Cuticular reticulation replicates the pattern of epidermal cells in lowermost Cambrian scalidophoran worms.

The cuticle of ecdysozoans (Panarthropoda, Scalidophora, Nematoida) is secreted by underlying epidermal cells and renewed via ecdysis. We explore here the relationship between epidermis and external cuticular ornament in stem-group scalidophorans from the early Cambrian of China (Kuanchuanpu Formation; ca 535 Ma) that had two types of microscopic polygonal cuticular networks with either straight or microfolded boundaries. Detailed comparisons with modern scalidophorans (priapulids) indicate that these networks faithfully replicate the cell boundaries of the epidermis. This suggests that the cuticle of early scalidophorans formed through the fusion between patches of extracellular material secreted by epidermal cells, as observed in various groups of present-day ecdysozoans, including arthropods. Key genetic, biochemical and mechanical processes associated with ecdysis and cuticle formation seem to have appeared very early (at least not later than 535 Ma) in the evolution of ecdysozoans. Microfolded reticulation is likely to be a mechanical response to absorbing contraction exerted by underlying muscles. The polygonal reticulation in early and extant ecdysozoans is clearly a by-product of the epidermal cell pavement and interacted with the sedimentary environment.

Hsa-miRNA-143-3p Reverses Multidrug Resistance of Triple-Negative Breast Cancer by Inhibiting the Expression of Its Target Protein Cytokine-Induced Apoptosis Inhibitor 1 In Vivo.

PURPOSE: Multidrug resistance (MDR) remains a major obstacle in the treatment of triple-negative breast cancer (TNBC) with conventional chemotherapeutic agents. A previous study demonstrated that hsa-miRNA-143-3p plays a vital role in drug resistance of TNBC. Downregulation of hsa-miRNA-143-3p upregulated the expression of its target protein cytokine-induced apoptosis inhibitor 1 (CIAPIN1) in order to activate MDR, while upregulation of hsa-miRNA-143-3p effectively enhances the sensitivity of drug-resistant TNBC cells to chemotherapeutics. The present study aimed to further verify these findings in vivo. METHODS: We established a hypodermic tumor nude mice model using paclitaxel-resistant TNBC cells. We expressed ectopic hsa-miRNA-143-3p under the control of a breast cancer-specific human mammaglobin promoter that guided the efficient expression of exogenous hsa-miRNA-143-3p only in breast cancer cells. Thereafter, we overexpressed hsa-miRNA-143-3p in xenografts using a recombinant virus system and quantified the expression of hsa-miRNA-143-3p, CIAPIN1 protein, and proteins encoded by related functional genes by western blot. RESULTS: We successfully completed the prospective exploration of the intravenous virus injection pattern from extensive expression to targeted expression. The overexpression of hsa-miRNA-143-3p significantly alleviated chemoresistance of TNBC by inhibiting viability. In addition, we observed that the expression of CIAPIN1 as a hsa-miRNA-143-3p target protein was remarkably decreased. CONCLUSION: We partly illustrated the mechanism underlying the hsa-miRNA-143-3p/CIAPIN1 drug resistance pathway. HsamiRNA-143-3p as a tumor suppressive microRNA may be a novel target to effectively reverse MDR of TNBC in vivo.

Cardiac Fibroblast-Specific Activating Transcription Factor 3 Promotes Myocardial Repair after Myocardial Infarction.

BACKGROUND: Myocardial ischemia injury is one of the leading causes of death and disability worldwide. Cardiac fibroblasts (CFs) have central roles in modulating cardiac function under pathophysiological conditions. Activating transcription factor 3 (ATF3) plays a self-protective role in counteracting CF dysfunction. However, the precise function of CF-specific ATF3 during myocardial infarction (MI) injury/repair remains incompletely understood. The aim of this study was to determine whether CF-specific ATF3 affected cardiac repair after MI. METHODS: Fifteen male C57BL/6 wild-type mice were performed with MI operation to observe the expression of ATF3 at 0, 0.5, 1.0, 3.0, and 7.0 days postoperation. Model for MI was constructed in ATF3TGfl/flCol1a2-Cre+ (CF-specific ATF3 overexpression group, n = 5) and ATF3TGfl/flCol1a2-Cre- male mice (without CF-specific ATF3 overexpression group, n = 5). In addition, five mice of ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre- were subjected to sham MI operation. Heart function was detected by ultrasound and left ventricular remodeling was observed by Masson staining (myocardial fibrosis area was detected by blue collagen deposition area) at the 28th day after MI surgery in ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre- mice received sham or MI operation. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect cell proliferation/cell cycle-related gene expression in cardiac tissue. BrdU staining was used to detect fibroblast proliferation. RESULTS: After establishment of an MI model, we found that ATF3 proteins were increased in the heart of mice after MI surgery and dominantly expressed in CFs. Genetic overexpression of ATF3 in CFs (ATF3TGfl/flCol1a2-Cre+ group) resulted in an improvement in the heart function as indicated by increased cardiac ejection fraction (41.0% vs. 30.5%, t = 8.610, P = 0.001) and increased fractional shortening (26.8% vs. 18.1%, t = 7.173, P = 0.002), which was accompanied by a decrease in cardiac scar area (23.1% vs. 11.0%, t = 8.610, P = 0.001). qRT-PCR analysis of CFs isolated from ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre- ischemic hearts revealed a distinct transcriptional profile in ATF3-overexpressing CFs, displaying pro-proliferation properties. BrdU-positive cells significantly increased in ATF3-overexpressing CFs than control CFs under angiotensin II stimuli (11.5% vs. 6.8%, t = 31.599, P = 0.001) or serum stimuli (31.6% vs. 20.1%, t = 31.599, P = 0.001). The 5(6)-carboxyfluorescein N-hydroxysuccinimidyl ester assay showed that the cell numbers of the P2 and P3 generations were higher in the ATF3-overexpressing CFs at 24 h (P2: 91.6% vs. 71.8%, t = 8.465, P = 0.015) and 48 h (P3: 81.6% vs. 51.1%, t = 9.029, P = 0.012) after serum stimulation. Notably, ATF3 overexpression-induced CF proliferation was clearly increased in the heart after MI injury. CONCLUSIONS: We identify that CF-specific ATF3 might contribute to be MI repair through upregulating the expression of cell cycle/proliferation-related genes and enhancing cell proliferation.

A Clinical Observation of Thymic Epithelial Tumor Metastatic to Breast.

BACKGROUND: Thymic carcinoma is prone to early metastasis and invasion, while its metastasis to the breast is particularly unique. CASE REPORT: We describe a case of thymic epithelial tumor metastatic to the breast fulfilling clinical diagnostic criteria. A 47-year-old female patient diagnosed with stage IV thymic carcinoma and previously treated with chemoradiation was diagnosed with metastatic breast cancer during a periodic review. Color Doppler ultrasonography showed a low-echo real occupancy in the breast. Pathological examination of the breast mass confirmed the diagnosis of thymic carcinoma metastasis. CONCLUSION: Hematogenous metastasis of thymic carcinoma to the breast is rare but not exceptional, and long-term survival can be expected with appropriate treatment.

[Effects of Phenol on Activity and Microfauna Community Structure of Activated Sludge].

In order to investigate the effects of phenol on activity and microfauna community structure of activated sludge, phenol with different concentrations were added into the wastewater for activated sludge culturing in a SBR reactor, then the activity parameters of TTC-ETS and INT-ETS of activated sludge were measured, and the dynamics of microfauna community was analyzed. The results indicated that TTC-ETS activity was more applicable to evaluate the effects of phenol on sludge activity than INT-ETS activity. The higher the concentration of phenol was, the more seriously the sludge activity was inhibited. When 50 mg·L-1 of phenol was added into the influent, the inhibition rate of sludge activity was (20.75±10.43)%, while it increased to (39.73±26.92)% with a great fluctuation at the phenol concentration of 100 mg·L-1. The inhibition rate of sludge activity fluctuated at about 40% in the later period of sludge culturing with 300 mg·L-1 of phenol. The inhibitory effects on microfauna community in activated sludge increased with increasing phenol concentration. Phenol had different effects on various groups of microfauna community, i.e., only one group (testate amoebae) was inhibited significantly at a low feeding concentration of phenol, many groups (sessile ciliates, testate amoebae, crawling ciliates, carnivorous ciliates) were inhibited at the phenol concentrations of 100 mg·L-1 and 300 mg·L-1, whereas a few groups (flagellates, nematodes, etc.) were promoted at the phenol concentration of 300 mg·L-1. There was a certain degree of relationship between sludge activity and microfauna under the influence of phenol, which means that Centropyxis aculeata, Plagiocampa mutabilis etc., may be bio-indicators for low sludge activity, and Epistylis lacustris, Bodo lens and Pleuromonas jaculans can be used as bio-indicators for high sludge activity in the activated sludge used to treat phenolic wastewater.

[Study on baking processing technology of hui medicine Aconitum flavum].

OBJECTIVE: To screen and optimize the processing technology of Aconitum flavum. METHODS: The acute-toxicity, anti-inflammatory and analgesic experiments were used as indexes. Four processing methods, including decoction, streaming, baking and processing with Chebulae Fructus decoction, were compared to screen the optimum processing method for Aconitum flavum. The baking time was also optimized. RESULTS: The optimal baked technology was that 1-2 mm decoction pieces was baked at 105 degrees C for 3 hours. CONCLUSION: The baking method is proved to be the optimal processing method of Aconitum flavum. It is shown that this method is simple and stable.