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Since silver nanoparticles (AgNPs) and polystyrene microplastics (PS-MP) share common environmental niches, their interactions can modulate their hazard impacts. Herein, we assessed the developmental toxicity of 1 mg/L PS-MP, 0.5 mg/L AgNPs and the mixtures of AgNPs and PS-MP on embryo-larval zebrafish. We found that AgNPs co-exposure with PS-MP remarkably decreased mortality rates, malformation rates, heart rates and yolk sac area, while it increased hatching rates and eye size compared to the AgNPs group. These phenomena revealed that the cell cycle, oxidative stress, apoptosis, lipid metabolism, ferroptosis and p53 signalling pathway were obviously affected by single AgNPs exposure at 96 hpf (hours post fertilization). Interestingly, all these effects were effectively ameliorated by co-exposure with PS-MP. The combination of transcriptomic and metabolomic analyses showed that the imbalance of DEGs (differentially expressed genes) and DEMs (differentially expressed metabolites) (PI, phosphatidylinositol and TAG-FA, triacylglycerol-fatty acid) disturbed both the cell cycle and lipid metabolism following single AgNPs exposure and co-exposure with PS-MP. These findings suggest that PS-MP attenuates the developmental toxicity of AgNPs on embryo-larval zebrafish. Overall, this study provides important insight into understanding the transcriptional responses and mechanisms of AgNPs alone or in combination with PS-MPs on embryo-larval zebrafish, providing a reference for ecological risk assessment of combined exposure to PS-MP and metal nanoparticles., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Anesthetic sevoflurane (Sev) causes cognitive dysfunction and neuronal death when used as an anesthetic during surgical procedures. Gynosaponin (GpS) was studied for its effects on brain morphology and cognitive behaviors in Sevanesthetized rats. The present study investigated whether GpS has an effect on Sev anesthesia-induced abnormalities in brain morphology and cognitive behaviors, as well as on apoptosis and inflammation of neurons in rats, and delved into the molecular mechanisms. Male Sprague-Dawley rats were induced by 3% Sev anesthesia, and GpS was injected into the rats via the tail vein. The in vitro model of Sev anesthesia was constructed by treating primary rat hippocampal neurons with 4.1% Sev in the presence of GpS (5, 10, and 20 μM). The neuroprotective effects of GpS against Sev-induced cognitive deficits in rats were evaluated using the open field and Morris water maze tests. The apoptosis of hippocampal neurons was observed using hematoxylin-eosin (HE staining and TUNEL assay. Cleaved caspase-3 expression and reactive oxygen species production in rat hippocampal tissue were measured by immunofluorescence. Apoptosis-related proteins and the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway were determined via Western blot. Pro-inflammatory factors tumor necrosis factor-α and interleukin-6 were measured via ELISA. Levels of malondialdehyde, superoxide dismutase and glutathione were assayed by commercial kits. Viability and apoptosis of hippocampal neurons were detected by Cell Counting Kit-8 and flow cytometry. Expression of cleaved caspase-3, B-cell leukemia/lymphoma 2 protein (Bcl-2) Bcl-2-associated protein (Bax) was determined by Western blot. GpS significantly reduced Sev-induced decline in short-term memory, learning and cognitive abilities, as well as neuronal degeneration apoptosis and inflammatory responses, GpS also lessened oxidative stress damage, and activated the PI3K/Akt/mTOR pathway (p<0.05). GpS therapy enhanced learning and memory abilities in rats suffering from Sev-induced cognitive deficits. The PI3K/Akt/mTOR pathway inhibitor LY294002 reversed the ameliorative effects of high-dose GpS on cognitive deficits and cell damage in primary hippocampal neurons in Sev anesthetized rats (p<0.05). We conclude that GpS ameliorates Sev-induced neurotoxicity and cognitive dysfunction by modulating the PI3K/Akt/mTOR pathway and alleviating neuronal apoptosis and oxidative stress.

Both epidemiological and animal studies suggest that adverse environment during pregnancy can change the offspring development programming, but it is difficult to achieve prenatal early warning. In this study we investigated the impact of prenatal dexamethasone exposure (PDE) on sperm quality and function of blood-testis barrier (BTB) in adult offspring and the underlying mechanisms. Pregnant rats were injected with dexamethasone (0.1, 0.2 and 0.4 mg·kg -1 ·d -1 , s.c.) from GD9 to GD20. After weaning (PW4), the pups were fed with lab chow. At PW12 and PW28, the male offspring were euthanized to collect blood and testes samples. We showed that PDE significantly decreased sperm quality (including quantity and motility) in male offspring, which was associated with impaired BTB and decreased CX43/E-cadherin expression in the testis. We demonstrated that PDE induced morphological abnormalities of fetal testicle and Sertoli cell development originated from intrauterine. By tracing to fetal testicular Sertoli cells, we found that PDE dose-dependently increased expression of histone lysine demethylases (KDM1B), decreasing histone 3 lysine 9 dimethylation (H3K9me2) levels of follistatin-like-3 (FSTL3) promoter region and increased FSTL3 expression, and inhibited TGFβ signaling and CX43/E-cadherin expression in offspring before and after birth. These results were validated in TM4 Sertoli cells following dexamethasone treatment. Meanwhile, the H3K9me2 levels of FSTL3 promoter in maternal peripheral blood mononuclear cell (PBMC) and placenta were decreased and its expression increased, which was positively correlated with the changes in offspring testis. Based on analysis of human samples, we found that the H3K9me2 levels of FSTL3 promoter in maternal blood PBMC and placenta were positively correlated with fetal blood testosterone levels after prenatal dexamethasone exposure. We conclude that PDE can reduce sperm quality in adult offspring rats, which is related to the damage of testis BTB via epigenetic modification and change of FSTL3 expression in Sertoli cells. The H3K9me2 levels of the FSTL3 promoter and its expression in the maternal blood PBMC can be used as a prenatal warning marker for fetal testicular dysplasia., (© 2024. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.)

Background: Hypertension is a prevalent cardiovascular disease characterized by elevated blood pressure and increased vascular resistance. HDAC inhibitors have emerged as potential therapeutic agents due to their ability to modulate gene expression and cellular processes. YPX-C-05, a novel hydroxamic acid-based HDAC inhibitor, shows promise in its vasodilatory effects and potential targets for hypertension treatment. In this study, we aimed to elucidate the mechanisms underlying YPX-C-05's vasodilatory effects and explore its therapeutic potential in hypertension., Methods: To determine the ex vivo vasodilatory effects of YPX-C-05, isolated aortic rings precontracted with phenylephrine were used. We assessed YPX-C-05's inhibitory effects on HDACs and its impact on histone H4 deacetylation levels in endothelial cells. Network pharmacology analysis was employed to predict putative targets of YPX-C-05 for hypertension treatment. To investigate the involvement of the PI3K/Akt/eNOS pathway, we employed enzyme-linked immunosorbent assay and to assess the levels of NO, ET-1, BH2, and BH4 in human umbilical vein endothelial cells. And we also analyzed the mRNA expression of eNOS and ET-1. Furthermore, Western blotting was conducted to quantify the phosphorylated and total Akt and eNOS levels in human umbilical vein endothelial cell lysates following treatment with YPX-C-05. In order to elucidate the vasodilatory mechanism of YPX-C-05, we employed pharmacological inhibitors for evaluation purposes. Furthermore, we evaluated the chronic antihypertensive effects of YPX-C-05 on N-omega-nitro-L-arginine-induced hypertensive mice in an in vivo model. Vascular remodeling was assessed through histological analysis., Results: Our findings demonstrated that YPX-C-05 exerts significant vasodilatory effects in isolated aortic rings precontracted with phenylephrine. Furthermore, YPX-C-05 exhibited inhibitory effects on HDACs and increased histone H4 acetylation in endothelial cells. Network pharmacology analysis predicted YPX-C-05 might activate endothelial eNOS via PI3K/Akt signaling pathway. Inhibition of the PI3K/Akt/eNOS pathway attenuated the vasodilatory effects of YPX-C-05, as evidenced by reduced levels of phosphorylated Akt and eNOS in human umbilical vein endothelial cell lysates. The chronic administration of YPX-C-05 in N-omega-nitro-L-arginine-induced hypertensive mice resulted in significant antihypertensive effects. Histological analysis demonstrated a reduction in vascular remodeling, further supporting the therapeutic potential of YPX-C-05 in hypertension., Conclusion: This study demonstrates for the first time that the novel hydroxamic acid-based HDAC inhibitor YPX-C-05 produces significant antihypertensive and vasodilatory effects through the PI3K/Akt/eNOS pathway. Our findings support the developing prospect of YPX-C-05 as a novel antihypertensive drug., Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest., (Copyright © 2023. Published by Elsevier Inc.)

More than 30% of fruits of Chinese Quince (Chaenomeles speciosa) and peach (Prunus persica) showed circular, water-soaked and brown spots in July 2022 in Kunming, Yunnan, China. The center of these spots was covered by a large number of earthy brown and oblate sporogeneous mycelium containing conidiophore and conidia, which were one-celled, limoniform, hyaline (13.73 to 22.77 x 8.17 to 12.84 µm, n=50). By September 2022, almost 100% of fruits showed symptoms. Later, most of them fell or a few stiff, black and mummified fruits were left on the trees. Fungal isolates were isolated by single-spore technique on Potato Dextrose agar (PDA) from the diseased fruits, and incubated at room temperature (20-28 °C) in darkness for 14 days. The colony was gray, smooth at margins, 7.6-8.0 cm in diameter. To fullfill Koch's postulates, mycelial plugs of one representative isolate YHD611 from Chinese Quince and another YHD610 from peach were used to inoculate three wounded and three non-wounded surface-disinfected fruits of both hosts at room temperature (19-27 °C), respectively. Three wounded and three non-wounded fruits inoculated with sterile PDA plugs served as the control. The wounded peaches appeared water-soaked and had brown lesions after three days of inoculation, then completely decayed after nine days, while non-wounded fruits showed symptoms after five days. The wounded fruits of Chinese Quince developed similar symptoms after eight days of inoculation, and completely decayed after 13 days, while non-wounded fruits showed obvious symptoms after 15 days. In a subsequent study, isolate YHD611 was inoculated to peach while isolate YHD610 was inoculated to Chinese Quince to understand host specificity of the isolates. The results showed that when peaches were infected with YHD611, symptoms were observed on wounded fruits after three days while on non-wounded fruits after five days. When Chinese Quince was infected with YHD610, symptoms were observed on wounded fruits after 14 days while on non-wounded fruits after 21 days. Fungal isolates from symptomatic fruits were identical to the original isolates. There were no symptoms on the control fruits of both hosts. Molecular identification was confirmed based on the sequences of internal transcribed spacer (ITS, primers ITS1 and ITS4) and β-tubulin (TUB2, primers Bt2a and Bt2b) genes (Niu et al. 2016). BLASTn analysis of the ITS (OQ15519and OQ155196) and TUB2 (OQ185202 and OQ185201) of YHD611 and YHD610 revealed a 100% sequence identity, respectively, to Monilia yunnanensis AH7-2 (KT735924.1 for ITS, KT736008.1 for TUB2). In the phylogenetic analyses based on ITS and TUB2 sequence data, the isolates YHD611 and YHD610 belonged to the M. yunnanensis clade. Based on morphological and molecular identification, both isolates were identified as M. yunnanensis, which was reported as the pathogen causing brown rot of plum, peach, apple and pear in Yunnan, China (Hu et al. 2011; Yin et al. 2015). To our knowledge, this is the first report of M. yunnanensis causing brown rot on the fruits of Chinese Quince in Yunnan, China. This study also reports that M. yunnanensis from Chinese Quince can infect peach, and the pathogen from peach can infect Chinese Quince. These findings suggest that M. yunnanensis can transfer from one host to another and causing serious economic losses in multiple fruit crops in Yunnan, China. References: Hu, M. J., et al. 2011. PLoS One. 6:e24990. Niu, C. W., et al. 2016. Mycosystema, 35(10):1. Yin, L. F., et al. 2015. Plant Dis. 99:1775.

Background: To develop a fully automatic framework for the diagnosis of cause for left ventricular hypertrophy (LVH) via cardiac cine images., Methods: A total of 302 LVH patients with cine MRI images were recruited as the primary cohort. Another 53 LVH patients prospectively collected or from multi-centers were used as the external test dataset. Different models based on the cardiac regions (Model 1), segmented ventricle (Model 2) and ventricle mask (Model 3) were constructed. The diagnostic performance was accessed by the confusion matrix with respect to overall accuracy. The capability of the predictive models for binary classification of cardiac amyloidosis (CA), hypertrophic cardiomyopathy (HCM) or hypertensive heart disease (HHD) were also evaluated. Additionally, the diagnostic performance of best Model was compared with that of 7 radiologists/cardiologists., Results: Model 3 showed the best performance with an overall classification accuracy up to 77.4% in the external test datasets. On the subtasks for identifying CA, HCM or HHD only, Model 3 also achieved the best performance with AUCs yielding 0.895-0.980, 0.879-0.984 and 0.848-0.983 in the validation, internal test and external test datasets, respectively. The deep learning model showed non-inferior diagnostic capability to the cardiovascular imaging expert and outperformed other radiologists/cardiologists., Conclusion: The combined model based on the mask of left ventricular segmented from multi-sequences cine MR images shows favorable and robust performance in diagnosing the cause of left ventricular hypertrophy, which could be served as a noninvasive tool and help clinical decision., (© 2023. The Author(s).)

The existence of latent viral reservoirs (LVRs), also called latent cells, has long been an acknowledged stubborn hurdle for effective treatment of HIV-1/AIDS. This stable and heterogeneous reservoir, which mainly exists in resting memory CD4 + T cells, is not only resistant to highly active antiretroviral therapy (HAART) but cannot be detected by the immune system, leading to rapid drug resistance and viral rebound once antiviral treatment is interrupted. Accordingly, various functional cure strategies have been proposed to combat this barrier, among which one of the widely accepted and utilized protocols is the so-called 'shock-and-kill' regimen. The protocol begins with latency-reversing agents (LRAs), either alone or in combination, to reactivate the latent HIV-1 proviruses, then eliminates them by viral cytopathic mechanisms (e.g., currently available antiviral drugs) or by the immune killing function of the immune system (e.g., NK and CD8+ T cells). In this review, we focuse on the currently explored small molecular LRAs, with emphasis on their mechanism-directed drug targets, binding modes and structure-relationship activity (SAR) profiles, aiming to provide safer and more effective remedies for treating HIV-1 infection.

Background: In newborns, propofol anesthesia is commonly utilized. Propofol is increasingly being shown to be effective and safe in treating procedural sedation and anesthesia in neonates. This research aims to evaluate the efficacy and safety of propofol in neonates using systematic review and meta-analysis methodologies., Methods: A thorough review and meta-analysis of studies on propofol anesthesia in neonates will be conducted. Conduct comprehensive searches in Web of Science, PubMed, Cochrane Library, EMBASE database, WanFang database, and Chinese biomedical literature database before May 25, 2021, to obtain published and qualified research. Two reviewers will assess the quality of the included papers and extract the data independently. Then, for meta-analysis, we will utilize RevMan 5.3 software., Results: This study will pool the data of separate trials to analyze the efficacy and safety of propofol in the treatment of procedural sedation/anesthesia in neonates., Conclusion: Our findings will give strong data for determining whether propofol is an effective treatment for procedural anesthesia in neonates., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Objective To make a preliminary pathological classification of lung adenocarcinoma with pure ground glass nodules(pGGN)on CT by using a deep learning model. Methods CT images and pathological data of 219 patients(240 lesions in total)with pGGN on CT and pathologically confirmed adenocarcinoma were collected.According to pathological subtypes,the lesions were divided into non-invasive lung adenocarcinoma group(which included atypical adenomatous hyperplasia and adenocarcinoma in situ and micro-invasive adenocarcinoma)and invasive lung adenocarcinoma group.First,the lesions were outlined and labeled by two young radiologists,and then the labeled data were randomly divided into two datasets:the training set(80%)and the test set(20%).The prediction Results of deep learning were compared with those of two experienced radiologists by using the test dataset. Results The deep learning model achieved high performance in predicting the pathological types(non-invasive and invasive)of pGGN lung adenocarcinoma.The accuracy rate in pGGN diagnosis was 0.8330(95% CI =0.7016-0.9157)for of deep learning model,0.5000(95% CI =0.3639-0.6361)for expert 1,0.5625(95% CI =0.4227-0.6931)for expert 2,and 0.5417(95% CI =0.4029-0.6743)for both two experts.Thus,the accuracy of the deep learning model was significantly higher than those of the experienced radiologists( P =0.002).The intra-observer agreements were good(Kappa values:0.939 and 0.799,respectively).The inter-observer agreement was general(Kappa value:0.667)( P =0.000). Conclusion The deep learning model showed better performance in predicting the pathological types of pGGN lung adenocarcinoma compared with experienced radiologists.

The dependence of tumor growth on neovascularization has become an important aspect of cancer biology. Tumor angiogenesis is one of the key mechanisms of tumorigenesis, growth and metastasis. The key events involved in this process are endothelial cell proliferation, migration, and vascular formation. Recent studies have revealed the importance of tumor-associated endothelial cells (TECs) in the development and progression of colorectal cancer (CRC), including epithelial proliferation, stem cell maintenance, angiogenesis, and immune remodeling. Decades of research have identified that the molecular basis of tumor angiogenesis includes vascular endothelial growth factors (VEGFs) and their receptor family, which are the main targets of antiangiogenesis therapy. VEGFs and their receptors play key roles in the pathology of angiogenesis, and their overexpression indicates poor prognosis in CRC. This article reviews the characteristics of the tumor vasculature and the role of TECs in different stages of CRC and immune remodeling. We also discuss the biological effects of VEGFs and their receptor family as angiogenesis regulators and emphasize the clinical implications of TECs in clinical treatment., Competing Interests: Conflict-of-interest statement: The authors have no conflicts of interest to declare., (©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.)

Rhabditis axei is a free-living nematode, which can occasionally invade into humans through drinking and contacting wastewater. It is usually parasitic in the digestive and urinary systems, causing the disease of rhabditelliasis axei. This paper reports a case of R. axei infection found in the urine routine examination.

In this study, thermally modified copper tailings (TMCT) were used to adsorb phosphate in aqueous solutions through experiments. The characterization of TMCT and unmodified copper tailings (UMCT) was done by scanning electron microscopy (SEM) and Brunauer-Emmett-Teller (BET) analysis. The effects of pH, adsorbent dosage, contact time, and initial phosphate concentrations on phosphate adsorption were investigated. We studied the adsorption ability of TMCT and UMCT at 298 K, and the Langmuir isotherm model closely described the adsorption isotherm data, indicating that the maximum adsorption capacity (Q max ) of the TMCT and UMCT was 14.25 mg g -1 and 2.08 mg g -1 , respectively. In addition, the adsorption isotherms of TMCT were analyzed at 288 K, 298 K, and 308 K, and the calculated Q max of phosphate were 9.83 mg g -1 at 288 K, 14.25 mg g -1 at 298 K, and 11.55 mg g -1 at 308 K. Finally, the concentration of copper in the effluent was checked, and the content was 130 mg L -1 . Then, the effluent was adsorbed by Eichhornia crassipes stem biochar; after adsorption, the concentration of the secondary effluent was 0.7 mg L -1 , which is lower than the grade II classification (1.0 mg L -1 ) of the integrated wastewater discharge standard (GB8978-1996). The results suggest that the TMCT can be effectively and environmentally friendly used to adsorb phosphate from aqueous solutions.

Objective: This study was performed to investigate the management of general anesthesia in an unusual case involving a patient with a broken tracheostomy tube presenting as an airway foreign body., Methods: We herein describe the anesthetic management of a patient with a broken tracheostomy tube. A 77-year-old Chinese man who had been involved in a car accident underwent a tracheostomy. One year later, he presented with cough and bleeding at the tracheostomy site. Preoperative evaluation revealed that the metal tracheostomy tube was lodged in his left main bronchus. General anesthesia was induced to maintain spontaneous breathing, and adequate topical anesthesia of the airway was administered., Results: The metal tracheostomy tube was successful removed, and a new tracheal tube was put in place., Conclusions: General anesthesia to maintain spontaneous breathing and adequate topical anesthesia of the airway can be safely used when removing broken tracheostomy tubes.

Background: Epidemiologic studies suggest the possibility of a modestly elevated risk of adverse neurodevelopmental outcomes in children exposed to anesthesia during early childhood. Sevoflurane is widely used in pediatric anesthetic practice because of its rapid induction and lower pungency. However, it is reported that sevoflurane leads to the long-term cognitive impairment. Some evidence revealed that the selective α2-adrenoreceptor agonist dexmedetomidine (DEX) exerts neuroprotective effects in various brain injury models of animals. But the role of DEX on sevoflurane-induced neuro-damage remains elusive., Materials and Methods: In our study, we isolated the hippocampal neuron cells from newborn neonatal rats and verified the purity of neurons by immunocytochemistry. We employed the flow cytometry and western blot to examine the effect of sevoflurane, DEX and α2-adrenergic receptor antagonist yohimbine on cell cycle distribution., Results: Immunocytochemistry results showed the purity of neurons > 94%, which provided a good model for neural pharmacology experiments. The exposure of sevoflurane-induced cell cycle arrest at S phase and suppressed the expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB). The addition of DEX suppressed sevoflurane-induced cell cycle arrest and the inhibitory of BDNF and TrkB expression. But the function of DEX was partly blocked by a α2 adrenergic receptor blocker yohimbine., Conclusion: Sevoflurane suppressed neuron cell proliferation via inhibiting the expression of BDNF and TrkB, and DEX relieved the neurotoxicity induced by sevoflurane via α2 adrenergic receptor. These findings provided new evidence that DEX exerted as a neuroprotective strategy in sevoflurane-induced neuro-damage, and provided new basis for the clinical application of DEX.

Farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily of ligand-activated transcription factors. As a metabolic regulator, FXR plays key roles in bile acid and cholesterol metabolism and lipid and glucose homeostasis. Therefore, FXR is a potential drug target for several metabolic syndromes, especially those related to lipidemia disorders. In the present study, we identified small molecule SIPI-7623, a derivative of an extract from Oriental wormwood (Artemisia capillaris), and found that it specifically upregulated the expression of cholesterol-7-alpha-hydroxylase (CYP7A1), downregulated the expression of sterol-regulatory element-binding protein 1c (SREBP-1c) in the liver, and inhibited the expression of ileal bile acid binding-protein (IBABP) in the ileum of rats. We found that inhibition of FXR by SIPI-7623 decreased the level of cholesterol and triglyceride. SIPI-7623 reduced the levels of cholesterol and triglyceride in in vitro HepG2 cell models, ameliorated diet-induced atherosclerosis, and decreased the serum lipid content on rats and rabbits model of atherosclerosis in vivo. Furthermore, SIPI-7623 decreased the extent of atherosclerotic lesions. Our resutls demonstrated that antagonism of the FXR pathway can be employed as a therapeutic strategy to treat metabolic diseases such as hyperlipidemia and atherosclerosis. In conclusion, SIPI-7623 could be a promising lead compound for development of drugs to treat hyperlipidemia and atherosclerosis., (Copyright © 2018 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.)

Objective To explore the effects of dermabrasion combined with ReCell ® on large superficial facial scars caused by burn, trauma and acnes.Methods Nineteen patients with large superficial facial scars were treated by the same surgeon with dermabrasion combined with ReCell ® . According to the etiology, patients were classified into post-burning group (n=5), post-traumatic group (n=7) and post-acne group (n=7). Fifteen patients completed the follow-ups, 5 patients in each group. Healing time, complication rate, the preoperative and 18-month-post-operative assessments using Patient Satisfaction Score (PSS), Vancouver Scar Scale (VSS), and Patient and Observer Scar Assessment Scale (POSAS) of each group were analyzed to compare the effect of the combined therapy on outcomes.Results The healing time of post-burning group (19.6±4.0 days), post-traumatic group (15.8±2.6 days), and post-acne group (11.4±3.1 days) varied remarkably (F=7.701, P=0.007). The complication rates were 60%, 20%, and 0 respectively. The post-operative POSAS improved significantly in all groups (P<0.05), where the most significant improvement was shown in the post-acne group (P<0.05). The post-operative PSS and VSS improved only in the post-traumatic group and post-acne group (all P<0.05), where the more significant improvement was also shown in the post-acne group (P<0.05).Conclusions The combined treatment of dermabrasion and ReCell ® has remarkable effect on acne scars, moderate effect on traumatic scars and is not suggested for burn scars. POSAS should be applied to assess the therapeutic effects of treatments for large irregular scars.

Regenerative medicine is an emerging discipline. Adipose tissue is a rich source of fat cells and mesenchymal stem cells, and autologous fat grafting has increasingly been applied in plastic surgeries and dermatological treatments. This paper reviews the latest advances in autologous fat grafting in scar revision.

Background: Data on the efficacy of the 23-valent pneumococcal polysaccharide vaccine (PPV-23) in preventing adult community-acquired pneumonia (CAP) among the target population of individuals aged over 65 years and high-risk individuals aged 19-64 years are conflicting. As the Advisory Committee on Immunization Practices (ACIP) has recently demonstrated PPV-23 is likely beneficial to immunocompromised adults by the Grading, Assessment, Development, and Evaluation (GRADE) framework, we conducted meta-analysis to examine its efficacy in an immunocompetent population., Methods: We searched the PUBMED, EMBASE, and Cochrane Library databases for randomized trials. Overall relative risks (RRs) with 95% confidential intervals (CIs) were calculated, and the Cochrane Q test (p, I(2)) was performed. Outcomes were assessed by the GRADE framework., Results: Seven randomized trials involving 156,010 participants were included in this meta-analysis. High-quality evidence revealed that PPV-23 was weakly associated with the prevention of all-cause pneumonia ([RR] 0.87, [95%CI] 0.76-0.98, p=0.11, I(2)=43%), especially among the target population ([RR] 0.72, [95%CI] 0.69-0.94, p=0.58 I(2)=0%), the elderly group aged over 40 years ([RR] 0.80, [95%CI] 0.69-0.94) and the Japanese population ([RR] 0.72, [95%CI] 0.59-0.88, p=0.24, I(2)=30%). The target population included adults aged over 65 years and patients at high risk of pneumonia due to chronic lung disease, chronic obstructive pulmonary disease or living in a nursing home. Protective trends of PPV-23 in the outcomes of pneumococcal pneumonia ([RR] 0.54, [95%CI] 0.18-1.65, p=0.01, I(2)=77%) and mortality due to pneumonia ([RR] 0.67, [95%CI] 0.43-1.04, p=0.67, I(2)=0%) were observed, although the results were statistically insignificant, possibly due to the small number of trials included. PPV-23 did not prevent all-cause mortality ([RR] 1.04, [95%CI] 0.87-1.24, p=0.95, I(2)=0%)., Conclusions: PPV-23 provided weak protection against all-cause pneumonia in an immunocompetent population, especially among the target population. The additional benefit of PPV-23 in preventing CAP further supports its application in the target population., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Cigarette smoking is known to have negative effects on tissue repair and healing. The aim of this study is to investigate the effects of nicotine in human umbilical cord mesenchymal stem cells (MSCs). After nicotine treatment, MSCs became pyknotic, vacuoles appeared in the cytoplasm and nucleus, and the nuclear boundary became fuzzy as observed using atomic force microscopy. Cell proliferation was inhibited in a dose-dependent manner (P < 0.05 for all concentrations). The proportion of apoptotic MSCs was significantly increased in a dose-dependent manner. The mitochondrial membrane potential was significantly decreased (P < 0.05). Nicotine-treated MSCs had a significantly higher G0/G1 ratio (P < 0.05). Peptide mass fingerprinting identified 27 proteins that were differentially expressed between MSCs with and without nicotine treatment. These nicotine exerted toxic effects on MSCs are likely related, at least in part, to the altered expression of multiple proteins that are essential to the health and proliferation of these cells., (© 2014 Wiley Periodicals, Inc.)

Introduction: Quercetin is widely distributed in plants and has been reported to have effects of anti-inflammation and anti-thrombosis. In this study, we evaluated the protective effect of quercetin on LPS-induced experimental DIC in rabbits, and tried to clarify its mechanism against DIC., Materials and Methods: LPS-induced DIC model in rabbits was established through continuous infusion of 100 ug · kg(-1) · h(-1) LPS for a period of 6h. Six groups were divided: quercetin-treated groups (0.5, 1.0, and 2.0 mg·kg(-1) · h(-1), respectively), LPS-control group, heparin-control group (100 IU · kg(-1) · h(-1)), and saline-control group. APTT, PT, and plasma FIB level were measured, the plasma levels of ALT, BUN, and TNF-α were detected, and the activity of Protein C and ATIII was recorded., Results: A continuous injection of LPS induced a gradual impairment of hemostatic parameters, a rise in plasma level of TNF-α, and damage in renal and hepatic function. The intravenous administration of quercetin significantly attenuated the increase of APTT, PT, ALT, BUN, and TNF-α, and the decrease of plasma FIB level and activity of Protein C and ATIII., Conclusion: Quercetin may have a protective effect against LPS-induced DIC in rabbits through anti-inflammation and anticoagulation., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Objective: To study and compare the anti-inflammatory effect and molecular mechanism of artemisinin and dihydroartemisinin., Method: Mouse mononuclear macrophage RAW264.7 cells were stimulated to release inflammatory mediators such as TNF-alpha, IL-6 and NO, in order to assess the drugs' inhibitory effect on macrophage's release of above inflammatory mediators. The levels of TNF-alpha and IL-6 were determined by ELISA and the cytotoxicity was determined by MTT method. The protein expression of iNOS, COX-2 and beta-actin were tested by Western blot. The enzymatic activity of COX-2 was determined by colorimetric method., Result: Dihydroartemisinin significantly inhibited LPS-induced release of TNF-alpha, IL-6 and NO from RAW264.7 in mice with the concentration range of 12.5 - 100 micromol x L(-1), and showed good dose dependence. Artemisinin only inhibited the IL-6 release to a certain extent., Conclusion: Dihydroartemisinin inhibits macrophages from releasing inflammatory factors TNF-alpha and IL-6 and inflammatory mediators NO by down-regulating iNOS protein. Artemisinin may help dihydroartemisinin to show its anti-inflammatory effect through metabolism.

A class of compact second-order finite difference algorithms is proposed for solving steady-state laminar natural convection in a square cavity using the stream-function-velocity (ψ-u) form of Navier-Stokes equations. The stream-function-velocity equation and the energy equation are all solved as a coupled system of equations for the four field variables consisting of stream function, two velocities, and temperature. Two strategies are considered for the discretizaton of the temperature equation, which are a second-order five-point compact scheme and a fourth-order nine-point compact scheme, respectively. The numerical capability of the presented algorithm is demonstrated by the application to natural convection in a square enclosure for a wide range of Rayleigh numbers (from 10(3) to 10(8)) and compared with some of the accurate results available in the literature. The presented schemes not only show second-order accurate, but also prove effective. For larger Rayleigh numbers, the algorithm combining the second-order compact scheme for the stream-function-velocity equation with the fourth-order compact scheme for the temperature equation performs more stably and effectively.

The pathogenesis of cachexia in patients with uremia is unknown. We tested the hypothesis that uremia-associated cachexia is caused by leptin signaling through the hypothalamic melanocortin receptor 4 (MC4-R). We performed either subtotal nephrectomy (N) or sham operations in WT, leptin receptor-deficient (db/db), and MC4-R knockout (MC4-RKO) mice. The animals were on 17% protein diets, and none of the uremic animals were acidotic. WT-N mice produced a classic syndrome of cachexia characterized by decreased food intake, increased metabolic rate, and loss of lean body mass. Corrected leptin levels were elevated. db/db mice and MC4-RKO mice resisted the cachexic effects of uremia on weight gain, body composition, and metabolic rate. Likewise, treatment of WT mice with intracranial agouti-related peptide reversed the cachexic effects of uremia on appetite, weight gain, body composition, and metabolic rate. Gene expression of ubiquitin C and proteasome subunits C2, C3, and C9 was not changed in the uremic animals, suggesting that other pathways are involved in this model of nonacidotic uremic cachexia. The results of this study suggest that elevated circulating levels of cytokines such as leptin may be an important cause of uremia-associated cachexia via signaling through the central melanocortin system.