Improving Tribological Properties of Multialkylated Cyclopentanes under Simulated Space Environment: Two Feasible Approaches

Space mechanisms require multialkylated cyclopentanes (MACs) more lubricious, more reliable, more durable, and better adaptive to harsh space environments. In this study, two kinds of additives were added into MACs for improving the tribological properties under simulated space environments: (a) solid nanoparticles (tungsten disulfide (WS₂), tungsten trioxide (WO₃), lanthanum oxide (La₂O₃), and lanthanum trifluoride (LaF₃)) for steel/steel contacts; (b) liquid additives like zinc dialkyldithiophosphate (ZDDP) and molybdenum dialkyldithiocarbamate (MoDTC) for steel/steel and steel/diamond-like carbon (DLC) contacts. The results show that, under harsh simulated space environments, addition of the solid nanoparticles into MACs allows the wear to be reduced by up to one order magnitude, while liquid additives simultaneously reduce friction and wear by 80% and 93%, respectively. Friction mechanisms were proposed according to surface/interface analysis techniques, such as X-ray photoelectron spectroscopy (XPS) and time-of-flight secondary ion mass spectroscopy (TOF-SIMS). The role of solid nanoparticles in reducing friction and wear mainly depends on their surface enhancement effect, and the liquid additives are attributed to the formation of tribochemical reaction film derived from ZDDP and MoDTC on the sliding surfaces

Simultaneous Removal of Soot and NO<i>_x</i> from Diesel Engines over Three-Dimensionally Ordered Macroporous ZSM-5-Supported MMnO_δ Catalysts

Three-dimensionally ordered macroporous (3DOM) ZSM-5 support was successfully designed and synthesized via a combination of seed- and steam-assisted methods. In addition, MMnOδ/3DOM ZSM-5 (M = Fe, Co, Ce, Pr, and W) catalysts were prepared using ZSM-5 as a carrier and showed good catalytic performance, which may be due to the catalysts’ unique pore structures and interactions between M and Mn. 3DOM ZSM-5-supported PrMnOδ possesses the best reaction performance for soot oxidation, with a lowest peak temperature of 430 °C, and the best low-temperature denitration performance, with a temperature window of 149–336 °C when NO conversion is 80%. This may be due to the catalyst’s better redox performance, abundant active oxygen and acidic sites, and the higher content of Mn4+ and OII/OI ratio compared with the other MMnOδ/3DOM ZSM-5 catalysts. Meanwhile, the high turnover frequency and low Ea over 3DOM ZSM-5-supported PrMnOδ also contributed to its high intrinsic activity. The corresponding reaction mechanisms were proposed according to in situ diffuse reflectance infrared Fourier transform spectroscopy analysis and other characterizations. At low temperature (<300 °C), the selective catalytic reduction reaction follows the Eley–Rideal and Langmuir–Hinshelwood mechanisms. At a high temperature, the mechanisms for soot combustion include active oxygen oxidation and NO2-assisted mechanisms

Decreased TUSC3 Promotes Pancreatic Cancer Proliferation, Invasion and Metastasis

<div><p>Pancreatic cancer is an aggressive disease with dismal prognosis. It is of paramount importance to understand the underlying etiological mechanisms and identify novel, consistent, and easy-to-apply prognostic factors for precision therapy. TUSC3 (tumor suppressor candidate 3) was identified as a potential tumor suppressor gene and previous study showed TUSC3 is decreased in pancreatic cancer at mRNA level, but its putative tumor suppressor function remains to be verified. In this study, TUSC3 expression was found to be suppressed both at mRNA and protein levels in cell line models as well as in clinical samples; decreased TUSC3 expression was associated with higher pathological TNM staging and poorer outcome. In three pairs of cell lines with different NF-κB activity, TUSC3 expression was found to be reversely correlated with NF-κB activity. TUSC3-silenced pancreatic cancer cell line exhibited enhanced potential of proliferation, migration and invasion. In an orthotopic implanted mice model, TUSC3 silenced cells exhibited more aggressive phenotype with more liver metastasis. In conclusion, the current study shows that decreased immunological TUSC3 staining is a factor prognostic of poor survival in pancreatic cancer patients and decreased TUSC3 promotes pancreatic cancer cell proliferation, invasion and metastasis. The reverse correlation between NF-κB activity and TUSC3 expression may suggest a novel regulation pattern for this molecule.</p></div

Decreased TUSC3 Promotes Pancreatic Cancer Proliferation, Invasion and Metastasis - Fig 3

<p><b>TUSC3 is decreased in pancreatic cancer cell lines both at mRNA level (A) and protein level (B)</b>.</p

TUSC3 expression is associated with clinical pathological staging and Ki67 index.

<p>TUSC3 expression is associated with clinical pathological staging and Ki67 index.</p

Decreased TUSC3 expression promotes tumor cell growth, migration and invasion.

<p>(A, B)TUSC3 is effectively knocked-down in Colo357 cell lines shown by (A) RT-PCR and (B) Western blot. (C, D) Proliferation is enhanced with TUSC3 knockdown, cell number counts are significantly different at 72 hours (Colo357 TUSC3 shRNA2 vs Colo357 Scramble p = 0.0086, Colo357 TUSC3 shRNA3 vs Colo357 Scramble p = 0.0011) (D). (E, F) Colony Formation is enhanced with TSUC3 knockdown (Colo357 TUSC3 shRNA2 vs Colo357 Scramble p<0.0001, Colo357 TUSC3 shRNA3 vs Colo357 Scramble p<0.0001). (G) Migration Test(Colo357 TUSC3 shRNA2 vs Colo357 Scramble p<0.0001, Colo357 TUSC3 shRNA3 vs Colo357 Scramble p<0.0001). (H, I) Invasion Test (Colo357 TUSC3 shRNA2 vs Colo357 Scramble p<0.0001, Colo357 TUSC3 shRNA3 vs Colo357 Scramble p<0.0001). (J) Wound healing test showed more rapid closure of the gap in TUSC3 silenced cells. All experiments were performed three times with representative figures shown as above.</p

Univariate and Multivariate Cox Proportional Hazard Analysis of Factors Affecting Recurrence-free and Overall Survival in Pancreatic Cancer.

<p>Univariate and Multivariate Cox Proportional Hazard Analysis of Factors Affecting Recurrence-free and Overall Survival in Pancreatic Cancer.</p

TUSC3 is regulated by NF-κB activity shown by three pairs of pancreatic cancer cell lines.

<p>(A) AsPC-1 and AsPC-1 mu with depressed NF-κB activity. (B) MDA p28 and MDA p28 mu with depressed NF-κB activity. (C) Colo357 and the daughter L3.6pl cell line with enhanced NF-κB activity. For each figure, left graph represents RT-PCR result, right graph represents Western blot for TUSC3.</p

TUSC3 is decreased in pancreatic cancer samples.

<p>(A) TUSC3 expression in non-neoplastic pancreatic tissues (acinar, duct and islets). (B) TUSC3 expression in pancreatic cancer cells. (C) Low TUSC3 expression in pancreatic cancer cells compared to islets. (D) Comparison of TUSC3 staining in primary PC and LN metastasis(paired t-test, p<0.001, n = 58). Original magnification×200.</p

TUSC3 silenced pancreatic tumor cells exhibit more potential of liver metastasis in an orthotopic Balb/C nude mouse model.

<p>(A) Gross appearance of the resected liver specimens from mice injected with two groups of TUSC3 silenced PC (Colo357 shRNA2 and Colo357 shRNA3) and control (Colo357 Scramble). Large liver metastases are visible in group Colo357 shRNA2 and Colo357 shRNA3. (B) The liver metastases were weighted and compared using t-test.</p