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To investigate correlation between abnormal replicative senescence of endometrial gland epithelial cells (EGECs) in shedding and non-shedding endometria and endometriosis cyst during menstruation. Musashi-1 expression, β-catenin expression, and EGECs ultrastructure in shedding and non-shedding endometrium when menstruation were observed through real-time PCR and transmission electron microscopy technologies. (1) Musashi-1 and β-catenin exhibited a high expression in shedding and non-shedding endometria in experimental group, showing a positive correlation between each other; and were significantly higher than that in control group. However; there was no correlation between these two in control group. (2) Transmission electron microscopy results: In experimental group, organelles in EGECs in shedding endometrium obtained were abundant on the first day of menstruation, nuclei were irregular, double nucleoli could be observed, and chromatin was rich. Furthermore, morphology of EGECs in non-shedding endometrium was irregular, organelles were abundant, basement membrane was irregular with abnormal curvature, and a large amount of collagenic fibers were found in intercellular spaces. On the fifth day of menstruation, the cilia and microvilli on secretory cells in endometrium increased and prolongated, and organelles became extremely rich. EGECs have potentials of division, proliferation, invasion and migration; and is associated with formation of endometriosis cysts.摘要 本研究目的是探究月经期间脱落和未脱落子宫内膜腺上皮细胞（endometrial gland epithelial cells, EGECs）的异常复制衰老与子宫内膜异位囊肿的相关性。通过实时PCR和透射电子显微镜技术观察月经期间脱落和未脱落子宫内膜中Musashi-1和β-catenin的表达以及EGECs的超微结构。（1）Musashi-1和β-catenin在实验组脱落和未脱落子宫内膜中存在高表达, 两者呈正相关, 并且显著高于对照组。然而, 在对照组中这两者之间无相关性。（2）透射电镜结果：实验组在月经第一天获得的脱落子宫内膜中EGECs所含的细胞器丰富, 细胞核不规则, 可见双核仁, 染色质丰富。此外, 在未脱落的子宫内膜中EGECs形态不规则, 细胞器丰富, 基底膜不规则, 曲率异常, 细胞间隙存在大量胶原纤维。在月经第5天, 子宫内膜分泌细胞上的纤毛和微绒毛增多并延长, 细胞器变得极为丰富。EGECs具有分裂、增殖、侵袭和迁移的潜力, 并且与子宫内膜异位囊肿的形成有关。.

Diatom examinations have been widely used to perform drowning diagnosis in forensic practice. However, current methods for recognizing diatoms, which use light or electron microscopy, are time-consuming and laborious and often result in false positive or negative decisions. In this study, we demonstrated an artificial intelligence (AI)-based system to automatically identify diatoms in conjunction with a classical chemical digestion approach. By employing transfer learning and data augmentation methods, we trained convolutional neural network (CNN) models on thousands or tens of thousands of tiles from digital whole-slide images of diatom smears. The results showed that the trained model identified the regions containing diatoms in the tiles. In an independent test, where the slide samples were collected in forensic casework, the best CNN model demonstrated a performance competitive with those of 5 forensic pathologists with experience in diatom quantification. This pilot study paves the way for future intelligent diatom examinations; many efficient diatom extraction methods could be incorporated into our automated system.

Bacterial surface layers (S-layers) are cell envelope structures ubiquitously found in gram-negative and gram-positive bacteria, including Lactobacillus. S-layers play a role in the determination and maintenance of cell shape as virulence factors, mediate cell adhesion, and regulate immature dendritic and T cells. In this study, we sought to understand the involvement of MAPK serine/threonine kinases in alterations in Endometrial epithelial cells (ESC) growth induced by Lactobacillus crispatus (L. crispatus) slpA, an S-layer protein. We applied various concentrations of L. crispatus to cultured ESCs and observed growth and changes in the phosphorylation status of ERK1/2, JNK, and p38. Similar experiments were conducted using L. crispatus lacking and overexpressing slpA. We found that ESC growth was altered by slpA primarily via ERK1/2. Our findings suggest that L. crispatus slpA promotes ESC growth mainly through an ERK1/2-dependent pathway.

Bimetallic nanoparticles are generally believed to have improved catalytic activity and stability due to geometric and electronic changes. In this work, biogenic-Pd (bio-Pd), biogenic-Pt (bio-Pt), and biogenic-PdPt (bio-PdPt) nanoparticles were synthesized by Shewanella oneidensis MR-1 in the absence or presence of quinone. Compared with direct microbial reduction process, the addition of anthraquinone-2,6-disulfonate (AQDS) could promote the reduction efficiency of Pd(II) or/and Pt(IV) and result in decrease of particles size. All kinds of nanoparticles could catalyze 4-nitrophenol reduction by NaBH4 and their catalytic activities took the following order: bio-PdPt (AQDS) ∼ bio-PdPt > bio-Pd (AQDS) > bio-Pd > bio-Pt (AQDS) ∼ bio-Pt. Moreover, the bio-PdPt (AQDS) nanoparticles could be reused for 6 cycles. We believe that this simple and efficient biosynthesis approach for synthesizing bimetallic bio-PdPt nanocatalysts is important for preparing active and stable catalysts.

G-protein coupled receptor 40 (GPR40) is a membrane-bound G-protein-coupled receptor with high binding affinity to medium- and long-chain free fatty acids (FFAs). Acute activation of GPR40 on pancreatic β-cells causes insulin secretion, whereas prolonged activation may contribute to a deterioration of the effect of saturated FFAs on β-cells. It has been documented that different types of FFAs produce various effects on insulin secretion; however, little information is available regarding the expression of GPR40 and its function after long-term exposure of β-cells to unsaturated FFAs. In the present study, GPR40 expression and function were assessed in INS-1 β-cells after 48 h exposure to different types of unsaturated FFAs. The mRNA and protein expression of GPR40 was increased significantly by long-term exposure of cells to polyunsaturated α-linolenic acid, but not to either oleic acid or linoleic acid. Immunocytochemistry revealed a reduction in the number of insulin-containing granules in cells treated with α-linolenic acid, which was correlated with an increase in cellular expression of GPR40. Basal and glucose-stimulated insulin secretion were markedly suppressed by 48 h treatment of cells with saturated palmitic acid, but not unsaturated α-linolenic acid. By testing various FFAs, it was found that FFA-induced suppression of basal and glucose-stimulated insulin secretion was attenuated by an increase in the degree of unsaturation of the FFAs and GPR40 expression in response to FFA treatment in INS-1 cells. The results of the present study indicate that long-term in vitro treatment of INS-1 rat pancreatic β-cells by unsaturated FFAs protects the cells against from gluco- and lipotoxicities and that this coincides with an increase in GPR40 expression.

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible immediate-early response protein 14 (Fn14) have been detected in several human tumors, and demonstrated to regulate multiple cellular responses, including proliferation, survival, migration, apoptosis and differentiation, suggesting roles in cancer. The objective of this study was to clarify the role of TWEAK/Fn14 in the development of human endometrial cancer. We found that TWEAK gene expression was down-regulated and Fn14 gene expression was up-regulated in human endometrial cancer specimens compared with that in normal endometrial specimens; TWEAK acting on Fn14 decreased cell viability by inducing apoptosis through caspase pathways in endometrial cancer cells. Our results suggest that Fn14 expression is high in endometrial cancers whereas local produced TWEAK may be low. TWEAK/Fn14 pathway activation may promote cancer cell apoptosis, which provides a new therapeutic target for human endometrial cancer treatment.

Magnetically recoverable noble metal nanoparticles are promising catalysts for chemical reactions. However, the chemical synthesis of these nanocatalysts generally causes environmental concern due to usage of toxic chemicals under extreme conditions. Here, Pd/Fe3O4, Au/Fe3O4 and PdAu/Fe3O4 nanocomposites are biosynthesized under ambient and physiological conditions by Shewanella oneidensis MR-1. Microbial cells firstly transform akaganeite into magnetite, which then serves as support for the further synthesis of Pd, Au and PdAu nanoparticles from respective precursor salts. Surface-bound cellular components and exopolysaccharides not only function as shape-directing agent to convert some Fe3O4 nanoparticles to nanorods, but also participate in the formation of PdAu alloy nanoparticles on magnetite. All these three kinds of magnetic nanocomposites can catalyze the reduction of 4-nitrophenol and some other nitroaromatic compounds by NaBH4. PdAu/Fe3O4 demonstrates higher catalytic activity than Pd/Fe3O4 and Au/Fe3O4. Moreover, the magnetic nanocomposites can be easily recovered through magnetic decantation after catalysis reaction. PdAu/Fe3O4 can be reused in at least eight successive cycles of 4-nitrophenol reduction. The biosynthesis approach presented here does not require harmful agents or rigorous conditions and thus provides facile and environmentally benign choice for the preparation of magnetic noble metal nanocatalysts.

Geobacter sulfurreducens was studied for the reduction of Pd(II) and production of Pd(0) nanoparticles capable of reducing Cr(VI). Transmission electronic microscopy, energy dispersive X-ray and X-ray diffraction analyses revealed that the nanoscale Pd(0) particles formed were associated with the cell surface and located inside the periplasm. The increase of cell dry weight (CDW):Pd ratio and addition of anthraquinone-2,6-disulfonate (AQDS) not only stimulated Pd(II) reduction, but also resulted in increase of nanoparticle number, decrease of particle diameter and improvement of Cr(VI) reduction efficiency. The relationship between reduction rate and initial Cr(VI) concentration (150-750 μM) followed Michaelis-Menten kinetics (Vmax=3.6 μmol h(-1) mg bio-Pd(-1) and Km=891.3 μM). These findings indicated the potential of using G. sulfurreducens cells for reclamation of palladium, formation of Pd(0) nanoparticles and efficient treatment of Cr(VI) pollution.

Obesity with excessive levels of circulating free fatty acids (FFAs) is tightly linked to the incidence of type 2 diabetes. Insulin resistance of peripheral tissues and pancreatic β-cell dysfunction are two major pathological changes in diabetes and both are facilitated by excessive levels of FFAs and/or glucose. To gain insight into the mitochondrial-mediated mechanisms by which long-term exposure of INS-1 cells to excess FFAs causes β-cell dysfunction, the effects of the unsaturated FFA linoleic acid (C 18:2, n-6) on rat insulinoma INS-1 β cells was investigated. INS-1 cells were incubated with 0, 50, 250 or 500 μM linoleic acid/0.5% (w/v) BSA for 48 h under culture conditions of normal (11.1 mM) or high (25 mM) glucose in serum-free RPMI-1640 medium. Cell viability, apoptosis, glucose-stimulated insulin secretion, Bcl-2, and Bax gene expression levels, mitochondrial membrane potential and cytochrome c release were examined. Linoleic acid 500 μM significantly suppressed cell viability and induced apoptosis when administered in 11.1 and 25 mM glucose culture medium. Compared with control, linoleic acid 500 μM significantly increased Bax expression in 25 mM glucose culture medium but not in 11.1 mM glucose culture medium. Linoleic acid also dose-dependently reduced mitochondrial membrane potential (ΔΨm) and significantly promoted cytochrome c release from mitochondria in both 11.1 mM glucose and 25 mM glucose culture medium, further reducing glucose-stimulated insulin secretion, which is dependent on normal mitochondrial function. With the increase in glucose levels in culture medium, INS-1 β-cell insulin secretion function was deteriorated further. The results of this study indicate that chronic exposure to linoleic acid-induced β-cell dysfunction and apoptosis, which involved a mitochondrial-mediated signal pathway, and increased glucose levels enhanced linoleic acid-induced β-cell dysfunction.

Reduction of pancreatic β-cell mass is a key element leading to type 2 diabetes. Obesity and overweight with high levels of lipids including cholesterol are tightly linked to type 2 diabetes. The direct impact of cholesterol on pancreatic β-cells, however, has not been extensively studied. In this study, MIN6 mouse β-cell line was used to test the effect of cholesterol on pancreatic β-cell apoptosis over different doses and durations. It was found that cholesterol dose- and time-dependently induced cell death of MIN6 cells above 160 μM after 6 h treatment in vitro. Annexin-V staining revealed that cholesterol treatment significantly induced apoptosis in MIN6 cells. Cholesterol treatment resulted in the loss of the ability to retain Rhodamine 123, indicating mitochondrial damage in MIN6 cells. Cholesterol-induced cell apoptosis and mitochondrial damage were blocked by low-temperature condition. In addition, glutathione also protected MIN6 cells from cholesterol-induced cell death. It is concluded that high level of cholesterol induces cell apoptosis in MIN6 cells, which is in part due to mitochondrial dysfunction. We suggest that excessive uptake of cholesterol in β-cells may contribute to β-cell apoptosis and dysfunction and the deterioration of type 2 diabetes.