Diallyl disulfide from garlic oil inhibits Pseudomonas aeruginosa virulence factors by inactivating key quorum sensing genes

Applied Microbiology and Biotechnology - Garlic oil can disrupt the quorum sensing (QS) pathways of the opportunistic pathogen Pseudomonas aeruginosa; however, the underlying mechanisms for this...     

Involvement of cell proliferation in the process of follicular atresia in the guinea pig

Cell morphology and proliferation was investigated in the atretic follicles during estrous cycles in the guinea pig. Ovarian samples on days 1, 4, 8, 12 and 16 of the estrous cycle in the guinea pig were taken in the morning for histologic staining with hematoxylin and eosin (HE), and immunohistochemical staining of the protein proliferating cell nuclear antigen (PCNA). The results indicated that the granulosa cells degenerated and eliminated first in atretic follicles, while the fibroblast-like cells appeared in the innermost layer of theca interna cells. When the fibroblast-like cells migrated to the antrum, they proliferated and formed a new tissue in peripheral to the zona pellucida of the oocyte. Our results also revealed that the orientation of the theca interna cell arrangement changed twice during the process of atresia, and the loose connective tissue in the antrum was critical for follicular atresia. Therefore, follicular atresia was not a simple process of cell death and elimination, but coexisted with cell proliferation. To our knowledge, we have for the first time confirmed cell proliferation and the presence of new tissue in atretic follicles in guinea pigs.     

鳞木目小孢子叶球山西鳞孢穗（新种）的解剖特征

描述了山西太原西山煤田太原组７号煤层煤核中一种鳞木目的小孢子叶球——山西鳞孢穗（新种）（Ｌｅｐｉｄｏｓｔｒｏｂｕｓｓｈａｎｘｉｅｎｓｅ ｓｐ． ｎｏｖ．）。其主要特征是：孢子叶球较小,长３．５ ｃｍ 以上,直径１．６～１．８ ｃｍ 。轴具管状中柱,孢子叶螺旋状着生于轴上。孢子叶柄长６～７ ｍ ｍ ,远端叶片长１．２ ｃｍ 以上。孢子叶柄具翅,翅长２～２．５ ｍ ｍ 。小孢子囊可能呈袋形,长与孢子叶柄相近,宽约４．５ ｍ ｍ ,高２～３ ｍ ｍ ,以其长度的约２／３着生于孢子叶柄的腹面上。成熟的孢子囊壁仅由一层柱状细胞构成。小孢子直径６８～７７ μｍ ,具三缝,远极面具短刺     

RFLP诊断方法的改进

RFLP(限制性片段长度多态)技术应用于遗传病的诊断始于1981年。在十年时间里,这一基因诊断技术和分析方法不断得到发展和改进。随着越来越多的致病基因和连锁DNA多态片段的分离和克隆,该技术在分析缺陷基因性质,携带者检出和产前诊断等方面将发挥重要作用.然而,RFLP技术复杂,耗费时间和费用较大,使其向临床推广应用面临很大局限性。因此,基因诊断的方法简化和技术改进大有必要。1985年首创的多聚酶链     

Flower-specific expression of <Emphasis Type="Italic">Arabidopsis</Emphasis><Emphasis Type="Italic">PCS1</Emphasis> driven by <Emphasis Type="Italic">AGAMOUS</Emphasis> second intron in tobacco decreases the fertility of transgenic plants

The PROMOTION OF CELL SURVIVAL 1 (PCS1) gene, encoding an aspartic protease, has an important role in determining the fate of cells in embryonic development and reproduction processes in Arabidopsis. To explore the potential function of the PCS1 gene in generating reproductive sterility, we placed the PCS1 gene under the control of an 1,869-bp nucleotide sequence from the 3′ end of the second intron (AG-I) of Arabidopsis AGAMOUS and CaMV 35S (–60) minimal promoter [AG-I-35S (–60)::PCS1], and introduced it into tobacco. RT–PCR results demonstrated that the PCS1 gene driven by AG-I-35S (–60) chimeric promoter was expressed only in anthers and carpels in the reproductive tissues of transgenic tobacco. Compared to wild-type plants, all AG-I-35S (–60) and AG-I-35S (–60)::PCS1 transgenic lines showed a normal phenotype throughout the vegetative growth phase. However, during the reproductive stage, most AG-I-35S (–60)::PCS1 transgenic plant anthers displayed delayed dehiscence, failed dehiscence, petalody and hypoplasia, and the pollen grains had different shapes and sizes with a distorted, shrunken, or collapsed morphology. Moreover, three transgenic lines, PCS1-1, PCS1-3 and PCS1-4, showed higher sterility than wild-type and AG-I-35S (–60) transgenic plants, respectively. These results showed that the construct of AG-I-35S (–60)::PCS1 was partially effective at preventing seed set and provided a novel sterility strategy.     

Mitochondrial dysfunction in platelets and hippocampi of senescence-accelerated mice

Senescence-accelerated mice (SAM) strains are useful models to understand the mechanisms of age-dependent degeneration. In this study, measurements of the mitochondrial membrane potential (Δψ_m) of platelets and the Adenosine 5^′-triphosphate (ATP) content of hippocampi and platelets were made, and platelet mitochondria were observed in SAMP8 (faster aging mice) and SAMR1 (aging resistant control mice) at 2, 6 and 9 months of age. In addition, an Aβ-induced (Amyloid beta-protein) damage model of platelets was established. After the addition of Aβ, the Δψ_m of platelets of SAMP8 at 1and 6 months of age were measured. We found that platelet Δψ_m, and hippocampal and platelet ATP content of SAMP8 mice decreased at a relatively early age compared with SAMR1. The platelets of 6 month-old SAMP8 showed a tolerance to Aβ-induced damages. These results suggest that mitochondrial dysfunction might be one of the mechanisms leading to age-associated degeneration in SAMP mice at an early age and the platelets could serve as a biomarker for detection of mitochondrial function and age related disease.     

Nkd2, a negative regulator of Wnt pathway, delays mitotic exit in Hela cell

Frequent amplification and abundant expression of Nkd2 has been identified in malignant peripheral nerve sheath tumors (MPNSTs), dominant for genomic instability, who is involved in both Wnt pathway and EGFR signaling pathway. As a negative regulator of Wnt pathway, Nkd2 suppresses Wnt signaling by binding to Dvl1 and causing its ubiquitination followed by 26S proteasome degradation. On the other hand, it interacts with TGF-α for its transportation to basolateral plasma membrane in polarized epithelial cells. It is of interest to determine if Nkd2 over-expression contributes to tumorigenesis and genomic instablity. In this paper, we found that cells expressing NKD2 delayed mitotic exit stage after double thymidine block synchronization, but aneuploidy was not detected in these cells. This was further confirmed by Western blotting. In nocodazole-synchronised cells, Cyclin B1 degradation was delayed with Nkd2 over-expression compared to control group. Given many previous publications showed that Wnt pathway components are involved in mitotic progression. Further investigation on Nkd2’s function in mitosis might give more clues on MPNSTs pathological progression.     

TGF-beta signaling promotes survival and repair in rat alveolar epithelial type 2 cells during recovery after hyperoxic injury

Hyperoxic rats treated with inosine during oxygen exposure have increased levels of active transforming growth factor (TGF)-beta in the bronchoalveolar lavage (BAL), yet alveolar epithelial type 2 cells (AEC2) isolated from these animals demonstrate less hyperoxia-induced DNA damage and increased expression of active Smad2. To determine whether TGF-beta1 signaling per se protected AEC2 against hyperoxic damage, freshly isolated AEC2 from hyperoxic rats were incubated with TGF-beta1 for 24 h and assayed for DNA damage by fluorescein-activated cell sorter analysis of TdT-mediated dUTP nick end labeling. TGF-beta1 was protective over a concentration range similar to that in BAL of inosine-treated hyperoxic animals (50-5,000 pg/ml). TGF-beta1 also augmented hyperoxia-induced DNA repair activity and cell migration, stimulated autocrine secretion of fibronectin, accelerated closure of a monolayer scratch wound, and restored hyperoxia-depleted VEGF secretion by AEC2 to normoxic levels. The TGF-beta receptor type I activin-like kinase-4, -5, and -7 inhibitor peptide SB-505124 abolished the protective effect of TGF-beta on hyperoxic DNA damage and increased TdT-mediated dUTP nick end labeling in normoxic cells. These data suggest that endogenous TGF-beta-mediated Smad signaling is required for AEC2 homeostasis in vitro, while exogenous TGF-beta1 treatment of hyperoxia-damaged AEC2 results in a cell that is equipped to survive, repair, migrate, secrete matrix, and induce new blood vessel formation more efficiently than AEC2 primed by hyperoxia alone.     

Effects of caffeine on in vivo and in vitro oocyte maturation in mice

The objective was to investigate, using a mouse model, the effects of caffeine on the number of ovulated oocytes, the rate of oocyte maturation, the susceptibility of oocytes to activating stimuli, spindle morphology, and distribution of cortical granules (CGs). Mice were given caffeine (150 mg/kg body weight ip) at various times relative to hCG (-2, 0, and +2h); in an in vitro study, 1, 5 or 10 mM caffeine was added to the maturation culture. Caffeine had no effect on the quality of oocytes in vivo maturation, but caffeine was detrimental to the quality of oocytes matured in vitro. Further studies are needed to determine caffeine concentration in follicles relative to that in culture medium.