Two-body charmed baryon decays involving decuplet baryon in the quark-diagram scheme

In the quark-diagram scheme, we study the charmed baryon decays of ${\bf B}_c\to {\bf B}^* M$, where ${\bf B}_c$ is $\Lambda_c^+$ or $\Xi_c^{+(0)}$, together with ${\bf B}^*$ ($M$) the decuplet baryon (pseudoscalar meson). It is found that only two $W$-exchange processes are allowed to contribute to ${\bf B}_c\to {\bf B}^* M$. Particularly, we predict ${\cal B}(\Lambda_c^+ \to \Sigma^{*0(+)} \pi^{+(0)})=(2.8\pm 0.4)\times 10^{-3}$, which respects the isospin symmetry. Besides, we take into account the $SU(3)$ flavor symmetry breaking, in order to explain the observation of ${\cal B}(\Lambda_c^+\to \Sigma^{*+}\eta)$. For the decays involving $\Delta^{++}(uuu)$, we predict ${\cal B}(\Lambda_c^+\to \Delta^{++} \pi^-,\Xi_c^+ \to \Delta^{++} K^-) =(7.0\pm 1.4,13.5\pm 2.7)\times 10^{-4}$ as the largest branching fractions in the singly Cabibbo-suppressed $\Lambda_c^+,\Xi_c^+\to{\bf B}^*M$ decay channels, respectively, which are accessible to the LHCb, BELLEII and BESIII experiments.Comment: 12 pages, 1 figure, 3 tables, version to appear in EPJ

Weekly induction intraperitoneal chemotherapy after primary surgical cytoreduction in patients with advanced epithelial ovarian cancer

BACKGROUND: Traditional intraperitoneal (IP) therapy administered simultaneously with intravenous (IV) chemotherapy in the primary setting has been well documented. This retrospective study was conducted to investigate the role of weekly IP therapy as an inducing intervention before front-line IV chemotherapy, particularly in patients with bulky residual disease after surgery. METHODS: A total of 426 patients with advanced ovarian cancer treated between 1990 and 1999, were reviewed. Follow-up data were available in 409 patients. Of whom, 230 patients received postoperative weekly IP therapy with a median cycles of 4, other 179 patients who did not receive any IP therapy were used as the control group. RESULTS: The median age of the patients was 51 years (range, 20–77 years). One hundred eighty-nine patients with stage III disease and 41 patients with stage IV disease were treated with postoperative IP therapy, respectively. Complications and toxicity were observed in 68 patients (29.5%), but there were no grade 4 toxicities and no patients died of complications or toxicities. In patients with residual disease > 1 cm, the median survival of those with IP delivery of chemotherapy and those without was 21.6 months and 18.8 months, respectively (hazard ratio [HR]= 0.69, P = 0.02). Whereas, in patients with residual disease ≤ 1 cm, the median survival was 46.8 months and 37.6 months, respectively (HR= 0.73, P = 0.09). Multivariate analysis suggested that the factors age ≤ 60 years, stage III, IP therapy and paclitaxel as front-line chemotherapy were associated with a better prognosis for patients with advanced ovarian cancer. CONCLUSION: Weekly postoperative IP therapy as an inducing intervention is practical for both physicians and patients with acceptable complications and associated with a lengthened survival of patients with advanced ovarian cancer. Whether this arm can be used in lieu of a traditional one needs further randomized trial to confirm the preliminary results

Diagnostic value of mammography density of breast masses by using deep learning

ObjectiveIn order to explore the relationship between mammographic density of breast mass and its surrounding area and benign or malignant breast, this paper proposes a deep learning model based on C2FTrans to diagnose the breast mass using mammographic density.MethodsThis retrospective study included patients who underwent mammographic and pathological examination. Two physicians manually depicted the lesion edges and used a computer to automatically extend and segment the peripheral areas of the lesion (0, 1, 3, and 5 mm, including the lesion). We then obtained the mammary glands’ density and the different regions of interest (ROI). A diagnostic model for breast mass lesions based on C2FTrans was constructed based on a 7: 3 ratio between the training and testing sets. Finally, receiver operating characteristic (ROC) curves were plotted. Model performance was assessed using the area under the ROC curve (AUC) with 95% confidence intervals (CI), sensitivity, and specificity.ResultsIn total, 401 lesions (158 benign and 243 malignant) were included in this study. The probability of breast cancer in women was positively correlated with age and mass density and negatively correlated with breast gland classification. The largest correlation was observed for age (r = 0.47). Among all models, the single mass ROI model had the highest specificity (91.8%) with an AUC = 0.823 and the perifocal 5mm ROI model had the highest sensitivity (86.9%) with an AUC = 0.855. In addition, by combining the cephalocaudal and mediolateral oblique views of the perifocal 5 mm ROI model, we obtained the highest AUC (AUC = 0.877 P < 0.001).ConclusionsDeep learning model of mammographic density can better distinguish benign and malignant mass-type lesions in digital mammography images and may become an auxiliary diagnostic tool for radiologists in the future

Cloning and analysis of a NBS-LRR disease resistance gene candidate PnAG1 from peanut ( Arachis hypogaea L.)

Background: Based on the conserved sequences of a known NBS resistance gene, a pair of degenerate primers was designed to amplify the NBS-LRR resistance gene from peanut using PCR and RACE methods. Results: Analyzing the amino acid sequence by BLAST on NCBI, which was deduced from the 1088bp-long gene named PnAG1-2, showed that it had a certain homology with some resistance proteins, among which Arachis cardenasii resistance protein gene had the highest homology (66%). Relative quantification PCR analysis indicated that PnAG1-2 gene expresses more in J11 (an A. flavus-resistant variety) than in JH1012 (an A. flavus-susceptible variety) when the harvest time was coming. Conclusions: In this study, the NBS-LRR resistance sequence was successfully cloned from peanut and prokaryotic expression was done on the gene, which provided a foundation for cultivating anti-A. flavus peanut varieties

An advanced biomass gasification technology with integrated catalytic hot gas cleaning. Part III: Effects of inorganic species in char on the reforming of tars from wood and agricultural wastes

Char is used directly as a catalyst for the catalytic reforming of tar during gasification. Experiments have been carried out to examine the effects of inorganics in char as a catalyst for the catalytic reforming of tar during the gasification of mallee wood, corn stalk and wheat straw in a pilot plant. The char catalyst was prepared from the pyrolysis of mallee wood at a fast heating rate. The catalytic activities of char and acid-washed char for tar reforming were compared under otherwise identical gasification conditions. For all biomass feedstocks tested for gasification, the tar contents in product gas could be drastically reduced by the catalyst, reaching a tar concentration level well below 100 mg/N m3. The acid-washed char also showed profound activity for tar reforming although its catalytic activity was definitely lower than the raw char. Both catalysts could effectively reform the aromatic ring systems (especially large aromatic ring systems with three or more fused benzene rings) in tars as is revealed using UV-fluorescence spectroscopy. The char itself was also partially gasified. After being used as a catalyst, the condensation of the aromatic rings and the accumulation of inorganic species led to drastic changes in char reactivity with O2 at 400 °C. The inorganic species in char tended to enhance the formation of H2 and CO during the reforming reactions in the catalytic reactor

Observation of GRB 221009A early afterglow in X/γ\gamma-ray energy band

The early afterglow of a Gamma-ray burst (GRB) can provide critical information on the jet and progenitor of the GRB. The extreme brightness of GRB 221009A allows us to probe its early afterglow in unprecedented detail. In this letter, we report comprehensive observation results of the early afterglow of GRB 221009A (from $T_0$+660 s to $T_0$+1860 s, where $T_0$ is the \textit{Insight}-HXMT/HE trigger time) in X/$\gamma$-ray energy band (from 20 keV to 20 MeV) by \textit{Insight}-HXMT/HE, GECAM-C and \textit{Fermi}/GBM. We find that the spectrum of the early afterglow in 20 keV-20 MeV could be well described by a cutoff power-law with an extra power-law which dominates the low and high energy bands respectively. The cutoff power-law $E_{\rm peak}$ is $\sim$ 30 keV and the power-law photon index is $\sim$ 1.8 throughout the early afterglow phase. By fitting the light curves in different energy bands, we find that a significant achromatic break (from keV to TeV) is required at $T_0$ + 1246$^{+27}_{-26}$ s (i.e. 1021 s since the afterglow starting time $T_{\rm AG}$=$T_0$+225 s), providing compelling evidence of a jet break. Interestingly, both the pre-break and post-break decay slopes vary with energy, and these two slopes become closer in the lower energy band, making the break less identifiable. Intriguingly, the spectrum of the early afterglow experienced a slight hardening before the break and a softening after the break. These results provide new insights into the understanding of this remarkable GRB.Comment: Accepted for publication in ApJ Letters on 19-Jan-2024, 11 pages, 7 figures and 2 table

TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells

The trafficking protein particle complex 4 (TRAPPC4) is implicated in vesicle-mediated transport, but its association with disease has rarely been reported. We explored its potential interaction with ERK2, part of the ERK1/2 complex in the Extracellular Signal-regulated Kinase/ Mitogen-activated Protein Kinase (ERK-MAPK) pathway, by a yeast two-hybrid screen and confirmed by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down. Further investigation found that when TRAPPC4 was depleted, activated ERK1/2 specifically decreased in the nucleus, which was accompanied with cell growth suppression and apoptosis in colorectal cancer (CRC) cells. Overexpression of TRAPPC4 promoted cell viability and caused activated ERK1/2 to increase overall, but especially in the nucleus. TRAPPC4 was expressed more highly in the nucleus of CRC cells than in normal colonic epithelium or adenoma which corresponded with nuclear staining of pERK1/2. We demonstrate here that TRAPPC4 may regulate cell proliferation and apoptosis in CRC by interaction with ERK2 and subsequently phosphorylating ERK1/2 as well as modulating the subcellular location of pERK1/2 to activate the relevant signaling pathway

Down-Regulation of GEP100 Causes Increase in E-Cadherin Levels and Inhibits Pancreatic Cancer Cell Invasion

AIMS: Invasion and metastasis are major reasons for pancreatic cancer death and identifying signaling molecules that are specifically used in tumor invasion is of great significance. The purpose of this study was to elucidate the role of GEP100 in pancreatic cancer cell invasion and metastasis and the corresponding molecular mechanism. METHODS: Stable cell lines with GEP100 knocked-down were established by transfecting GEP100 shRNA vector into PaTu8988 cells and selected by puromycin. qRT-PCR and Western blot were performed to detect gene expression. Matrigel-invasion assay was used to detect cancer cell invasion in vitro. Liver metastasis in vivo was determined by splenic injection of indicated cell lines followed by spleen resection. Immunofluorescence study was used to detect the intracellular localization of E-cadherin. RESULTS: We found that the expression level of GEP100 protein was closely related to the invasive ability of a panel of 6 different human pancreatic cancer cell lines. Down-regulation of GEP100 in PaTu8988 cells significantly decreased invasive activity by Matrigel invasion assay, without affecting migration, invasion and viability. The inhibited invasive activity was rescued by over-expression of GEP100 cDNA. In vivo study showed that liver metastasis was significantly decreased in the PaTu8988 cells with GEP100 stably knocked-down. In addition, an epithelial-like morphological change, mimicking a mesenchymal to epithelial transition (MET) was induced by GEP100 down-regulation. The expression of E-cadherin protein was increased 2-3 folds accompanied by its redistribution to the cell-cell contacts, while no obvious changes were observed for E-cadherin mRNA. Unexpectedly, the mRNA of Slug was increased by GEP100 knock-down. CONCLUSION: These findings provided important evidence that GEP100 plays a significant role in pancreatic cancer invasion through regulating the expression of E-cadherin and the process of MET, indicating the possibility of it becoming a potential therapeutic target against pancreatic cancer