Stimulation of anterior thalamic nucleus protects hippocampus neural injury in kainic acid-induced epileptic rats

Anterior nucleus of thalamus (ANT) stimulation has been proved to be effective in the treatment of refractory epilepsy, but the underlying mechanisms remain to be elucidated. We examined the role of ANT stimulation on hippocampal neuron death after seizures induced by kainic acid (KA). Our data showed that ANT stimulation could significantly rescue neurons from death induced by seizures, by reducing the release of cytochrome c (cyto c) and also via apoptosis-inducing factor (AIF) induced by seizures through inhibiting the activated caspase-9 and caspase-3. Our data suggest that ANT stimulation may protect against neuronal loss and reduce neuronal injury in the ipsilateral CA3 region of the hippocampus in the KA-induced epileptic rats, and the underlying mechanism may be mediated by inhibiting mitochondrial caspase-dependent (cyto c release and the subsequent cleavage of caspase-) and caspase-independent (nuclear translocation of AIF) apoptosis pathways

Hepcidin and sports anemia

Iron is an important mineral element used by the body in a variety of metabolic and physiologic processes. These processes are highly active when the body is undergoing physical exercises. Prevalence of exercise-induced iron deficiency anemia (also known as sports anemia) is notably high in athletic populations, particularly those with heavy training loads. The pathogenesis of sports anemia is closely related to disorders of iron metabolism, and a more comprehensive understanding of the mechanism of iron metabolism in the course of physical exercises could expand ways of treatment and prevention of sports anemia. In recent years, there have been remarkable research advances regarding the molecular mechanisms underlying changes of iron metabolism in response to physical exercises. This review has covered these advances, including effects of exercise on duodenum iron absorption, serum iron status, iron distribution in organs, erythropoiesis, and hepcidin’s function and its regulation. New methods for the treatment of exercise-induced iron deficiency are also discussed

Single machine scheduling with exponential time-dependent learning effect and past-sequence-dependent setup times

AbstractIn this paper we consider the single machine scheduling problem with exponential time-dependent learning effect and past-sequence-dependent (p-s-d) setup times. By the exponential time-dependent learning effect, we mean that the processing time of a job is defined by an exponent function of the total normal processing time of the already processed jobs. The setup times are proportional to the length of the already processed jobs. We consider the following objective functions: the makespan, the total completion time, the sum of the quadratic job completion times, the total weighted completion time and the maximum lateness. We show that the makespan minimization problem, the total completion time minimization problem and the sum of the quadratic job completion times minimization problem can be solved by the smallest (normal) processing time first (SPT) rule, respectively. We also show that the total weighted completion time minimization problem and the maximum lateness minimization problem can be solved in polynomial time under certain conditions

N′-(5-ethoxycarbonyl-3,4-dimethyl-pyrrol-2-yl-methylidene)-4-hydroxybenzohydrazide monohydrate, C17H21N3O5

Abstract C17H21N3O5, monoclinic, P21/n (no. 14), a = 9.2278(16) Å, b = 15.093(3) Å, c = 12.698(2) Å, β = 105.195(12)°, V = 1706.7(5) Å3, Z = 4, R gt(F) = 0.0553, wR ref(F 2) = 0.1662, T = 296 K

Bis[N-benzyl-2-(quinolin-8-yl­oxy)acetamide] monohydrate

In the title compound, 2C18H16N2O2·H2O, the dihedral angles between the quinoline rings and the benzene rings in the two independent acetamide mol­ecules are 80.09 (5) and 61.23 (5)°. The crystal packing is stablized by O—H⋯N and N—H⋯O hydrogen bonds between the acetamide and water mol­ecules

ECHS1 interacts with STAT3 and negatively regulates STAT3 signaling

AbstractSignal transducer and activator of transcription 3 (STAT3) is a critical transcriptional factor in a variety of cellular processes, and is frequently over-activated in a range of human tumors. However, the processes that regulate STAT3 activation need to be further clarified. With a yeast two-hybrid screening, we identified enoyl-CoA hydratase short chain 1 (ECHS1) as a novel STAT3 binding protein. We further confirmed the interaction between STAT3 and ECHS1 by GST-pull down and co-immnunoprecipitation. Importantly, we found that ECHS1 specifically represses STAT3 activity and negatively regulates the expression of several target genes of STAT3 through inhibiting STAT3 phosphorylation. Therefore, our findings will provide new insights into the mechanism of STAT3 signaling regulation.Structured summary of protein interactionsSTAT3physically interactswithECHS1bypull down(View interaction)STAT3physically interactswithECHS1bytwo hybrid(View Interaction:1,2)ECHS1physically interactswithSTAT3byanti tag co immunoprecipitation(View Interaction:1,2)STAT3physically interactswithECHS1byanti bait co immunoprecipitation(View interaction

Ethyl 3,4-dimethyl-1H-pyrrole-2-carboxyl­ate

The non-H atoms of the title compound, C9H13NO2, are almost coplanar (r.m.s. deviation = 0.0358 Å). Weak inter­molecular N—H⋯O hydrogen bonds link the mol­ecules into zigzag chains along the b axis with graph-set motif C(5). The chains are further linked into a three-dimensional network by C—H⋯O hydrogen bonds and C—H⋯π inter­actions

High-frequency stimulation of nucleus accumbens changes in dopaminergic reward circuit

Deep brain stimulation (DBS) of the nucleus accumbens (NAc) is a potential remedial therapy for drug craving and relapse, but the mechanism is poorly understood. We investigated changes in neurotransmitter levels during high frequency stimulation (HFS) of the unilateral NAc on morphine-induced rats. Sixty adult Wistar rats were randomized into five groups: the control group (administration of saline), the morphine-only group (systematic administration of morphine without electrode implantation), the morphine-sham-stimulation group (systematic administration of morphine with electrode implantation but not given stimulation), the morphine-stimulation group (systematic administration of morphine with electrode implantation and stimulation) and the saline-stimulation group (administration of saline with electrode implantation and stimulation). The stimulation electrode was stereotaxically implanted into the core of unilateral NAc and microdialysis probes were unilaterally lowered into the ipsilateral ventral tegmental area (VTA), NAc, and ventral pallidum (VP). Samples from microdialysis probes in the ipsilateral VTA, NAc, and VP were analyzed for glutamate (Glu) and caminobutyric acid (GABA) by high-performance liquid chromatography (HPLC). The levels of Glu were increased in the ipsilateral NAc and VP of morphine-only group versus control group, whereas Glu levels were not significantly changed in the ipsilateral VTA. Furthermore, the levels of GABA decreased significantly in the ipsilateral NAc, VP, and VTA of morphineonly group when compared with control group. The profiles of increased Glu and reduced GABA in morphine-induced rats suggest that the presence of increased excitatory neurotransmission in these brain regions. The concentrations of the Glu significantly decreased while the levels of GABA increased in ipsilateral VTA, NAc, and VP in the morphine-stimulation group compared with the morphine-only group. No significant changes were seen in the morphine-sham stimulation group compared with the morphine-only group. These findings indicated that unilateral NAc stimulation inhibits the morphineinduced rats associated hyperactivation of excitatory neurotransmission in the mesocorticolimbic reward circuit

2-Chloro-N-methyl-N-phenyl­acetamide

In the title compound, C9H10ClNO, the non-H atoms, excluding the phenyl group, are almost coplanar (r.m.s. deviation of the non-H atoms = 0.1015 Å). The dihedral angle formed between this plane and the benzene ring is 87.07 (5)°. Weak inter­molecular C—H⋯O inter­actions help to stabilize the packing