Sulfate-reducing bacteria (SRB) mediated carbonate dissolution and arsenic release: Behavior and mechanisms.

Carbonate bound arsenic act as an important reservoir for arsenic (As) in nature aquifers. Sulfate-reducing bacteria (SRB), one of the dominant bacterial species in reductive groundwater, profoundly affects the biogeochemical cycling of As. However, whether and how SRB act on the migration and transformation of carbonate bound arsenic remains to be elucidated. Batch culture experiment was employed using filed collected arsenic bearing calcite to investigate the release and species transformation of As by SRB. We found that arsenic in the carbonate samples mostly exist as inorganic As(V) (93.92 %) and As(III). The present of SRB significantly facilitated arsenic release from carbonates with a maximum of 22.3 µg/L. The main release mechanisms of As by SRB include 1) calcite dissolution and the liberate of arsenic in calcite lattices, and 2) the break of H-bonds frees arsenic absorbed on carbonate surface. A redistribution of arsenic during culture incubation took place which may due to the precipitation of As2Sx or secondary FeAl minerals. To our best knowledge, it is the first experimental study focusing on the release of carbonate bound arsenic by SRB. This study provides new insights into the fate and transport of arsenic mediated by microorganism within high arsenic groundwater-sediment system.

Track Fastener Defect Detection Model Based on Improved YOLOv5s.

Defect detection of track fasteners is a prerequisite for safe and reliable railroad operation. The traditional manual visual inspection method has been unable to meet the growing demand for railroad network inspection in China. To achieve the need for accurate, fast, and intelligent detection of rail fasteners, this paper proposes a rail fastener defect detection model based on improved YOLOv5s. Firstly, the convolutional block attention module (CBAM) is added to the Neck network of the YOLOv5s model to enhance the extraction of essential features by the model and suppress the information of minor features. Secondly, a weighted bidirectional feature pyramid network (BiFPN) is introduced to realize the multi-scale feature fusion of the model. Finally, the K-means++ algorithm is used to re-cluster the dataset to obtain the anchor box suitable for the fastener dataset and improve the positioning ability of the model. The experimental results show that the improved model achieves an average mean precision (mAP) of 97.4%, a detection speed of 27.3 FPS, and a model memory occupancy of 15.5 M. Compared with the existing target detection model, the improved model has the advantages of high detection accuracy, fast detection speed, and small model memory occupation, which can provide technical support for edge deployment of rail fastener defect detection.

Characterization of nine polyphenols in fruits of Malus pumila Mill by high-performance liquid chromatography.

Polyphenols are important bioactive substances in apple. To explore the profiles of the nine representative polyphenols in this fruit, a high-performance liquid chromatography method has been established and validated. The validated method was successfully applied for the simultaneous characterization and quantification of these nine apple polyphenols in 11 apple extracts, which were obtained from six cultivars from Shaanxi Province, China. The results showed that only abscission of the Fuji apple sample was rich in the nine apple polyphenols, and the polyphenol contents of other samples varied. Although all the samples were collected in the same region, the contents of nine polyphenols were different. The proposed method could serve as a prerequisite for quality control of Malus products.

Cystatin C is a moderate predictor of acute kidney injury in the early stage of traumatic hemorrhagic shock.

Patients with traumatic hemorrhagic shock are highly susceptible to the development of acute kidney injury (AKI), but little data are available regarding the changes in cystatin C (CysC) in patients with traumatic hemorrhagic shock. The aim of the present study, therefore, was to investigate whether CysC has a higher value than serum creatinine (SCr) and urea for use in monitoring glomerular function in traumatic hemorrhagic shock. Data from a cohort of patients with traumatic hemorrhagic shock, who had been admitted to a trauma center, were collected. Receiver operating characteristic (ROC) curve analysis was used to determine the diagnostic value of serum CysC, SCr and urea for the identification of renal dysfunction, and the data were expressed as the area under the curve (AUC). CysC was not significantly affected by gender, age, mechanism of injury or time between injury and arrival at the center in the patients with traumatic hemorrhagic shock. The CysC level of the patients was significantly higher than that of the normal subjects (1.10±0.36 vs. 0.91±0.34 mg/l); the SCr and urea levels of the patients were also significantly increased compared with those of the normal subjects. Nonparametric ROC plots of the sensitivity and specificity of SCr, CysC and urea for the detection of AKI revealed AUC values of 0.901 [95% confidence interval (CI), 0.791-1.000], 0.728 (95% CI, 0.570-0.886) and 0.709 (95% CI, 0.552-0.865) for SCr, CysC and urea, respectively. No significant correlation between mortality and CysC, SCr or urea was found. These data indicate that the level of CysC is significantly increased in the early stage of traumatic hemorrhagic shock and that CysC can be used as a marker to predict AKI; however, the diagnostic utility of CysC remains lower than that of SCr in the early stage of the condition.

Anatomical variations of the upper thoracic sympathetic chain.

The aim is to clearly delineate the upper thoracic sympathetic chains and neural connections between the chains and ventral rami of the thoracic nerves, and to provide an anatomical foundation for successful upper thoracic sympathicotomy for treating upper essential hyperhidrosis. The upper thoracic sympathetic chains, upper five intercostal nerves, and neural connections between them in 50 halves of 25 adult cadavers have been dissected, measured, and mapped. The stellate ganglion had an incidence of 80%. The second to the fourth thoracic sympathetic ganglia were commonly located in the corresponding intercostal spaces with the presence of 92%, 68%, and 50%, respectively. The incidence of the first and second intercostal rami was 40% and 6%, and that of the ascending or descending rami from the second, third and fourth ganglia was 54%, 24%, and 14%, respectively. Additional rami communicantes joined the ventral ramus of the 1st thoracic nerve proximal to the point where the latter gave a branch to the brachial plexus. The farthest horizontal distance from the sympathetic chain to the junction between the additional rami communicantes and the second to the fourth intercostal nerves was 29.1 mm. Only 16% of cadavers had similar anatomy bilaterally. Anatomical variations of the upper thoracic sympathetic trunk in relation to intercostal nerves, which may be one of the causes resulting in surgical failures and recurrences, were striking. Attention should be given to such anatomical variations when planning thoracic sympathicotomy.

[Level of microwave radiation from mobile phone base stations built in residential districts].

OBJECTIVE: To investigate the condition of microwave radiation pollution from mobile phone base station built in populated area. METHODS: Random selected 18 residential districts where had base station and 10 residential districts where had no base stations. A TES-92 electromagnetic radiation monitor were used to measure the intensity of microwave radiation in external and internal living environment. RESULTS: The intensities of microwave radiation in the exposure residential districts were more higher than those of the control residential districts (p < 0.05). There was a intensity peak at about 10 m from the station, it would gradually weaken with the increase of the distance. The level of microwave radiation in antenna main lobe region is not certainly more higher than the side lobe direction, and the side lobe direction also is not more lower. At the same district, where there were two base stations, the electromagnetic field nestification would take place in someplace. The intensities of microwave radiation outside the exposure windows in the resident room not only changed with distance but also with the height of the floor. The intensities of microwave radiation inside the aluminum alloys security net were more lower than those of outside the aluminum alloys security net (p < 0.05), but the inside or outside of glass-window appears almost no change (p > 0.05). CONCLUSIONS: Although all the measure dates on the ground around the base station could be below the primary standard in "environment electromagnetic wave hygienic standard" (GB9175-88), there were still a minorities of windows which exposed to the base station were higher, and the outside or inside of a few window was even higher beyond the primary safe level defined standard. The aluminum alloys security net can partly shield the microwave radiation from the mobile phone base station.

Cleavage of p53-vimentin complex enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis of rheumatoid arthritis synovial fibroblasts.

Rheumatoid arthritis synovial fibroblasts (RASFs) contribute to arthritic cartilage degradation. Although RASFs are normally resistant to apoptosis, Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based gene therapy has been successfully used in a mouse model of arthritis. We investigated this further by treating human RASFs with nontoxic doses of the proteasome inhibitor lactacystin. Treatment induced cytosolic accumulation of p53 and enhanced the susceptibility of RASFs to apoptosis mediated by TRAIL-R2 (DR5) but not Fas. A specific role for p53 in TRAIL-R2-mediated apoptosis was indicated by the ability of p53 siRNA to significantly reduce RASF apoptosis and by the reduced apoptosis of RASFs bearing p53 mutations on treatment with anti-DR5 antibody or anti-DR5 antibody plus lactacystin. p53 immunoprecipitation followed by mass spectrometry identified a vimentin-p53 complex, an interaction that was confirmed by reciprocal vimentin-p53 immunoprecipitation and by co-immunofluorescence. Interestingly, human caspase-4 cleaved human vimentin, and blockade of caspase-4 with a chemical inhibitor or with specific siRNA significantly inhibited TRAIL-R2-mediated apoptosis of RASFs. Furthermore, blockade of caspase-4 was paralleled by persistence of a cytosolic pattern of p53 and absence of p53 translocation to the nucleus. Taken together, our findings suggest a unique role for caspase-4 in cleaving vimentin and releasing cytosolic p53 for nuclear translocation, events that may regulate the sensitivity of RASFs to receptor-mediated apoptosis.

Regulation of apoptosis proteins in cancer cells by ubiquitin.

Ubiquitin inhibitors act at many levels to enhance apoptosis signaling. For TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling, there are at least five mechanisms by which apoptosis are regulated by the ubiquitin-proteasome pathway. First, proteasome inhibitors can decrease Fas-like inhibitor protein (FLIP) protein levels in tumors, resulting in increased apoptosis signaling due to increased caspase-8 activation. This appears to involve the ubiquitin ligase TNF receptor activation factor-2 (TRAF2) and acts indirectly by causing cell-cycle arrest at a stage where there is high degradation of the FLIP-TRAF2 complex. Second, the regulation of the proapoptotic Bcl-2 family member BAX occurs indirectly. Apoptosis signaling and caspase activation results in a confirmation change in the normally monomeric BAX, which exposes the BH3 domain of BAX, leading to dimerization and resistance to ubiquitin degradation. BAX then translocates into the mitochondria, resulting in the release of proapoptotic mitochondrial factors such as cytochrome c and second mitochondria-derived activator of caspase (SMAC). This results in the activation of caspase-9 and formation of the apoptosome and efficient apoptosis signaling. A third mechanism of the regulation of TRAIL signaling in the ubiquitin-proteasome pathway is mediated by the inhibitor of apoptosis proteins (IAP) E3 ligases. These IAPs can directly bind to caspases but also can act as ubiquitin ligases for caspases, resulting in the degradation of these caspases. IAP binding to caspases can be inhibited by SMAC, which exhibits a caspase-9 homology domain. The fourth mechanism for apoptosis activation by proteasome inhibitors is through the stabilization of the inhibitor of the kappaB (IkappaB)/NF-kappaB complex and prevention of nuclear translocation of the antiapoptosis transcription factor NF-kappaB. During TRAIL-DR4, DR5 signaling, this pathway is activated by interactions of activated Fas-associated death domain with activated receptor-interacting protein (RIP), which in turn activates NF-kappaB-inducing kinase and phosphorylates IkappaB. Therefore, the inhibition of IkappaB degradation blocks this RIP-mediated antiapoptosis signaling event. Last, p53 protein levels, and susceptibility to apoptosis, can be deregulated by the human homolog Hdm2 (Mdm2) E3 ligase. This process is inhibited by p53 phosphorylation and by sequestration of Mdm2 by ARF. Better mechanisms to inhibit the ubiquitin-proteasome pathway targeted at the ubiquitin-proteasome degradation process itself, or more specifically at the E3 ligases known to modulate and downregulate proapoptosis pathways will lead to the enhancement of TRAIL apoptosis signaling and better cancer therapeutic outcomes act through this pathway.

[Effect of ubiquitin-proteasome pathway on TRAIL inducing apoptosis].

OBJECTIVE: To determine the influence of ubiquitin-proteasome in regulating the TRAIL-mediated apoptosis. METHODS: RASF cells and SCID mice were divided into 4 groups treated with PBS,anti-DR5, lactacystin, and anti-DR5 plus lactacystin. The apoptosis of cells was detected with Hoechst 33342 and TUNEL. The effect of caspase inhibitor on cell apoptosis was analysed with Hoechst 33342 and Luminescent ATP Lite. RESULTS: Block ubiquitin-proteasome with lactacystin, a highly specific and irreversible proteasome inhibitor, induced 95% cell apoptosis both in vitro and in vivo. In contrast, there was no apoptosis of cells after the treatment with anti-DR5 antibody or lactacystin alone. CONCLUSION: The inhibition of ubiquitin-proteasome pathway can sensitize rheumatoid arthritis synovial fibroblast cells to TRAIL- induced apoptosis, and the activation of caspase 8 and caspase 4 is necessary in this process.