Efficacy of Arthroscopy-Assisted Minimally Invasive Surgery in the Treatment of Patients with Tibial Plateau Fractures.

Objective: This study analyzes the therapeutic effect of arthroscopy-assisted minimally invasive surgery in patients with tibial plateau fractures (TPFs) and its influence on knee function and range of motion (ROM) recovery. Methods: This study enrolled 84 patients with TPFs admitted to the researchers' hospital between March 2021 and May 2022 as the study subjects, including 42 patients treated with open reduction and internal fixation (observation group) and 42 patients treated with arthroscopy-assisted minimally invasive surgery (experimental group). Then, perioperative indexes, knee symptom scores, knee function scores, knee ROM, and postoperative complications were compared between these two groups. Results: Surgery time was significantly shorter, intraoperative bleeding was less, and the time of the first off-bed activity was signally earlier in the experimental group than in the observation group (P < .05). All postoperative Lysholm and Rasmussen scores in both groups increased compared with preoperative scores, and the degree of increase was higher in the experimental group than in the observation group (P < .05). The range of flexion, extension, and internal/external rotation angles of patients was more extensive in both groups after surgery than before surgery, and the improvement of the experimental group was greater than that of the observation group (P < .05). The experimental group had a considerably lower incidence of postoperative complications than the observation group (P < .05). Conclusion: Arthroscopy-assisted minimally invasive surgery is highly effective in treating TPFs. Specifically, this surgery further improves knee symptoms, promotes the recovery of knee function, elevates knee ROM, and reduces the risk of postoperative complications compared to traditional open reduction and internal fixation.

Effects of mesencephalic astrocyte-derived neurotrophic factor on sepsis-associated acute kidney injury.

BACKGROUND: To determine the protective role of mesencephalic astrocyte-derived neurotrophic factor (MANF) in regulating sepsis-associated acute kidney injury (S-AKI). METHODS: A total of 96 mice were randomly divided into the control group, control+MANF group, S-AKI group, and S-AKI+MANF group. The S-AKI model was established by injecting lipopolysaccharide (LPS) at 10 mg/kg intraperitoneally. MANF (200 µg/kg) was administered to the control+MANF and S-AKI+MANF groups. An equal dose of normal saline was administered daily intraperitoneally in the control and S-AKI groups. Serum and kidney tissue samples were obtained for biochemical analysis. Western blotting was used to detect the protein expression of MANF in the kidney, and enzyme-linked immunosorbent assay (ELISA) was used to determine expression of MANF in the serum, pro-inflammatory cytokines (tumor necrosis factor-α [TNF-α] and interleukin-6 [IL-6]). Serum creatinine (SCr), and blood urea nitrogen (BUN) were examined using an automatic biochemical analyzer. In addition, the kidney tissue was observed for pathological changes by hematoxylin-eosin staining. The comparison between two groups was performed by unpaired Student's t-test, and statistics among multiple groups were carried out using Tukey's post hoc test following one-way analysis of variance (ANOVA). A P-value <0.05 was considered statistically significant. RESULTS: At the early stage of S-AKI, MANF in the kidney tissue was up-regulated, but with the development of the disease, it was down-regulated. Renal function was worsened in the S-AKI group, and TNF-α and IL-6 were elevated. The administration of MANF significantly alleviated the elevated levels of SCr and BUN and inhibited the expression of TNF-α and IL-6 in the kidney. The pathological changes were more extensive in the S-AKI group than in the S-AKI+MANF group. CONCLUSION: MANF treatment may significantly alleviate renal injury, reduce the inflammatory response, and alleviate or reverse kidney tissue damage. MANF may have a protective effect on S-AKI, suggesting a potential treatment for S-AKI.

Multi-type emission factors quantification of black carbon from agricultural machinery based on the whole tillage processes in China.

Black carbon (BC), as one of the short-lived climate pollutants, is becoming more prominent contribution from non-road mobile source, especially for agricultural machinery (AM) in China. However, the understanding of BC emissions from AM is still not clear, and the BC emission factors (EFs) are also limited. In this study, we conducted real-world measurements on twenty AM to investigate the instantaneous BC emission characteristics and quantify BC EFs under the whole tillage processes. We find the instantaneous BC emissions and fuel consumptions are obvious differences and present good synchronization under different tillage processes. Multi-type (CO2-, fuel-, distance-, time-, and area-based) EFs of BC are developed, which are significantly affected by different tillage processes and emission standards of the used AM. While AM conducting rotary tillage, ploughing, harvest corn and harvest wheat on the same area of land, total BC emissions by using the China III emission standard AM will be reduced by 56%, 36%, 88%, and 87% than those by using China II emission standard AM, respectively. Furthermore, for corn and wheat production under the whole tillage processes, BC EFs are 16.90 (6.03-39.12) g/hm2 and 18.18 (5.91-38.69) g/hm2, CO2 EFs are 112.64 (72.07-195.98) g/hm2 and 103.72 (71.47-167.02) g/hm2, respectively. We estimate the BC and CO2 emissions from wheat and corn productions based on the average area-based EFs. The large fluctuation ranges of BC and CO2 emissions in different tillage processes and the whole processes can reflect that the use of AM in China is uneven. It also indicates that there is a large space for BC and CO2 emission reduction and optimization. Therefore, more attention should be paid to the control of BC and CO2 emissions from AM. We believe that the recommended multi-type EFs are applicable for the quantification of BC emissions from AM in China and other countries.

Aberrant expression of GSTM5 in lung adenocarcinoma is associated with DNA hypermethylation and poor prognosis.

BACKGROUND: Glutathione-S transferases (GSTs) comprise a series of critical enzymes involved in detoxification of endogenous or xenobiotic compounds. Among several GSTs, Glutathione S-transferases mu (GSTM) has been implicated in a number of cancer types. However, the prognostic value and potential functions of the GSTM family genes have not been investigated in lung adenocarcinoma (LUAD). METHODS: We examined the expression of GSTM5 in LUAD and identified associations among GSTM5 expression, clinicopathological features, survival data from the Cancer Genome Atlas (TCGA). The correlation between GSTM5 DNA methylation and its expression was analyzed using the MEXPRESS tool and UCSC Xena browser. The methylation status of GSTM5 in the promoter region in lung cancer cells was measured by methylation-specific PCR (MSP). After 5-aza-2'-deoxycytidine treatment of lung cancer cells, expression of GSTM5, cell proliferation and migration were assessed by RT-PCR, CCK-8 and transwell assays, respectively. RESULTS: The results showed that GSTM5 was abnormally down-regulated in LUAD patients' tissues, and patients with low GSTM5 expression level had significantly shorter OS. Cox regression analyses revealed that GSTM5 was associated with overall survival (OS) of LUAD patients, which expression was an independent prognostic indicator in terms of OS (hazard ratio: 0.848; 95% CI: 0.762-0.945; P = 0.003). In addition, we found the promoter region of GSTM5 was hypermethylated in the tumor tissue compared with adjacent normal tissues, and the average methylation level of GSTM5 were moderately correlated with its expression. Moreover, methylation-specific PCR also showed that the GSTM5 gene promoter was hypermethylated in lung cancer cells, and treatment with 5-Aza-CdR can restore the gene expression and inhibit cell proliferation and migration. Finally, Gene Set Enrichment Analysis (GSEA) revealed that low GSTM5 expression was significantly related to DNA repair pathways. CONCLUSION: Our data demonstrate that low GSTM5 expression and its high DNA methylation status may act as a novel putative molecular target gene for LUAD.

Quantitative of instantaneous BC emissions based on vehicle specific power from real-world driving diesel trucks in China.

In-depth exploration of the potential links between instantaneous black carbon (BC) emissions and driving parameters from real-world diesel trucks (DTs) is a key step toward development of a highly flexible vehicle emissions estimation system. In this study, we conducted real-world measurements on 22 DTs with mainstream types and emission standards, and obtained instantaneous data of BC emissions and vehicle driving. Since vehicle specific power (VSP) is an excellent surrogate for engine load, we characterize the instantaneous BC emissions and VSP distributions, and then establish links between VSP and fuel consumption, VSP and BC emission rates, VSP and BC emission factors (EFs), respectively. We find that BC emission rates of China V light-duty DTs installed with diesel particulate filter (DPF) are significantly lower (2 to 3 orders of magnitude) than those with China III and China IV. Frequent acceleration and deceleration of vehicles maybe the main reason leads to high BC emissions. The distribution of VSP is mainly concentrated in the ranges of -30 to 35 kW/t in the scope of this study. We find that VSP and BC EFs did not show a consistent pattern for all tested DTs, and BC EFs present obvious fluctuations with the VSP variation. The average fuel-based BC EFs vary by factors of 2.27-8.25 from the lowest to highest EFs. Through a fitting of the third-order polynomial function, we finally quantify and provide fitting formulas of BC EFs and VSP under more detailed categorization. Our results can provide important data support for accurate quantification of BC EFs, and even emission inventory calculations.

Non-negligible emissions of black carbon from non-road construction equipment based on real-world measurements in China.

Non-road construction equipment (NRCE) has become a vital contributor to urban air pollutants with the rapid urbanization in China. Black carbon (BC), as a key pollutant emitted from NRCE (mainly diesel-fueled), has attracted considerable concerns due to adverse impacts on climate change, visibility, and human health. However, the understanding of its emissions is still unclear based on limited research results. In this study, we conducted real-world measurements on BC emissions from 12 excavators and 9 loaders to characterize the variation and quantify fuel-based emission factors (EFs) by using a synchronous platform based on PEMS (SP-PEMS). We analyzed the impacts of key factors (operation mode, emission standard, and engine rated power) on BC emission comprehensively. High BC emission in working mode may be mainly owing to the increase of fuel consumption and the deterioration of air-fuel ratio. With more stringent emission standards, BC EFs of all tested NRCE present significant decreasing trends. Interestingly, NRCE with high rated power generally exhibits lower BC emissions. Through comparison, we find BC EFs in this study are generally higher than elemental carbon (EC) EFs reported in previous studies, which will lead BC emissions from NRCE to be underestimated while EC EFs are used instead of BC EFs. Furthermore, BC EFs of NRCE with Stage III are significantly higher (1-3 orders of magnitude) than those of on-road diesel trucks with the current mainstream emission standards of China IV and China V, which reinforces the urgency and importance of controlling BC emissions from NRCE in China. Finally, we recommend BC EFs of excavators and loaders under different emission standards and operation modes, and which preliminarily fills the gap in localized BC EFs of typical NRCE to relieve the urgent needs for emission inventory calculation.

Sera and lungs metabonomics reveals key metabolites of resveratrol protecting against PAH in rats.

Pulmonary arterial hypertension (PAH) is a type of high morbidity and mortality disease. Currently, the intrinsic metabolic alteration and potential mechanism of PAH are still not fully uncovered. Previously, we have found that polyphenol resveratrol (Rev) reversed the remodeling of the pulmonary vasculature and decreased the number of mitochondria in pulmonary arterial smooth muscle cells (PASMCs) (Lei Yu et al. (2017)). However, potential effects of Rev on the changed metabolic molecules derived from lung tissue and serum have no fully elucidated. Thus, we conducted a systematic elaboration through the metabonomics method. Various of metabolites in different pathways including amino acid metabolism, tricarboxylic acid cycle (TCA), acetylcholine metabolism, fatty acid metabolism and biosynthesis in male Wistar rats' sera and lung tissues were explored in three groups (normal group, PAH group, PAH and Rev treatment group). We found that leucine and isoleucine degradation, valine, leucine and isoleucine biosynthesis, tryptophan metabolism and aminoacyl-tRNA biosynthesis were involved in the development of PAH. Hydroxyphenyllactic, isopalmitic acid and cytosine might be significant key metabolites. Further work in this area may inform personalized treatment approaches in clinical practice of PAH through elucidating pathophysiology mechanisms of experimental verification.

Polycyclic and nitro-polycyclic aromatic hydrocarbon pollution characteristics and carcinogenic risk assessment of indoor kitchen air during cooking periods in rural households in North China.

Medium-flow atmospheric samplers were used to collect particulate (PM2.5) and gaseous samples from the indoor kitchen of each of 35 randomly selected rural houses in North China while a meal was being cooked. The concentrations of 16 polycyclic aromatic hydrocarbons (PAHs) and 9 nitro-PAHs (NPAHs) in the samples were quantified by high-performance liquid chromatography (HPLC). This study provided the real PAH and NPAH pollution characteristics and carcinogenic risk produced by cooking in rural indoor kitchens in North China. The mean PAH and NPAH concentrations in air in the indoor kitchens during cooking periods were 4049.1 and 1741.6 ng/m3, respectively. The PAH and NPAH concentrations were lower in the particulate phase than the gaseous phase. The mean PAH and NPAH concentrations were much higher for cooking using coal than for cooking using liquefied petroleum gas (LPG) or electricity. The PAH and NPAH benzo[a]pyrene toxic equivalent (TEQBaP) concentrations for cooking using coal were 1823.3 and 2760.9 ng/m3, respectively. Lower PAH and NPAH concentrations were found in kitchens with than without range hoods. Range hoods decreased the PAH and NPAH TEQBaP concentrations by 68.8% and 61.9%, respectively. Appropriate fuel and ventilation choice will improve air pollution in indoor kitchens during cooking. The results provide important evidence for changing cooking habits and developing policies for cooking in rural China.

Down-regulation of lncRNA Gas5 promotes hypoxia-induced pulmonary arterial smooth muscle cell proliferation by regulating KCNK3 expression.

Pulmonary hypertension (PH) is a progressive and potentially serious lung disease, defined by an abnormal elevation of pulmonary arterial pressure. PH occurs for many reasons, and hypoxia is considered as an important stimulus for the disease. Proliferation and migration of pulmonary artery smooth muscular cells (PASMCs) in the small peripheral pulmonary arteries are common characteristic features in hypoxia-induced PH (HPH). However, the mechanisms involved in the hypoxia-induced cell proliferation and migration are not clear. The aim of the present study was to investigate the role of lncRNA Gas5 in the hypoxia-stimulated proliferation and migration of human PASMCs (hPASMCs). We found that the expression of Gas5 was down-regulated in a rat model with hypoxia and in cultured hypoxic hPASMCs, and silence of Gas5 significantly promoted hPASMCs proliferation and migration in both normal and hypoxia condition. Subsequent studies revealed that miR-23b-3p interacted with Gas5 by directly targeting the miRNA-binding site in the Gas5 sequence, and qRT-PCR results showed miR-23b-3p and Gas5 could affect each other's expression, respectively. Further study demonstrated that Gas5 acted as a competing endogenous RNA (ceRNA) for miR-23b-3p to modulate the KCNK3 expression, and these interactions led to promotion of hPASMCs proliferation and migration. This study identified that Gas5/miR-23b-3p/KCNK3 axis may be a mechanism that hypoxia-induced PASMCs proliferation and migration, providing a strategy for clinical treatment of HPH in the future.

Dacomitinib, a new pan-EGFR inhibitor, is effective in attenuating pulmonary vascular remodeling and pulmonary hypertension.

Accumulating evidence suggests that epidermal growth factor receptor (EGFR) plays a role in the progression of pulmonary arterial hypertension (PAH). Clinically-approved epidermal growth factor inhibitors such as gefitinib, erlotinib, and lapatinib have been explored for PAH. However, None of them were able to attenuate PAH. So, we explored the role of dacomitinib, a new pan-EGFR inhibitor, in PAH. Adult male Sprague-Dawley rats were used to study hypoxia- or monocrotaline-induced right ventricular remodeling as well as systolic function and hemodynamics using echocardiography and a pressure-volume admittance catheter. Morphometric analyses of lung vasculature and pressure-volume vessels were performed. Immunohistochemical staining, flow cytometry, and viability, as well as scratch-wound, and Boyden chamber migration assays were used to identify the roles of dacomitinib in pulmonary artery smooth muscle cells (PASMCs). The results revealed that dacomitinib has a significant inhibitory effect on the thickening of the media, adventitial collagen increased. Dacomitinib also has a significant role in attenuating pulmonary artery pressure and right ventricular hypertrophy. Additionally, dacomitinib inhibits hypoxia-induced proliferation, migration, autophagy and cell cycle progression through PI3K-AKT-mTOR signaling in PASMCs. Our study indicates that dacomitinib inhibited hypoxia-induced cell cycle progression, proliferation, migration, and autophagy of PASMCs, thereby attenuating pulmonary vascular remodeling and development of PAH via the PI3K-AKT-mTOR signaling pathway. Overall, dacomitinib may serve as new potential therapeutic for the treatment of PAH.

Reverse the down regulation of miR-92b-3p by hypoxia can suppress the proliferation of pulmonary artery smooth muscle cells by targeting USP28.

MiR-92b-3p has been shown to take part in several disease by regulate proliferation, apoptosis, differentiation and metastasis. However, the role of miR-92b-3p in pulmonary arterial hypertension (PAH) has not been illustrated clearly. Here, we found the level of miR-92b-3p which mainly located in the smooth muscle layer was down-regulation under hypoxic condition. It can inhibit pulmonary artery smooth muscle cells (PASMCs) proliferation and cell cycle progression. Through luciferase assay, miR-92b-3p bound to the 3'-UTR of USP28. we found that there was a significant negative relation between the level of miR-92b-3p and USP28 at protein level and reversed the down regulation of miR-92b-3p by hypoxia can suppress the proliferation of pulmonary artery smooth muscle cells by targeting USP28. These results suggested that miR-92b-3p acted a potential proliferation regulator in PASMCs and it maybe a novel treatment target of PAH.

Characterization and carcinogenic risk assessment of polycyclic aromatic and nitro-polycyclic aromatic hydrocarbons in exhaust emission from gasoline passenger cars using on-road measurements in Beijing, China.

The polycyclic aromatic hydrocarbon (PAH) and nitro-polycyclic aromatic hydrocarbon (NPAH) emissions from 16 gasoline passenger cars, encompassing five emission standards and two driving conditions, were tested using a portable emission measurement system (PEMS) in Beijing under on-road conditions. In total, 16 PAHs and 9 NPAHs were quantified in both the gaseous and particulate phases by high-performance liquid chromatography (HPLC). The results indicated that lower PAH and NPAH emissions were observed with improved emission standards, especially for China 3 to China 5 vehicles (P < 0.05). Higher emission factors (EFs) were detected on nonhighway roads than on highway roads due to incomplete combustion. Although most PAHs and NPAHs were in the gas-phase, the TEQBaP of the particulate-phase PAHs was 4.2 times higher than that of the gas-phase PAHs, whereas the opposite pattern was observed for NPAHs. The TEQBaP EFs on nonhighway roads were 1.0-2.3 times higher than those on highway roads. The results of this study will be valuable for estimating the emissions and performing carcinogenic risk assessment of PAHs and NPAHs from urban gasoline passenger cars on roads. Formulating more stringent regulations and emission control technologies for PAHs and NPAHs is important.

Better rotational control but similar outcomes with the outside-in versus the transtibial drilling technique for anterior cruciate ligament reconstruction: a systematic review of comparative trials.

INTRODUCTION: This study was a systematic review comparing the clinical outcomes of using the transtibial (TT) versus the outside-in (OI) technique for anterior cruciate ligament (ACL) reconstruction. MATERIALS AND METHODS: A comprehensive literature search was conducted using multiple databases, including Medline, Embase, and Cochrane. All databases were searched from the earliest records through August 2017 using the following Boolean operators: transtibial AND (outside-in OR out-in OR two incisions) AND anterior cruciate ligament. All prospective and retrospective controlled trials were retrieved that directly compared physical examination and knee function scores and patient-rated outcomes between the TT and OI techniques. RESULTS: Four prospective and three retrospective articles were identified by the search, and the findings suggested that the OI was superior to the TT technique for preparing the femoral tunnel based on the pivot shift test (p = 0.05). There was no statistically significant difference between the two treatment groups in International Knee Documentation Committee (IKDC) grades, IKDC scores, Lysholm scores, Tegner scores, or the Lachman test. CONCLUSIONS: No statistically significant differences were found in clinical functional results when comparing patients who underwent ACL reconstruction with the TT or OI techniques. However, the OI technique was found to be advantageous in conferring increased rotational stability as revealed by the pivot shift test. Additional studies with larger sample sizes are needed to make more precise conclusions. LEVEL OF EVIDENCE: Therapeutic study (systematic review), Level III.

Antitumor activity of adenoviral vector containing T42 and 4xT42 peptide gene through inducing apoptosis of tumor cells and suppressing angiogenesis.

The T42 peptide, generated from two active fragments of tumstatin, has been shown to have anti­tumor activity. The adenoviral vector is the most frequently used vector in research and clinical trials for gene therapy. In the present study, the anti­tumor activity of the T42 peptide and quadruple T42 (4xT42) peptide adenoviral vectors were elucidated for the first time, to the best of our knowledge. Human embryonic kidney 293 cells were infected with plasmid adenovirus (pAd)­enhanced green fluorescent protein (EGFP)­T42 or pAd­EGFP­4xT42 and the expression of the T42 and 4xT42 genes was confirmed by the identification of GFP expression and reverse transcription polymerase chain reaction experiments. The anti­cancer effects of pAd­EGFP­T42 and pAd­EGFP­4xT42 on breast cancer cells in vivo and in vitro were subsequently investigated. The results indicated that the packaging of the recombinant adenoviruses with the viral titer was successful, following purification at 5x109 plaque forming units/ml. The results also revealed that the recombinant adenoviruses promoted apoptosis in MCF­7 breast cancer cells and inhibited cancer growth. Through the analysis of caspase­3, B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein expression, it was demonstrated that the T42/4xT42 peptide may induce apoptosis via the mitochondrial pathway. In addition, mouse xenograft experiments confirmed that the T42 peptide inhibited tumor growth and reduced angiogenesis in vivo. In conclusion, the results of the present study indicated that the T42 and 4xT42 peptide genes, transfected by a recombinant adenovirus, may provide a potential novel strategy for the treatment of breast cancer.