Epidemiology and prognostic factors for new-onset deep venous thrombosis after unicompartmental knee arthroplasty: a retrospective study.

BACKGROUND: Patients who underwent knee joint arthroplasty were at risk of venous thromboembolic events (VTEs), however, less studies were conducted to demonstrate the epidemiology and risk factors of deep venous thrombosis (DVT) following unicompartmental knee arthroplasty (UKA). Objective of this study was to explore the incidence and prognostic factors of DVT after UKA. METHODS: Patients who underwent primary UKA from December 2018 to June 2022 were recruited in this study. Demographic characteristics, operation related variables and laboratory index were extracted and analyzed. Receiver operating characteristic analysis was performed to detect the optimum cut-off value for variables of interest. Univariate and multivariate logistic analysis were performed to identify risk factors of DVT. RESULTS: 351 UKAs with a mean age of 65.4 ± 7.1 years were reviewed. After 12.9 ± 11.2 months follow-up, 35 DVTs were confirmed which indicating an incidence of 9.9%. The results showed that occupation (agricultural laborer) (P = 0.008), disease duration > 8.5 years (P = 0.035), operation time > 169 min (P = 0.003), intraoperative blood loss > 102 ml (P < 0.001), BMI > 26.8 kg/m 2 (P = 0.001), preoperative D-dimer > 0.29 mg/L (P = 0.001), prothrombin time < 10.7 s (P = 0.033) and INR < 0.98 (P = 0.032) between DVT and Non-DVT group were significantly different. Multivariate logistic regression analysis showed intraoperative blood loss > 102 ml (OR, 3.707; P, 0.001), BMI > 26.8 kg/m 2 (OR, 4.664; P, 0.004) and D-dimer > 0.29 mg/L (OR, 2.882; P, 0.009) were independent risk factors of DVT after UKA. CONCLUSION: The incidence of DVT in the present study was 9.9%, extensive intraoperative blood loss, advanced BMI and high level of D-dimer would increase the risk of lower extremity thrombosis by 2-4 times.

The efficacy of unicondylar knee arthroplasty for medial compartment arthritis of the knee combined with anterior cruciate ligament dysfunction.

BACKGROUND: To investigate the outcome and prognosis after Unicondylar knee arthroplasty (UKA) in patients with medial compartment arthritis of the knee combined with anterior cruciate ligament(ACL) dysfunction. METHODS: A total of 122 patients diagnosed with knee osteoarthritis and treated with medial mobile platform unicondylar replacement at our center from January 2019 to December 2021 were retrospectively included in the study, and were divided into two groups according to ACL function, namely the normal ACL function group (ACLF) and the poor ACL function (N-ACLF) group. The postoperative results and prognosis of the two groups were evaluated and compared. RESULTS: This study included 122 patients who underwent UKA surgery. There were no statistical differences in preoperative and postoperative posterior tibial tilt angle, knee mobility, KOOS, and prognosis between the two groups (P > 0.05). CONCLUSION: For medial compartment arthritis of the knee combined with ACL malfunction, surgery resulted in pain relief, improved quality of life and a good prognosis for such patients. It is hoped that clinicians will perform UKA in patients with ACL dysfunction after a comprehensive evaluation to improve their quality of life.

Association of mitochondrial DNA variation with high myopia in a Han Chinese population.

High myopia (HM), which is characterized by oxidative stress, is one of the leading causes of visual impairment and blindness across the world. Family and population genetic studies have uncovered nuclear-genome variants in proteins functioned in the mitochondria. However, whether mitochondrial DNA mutations are involved in HM remains unexplored. Here, we performed the first large-scale whole-mitochondrial genome study in 9613 HM cases and 9606 control subjects of Han Chinese ancestry for identifying HM-associated mitochondrial variants. The single-variant association analysis identified nine novel genetic variants associated with HM reaching the entire mitochondrial wide significance level, including rs370378529 in ND2 with an odds ratio (OR) of 5.25. Interestingly, eight out of nine variants were predominantly located in related sub-haplogroups, i.e. m.5261G > A in B4b1c, m.12280A > G in G2a4, m.7912G > A in D4a3b, m.94G > A in D4e1, m.14857 T > C in D4e3, m.14280A > G in D5a2, m.16272A > G in G2a4, m.8718A > G in M71 and F1a3, indicating that the sub-haplogroup background can increase the susceptible risk for high myopia. The polygenic risk score analysis of the target and validation cohorts indicated a high accuracy for predicting HM with mtDNA variants (AUC = 0.641). Cumulatively, our findings highlight the critical roles of mitochondrial variants in untangling the genetic etiology of HM.

Incidence and risk factors for surgical site infection after medial opening-wedge high tibial osteotomy using a locking T-shape plate.

Medial opening-wedge high tibial osteotomy (MOWHTO) is a well-established surgical method for treatment of isolated medial compartment osteoarthritis with varus deformity, but the surgical outcomes may be compromised by surgical site infection (SSI). This study aimed to investigate the incidence and the risk factors for SSI after MOWHTO. This retrospective study included consecutive patients who underwent MOWHTO for isolated medial compartment osteoarthritis with varus deformity in two tertiary referral hospitals from January 2019 and June 2021. Patients who developed SSI within 12 months of surgery were identified by inquiring the medical records for index hospitalisation, notes of after-discharge outpatient visits, or records of readmission for treatment of SSI. Univariate comparisons were performed to detect the differences between SSI and non-SSI groups, and multivariate logistic regression analysis was used to identify the independent risk factors. Six hundred sixteen patients with 708 procedures were included and 30 (4.2%) cases of SSI occurred, with 0.6% rate for deep SSI and 3.6% for superficial. Univariate analyses showed significant difference between groups in terms of morbidity obesity (≥32 kg/m2 ) (20.0% vs 8.9%), comorbid diabetes (26.7% vs 11.1%), active smoking (20.0% vs 6.3%), time from admission to operation (5.2 ± 4.0 vs 4.1 ± 3.0), size of osteotomy ≥12 mm (40.0% vs 20.0%), type of bone grafting and lymphocyte count (2.1 ± 0.5 vs 1.9 ± 0.6). However, in the multivariate analysis, only active smoking (OR, 3.4; 95% CI, 1.4-10.2), size of osteotomy ≥12 mm (OR, 2.8; 95% CI, 1.3-5.9) and allogeneic/artificial vs no bone grafting (OR, 2.4; 95% CI, 1.0-10.8) remained significant. SSI was not uncommon after MOWHTO, but the majority was superficial. The identified three independent factors, including smoking, size of osteotomy ≥12 mm and allogeneic/artificial bone grafting would help risk assessment and stratification, target risk factor modification and clinical surveillance, and inform patient counselling.

Incidence and risk factors of delayed wound healing in patients who underwent unicompartmental knee arthroplasty.

Unicompartmental knee arthroplasty (UKA) has been proven as an ideal alternative surgical procedure to treat symptomatic isolated knee osteoarthritis, and recently this technique has gained its popularity. However, postoperative complications would inevitably compromise the effectiveness and patients' satisfaction. The objective of this study is to demonstrate the incidence and risk factors of delayed wound healing (DWH) after UKA. This retrospective cohort study was conducted from February 2021 to May 2022 and a total of 211 patients were enrolled. Demographic characteristics, operation-related variables, and laboratory indexes were extracted. Receiver operating characteristic analysis was performed to detect the optimum cut-off value for continuous variables. Univariate and multivariate logistic regression analysis was performed to demonstrate the risk factors of DWH. There were 155 female and 56 male patients with an average age of 64. 6 ± 6.9 years included in this study. After 6.6 ± 4.9 months' follow-up, 12 cases of DWH were observed which indicated an incidence of DWH of 5.7%, mean wound healing duration for 12 patients was 43.1 ± 19.3 days. In the univariate analysis, age > 62.5 years, postoperative hospital stay < 5.5 days, surgical incision < 10.5 cm, barbed suture, body mass index (BMI) > 32.0 kg/m2 , operation duration > 102.5 minutes, intraoperative blood loss > 102.5 mL, preoperative white blood cell count > 5.95*109 /L, preoperative seroglobulin (GLB) > 29.6 g/L, postoperative total protein < 63.4 g/L, postoperative serum albumin < 36.4 g/L, and postoperative GLB > 26.8 g/L were significantly different between patients with and without DWH (P < .05). In final multivariate logistic analysis, results showed that intraoperative blood loss > 102.5 mL (odds ratio [OR], 3.09; P = .001), postoperative hospital stay < 5.5 days (OR, 1.74; P = .014), surgical incision < 10.5 cm (OR, 1.67; P = .000), and BMI > 32.0 kg/m2 (OR, 4.47; P = .022) were independent risk factors for DWH. DWH prolongs hospital stay in UKA patients and increases healthcare expenditure; also affected the implementation schedule of postoperative functional exercise plans. Surgeons should identify patients at risk, meanwhile, make timely and correct clinical interventions to decrease the incidence of this complication.

Apaf-1 interacting protein, a new target of microRNA-146a-3p, promotes prostate cancer cell development via the ERK1/2 pathway.

The Apaf-1 interacting protein (APIP), a ubiquitously expressed antiapoptotic molecule, is aberrantly expressed and of great significance in various cancers. However, little is known regarding the potential value and underlying mechanisms of APIP in prostate cancer. Here, we demonstrated that APIP expression is significantly upregulated in prostate cancer cell lines. APIP overexpression promoted tumor cell proliferation and migration and induced extracellular regulated protein kinases 1/2 (ERK1/2) activation. Pharmacological inhibition of ERK1/2 signaling reversed APIP-induced increase in cell proliferation and migration induced by APIP overexpression. Expression of APIP was hampered by miR-146a-3p. A dual luciferase reporter gene assay identified the regulatory relationship between APIP and miR-146a-3p in prostate cancer, suggesting that APIP is a direct target of miR-146a-3p. miR-146a-3p reduced cell proliferation and migration in prostate cancer. Furthermore, miR-146a-3p inhibited ERK1/2 activation. Application of an ERK1/2 inhibitor reversed the increase in cell proliferation and migration induced by miR-146a-3p inhibition. In summary, this study focused on the role of APIP in regulating cell growth and migration and proposes a theoretical basis for APIP as a promising biomarker in prostate cancer development.

GDI2 is a target of paclitaxel that affects tumorigenesis of prostate cancer via the p75NTR signaling pathway.

BACKGROUND: Prostate cancer (PCa) refers to malignant tumors derived from prostate epithelial cells, whose morbidity and mortality rates have been increasing every year. Although new drugs for treating prostate cancer continue to emerge, the unclear mechanism underlying drug targets limits this therapy, thereby constraining identification of effective therapeutic targets. Although GDP dissociation inhibitor 2(GDI2) is highly expressed and closely associated with occurrence and development of many tumors, its role in prostate cancer remains unclear. In this study, we investigated the role of GDI2 and elucidated its underlying mechanism of action in prostate cancer. Moreover, we screened chemotherapeutic drugs that affect GDI2 expression with a view of identifying novel targets for diagnosis and treatment of prostate cancer. METHODS: We performed sequence analyses and functional assays to precisely elucidate the GDI2 role in prostate cancer. Moreover, we induced tumorigenesis in nude mice to verify the role of GDI2 in vivo. Finally, we used the CCK8 assay to ascertain the most suitable IC50 across the three drugs and performed quantitative real time polymerase chain reaction (qRT-PCR) and Western Blot to analyze the effects of drugs on expression of GDI2, p75NTR, and p-NFκB. RESULTS: GDI2 was up-regulated in prostate cancer cells and tissues. Knocking down GDI2 suppressed cell proliferation but promoted cell apoptosis. Interestingly, knocking down GDI2 activated the p75NTR signaling pathway, indicating, for the first time, that p75NTR is negatively correlated with GDI2 expression. CONCLUSION: Taken together, these results indicate that GDI2 is a therapeutic target of paclitaxel. Knocking down of GDI2 inhibits cell proliferation and promotes cell apoptosis via the p75NTR signaling pathway in prostate cancer. Notably, paclitaxel inhibits GDI2 expression, implying that GDI2 may be a promising therapeutic target in prostate cancer.

CPEB1 enhances erastin-induced ferroptosis in gastric cancer cells by suppressing twist1 expression.

The induction of ferroptosis is considered a new strategy for cancer treatment. Cytoplasmic polyadenylation element binding protein 1 (CPEB1) is a post-transcriptional regulatory factor, whose low expression has been reported to link to the enhanced metastasis and angiogenesis of gastric cancer (GC). In this study, to explore the role of CPEB1 in ferroptosis, GC cells with overexpressed or silenced CPEB1 expression were treated with erastin, a classic ferroptosis inducer. The results showed that erastin dose-dependently decreased the viability of four GC cell lines (AGS, SNU-1, Hs-746 T, and HGC-27), suggesting that ferroptosis could be triggered in these GC cells. Interestingly, HGC-27 cells overexpressing CPEB1 were more sensitive to erastin, generated more lipid reactive oxygen species (ROS) and malondialdehyde (MDA), and their glutathione peroxidase 4 (Gpx4) expression and GSH content were reduced. Contrarily, CPEB1-silenced AGS cells were more resistant to erastin. Mechanically, we demonstrated that CPEB1 overexpression reduced the expression of twist1, an inhibitor of activating transcription factor 4 (ATF4), thereby activating the ATF4/ChaC Glutathione Specific Gamma-Glutamylcyclotransferase 1 (CHAC1) pathway (CHAC1, a molecule known to induce GSH degradation). Furthermore, re-expression of twist1 in GC cells impaired the effects of CPEB1 overexpression in presence of erastin. Additionally, similar to the in vitro results, the growth-inhibiting effects of erastin on GC xenografted tumors were also augmented by CPEB1 overexpression in vivo. Collectively, we demonstrate that CPEB1 facilitates erastin-induced ferroptosis by inhibiting twist1.

Vitamin C Prevents Hydrocortisone-Induced Injury in HMEC-1 through Promoting Bestrophin-3 Expression.

OBJECTIVE: To investigate the protective effects and underlying mechanisms of Vitamin C (VC) on hydrocortisone (HC)-induced cell injury in human microvascular endothelial cells (HMEC). METHODS: Cell viability was measured by CCK-8 assay and the expression of Best-3 was detected by Western blotting assay. The experiment was divided into normal control, HC injury group, VC treatment groups, HC + Best-3 siRNA group, HC + VC + Best-3 siRNA group, HC + pcDNA3.1 Best-3 group, and HC + VC + pcDNA3.1 Best-3 group. RESULTS: HC inhibited HMEC-1 cell viability was balanced with lower expression of Best-3 in a dose-dependent manner. Conversely, VC promoted HMEC-1 cell viability was paralleled to higher expression of Best-3 in a dose-dependent manner. Silencing Best-3 with Best-3 siRNA inhibited HMEC-1 cell viability, however, over-expression of Best-3 with pcDNA3.1 Best-3 promoted HMEC-1 cell viability. Moreover, VC and over-expression of Best-3 prevented HC-induced HMEC-1 cell apoptosis; however, silencing Best-3 further enhanced HC-induced HMEC-1 cell apoptosis. HC reduced Best-3 expression, which was alleviated by VC treatment. HC treatment decreased Bcl-2 expression, facilitated Bax expression. Both of VC and over-expression of Best-3 promoted Bcl-2 expression and decreased Bax expression. Additionally, VC and Best-3 expression have a synergistic effect. CONCLUSIONS: VC can efficiently attenuate HC-induced HMEC-1 cell injury, which may be related to promote Best-3 expression.

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma.

BACKGROUND/AIMS: Hepatocellular carcinoma (HCC) has a high morbidity as well as mortality and is believed to be one of the most prevalent cancers worldwide. The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in numerous cancers, including HCC. This study aimed to explore the role of MALAT1 in HCC progression. METHODS: The expression levels of MALAT1 and Vimentin in HCC tissues and relative pair-matched adjacent normal liver tissues were analyzed by RT-PCR, and immunohistochemistry. Using bioinformatics analysis and dual-luciferase assay, we examined the correlation between MALAT1 and miR-30a-5p. Dual-luciferase assay and western blotting suggested that Vimentin was a target of miR-30a-5p. A wound healing assay and transwell assays were employed to determine the effect of MALAT1 and miR-30a-5p on cell migration and invasion in HCC. RESULTS: Our data demonstrated that the levels of MALAT1 and Vimentin were upregulated in HCC tissues and that miR-30a-5p was a direct target of MALAT1. Silenced MALAT1 and overexpressed miR-30a-5p each inhibited cell migration and invasion. Additionally, dual-luciferase assay and western blotting demonstrated that MALAT1 could competitively sponge miR-30a-5p and thereby regulate Vimentin. CONCLUSION: Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion. Therefore, the MALAT1-miR-30a-5p-Vimentin axis is a potential therapeutic target and molecular biomarker in HCC.

MicroRNA-98 regulates osteogenic differentiation of human bone mesenchymal stromal cells by targeting BMP2.

To study the effects of microRNA-98 (miR-98) on human bone mesenchymal stromal cells (hBMSCs). The patients undergoing hip arthroplasty were selected by inclusion/exclusion criteria for this study. The extracted hBMSCs were detected of osteogenic differentiation by alizarin red S staining, and of cell phenotype by flow cytometry. Bioinformatics, dual luciferase report, western blotting, RT-PCR and immunoblotting were used in our study. The hBMSCs were divided into miR-98 mimics, miR-98 negative control (NC), miR-98 inhibitors, Mock and miR-98 inhibitors + siBMP2 groups. Human bone mesenchymal stromal cells were extracted and purified in vitro and had specific cytological morphology, surface markers and abilities of self-renewal and differentiation. Compared with the NC group and Mock group, the miR-98 mimics group showed increased miR-98 level while the miR-98 inhibitors group decreased miR-98 level (both P < 0.01). Dual luciferase reporter showed BMP2 was the target gene of miR-98. The levels of mRNA and protein expression of BMP2, protein expression of RUNX2, alkaline phosphatase activity and osteocalcin content significantly decreased in the miR-98 mimics group while increased in the miR-98 inhibitors group and showed no changes in the NC group and Mock group (all P < 0.05). The miR-98 mimics group showed obviously declined stained red particles and the miR-98 inhibitors group showed opposite result. After lowering the expression of miR-98, osteogenic differentiation ability of hBMSCs rose, which was weakened by the transfection with siBMP2. miR-98 may regulate osteogenic differentiation of hBMSCs by targeting BMP2.

Tunable emission, energy transfer and charge compensation in SrMoO4:Sm(3+),Tb(3+),Na(+) phosphor.

A series of SrMoO4:Sm(3+),Tb(3+),Na(+) phosphors was synthesized using a high-temperature solid-state reaction method in air. On excitation at 290 nm, SrMoO4:Sm(3+),Tb(3+) phosphor emitted light that varied systematically from green to reddish-orange on changing the Sm(3+) and Tb(3+) ion concentrations. The emission intensities of SrMoO4:Sm(3+) and SrMoO4:Sm(3+),Tb(3+) phosphors were increased two to four times due to charge compensation when Na(+) was added as a charge compensator. The luminescence mechanism and energy transfer could be explained using energy-level diagrams of the MoO4(2-) group, Sm(3+) and Tb(3+) ions. SrMoO4:Sm(3+),Tb(3+),Na(+) could be used as reddish-orange phosphor in white light-emitting diodes (LEDs) based on an ~ 405 nm near-UV LED chip. This research is helpful in adjusting and improving the luminescence properties of other phosphors.

Involvement of nephrin in human placental trophoblast syncytialization.

The placenta has numerous functions, such as transporting oxygen and nutrients and building the immune tolerance of the fetus. Cell fusion is an essential process for placental development and maturation. In human placental development, mononucleated cytotrophoblast (CTB) cells can fuse to form a multinucleated syncytiotrophoblast (STB), which is the outermost layer of the placenta. Nephrin is a transmembrane protein that belongs to the Ig superfamily. Previous studies have shown that nephrin contributes to the fusion of myoblasts into myotubes in zebrafish and mice, presenting a functional conservation with its Drosophila ortholog sticks and stones. However, whether nephrin is involved in trophoblast syncytialization remains unclear. In this study, we report that nephrin was localized predominantly in the CTB cells and STB of human placenta villi from first trimester to term pregnancy. Using a spontaneous fusion model of primary CTB cells, the expression of nephrin was found to be increased during trophoblast cell fusion. Moreover, the spontaneous syncytialization and the expression of syncytin 2, connexin 43, and human chorionic gonadotropin beta were significantly inhibited by nephrin-specific siRNAs. The above results demonstrate that nephrin plays an important role in trophoblast syncytialization.

Luminescence properties of red-emission Mg4 Nb2 O9:Eu3+ phosphor.

Red-emitting Mg4 Nb2 O9 :Eu(3+) phosphor is synthesized via a solid-state reaction method in air, and its crystal structure and luminescence are investigated. The phosphor can be excited efficiently by ~ 395 nm light, coupled well with a ~ 395 nm near-ultraviolet chip and emits red light at ~ 613 nm with sharp spectra due to (5) D0 → (7) F2 transition of the Eu(3+) ion. Mg4 Nb2 O9 :Eu(3+) phosphor sintered at 1350 ºC shows Commission international de I'Eclairage (CIE) chromaticity coordinates of x = 0.6354, y = 0.3592, and is a potential red-emitting phosphor candidate for white light-emitting diodes (W-LEDs) under ~ 395 nm near-ultraviolet LED chip excitation.

Screening Mutations of the Monogenic Syndromic High Myopia by Whole Exome Sequencing From MAGIC Project.

Purpose: This observational study aimed to identify mutations in monogenic syndromic high myopia (msHM) using data from reported samples (n = 9370) of the Myopia Associated Genetics and Intervention Consortium (MAGIC) project. Methods: The targeted panel containing 298 msHM-related genes was constructed and screening of clinically actionable variants was performed based on whole exome sequencing. Capillary sequencing was used to verify the identified gene mutations in the probands and perform segregation analysis with their relatives. Results: A total of 381 candidate variants in 84 genes and 85 eye diseases were found to contribute to msHM in 3.6% (335/9370) of patients with HM. Among them, the 22 genes with the most variations accounted for 62.7% of the diagnostic cases. In the genotype-phenotype association analysis, 60% (201/335) of suspected msHM cases were recalled and 25 patients (12.4%) received a definitive genetic diagnosis. Pathogenic variants were distributed in 18 msHM-related diseases, mainly involving retinal dystrophy genes (e.g. TRPM1, CACNA1F, and FZD4), connective tissue disease genes (e.g. FBN1 and COL2A1), corneal or lens development genes (HSF4, GJA8, and MIP), and other genes (TEK). The msHM gene mutation types were allocated to four categories: nonsense mutations (36%), missense mutations (36%), frameshift mutations (20%), and splice site mutations (8%). Conclusions: This study highlights the importance of thorough molecular subtyping of msHM to provide appropriate genetic counselling and multispecialty care for children and adolescents with HM.

Exome-wide association study identifies KDELR3 mutations in extreme myopia.

Extreme myopia (EM), defined as a spherical equivalent (SE) ≤ -10.00 diopters (D), is one of the leading causes of sight impairment. Known EM-associated variants only explain limited risk and are inadequate for clinical decision-making. To discover risk genes, we performed a whole-exome sequencing (WES) on 449 EM individuals and 9606 controls. We find a significant excess of rare protein-truncating variants (PTVs) in EM cases, enriched in the retrograde vesicle-mediated transport pathway. Employing single-cell RNA-sequencing (scRNA-seq) and a single-cell polygenic burden score (scPBS), we pinpointed PI16 + /SFRP4+ fibroblasts as the most relevant cell type. We observed that KDELR3 is highly expressed in scleral fibroblast and involved in scleral extracellular matrix (ECM) organization. The zebrafish model revealed that kdelr3 downregulation leads to elongated ocular axial length and increased lens diameter. Together, our study provides insight into the genetics of EM in humans and highlights KDELR3's role in EM pathogenesis.

Seasonally variable intestinal metagenomes of the red palm weevil (Rhynchophorus ferrugineus).

The intestinal microbes residing in the red palm weevil (RPW, Rhynchophorus ferrugineus) larva consume tender interior fibrous tissues of date palm trunks. The understanding of such microbiota at molecular level provides vital clues for the biological control of this devastating pest. Using pyrosequencing and shotgun strategy, we first study taxonomic profiles of the microbiota sampled at different months (March, July and November), and then confirm the impact of high-temperature stress on the microbial populations based on data from 16S rRNA amplicons using both field and laboratory samples. We further identify Klebsiella pneumoniae in November and Lactococcus lactis in July as the dominant species of the microbiota. We find that the RPW gut microbiota degrades polysaccharides and sucrose with hydrolases and that different active bacterial species in November and July are responsible for the symbiotic relationship between the microbiota and the host. Our results provide vital information for pest control and cellulolytic bacterial species characterization.

[Epithelial-mesenchymal transition in prostate cancer].

Prostate cancer (PCa) is a common disease in elderly men, its incidence ranking the second among all malignancies in males in Western countries and increasing in China in the last decade. Tumor metastasis is the main cause of death of PCa patients. In the development and progression of tumor, the tumorous cells in the infiltration area interact with their microenvironment, undergo epithelial-mesenchymal transition (EMT) and consequently cause distant metastases. So to study the role of EMT in the development and progression of tumor is of great significance for the treatment of PCa. This article reviews the relevant literature of the last 3 years and gives an overview of the factors affecting EMT in prostate cancer, aiming at a therapeutic target.

Medial open-wedge high tibial osteotomy for the treatment of degenerative varus knee osteoarthritis in geriatric patients: a retrospective study.

HTO has proven to be a cost-effective surgical procedure in the treatment of KOA, but few investigations have studied radiological changes and clinical effectiveness of OWHTO in geriatric patients. 76 patients were recruited in this retrospective study. According to the age, patients were divided into two groups (≤ 60, Group "Young"; > 60, Group "Geriatric"). Demographic data, radiological imaging and postoperative complications were analyzed. Kellgren-Lawrence grade (K-L), weight-bearing line ratio (WBLR); posterior tibial slope angle (PTS); American knee score (AKS); Western Ontario and McMaster Universities Arthritis Index (WOMAC) and visual analog scale (VAS) were introduced to estimate the clinical outcome of OWHTO. There were 18 male and 58 female patients in the present study with a mean age of 58.5 ± 9.2 years (ranges from 40 to 82 years); the average age was 51.4 ± 4.1 years and 67.3 ± 4.9 years for group Y and G respectively, 44.7% and 31.5% patients were older than 60 and 65 years. BMI for the 76 patients was 26.6 ± 3.2 kg/m2, and geriatric patients were more likely accompanied by one or more comorbidities (70.6 vs. 45.2%). There were 34 and 42 patients in group Geriatric and group Young respectively, and no significant difference of MPTA, WBLR, PTS and WOMAC, VAS, AKS and ROM between the two group (P > 0.05) were found. After more than a two-year follow-up period, postoperative WBLR, AKS, WOMAC and VAS were much more desired than preoperative, and no significant difference of these variables between the young and geriatric group (P > 0.05), however, elderly patients were more likely to suffer from a longer bone union time. OWHTO can avoid geriatric patients from undergoing secondary knee surgery in the short term, however the survival rate of OWHTO in geriatric patients should be ultimately clarified by different studies.

Long non-coding RNA AC245100.4 activates the PI3K/AKT pathway to promote PCa cell proliferation by elevating PAR2.

Background: Prostate cancer (PCa) is among the most generally diagnosed cancers in males. A long non-coding RNA (lncRNA) called AC245100.4 has been discovered and linked to PCa carcinogenesis. However, its specific and potential mechanism is uncertain in PCa. In this research, we investigated the role of AC245100.4 in cell proliferation and the underlying mechanism in PCa cells. Methods: qRT-PCR assays were utilized to detect AC245100.4 expression and confirm its downstream target. The pathways related to AC245100.4 were identified by RAP-MS. PCa cell proliferation was experimented by Cell Counting Kit-8 and Colony formation assays. Western blot was performed to detect PAR2, AKT, p-AKT, Cyclin D1 and PCNA expression. Results: AC245100.4/PAR2 overexpression promotes PCa cell proliferation and the opposite results are obtained after AC245100.4/PAR2 knockdown. Mechanistically, we found that PAR2 is confirmed as the AC245100.4 downstream target and AC245100.4 promotes PCa cell proliferation by regulating PAR2. AC245100.4 promotes PCa cell proliferation via PI3K/AKT pathway. Rescue assays validated that PAR2 knockdown reversed the impact of AC245100.4 overexpression on increasing p-AKT protein levels. Conclusion: This research revealed that AC245100.4 enhances cell proliferation in PCa cells through modulating the PAR2/PI3K/AKT axis, which may offer novel tumor markers and potential therapeutic targets for PCa.