1%, the specificity is 84.2%. Conclusion: The value of D-dimer in the diagnosis of chronic PJI of knee joint is higher than that of hip joint, but the value of D-dimer in the diagnosis of chronic PJI is not better than ESR and CRP.

Effect of miR-26b on gestational diabetes mellitus in rats via PI3K/Akt signaling pathway.

OBJECTIVE: The aim of this study was to explore the influence of micro ribonucleic acid (miR)-26b on gestational diabetes mellitus in rats via the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathway. MATERIALS AND METHODS: A total of 60 healthy pregnant female rats were randomly divided into three groups, including group A (normal group), group B (model group), and group C (model + miR-26b group). The differences in fasting blood glucose (FBG), C-reactive protein (CRP), and phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) among the three groups were analyzed via serum CRP test, morphological observation, quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR), and Western blotting, respectively. RESULTS: The levels of FBG ad CRP were significantly up-regulated in group B when compared with group A (p<0.01). Meanwhile, they increased significantly in group C when compared with group B (p<0.01). Rats in group A exhibited smooth and flat thoracic aortic intimas, as well as neatly arranged smooth muscle cells at the media layer. However, rats in group B showed fractured intimas with enlarged junction gaps, as well as necrotic and detached endothelial cells. Compared with group B, group C exhibited extremely poorly arranged cells at all the layers, rough and rugged intimas, larger areas of necrotic and detached endothelial cells, and markedly worsened lesions. QRT-PCR results indicated that the expression of phosphorylated-PI3K (p-PI3K) was significantly lower in group B than that of group A (p=0.04). Meanwhile, it was markedly lower in group C than that in group B (p=0.04). The expression of p-Akt was remarkably lower in group B than group A (p=0.04), which was also significantly lower in group C than group B (p=0.04). Compared with group A, the expressions of p-PI3K and p-Akt in the thoracic aorta of group B were evidently down-regulated (p<0.01). Furthermore, they decreased markedly in group C when compared with group B (p<0.01). CONCLUSIONS: MiR-26b accelerates the progression of gestational diabetes by inhibiting the PI3K/Akt signaling pathway.

Effect of TGF-ß1 on myocardial cell apoptosis in rats with acute myocardial infarction via MAPK signaling pathway.

OBJECTIVE: Transforming growth factor beta 1 (TGF-ß1) can promote myocyte hypertrophy, thus playing an important role in ventricular remodeling after myocardial infarction (MI). MATERIALS AND METHODS: In this study, the model of MI was established in rats through ligating the left anterior descending coronary artery. Subsequently, the messenger ribonucleic acid (mRNA) and protein expression levels of TGF-ß1 in myocardial cells in both model group and sham operation group were determined. The effects of TGF-ß1 treatment on myocardial cell apoptosis in MI rats were explored. Moreover, the changes of mitogen-activated protein kinase (MAPK) signaling pathway in rats with acute MI were verified. In addition, the protein expressions of phosphorylated-MAPK kinases 3/6 (p-MKK3/6) and MKK3/6 in myocardial cells of the two groups were analyzed. RESULTS: The mRNA and protein expression levels of TGF-ß1 in myocardial cells of acute MI rats were significantly higher than those in the sham operation group (p<0.01). After treatment with TGF-ß1, the expression level of B-cell lymphoma 2 (Bcl-2) associated X protein (Bax) was obviously down-regulated. The Bax/Bcl-2 ratio was notably lower than that in control group (p<0.01). Meanwhile, the proportion of apoptotic cells decreased remarkably (p<0.01). In the model group, no evident change was observed in the protein expression level of MKK3/6, whereas the levels of p-MKK3/6 were prominently up-regulated (p<0.01). CONCLUSIONS: TGF-ß1 can activate MKK3/6 in the MAPK signaling pathway to resist the apoptosis of myocardial cells in acute MI rats.

LncRNATCF7 up-regulates DNMT1 mediated by HPV-18 E6 and regulates biological behavior of cervical cancer cells by inhibiting miR-155.

OBJECTIVE: This work aimed to study the mechanism of lncRNATCF7 upregulating DNMT1 mediated by HPV-18 E6 and regulating the biological behavior of cervical cancer cells by inhibiting miR-155. PATIENTS AND METHODS: HPV-16 E6 enhanced DNMT1 expression in cervical cancer cells, which was detected by Western blotting. The expression of miR-155 in cervical cancer was detected by qPCR, the interaction between TCF-7 and miR-155 by Dual-luciferase reporter gene. The changes in invasion ability of cervical cancer cells and the effect of miR-155 on the invasion ability of cervical cancer cells after inhibiting TCF-7 were detected by the transwell invasion assay, while changes in migration ability of cervical cancer cells and the effect of miR-155 on migration ability of cervical cancer cells after inhibiting TCF-7 were observed by the scratch assay. The effect of inhibiting TCF-7 on the tumor size and volume of cervical cancer was detected by the subcutaneous tumor formation in nude mice. RESULTS: E6 expression was significantly inhibited by E6 siRNA. The knockdown of endogenous HPV-16 E6 markedly inhibited the expression of DNMT1; TCF-7 specifically bound to the 3' UTR of miR-155; inhibition of TCF-7 can inhibit invasion and migration of cervical cancer cells; enhanced miR-155 after the inhibition of TCF-7 can promote the invasion and migration of cervical cancer cells; compared with NC group, the tumor volume and weight of TCF-7-siRNA group tumor-bearing was significantly reduced. CONCLUSIONS: TCF-7 plays an important role in the development of cervical cancer. TCF-7 can target miR-155 to regulate the invasion and migration of cervical cancer cells.

Investigating the expression of miRNA-133 in animal models of myocardial infarction and its effect on cardiac function.

OBJECTIVE: This study aimed to investigate the expression of miR-133 in animal models of myocardial infarction and its effect on cardiac function. MATERIALS AND METHODS: Forty-five male-specific pathogen-free (SPF) C57/BL6 mice were selected, among which 35 were made for animal models of myocardial infarction and were enrolled into Model Group and another 10 were enrolled into Blank Control Group. Seven mice died in the model making. Ten mice randomly selected from the 28 mice successfully modeled were transfected with adenovirus carrying miRNA-133 and set as Virus Group, while the remaining 18 mice were randomly divided into Virus No-load Group and Model Group. Mice in Virus Group were transfected with adenovirus carrying miRNA-133, while those in Virus No-load Group were transfected with empty viral vectors without miRNA-133. The left ventricular ejection fraction (LVEF) and fractional shortening (FS) of the mice weeks after the infection were recorded and evaluated by echocardiography. The relative expression levels of miR-133 in the heart tissues of the four groups of mice were compared by Real Time-Polymerase Chain Reaction (RT-PCR). RESULTS: The miR-133 expressions in Blank Control Group and Virus Group were higher than that of Model Group (p<0.05). Then, the myocardial infarction area of mice was compared. The LVEF and FS values of mice in Model Group, Virus No-load Group, and Virus Group were significantly lower than those in Blank Control Group, with the LVEF and FS values of Virus Group higher than that of Model Group and Virus No-load Group (p<0.05). The swimming time of Blank Control Group was significantly higher than that of Model Group and Virus Group (p<0.05), with Virus Group and Virus No-load Group having a greatly longer swimming time than Model Group (p<0.05). The myocardial infarction area of mice in Virus Group was significantly smaller than that in Model Group and Virus No-load Group, the difference was statistically significant (p<0.05). There was no significant difference in myocardial infarction area of mice between Model Group and Virus No-load Group (p>0.05). CONCLUSIONS: MiR-133 was in a low expression state in the mice models of myocardial infarction and the overexpression of miR-133 could significantly improve the cardiac function index and motor function, as well as reduce the myocardial infarction area of mice with myocardial infarction. This could inspire new molecular therapy for the treatment of myocardial infarction.

MicroRNA-490-3p inhibits inflammation and apoptosis induced by spinal cord injury via targeting MK2.

OBJECTIVE: To investigate the regulatory role of microRNA-490-3p in the recovery process of spinal cord injury (SCI) and its underlying mechanism. PATIENTS AND METHODS: Expression levels of microRNA-490-3p and MK2 in peripheral blood of SCI patients and healthy controls were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Glial cells C8-D1A and C8-B4 were induced by H2O2 for constructing in vitro SCI model, followed by detection of microRNA-490-3p and MK2 levels. After glial cells were transfected with microRNA-490-3p mimic or inhibitor, respectively, cell apoptosis and levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected. Bioinformatics was used to predict the binding site between microRNA-490-3p and MK2, which was further verified by dual-luciferase reporter gene assay. After construction of MK2 overexpression plasmid, rescue experiments were carried out to confirm the regulatory effect of microRNA-490-3p on MK2 in mediating SCI recovery. RESULTS: MicroRNA-490-3p expression was remarkably lower, whereas MK2 expression was higher in peripheral blood of SCI patients than those of healthy controls. Downregulated microRNA-490-3p and upregulated MK2 were observed in glial cells after H2O2 induction in C8-D1A and C8-B4 cells. Overexpression of microRNA-490-3p remarkably decreased levels of TNF-α and IL-6, as well as alleviated apoptosis in glial cells. Both protein and mRNA levels of MK2 were negatively regulated by microRNA-490-3p. Dual-luciferase reporter gene assay confirmed that MK2 was the target gene of microRNA-490-3p. Finally, rescue experiments verified that the regulatory effects of microRNA-490-3p on alleviating inflammation and apoptosis after SCI were reversed by MK2 overexpression. CONCLUSIONS: MicroRNA-490-3p is lowly expressed in glial cells after SCI. Overexpression of microRNA-490-3p alleviates inflammation and apoptosis via targeting MK2, thereafter promoting SCI recovery.

[The anti-inflammatory effect of hesperetin on lung damage induced by paraquat in rats].

Objective: To investigate the anti-inflammatory effect of hesperetin (HSP) on lung damage induced by paraquat (PQ) in rats by detecting the levels of inflammatory makers in rat lung tissues. Methods: 140 Wistar male rats were randomly divided into negative control group, HSP control group, HSP control group, paraquat model group, pirfenidone (PDF) positive control group, and 100, 200, 400 mg/kg HSP treatment groups. All groups were exposed to 50mg/kg paraquat by oral gavage except for the negative control group and HSP control group. After 24 hours, the rats in each group were given drug intervention once daily. 10 rats were randomly sacrificed at 7th day and 28th day after exposure to paraquat respectively. 3 rats were randomly selected from them and HE, Masson staining were used to observe the pathological changes in the lungs of each group. Each group randomly selected 6 rats at two time points to detect the levels of TGF-ß(1), TNF-α, IL-4, IL-10, IL-1ß and IFN-γ in rat lung tissues. Results: Histopathological examination found that the lung injury were reduced in the rats of PDF positive control group and all HSP treatment groups. Compared with the negative control group, the levels of TGF-ß1, IL-1ß, TNF-α, IL-4, and IL-10 in rat lung tissues were significantly increased (P<0.05, P<0.01) after PQ exposure at two points in time, and there was no significant difference in the level of IFN-γ in lung tissues compared with the negative control group (P>0.05) . The levels of TGF-ß1, IL-1ß, IL-4, IL-10 and TNF-α in the lung tissues of rats on the 7th day in different dose treatment groups of HSP were reduced compared with those in the PQ model group with varying degrees (P<0.05, P<0.01) . The level of IFN-γ in lung tissues of rats were not significantly different from that of model group (P>0.05) . The levels of TGF-ß(1) and TNF-α in lung tissue of rats on the 28th day in PDF positive control group and different dose treatment groups of HSP were reduced compared with those in the PQ model group with varying degrees (P<0.05, P<0.01). The levels of IFN-γ in the rat lung tissues were increased compared with those in the PQ model group (P<0.05). Besides, there were no significant in the levels of IL-1ß, IL-4 and IL-10 in lung tissues compared with PQ model group (P>0.05). Conclusion: HSP can reduce lung damage induced by PQ in rats by inhibiting the release of inflammatory factors and promoting the secretion of anti-inflammatory factors.

[Expression of C-fos in nasopharyngeal carcinoma and the relationship with chemosensitivity and prognosis].

Objective:To investigate the expression of C-fos in patients with nasopharyngeal carcinoma(NPC), and analyze the relationship between the expression of C-fos and the clinical characteristics, chemosensitivity and prognosis. Method:Clinical and follow-up data of 75 NPC patients was analyzed retrospectively. The expression of C-fos was detected by immunohistochemical assay, and chemosensitivity was detected by ATP bioluminescent anticancer drug sensitivity detection technology. The relationship between them was studied.Result:The expression of C-fos in NPC was statistically higher than that in the control nasopharyngeal mucosa(P<0.001). It was found that C-fos had no statistical relationship with the gender, age, pathologic type, clinical stage of tumor classification, lymph node status, metastasis status and overall stage of NPC patients(P>0.05). NPC had different chemosensitivity with 8 anticancer drugs(P<0.001).There was a significant difference in chemosensitivity of paclitaxel between the high expression of C-fos group and the low expression of C-fos group(P=0.036). The rate of tumor progression was significantly higher in NPC patients with high expression of C-fos than in the low expression group(P=0.014).There was no significant difference in overall survival between the two groups(P=0.076). Conclusion:C-fos is highly expressed in NPC tissues, and the high expression of C-fos in NPC tissues may be related to tumor progression and resistance to paclitaxel.

Regulatory effect of miRNA on multi-directional differentiation ability of mesenchymal stem cell in treatment of osteoporosis.

This study was designed to evaluate the effect of miRNA acting in regulating multi-directional differentiation ability of mesenchymal stem cell in treatment of osteoporosis (OP), with the aim of finding a new idea and approach for clinical treatment of OP. Estrogen deficiency-induced OP mice model was established by means of ovariectomy (OVX). Additionally, a sham group was set up for control. Bone Marrow Mesenchymal Stem Cells (BMMSCs) of OVX group (O/BMMSCs) and BMMSCs of sham group (S/BMMSCs) were separately cultured. Then surface markers of BMMSCs were detected. Multi-directional differentiation ability was identified in the two groups by giving cells targeted induced stimulation. It was found that the bone trabecula, bone density and bone volume fraction of distal femoral metaphysis in the OVX group were much lower than those of the sham group. Moreover, trabecular bone space in the OVX group became larger; O/BMMSCs and S/BMMSCs both had normal expression of surface markers as well as potentials of osteogenic and adipogenic differentiation; O/BMMSCs had a weaker osteogenic capability but a stronger adipogenic capability than S/BMMSCs. All the findings suggest that the regulatory effect of miRNA on multi-directional differentiation ability plays a vital role in the treatment of OP, and there is a close correlation between them; deficiency or functional defect of BMMSCs can result in the occurrence of OP.

Correlation between PPARg2 gene Pro12Ala polymorphism and cerebral infarction in an Inner Mongolian Han Chinese population.

The variant of PPAR-g2 has been shown to promote the increase of carotid IMT in patients suffering from cerebral infarction and the Pro12Ala polymorphism in the peroxisome proliferator-activated receptorg2 (PPARg2) gene may be associated with cerebral infarction. However, due to the different genetic background, race, and regional variations of cerebral infarction patient, the results of investigations into this subject differ. The aim of this study was to investigate this polymorphism in relation to cerebral infarction among the Inner Mongolian Han Chinese population. A total of 574 Han Chinese individuals from Inner Mongolian were selected randomly, including 302 patients with cerebral infarction and 272 healthy controls. Polymerase chain reaction-restriction fragment length polymorphism was used to determine genotypes of the PPARg2 Pro12Ala variant and results were confirmed by direct sequencing. Genotype frequencies were found to be 90.7 and 91.9% for P/P, 8.6 and 7.7% for P/A, and 0.7 and 0.4 for A/A in the cerebral infarction and control groups, respectively. No statistically significant differences in genotype distribution were observed between the two groups (P > 0.05). Moreover, PPARg2 Pro12Ala genotype was not significantly associated with altered fasting blood glucose, blood pressure, or serum lipid profiles. After adjustment for gender, body mass index, and smoking habit, logistic regression was used to analyze the relationship between the Pro12Ala polymorphism and cerebral infarction (odds ratio = 0.888, 95% confidence interval = 0.106-7.460, P > 0.05), revealing that this variant was not the main pathogenic factor involved. Therefore, the Pro12Ala mutation of PPARg2 may not be associated with cerebral infarction in the Inner Mongolian Han Chinese population.