Parental Care System and Brood Size Drive Sex Difference in Reproductive Allocation:An Experimental Study on Burying Beetles

Life-history theory predicts that increased resource allocation in current reproduction comes at the cost of survival and future reproductive fitness. In taxa with biparental care, each parent can adjust investment on current reproduction according to changes in their partner’s effort, but these adjustments may be different for males and females as they may have different reproductive strategies. Numerous theoretical and empirical studies have proposed the mechanism underlying such adjustments. In addition, the value of the brood or litter (brood size) has also been suggested to affect the amount of care through manipulation of brood size. While the two conditions have been studied independently, the impact of their interplay on potential sex-dependent future reproductive performance remains largely unknown. In this study, we simultaneously manipulated both care system (removal of either parent vs. no removal) and brood size in a burying beetle (Nicrophorus vespilloides) to understand their joint effect on reproductive allocation and trade-off between current and future reproduction. Our results show that males compensated for mate loss by significantly increasing the level of care regardless of brood size, while females exhibited such compensation only for small brood size. Additionally, with an increase in allocation to current reproduction, males showed decreased parental investment during the subsequent breeding event as a pair. These findings imply a dual influence of parental care system and brood size on allocation in current reproduction. Moreover, the impact of such adjustments on sex-dependent differences in future reproduction (parental care, larvae number, and average larval mass at dispersal) is also demonstrated. Our findings enhance the understanding of sex roles in parental investment and highlight their importance as drivers of reproductive allocation

Localization of Fusobacterium nucleatum in oral squamous cell carcinoma and its possible directly interacting protein molecules: A case series

Introduction. While 15 to 20% of cancers are associated with microbial infection, the relationship between oral microorganisms and oral squamous cell carcinoma (OSCC) remains unclear. The location of bacteria in a tumor is closely related to its carcinogenic mechanism. The aim of this study was to analyse bacterial diversity in clinical OSCC tissue samples and tumor distant normal tissues, locate target bacteria, and search for proteins that may interact with target bacteria. Materials and Methods. The 16S rDNA method was used to analyse bacterial diversity in clinical OSCC tissue samples and tumor distant normal tissues. Correlations between Fusobacterium abundance and clinicopathological characteristics were analysed using the χ2 test. The position of target bacteria was analysed by fluorescence in situ hybridization (FISH), and the expression of CK, CD31, CD45, CD68, cyclin D1, βcatenin, E-cadherin, NF-κB, and HIF-1α was analysed by immunohistochemistry (IHC) in OSCC tumor tissues and tumor distant normal tissues. Results. The 16S rDNA results showed that the detected amount of Fusobacterium in OSCC tumor tissues was significantly larger than that in tumor distant normal tissues. High expression of Fusobacterium was significantly correlated with the lifestyle-related oral risk habits, including smoking (p=0.036) and alcohol consumption (p=0.022), but did not correlate with patient sex, age, tumor laterality, tumor size, grade or TNM stage. Fusobacterium nucleatum was enriched in tumor stroma, where CD31+ blood vessels and inflammatory cells (including CD45+ leukocytes and CD68+ macrophages) were densely distributed. Cyclin D1 was mainly expressed in the nucleus of tumor cells. β-catenin was expressed in the tumor cell membrane and was positively expressed in tumor interstitial vascular endothelial cells. E-cadherin was mainly expressed in tumor cell membranes. NF-κB was positively expressed in the cytoplasm of tumor cells, tumor interstitial cells and myo-fibrocytes. HIF-1α was mainly expressed in the cytoplasm of tumor interstitial cells. HIF-1α was highly expressed where Fusobacterium nucleatum was densely distributed. Conclusion. According to our study, the detected amount of Fusobacterium in OSCC tumor tissues was significantly larger than that in tumor distant normal tissues, and Fusobacterium nucleatum might aggravate inflammation and hypoxia by interacting with NF-κB and HIF-1α in OSCC

Impact of forest fire on radial growth of tree rings and their element concentrations of Pinus sylvestris and Larix gmelinii in northern China

AimsThrough analyzing the responses of the radial growth and element concentrations (B, Mg, Al, K, Ca, Mn, Fe, Zn, Na, P, Ni, and Cu) of tree rings of two dominant tree species to forest fires, we aimed to investigate the relationship between tree rings and the fires. MethodsWe sampled wood cores of Pinus sylvestris and Larix gmelinii in the northern forest region of China, where forest fires happened in 1990 and 2008. The ring-width growth of P. sylvestris and L. gmelinii from 1986 to 1995 and 2004 to 2013 in two sites of Tahe County were measured. Element concentrations in tree rings were determined using inductively coupled plasma mass spectrometry (ICP-MS). ResultsOur results showed that tree-ring radial growth was largely reduced after the fire, together with the increase in concentrations of B, Al, Mn, and Fe but the decrease in some samples in K. Strong correlations were observed between tree-ring growth and concentrations of Mg and Mn of P. sylvestris and Znof L. gmelinii. DiscussionThe results provide evidence that variations in tree-ring growth and element concentrations, particularly concentrations of B, Al, Mn, and Fe, are potentially useful to monitor forest fires, which add new insights into the study of forest fire history

Implications of C1q/TNF-related protein superfamily in patients with coronary artery disease.

The C1q complement/TNF-related protein superfamily (CTRPs) displays differential effects on the regulation of metabolic homeostasis, governing cardiovascular function. However, whether and how they may serve as predictor/pro-diagnosis factors for assessing the risks of coronary artery disease (CAD) remains controversial. Therefore, we performed a clinical study to elaborate on the implication of CTRPs (CTRP1, CTRP5, CTRP7, and CTRP15) in CAD. CTRP1 were significantly increased, whereas CTRP7 and CTRP15 levels were decreased in CAD patients compared to the non-CAD group. Significant differences in CTRP1 levels were discovered between the single- and triple-vascular-vessel lesion groups. ROC analysis revealed that CTRP7 and CTRP15 may serve as CAD markers, while CTRP1 may serve as a marker for the single-vessel lesion of CAD. CTRP1 and CTRP5 can serve as markers for the triple-vessel lesion. CTRP1 may serve as an independent risk predictor for triple-vessel lesion, whereas CTRP15 alteration may serve for a single-vessel lesion of CAD. CTRP1 may serve as a novel superior biomarker for diagnosis of severity of vessel-lesion of CAD patients. CTRP7, CTRP15 may serve as more suitable biomarker for the diagnosis of CAD patients, whereas CTRP5 may serve as an independent predictor for CAD. These findings suggest CTRPs may be the superior predictive factors for the vascular lesion of CAD and represent novel therapeutic targets against CAD

Determination of key enzymes for threonine synthesis through in vitro metabolic pathway analysis

Figure S1. The pathway flux (J) in the in vitro system when one enzyme concentration was increased. (A) The pathway flux when purified ThrA was added to the crude enzyme extract. (B) The pathway flux when purified Asd was added to the crude enzyme extract. (C) The pathway flux when purified ThrB was added to the crude enzyme extract. (D) The pathway flux when purified ThrC was added to the crude enzyme extract

Anthropogenic influence on 2018 summer persistent heavy and daily extreme rainfall in central western China

Anthropogenic forcing has reduced the probability of summer persistent heavy rainfall in central western China similar to 2018 by ~47%, but increased that of daily extremes by ~1.5 times, based on HadGEM3-GA6 ensembles

Programmed cell death and lipid metabolism of macrophages in NAFLD

Non-alcoholic fatty liver disease (NAFLD) has now become the leading chronic liver disease worldwide with lifestyle changes. This may lead to NAFLD becoming the leading cause of end-stage liver disease in the future. To date, there are still no effective therapeutic drugs for NAFLD. An in-depth exploration of the pathogenesis of NAFLD can help to provide a basis for new therapeutic agents or strategies. As the most important immune cells of the liver, macrophages play an important role in the occurrence and development of liver inflammation and are expected to become effective targets for NAFLD treatment. Programmed cell death (PCD) of macrophages plays a regulatory role in phenotypic transformation, and there is also a certain connection between different types of PCD. However, how PCD regulates macrophage polarization has still not been systematically elucidated. Based on the role of lipid metabolic reprogramming in macrophage polarization, PCD may alter the phenotype by regulating lipid metabolism. We reviewed the effects of macrophages on inflammation in NAFLD and changes in their lipid metabolism, as well as the relationship between different types of PCD and lipid metabolism in macrophages. Furthermore, interactions between different types of PCD and potential therapeutic agents targeting of macrophages PCD are also explored

Macrophage CGI-58 Deficiency Activates ROS-Inflammasome Pathway to Promote Insulin Resistance in Mice

SummaryOvernutrition activates a proinflammatory program in macrophages to induce insulin resistance (IR), but its molecular mechanisms remain incompletely understood. Here, we show that saturated fatty acid and lipopolysaccharide, two factors implicated in high-fat diet (HFD)-induced IR, suppress macrophage CGI-58 expression. Macrophage-specific CGI-58 knockout (MaKO) in mice aggravates HFD-induced glucose intolerance and IR, which is associated with augmented systemic/tissue inflammation and proinflammatory activation of adipose tissue macrophages. CGI-58-deficient macrophages exhibit mitochondrial dysfunction due to defective peroxisome proliferator-activated receptor (PPAR)γ signaling. Consequently, they overproduce reactive oxygen species (ROS) to potentiate secretion of proinflammatory cytokines by activating NLRP3 inflammasome. Anti-ROS treatment or NLRP3 silencing prevents CGI-58-deficient macrophages from oversecreting proinflammatory cytokines and from inducing proinflammatory signaling and IR in the cocultured fat slices. Anti-ROS treatment also prevents exacerbation of inflammation and IR in HFD-fed MaKO mice. Our data thus establish CGI-58 as a suppressor of overnutrition-induced NLRP3 inflammasome activation in macrophages