Growth and feeding rates of the newly hatched larval ctenophore Mnemiopsis leidyi A. Agassiz (Ctenophora, Lobata)

Mnemiopsis leidyi: larvae depend on microplankton (<200 µm) prey duringthe first few days following hatching until larvae are >0.5mm in length and can successfully capture and consume mesozooplanktonprey. Feeding and growth rates of newly hatched M. leidyi larvaewere measured in controlled laboratory experiments. When fednatural microplankton assemblages, newly hatched larvae consumedsignificant quantities of both autotrophic and heterotrophicprey, including diatoms, phototrophic, heterotrophic and mixotrophicdinoflagellates, euglenoid flagellates, aloricate and tintinnidciliates, and rotifers. Average per capita clearance rates were1.99–7.59 mL individual^–1 h^–1 ( = 4.01 mL individual^–1 h^–1; SD = 1.95)and total per capita ingestion was 0.01–4.70 µgC individual^–1 day^–1 x 10² ( = 0.83 µg C individual^–1 day^–1 x 10²; SD =1.89). Larval growth rates were –0.13 to 0.56 mm individual^–1day^–1 (equivalent to –1.72 to 4.33 µg C individual^–1day^–1) over a range of larval sizes from 0.5 (<0.5µg C) to 5 mm (85 µg C). A diet consisting entirelyof microplankton prey supported larval growth for >2 weeks,and growth rate decreased when larvae reached 4–5 mm inlength, corresponding to the beginning of their morphologicaltransition from tentaculate to lobate feeding mode. The grossgrowth efficiency of larvae fed natural microplankton assemblageswas 3%.     

Ectoparasites of Chevrier's field mouse, Apodemus chevrieri, in a focus of plague in southwest China

Chevrier's field mouse, Apodemus chevrieri Milne-Edwards (Rodentia: Muridae), has been identified as the main wild reservoir of plague in the sylvatic plague focus of Yunnan Province, southwest China. Here, the ectoparasite communities of A. chevrieri and the potential medical and veterinary importance of these ectoparasites are described. A high proportion (66%) of 321 mice were found to be infested with ectoparasites. A total of 81 species of ectoparasite, including 48 species of chigger mite, 25 species of mesostigmatid (gamasid) mite, six species of flea and two species of sucking louse were collected. Most species of ectoparasite were relatively uncommon, but a few were abundant. Within this ectoparasite complex, 16 species have previously been reported to be vectors of human disease agents. Apodemus chevrieri would appear therefore to be a natural reservoir for plague bacilli and epidemic haemorrhagic fever (Korean haemorrhagic fever) viruses.     

四川石棉县蝴蝶资源调查报告

报道四川石棉城区及5个乡的蝶类调查情况。通过10多年的调查和标本采集,获标本600余号,整理出10科99种。     

CircRNA fibroblast growth factor receptor 3 promotes tumor progression in non-small cell lung cancer by regulating Galectin-1-AKT/ERK1/2 signaling

The dysregulation of circular RNA (circRNA) expression is involved in the progression of several cancers, including non-small cell lung cancer (NSCLC). However, the role and underlying molecular mechanisms of circRNA FGFR3 (circFGFR3) in NSCLC progression remains unknown. Here, we used quantitative real-time polymerase chain reaction to validate that circFGFR3 expression was higher in NSCLC tissues than in the paratumor tissues. Furthermore, our study indicated that the forced circFGFR3 expression promoted NSCLC cell invasion and proliferation. Mechanistically, we found that circFGFR3 promoted NSCLC cell invasion and proliferation via competitively combining with miR-22-3p to facilitate the galectin-1 (Gal-1), p-AKT, and p-ERK1/2 expressions. Clinically, we revealed that the high circFGFR3 expression correlates with the poor clinical outcomes in patients with NSCLC. Together, these data provide mechanistic insights into the circFGFR3-mediated regulation of both the AKT and ERK1/2 signaling pathways by sponging miR-22-3p and increasing Gal-1 expression.     

Downregulation of long non-coding RNA TUG1 suppresses tumor growth by promoting ubiquitination of MET in diffuse large B-cell lymphoma

Molecular and Cellular Biochemistry - Long non-coding RNAs (lncRNAs) can modulate gene expression through different mechanisms, but the fundamental molecular mechanism between lncRNAs and MET...     

Mutations in CKAP2L,the Human Homolog of the Mouse Radmis Gene,Cause Filippi Syndrome

Filippi syndrome is a rare, presumably autosomal-recessive disorder characterized by microcephaly, pre- and postnatal growth failure, syndactyly, and distinctive facial features, including a broad nasal bridge and underdeveloped alae nasi. Some affected individuals have intellectual disability, seizures, undescended testicles in males, and teeth and hair abnormalities. We performed homozygosity mapping and whole-exome sequencing in a Sardinian family with two affected children and identified a homozygous frameshift mutation, c.571dupA (p.Ile191Asnfs^∗6), in CKAP2L, encoding the protein cytoskeleton-associated protein 2-like (CKAP2L). The function of this protein was unknown until it was rediscovered in mice as Radmis (radial fiber and mitotic spindle) and shown to play a pivotal role in cell division of neural progenitors. Sanger sequencing of CKAP2L in a further eight unrelated individuals with clinical features consistent with Filippi syndrome revealed biallelic mutations in four subjects. In contrast to wild-type lymphoblastoid cell lines (LCLs), dividing LCLs established from the individuals homozygous for the c.571dupA mutation did not show CKAP2L at the spindle poles. Furthermore, in cells from the affected individuals, we observed an increase in the number of disorganized spindle microtubules owing to multipolar configurations and defects in chromosome segregation. The observed cellular phenotypes are in keeping with data from in vitro and in vivo knockdown studies performed in human cells and mice, respectively. Our findings show that loss-of-function mutations in CKAP2L are a major cause of Filippi syndrome.     

Sex- and age-dependent effects of Gpr30 genetic deletion on the metabolic and cardiovascular profiles of diet-induced obese mice

The G protein-coupled receptor 30 (GPR30) has been claimed as an estrogen receptor. However, the literature reports controversial findings and the physiological function of GPR30 is not fully understood yet. Consistent with studies assigning a role of GPR30 in the cardiovascular and metabolic systems, GPR30 expression has been reported in small arterial vessels, pancreas and chief gastric cells of the stomach. Therefore, we hypothesized a role of GPR30 in the onset and progression of cardiovascular and metabolic diseases. In order to test our hypothesis, we investigated the effects of a high-fat diet on the metabolic and cardiovascular profiles of Gpr30-deficient mice (GPR30-lacZ mice). We found that GPR30-lacZ female, rather than male, mice had significant lower levels of HDL along with an increase in fat liver accumulation as compared to control mice. However, two indicators of cardiac performance assessed by echocardiography, ejection fraction and fractional shortening were both decreased in an age-dependent manner only in Gpr30-lacZ male mice. Collectively our results point to a potential role of Gpr30 in preserving lipid metabolism and cardiac function in a sex- and age-dependent fashion.     

Targeting IL-10 in Auto-immune Diseases

IL-10 is a multifunctional cytokine secreted by a variety of cells. It not only inhibits activation of monocyte/macrophage system and synthesis of monocyte cytokine and inflammatory cytokine but also promotes the proliferation and maturation of non-monocyte-dependent T cell, stimulating proliferation of antigen-specific B cell. Increasing evidence indicates that IL-10 plays an important role in both the onset and development of auto-immune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjogren’s syndrome (SS), multiple sclerosis (MS), Crohn’s disease (CD), and psoriasis. However, the exact mechanisms of IL-10 in auto-immune diseases remain unclear. In the present review, we will summarize the biological effects of IL-10, as well as its role and therapeutic potential in auto-immune diseases.