Generation of Glycosyl Radicals from Glycosyl Sulfoxides and Its Use in the Synthesis of C-linked Glycoconjugates.

We here report glycosyl sulfoxides appended with an aryl iodide moiety as readily available, air and moisture stable precursors to glycosyl radicals. These glycosyl sulfoxides could be converted to glycosyl radicals by way of a rapid and efficient intramolecular radical substitution event. The use of this type of precursors enabled the synthesis of various complex C-linked glycoconjugates under mild conditions. This reaction could be performed in aqueous media and is amenable to the synthesis of glycopeptidomimetics and carbohydrate-DNA conjugates.

Bioinspired Transition-Metal Complexes as Electrocatalysts for the Oxygen Reduction Reaction.

The oxygen reduction reaction (ORR) is one of the most important reactions in life processes and energy conversion systems. To alleviate global warming and the energy crisis, the development of high-performance electrocatalysts for the ORR for application in energy conversion and storage devices such as metal-air batteries and fuel cells is highly desirable. Inspired by the biological oxygen activation/reduction process associated with heme- and multicopper-containing metalloenzymes, iron and copper-based transition-metal complexes have been extensively explored as ORR electrocatalysts. Herein, an outline into recent progress on non-precious-metal electrocatalysts for the ORR is provided; these electrocatalysts do not require pyrolysis treatment, which is regarded as desirable from the viewpoint of bioinspired molecular catalyst design, focusing on iron/cobalt macrocycles (porphyrins, phthalocyanines, and corroles) and copper complexes in which the ORR activity is tuned by ligand variation/substitution, the method of catalyst immobilization, and the underlying supporting materials. Current challenges and exciting imminent developments in bioinspired ORR electrocatalysts are summarized and proposed.

Titanium Dioxide-Grafted Copper Complexes: High-Performance Electrocatalysts for the Oxygen Reduction Reaction in Alkaline Media.

The sluggish kinetics of the oxygen reduction reaction (ORR) at the cathodes of fuel cells significantly hampers fuel cell performance. Therefore, the development of high-performance, non-precious-metal catalysts as alternatives to noble metal Pt-based ORR electrocatalysts is highly desirable for the large-scale commercialization of fuel cells. TiO2 -grafted copper complexes deposited on multiwalled carbon nanotubes (CNTs) form stable and efficient electrocatalysts for the ORR. The optimized catalyst composite CNTs@TiO2 -ZA-[Cu(phen${{^{{\rm NO}{_{2}}}}}$)(BTC)] shows surprisingly high selectivity for the 4 e(-) reduction of O2 to water (approximately 97 %) in alkaline solution with an onset potential of 0.988 V vs. RHE, and demonstrates superior stability and excellent tolerance for the methanol crossover effect in comparison to a commercial Pt/C catalyst. The copper complexes were grafted onto the surface of TiO2 through coordination of an imidazole-containing ligand, zoledronic acid (ZA), which binds to TiO2 through its bis-phosphoric acid anchoring group. Rational optimization of the copper catalyst's ORR performance was achieved by using an electron-deficient ligand, 5-nitro-1,10-phenanthroline (phen${{^{{\rm NO}{_{2}}}}}$), and bridging benzene-1,3,5-tricarboxylate (BTC). This facile approach to the assembly of copper catalysts on TiO2 with rationally tuned ORR activity will have significant implications for the development of high-performance, non-precious-metal ORR catalysts.

Covalent grafting of carbon nanotubes with a biomimetic heme model compound to enhance oxygen reduction reactions.

The oxygen reduction reaction (ORR) is one of the most important reactions in both life processes and energy conversion systems. The replacement of noble-metal Pt-based ORR electrocatalysts by nonprecious-metal catalysts is crucial for the large-scale commercialization of automotive fuel cells. Inspired by the mechanisms of dioxygen activation by metalloenzymes, herein we report a structurally well-defined, bio-inspired ORR catalyst that consists of a biomimetic model compound-an axial imidazole-coordinated porphyrin-covalently attached to multiwalled carbon nanotubes. Without pyrolysis, this bio-inspired electrocatalyst demonstrates superior ORR activity and stability compared to those of the state-of-the-art Pt/C catalyst in both acidic and alkaline solutions, thus making it a promising alternative as an ORR electrocatalyst for application in fuel-cell technology.

Yangxin Decoction combined acupuncture on blood lipid metabolism in Qi Deficiency and Blood Stasis type of Chest Bi-Syndrome: A protocol of systematic review.

BACKGROUND: In recent years, clinical studies about Yangxin Decoction combined acupuncture (YXDA) for the treatment of Qi Deficiency and Blood Stasis type of Chest Bi-Syndrome (CBS-QDBS) has been increased, but the results are different. The aim of this study is to investigate the effect of YXDA on blood lipid metabolism (BLMB) in patients with CBS-QDBS. METHODS: We will collect any randomized controlled trials that assess the effect of YXDA on BLMB in CBS-QDBS from PUBMED, EMBASE, Cochrane Library, PsycINFO, CINAHL, Allied and Complementary Medicine Database, and China National Knowledge Infrastructure. All of these databases will be searched from their initial time to the present. All language limitation will be imposed. Literature selection, information collection, and risk of bias assessment will be performed independently by two authors, respectively. All data analysis will be undertaken using RevMan 5.3 Software. RESULTS: This study will summarize the systematic nature of the literature search and its methods for assessing study quality and analyzing all relevant outcome data. Considering the inconsistent results, this study will improve the existing evidence on the effect of YXDA on BLMB in CBS-QDBS. CONCLUSION: The findings of this study will present the latest evidence of YXDA on BLMB in patients with CBS-QDBS. STUDY REGISTRATION: INPLASY202070047.

[Testosterone induces different-featured prostate hyperplasia in castrated and uncastrated mice].

OBJECTIVE: To study the different features of hyperplasia in castrated and uncastrated mice after testosterone (T) treatment. METHODS: Forty-eight BALB/c mice were randomly divided into 6 groups of 8 in each: castrated (A), uncastrated (B) , castrated + low T (C), uncastrated + low T (D), castrated + high T (E), uncastrated + high T (F). Groups C and D were treated with testosterone solution at the dose of 12.5 mg/(kg d) and Groups E and F at 125 mg/(kg d) for 20 consecutive days, while Groups A and B received saline only. All the mice were sacrificed on the 21st day, their ventral and dorsal prostate glands weighed and their pathological features studied. RESULTS: Atrophic prostates were observed in Group A, but normal in Group B; prostatic hyperplasia was found in both Group C and D, but more obvious in the latter (P <0.05); and a slightly higher degree of hyperplasia was noted in Groups E and F than in C and D. There was an increase in serum T and vascular endothelial growth factor (VEGF) concentration and a decrease in serum estrogen (E2) concentration in the testosterone treated groups. CONCLUSION: Both castrated and uncastrated mice develop prostate hyperplasia after short-term testosterone treatment, although in different degrees and with different features, which may help further the studies on the association of castration and androgen with prostate diseases.

[Estimation of tissue's blood oxygen parameters from visible absorption spectrum of tissues by artificial neural network].

Total hemoglobin concentration (THC) and hemoglobin oxygen saturation (SO2) are essential parameters to doctors who wonder patients' hematogenous conditions and oxygen supplies and consumptions. Instruments presently used for measuring these parameters have big size of detecting probes that limit their applications to inner bodies. An optical probe involving two fibers with source-detector separations of one hundred micrometers was developed in the present study for purpose of minimally invasive inner detecting, which uses steady-state, broadband (300-1 000 nm) light source. The source light is delivered to targets through one fiber and the reflected light from the targets is collected and transferred to a spectrometer through the other fiber. Reflectance spectrum is obtained from the spectrometer. The method of reading THC and SO2 from the reflectance spectrum was developed using liquid-tissue phantoms containing intralipid and blood. Firstly, reflex spectrum of intralipid was recorded before mixtures of intralipid and blood with different THC were made as tissue phantoms. Then the fiber optical spectrometer was used to obtain reflex spectra as the phantoms' SO2 changed; simultaneously their corresponding THC and SO2 were recorded as the scale values by an oximeter. Differences of reflex spectra in 520-590 nm between intralipid and tissue models were proved reliably. Secondly, after data collections of absorption spectra and scale values were finished, two artificial neural networks (ANN) were build to model the relationship between scale values and absorption spectra. After being trained, the ANNs could output THC and SO2 correctly when an absorption spectrum was input. The ANNs produced errors of less than 4 micromol x L(-1) for THC and 5% for SO2. In vivo and minimally invasive measurements of THC and SO2 of brain tissues in different depth were finished on 30 rats by this specific system with the ANNs. The probe was inserted stereotactically to a depth of 6 mm with measurements obtained every 0.2 mm. SO2 of gray mater and white mater of rats was respectively obtained as 0.60-0.70 and 0.45-0.55. The highest THC, 110 micromol x L(-1) was measured around rat cortex. THC of brain tissue in other depth is 70-90 micromol x L(-1). These values agree well with reported data. This simple, inexpensive method deserves further study to establish its efficacy for THC and SO2 measurements of inner body.

[Corrigendum] 5­bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2­one induces apoptosis in T24 human bladder cancer cells through mitochondria-dependent signaling pathways.

Following the publication of this article, an interested reader drew to our attention that Fig. 1, which described the effects of 5-bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2-one (BHP) on T24 bladder carcinoma cell morphology and viability, contained a pair of panels showing identical data. After having re-examined our original data, we realize that the control data (showing 0 µM BHP) were inadvertently also included in Fig. 1 for the panel that was intended to show the effect of adding 10 µM BHP to the cells. A corrected version of Fig. 1, featuring the correct data for the addition of 10 µM BHP to the cells, is shown here. The error did not affect the conclusions reported in this study. We sincerely apologize for this mistake, and thank the reader of our article who drew this matter to our attention. Furthermore, we regret any inconvenience this mistake has caused. [the original article was published in the Molecular Medicine Reports 15: 153-159, 2016; DOI: 10.3892/mmr.2016.5991].

5­bromo­3­(3­hydroxyprop­1­ynyl)­2H­pyran­2­one induces apoptosis in T24 human bladder cancer cells through mitochondria-dependent signaling pathways.

The present study was performed to investigate the effect of 5-bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2-one (BHP) on the induction of apoptosis and cell cycle arrest in T24 human bladder carcinoma cells. An MTT assay was used to investigate the inhibition of cell proliferation. Flow cytometry was used to observe alterations in the cell cycle, generation of reactive oxygen species (ROS), alterations in mitochondrial membrane potential (MMP) and induction of apoptosis in the T24 cells following BHP treatment. Western blot analysis was performed for the determination of expression levels of apoptotic proteins, and 4,6­diamidino­2­phenylindole dihydrochloride staining was used to observe apoptosis and DNA damage. The results demonstrated that treatment of the bladder cancer cells with BHP enhanced the activation of caspases and increased the production of ROS. It also caused damage to DNA, reduced MMP, and increased the secretion of endonuclease G and apoptosis­inducing factor from the mitochondria. The expression levels of cyclin E and cell division cycle 25C were reduced, whereas the expression levels of p21 and phosphorylated p53 were increased in the BHP­treated cells. In addition, treatment with BHP caused cell cycle arrest at the G0/G1 phase, increased the expression levels of B cell lymphoma­2 (Bcl­2)­associated X protein and poly(ADP­ribose) polymerase, decreased the expression of Bcl­2 and ultimately induced apoptosis of the T24 cells. Thus, BHP inhibited the proliferation of bladder cancer cells by inducing cell apoptosis through the mitochondrial pathway.

Effect of Rac1 downregulation mediated by shRNA on the biological behaviour of human cervical cancer cells.

OBJECTIVE: The function of Ras-related C3 botulinum toxin substrate1 (Rac1) in the progression of cervical cancer is unclear. This study used RNA interference technology to explore the involvement of Rac1 in the regulation of cervical cancer cells. METHODS: A short hairpin (sh) RNA plasmid targeting Rac1 was constructed and transfected into HeLa cells. Rac1 mRNA and protein levels were investigated by reverse transcription-polymerase chain reaction and Western blot, respectively. Cell proliferation and cisplatin chemosensitivity were determined using the methyl thiazolyl tetrazolium assay. The Matrigel™ assay and flow cytometry were used to assess cell invasion and apoptosis, respectively. The concentration of matrix metalloproteinase (MMP)-2 in cell supernatants was detected by enzyme-linked immunosorbent assay. RESULTS: Rac1 expression was significantly downregulated at the mRNA and protein levels in HeLa cells transfected with Rac1 shRNA, and the cell proliferation and invasion capability of cells was decreased. Rac1 downregulation was associated with a decrease in MMP-2 secretion, and increased cell chemosensitivity to cisplatin and cisplatin-induced apoptosis. CONCLUSIONS: Rac1 may play an important role in cervical cancer progression and could be a potential target for anticancer therapy.