Emodin ameliorates matrix degradation and apoptosis in nucleus pulposus cells and attenuates intervertebral disc degeneration through LRP1 in vitro and in vivo.

Low back pain (LBP) is the leading cause of disability worldwide, with a strong correlation to intervertebral disc degeneration (IDD). Inflammation-induced extracellular matrix (ECM) degradation plays a major role in IDD's progression. Emodin, known for its anti-inflammatory effects and ability to inhibit ECM degradation in osteoarthritis, but its role in IDD is unclear. Our study aimed to explore emodin's role and mechanisms on IDD both in vivo and in vitro. We discovered that emodin positively regulated anabolic markers (COL2A1, aggrecan) and negatively impacted catabolic markers (MMP3, MMP13) in nucleus pulposus cells, while also inhibiting cell apoptosis under inflammation environment. We revealed that emodin inhibits inflammation-induced NF-ĸB activation by suppressing the degradation of LRP1 via the proteasome pathway. Additionally, LRP1 was validated as essential to emodin's regulation of ECM metabolism and apoptosis, both in vitro and in vivo. Ultimately, we demonstrated that emodin effectively alleviates IDD in a rat model. Our findings uncover the novel pathway of emodin inhibiting ECM degradation and apoptosis through the inhibition of NF-κB via LRP1, thus alleviating IDD. This study not only broadens our understanding of emodin's role and mechanism in IDD treatment but also guides future therapeutic interventions.

Comprehensive analysis of angiogenesis pattern and related immune landscape for individual treatment in osteosarcoma.

Postoperative recurrence and metastasis are the main reasons for the poor prognosis of osteosarcoma (OS). Currently, an ideal predictor for not only prognosis but also drug sensitivity and immunotherapy responses in OS patients is urgently needed. Angiogenesis plays a crucial role in tumour progression, which suggests its immense potential for predicting prognosis and responses to immunotherapy for OS. Angiogenesis patterns in OS were explored in depth in this study to construct a prognostic model called ANGscore and clarify the underlying mechanism involved in the immune microenvironment. The efficacy and robustness of the model were validated in multiple datasets, including bulk RNA-seq datasets (TARGET-OS, GSE21257), a single-cell RNA-seq dataset (GSE152048) and immunotherapy-related datasets (GSE91061, GSE173839). OS patients with a high ANGscore had a worse prognosis, accompanied by the immune desert phenotype. Pseudotime and cellular communication analyses in scRNA-seq data revealed that as the ANGscore increased, the malignant degree of cells increased, and IFN-γ signalling was involved in tumour progression and regulation of the tumour immune microenvironment. Furthermore, the ANGscore was associated with immune cell infiltration and the response rate to immunotherapy. OS patients with high ANGscore might be resistant to uprosertib, and be sensitive to VE821, AZD6738 and BMS.345541. In conclusion, we established a novel ANGscore system by comprehensively analysing the expression pattern of angiogenesis genes, which can accurately differentiate the prognosis and immune characteristics of OS populations. Additionally, the ANGscore can be used for patient stratification during immunotherapy, and guide individualized treatment strategies.

JAC4 Alleviates Rotenone-Induced Parkinson's Disease through the Inactivation of the NLRP3 Signal Pathway.

Parkinson's disease (PD) is the fastest-growing neurodegeneration disease, characterized typically by a progressive loss of dopaminergic neurons in the substantia nigra, and there are no effective therapeutic agents to cure PD. Rotenone (Rot) is a common and widely used pesticide which can directly inhibit mitochondrial complex I, leading to a loss of dopaminergic neurons. Our previous studies proved that the JWA gene (arl6ip5) may play a prominent role in resisting aging, oxidative stress and inflammation, and JWA knockout in astrocytes increases the susceptibility of mice to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. JWA-activating compound 4 (JAC4) is a small-molecule activator of the JWA gene, but its role in and mechanism against PD have not yet been clarified. In the present study, we showed that the JWA expression level is strongly related to tyrosine hydroxylase (TH) in different growth periods of mice. Additionally, we constructed models with Rot in vivo and in vitro to observe the neuroprotective effects of JAC4. Our results demonstrated that JAC4 prophylactic intervention improved motor dysfunction and dopaminergic neuron loss in mice. Mechanistically, JAC4 reduced oxidative stress damage by reversing mitochondrial complex I damage, reducing nuclear factor kappa-B (NF-κB) translocation and repressing nucleotide-binding domain, leucine-rich-containing family and pyrin domain-containing-3 (NLRP3) inflammasome activation. Overall, our results provide proof that JAC4 could serve as a novel effective agent for PD prevention.

JP1 normalizes tumor vasculature to suppress metastasis and facilitate drug delivery by inhibiting IL-8.

Tumor vascular normalization prevents tumor cells from breaking through the basement membrane and entering the vasculature, thereby inhibiting metastasis initiation. In this study, we report that the antitumor peptide JP1 regulated mitochondrial metabolic reprogramming through AMPK/FOXO3a/UQCRC2 signaling, which improved the tumor microenvironment hypoxia. The oxygen-rich tumor microenvironment inhibited the secretion of IL-8 by tumor cells, thereby promoting tumor vascular normalization. The normalized vasculature resulted in mature and regular blood vessels, which made the tumor microenvironment form a benign feedback loop consisting of vascular normalization, sufficient perfusion, and an oxygen-rich microenvironment, prevented tumor cells from entering the vasculature, and inhibited metastasis initiation. Moreover, the combined therapy of JP1 and paclitaxel maintained a certain vascular density in the tumor and promoted tumor vascular normalization, increasing the delivery of oxygen and drugs and enhancing the antitumor effect. Collectively, our work highlights the antitumor peptide JP1 as an inhibitor of metastasis initiation and its mechanism of action.

TAK-715 alleviated IL-1ß-induced apoptosis and ECM degradation in nucleus pulposus cells and attenuated intervertebral disc degeneration ex vivo and in vivo.

BACKGROUND: Intervertebral disc degeneration (IDD) is one of the most common disorders related to the spine. Inflammation, apoptosis and extracellular matrix (ECM) degradation contribute to disc degeneration in nucleus pulposus cells (NPCs). This study focused on the role and mechanism of the p38 inhibitor TAK-715 in intervertebral disc degeneration. METHODS: NPCs were treated with IL-1ß to mimic apoptosis, followed by the addition of TAK-715. It was determined that apoptosis, inflammatory mediators (COX-2), inflammatory cytokines (HMGB1), and ECM components (collagen II, MMP9, ADAMTS5, and MMP3) existed in NPCs. In addition, the p38MAPK signaling pathways were examined. The role of TAK-715 in vivo was determined by acupuncture-induced intervertebral disc degeneration. Following an intradiscal injection of TAK-715, MRI and a histopathological analysis were conducted to assess the degree of degeneration. RESULTS: IL-1ß-induced apoptosis was alleviated by TAK-715 in vitro, and antiapoptotic proteins were upregulated. Furthermore, TAK-715 blocked IL-1ß-induced inflammatory mediator production (COX-2) and inflammatory cytokine production (HMGB1) and degraded the ECM (collagen II, MMP9, ADAMTS5, and MMP3). By inhibiting the phosphorylation of p38, TAK-715 exerted its effects. In a rat tail model, TAK-715 ameliorates puncture-induced disc degeneration based on MRI and histopathology evaluations. CONCLUSION: TAK-715 attenuated intervertebral disc degeneration in vitro and in vivo, suggesting that it might be an effective treatment for IDD.

Crystal structure of transcription factor TGA7 from Arabidopsis.

TGA family of transcription factors play important roles in the systemic acquired resistance (SAR) in plants. In SAR, TGA7 binds to the activation sequence-1 (as-1) in the promoter region of SAR related genes and regulates their expressions in an NPR1 dependent manner. Despite its important roles in plant immunity, the molecular mechanism for DNA binding of TGA7 remains unclear. In the present work, we resolved the crystal structure of TGA7 dimers at a resolution of 2.06 Å, in which each monomer binds one molecule of palmitate. Further biochemical studies revealed that TGA7 specifically binds to the TGACG boxes of as-1 DNA in the form of homodimers, and it has specific requirements for the relative spacing and orientation of the two TGACG boxes. Moreover, we built a TGA7-DNA complex model and confirmed by site-directed mutagenesis that amino acid residue R109 in the DNA binding domain (DBD) of TGA7 is a key residue responsible for DNA recognition. Our work offers a good example for structural and functional studies of TGA proteins, and provides key clues to understand the DNA binding mechanism of TGA proteins in the SAR.

AOSRV: Development and preliminary performance assessment of a new robotic system for autonomous percutaneous vertebroplasty.

BACKGROUND: Percutaneous vertebroplasty (PVP) is one of the most effective treatments for patients with vertebral fracture that need surgical treatment, and surgical robotics are promising tools to provide surgeons with improved precision, surgical efficiency and reduce radiation exposure. However, there are currently few robotics that are developed to help assist with PVP. METHODS: A new spinal surgical robotic system 'AOSRV' for autonomous vertebral puncture and bone cement injection was designed and customised in this study. To investigate its practical abilities and the advantages, we performed single-segment/double-segment PVP simulation surgeries on pig spinal specimens manually and using AOSRV. RESULTS: By contrast with the freehand group (FG) in single-segment (SS)/double-segment (DS) surgery, the robotic group (RG) was superior in the operation time (RGSS = 21.14 ± 4.11 min, FGSS = 33.17 ± 6.83 min; RGDS = 42.39 ± 7.31 min, FGDS = 62.86 ± 20.39 min), puncture adjustments (RGSS = 2.30 ± 1.77, FGSS = 14.86 ± 5.46; RGDS = 3.91 ± 1.76, FGDS = 20.00 ± 7.76), intraoperative fluoroscopies (RGSS = 4.10 ± 1.52, FGSS = 20.57 ± 5.44; RGDS = 7.82 ± 1.40, FGDS = 25.91 ± 7.23) and bone cement leakage rate (RGSS = 30%, FGSS = 71.4%; RGDS = 38.6%, FGDS = 83.3%). CONCLUSIONS: AOSRV was successfully developed and had a promising preliminary performance. An innovative attempt was made for the blank space of the autonomous vertebroplasty surgical robotics, and it may shed a light on more promising applications in the future.

Glomus tumor of uncertain malignant potential within the cervical spine: a case report.

The case report details the first glomus tumor (GT) of uncertain malignant potential within the cervical spine. The patient had been experiencing neck pain and numbness of the left side of her body for 3 months. Magnetic resonance imaging (MRI) revealed a lesion with the dimensions 22 mm × 11 mm in the left side of the intervertebral foramen and epidural of C1-5. When the patient appeared aggravating symptoms, we performed an emergency surgery to relieve the spinal cord compression resulting from the growing tumor. During the surgery, a grey-brown friable tumor was observed, and the tumor was located both outside and inside of the cervical spine. Morphological and immunohistochemical (IHC) analysis showed that the lesion was a globular tumor with uncertain malignant potential. After the surgery, the patient received adjuvant radiotherapy consisting of 58.9 Gy in 23 fractions postoperatively. The MRI at 4 months after the surgery showed a progression of the tumor, at which point the patient ceased treatment. GT of uncertain malignant potential within the cervical spine lacks specific clinical manifestations and reliable non-invasive means of examination, so its diagnosis depends on pathological biopsy and IHC examination. Surgical excision is the first treatment to relieve the symptoms of nerve compression. Further research of postoperative radiotherapy and chemotherapy is required to improve treatment options.

JP3 enhances the toxicity of cisplatin on drug-resistant gastric cancer cells while reducing the damage to normal cells.

Background: Cisplatin (DDP) is a highly effective chemotherapeutic agent to most solid tumors including gastric cancer (GC), however, its clinical value is limited due to severe toxic side effects and secondary drug resistance. JP3, a JWA protein based MMP2-targeted polypeptide, known to inhibit the growth of GC in vivo. However, the bidirectional effects of JP3 in DDP-resistant GC and normal cells have not been demonstrated. The present study aims to investigate the actions of JP3 on protecting normal cells from the toxicity of DDP while enhancing its anti-tumor effects on GC cells. Methods: Routine laboratory experimental methods including CCK-8 assay, Western blotting, Hoechst staining, immunofluorescence (IF) and qRT-PCR were used in mechanism investigation; protein docking analysis and coimmunoprecipitation (Co-IP) were used for prediction and confirmation of interactions between JP3 and CK2. Mouse xenograft model was used for screening the treatment of JP3 plus DDP on GC growth. Results: DDP showed similar toxicities to normal cells and DDP-resistant GC cells; JP3 competitively inhibited the binding of XRCC1 to CK2, reduced the DNA repair and anti-apoptosis capacity of DDP-resistant GC cells in combination with DDP treatment; meanwhile, JP3 protected normal cells from DDP-induced oxidative stress and DNA damage through ERK/Nrf2 signaling. JP3 combined with DDP showed similar bidirectional effects in vivo. Conclusions: JP3 enhanced the inhibitory effects of DDP on tumor growth while reduced toxic side effects of DDP on normal cells. The results of this study provide a new insight for the treatment of drug-resistant GC.

A broadband all-fiber integrated graphene photodetector with CNT-enhanced responsivity.

Carbon-based nanomaterials such as carbon nanotubes (CNTs) and graphene have great potential for high-performance all-carbon photodetectors due to their unique optical and electronic properties. Here, we assemble a hybrid CNT/graphene film prepared by depositing CNTs on a single layer graphene with a side-polished optical fiber to achieve a novel all-fiber integrated photodetector. Because CNTs strongly enhanced the interaction between graphene and the fiber mode, the photodetector shows an extra-high photoresponsivity over the visible and infrared region. Especially at 1550 nm, the photoresponsivity is found to be ∼1.48 × 105 A W-1, which is 6.5 times larger than those of photodetectors without CNTs. These findings provide a highly versatile, reproducible, and low-cost platform to integrate novel zero-, one-, and two-dimensional materials into optical fibers and deliver more sophisticated functionalities.

A broadband and low-power light-control-light effect in a fiber-optic nano-optomechanical system.

The coupling of the optical and mechanical degrees of freedom using optical force in nano-devices offers a novel mechanism to implement all-optical signal processing. However, the ultra-weak optical force requires a high pump optical power to realize all-optical processing. For such devices, it is still challenging to lower the pump power and simultaneously broaden the bandwidth of the signal light under processing. In this work, a simple and cost-effective optomechanical scheme was demonstrated that was capable of achieving a broadband (208 nm) and micro-Watt (∼624.13 µW) light-control-light effect driven by a relatively weak optical force (∼3 pN). In the scheme, a tapered nanofiber (TNF) was evanescently coupled with a substrate, allowing the pump light guided in the TNF to generate a strong transverse optical force for the light-control-light effect. Additionally, thanks to the low stiffness (5.44 fN nm-1) of the TNF, the light-control-light scheme also provided a simple method to measure the static weak optical force with a minimum detectable optical force down to 380.8 fN. The results establish TNF as a cost-effective scheme to break the limitation of the modulation wavelength bandwidth (MWB) at a low pump power and show that the TNF-optic optomechanical system can be well described as a harmonic oscillator.

Oxidative stress, apoptosis, and cell cycle arrest are induced in primary fetal alveolar type II epithelial cells exposed to fine particulate matter from cooking oil fumes.

Epidemiological studies demonstrate a linkage between morbidity and mortality and particulate matter (PM), particularly fine particulate matter (PM2.5) that can readily penetrate into the lungs and are therefore more likely to increase the incidence of respiratory and cardiovascular diseases. The present study investigated the compositions of cooking oil fume (COF)-derived PM2.5, which is the major source of indoor pollution in China. Furthermore, oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest induced by COF-derived PM2.5 in primary fetal alveolar type II epithelial cells (AEC II cells) were also detected. N-acetyl-L-cysteine (NAC), a radical scavenger, was used to identify the role of oxidative stress in the abovementioned processes. Our results suggested that compositions of COF-derived PM2.5 are obviously different to PM2.5 derived from other sources, and COF-derived PM2.5 led to cell death, oxidative stress, apoptosis, and G0/G1 cell arrest in primary fetal AEC II cells. Furthermore, the results also showed that COF-derived PM2.5 induced apoptosis through the endoplasmic reticulum (ER) stress pathway, which is indicated by the increased expression of ER stress-related apoptotic markers, namely GRP78 and caspase-12. Besides, the induction of oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest was reversed by pretreatment with NAC. These findings strongly suggested that COF-derived PM2.5-induced toxicity in primary fetal AEC II cells is mediated by increased oxidative stress, accompanied by ER stress which results in apoptosis.

Maternal exposure to fine particulate matter (PM2.5) and pregnancy outcomes: a meta-analysis.

A growing body of evidence has investigated the association between maternal exposure to PM2.5 (particulate matter with aerodynamic diameter 2.5 µm) during pregnancy and adverse pregnancy outcomes. However, the results of those studies are not consistent. To synthetically quantify the relationship between maternal exposure to PM2.5 during pregnancy and pregnancy outcomes (the change in birth weight, low birth weight (LBW), preterm birth (PTB), small for gestational age (SGA), and stillbirth), a meta-analysis of 25 published observational epidemiological studies that met our selection criteria was conducted. Results suggested a 10 µg/m(3) increase in PM2.5 was positively associated with LBW (odds ratio (OR) = 1.05; 95 % confidence interval (CI), 1.02-1.07), PTB (OR = 1.10; 95 % CI, 1.03-1.18), and SGA (OR = 1.15; 95 % CI, 1.10-1.20) based on entire pregnancy exposure, and pooled estimate of decrease in birth weight was 14.58 g (95 % CI, 9.86-19.31); however, there was no evidence of a statistically significant effect of per 10 µg/m(3) increase in PM2.5 exposure on the risk of stillbirth (OR = 1.18; 95 % CI, 0.69-2.04). With respect to three different gestation periods, no significant risks were found in PTB, stillbirth, and the first trimester on the change of birth weight with a 10 µg/m(3) increase in PM2.5. In this study, a comprehensive quantitative analysis of the results show that PM2.5 can increase the risk of LBW, PTB, and SGA; pregnant women need to take effective measures to reduce PM2.5 exposure.

Calcium overload and in vitro apoptosis of the C6 glioma cells mediated by sonodynamic therapy (hematoporphyrin monomethyl ether and ultrasound).

UNLABELLED: The objective of this study was to investigate the role of intracellular calcium overload in the in vitro apoptosis of C6 glioma cells mediated by low level ultrasound and hematoporphyrin monomethyl ether (HMME) therapy. The frequency of ultrasound was optimized by the cell viability assay using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The apoptotic rate, reactive oxygen species (ROS) and decreased mitochondrial membrane potential (MMP) were determined by flow cytometry. Morphological changes were observed by the transmission electron microscope. Concentrations of intracellular Ca2+, [Ca2+]i were detected by a confocal microscopic laser scanning, and the release of cytochrome-c (cyt-c) was measured by western blotting. RESULTS: The SDT-mediated apoptotic effect involved an overload of [Ca2+]i derived from the intra- and extracellular sources during the early progression of apoptotosis. The process was associated with an increased ROS production, a decreased MMP, and a release of cyt-c. In conclusion,the combined use of low level ultrasound and HMME improved the apoptotic rate of C6 glioma cells mediated by ultrasound alone. The [Ca2+]i overload involving activation of mitochondrial signaling played a pivotal role in the SDT-induced apoptosis.

Plasminogen activator inhibitor-1 -675 4G/5G polymorphism and polycystic ovary syndrome risk: a meta analysis.

PURPOSE: Several studies have reported that excessive amounts of plasminogen activator inhibitor-1(PAI-1) might increase the incidence of polycystic ovary syndrome(PCOS), but so far the published results were inconsistent. The aim of this study was to further investigate the association between PAI-1 gene polymorphism and the susceptibility to PCOS by performing a meta-analysis. METHODS: A comprehensive literature search for relevant studies was conducted on google scholar, PubMed, the Chinese National Knowledge Infrastructure (CNKI) and the Chinese Biomedical Literature Database (CBM). This meta-analysis was performed using the STATA 11.0 software and the pooled odds ratio (OR) with 95% confidence interval (CI) was calculated. RESULTS: Ten case-control studies were included in this meta-analysis with a total of 2,079 cases and 1,556 controls. The results showed that PAI-1 -675 4G/5G polymorphism may increase the risk of PCOS, especially among Asian populations. However, there was no statistically significant association between the polymorphism and PCOS risk in Caucasians. CONCLUSION: Our meta-analysis suggests that PAI-1 -675 4G/5G polymorphism may contribute to increasing susceptibility to PCOS in Asians. Detection of the PAI-1 gene polymorphism might be a promising biomarker for the susceptibility of PCOS.

The apoptotic pathways effect of fine particulate from cooking oil fumes in primary fetal alveolar type II epithelial cells.

Apoptosis occurs along three major pathways: (i) an extrinsic pathway, mediated by death receptors; (ii) an intrinsic pathway centered on mitochondria; and (iii) an ER-stress pathway. We investigated the apoptotic pathway effects of cooking oil fumes (COF) in fetal lung type II-like epithelium cells (AEC II). Exposure to COF caused up-regulation of the pro-apoptotic protein Bax and down-regulation of the anti-apoptotic protein Bcl-2. COF induced the mitochondrial permeability transition, an early event in apoptosis; cytochrome c was translocated from the mitochondria to the cytoplasm and nucleus. Caspase-9 and caspase-3 were activated, as a consequence of the mitochondrial permeability transition. The death receptor apoptotic pathway was triggered by COF, as indicated by a change in Fas expression, resulting in increased caspase-8 content. COF exposure arrested the cell cycle the at G0-G1 phase. In summary, COF can lead to apoptosis via mitochondrial and death receptor pathways in AEC II cells.

The association between the C-509T and T869C polymorphisms of TGF-ß1 gene and the risk of asthma: a meta-analysis.

Asthma is a complex multigenic disease in which gene-environment interactions play a critical role in disease onset and progression. Transforming growth factor-ß1 (TGF-ß1) is one of several candidate locus for the pathogenesis of asthma, and is highly polymorphic. To derive a more precise estimation of the relationship between the T869C and C-509T polymorphisms of the TGF-ß1 gene and asthma, a meta-analysis of 24 published case-control studies was conducted. 20 studies for C-509T polymorphism and 8 studies for T869C polymorphism were included. The pooled odds ratios were calculated respectively for allele contrasts, additive genetic model, dominant genetic model and recessive genetic model. Subgroup analyses were also performed by ethnicity, age, atopic status and asthma severity for two gene polymorphisms. In regard to T869C polymorphism, significant associations with asthma were observed in recessive (OR 1.23, 95%CI 1.00-1.51 and P=0.047), additive and allele models. In the subgroup analysis by age, significant risks were also found in the recessive model for adults (OR 1.31, 95%CI 1.02-1.69 and P=0.032), atopic asthma (OR 1.63, 95%CI 1.07-2.49 and P=0.023). With respect to C-509T polymorphism, significant associations with asthma were demonstrated in the overall analysis and subgroup analyses in the dominant model for Asian (OR 1.37, 95%CI 1.04-1.81 and P=0.025), Adults (OR 1.26, 95%CI 1.02-1.56 and P=0.035), Children (OR 1.19, 95%CI 1.01-1.40 and P=0.034). Potentially functional TGF-ß1 C-509T and T869C polymorphisms may be risk factors for asthma susceptibility.

Actinopolyspora dayingensis sp. nov., a novel halophilic actinomycete isolated from a hypersaline lake.

A novel halophilic, filamentous actinomycete, designated TRM 4064(T), was isolated from a hypersaline habitat in Sichuan Province, China. Phylogenetic analysis based on an almost-complete 16S rRNA gene sequence of strain TRM 4064(T) showed that it was most closely related to Actinopolyspora mortivallis (99.1 % sequence similarity). The sequence similarities between strain TRM 4064(T) and other Actinopolyspora species with validly-published names were <97.0 %. However, it had relatively low mean values for DNA-DNA relatedness with the A. mortivallis DSM 44261(T) (23.2 %). Optimal growth occurred at 37 °C, pH 7.0 and in the presence of 13 % (w/v) NaCl. The whole-cell sugar pattern consists of xylose, glucose, ribose and arabinose. The predominant menaquinones are MK-10(H4) (38.2 %), MK-9(H4) (25.1 %), MK-9(H2) (28.6 %) and MK-8(H4) (7.3 %). The major fatty acids are anteiso-C17:0 (36.9 %) and iso-C17:0 (19.3 %). The diagnostic phospholipids detected were diphosphatidylglycerol (DPG), phosphatidylglycerol (PG), phosphatidylcholine (PC), phosphatidylinositol (PI) and two unknown phospholipids. The G+C content of the genomic DNA of the type strain is 66.3 mol%. Strain TRM 4064(T) therefore represents a novel species of the genus Actinopolyspora, for which the name Actinopolyspora dayingensis sp. nov. is proposed. The type strain is TRM 4064(T) (= KCTC 19979(T) = CCTCC AA 2010010(T)).

Toxic effect of cooking oil fumes in primary fetal pulmonary type II-like epithelial cells.

Epidemiological studies indicated that there is an increased risk of respiratory tract cancer among cooks and bakers. The cooking oil fumes are believed to conduct this risk, and many studies have focused on evaluating the mutagenicity and finding the mutagenic components in oil fumes. COFs contains two major classes of compounds. One class consists of polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene, benzo[b]fluoranthene, fluoranthene, and benzo[g,h,i]perylene. BaP is a known immunosuppressant. It can also alter cell cycle progression, induce inflammation, and impair DNA repair and apoptotic processes leading to aberrant cellular functioning. This study investigates the effect of toxicity of cooking oil fumes (COFs) in primary ICR mice' fetal lung type II-like epithelium cells (AEC II). The cells were cultured in different concentrations (0, 12.5, 25, 50, 100, and 200µg/ml) of COFs for different time periods. The results showed that cell viability decreased in a dose- and time- dependent manner, which is accompanied by increased malondialdehyde (MDA) level and decreased superoxide dismutase (SOD) and glutathione (GSH) activities. Moreover, comet assay suggested DNA damage, as well as increased production of DNA adducts induced by PAHs. The present study also shows that COFs may disturb cell cycles even at a very low dose. In summary, the present study indicates that COFs may lead to toxicity in AEC II cells.