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SUMMARY Aims: To investigate the mechanism behind cytotoxic edema formation following subarachnoid hemorrhage (SAH). Methods: We explored the role of aquaporin-4 (AQP4), inwardly rectifying K+ 4.1 (Kir4.1) channels and their upstream orchestrators p53 and p38MAPK in this process. A p53 inhibitor, pifithrin-α (PFT-α) was administered intraperitoneally to rats undergoing SAH by endovascular perforation. Totally, 98 male SD rats were categorized into sham, SAH, SAH+ dimethyl sulfoxide (DMSO), SAH+ 0.2 or 2.0 mg/kg PFT-α groups. At 24 h after SAH, MRI (diffusion-weighted imaging [DWI]), immunohistochemistry, and Western blot were used. Results: MRI (DWI) showed a significant cytotoxic edema in the brain following SAH with PFT-α therapy reducing it. Immunohistochemistry and Western blot showed an increased level of p53, phosphorylated-p38MAPK and AQP4 and a reduced level of Kir4.1; all of which could be reversed following PFT-α treatment. Treble labeling staining revealed colocalization of p53 with phosphorylated-p38MAPK and unmatched expression of AQP4 and Kir4.1 within astrocyte cells. Conclusion: These results indicated p53 mediates the formation of cytotoxic edema in the brain following SAH; an uncoupling expression of AQP4 and Kir4.1 on astrocytic end feets orchestrated by p38MAPK was partly responsible. [ABSTRACT FROM AUTHOR]

With the development of assisted reproductive technology and genetic analysis technology, the preimplantation genetic screening (PGS) is used to detect the numerical chromosomal abnormalities (aneuploid) in embryos, so as to improve pregnancy outcomes of in vitro fertilization -embryo transfer (IVF -ET). New methods and technologies have been used in PGS, such as blastocyst stage biopsy, comparative genomic hybridization, microarrays and next generation sequencing, which increase the diagnose accuracy and decrease the risk of misdiagnosis. At the same time, PGS is also facing many challenges. The clinical application of PGS was reviewed in this article. [ABSTRACT FROM AUTHOR]

Aims Programmed Cell Death 5 ( PDCD5) is a protein that accelerates apoptosis in different types of cells in response to various stimuli and is down-regulated in many cancer tissues. We hypothesized in this study that down-regulating PDCD5 can protect the brain from ischemic damage by inhibiting PDCD5-induced apoptotic pathway. Methods One hundred and sixty male Sprague-Dawley rats were randomly assigned to five groups: Sham surgery (n = 25), MCAO (n = 45), MCAO+rh PDCD5 (Rh PDCD5) (n = 30), MCAO+control si RNA (n = 30), and MCAO+ PDCD5 si RNA (n = 30). At 24 h following MCAO, immunohistochemistry and Western blot were performed. Results PDCD5 si RNA reduced the infarct volume, improved neurological deficits, improved cerebral blood flow ( CBF), and reduced Evans blue extravasation. Meanwhile, over-expression of PDCD5 protein with recombinant human PDCD5 (rh PDCD5) had an opposite effect. Immunohistochemistry and Western blot demonstrated PDCD5 si RNA decreased the expressions of key proapoptotic proteins such as p53, Bax/Bcl-2, and cleaved caspase-3 in the penumbra areas, whereas rh PDCD5 increased cell apoptosis. Double fluorescence labeling showed the positive immunoreactive materials of PDCD5 were partly colocalized with MAP2, GFAP, CD34, p53, and caspase-3 in the penumbra areas in brain. Conclusions PDCD5-induced apoptosis and over-expression of PDCD5 are harmful to the ischemic neurons in vivo. Meanwhile, the inhibition of PDCD5 may be protective via reducing the apoptotic-related protein such as p53, Bax, and caspase-3. This observation may have potential for the treatment of ischemic cerebral stroke. [ABSTRACT FROM AUTHOR]

• Swollen-induced in-situ encapsulation of catalysts in cross-linked polysiloxane elastomers polymer. • Silicone rubber-based microchannel reactor was employed for asymmetric transforms. • Cross-linked polysiloxane elastomers was proved to be easily recycled by filtration or pick-up,reused by several times and exhibits excellent enantioselectivities 94–96% ees The immobilization of molecular catalysts to fabricate heterogeneous catalysts for catalytic asymmetric transformations is extremely important and has attracted great attentions. Herein we developed a simple and new strategy for the heterogenization of homogeneous molecular complexes into the cross-linked polymer. It is demonstrated for the first time that the cross-linked polysiloxane elastomers can be applied for the swollen-induced in-situ encapsulation of homogeneous catalysts with or without chiral ligands. The swollen-induced in-situ encapsulation of silver catalyst system in the cross-linked polysiloxane elastomers led to the formation of silicone rubber-based hierarchically porous that could be used in asymmetric [3+2] cycloaddition, asymmetric tandem conjugate addition−elimination reaction and oxidation of hydrosilanes to silanols. The swollen-induced in-situ encapsulation of chiral silver complex in the cross-linked polysiloxane elastomers was proved to be easily recycled by filtration or pick-up and reused by several times. The simplest heterogeneous catalysis by the strategy of swollen-induced in-situ encapsulation can be extended to the encapsulation of chiral metal catalysts into different polymeric materials for the heterogenization of homogeneous catalysis. [Display omitted] [ABSTRACT FROM AUTHOR]

Organosilicon compounds are important reagents and synthetic intermediates that play a key role in the construction of new materials and complex products. Here we show a highly diastereoselective rhodium‐catalyzed cycloisomerization of 1,6‐dienes, in which the use of (EtO)3SiH accelerates the intramolecular cyclization reaction to afford a novel spiro‐fused succinimide and pyrazolone derivatives in moderate to excellent yields as a single diastereoisomer. The proposed mechanism involves an active Rh−H species from the hydrosilane that is the H‐donor in this spiro‐type cycloisomerization reaction. [ABSTRACT FROM AUTHOR]

Aims Inflammation and apoptosis play important roles in increasing vascular permeability following subarachnoid hemorrhage (SAH). The objective of this study was to evaluate whether urinary trypsin inhibitor (UTI), a serine protease inhibitor, attenuates vascular permeability by its antiinflammatory and antiapoptotic effects after experimental SAH. Methods Subarachnoid hemorrhage models were established in adult male Sprague-Dawley rats by endovascular perforation. UTI was administered by intraperitoneal injection immediately following SAH. Brain edema was assessed by magnetic resonance imaging (MRI) at 24 h after SAH. Neurological deficits, brain water content, vascular permeability, malondialdehyde (MDA) concentration, and myeloperoxidase (MPO) activity were evaluated. Immunohistochemical staining and Western blot were used to explore the underlying protective mechanism of UTI. Results Urinary trypsin inhibitor 50,000 U/kg significantly attenuated brain edema and neurological deficits and reduced vascular permeability at 24 h after SAH. MDA concentration and MPO activity in hippocampus were significantly decreased with UTI treatment. Furthermore, the levels of phosphorylated JNK, NF-κB (p65), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and proapoptotic protein p53, caspase-3 were elevated in the microvascular endothelial cells of the hippocampus after SAH, which were alleviated with UTI treatment. Conclusion Urinary trypsin inhibitor reduced vascular permeability after SAH through its antiinflammatory and antiapptotic effects via blocking the activity of JNK, NF-κB, and p53. [ABSTRACT FROM AUTHOR]

Objective: To clarify the relationship between oocyte maturation and mitochondria distribution and assess the effects of in vitro maturation (IVM) on the distribution of mitochondria in human oocytes. Design: Prospective randomized trial. Setting: Hospital-based IVF center. Patient(s): One hundred fifty-eight patients undergoing intracytoplasmic sperm injection (ICSI) treatment for male factors or combined with oviduct infertility and fifteen patients undergoing controlled ovarian hyperstimulation followed by coitus or IUI. Intervention(s): Of all the 284 immature oocytes, 140 were fixed directly. The others were prepared for IVM before they were fixed. All the 21 oocytes matured in vivo were fixed directly and stained for mitochondria. Both immature and mature oocytes were stained by Mito Tracker Green FM. The distribution of mitochondria was observed using a confocal laser scanning microscope. Main Outcome Measure(s): Mitochondrial distribution. Result(s): Three mitochondria distribution patterns were identified: peripheral, semiperipheral, and evenly diffused. A peripheral distribution of mitochondria was presented by 64.1% (50/78) of the germinal vesicle (GV) oocytes; 45.2% (28/62) of the meiosis I oocytes maintained the peripheral distribution; and 38.7% (24/62) presented a diffused status. After IVM, 75.5% (80/106) of the oocytes displayed an evenly diffused type of distribution. The mitochondria were more abundant in the inner cytoplasm than in the peripheral region in most of the oocytes matured in vivo. Conclusion(s): There are obvious changes in the distribution of mitochondria in human oocytes before and after maturation. Distribution of mitochondria in oocytes matured in vitro is slightly different from that of oocytes matured in vivo. The results may partially explain the reduced developmental potential of oocytes matured in vitro compared with those matured in vivo. [Copyright &y& Elsevier]