Prelamin A overexpression promotes detrusor calcification/aging in urinary incontinence via prelamin A accumulation.

Urinary incontinence (UI) is known as a distressing condition particularly among older adults, and negatively associated with health-related quality of life in both males and females. Prelamin A accumulation has been found in all progeroid laminopathies and is obviously linked to cell and organism aging. Therefore, this study was expected to investigate the effect of prelamin A on detrusor on UI. Prelamin A expression in clinical and animal samples was detected. To investigate the degree of prelamin A accumulation and detrusor calcification/aging, the detrusor cells were subcultured separately into low and high passage. The low-passage subculture cells were treated with transfection of overexpressed prelamin A plasmid, and transfection of overexpressed prelamin A plasmid and application of farnesyl transferase inhibitor (FTIs) H-9279, respectively. Zmpste24, Icmt and lamin A/C expression were detected to explore how prelamin A affected detrusor calcification/aging. Prelamin A was overexpressed in aged detrusor cells, indicating prelamin A expression was positively related to the age of subjects. The degree of prelamin A accumulation and detrusor calcification/aging was higher in aged rats and high passage subculture cells. Zmpste24, Icmt and lamin A/C were poorly expressed in cells transfected with overexpressed prelamin A, as well as cell proliferation activity decreased and calcium deposition and apoptotic rate increased. Furthermore, we also found that the effect of overexpressed prelamin A was lost when cells were treated with H-9279. These findings provide evidence that prelamin A overexpression impairs degradation of its farnesylated form, thus causing prelamin A accumulation which induces detrusor calcification/aging in UI.

MicroRNA-27a Suppresses Detrusor Fibrosis in Streptozotocin-Induced Diabetic Rats by Targeting PRKAA2 Through the TGF-ß1/Smad3 Signaling Pathway.

BACKGROUND/AIMS: We examined the effects of microRNA-27a (miR-27a) on detrusor fibrosis in streptozotocin (STZ)-induced diabetic rats. METHODS: Eighty healthy Sprague-Dawley (SD) rats were randomly allocated into control, diabetic, miR-27a mimics, mimics control, miR-27a inhibitors, inhibitors control, siRNA-PRKAA2 (siPRKAA2) and inhibitors + siPRKAA2 groups (the latter 7 groups were established as STZ-induced diabetic rat models and treated in different manners). Detrusor cell apoptosis in bladder tissues was determined through terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining. Detrusor cells were assigned to the blank, miR-27a mimics, mimics control, miR-27a inhibitors, inhibitors control, siPRKAA2 and inhibitors + siPRKAA2 groups. Flow cytometry determined the cell cycle stage and apoptosis. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting (WB) were used to assess the expression of miR-27a, PRKAA2, TGF-ß1, Smad3, p-Smad3, fibronectin (FN), connective tissue growth (CTGF), and collagen-I (COL-I) in tissues and cells. RESULTS: Compared with the control group, the diabetic, miR-27a mimics, and siPRKAA2 groups showed reduced weight and PRKAA2 expression, but elevated blood glucose, serum creatinine (sCr), blood urea nitrogen (BUN), cell apoptosis, and expression of TGF-ß1, Smad3, FN, COL-I, CTGF, and p-Smad3. The opposite trend was observed in the miR-27a inhibitors group. PRKAA2 is a target gene of miR-27a. Compared to the blank group, the miR-27a mimics and siPRKAA2 groups indicated markedly increased TGF-ß1, Smad3, FN, COL-I, CTGF and p-Smad3 expression; decreased PRKAA2 expression; and increased cell apoptosis. The miR-27a inhibitors group showed the opposite trend. CONCLUSION: These results indicate that miR-27a may contribute to detrusor fibrosis in STZ-induced diabetic rats by targeting PRKAA2 via the TGF-ß1/Smad3 signaling pathway.

Lung cancer cell-intrinsic IL-15 promotes cell migration and sensitizes murine lung tumors to anti-PD-L1 therapy.

BACKGROUND: IL-15 plays a vital role in enhancing NK cell- and T-cell-mediated antitumor immune responses; however, the direct effect of IL-15 on tumor cells has not been fully elucidated. Herein, we investigated the effect of IL-15 on lung adenocarcinoma cells. METHODS: Silencing and overexpression techniques were used to modify endogenous IL-15 expression in tumor cells. Transwell assays were used to assess tumor cell migration and invasion; a live-cell analysis system was used to evaluate cell motility; cellular morphological changes were quantified by confocal fluorescence microscopy; the molecular mechanisms underlying the effect of IL-15 on tumor cells were analyzed by western blotting; and RhoA and Cdc42 activities were evaluated by a pulldown assay. NCG and C57BL/6 mouse models were used to evaluate the functions of IL-15 in vivo. RESULTS: Cancer cell-intrinsic IL-15 promoted cell motility and migration in vitro and metastasis in vivo via activation of the AKT-mTORC1 pathway; however, exogenous IL-15 inhibited cell motility and migration via suppression of the RhoA-MLC2 axis. Mechanistic analysis revealed that both the intracellular and extracellular IL-15-mediated effects required the expression of IL-15Rα by tumor cells. Detailed analyses revealed that the IL-2/IL-15Rß and IL-2Rγ chains were undetected in the complex formed by intracellular IL-15 and IL-15Rα. However, when exogenous IL-15 engaged tumor cells, a complex containing the IL-15Rα, IL-2/IL-15Rß, and IL-2Rγ chains was formed, indicating that the differential actions of intracellular and extracellular IL-15 on tumor cells might be caused by their distinctive modes of IL-15 receptor engagement. Using a Lewis lung carcinoma (LLC) metastasis model, we showed that although IL-15 overexpression facilitated the lung metastasis of LLC cells, IL-15-overexpressing LLC tumors were more sensitive to anti-PD-L1 therapy than were IL-15-wild-type LLC tumors via an enhanced antitumor immune response, as evidenced by their increased CD8+ T-cell infiltration compared to that of their counterparts. CONCLUSIONS: Cancer cell-intrinsic IL-15 and exogenous IL-15 differentially regulate cell motility and migration. Thus, cancer cell-intrinsic IL-15 acts as a double-edged sword in tumor progression. Additionally, high levels of IL-15 expressed by tumor cells might improve the responsiveness of tumors to immunotherapies.

TGFß Antagonizes IFNγ-Mediated Adaptive Immune Evasion via Activation of the AKT-Smad3-SHP1 Axis in Lung Adenocarcinoma.

IFNγ-mediated signaling in tumor cells can induce immunosuppressive responses and cause tumor resistance to immunotherapy. Blocking TGFß promotes T lymphocyte infiltration and turns immunologically cold tumors into hot tumors, thereby improving the efficacy of immunotherapy. Several studies have shown that TGFß inhibits IFNγ signaling in immune cells. We thus sought to determine whether TGFß affects IFNγ signaling in tumor cells and plays a role in the development of acquired resistance to immunotherapy. TGFß stimulation of tumor cells increased SHP1 phosphatase activity in an AKT-Smad3-dependent manner, decreased IFNγ-mediated tyrosine phosphorylation of JAK1/2 and STAT1, and suppressed the expression of STAT1-dependent immune evasion-related molecules, e.g., PD-L1, IDO1, herpes virus entry mediator (HVEM), and galectin-9 (Gal-9). In a lung cancer mouse model, dual blockade of TGFß and PD-L1 led to superior antitumor activity and prolonged survival compared with anti-PD-L1 therapy alone. However, prolonged combined treatment resulted in tumor resistance to immunotherapy and increased expression of PD-L1, IDO1, HVEM, and Gal-9. Interestingly, after initial anti-PD-L1 monotherapy, dual TGFß and PD-L1 blockade promoted both immune evasion gene expression and tumor growth compared with that in tumors treated with continuous PD-L1 monotherapy. Alternatively, treatment with JAK1/2 inhibitor following initial anti-PD-L1 therapy effectively suppressed tumor growth and downregulated immune evasion gene expression in tumors, indicating the involvement of IFNγ signaling in immunotherapy resistance development. These results demonstrate an unappreciated effect of TGFß on the development of IFNγ-mediated tumor resistance to immunotherapy. SIGNIFICANCE: Blocking TGFß facilitates IFNγ-mediated resistance to anti-PD-L1 therapy due to the role of TGFß in inhibiting IFNγ-induced immunoevasion by increasing SHP1 phosphatase activity in tumor cells.

A Mesozoic fossil lagerstätte from 250.8 million years ago shows a modern-type marine ecosystem.

Finely preserved fossil assemblages (lagerstätten) provide crucial insights into evolutionary innovations in deep time. We report an exceptionally preserved Early Triassic fossil assemblage, the Guiyang Biota, from the Daye Formation near Guiyang, South China. High-precision uranium-lead dating shows that the age of the Guiyang Biota is 250.83 +0.07/-0.06 million years ago. This is only 1.08 ± 0.08 million years after the severe Permian-Triassic mass extinction, and this assemblage therefore represents the oldest known Mesozoic lagerstätte found so far. The Guiyang Biota comprises at least 12 classes and 19 orders, including diverse fish fauna and malacostracans, revealing a trophically complex marine ecosystem. Therefore, this assemblage demonstrates the rapid rise of modern-type marine ecosystems after the Permian-Triassic mass extinction.

Dearomatization/Deiodination of o-Iodophenolic Compounds with α,ß-Unsaturated Imines for Accessing Benzofuran Derivatives.

A dearomatization/deiodination/rearomatization strategy for the [3 + 2] cyclization of o-iodophenolic substrates with α,ß-unsaturated imines to construct various dihydrobenzofuran-related skeletons has been established. Tolerance to different functional groups has been tested. Mechanistic studies revealed that this domino reaction was possibly realized by the deiodination and tautomerization of the key dearomatized intermediate to generate a free phenolic O radical. Moreover, an anticancer agent 4 and an α-glucosidase inhibitor 5 with high bioactivities were successfully synthesized using this novel protocol.

Application of electromagnetic navigation bronchoscopy-guided microwave ablation in multiple pulmonary nodules: a single-centre study.

OBJECTIVES: Electromagnetic navigation bronchoscopy (ENB)-guided microwave ablation is a minimally invasive technology for treating pulmonary lesions. This study analysed the short-term safety and efficacy of ENB-guided microwave ablation in multiple pulmonary nodules (MPNs). METHODS: This retrospective study reports a single-centre experience with ENB-guided microwave ablation for MPNs. Clinical, surgical and pathological data were obtained for patients who underwent ENB-guided microwave ablation from 23 December 2019 to 23 June 2021. The primary end points were technical safety and efficiency. RESULTS: The study assessed 65 patients who underwent ENB-guided microwave ablation, 57 of whom simultaneously underwent video-assisted thoracic surgery. In total, 216 nodules were treated. Of 96 nodules treated by ENB-guided microwave ablation, 94 nodules had ground-glass opacity. Ablation efficiency was confirmed by hybrid cone-beam computed tomography. Of 120 nodules surgically removed, 106 nodules had ground-glass opacity. The mean nodule size was 7.9 mm in ablated nodules and 10.2 mm in resected nodules. Distance between nodules and pleura or fissure was 17.45 mm in ablated nodules and 7.29 mm in resected nodules. The overall malignancy rate was 47.7% (103/216); the complication rate was low (65 patients). At short-term follow-up, the post-ablation target zone shrank by 1 week and stabilized after 4-6 months. No local recurrence or enlargement of other pulmonary nodules was noted. CONCLUSIONS: To treat MPNs, ENB-guided microwave ablation is safe and efficient. The combination of this treatment and video-assisted thoracic surgery is a potential application, which can preserve as much pulmonary function as possible and treat MPNs to the maximum extent.

A new perleidid neopterygian fish from the Early Triassic (Dienerian, Induan) of South China, with a reassessment of the relationships of Perleidiformes.

Neopterygii is the largest clade of ray-finned fishes, including Teleostei, Holostei, and their closely related fossil taxa. This clade was first documented in the Early Carboniferous and underwent rapid evolutionary radiation during the Early to Middle Triassic. This article describes a new perleidid neopterygian species, Teffichthys elegans sp. nov., based on 13 well-preserved specimens from the lower Daye Formation (Dienerian, Induan) in Guizhou, China. The new species documents one of the oldest perleidids, providing insights into the early diversification of this family. The results of a phylogenetic analysis recover Teffichthys elegans sp. nov. as the sister taxon to Teffichthys madagascariensis within the Perleididae. T. elegans sp. nov. shares three derived features of Perleididae: the length of the anteroventral margin of the dermohyal nearly half the length of the anterodorsal margin of the preopercle; the anteroventral margin of the preopercle nearly equal to the anterior margin of the subopercle in length; and the anteroventral margin of the preopercle one to two times as long as the anterodorsal margin of the preopercle. It possesses diagnostic features of Teffichthys but differs from T. madagascariensis by the following features: presence of three supraorbitals; six pairs of branchiostegal rays; relatively deep anterodorsal process of subopercle; absence of spine on the posterior margin of the jugal; and pterygial formula of D26/P14, A22, C36/T39-41. The Perleidiformes are restricted to include only the Perleididae, and other previously alleged 'perleidiform' families (e.g., Hydropessidae and Gabanellidae) are excluded to maintain the monophyly of the order. Similar to many other perleidids, T. elegans sp. nov. was likely a durophagous predator with dentition combining grasping and crushing morphologies. The new finding also may indicate a relatively complex trophic structure of the Early Triassic marine ecosystem in South China.

Impacts of underwater topography on the distribution of microplastics in lakes: A case from Dianchi Lake, China.

The spatial distribution of microplastics and the factors influencing their distribution in lakes are important aspects of plastics pollution studies. This study investigated the impacts of lake underwater topography on the spatial distribution of microplastics in Dianchi Lake in China. Data on spatial distribution of microplastics were obtained by pump sampling, microscopic examination, and polymer identification. Parameters of underwater topography were extracted from an isobaths map of Dianchi Lake. The relationships between underwater topography and the abundance of microplastics were analyzed. The results showed that for the northern part of the lake, water depth, slope gradient, relief, roughness and surface curvature have significant relationships with the spatial distribution of microplastics. In the southern part, only roughness showed a significant relationship. The roughness is the only important factor which impacts the microplastics distribution in both parts of the lake and the whole lake. These differences between the northern part and the southern part of the lake are related to the stronger circular currents in the southern part of the lake. These results showed that the impacts of underwater topography manifest themselves well when lake currents are weak, and these impacts are reduced or muted when lake currents are strong. Our research results provide a good reference for understanding distribution and migration principle of microplastics in lakes.

IFN-γ activates the tumor cell-intrinsic STING pathway through the induction of DNA damage and cytosolic dsDNA formation.

Stimulator of interferon genes (STING) pathway activation predicts the effectiveness of targeting the PD-1/PD-L1 axis in lung cancer. Active IFN-γ signaling is a common feature in tumors that respond to PD-1/PD-L1 blockade. The connection between IFN-γ and STING signaling in cancer cells has not been documented. We showed that IFN-γ caused DNA damage and the accumulation of cytosolic dsDNA, leading to the activation of the cGAS- and IFI16-dependent STING pathway in lung adenocarcinoma cells. IFN-γ-induced iNOS expression and nitric oxide production were responsible for DNA damage and STING activation. Additional etoposide treatment enhanced IFN-γ-induced IFN-ß and CCL5 expression. Tumor-infiltrating T cells stimulated with a combination of anti-CD3 and anti-PD-1 antibodies caused STING activation and increased IFN-ß and CCL5 expression in lung adenocarcinoma. These effects were abrogated by the addition of an IFN-γ neutralizing antibody. Our results suggest that the activation of tumor-infiltrating T cells could alter the tumor microenvironment via the IFN-γ-mediated activation of STING signaling in cancer cells.

IFN-γ-induced ER stress impairs autophagy and triggers apoptosis in lung cancer cells.

Interferon-gamma (IFN-γ) is a major effector molecule of immunity and a common feature of tumors responding to immunotherapy. Active IFN-γ signaling can directly trigger apoptosis and cell cycle arrest in human cancer cells. However, the mechanisms underlying these actions remain unclear. Here, we report that IFN-γ rapidly increases protein synthesis and causes the unfolded protein response (UPR), as evidenced by the increased expression of glucose-regulated protein 78, activating transcription factor-4, and c/EBP homologous protein (CHOP) in cells treated with IFN-γ. The JAK1/2-STAT1 and AKT-mTOR signaling pathways are required for IFN-γ-induced UPR. Endoplasmic reticulum (ER) stress promotes autophagy and restores homeostasis. Surprisingly, in IFN-γ-treated cells, autophagy was impaired at the step of autophagosome-lysosomal fusion and caused by a significant decline in the expression of lysosomal membrane protein-1 and -2 (LAMP-1/LAMP-2). The ER stress inhibitor 4-PBA restored LAMP expression in IFN-γ-treated cells. IFN-γ stimulation activated the protein kinase-like ER kinase (PERK)-eukaryotic initiation factor 2a subunit (eIF2α) axis and caused a reduction in global protein synthesis. The PERK inhibitor, GSK2606414, partially restored global protein synthesis and LAMP expression in cells treated with IFN-γ. We further investigated the functional consequences of IFN-γ-induced ER stress. We show that inhibition of ER stress significantly prevents IFN-γ-triggered apoptosis. CHOP knockdown abrogated IFN-γ-mediated apoptosis. Inhibition of ER stress also restored cyclin D1 expression in IFN-γ-treated cells. Thus, ER stress and the UPR caused by IFN-γ represent novel mechanisms underlying IFN-γ-mediated anticancer effects. This study expands our understanding of IFN-γ-mediated signaling and its cellular actions in tumor cells.

CD8+CD57+ T cells exhibit distinct features in human non-small cell lung cancer.

BACKGROUND: The repetitive antigen stimulation during chronic infection often leads to the accumulation of CD8+CD57+ T cells. These cells express high levels of interferon-γ, granzyme B and perforin with elevated cytolytic effect, and are considered as the most potent cells for combating chronical viral infection. The status of CD8+CD57+ T cells in non-small cell lung cancer (NSCLC) has not been well defined. METHODS: We used flow cytometry and undertook a systemic approach to examine the frequency, immunophenotyping and functional properties of CD8+CD57+ T cells in the peripheral blood, tumor tissue and the corresponding normal tissue, as well as lung draining lymph nodes, of patients with NSCLC. RESULTS: CD57+ T cells expressed high levels of programmed cell death-1 (PD-1) in all tested compartments and were predominantly CD8+ T cells. These cells in the peripheral blood displayed a terminally differentiated phenotype as defined by loss of CD27 and CD28 while expressing KLRG1. CD8+CD57+ T cells exhibited enhanced cytotoxic potencies and impaired proliferative capability. Unlike CD57+ T cells in the peripheral blood, a significant proportion of CD57+ T cells in the primary tumors expressed CD27 and CD28. CD8+CD57+ T cells in tumors lacked cytotoxic activity. The proliferative activity of these cells was also impaired. CD8+CD57+ T cells in the corresponding normal lung tissues shared similarities with their counterparts in peripheral blood rather than their counterparts in tumors. The vast majority of CD8+CD57+ T cells in lung draining lymph nodes were positive for CD27 and CD28. These cells were unable to produce perforin and granzyme B, but their proliferative activity was preserved. CD8+CD57+ T cells in tumors displayed an inferior response to PD-1 blockade compared with their CD8+CD57- counterparts. Interleukin (IL)-15 preferentially restored the effector function of these cells. Additionally, IL-15 was able to restore the impaired proliferative activity of CD8+CD57+ T cells in tumors and peripheral blood. CONCLUSIONS: Our data indicate that the failure of the immune system to fight cancer progression could be a result of impaired CD8+ T-cell functional maturation into fully differentiated effector T cells within the tumor microenvironment. Boosting IL-15 activity might promote tumor-reactive CD8+ T-cell functional maturation while preserving their proliferative activity.

[Construction and characterization of type I fimbriae fimH deletion mutant from avian pathogenic Escherichia coli].

The wild type avian pathogenic Escherichia coli (APEC) isolate A2 (Serotype O2:K89) was selected as the prototype of the (APEC) Type I Fimbriae. Based on the original sequences of Type I Fimbriae operon gene clusters in the GenBank,we generated PCR products by using primers with the homologies extension of fimH gene to be deleted and template plasmid pKD3 carrying selectable antibiotic chloramphenicol resistance (cat) gene that is flanked by FRT (FLP recognition target) sites. By using the PCR products, the A2 deltafimH::Cat deletion mutant from A2 isolate was constructed by lambdaRed-mediated recombination system in the flanking homologies. After selection, the resistance gene located in the A2deltafimH::Cat mutant was eliminated in the second recombination, by using a helper plasmid pCP20, a temperature-sensitive one encoding and expressing the FLP recombinase, which acts on the directly repeated FRT sites flanking the resistance gene. The A2deltafimH mutant obtained was further confirmed by fimH PCR amplification and sequencing. The A2deltafimH mutant with the deletion of fimH adhesin in the fim gene cluster lost the ability of agglutination reaction with both guinea pig erythrocytes and yeast cells. The A2deltafimH deletion mutant restored the agglutination ability of both binding guinea pig erythrocytes and yeast cells when transfected the compatible recombinant plasmid pBR322-fimH with fimH insert in the fimH complementation assay. Very similar to the wild type A2 isolate, The obtained binding activity from the A2deltafimH mutant in the complementation assay was completely inhibited when pretreated with 0.5% mannose solution. Compared with the wild type isolate, the A2deltafimH mutant grew slowly during all stages of growth. This work provides the basis for us to study the molecular pathogenesis mechanisms of interaction between the APEC Type I Fimbriae and susceptible host cells, extra-intestinal infection, prevention and control of the APEC-caused disease.

Effects of indole alkaloids from leaf of Alstonia scholaris on post-infectious cough in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Leaf of Alstonia scholaris (L.) R. Br. (Apocynaceae), a wide used ethic-medicine in many Asia and Africa counties, has also been recorded as the common traditional Chinese medicine for treatment of illnesses in respiratory system by Dai people. AIM OF THE STUDY: To provide experimental data of clinical adaption of total indole alkaloids (TA) from leaf of A. scholaris for treating post-infectious cough in phase II clinical trial. MATERIALS AND METHODS: To model post-infectious cough, all animals except control group were instilled intra-tracheal with lipopolysaccharide (LPS) (80 µg/50 µL/mouse), followed by subsequent exposure to cigarette smoke (CS) for 30 min per day for a total of 30 days. Mice were orally given TA at dose of 10, 25, 50 mg/kg, and four main alkaloids (Sch: scholaricine, Epi: 19-epischolaricine, Val: vallesamine, Pic: picrinine) once daily. Cellular infiltration was assessed in the broncho-alveolar lavage fluid (BALF). Expression of interleukin-6 (IL-6) and C-reactive protein (CRP) in the serum was determined, the superoxide dismutase (SOD) activity as well as malondialdehyde (MDA) content in the serum and homogenate were examined. Finally, histopathological examination in the lungs was assessed by H. E. staining. RESULTS: After administration of TA and four major alkaloids respectively, the symptoms of cough in mice were obviously attenuated. Total white blood cells (WBC) and neutrophils (NEU) amounts in BALF were reduced obviously and the pathological damage of lung was also attenuated. There was also significant reduction in IL-6, CRP, MDA and a marked improvement in SOD. CONCLUSIONS: The efficacy of indole alkaloids against post-infectious cough (PIC) was shown in the down-regulation of inflammatory cells, cytokines, and the balance of antioxidants. What's more, the pharmacological effects of TA were better than single indole alkaloid, which might be related to the synergic effect of four major alkaloids.

[Display of the F18 fimbrial adhesin on the bacterial surface using type V secretion system and characterization of the binding domain of the adhesin].

The beta domains of autotransporters (also called type V secretion system) have been demonstrated to be feasible tools to display foreign passenger domain on the bacterial surface. In the present work, using the DNA manipulation the type V secretion system MisL displaying the binding doamin FedF1 of the F18ab fimbrial adhesion was constructed, and the full length adhesin FedF of F18ab fimbriae and the FedF mutant (with the 88th and 89th amino acid residues changed from Histadine to Alamine) on the surface of E. coli DH5alpha, respectively. The recombinant E. coli DH5alpha with the different recombinant plasmids of pnirBMisL-fedF1, pnirBMisL-fedF and pnirBMisL-fedF(M) were induced at anaerobic conditions. After induction, the binding doamin FedF1 of the FedF and adhesin FedF displayed on the surface of E. coli DH5alpha were tested for their agglutination and adhesion capability with the anti-rabbit sera against FedF subunit or the small intestinal epithelial cells from susceptible piglets. The results showed that the pnirBMisL-fedF1 or pnirBMisL-fedF recombinant bacteria could agglutinate with the anti-rabbit sera against FedF subunit and adhere to the small intestinal epithelial cells well. But the recombinant bacterial strain with the recombinant plasmid pnirBMisL-fedF(M) completely abolished the agglutination characteristic and receptor adhesiveness. These results confirmed that the binding doamin FedF1 of the F18ab fimbrial adhesin and the adhesin FedF of F18ab fimbriae could be transported and displayed functionally on the surface of E. coli DH5alpha by using type V secretion system and the His-88 and His-89 amino acid residues located in the FedF adhesin were important for the formation of the binding domain of the adhesin FedF of Fl8ab fimbriae.

Work-Related Musculoskeletal Disorders and Risk Factors among Chinese Medical Staff of Obstetrics and Gynecology.

Medical staff in the department of obstetrics and gynecology are a group of professionals reportedly at high risk of work-related musculoskeletal disorders (WMSD), however, little is known about the current status of this problem in China. The aim of this study was to investigate prevalence and risk factors of work-related musculoskeletal disorders among this population in China. A self-developed questionnaire was distributed to 1017 obstetrics and gynecology practitioners to collect information on musculoskeletal symptoms and relevant factors. Prevalence and severity of work-related musculoskeletal disorders in different parts of the body were calculated and the relationship between personal and ergonomic factors and work-related musculoskeletal disorders was analyzed using Chi-square test and unconditional logistic regression models. The results indicated a high prevalence of 85.5% among the subjects, with the shoulder (n = 575, 62.0%), neck (n = 560, 60.3%) and lower back (n = 504, 54.3%) being the three most affected regions. Individual, postural, work-environmental as well as psychosocial factors were recognized to be associated with WMSDs in different body parts. Therefore, attention must be given to the problem of musculoskeletal disorders among Chinese obstetrics and gynecology staff. It is recommended to develop good life habits, improve work environment, adjust work organization as well as train on proper postures in their daily operation.

Mass spectrometric monitoring of interfacial photoelectron transfer and imaging of active crystalline facets of semiconductors.

Monitoring of interfacial electron transfer (ET) in situ is important to understand the ET mechanism and designing efficient photocatalysts. We describe herein a mass spectrometric approach to investigate the ultrafast transfer of photoelectrons that are generated by ultraviolet irradiation on surfaces of semiconductor nanoparticles or crystalline facets. The mass spectrometric approach can not only untargetedly detect various intermediates but also monitor their reactivity through associative or dissociative photoelectron capture dissociation, as well as electron detachment dissociation of adsorbed molecules. Proton-coupled electron transfer and proton-uncoupled electron transfer with radical initiated polymerization or hydroxyl radical abstraction have been unambiguously demonstrated with the mass spectrometric approach. Active crystalline facets of titanium dioxide for photocatalytic degradation of juglone and organochlorine dichlorodiphenyltrichloroethane are visualized with mass spectrometry imaging based on ion scanning and spectral reconstruction. This work provides a new technique for studying photo-electric properties of various materials.

Titanium Dioxide Photocatalytic Polymerization of Acrylamide for Gel Electrophoresis (TIPPAGE) of Proteins and Structural Identification by Mass Spectrometry.

Polyacrylamide gel electrophoresis (PAGE) coupled with mass spectrometry has been well established for separating, identifying and quantifying protein mixtures from cell lines, tissues or other biological samples. The copolymerization process of acrylamide and bis-acrylamide is the key to mastering this powerful technique. In general, this is a vinyl addition reaction initiated by free radical-generating reagents such as ammonium persulfate (APS) and tetramethylethylenediamine (TEMED) under basic pH and degassing experimental condition. We report herein a photocatalytic polymerization approach that is based on photo-generated hydroxyl radicals with nanoparticles of titanium dioxide. It was shown that the polymerization process is greatly accelerated in acidic condition when ultraviolet light shots on the gel solution containing TiO2 nanoparticles without degassing. This feature makes it very useful in preparing Triton X-100 acid urea (TAU) gel that has been developed for separating basic proteins such as histones and variants in acidic experimental condition. Additionally, the presence of titanium dioxide in the gel not only improves mechanistic property of gels but also changes the migration pattern of different proteins that have different affinities to titanium dioxide.

Mercury arc lamp based super-resolution imaging with conventional fluorescence microscopes.

We present an implementation of localization based three-dimensional super-resolution imaging on a regular microscope. We retain the original arc lamp as the photoactivation light source, and incorporate an inexpensive diode laser for imaging. As alterations to the standard microscope is minimal, this optical setup can be easily adapted in a typical research laboratory and even undergraduate teaching experiments, providing an inexpensive system for students and research scientists who require such super resolution capabilities. With this simple design, a spatial resolution of better than 40 nm at a reasonable frame rate has been achieved, adequate for most routine applications.

Desulfonylation of tosyl amides through catalytic photoredox cleavage of N-S bond under visible-light irradiation.

All lit up: A novel and efficient desulfonylation method of tosyl amides has been developed by means of visible-light-promoted reductive cleavage of N-S bonds. This method has a broad substrate scope, good functional group tolerance, and excellent yields.