Enhanced Hippocampus-Nidopallium Caudolaterale Interaction in Visual-Spatial Associative Learning of Pigeons.

Learning the spatial location associated with visual cues in the environment is crucial for survival. This ability is supported by a distributed interactive network. However, it is not fully understood how the most important task-related brain areas in birds, the hippocampus (Hp) and the nidopallium caudolaterale (NCL), interact in visual-spatial associative learning. To investigate the mechanisms of such coordination, synchrony and causal analysis were applied to the local field potentials of the Hp and NCL of pigeons while performing a visual-spatial associative learning task. The results showed that, over the course of learning, theta-band (4-12 Hz) oscillations in the Hp and NCL became strongly synchronized before the pigeons entered the critical choice platform for turning, with the information flowing preferentially from the Hp to the NCL. The learning process was primarily associated with the increased Hp-NCL interaction of theta rhythm. Meanwhile, the enhanced theta-band Hp-NCL interaction predicted the correct choice, supporting the pigeons' use of visual cues to guide navigation. These findings provide insight into the dynamics of Hp-NCL interaction during visual-spatial associative learning, serving to reveal the mechanisms of Hp and NCL coordination during the encoding and retrieval of visual-spatial associative memory.

Performance Baseline of Phase Transfer Entropy Methods for Detecting Animal Brain Area Interactions.

Objective: Phase transfer entropy (TEθ) methods perform well in animal sensory-spatial associative learning. However, their advantages and disadvantages remain unclear, constraining their usage. Method: This paper proposes the performance baseline of the TEθ methods. Specifically, four TEθ methods are applied to the simulated signals generated by a neural mass model and the actual neural data from ferrets with known interaction properties to investigate the accuracy, stability, and computational complexity of the TEθ methods in identifying the directional coupling. Then, the most suitable method is selected based on the performance baseline and used on the local field potential recorded from pigeons to detect the interaction between the hippocampus (Hp) and nidopallium caudolaterale (NCL) in visual-spatial associative learning. Results: (1) This paper obtains a performance baseline table that contains the most suitable method for different scenarios. (2) The TEθ method identifies an information flow preferentially from Hp to NCL of pigeons at the θ band (4-12 Hz) in visual-spatial associative learning. Significance: These outcomes provide a reference for the TEθ methods in detecting the interactions between brain areas.

The Emerging Role of Ferroptosis in Liver Diseases.

Ferroptosis is a newly discovered type of cell death mediated by iron-dependent lipid peroxide. The disturbance of iron metabolism, imbalance of the amino acid antioxidant system, and lipid peroxide accumulation are considered distinct fingerprints of ferroptosis. The dysregulation of ferroptosis has been intensively studied in recent years due to its participation in various diseases, including cancer, kidney injury, and neurodegenerative diseases. Notably, increasing evidence indicates that ferroptosis plays different roles in a wide spectrum of liver diseases. On the one hand, inhibiting ferroptosis may counteract the pathophysiological progression of several liver diseases, such as alcoholic liver injury, nonalcoholic steatosis hepatitis and fibrosis. On the other hand, inducing ferroptosis may restrict the emergence of secondary resistance to current medicines, such as sorafenib, for hepatocellular carcinoma (HCC) therapy. Here, we summarize the biological characteristics and regulatory signalling pathways of ferroptosis involved in liver disease. The current available medical agents targeting ferroptosis, including inducers or inhibitors applied in liver diseases, are also reviewed. This work aims to provide new insight into the emerging role of pathogenesis and therapeutic approaches for liver diseases.

Effect of annonaceous acetogenin mimic AA005 on proliferative inhibition of leukemia cells in vitro and its possible mechanisms / 中国实验血液学杂志

This study was aimed to investigate the biological behavior of annonaceous acetogenin mimic AA005 in various kinds of leukemia cells and further elaborated its possible mechanisms in acute promyelocytic leukemia (APL) cell line NB4. The proliferative inhibition of leukemia cells was measured by CCK-8 method. Cell death was determined by trypan blue. Cell morphological features of NB4 treated with AA005 were examined by microscopy after Wright's staining. The form of cell death was measured by flow cytometry. Proteins PARP-1 and caspase-3 were detected by Western blot. Flow cytometry was used to detect the cell cycle arrest induced by AA005 of low concentration. The results showed that AA005 (> 200 nmol/L) significantly inhibited proliferation of all tested leukemia cell lines in a concentration-dependent manner. The vast majority of cells went to die after leukemia cell lines of NB4, U937 and K562 were treated with different concentration of AA005 for 48 h. Typical morphologic changes significantly appeared in NB4 cells after AA005 treatment. AA005 almost simultaneously induced early apoptosis and late apoptosis. The little cleavage of PARP-1 and activation of caspase-3 happened in AA005-induced cell death, and caspase-3 inhibitor Z-VAD-fmk could not block the cell death. The non-toxic concentrations of AA005 (< 200 nmol/L) caused NB4 cells G(2)/M-phase arrest. It is concluded that annonaceous acetogenin mimic AA005 induces significant proliferative inhibition of various leukemia cell lines in a concentration-dependent manner, which may be associated with cell death and G(2)/M-phase arrest induced by AA005.

Generation of trans-arachidonic acid under nitrative stress is associated with upregulation of thromponsdin-1 in diabetic rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Trans-arachidonic acids (TAAs), newly discovered markers of nitrative stress and the major products of nitrogen dioxide (NO2(·))-mediated isomerization of arachidonic acid (AA), represent a new mechanism of NO2(·)-induced toxicity. It has been reported that TAAs were generated in oxygen-induced microvascular degeneration model and TAAs were also generated in a diabetic retinopathy (DR) model. In this study, we examined high glucose-induced nitrative stress damage and TAAs levels and explored the possible mechanisms for DR caused by reactive nitrogen species.</p><p><b>METHODS</b>Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ) at 60 mg/kg. Bovine retinal capillary endothelial cells (BRECs) were selectively cultured and incubated with normal or high glucose. The serum TAAs and AA in diabetic rats were measured by the gas chromatography and mass spectrometry (GC/MS) method. The ratio of peak area of TAAs to AA with selected ion of 79 was estimated by a group t-test. Thrombospondin-1 (TSP-1) in the rat retinas and BRECs extracts were examined by Western blotting. The phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) protein was examined by Western blotting in BRECs incubated with high glucose.</p><p><b>RESULTS</b>The TAAs to AA ratio (TAAs/AA) was significantly increased in the serum at 8, 12 and 16 weeks after STZ injection (P < 0.05), with no noticeable change found at 2 or 4 weeks (P > 0.05). Expression of TSP-1 in the retina of diabetic rats was progressively elevated according to the duration of diabetes. TSP-1 expression was increased in BRECs incubated with high glucose at 48 hours. Moreover, high glucose also increased ERK1/2 expression, which peaked at 30 minutes and then decreased in the following 48 hours.</p><p><b>CONCLUSION</b>An elevation of TAAs/AA is associated with high glucose-induced nitrative stress, which probably involves upregulation of TSP-1 through activating ERK1/2.</p>