Chiral Brønsted Acid-Catalyzed Asymmetric Reaction via Vinylidene Ortho-Quinone Methides.

Vinylidene ortho-quinone methides (VQMs) have been proven to be versatile and crucial intermediates in the catalytic asymmetric reaction in last decade, and thus have drawn considerable concentrations on account of the practical application in the construction of enantiomerically pure functional organic molecules. However, in comparison to the well established chiral Brønsted base-catalyzed asymmetric reaction via VQMs, chiral Brønsted acid-catalyzed reaction is rarely studied and there is no systematic summary to date. In this review, we summarize the recent advances in the chiral Brønsted acid-catalyzed asymmetric reaction via VQMs according to three types of reactions: a) intermolecular asymmetric nucleophilic addition to VQMs; b) intermolecular asymmetric cycloaddition of VQMs; c) intramolecular asymmetric cyclization of VQMs.

[Toll-like Receptor Agonists in Radiation Protection].

Ionizing radiation causes the massive apoptosis of human tissue cells,leading to dysfunction of the gastrointestinal tract and hematopoietic system.Thus,high-efficiency,low-toxicity radiation protection drugs are urgently needed.Toll-like receptor agonists have been developed based on the anti-apoptotic mechanism of tumor cells in recent years,which exert their radioprotective effects by activating downstream pathways,mainly nuclear factor-κB.

[Expression of Peroxiredoxin-6 Gene in Patients with Acute Myeloid Leukemia and Its Clinical Significance].

Objective: To study the expression of Peroxiredoxin-6 (Prdx6) gene in elderly patients with acute myeloid leukemia (AML) and its clinical significance.

Methods: The expression level of Prdx6 in bone marrow cells of 33 cases of AML, 8 cases of CML and 11 cases of other blood diseases was detected by PCR. The correlation of the abnormal expression of Prdx6 with patient age and blood routine parameters was further analyzed.

Transplantation of bone marrow mesenchymal stem cells promotes learning and memory functional recovery and reduces hippocampal damage in rats with alcohol-associated dementia.

Background: Chronic ethanol exposure leads to permanent damage to the central nervous system and produces cognitive deficits such as learning and memory impairment. The present study was designed to explore the therapeutic effect of bone marrow mesenchymal stem cells (BMMSCs) on a rat model of alcohol-associated dementia (AAD).

Methods: Bone marrow mesenchymal stem cells were prelabeled with 4',6-diamidino-2-phenylindole and directly transplanted into the hippocampus of AAD rats, an important site of alcohol effects that lead to cognitive deficits.

Hydrogen sulfide inhibits opioid withdrawal-induced pain sensitization in rats by down-regulation of spinal calcitonin gene-related peptide expression in the spine.

Hyperalgesia often occurs in opioid-induced withdrawal syndrome. In the present study, we found that three hourly injections of DAMGO (a μ-opioid receptor agonist) followed by naloxone administration at the fourth hour significantly decreased rat paw nociceptive threshold, indicating the induction of withdrawal hyperalgesia. Application of NaHS (a hydrogen sulfide donor) together with each injection of DAMGO attenuated naloxone-precipitated withdrawal hyperalgesia.

Chronic morphine treatment induces over-expression of HSP70 in mice striatum related with abnormal ubiquitin-proteasome degradation.

Background: It has been shown that opioid dependence-related neuronal plasticity may rely not only on protein synthesis, but also on protein degradation, mainly mediated by ubiquitin-proteasome system (UPS). The aim of the present study was to determine the effect of morphine on the regulation of protein degradation in the brain and to determine which proteins are involved in the underlying mechanism.

Methods: Mice were given chronic morphine administration and the state of morphine dependence was confirmed by induction of naloxone-precipitated withdrawal jumping.

Hydrogen sulfide attenuates opioid dependence by suppression of adenylate cyclase/cAMP pathway.

Aims: The best-established mechanism of opioid dependence is the up-regulation of adenylate cyclase (AC)/cAMP pathway, which was reported to be negatively regulated by hydrogen sulfide (H2S), a novel endogenous neuromodulator. The present study was, therefore, designed to determine whether H2S is able to attenuate the development of opioid dependence via down-regulating AC/cAMP pathway.

Results: We demonstrated that application of sodium hydrosulphide (NaHS) and GYY4137, two donors of H2S, significantly alleviated naloxone-induced robust withdrawal jumping (the most sensitive and reliable index of opioid physical dependence) in morphine-treated mice.

Effects of chronic morphine treatment on protein expression in rat dorsal root ganglia.

The initial aim of this study was to identify protein changes in the dorsal root ganglia (DRG) associated with long-term morphine treatment. We carried out a differential proteomics analysis on samples from the DRG of control and morphine-dependent rats (5-40 mg/kg, subcutaneously, twice daily for 28 days) after 4 days of morphine withdrawal. Proteins showing a statistically significant variation between the two groups were selected for identification by mass spectrometric analysis.

Chronic morphine administration induces over-expression of aldolase C with reduction of CREB phosphorylation in the mouse hippocampus.

In recent studies, alterations in the activity and expression of metabolic enzymes, such as those involved in glycolysis, have been detected in morphine-dependent patients and animals. Increasing evidence demonstrates that the hippocampus is an important brain region associated with morphine dependence, but the molecular events occurring in the hippocampus following chronic exposure to morphine are poorly understood. Aldolase C is the brain-specific isoform of fructose-1, 6-bisphosphate aldolase which is a glycolytic enzyme catalyzing reactions in the glycolytic, gluconeogenic, and fructose metabolic pathways.

2-Methyl-7-nitro-2,3-dihydro-1-benzofuran.

The dihydro-furan ring of the title compound, C(9)H(9)NO(3), adopts an envelope conformation. The nitro group is twisted slightly away from the attached benzene ring [dihedral angle = 21.9 (1)°].

1-Hydroxymethyl-1-methylethan-aminium chloride.

The asymmetric unit of the title compound, C(4)H(12)NO(+)·Cl(-), contains two independent ion pairs. Weak intra-molecular C-H⋯O and N-H⋯O hydrogen bonds result in the formation of three five-membered rings, which have envelope conformations. The crystal structure contains intermolecular O-H⋯Cl, N-H⋯O, N-H⋯Cl and O-H⋯O hydrogen bonds.

[Hydroquinone inhibits NF-kappaB expression in human bone marrow stromal cells in vitro].

This study was aimed to investigate whether hydroquinone (HQ) can inhibit NF-kappaB expression activated by phorbol myristate acetate (PMA), and to explore the relationship between the mechanism and the hematology toxicity of benzene tentatively. The human bone marrow stromal cells (BMSC) were harvested by in vitro culture and their change of morphology were observed. The activity and protein expression of NF-kappaB p65 extracted from those BMSC were measured with immunohistochemistry and TransAM P65 kit.