Discriminative Grandparental Investment in China : Evidence from an Undergraduate Questionnaire Study.

Many studies in Western societies show a pattern of discriminative grandparental investment as follows: maternal grandmothers (MGMs) > maternal grandfathers (MGFs) > paternal grandmothers (PGMs) > paternal grandfathers (PGFs). This pattern is in line with the expectation from evolutionary reasoning. Yet whether or not this pattern applies in China is in question. The present study was based on a questionnaire survey at a university in Central China (N = 1,195). Results show that (1) when grandparent-grandchild residential distance during grandchildren's childhood is controlled, in the case of grandsons and granddaughters as a whole and granddaughters only, both grandparental caregiving and grandchildren's emotional closeness to grandparents display a rank order of MGM > MGF > PGM > PGF, but in the case of grandsons only, this order is not statistically significant. (2) There are stable relationships between grandparental caregiving/grandchildren's emotional closeness and residential distance/similarity in appearance. (3) The effects of residential distance on either PGFs' or PGMs' caregiving exceed those on either MGFs' or MGMs'. (4) The PGF and PGM prefer grandsons to granddaughters in their caregiving, whereas the MGF and MGM do not have a sex preference, and (5) the fact that the PGF and PGM invest more in grandsons than in granddaughters does not depend on grandsons' duration of living in a rural area. Our results suggest that (1) in general, the Chinese display a pattern of differential grandparental investment predicted by an evolutionary perspective, (2) the evolutionary perspective that combines the two factors of paternal uncertainty and sex-specific reproductive strategies is applicable to grandparental investment in China, and (3) the traditional son-preference culture also plays some role in affecting grandparental investment in China, though the roles of culture and urban-rural cultural difference should not be exaggerated.

Reduced smooth muscle-fibroblasts transformation potentially decreases intestinal wound healing and colitis-associated cancer in ageing mice.

Cancer and impaired tissue wound healing with ageing are closely related to the quality of life of the elderly population. Given the increased incidence of cancer and the population ageing trend globally, it is very important to explore how ageing impairs tissue wound healing and spontaneous cancer. In a murine model of DSS-induced acute colitis and AOM/DSS-induced colitis-associated cancer (CAC), we found ageing significantly decreases intestinal wound healing and simultaneous CAC initiation, although ageing does not affect the incidence of AOM-induced, sporadic non-inflammatory CRC. Mechanistically, reduced fibroblasts were observed in the colitis microenvironment of ageing mice. Through conditional lineage tracing, an important source of fibroblasts potentially derived from intestinal smooth muscle cells (ISMCs) was identified orchestrating intestinal wound healing and CAC initiation in young mice. However, the number of transformed fibroblasts from ISMCs significantly decreased in ageing mice, accompanied by decreased intestinal wound healing and decreased CAC initiation. ISMCs-fibroblasts transformation in young mice and reduction of this transformation in ageing mice were also confirmed by ex-vivo intestinal muscular layer culture experiments. We further found that activation of YAP/TAZ in ISMCs is required for the transformation of ISMCs into fibroblasts. Meanwhile, the reduction of YAP/TAZ activation in ISMCs during intestinal wound healing was observed in ageing mice. Conditional knockdown of YAP/TAZ in ISMCs of young mice results in reduced fibroblasts in the colitis microenvironment, decreased intestinal wound healing and decreased CAC initiation, similar to the phenotype of ageing mice. In addition, the data from intestine samples derived from inflammatory bowel disease (IBD) patients show that activation of YAP/TAZ also occurs in ISMCs from these patients. Collectively, our work reveals an important role of the ageing stromal microenvironment in intestinal wound healing and CAC initiation. Furthermore, our work also identified a potential source of fibroblasts involved in colitis and CAC.

Emerging roles of circular RNAs in tuberculosis.

Tuberculosis (TB) remains a major global health issue, resulting in around 1.5 million people deaths each year. Better diagnostic and therapeutic tools are urgently needed. Circular RNAs (circRNAs) are a new class of noncoding RNAs with a covalently closed structure, and exhibit a tissue-, cell-, and developmental stage-specific expression pattern. Recently, circRNAs were thought to be regulatory molecules implicated in the onset and progression of a series of human diseases including tuberculosis. In tuberculosis, circRNAs have been shown to regulate host anti-TB immune responses, such as decreasing monocyte apoptosis, enhancing autophagy and promoting macrophage polarization. Importantly, circRNAs are physically stable and abundant in several types of body fluids. Therefore they are considered as promising minimally-invasive biomarkers. In this review, we focus on the recent advances in the immune regulatory roles of circRNAs, as well as their potential diagnostic value in TB.

[Effects of Msp on the Proliferation, Migration and Invasion of Human Non-small Cell Lung Cancer Cells].

OBJECTIVES: To determine the effects of macrophage stimulating protein (Msp) on the proliferation, migration and invasion of human non-small cell lung cancer cells PC14. METHODS: The eukaryotic expression vector for st1was constructed and transfected into Msp(-)and RON(-)human non-small cell lung cancer cells PC14. The expression of st1mRNA in PC14 cells was observed by RT-PCR. The expression levels of Msp protein in PC14, PC14-st1-pEGFP-N1 and PC14-pEGFP-N1 groups as well as the expression of RON in PC14 and SKBR-3 cells were detected by Western blot. RAW264.7 (mouse monocyte macrophage) and SKBR-3 cells were cultured in the supernatant of cells(PC14, PC14-st1-pEGFP-N1and PC14-pEGFP-N1 groups)and tested with Transwell microporous membrane, through which the biologic activity of Msp was evaluated by calculating the cell number migrated. The proliferation of PC14 was measured by MTT assay. The capabilities of PC14 to migrate and invade were measured by Transwell chamber and Matrigel invasion tests, respectively. RESULTS: The expressions of mRNA and protein of Mst1 in PC14 were stable after transfection with Mst1. Msp (PC14-st1 -pEGFP-N1 group) promoted the migration of RON (+) cells (SKBR-3 and RAW264.7). Compared with PC14 and PC14-pEGFP-N1 groups, the proliferation, migration and invasion of PC14 cells in PC14-st1 -pEGFP-N1 group were inhibited significantly. CONCLUSIONS: Msp can promote the migration of RON (+) cancer cells in paracrine secretion manner and inhibit the proliferation, migration and invasion of human non-small cell lung cancer cells PC14 in an unknown way.

[The Correlation Between MicroRNAs in Serum and the Extent of Liver Injury].

OBJECTIVES: To investigate the correlation between the absolute quantification of the microRNAs (miR-122, miR-451, miR-92a, miR-192) in serum during acute liver injury and the extent of liver injury on rat models of CCl4 induced acute liver injury and mice models of acetaminophen (APAP) induced acute liver injury. Furthermore, to investigate the correlation between the absolute quantification of microRNAs in serum and the drug induced liver injury pathological scoring system (DILI-PSS). METHODS: The acute liver injury model in rat by CCl4 (1.5 mL/kg), and the acute liver injury model in mice by APAP (160 mg/kg) were established. The serum at different time points on both models were collected respectively. The absolute quantification of microRNAs in serum were detected by using MiRbayTM SV miRNA Assay kit. Meanwhile, the pathological sections of liver tissue of the mice at each time point were collected to analyze the correlation between microRNAs and the degree of liver injury. RESULTS: In CCl4-induced rat acute liver injury model and APAP induced mouse acute liver injury, miR-122 and miR-192 appeared to be rising significantly, which remained the highest level at 24 h after treatment, and declined to the normal level after 72 h. In CCl4-induced rat acute liver injury model, the change of miR-92a was fluctuated and had no apparent rules, miR-451 declined gradually, but not obviously. In mice acute liver injury model induced by APAP, miR-92a and miR-451 in the progress of liver injury declined gradually, reached the lowest point at 48 h, and then recovered. The result of correlation analysis indicated that miR-122 and miR-192 presented a good positive correlation with the DILI-PSS ( r=0.741 3, P<0.05; r=0.788 3, P<0.01). CONCLUSIONS: The absolute quantification of miR-122 and miR-192 in serum has the highest level in 24 h, then decrease in 72 h, in both drug-induced and chemical liver injury. In addition, both the two microRNAs have good correlation with DILI-PSS in APAP-induced liver injury models.