Regulatory role of PDK1 via integrated gene analysis of mitochondria-immune response in periodontitis.

AIMS: To investigate the association between mitochondrial events and immune response in periodontitis and related regulatory genes. MAIN METHODS: Gene expression profiles in gingival tissues were retrieved from the Gene Expression Omnibus. Mitochondria-immune response-related differentially expressed genes (MIR-DEGs) between the healthy and periodontitis samples were determined. WGCNA, GO, and KEGG were used to investigate the function and the enriched pathways of MIR-DEGs. The correlation between MIR-DEGs expression and clinical probing pocket depth was analyzed. The MIR-DEGs were further identified and verified in animal samples. A periodontitis model was established in C57BL/6 mice with silk ligation. Micro-computed tomography was used to assess alveolar bone loss. Western blot, quantitative real-time polymerase chain reaction, and immunohistochemical analyses further validated the differential expression of the MIR-DEGs. KEY FINDINGS: A total of ten MIR-DEGs (CYP24A1, PRDX4, GLDC, PDK1, BCL2A1, CBR3, ARMCX3, BNIP3, IFI27, and UNG) were identified, the expression of which could effectively distinguish patients with periodontitis from the healthy controls. Enhanced immune response was detected in the periodontitis group with that in the healthy controls, especially in B cells. PDK1 was a critical MIR-DEG correlated with B cell immune response and clinical periodontal probing pocket depth. Both animal and clinical periodontal samples presented higher gene and protein expression of PDK1 than the control samples. Additionally, PDK1 colocalized with B cells in both animal and clinical periodontal tissues. SIGNIFICANCE: Mitochondria participate in the regulation of the immune response in periodontitis. PDK1 may be the key mitochondria-related gene regulating B-cell immune response in periodontitis.

3-methyl-1H-indol-1-yl dimethylcarbamodithioate attenuates periodontitis through targeting MAPK signaling pathway-regulated mitochondrial function.

Periodontitis, the second most common oral disease, is primarily initiated by inflammatory responses and osteoclast differentiation, in which the MAPK signaling pathway and mitochondrial function play important roles. 3-methyl-1H-indol-1-yl dimethylcarbamodithioate (3o), a hybrid of indole and dithiocarbamate, was first synthesized by our group. It has shown anti-inflammatory activity against lipopolysaccharide-induced acute lung injury. However, it is not known if 3o can exert effects in periodontitis. In vitro study: LPS-induced macrophage inflammation initiation and a receptor activator of nuclear factor κB ligand-stimulated osteoclast differentiation model were established. Cell viability, inflammatory cytokines, osteoclast differentiation, the MAPK signaling pathway, and mitochondrial function before and after treatment with 3o were investigated. In vivo study: Alveolar bone resorption, inflammatory cytokine expression, osteoclast differentiation, and the underlying mechanisms were assessed in mice with periodontitis. Inflammatory cytokine expression and osteoclast differentiation appeared downregulated after 3o treatment. 3o inhibited the MAPK signaling pathway and restored mitochondrial function, including mitochondrial reactive oxygen species, mitochondrial membrane potential, and ATP production. Meanwhile, 3o reduced inflammation activation and bone resorption in mice with periodontitis, reflected by the decreased expression of inflammatory cytokines and osteoclasts, implying that 3o inhibited the MAPK signaling pathway and the mitochondrial oxidative DNA damage marker 8-OHdG. These results highlight the protective role of 3o in periodontitis in mice and reveal an important strategy for preventing periodontitis.

Mitochondrial impairment and downregulation of Drp1 phosphorylation underlie the antiproliferative and proapoptotic effects of alantolactone on oral squamous cell carcinoma cells.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of the most prevalent and fatal oral cancers. Mitochondria-targeting therapies represent promising strategies against various cancers, but their applications in treating OSCC are limited. Alantolactone (ALT) possesses anticancer properties and also regulates mitochondrial events. In this study, we explored the effects of ALT on OSCC and the related mechanisms. METHODS: The OSCC cells were treated with varying concentrations and duration of ALT and N-Acetyl-L-cysteine (NAC). The cell viability and colony formation were assessed. The apoptotic rate was evaluated by flow cytometry with Annexin V-FITC/PI double staining. We used DCFH-DA and flow cytometry to detect reactive oxygen species (ROS) production and DAF-FM DA to investigate reactive nitrogen species (RNS) level. Mitochondrial function was reflected by mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and ATP levels. KEGG enrichment analyses determined the mitochondrial-related hub genes involved in OSCC progression. Dynamin-related protein 1 (Drp1) overexpression plasmids were further transfected into the cells to analyze the role of Drp1 in OSCC progression. Immunohistochemistry staining and western blot verified the expression of the protein. RESULTS: ALT exerted anti-proliferative and pro-apoptosis effects on OSCC cells. Mechanistically, ALT elicited cell injury by promoting ROS production, mitochondrial membrane depolarization, and ATP depletion, which were reversed by NAC. Bioinformatics analysis showed that Drp1 played a crucial role in OSCC progression. OSCC patients with low Drp1 expression had a higher survival rate. The OSCC cancer tissues presented higher phosphorylated-Drp1 and Drp1 levels than the normal tissues. The results further showed that ALT suppressed Drp1 phosphorylation in OSCC cells. Moreover, Drp1 overexpression abolished the reduced Drp1 phosphorylation by ALT and promoted the cell viability of ALT-treated cells. Drp1 overexpression also reversed the mitochondrial dysfunction induced by ALT, with decreased ROS production, and increased mitochondrial membrane potential and ATP level. CONCLUSIONS: ALT inhibited proliferation and promoted apoptosis of oral squamous cell carcinoma cells via impairment of mitochondrial homeostasis and regulation of Drp1. The results provide a solid basis for ALT as a therapeutic candidate for treating OSCC, with Drp1 being a novel therapeutic target in treating OSCC.

Activation of PGC-1α-dependent mitochondrial biogenesis supports therapeutic effects of silibinin against type I diabetic periodontitis.

AIM: To investigate whether silibinin impacts diabetic periodontitis (DP) via mitochondrial regulation. MATERIALS AND METHODS: In vivo, rats were divided into control, diabetes, DP and DP combined with silibinin groups. Diabetes and periodontitis were induced by streptozocin and silk ligation, respectively. Bone turnover was evaluated by microcomputed tomography, histology and immunohistochemistry. In vitro, human periodontal ligament cells (hPDLCs) were exposed to hydrogen peroxide (H2 O2 ) with or without silibinin. Osteogenic function was analysed by Alizarin Red and alkaline phosphatase staining. Mitochondrial function and biogenesis were investigated by mitochondrial imaging assays and quantitative polymerase chain reaction. Activator and lentivirus-mediated knockdown of peroxisome proliferator-activated receptor gamma-coactivator 1-alpha (PGC-1α), a critical regulator of mitochondria biogenesis, was used to explore the mitochondrial mechanisms. RESULTS: Silibinin attenuated periodontal destruction and mitochondrial dysfunction and enhanced mitochondrial biogenesis and PGC-1α expression in rats with DP. Meanwhile, silibinin promoted cell proliferation, osteogenesis and mitochondrial biogenesis and increased the PGC-1α level in hPDLCs exposed to H2 O2 . Silibinin also protected PGC-1α from proteolysis in hPDLCs. Furthermore, both silibinin and activator of PGC-1α ameliorated cellular injury and mitochondrial abnormalities in hPDLCs, while knockdown of PGC-1α abolished the beneficial effect of silibinin. CONCLUSIONS: Silibinin attenuated DP through the promotion of PGC-1α-dependent mitochondrial biogenesis.

Silibinin Attenuates Experimental Periodontitis by Downregulation of Inflammation and Oxidative Stress.

Periodontitis is an oral microbiota-induced inflammatory disease, in which inflammation and oxidative stress play a critical role. Silibinin (SB), a Silybum marianum-derived compound, exhibits strong anti-inflammatory and antioxidative properties. We adopted a rat ligature-induced periodontitis model and a lipopolysaccharide- (LPS-) stimulated human periodontal ligament cells (hPDLCs) model to evaluate the protective effects of SB. In the in vivo model, SB reduced alveolar bone loss and apoptosis of PDLCs in the periodontal tissue. SB also maintained the expression of nuclear factor-E2-related factor 2 (Nrf2), a key regulator of cellular resistance to oxidative stress, and attenuated lipid, protein, and DNA oxidative damages in the periodontal lesion area. Meanwhile, in the in vitro model, SB administration reduced the production of intracellular reactive oxidative species (ROS). Furthermore, SB exerted a strong anti-inflammatory property in both in vivo and in vitro models by inhibiting the expression of inflammatory mediators including nuclear factor-κB (NF-κB) as well as nucleotide binding oligomerization domain- (NOD-) like receptor family pyrin domain-containing 3 (NLRP3) and downregulating the levels of proinflammatory cytokines. This study, for the first time, demonstrates that SB exhibits the anti-inflammatory and antioxidative properties against periodontitis by downregulating the expression of NF-κB and NLRP3 and upregulating Nrf2 expression, suggesting a promising potential clinical application of SB in periodontitis.

CypD-mediated mitochondrial dysfunction contributes to titanium ion-induced MC3T3-E1 cell injury.

Titanium (Ti) ion can stimulate osteoblast apoptosis and therefore have a high potential to play a negative role in the aseptic loosening of implants. Mitochondrial abnormalities are closely related to osteoblast dysfunction. However, the mitochondrial molecular mechanism of Ti ion induced osteoblastic cell apoptosis is still unclear. This study investigated in vitro mitochondrial oxidative stress (mtROS) mediated mitochondrial dysfunction involved in Ti ion-induced apoptosis of murine MC3T3-E1 osteoblastic cells. In addition to reducing mitochondrial membrane potential (MMP) and decreasing adenosine triglyceride production, exposure to Ti ions increased mitochondrial oxidative stress. Moreover, mitochondrial abnormalities significantly contributed to Ti ion induction of osteoblastic cellular apoptosis. A mitochondria-specific antioxidant, mitoquinone (MitoQ), alleviated Ti ion-induced mitochondrial dysfunction and apoptosis in osteoblastic cells, indicating that Ti ion mainly induces mitochondrial oxidative stress to produce a cytotoxic effect on osteoblasts. Here we show that the primary regulator of mitochondrial permeability transition pore (mPTP), cyclophilin D (CypD), is involved in mitochondrial dysfunction and osteoblast cell apoptosis induced by Ti ion. Overexpression of CypD exacerbates osteoblast apoptosis and impairs osteogenic function. Moreover, detrimental effects of CypD were rescued by cyclosporin A (CsA), an inhibitor of CypD, which shows its protective effect on mitochondrial and osteogenic osteoblast functions. Based on new insights into the mitochondrial mechanisms underlying Ti ion-induced apoptosis of osteoblastic cells, the findings of this study lay the foundation for the clinical use of CypD inhibitors to prevent or treat implant failure.

Independent and Interactive Effects of Environmental Conditions on Aerosolized Surrogate SARS-CoV-2 - Beijing, China, June to September 2020.

What is already known about this topic?: Environmental factors such as temperature and humidity play important roles in the transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via droplets/aerosols. What is added by this report?: Higher relative humidity (61%-80%), longer spreading time (120 min), and greater dispersal distance (1 m) significantly reduced SARS-CoV-2 pseudovirus loads. There was an interaction effect between relative humidity and spreading time. What are the implications for public health practice?: The findings contribute to our understanding of the impact of environmental factors on the transmission of SARS-CoV-2 via airborne droplets/aerosols.

Cationic antimicrobial peptide NRC-03 induces oral squamous cell carcinoma cell apoptosis via CypD-mPTP axis-mediated mitochondrial oxidative stress.

Pleurocidin-family cationic antimicrobial peptide NRC-03 exhibits potent and selective cytotoxicity towards cancer cells. However, the anticancer effect of NRC-03 in oral squamous cell carcinoma (OSCC) and the molecular mechanism of NRC-03 induced cancer cell death is still unclear. This study focused to investigate mitochondrial oxidative stress-mediated altered mitochondrial function involved in NRC-03-induced apoptosis of OSCC cells. NRC-03 entered the OSCC cells more easily than that of normal cells and bound to mitochondria as well as the nucleus, causing cell membrane blebbing, mitochondria swelling, and DNA fragmentation. NRC-03 induced high oxygen consumption, reactive oxygen species (ROS) release, mitochondrial dysfunction, and apoptosis in OSCC cells. Non-specific antioxidant N-acetyl-l-cysteine (NAC), or mitochondria-specific antioxidant mitoquinone (MitoQ) alleviated NRC-03-induced apoptosis and mitochondrial dysfunction indicated that NRC-03 exerts a cytotoxic effect in cancer cells via inducing cellular and mitochondrial oxidative stress. Moreover, the expression of cyclophilin D (CypD), the key component of mitochondrial permeability transition pore (mPTP), was upregulated in NRC-03-treated cancer cells. Blockade of CypD by siRNA-mediated depletion or pharmacological inhibitor cyclosporine A (CsA) significantly suppressed NRC-03-induced mitochondrial oxidative stress, mitochondrial dysfunction, and apoptosis. NRC-03 also activated MAPK/ERK and NF-κB pathways. Importantly, intratumoral administration of NRC-03 inhibited the growth of CAL-27 cells-derived tumors on xenografted animal models. Taken together, our study indicates that NRC-03 induces apoptosis in OSCC cells via the CypD-mPTP axis mediated mitochondrial oxidative stress.

Detection of the SARS-CoV-2 Delta Variant in the Transboundary Rivers of Yunnan, China.

Ruili and Longchuan, two border counties in southwestern China, are facing epidemic control challenges due to the high rate of COVID-19 infections originating from neighboring Myanmar. Here, we aimed to establish the applicability of wastewater and environmental water surveillance of SARS-CoV-2 and conduct whole-genome sequencing (WGS) to trace the possible infection origin. In August 2021, total 72 wastewater and river water samples were collected from 32 sampling sites. SARS-CoV-2 ORF1ab and N genes were measured by RT-qPCR. We found that 19 samples (26.39%) were positive, and the viral loads of ORF1ab and N genes were 6.62 × 102-2.55×105 and 1.86 × 103-2.32 × 105 copies/L, respectively. WGS further indicated the sequences in two transboundary river samples, and one hospital wastewater sample belonged to the delta variant, suggesting that the infection source might be areas with high COVID-19 delta variant incidence in Southeast Asia (e.g., Myanmar). We reported for the first time the detection and quantification of SARS-CoV-2 RNA in the transboundary rivers of Myanmar-China. Our findings demonstrate that wastewater and environmental water may provide independent and nonintrusive surveillance points to monitor the global spread of emerging COVID-19 variants of concern, particularly in high-risk regions or border areas with considerable epidemic challenges and poor wastewater treatment facilities.

Wearing time and respiratory volume affect the filtration efficiency of masks against aerosols at different sizes.

Face masks are critical in preventing the spread of respiratory infections including coronavirus disease 2019 (COVID-19). Different types of masks have distinct filtration efficiencies (FEs) with differential costs and supplies. Here we reported the impact of breathing volume and wearing time on the inward and outward FEs of four different mask types (N95, surgical, single-use, and cloth masks) against various sizes of aerosols. Specifically, 1) Mask type was an important factor affecting the FEs. The FEs of N95 and surgical mask were better than those of single-use mask and cloth mask; 2) As particle size decreased, the FEs tended to reduce. The trend was significantly observed in FEs of aerosols with particle size < 1 µ m ; 3) After wearing N95 and surgical masks for 0, 2, 4, and 8 h, their FEs (%) maintained from 95.75 ± 0.09 to 100 ± 0 range. While a significant decrease in FEs were noticed for single-use masks worn for 8 h and cloth masks worn >2 h under deep breathing (30 L/min); 4) Both inward and outward FEs of N95 and surgical masks were similar, while the outward FEs of single-use and cloth masks were higher than their inward FEs; 5) The FEs under deep breathing was significantly lower than normal breathing with aerosol particle size <1 µ m. In conclusion, our results revealed that masks have a critical role in preventing the spread of aerosol particles by filtering inhalation, and FEs significantly decreased with the increasing of respiratory volume and wearing time. Deep breathing may cause increasing humidity and hence decrease FEs by increasing the airflow pressure. With the increase of wearing time, the adsorption capacity of the filter material tends to be saturated, which may reduce FEs. Findings may be used to provide information for policies regarding the proper use of masks for general public in current and future pandemics.

Hydroxytyrosol prevents periodontitis-induced bone loss by regulating mitochondrial function and mitogen-activated protein kinase signaling of bone cells.

Reactive oxygen species (ROS) overproduction promotes the alveolar bone loss during the development of periodontitis. Mitochondria are the principal source of ROS. Hydroxytyrosol (HT), a natural phenolic compound present in olive oil, is well known for its antioxidant and mitochondrial-protective prosperities. Nonetheless, the impact of HT on periodontitis and its related mechanisms underlying bone cell behavior remains unknown. Osteoclasts differentiated from RAW264.7 model and oxidative stress (OS) induced pre-osteoblast MC3T3-E1 cell injury model were treated with and without HT. Cell viability, apoptosis, differentiation, mitochondrial function along with mitogen-activated protein kinase (MAPK) signaling pathway were investigated. Meanwhile, the effect and related mechanisms of HT on bone loss in mice with periodontitis were also detected. HT inhibited osteoclast differentiation and prevented OS induced pre-osteoblast cells injury via regulating mitochondrial function as well as ERK and JNK signaling pathways. Moreover, HT attenuated the alveolar bone loss, increased bone forming activity, inhibited the osteoclasts differentiation and decreased the level of OS in mice with periodontitis. Our findings, for the first time, revealed a novel function of HT in bone remodeling of periodontitis, and highlighted its therapeutical potential for the prevention/treatment of periodontitis.

[Responses of radial growth of Quercus mongolica to stand density and climatic factors in a mountainous area of eastern Liaoning Province, China]. / è¾½ä¸œå±±åŒºè’™å¤æ Žå¾„å‘ç”Ÿé•¿å¯¹æž—åˆ†å¯†åº¦å’Œæ°”å€™å› å­çš„å“åº”.

To explore the effects of stand density and climatic factors on radial growth of Quercus mongolica, we used tree ring chronology to examine the radial growth changes in a secondary Q. mongolica forest under different levels of stand density (thinning). The meteorological data combined with the driving factors of Q. mongolica growth were analyzed. The results showed that the radial growth of Q. mongolica was significantly affected by stand density. The mean annual radial growth of Q. mongolica was 3.12 mm in low-density virgin forest, 1.55 and 1.42 mm in the two medium-density secondary forests, respectively, and 0.96 mm in high-density secondary forest. The thinning intensity of 20% had a limited effect on promoting the radial growth recovery of high-density forest (1900 trees·hm-2), but had a significant effect on medium-density forest (1600 trees·hm-2). The radial growth of Q. mongolica was sensitive to the precipitation changes in January and February of the current year. Thinning reduced the sensitivity of Q. mongolica radial growth to climate. Under scenarios of climate warming and drying, density regulation could be beneficial in mitigating the adverse effects of climate change on the growth of Q. mongolica.

Crosstalk between reactive oxygen species and Dynamin-related protein 1 in periodontitis.

Excessive generation of reactive oxygen species (ROS) have great impacts on the development of periodontitis. Dynamin-related protein 1 (Drp1) mediated mitochondrial fission is the main reason and the result of excessive ROS generation. However, whether Drp1 and crosstalk between ROS and Drp1 contribute to the process of periodontitis remains elusive. We herein investigated the role and functional significance of crosstalk between ROS and Drp1 in periodontitis. Firstly, human periodontal ligament cells (hPDLCs) were treated with hydrogen peroxide (H2O2) and ROS inhibitor N-acetyl-cysteine (NAC) or Drp1 inhibitor mitochondrial division inhibitor 1 (Mdivi-1). Cell viability, apoptosis, osteogenic differentiation, expression of Drp1, and mitochondrial function were investigated. Secondly, mice with periodontitis were treated with NAC or Mdivi-1. Finally, gingival tissues were collected from periodontitis patients and healthy individuals to evaluate ROS and Drp1 levels. H2O2 induced cellular injury and inflammation, excessive ROS production, mitochondrial abnormalities, and increased expression of p-Drp1 and Drp1 in hPDLCs, which could be reversed by NAC and Mdivi-1. Moreover, both NAC and Mdivi-1 ameliorated tissue damage and inflammation, and decreased expression of p-Drp1 and Drp1 in mice with periodontitis. More importantly, patients with periodontitis presented significantly higher levels of ROS-induced oxidative damage and p-Drp1 than that in healthy individuals and correlated with clinical parameters. In summary, ROS-Drp1 crosstalk greatly promotes the development of periodontitis. Pharmacological blockade of this crosstalk might be a novel therapeutic strategy for periodontitis.

Risk factors and on-site simulation of environmental transmission of SARS-CoV-2 in the largest wholesale market of Beijing, China.

From June 11, 2020, a surge in new cases of coronavirus disease 2019 (COVID-19) in the largest wholesale market of Beijing, the Xinfadi Market, leading to a second wave of COVID-19 in Beijing, China. Understanding the transmission modes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the personal behaviors and environmental factors contributing to viral transmission is of utmost important to curb COVID-19 rise. However, currently these are largely unknown in food markets. To this end, we completed field investigations and on-site simulations in areas with relatively high infection rates of COVID-19 at Xinfadi Market. We found that if goods were tainted or personnel in market was infected, normal transaction behaviors between sellers and customers, daily physiological activities, and marketing activities could lead to viral contamination and spread to the surroundings via fomite, droplet or aerosol routes. Environmental factors such as low temperature and high humidity, poor ventilation, and insufficient hygiene facilities and disinfection practices may contribute to viral transmission in Xinfadi Market. In addition, precautionary control strategies were also proposed to effectively reduce the clustering cases of COVID-19 in large-scale wholesale markets.

Aerosol transmission of SARS-CoV-2? Evidence, prevention and control.

As public health teams respond to the pandemic of coronavirus disease 2019 (COVID-19), containment and understanding of the modes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission is of utmost importance for policy making. During this time, governmental agencies have been instructing the community on handwashing and physical distancing measures. However, there is no agreement on the role of aerosol transmission for SARS-CoV-2. To this end, we aimed to review the evidence of aerosol transmission of SARS-CoV-2. Several studies support that aerosol transmission of SARS-CoV-2 is plausible, and the plausibility score (weight of combined evidence) is 8 out of 9. Precautionary control strategies should consider aerosol transmission for effective mitigation of SARS-CoV-2.

Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3ß-Nrf2 Signaling Pathway.

Osteoblasts dysfunction, induced by oxidative stress (OS), is one of major pathological mechanisms for osteoporosis. Curcumin (Cur), a bioactive antioxidant compound, isolated from Curcumin longa L, was regarded as a strong reactive oxygen species (ROS) scavenger. However, it remains unveiled whether Cur can prevent osteoblasts from OS-induced dysfunction. To approach this question, we adopted a well-established OS model to investigate the preventive effect of Cur on osteoblasts dysfunction by measuring intracellular ROS production, cell viability, apoptosis rate and osteoblastogenesis markers. We showed that the pretreatment of Cur could significantly antagonize OS so as to suppress endogenous ROS production, maintain osteoblasts viability and promote osteoblastogenesis. Inhibiting Glycogen synthase kinase (GSK3ß) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3ß-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3ß-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3ß-Nrf2 signaling and provide a promising way for osteoporosis treatment.

The Safety and Feasibility of Enhanced Recovery after Surgery in Patients Undergoing Pancreaticoduodenectomy: An Updated Meta-Analysis.

BACKGROUND: Enhanced recovery after surgery (ERAS) is a multimodal, multidisciplinary, evidence-based approach to care for surgical patients and aims at optimizing the perioperative management and outcomes. The ERAS approach was first implemented in colorectal surgery patients; however, the reported applications in pancreatoduodenectomy patients are limited. In recent years, studies on ERAS for patients undergoing pancreaticoduodenectomy have been published. The accumulation of new randomized controlled trials and high-quality case-control studies stimulated us to update the analysis. Our study comprehensively collected data to provide the best evidence summary for the clinic. AIM: To evaluate the safety and feasibility of enhanced recovery after surgery in the perioperative management of pancreatoduodenectomy patients. METHODS: A systematic literature search of PubMed, Embase, and the Cochrane Library was performed up to July 2019. All randomized controlled trials and case-control studies that applied ERAS for patients undergoing pancreaticoduodenectomy were considered for inclusion in this study. The patients were divided into two groups: patients who received the ERAS perioperative management approach were defined as the ERAS group and patients who received the traditional perioperative management approach were defined as the control group. All statistical analyses were conducted using the Revman5.3 software, and the outcomes were calculated as odds ratios or weighted mean differences with their corresponding 95% confidence intervals. A funnel plot was created to assess publication bias. Subgroup and sensitivity analyses were performed to explore the sources of heterogeneity. RESULTS: A total of 20 studies involving 3613 patients (1914 patients in the ERAS group vs. 1699 patients in the control group) were included in this study. Among the 20 studies, 4 were randomized controlled trials, and 16 were case-control studies. The overall postoperative complication rate was significantly lower in the ERAS group (OR = 0.62, 95% CI: 0.53-0.74, P < 0.00001) than in the control group. In addition, the minor complication rate (Clavien-Dindo I-II) was also lower in the ERAS group (OR = 0.70, 95% CI: 0.58-0.86, P = 0.0005). The patients in the ERAS group had a lower incidence of delayed gastric emptying (OR = 0.51, 95% CI: 0.42-0.63, P < 0.00001) and shorter length of hospital stay (WMD = -4.27, 95% CI: -4.81~-3.73, P < 0.00001) than in the control group. The rates of pancreatic fistula (regardless of Grade A/B/C), wound infections, abdominal abscesses, readmission, reoperation, and morbidity were not significantly different between the two groups. CONCLUSION: The ERAS approach is safe and effective in the perioperative management of patients undergoing pancreaticoduodenectomy and helps to accelerate the postoperative recovery and improve prognosis.

Comparison of culturable antibiotic-resistant bacteria in polluted and non-polluted air in Beijing, China.

BACKGROUND: Air pollution has been a serious health issue in Beijing for years. Airborne antibiotic-resistant bacteria could be a potential health crisis as reserve of antibiotic resistance transmission in environment. The composition and antibiotic resistance pattern of culturable bacterial community and how these are affected by air pollution remain unclear. OBJECTIVES: This study aimed to compare the compositions and antibiotic resistance patterns of culturable bacteria in polluted and non-polluted weather conditions in Beijing. METHODS: Air samples were collected indoors and outdoors during polluted and non-polluted weather using six-stage Andersen Samplers. For each isolated bacterium, the 16S ribosomal RNA gene was amplified, sequenced, and blasted against the National Center for Biotechnology Information database Antibiotic resistance was conducted by antimicrobial susceptibility testing. RESULTS: Bacterial concentration in polluted weather was significantly higher than in non-polluted weather, both indoors and outdoors (P < 0.05). Gram-positive bacteria (GPB) were dominant in both weathers but gram-negative bacteria (GNB) were more abundant in polluted weather than non-polluted weather both indoors and outdoors. Multidrug-resistant (MDR) bacteria occupied 23.7% of all bacterial isolates, 22.4% of isolates from polluted weather and 27.8% of isolates from non-polluted weather. Penicillins were resisted by 72.4% and 83.3% of isolates from polluted and non-polluted weather, respectively. CONCLUSIONS: The bacterial concentration was significantly higher in polluted weather, compared to non-polluted weather. Polluted weather is correlated with changes in the bacterial composition in the air, with a greater abundance of GNB. Penicillins was resisted by over 70% of bacterial isolates. The abundance of MDR bacteria suggested potential risks for human health.

Oxidative stress-related biomarkers in saliva and gingival crevicular fluid associated with chronic periodontitis: A systematic review and meta-analysis.

AIM: Oxidative stress (OS) biomarkers have been detected in saliva and gingival crevicular fluid (GCF) during chronic periodontitis (CP) progression; however, the relationship between OS biomarkers and CP progression remains elusive. The purpose of this meta-analysis is to investigate the relationship between local OS biomarkers and CP. METHODS: This review was conducted through a systematic search from three databases. Studies on CP participants were included as an experimental group, and studies on periodontally healthy (PH) participants were included as a control. Mean effects were expressed as standardized mean difference with their associated 95% confidence intervals. RESULTS: From a total of 2,972 articles, 32 articles fulfilled the inclusion criteria. We found a significant decrease of total antioxidant capacity and a significant increase of malondialdehyde (MDA), nitric oxide, total oxidant status (TOS), and 8-hydroxy-deoxyguanosine levels in the saliva of CP patients. Moreover, we also found an elevation of MDA level in GCF of CP group when compared with the PH group. There were no significant differences of salivary and GCF superoxide dismutase levels, salivary glutathione peroxidase level, and GCF TOS level between two groups. However, a high heterogeneity was observed among evaluated studies. CONCLUSIONS: Despite the limitations of this study, the result of our meta-analysis supported the rationale that there was a direct link between CP and OS-related biomarkers' levels in the local site, indicating the important role of OS in the onset and development of CP.