In-situ study of the influence of additives on the growth behavior of copper electrodeposits on copper single crystal

Trace organic additives are known to be essential in obtaining desired metal electrodeposits in the microelectronic industry, however, fundamental design principles for their use and a scientific understanding of their interaction during electrodeposition is lacking. In the present study we investigated electrodeposition of copper on the Cu(100) surface in air-saturated or dearated acid-sulfate plating solutions containing several combinations of chloride and additives benzotriazole (BTA) and 3-mercapto propane sulfonic acid (MPSA) under galvanostatic pulse-current conditions. The electrodeposition process was followed using in-situ atomic force microscopy (AFM). AFM images were quantitatively analyzed by pattern-recognition and scaling procedures. In the absence of additives, copper deposits grew in a layer-by-layer mode from the earliest stage of deposition. The surface consisted of smooth terraces separated by steps. The scaling analysis result was consistent with a process dominated by surface diffusion and step growth. In chloride containing solutions, square-pyramidal mounds were initiated and grew to cover the surface. Mound slope increased with deposition time with no indication of reaching a steady-state value. This growth mode was consistent with a surface diffusion mechanism. The scaling result was similar to the additive-free system, but indicated that surface diffusion was more dominant in the presence of chloride. BTA inhibited the surface and produced nucleation-limited growth at hemispheroidal centers whose height to base radius aspect ratio increased linearly with deposition time. Nucleation and growth of three-dimensional nodules started randomly across the entire surface. The nodules were smaller in size than the mounds observed without BTA. The number and density of nodules were much higher than the mounds density. The deposit growth was dominated by a roughening mechanism that can be described by the random roughening term of a stochastic model. In the presence of MPSA, growth was not confined to nucleation centers, and the (100) symmetry was visible in the main features. However, pyramidal mounds did not develop. None of the existing models described sufficiently the surface growth mechanism for this case. Roughening of copper deposits in oxygen-free solution was faster than in oxygen-saturated solution. The results of scaling analysis and pattern-recognition analysis were in agreement with kinetic studies conducted by other researchers. The presence of dissolved oxygen in solutions did not remarkably affect the scaling behavior for each examined solution

Microorganisms in coastal wetland sediments: a review on microbial community structure, functional gene, and environmental potential

Coastal wetlands (CW) are the junction of the terrestrial and marine ecosystems and have special ecological compositions and functions, which are important for maintaining biogeochemical cycles. Microorganisms inhabiting in sediments play key roles in the material cycle of CW. Due to the variable environment of CW and the fact that most CW are affected by human activities and climate change, CW are severely degraded. In-depth understanding of the community structure, function, and environmental potential of microorganisms in CW sediments is essential for wetland restoration and function enhancement. Therefore, this paper summarizes microbial community structure and its influencing factors, discusses the change patterns of microbial functional genes, reveals the potential environmental functions of microorganisms, and further proposes future prospects about CW studies. These results provide some important references for promoting the application of microorganisms in material cycling and pollution remediation of CW

Inhibition of Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Zeta (YWHAZ) Overcomes Drug Resistance and Tumorigenicity in Ovarian Cancer

Background/Aims: Cancer stem-like cells are the main cause of tumor occurrence, progression, and therapeutic resistance. However, the precise signals required for the maintenance of the stem-like traits of these cells in ovarian cancer remain elusive. We have thus worked to elucidate the functional role of Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ), a gene encoding the 14-3-3ζ protein, in the regulation of multidrug resistance and stem cell-like traits in ovarian cancer. Methods: We detected the YWHAZ levels in human ovarian cancer specimens and cell lines using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blots. MTS assays, soft agar colony formation assays, migration assays, cell cycle analysis, sphere formation assays, and flow cytometry were applied to investigate the functional role of YWHAZ in ovarian cancer. Results: Our data reveals substantially increased YWHAZ expression in both cisplatin- and paclitaxel-resistant ovarian cancer cells. Silencing YWHAZ restored the sensitivity of resistant ovarian cancer cells to cisplatin and paclitaxel. Furthermore, in vitro studies showed that down-regulation of YWHAZ inhibited cell cycle progression, migration, and the expression of stem cell markers. Moreover, tumorigenicity was suppressed in tumor-bearing BALB/c nude mice following YWHAZ knockdown. Additionally, we demonstrated that the expression of YWHAZ was directly down-regulated by miR-30e in resistant ovarian cancer cells. Conclusion: Our results have led to new insights into the essential role of YWHAZ in the regulation of tumourigenesis, stem-like traits, and drug resistance in ovarian cancer, thereby helping to identify a potential target for ovarian cancer therapy

Survival outcomes of stage I colorectal cancer:development and validation of the ACEPLY model using two prospective cohorts

BACKGROUND: Approximately 10% of stage I colorectal cancer (CRC) patients experience unfavorable clinical outcomes after surgery. However, little is known about the subset of stage I patients who are predisposed to high risk of recurrence or death. Previous evidence was limited by small sample sizes and lack of validation. METHODS: We aimed to identify early indicators and develop a risk stratification model to inform prognosis of stage I patients by employing two large prospective cohorts. Prognostic factors for stage II tumors, including T stage, number of nodes examined, preoperative carcinoma embryonic antigen (CEA), lymphovascular invasion, perineural invasion (PNI), and tumor grade were investigated in the discovery cohort, and significant findings were further validated in the other cohort. We adopted disease-free survival (DFS) as the primary outcome for maximum statistical power and recurrence rate and overall survival (OS) as secondary outcomes. Hazard ratios (HRs) were estimated from Cox proportional hazard models, which were subsequently utilized to develop a multivariable model to predict DFS. Predictive performance was assessed in relation to discrimination, calibration and net benefit. RESULTS: A total of 728 and 413 patients were included for discovery and validation. Overall, 6.7% and 4.1% of the patients developed recurrences during follow-up. We identified consistent significant effects of PNI and higher preoperative CEA on inferior DFS in both the discovery (PNI: HR = 4.26, 95% CI: 1.70–10.67, p = 0.002; CEA: HR = 1.46, 95% CI: 1.13–1.87, p = 0.003) and the validation analysis (PNI: HR = 3.31, 95% CI: 1.01–10.89, p = 0.049; CEA: HR = 1.58, 95% CI: 1.10–2.28, p = 0.014). They were also significantly associated with recurrence rate. Age at diagnosis was a prominent determinant of OS. A prediction model on DFS using Age at diagnosis, CEA, PNI, and number of LYmph nodes examined (ACEPLY) showed significant discriminative performance (C-index: 0.69, 95% CI:0.60–0.77) in the external validation cohort. Decision curve analysis demonstrated added clinical benefit of applying the model for risk stratification. CONCLUSIONS: PNI and preoperative CEA are useful indicators for inferior survival outcomes of stage I CRC. Identification of stage I patients at high risk of recurrence is feasible using the ACEPLY model, although the predictive performance is yet to be improved. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12916-022-02693-7

Haploinsufficiency of SIRT1 Enhances Glutamine Metabolism and Promotes Cancer Development

SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, plays a vital role in the regulation of metabolism, stress responses, and genome stability. However, the role of SIRT1 in the multi-step process leading to transformation and/or tumorigenesis, as either a tumor suppressor or tumor promoter, is complex and maybe dependent upon the context in which SIRT1 activity is altered, and the role of SIRT1 in tumor metabolism is unknown. Here we demonstrate that SIRT1 dose-dependently regulates cellular glutamine metabolism and apoptosis, which in turn differentially impact cell proliferation and cancer development. Heterozygous deletion of Sirt1 induces c-Myc expression, enhancing glutamine metabolism and subsequent proliferation, autophagy, stress resistance and cancer formation. In contrast, homozygous deletion of Sirt1 triggers cellular apoptotic pathways, increases cell death, diminishes autophagy, and reduces cancer formation. Consistent with the observed dose-dependence in cells, intestine-specific Sirt1 heterozygous mice have enhanced intestinal tumor formation, whereas intestine-specific Sirt1 homozygous knockout mice have reduced development of colon cancer. Furthermore, SIRT1 reduction but not deletion is associated with human colorectal tumors, and colorectal cancer patients with low protein expression of SIRT1 have a poor prognosis. Taken together, our findings indicate that the dose-dependent regulation of tumor metabolism and possibly apoptosis by SIRT1 mechanistically contributes to the observed dual roles of SIRT1 in tumorigenesis. Our study highlights the importance of maintenance of a suitable SIRT1 dosage for metabolic and tissue homeostasis, which will have important implications in SIRT1 small molecule activators/inhibitors based therapeutic strategies for cancers

Electrochemical Acceptorless Dehydrogenation of N‑Heterocycles Utilizing TEMPO as Organo-Electrocatalyst

Catalytic acceptorless dehydrogenation (CAD) has been a basically important organic transformation to ubiquitous unsaturated compounds without the usage of a sacrificial hydrogen acceptor. In this work, we successfully developed the first electrochemical acceptorless dehydrogenation (ECAD) of N-heterocycles using TEMPO as the organo-electrocatalyst. We have achieved the catalytic dehydrogenation of N-heterocycles in an anode and the release of H₂ in a cathode using an undivided-cell system. A variety of six-membered and five-membered nitrogen-heteroarenes can be synthesized in good yields in this system. In addition, this protocol can also be used in the application of important molecular synthesis. Our electrochemical strategy provides a mild and metal-free route for (hetero)­aromatic compounds synthesis via the CAD strategy

Nickel-Catalyzed Reductive Cross-Coupling of Aryl Bromides with Alkyl Bromides: Et₃N as the Terminal Reductant

Reductive cross-coupling has emerged as a direct method for the construction of carbon–carbon bonds. Most cobalt-, nickel-, and palladium-catalyzed reductive cross-coupling reactions to date are limited to stoichiometric Mn(0) or Zn(0) as the reductant. One nickel-catalyzed cross-coupling paradigm using Et₃N as the terminal reductant is reported. By using this photoredox catalysis and nickel catalysis approach, a direct Csp²–Csp³ reductive cross-coupling of aryl bromides with alkyl bromides is achieved under mild conditions without stoichiometric metal reductants