代谢相关性脂肪肝(MAFLD)是临床常见的与肥胖、糖尿病、遗传等密切相关的以肝内脂肪堆积为特点的慢性肝病.铁死亡是一种铁依赖性和脂质过氧化驱动的程序性细胞死亡方式.由于铁超载和氧化应激是导致肝脏损伤及疾病进展的主要诱因,也是MAFLD的表现之一,因此铁死亡在MAFLD中的作用受到密切关注,多项研究证实中医药可以通过纠正铁死亡失衡改善MAFLD.该文对铁死亡在中医药治疗MAFLD中的作用机制进行综述.

胃血管球瘤是一种罕见的起源于胃动静脉吻合壁的软组织间叶源性肿瘤,常因缺乏特异性症状及影像学表现而不易诊断.本文回顾1例胃血管球瘤继行远端胃切除术的临床病例并复习相关文献,以期提升对此类疾病的认识.

One of the main nanomaterials is gold nanoparticle. During current researches, it has been indicated that these nanoparticles have high cytotoxic activities against abnormal cancer cells. Gold nanoparticles are composed of silver surrounded by oxygen networks. This nanoparticle has the antioxidant behaviors including superoxidase dismutase, catalytic enzyme activity, nitric oxide and hydroxyl radical inhibition, as well as oxidant behaviors that determine several conditions such as the pH of the environment, the type of activity of this nanoparticle. In the present study, gold nanoparticles were green-synthesized using the aqueous extract of Alhagi maurorum leaf aqueous extract. The synthesized AuNPs were characterized by analytical techniques including TEM, XRD, EDX, FE-SEM and UV-vis., and FT-IR. The nanoparticles were formed in a spherical shape in the average size of 18.36 nm. In the oncological part of the recent study, the treated cells with AuNPs were assessed by MTT assay for 48 h about the cytotoxicity and anti-gastric carcinoma properties on normal (HUVEC) and gastric carcinoma cell lines i.e. GC1415, GC1436, NCI-N87 and MKN45. The viability of gastric carcinoma cell lines reduced dose -dependently in the presence of AuNPs. The IC50 of AuNPs were 44, 125, 45, and 22 mu g/mL against GC1415, GC1436, NCI-N87 and MKN45 cell lines, respectively. In the antioxidant test, the IC50 of AuNPs and BHT against DPPH free radicals were 48 and 37 mu g/mL, respectively.

1Department of Gastroenterology, Tianjin Nankai Hospital, Tianjin, People’s Republic of China; 2Department of Traditional Chinese Medicine, Chen Tangzhuang Community Health Service Center, Hexi District, Tianjin, People’s Republic of China Background: Many studies have confirmed that circular (circRNA) is involved in the development of gastric cancer (GC). However, the role of circFLNA in the progression of GC remains unclear. Methods: Quantitative real-time PCR (qRT-PCR) was used to measure the relative expression of circFLNA, microRNA (miR)-646 and 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 2 (PFKFB2). Cell counting kit 8 (CCK8) assay, transwell assay and flow cytometry were performed to determine the proliferation, migration, invasion and apoptosis of cells, respectively. GC tumor xenograft models were built to confirm the function of circFLNA silencing on GC tumor growth in vivo. Furthermore, the lactate production, glucose consumption, ATP level and glucose uptake were detected to assess the glycolysis of cells. Then, the interaction between miR-646 and circFLNA or PFKFB2 was confirmed using dualluciferase reporter assay. RNA immunoprecipitation (RIP) assay was used to verify the interaction between miR-646 and circFLNA further. In addition, Western blot (WB) analysis was employed to detect the relative protein expression of PFKFB2. Results: Our results found that circFLNA was upregulated in GC tissues and cells. Silencing of circFLNA could suppress the proliferation, migration, invasion, glycolysis, and enhance the apoptosis of GC cells. Also, circFLNA knockdown reduced GC tumor volume and weight in vivo. Further experiments revealed that circFLNA could sponge miR-646, and miR-646 could target PFKFB2. The rescue experiments indicated that miR-646 inhibitor could reverse the suppressive effect of circFLNA silencing on GC progression, and PFKFB2 overexpression also could invert the inhibition effect of miR-646 on GC progression. Conclusion: Our data concluded that circFLNA played a pro-cancer role in GC, which suggested that circFLNA might be a potential biomarker for GC treatment.

Increasing studies have demonstrated that microRNAs (miRNAs) are associated with the metastasis of gallbladder carcinoma (GBC). Recently, miR-324-5p has been reported to be a tumour-suppressive miRNA in many types of malignant cancer. However, the biological function and molecular mechanism of miR-324-5p in GBC still remain largely unknown. Here, we found that miR-324-5p expression was notably down-regulated in both GBC tissues and cells compared with that in normal controls. Downregulated miR-324-5p expression was negatively associated with the status of local invasion and lymph node metastasis and predicted a poor prognosis in GBC patients. Further functional assays revealed that restoration of miR-324-5p significantly suppressed GBC cell migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and impeded the metastasis of GBC cells in vivo. Moreover, RNA immunoprecipitation (RIP) and dual-luciferase reporter assay confirmed that the transforming growth factor beta 2 (TGFB2) was a direct target gene of miR-324-5p in GBC cells. Mechanically, small interfering RNA (siRNA)-mediated knockdown of TGFB2 partially phenocopied the inhibitory effects of miR-324-5p overexpression on GBC cell metastatic phenotypes. In summary, our findings demonstrated that miR-324-5p targets TGFB2 expression to inhibit GBC cell metastatic behaviors, and implying miR-324-5p as a potential biomarker for diagnostic and therapeutic strategies in GBC.

The development of an effective therapeutic intervention for liver cancer is a worldwide challenge that remains to be adequately addressed. Of note, TP53, which encodes the p53 protein, is an important tumor suppressor gene, 61% of TP53 is functionally inactivated in liver cancer. Recombinant human adenovirus p53 (rAd-p53) is the first commercial product that has been used for gene therapy. In the present study, the combined mechanistic effects of rAd-p53 and curcumin, a naturally occurring compound with previously reported anti-inflammatory, antioxidant and anti-cancer properties, were assessed in liver cancer cells, using HepG2 cells as the model cell line. The administration of either curcumin or rAd-p53 promoted apoptosis, suppressed epithelial-mesenchymal transition (EMT) and blocked G2/M phase progression in HepG2 cells, which were potentiated further when both agents were applied together. Combined rAd-p53 and curcumin treatment resulted in higher p53 (P<0.01) and p21 (P<0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on TP53 expression. Additionally, curcumin and rAd-p53 were demonstrated to regulate the activation of mitogen-activated protein kinases (MAPKs) ERK1/2, p38 MAPK and JNK. These results indicated that the combination of rAd-p53 with curcumin synergistically potentiates apoptosis and inhibit EMT compared with either rAd-p53 or curcumin treatment alone via the regulation of TP53 regulation. Mechanistically, this effect on TP53 expression may involve the ERK1/2, p38 MAPK and JNK signaling pathways. The current study provides new insights that can potentially advance the development of therapeutic strategies for liver cancer treatment.

Male breast cancer (MBC) is a rare disease and accounts for <1 % of all breast cancers.

Purpose: To validate a simple portal dose calculator for plan QA and in‐vivo dosimetry. Methods: We model portal dose as a function of the fluence map, patient attenuation, patient scatter and portal response. Fluence maps are reconstructed using control‐point sequence in RTPlan. Patient attenuation is calculated via ray‐tracing through the patient CT. The effect of patient scatter and portal response is modeled by convolution, where the convolution kernel is derived from the commissioning measurements of different beam energies, different field sizes, different phantom thickness, and different source to image distances (SIDs). For various IMRT/3D plan, phantom and patient geometry, both in‐air and in‐transit portals were calculated. The calculations were compared with portal measurements. The Gamma Index of measurements against predicted portals with various dose difference (DD) criteria (1%, 2%, 3%, 4%, 5%, etc) and distance to agreement (DTA) criteria (1 mm, 2 mm, 3 mm, 4 mm, 5 mm, etc) were calculated. The Gamma pass rates of various DD and DTA criteria were evaluated and formed a Gamma table. Results: For various IMRT beams, the head, body and lung phantoms, the in‐air and in‐transit portal calculations matched well with portal measurements. The Gamma pass rates for in‐air portal are above 97% for 2 mm, 2% criteria and above 99% for 3 mm, 3% criteria. The Gamma pass rates for in‐transit portal were above 90% for 2 mm, 2% criteria and above 95% for 3 mm, 3% criteria. Conclusion: The simple portal dose calculation model is validated via phantom measurements. The model could be used in clinic for in‐air and intransit portal prediction.

OBJECTIVE:Male breast cancer (MBC) is a rare disease, with clinical and prognostic features still controversial. The aim of this study was to discuss the clinical characteristics and prognosis of MBC.METHODS:Clinical data related to 71 MBC patients was reviewed.RESULTS:The radio of MBC to female breast cancer (FBC) was 42:10 000. Age related to the diagnosis of MBC ranged from 43 to 84 years with the median age as 62 years old, older than the FBC patients (t = 6.355, P = 0.000). The percentage of invasive ductal carcinoma in MBC patients was much higher than in FBC patients (χ(2) = 29.875, P = 0.000). The positive rate of estrogen receptor (ER) was significantly higher than those in FBC patients and the positive rates of human epidermal growth factor receptor-2 (HER-2) were less frequently (χ(2) = 3.741, P = 0.048 and χ(2) = 12.845, P = 0.002) seen. Data from the univariate and multivariate analysis showed that the 3-, 5- and 10-year survival rates of MBC were 82.6%, 74.0% and 47.4% respectively, significantly higher than those in FBC patients (P = 0.004, P = 0.046). Patients with positive HER-2 showed worse prognosis than HER-2 negative patients in MBC patients (χ(2) = 4.219, P = 0.040).CONCLUSION:There were significant clinic-pathologic and prognostic differences between FBC and MBC patients. The HER-2 positivity seemed to be an important factor for the prognosis and treatment of patients with MBC.