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Anemia is a hematological disorder that adversely affects the health of millions of people worldwide. Although many variables influence the development and exacerbation of anemia, one major contributing factor is the impairment of erythropoiesis. Normal erythropoiesis is highly regulated by the zinc finger transcription factor GATA-1. Disruption of the zinc finger motifs in GATA-1, such as produced by germline mutations, compromises the function of this critical transcription factor and causes dyserythropoietic anemia. Herein, we utilize a combination of in vitro and in vivo studies to provide evidence that arsenic, a widespread environmental toxicant, inhibits erythropoiesis likely through replacing zinc within the zinc fingers of the critical transcription factor GATA-1. We found that arsenic interacts with the N- and C-terminal zinc finger motifs of GATA-1, causing zinc loss and inhibition of DNA and protein binding activities, leading to dyserythropoiesis and an imbalance of hematopoietic differentiation. For the first time, we show that exposures to a prevalent environmental contaminant compromises the function of a key regulatory factor in erythropoiesis, producing effects functionally similar to inherited GATA-1 mutations. These findings highlight a novel molecular mechanism by which arsenic exposure may cause anemia and provide critical insights into potential prevention and intervention for arsenic-related anemias.

Midazolam is widely used as a sedative and anesthetic induction agent by modulating the different GABA receptors in the central nervous system. Studies have also shown that midazolam has an anticancer effect on various tumors. In a previous study, we found that midazolam could induce MA-10 mouse Leydig tumor cell apoptosis by activating caspase cascade. However, the detailed mechanism related to the upstream and downstream pathways of the caspase cascade, such as endoplasmic reticulum (ER) stress, autophagy, and p53 pathways plus cell cycle regulation in MA-10 mouse Leydig tumor cells, remains elusive. Flow cytometry assay and Western blot analyses were exploited. Midazolam significantly decreased cell viability but increased sub-G1 phase cell numbers in MA-10 cells (P<0.05). Annexin V/propidium iodide double staining further confirmed that midazolam induced apoptosis. In addition, expressions of Fas and Fas ligand could be detected in MA-10 cells with midazolam treatments, and Bax translocation and cytochrome c release were also involved in midazolam-induced MA-10 cell apoptosis. Moreover, the staining and expression of LC3-II proteins could be observed with midazolam treatment, implying midazolam could induce autophagy to control MA-10 cell apoptosis. Furthermore, the expressions of p-EIF2α, ATF4, ATF3, and CHOP could be induced by midazolam, indicating that midazolam could stimulate apoptosis through ER stress in MA-10 cells. Additionally, the expressions of cyclin A, cyclin B, and CDK1 could be inhibited by midazolam, and the phosphorylation of p53, P27, and P21 could be adjusted by midazolam, suggesting that midazolam could manage cell cycle through the regulation of p53 pathway to induce apoptosis in MA-10 cells. Midazolam could induce cell apoptosis through the activation of ER stress and the regulation of cell cycle through p53 pathway with the involvement of autophagy in MA-10 mouse Leydig tumor cells.

Midazolam (MDZ) has powerful hypnosis, amnesia, anti-anxiety and anticonvulsant effects. Studies have shown that prenatally developmental toxicity of diazepam can be observed in many organs/tissues. However, it remains elusive in male reproductive system. TM3 mouse Leydig progenitor cell line was used to determine whether MDZ has any unfavorable effects. Midazolam significantly decreased cell viability in dose- and time-dependent manners in TM3 cells. In flow cytometry analysis, midazolam significantly increased subG1 phase cell numbers, and annexin V/PI double staining assay further confirmed that MDZ induced apoptosis in TM3 cells. Moreover, MDZ significantly induced the expression of caspase-8 and -3 proteins and the phosphorylation of JNK, ERK1/2 and p38. Besides, MDZ didn't activate Akt pathway in TM3 cells. Furthermore, the expressions of p-EIF2α, ATF4, ATF3 and CHOP were induced by midazolam, suggesting that midazolam could induce apoptosis through endoplasmic reticulum (ER) stress in TM3 cells. Additionally, the expressions of cyclin A, cyclin B and CDK1 were inhibited by midazolam through the regulation of p53 in TM3 cells, indicating that midazolam could regulate cell cycle to induce apoptosis. Midazolam could activate caspase, MAPKs and ER stress pathways and impede Akt pathway and cell cycle to induce apoptosis in TM3 mouse Leydig progenitor cells.

Propofol is an anesthetic agent moderating GABA receptors in the nervous system. A number of studies have demonstrated that propofol exerts a negative effect on neural stem cell development in the neonatal mouse hippocampus. However, to the best of our knowledge, there is no study available to date illustrating whether neonatal exposure to propofol affects Leydig stem/progenitor cell development for normal male reproductive development and functions, and the regulatory mechanism remains elusive. In the present study, TM3 cells, a mouse Leydig stem/progenitor cell line, was treated with propofol. The data illustrated that propofol significantly reduced TM3 cell viability. TM3 subG1 phase cell numbers were significantly increased by propofol assayed by flow cytometric analysis. Annexin V/PI double staining assay of the TM3 Leydig cells also demonstrated that propofol increased TM3 cell apoptosis. In addition, cleaved caspase-8, -9 and -3 and/or poly(ADP-ribose) polymerase (PARP) were significantly activated by propofol in the TM3 cells. Furthermore, the expression levels of phospho-JNK, phospho-ERK1/2 and phospho-p38 were activated by propofol in the TM3 cells, indicating that propofol induced apoptosis through the mitogen-activated protein kinase (MAPK) pathway. Additionally, propofol diminished the phosphorylation of Akt to increase the apoptosis of TM3 cells. On the whole, the findings of the present study demonstrate that propofol induces TM3 cell apoptosis by activating caspases and MAPK pathways, as well as by inhibiting the Akt pathway in TM3 cells. These findings illustrate that propofol affects the viability of Leydig stem/progenitor cells possibly related to the development of the male reproductive system.

In the western world, there is an increasing trend of occurrence in testicular cancer. Treatment of malignant testicular cancer is primarily combined surgery with various chemical drugs. Propofol has been frequently used as an anesthetic and sedative induction agent, which could modulate different γ-aminobutyric acid receptors in the central nervous system. Studies demonstrated that propofol activates endoplasmic reticulum stress to induce apoptosis in lung cancer. However, it remains elusive whether propofol regulates caspase and/or mitogen-activated protein kinase (MAPK) pathways to induce apoptosis in Leydig tumor cells. In the present study, MA-10 mouse Leydig tumor cells were treated with propofol, and possible signal pathways associated with apoptosis were investigated. Results demonstrated that increasing dosage of propofol (300-600 µM) for 24 h significantly decreased cell viability in MA-10 cells (P<0.05). In flow cytometry analysis, the amount of sub-G1 phase cell numbers in MA-10 cells was significantly increased by propofol (P<0.05). Additionally, Annexin V/propidium iodide double staining further confirmed that propofol could induce MA-10 cell apoptosis. Furthermore, cleaved caspase-8, −9 and −3, and/or poly(ADP-ribose) polymerase were significantly activated following treatment of propofol in MA-10 cells. In addition, c-Jun N-terminal kinase, extracellular signal-regulated kinase 1/2, and p38 were significantly activated by propofol in MA-10 cells (P<0.05), indicating that propofol may induce apoptosis through the MAPK pathway. Additionally, propofol diminished the phosphorylation of Akt to activate apoptosis in MA-10 cells. In conclusion, propofol may induce MA-10 cell apoptosis by activating caspase and MAPK pathways, and inhibiting the Akt pathway in MA-10 cells, demonstrating that propofol may be a potential anticancer agent against Leydig cell cancer.

Organophilic montmorillonite was prepared using ion‐exchange method between sodium ions in clay layers and four kind of quaternary ammonium salt. The montmorillonite has the largest d001‐spacing, as determined by X‐ray diffraction in modified by di(hydrogenated tallowalkyl) dimethyl ammonium chloride. Polystyrene montmorillonite nanocomposites were obtained by suspension and emulsion polymerization of styrene in the dispersed organophilic montmorillonite. The d001‐spacing of clay was determined by X‐ray diffraction (XRD). The thermal stability of organophilic montmorillonite was investigated by thermogravimetric analysis (TGA). POLYM. COMPOS., 2008. © 2008 Society of Plastics Engineers

Fe3O4/MWCNTs nanocomposites were prepared by chemical oxidation coprecipitation method and developed as highly efficient heterogeneous Fenton-like catalyst. XRD results revealed that Fe3O4 nanoparticles deposited onto MWCNTs surface remained the inverse spinel crystal structure of cubic Fe3O4 phase. The FTIR characteristic peaks of MWCNTs weakened or disappeared due to the anchor of Fe3O4 nanoparticles and Fe–O peak at 570 cm–1 was indicative of the formation of Fe3O4. TEM observation revealed that Fe3O4 nanoparticles were tightly anchored by MWCNTs. The Fenton-like catalytic activity of Fe3O4/MWCNTs nanocomposites for the discoloration of methyl orange (MO) was much higher than that of Fe3O4 nanoparticles. The process optimization of this heterogeneous Fenton-like system was implemented by response surface methodology (RSM). The optimum conditions for MO discoloration were determined to be of 12.3 mmol/L H2O2 concentration, 2.9 g/L catalyst dosage, solution pH 2.7 and 39.3 min reaction time, with the maximum predicted value for MO discoloration ratio of 101.85%. The corresponding experimental value under the identical conditions was obtained as 99.86%, which was very close to the predicted one with the absolute deviation of 1.99%.

Background：Ossification of the ligamentum flavum （OLF） is being increasingly recognized as a cause of thoracic myelopathy.This study was to describe a rare clinical entity of spinal cord kinking （SK） in thoracic myelopathy secondary to OLF.Methods：The data of 95 patients with thoracic myelopathy secondary to OLF were analyzed retrospectively.The incidence and location of SK were determined using preoperative magnetic resonance imaging （MRI）.The clinical presentation and radiological characteristics in patients with SK were analyzed.Posterior en bloc laminectomy with OLF was performed,and the surgical results were evaluated.Results：SK was found in seven patients （7.4％） based on preoperative MRI.The patients included one male and six females with an average age of 55.6 years （range,48-64 years）.Five patients presented with radiculomyelopathy and two presented with typical thoracic myelopathy of spastic paraparesis.In all cases,the kinking was located just above the end of the spinal cord where the conus medullaris （CM） was compressed by the OLF.The degree of SK varied from mild to severe.The tip of the CM was located between the upper third of T1 1 to the lower third of L 1,above the lower edge of L 1.With an average follow-up of 30.4 months,the modified Japanese Orthopedic Association score significantly improved from 5.7 ± 1.8 preoperatively to 8.9 ± 1.4 postoperatively （t =12.05;P ＜ 0.0001） with an improvement rate of 63.1 ± 12.3％.Conclusions：SK is a rare radiological phenomenon.It is typically located at the thoracolumbar junction,where the CM is compressed by the OLF.Our findings indicate that these patients may benefit from a posterior decompressive procedure.

本文介绍一例87岁男性患者,右腋下肿物4年,通过电子计算机断层扫描（CT）、磁共振成像（MRI）、正电子发射计算机断层显像（PET-CT）和肿物穿刺活检免疫组化确诊为副乳腺癌。进行肿物手术切除,术后内分泌辅助治疗。男性副乳腺癌的案例少见,只有零星的文献报道。在1975~2015年中国医院知识库和Pub Med文献数据库记录中,本文的患者是年龄最大的男性副乳腺患者。

With the climate constantly changing, plants suffer more frequently from various abiotic and biotic stresses. However, they have evolved biosynthetic machinery to survive in stressful environmental conditions. Flavonoids are involved in a variety of biological activities in plants, which can protect plants from different biotic (plant-parasitic nematodes, fungi and bacteria) and abiotic stresses (salt stress, drought stress, UV, higher and lower temperatures). Flavonoids contain several subgroups, including anthocyanidins, flavonols, flavones, flavanols, flavanones, chalcones, dihydrochalcones and dihydroflavonols, which are widely distributed in various plants. As the pathway of flavonoid biosynthesis has been well studied, many researchers have applied transgenic technologies in order to explore the molecular mechanism of genes associated with flavonoid biosynthesis; as such, many transgenic plants have shown a higher stress tolerance through the regulation of flavonoid content. In the present review, the classification, molecular structure and biological biosynthesis of flavonoids were summarized, and the roles of flavonoids under various forms of biotic and abiotic stress in plants were also included. In addition, the effect of applying genes associated with flavonoid biosynthesis on the enhancement of plant tolerance under various biotic and abiotic stresses was also discussed.