Interfacial magnetic spin Hall effect in van der Waals Fe3GeTe2/MoTe2 heterostructure.

The spin Hall effect (SHE) allows efficient generation of spin polarization or spin current through charge current and plays a crucial role in the development of spintronics. While SHE typically occurs in non-magnetic materials and is time-reversal even, exploring time-reversal-odd (T-odd) SHE, which couples SHE to magnetization in ferromagnetic materials, offers a new charge-spin conversion mechanism with new functionalities. Here, we report the observation of giant T-odd SHE in Fe3GeTe2/MoTe2 van der Waals heterostructure, representing a previously unidentified interfacial magnetic spin Hall effect (interfacial-MSHE). Through rigorous symmetry analysis and theoretical calculations, we attribute the interfacial-MSHE to a symmetry-breaking induced spin current dipole at the vdW interface. Furthermore, we show that this linear effect can be used for implementing multiply-accumulate operations and binary convolutional neural networks with cascaded multi-terminal devices. Our findings uncover an interfacial T-odd charge-spin conversion mechanism with promising potential for energy-efficient in-memory computing.

Cd44v6 acts as a directional responding factor in the process of transcoelomic metastasis from gastric carcinoma to Krukenberg tumor.

INTRODUCTION: Due to the limited number of studies focusing on the optimal treatment of multiple Krukenberg tumor (KT)-gastric carcinoma (KT - GC), it is necessary to conduct large-scale studies to confirm the definite role of serum tumor markers in the diagnosis and prognosis of KT. Moreover, the clinical significance of variant 6 of CD44 (CD44v6) in transcoelomic metastasis should be considered. AREAS COVERED: This review covers molecular pre-cancer diagnosis, gastric carcinoma metastasis, and anti-cancer treatments. Additionally, gastrointestinal cancer metastasis is a key area for improvement. EXPERT OPINION: The detection of CD44v6 differs in the World Health Organization Classification of Gastric Adenocarcinoma, the Lauren Classification of Gastric Adenocarcinoma, and the anatomic location of gastric adenocarcinoma. The results were compared among the three groups. The mechanism of gastric adenocarcinoma metastasis still requires further elucidation. CD44v6 molecular detection helps clarify the pre-cancer diagnosis of KT before seeding. If subsequent studies confirm its role as a signaling molecule, it could pave the way for new research directions in clinical practice; however, additional academic confirmation is necessary.

Pressure-Tuning Superconductivity in Noncentrosymmetric Topological Materials ZrRuAs.

Recently, the hexagonal phase of ternary transition metal pnictides TT'X (T = Zr, Hf; T' = Ru; X = P, As), which are well-known noncentrosymmetric superconductors, were predicted to host nontrivial bulk topology. In this work, we systematically investigate the electronic responses of ZrRuAs to external pressure. At ambient pressure, ZrRuAs show superconductivity with Tc ~ 7.74 K, while a large upper critical field ~ 13.03 T is obtained for ZrRuAs, which is comparable to the weak-coupling Pauli limit. The resistivity of ZrRuAs exhibits a non-monotonic evolution with increasing pressure. The superconducting transition temperature Tc increases with applied pressure and reaches a maximum value of 7.93 K at 2.1 GPa, followed by a decrease. The nontrivial topology is robust and persists up to the high-pressure regime. Considering both robust superconductivity and intriguing topology in this material, our results could contribute to studies of the interplay between topological electronic states and superconductivity.

ß-Elemene Promotes Apoptosis Induced by Hyperthermia via Inhibiting HSP70.

Thermotherapy has been presented as a promising strategy to be used as an effective nonsurgical technique for colorectal carcinoma. Although this strategy presents several advantages, including low toxicity and high repeatability, thermotherapy often needs to be combined with other therapies because residual tumor cells that survive hyperthermal treatment often lead to relapse. In this study, we evaluated the effects of ß-elemene, which has been proven to have the potential to reverse chemotherapy drug resistance, on promoting the antitumor effects of hyperthermia. ß-elemene treatment significantly promoted apoptosis after 2 hours of hyperthermia treatment and blocked cell cycle phases at G1/G0. ß-elemene also significantly decreased colony formation and tumor formation abilities after hyperthermia treatment. ß-elemene treatment significantly decreased HSP70, but not HSP90 or HSP27, induced by hyperthermia treatment without disturbing HSP70 mRNA. It was also found that ß-elemene decreased phosphorylated ERK1/2 induced by hyperthermia. Regain of HSP70 reversed ß-elemene-mediated apoptosis, indicating that ß-elemene may induce apoptosis by decreasing HSP70. Moreover, ß-elemene treatment significantly decreased invasion capacity by decreasing the EMT, which was induced by hyperthermia treatment. Taken together, our results offer a potential strategy for CRC therapy via the combination of hyperthermia and ß-elemene.

Highly Invasive and Metastatic High-grade Endometrial Stromal Sarcoma With BCOR Gene Alterations: A Case Report.

BACKGROUND: The coexistence of a uterine leiomyosarcoma and a high-grade endometrial stromal sarcoma (HGESS) is extremely rare, especially when one of the components causes metastasis. CASE REPORT: A 46-year-old female with aggravated abdominal pain for more than 4 months was diagnosed with uterine malignant mesenchymal tumor composed of predominantly a leiomyosarcoma (99%) and a minor component of HGESS with BCL6 corepressor (BCOR) gene alterations (1%), with ovarian and pelvic metastases. RESULTS: The volume of HGESS with BCOR gene alterations accounted for less than 1% of the tumor mass but caused ovarian and pelvic metastases. CONCLUSION: HGESS with BCOR gene alterations is extremely aggressive. We suggest that when both components of HGESS with BCOR gene alterations and uterine leiomyosarcoma are present in one patient, the HGESS with BCOR gene alterations needs to be highlighted in the pathological report, even if it accounts for less than 1% of the tumor volume.

Case Report: A Primary Right Ventricular Vascular Malformation Presenting as a Mass.

Primary right ventricular vascular malformation is a rare primary benign anomaly in heart in nature. Due to the extremely low incidence and the progress on the classification of vascular malformation, a few cases were reported in the literatures. In the current case study, a 55-year-old women presented with a cardiac mass that was identified in right ventricle during a routine medical checkup. Magnetic resonance imaging demonstrated a well-circumscribed mass attached to the interventricular septum. Median sternotomy for the surgical resection of the mass and a cardiopulmonary bypass were performed. The intraoperative transesophageal echocardiogram showed that the mass had been successfully removed. The patient recovered well and was discharged from hospital 9 days after the surgery. The pathological diagnosis was primary cardiac arteriovenous malformation. No mass recurrence was shown by echocardiography during the 13 months' follow-up.

Comparative mRNA/micro-RNA co-expression network drives melanomagenesis by promoting epithelial-mesenchymal transition and vasculogenic mimicry signaling.

This study aimed to identify a novel disease-associated differentially co-expressed mRNA-microRNA (miRNA) that is associated with vasculogenic mimicry (VM) and epithelial-to-mesenchymal transition (EMT) network at different stages of melanoma. By applying weighted gene co-expression network analysis, we constructed a VM+EMT biological network with the available microarray dataset downloaded from a public database. Quantitative real-time PCR, immunohistochemical staining, and CD31-periodic acid solution dual staining were performed to confirm the expression of genes associated with EMT and VM formation in subjects with malignant melanoma (n = 18) and primary melanoma (n = 13) and in healthy subjects (n = 10). Our findings suggested that phosphatidylserine-specific phospholipase A1-alpha (PLA1A) and dermokine (DMKN) genes function as oncogenes that trigger VM and EMT processes during melanomagenesis on interaction with miR-370, miR-563, and miR-770-5p. PLA1A and DMKN genes can be considered potential VM+EMT network-based diagnostic biomarkers for distinguishing between melanoma patients. We postulate that a network with altered PLA1A/miR-563 and DMNK/miR-770-5p/miR-370 may contribute to melanomagenesis by triggering the EMT signaling pathway and VM formation. This study provides a potentially valuable approach for the early diagnosis and prognosis of melanoma progression.

Positive Association Between Serum Insulin-Like Growth Factor-1 and Cognition in Patients with Cerebral Small Vessel Disease.

Cognitive impairment is one of the main complications of cerebral small vessel disease (CSVD). Serum insulin-like growth factor-1 (IGF-1) might serve as a marker for the risk of cognitive decline in patients with CSVD. We investigated the association of IGF-1 with the development of cognitive impairment in patients with CSVD. We included 216 patients with CVSD (mean age, 67.57 ± 8.53 years; 31.9% female). We compared 117 (54.2%) patients who developed cognitive impairment with 99 (45.8%) patients without cognitive impairment. Patients who developed cognitive impairment had significantly lower levels of IGF-I (p < 0 .001), suggesting that altered IGF-1 signaling may be a risk factor for cognitive decline in patients with CSVD.

PLA1A expression as a diagnostic marker of BRAF-mutant metastasis in melanoma cancer.

BRAF and NRAS are the most reported mutations associated to melanomagenesis. The lack of accurate diagnostic markers in response to therapeutic treatment in BRAF/NRAS-driven melanomagenesis is one of the main challenges in melanoma personalized therapy. In order to assess the diagnostic value of phosphatidylserine-specific phospholipase A1-alpha (PLA1A), a potent lysophospholipid mediating the production of lysophosphatidylserine, PLA1A mRNA and serum levels were compared in subjects with malignant melanoma (n = 18), primary melanoma (n = 13), and healthy subjects (n = 10). Additionally, the correlation between histopathological subtypes of BRAF/NRAS-mutated melanoma and PLA1A was analyzed. PLA1A expression was significantly increased during melanogenesis and positively correlated to disease severity and histopathological markers of metastatic melanoma. PLA1A mRNA and serum levels were significantly higher in patients with BRAF-mutated melanoma compared to the patients with NRAS-mutated melanoma. Notably, PLA1A can be used as a diagnostic marker for an efficient discrimination between naïve melanoma samples and advanced melanoma samples (sensitivity 91%, specificity 57%, and AUC 0.99), as well as BRAF-mutated melanoma samples (sensitivity 62%, specificity 61%, and AUC 0.75). Our findings suggest that PLA1A can be considered as a potential diagnostic marker for advanced and BRAF-mutated melanoma.

Combined large cell neuroendocrine carcinoma of the lung associated with low-grade fetal adenocarcinoma without ß-catenin mutation: a case report.

We report a case of combined large cell neuroendocrine carcinoma of the lung associated with low-grade fetal adenocarcinoma (L-FLAC) without ß-catenin mutation in exon 3. A 33-year-old man presented at the hospital with a more than 5-month history of cough with no obvious cause. Computed tomography revealed a large, solid, round mass located in the upper lobe of the right lung. Microscopic examination showed two tumor components: large cell neuroendocrine carcinoma and low-grade fetal adenocarcinoma. Immunohistochemistry ofthe fetal adenocarcinoma showed abnormal nuclear/cytoplasmic expression of ß-catenin, but no exon 3 mutation in ß-catenin. Our findings provide further insight into the pathologic mechanism of FLAC.

Erastin induces apoptotic and ferroptotic cell death by inducing ROS accumulation by causing mitochondrial dysfunction in gastric cancer cell HGC­27.

Erastin, a classical inducer of non­apoptotic cell death, exerts cytotoxicity in several types of cancer cells, including gastric cancer cells, by depleting glutathione, which is a primary cellular antioxidant, thus causing reactive oxygen species (ROS) accumulation. Although numerous studies have focused on the non­apoptotic cell death induced by erastin, whether erastin induces apoptosis remains unknown. The present study confirmed the cytotoxicity of erastin in HGC­27 cells and used a 30% inhibitory concentration (IC30, approximately 6.23 µM) for further analysis. The cell cycle analysis revealed that 6.23 µM of erastin inhibited proliferation by blocking the cell cycle at the G1/G0 phase. Further analysis also showed that 6.23 µM of erastin clearly inhibited HGC­27 malignant behaviors, including migration, invasion, colony formation and tumor formation in soft agar. The observation of ROS accumulation due to erastin treatment led to determination of the effects of erastin on mitochondrial function and, as expected, erastin treatment decreased transcriptional activity and ATP production in mitochondria and disrupted the mitochondrial potential; these effects were reversed by the addition of the ROS scavenger NAC. To evaluate the effect of erastin in inducing apoptosis, HGC­27 cells were treated with 6.23 µM of erastin for 7 days and then analyzed. Evident apoptotic cell death was induced by erastin and this apoptosis was reversed by the addition of an apoptosis inhibitor (zVAD) or NAC but not by the addition of a ferroptosis inhibitor (ferrostatin­1). Furthermore, the detection of caspase­3 and poly (adenosine diphosphate­ribose) polymerase (PARP) also confirmed that treatment with erastin promoted the cleavage of caspase­3 and PARP, which are hallmarks of apoptosis. Taken together, the present study revealed that a low dose of erastin inhibited malignant behavior and induced apoptosis by causing mitochondrial dysfunction.

Long non­coding RNA growth arrest­specific 5 (GAS5) acts as a tumor suppressor by promoting autophagy in breast cancer.

Growth arrest­specific 5 (GAS5) is a known tumor suppressor which negatively regulates cell survival and malignancy in several cancer cell types. The present study aimed to establish the correlation between GAS5 and unc­51 like autophagy activating kinase (ULK)1/2, two key regulators of autophagy initiation in breast cancer (BC). To address this, expression levels of these genes were quantitively analyzed in BC clinical samples by performing reverse transcription­quantitative PCR. GAS5 was downregulated in BC clinical samples compared with adjacent samples and was positively correlated with ULK1/2. Detection methods including cell cycle analysis, annexin V­FITC/PI double staining and flow cytometry analysis, Transwell cell invasion assay, transfection and western blotting were used for BC cells. In MCF­7 cells, it was also observed that overexpression of GAS5 upregulated ULK1/2 protein levels without disturbing other autophagy initiation­associated proteins and inhibited cell proliferation, invasion and tumor formation. These effects were reversed by blocking autophagy with 3­methyladenine (3­MA). These results demonstrated that the suppressive effects of overexpressed GAS5 were mediated via autophagy induction, at least in part. Overexpression of GAS5 induced chemoresistance to cisplatin, which was not reversed by 3­MA­mediated inhibition of autophagy, indicating that GAS5 promotes chemosensitivity in an autophagy­independent manner. Collectively, these results indicated that GAS5 contributes to the pathogenesis of BC potentially by promoting autophagy. However, the mechanism by which GAS5 functions as a tumor suppressor in an autophagy­independent manner remains unknown.

Inflammatory Fibroid Polyp: An Unusual Cause of Abdominal Pain in the Upper Gastrointestinal Tract a Case Report.

Inflammatory fibroid polyps (IFPs) tend to occur in the gastrointestinal tract, and they are rare and benign neoplasms. In general, IFPs often come from epithelial tissue. The gastric antrum is the most common location. Endoscopic ultrasound (EUS) often shows a predominantly hypoechoic mass with well-defined borders originating from the submucosal area. Here, we report the case of a 46-year-old woman with abdominal pain who underwent computed tomography (CT), endoscopic ultrasound and endoscopic submucosal dissection (ESD) of resected specimens; the diagnosis was ultimately an inflammatory fibroid polyp. She is currently in clinical remission.

Rab-like protein 1 A is upregulated by cisplatin treatment and partially inhibits chemoresistance by regulating p53 activity.

Rab-like protein 1 A (RBEL1A), which is a predominant isoform of RBEL1, has been identified to serve an important function in breast tumorigenesis and may be upregulated in breast tumor cells. RBEL1A may block the transcriptional activity of p53, which is important in the induction of cisplatin sensitivity. Previous studies supported the association between the induction of chemoresistance and the inhibition of p53 by RBEL1A. However, the response of RBEL1A to chemotreatment and its interaction with p53 remains to be investigated. The present study revealed that the cisplatin treatment induced the expression of RBEL1A in MCF-7 cells. Consistent with previous studies, the present study demonstrated that cisplatin treatment and RBEL1A overexpression blocked the oligomerization of p53 in MCF-7 cells and led to a decrease of the transcriptional activity of p53 and its downstream target gene p21. Additionally, upregulation of RBEL1A decreased the protein level of p53 by promoting the ubiquitination of p53. A cytotoxicity assay demonstrated that upregulation of RBEL1A partially contributed to chemosensitivity via inhibiting p53 in MCF-7 cells. A pG13L (p53-responsive reporter plasmid) luciferase reporter and co-immunoprecipitation assay revealed that upregulation of RBEL1A led to an inhibition of the transcriptional activity of p53 or its target gene p21. Analysis of cellular proliferation, cell cycle and invasion also confirmed the regulatory activity of RBEL1A on the malignancy of breast cancer cells. Taken together, these results suggest that the induction of RBEL1A following cisplatin treatment may partially inhibit chemosensitivity in a p53-dependent manner.

HLJ1 is a novel biomarker for colorectal carcinoma progression and overall patient survival.

The implication of HLJ1, a member of the heat shock protein-40 chaperone family, in colorectal carcinoma (CRC) remains unclear. The aim of this study was to determine the dynamic changes of HLJ1 in CRC both in vitro and in vivo, and the relationship between its level and the survival rate of CRC patients. Both real-time RT-PCR and Western blot were used to detect the expression of HLJ1 in CRC cells, while the distribution of HLJ1 in CRC and its adjacent normal mucosa tissues from CRC patients was determined with immunohistochemistry. Moreover, MTT and in vitro invasive assays were performed to determine the effect of HLJ1 overexpression on cell proliferation and invasion of CRC cells. The results indicated that in highly metastatic CRC cells, the HLJ1 expression was lower than that in lowly metastatic ones, and that the overexpression of HLJ1 significantly inhibited CRC cell proliferation and invasion in vitro. Interestingly, the HLJ1 expression was significantly down-regulated in CRC or lymphatic metastatic tissues from patient, compared to that in the normal mucosa (P<0.05), and the HLJ1 expression was correlated strongly with lymph metastasis, Dukes' stage, and remote metastasis (P<0.05). Most surprisingly, patients with a higher HLJ1 level had a better overall survival rate, compared to that in patients with lower HLJ1 level (P<0.05). Based on all these findings, we conclude that HLJ1 is a strong tumor suppressor for CRC, and thus the down-regulation of the HLJ1 expression may be used as a biomarker to predict clinical outcome of patients with CRC.

[Analysis of soil respiration and influence factors in wheat farmland under conservation tillage in southwest hilly region].

In order to investigate the effect of conservation tillage on soil respiration in dry cropping farmland in southwest purple hilly region, the LI6400-09 respiratory chamber was adopted in the experiment conducted in the experimental field in Southwest University in Beibei, Chongqing. The respiration and the hydrothermal and biotic factors of soil were measured and analyzed during the growth period of wheat in the triple intercropping system of wheat/maize/soybean. There were four treatments including T (traditional tillage), R (ridge tillage), TS (traditional tillage + straw mulching) and RS (ridge tillage + straw mulching), which were all in triplicates. The results indicated that the soil respiration rate changed in the range of 1.100-2.508 micromol x (m2 x s)(-1) during the reproductive growth stage of wheat. There were significant differences in soil respiration rate among different treatments, which could be ranked as RS > R > TS > T. The soil temperature in the 10cm layer was ranked as T > R > TS > RS. The relationship between soil respiration and soil temperature fitted well with an exponential function, in which the Q10 values were 1.25, 1.20, 1.31 and 1.26, respectively. The soil moisture in the 5cm layer was ranked as TS > RS > T > R. The best fitting model between soil moisture and soil respiration was a parabolic curve, indicating the presence of soil moisture with the strongest soil respiration. The response threshold of wheat to soil moisture was 14.80%-17.47% during the reproductive stage. The dominant groups of soil animals were Collembola and Acarina, which were correlated with soil respiration to some extent. The correlation was high in the treatments T and R, ranged from 0.669-0.921, whereas there was no remarkable correlation in the other treatments.