The Laplacian energy of random graphs

Gutman {\it et al.} introduced the concepts of energy \En(G) and Laplacian energy \EnL(G) for a simple graph $G$, and furthermore, they proposed a conjecture that for every graph $G$, \En(G) is not more than \EnL(G). Unfortunately, the conjecture turns out to be incorrect since Liu {\it et al.} and Stevanovi\'c {\it et al.} constructed counterexamples. However, So {\it et al.} verified the conjecture for bipartite graphs. In the present paper, we obtain, for a random graph, the lower and upper bounds of the Laplacian energy, and show that the conjecture is true for almost all graphs.Comment: 14 page

The vertical influence of temperature and precipitation on snow cover variability in the Central Tianshan Mountains, Northwest China

Seasonal snow cover in mountainous regions will affect local climate and hydrology. In this study, we assessed the role of altitude in determining the relative importance of temperature and precipitation in snow cover variability in the Central Tianshan Mountains. The results show that: (1) in the study area, temperature has a greater influence on snow cover than precipitation during most of the time period studied and in most altitudes. (2) In the high‐elevation area, there is a threshold altitude of 3900±400 m, below which temperature is negatively while precipitation is positively correlated to snow cover, above which the situation is the opposite. Besides, this threshold altitude decreases from snow accumulated period to snow stable period and then increases from snowmelt period to snow‐free period. (3) Below 2000 m, there is another threshold altitude of 1400±100 m during the snow stable period, below (above) which precipitation (temperature) is the main driver of snow cover

Xue-Jie-San restricts ferroptosis in Crohn’s disease via inhibiting FGL1/NF-κB/STAT3 positive feedback loop

Crohn’s disease (CD) is an incurable inflammatory bowel disease due to unclear etiology and pathogenesis. Accumulating evidences have shown the harmful role of ferroptosis in CD onset and development. Additionally, fibrinogen-like protein 1 (FGL1) has been verified to be a potential therapeutic target of CD. Xue-Jie-San (XJS) is an effective prescription for treating CD. However, its therapeutic mechanism has not been fully elucidated. This study aimed to determine whether XJS alleviating CD via regulating ferroptosis and FGL1 expression. A colitis rat model was induced by 2,4,6-trinitrobenzene sulfonic acid and treated with XJS. The disease activity indices of the colitis rats were scored. Histopathological damage was assessed using HE staining. ELISA was performed to examine inflammatory cytokines. Transmission electron microscopy was utilized to observe ultrastructure changes in intestinal epithelial cells (IECs). Iron load was evaluated by examining iron concentrations, the expressions of FPN, FTH and FTL. Lipid peroxidation was investigated through detecting the levels of ROS, 4-HNE, MDA and PTGS2. Furthermore, the SLC7A11/GSH/GPX4 antioxidant system and FGL1/NF-κB/STAT3 signaling pathway were examined. The results showed that colitis was dramatically ameliorated in the XJS-treated rats as evidenced by relief of clinical symptoms and histopathological damages, downregulation of pro-inflammatory cytokines IL-6, IL-17 and TNF-α, and upregulation of anti-inflammatory cytokine IL-10. Furthermore, XJS administration led to ferroptosis inhibition in IECs by reducing iron overload and lipid peroxidation. Mechanistically, XJS enhanced the SLC7A11/GSH/GPX4 antioxidant system negatively regulated by the FGL1/NF-κB/STAT3 positive feedback loop. In conclusion, XJS might restrain ferroptosis in IECs to ameliorate experimental colitis by inhibition of FGL1/NF-κB/STAT3 positive feedback loop

Urea-induced ROS generation causes insulin resistance in mice with chronic renal failure.

Although supraphysiological concentrations of urea are known to increase oxidative stress in cultured cells, it is generally thought that the elevated levels of urea in chronic renal failure patients have negligible toxicity. We previously demonstrated that ROS increase intracellular protein modification by O-linked β-N-acetylglucosamine (O-GlcNAc), and others showed that increased modification of insulin signaling molecules by O-GlcNAc reduces insulin signal transduction. Because both oxidative stress and insulin resistance have been observed in patients with end-stage renal disease, we sought to determine the role of urea in these phenotypes. Treatment of 3T3-L1 adipocytes with urea at disease-relevant concentrations induced ROS production, caused insulin resistance, increased expression of adipokines retinol binding protein 4 (RBP4) and resistin, and increased O-GlcNAc–modified insulin signaling molecules. Investigation of a mouse model of surgically induced renal failure (uremic mice) revealed increased ROS production, modification of insulin signaling molecules by O-GlcNAc, and increased expression of RBP4 and resistin in visceral adipose tissue. Uremic mice also displayed insulin resistance and glucose intolerance, and treatment with an antioxidant SOD/catalase mimetic normalized these defects. The SOD/catalase mimetic treatment also prevented the development of insulin resistance in normal mice after urea infusion. These data suggest that therapeutic targeting of urea-induced ROS may help reduce the high morbidity and mortality caused by end-stage renal disease