Appendicitis tends to be complicated during the COVID-19 epidemic: A multicentre retrospective study.

Background: In past studies, non-medical factors in the social-healthcare-patient triad associated with the prevalence of COVID-19 have led to delays in the presentation of patients with acute appendicitis and an increase in complications. However, as research progresses, there is increasing evidence of a clinical association between COVID-19 and the development of acute appendicitis. Methods: The effect of COVID-19 prevalence and associated factors on acute appendicitis in the control (2016-2019) and exposed (2020-2023) groups was derived from a retrospective study of 3070 patients with acute appendicitis from 2016 to 2023. Results: After the implementation of the restrictions, the rate of acute appendicitis visits in the exposed group compared to the control group dropped sharply in the initial period (P = 0.047) and recovered gradually with the relaxation of the restrictions. Similar changes occurred in the number of acute complicated appendicitis visits. In addition, after the lifting of restrictions and the COVID-19 outbreak, the proportion of acute complicated appendicitis in the exposed group increased significantly (P < 0.001) and an increase in the number of complicated appendicitis visits was observed (P < 0.001) compared with the control group. In addition, the age distribution of acute appendicitis during this period showed an ageing trend (P = 0.001). Conclusion: COVID-19 infections may be more likely to progress to complicated appendicitis after an episode of appendicitis, even if they have been cured for the same period of time. In addition, the proportion of elderly patients with appendicitis increased after the COVID-19 epidemic.

Ribosome production factor 2 homolog promotes migration and invasion of colorectal cancer cells by inducing epithelial-mesenchymal transition via AKT/Gsk-3ß signaling pathway.

Colorectal cancer (CRC) is one of the most common malignancies of the gastrointestinal tract, and its prognosis is closely related to the degree of tumor invasion and metastasis. Ribosome production factor 2 homolog (RPF2) plays an important role in the process of ribosome biogenesis; however, its biological function in the progression of malignant tumors including CRC remains unknown. It was found that RPF2 expression was significantly higher in CRC tissues than in the adjacent normal tissue, using mRNA chip technology. This study aimed to explore the role of RPF2 in the invasion and migration of CRC cells and investigate its probable molecular mechanism. The results demonstrated that RPF2 is not only highly expressed in CRC tissues and cell lines but can also activate the AKT/GSK-3ß signaling pathway through direct interaction with CARM1, promoting epithelial-mesenchymal transition, and consequently enhancing the migration and invasion abilities of CRC cells in vitro and in vivo. Thus, we speculated that RPF2 may become a novel therapeutic target for suppression of local invasion and distant metastasis of CRC.

Vasohibin 2 promotes malignant behaviors of pancreatic cancer cells by inducing epithelial-mesenchymal transition via Hedgehog signaling pathway.

BACKGROUND: Based on previous findings, we hypothesized that Vasohibin 2 (VASH2) protein may induce epithelial-mesenchymal transition (EMT) of pancreatic cancer (PC) cells by promoting the malignant behaviors of these cells. The present study aimed to test this hypothesis and explore the possible mechanisms involved. METHODS: The expression of VASH2 in PC tissues and cell lines was detected by quantitative real-time PCR and Western blot. PC cells with overexpression or knockdown of VASH2 were used to examine the involvement of VASH2 in EMT by detecting the expression of epithelial (E-cadherin) and mesenchymal (vimentin) markers and EMT-related transcription factor ZEB1/2, in gemcitabine resistance and tumor cell invasion by apoptosis and invasion assays, and in cancer stem cell-like phenotypes by detecting the proportion of CD24+ CD44+ and side population (SP) cells in PC cells with flow cytometry. The impact of VASH2 overexpression and knockdown on components of the Hedgehog signaling pathway was also assessed. RESULTS: We found that VASH2 was highly expressed in PC tissues and cells. It promoted the EMT of PC cells by altering ZEB1/2 expression. VASH2 also stimulated invasion and chemotherapeutic resistance of PC cells and increased the proportion of cancer stem-like cells in PC cells. VASH2 did so by upregulating the expression of multiple molecules in the Hedgehog signaling pathway of PC cells. CONCLUSION: VASH2 promotes malignant behaviors of PC cells by inducing EMT via activation of the Hedgehog signaling pathway.

Curcumin Suppresses the Colon Cancer Proliferation by Inhibiting Wnt/ß-Catenin Pathways via miR-130a.

Curcumin exhibits anti-tumor effects in several cancers, including colorectal carcinoma (CRC), but the detailed mechanisms are still unclear. Here we studied the mechanisms underlying the anti-tumor effect of curcumin in colon cancer cells. SW480 cells were injected into mice to establish the xenograft tumor model, followed by evaluation of survival rate with the treatment of curcumin. The expression levels of ß-catenin, Axin and TCF4 were measured in the SW480 cells in the absence or presence of curcumin. Moreover, miRNAs related to the curcumin treatment were also detected in vitro. Curcumin could suppress the growth of colon cancer cells in the mouse model. This anti-tumor activity of curcumin was exerted by inhibiting cell proliferation rather than promoting cell apoptosis. Further study suggested that curcumin inhibited cell proliferation by suppressing the Wnt/ß-catenin pathway. MiR-130a was down-regulated by curcumin treatment, and overexpressing miR-130a could abolish the anti-tumor activity of curcumin. Our study confirms that curcumin is able to inhibit colon cancer by suppressing the Wnt/ß-catenin pathways via miR-130a. MiR-130a may serve as a new target of curcumin for CRC treatment.

Simultaneous Detection of α-Fetoprotein and Carcinoembryonic Antigen Based on Si Nanowire Field-Effect Transistors.

Primary hepatic carcinoma (PHC) is one of the most common malignancies worldwide, resulting in death within six to 20 months. The survival rate can be improved by effective treatments when diagnosed at an early stage. The α-fetoprotein (AFP) and carcinoembryonic antigen (CEA) have been identified as markers that are expressed at higher levels in PHC patients. In this study, we employed silicon nanowire field-effect transistors (SiNW-FETs) with polydimethylsiloxane (PDMS) microfluidic channels to simultaneously detect AFP and CEA in desalted human serum. Dual-channel PDMS was first utilized for the selective modification of AFP and CEA antibodies on SiNWs, while single-channel PDMS offers faster and more sensitive detection of AFP and CEA in serum. During the SiNW modification process, 0.1% BSA was utilized to minimize nonspecific protein binding from serum. The linear dynamic ranges for the AFP and CEA detection were measured to be 500 fg/mL to 50 ng/mL and 50 fg/mL to 10 ng/mL, respectively. Our work demonstrates the promising potential of fabricated SiNW-FETs as a direct detection kit for multiple tumor markers in serum; therefore, it provides a chance for early stage diagnose and, hence, more effective treatments for PHC patients.

Sorafenib and DE605, a novel c-Met inhibitor, synergistically suppress hepatocellular carcinoma.

Sorafenib, an oral multikinase inhibitor of Raf, VEGF and PDGF receptor signaling is approved for advanced hepatocellular carcinoma (HCC). One strategy to improve HCC therapy is to combine agents that target key signaling pathways. Aberrant mesenchymal-epithelial transition factor (c-Met) activation is associated with a variety of human malignancies and therefore represents a target for therapy. In this study, we investigated a novel c-Met inhibitor, DE605, together with sorafenib in hepatocellular carcinoma cells in vitro and in vivo. DE605 and sorafenib synergistically induced apoptosis in hepatocellular carcinoma cells. Mechanistically, DE605 activated the FGFR3/Erk pathway, which in turn was inhibited by sorafenib, resulting in synergism. Finally, DE605 and sorafenib significantly inhibited growth of PLC/PRF/5 hepatocellular carcinoma tumor xenografts in athymic nude mice. Importantly, no obvious weight loss (toxicity) was detected. Thus in combination, DE605 and sorafenib target complementary anti-apoptotic pathways and synergistically suppress HCC, providing the rationale for clinical studies with this novel combination.

Endoscopic surgical treatment of bromhidrosis: a report of 18 consecutive patients from 2010 to 2013.

BACKGROUND: The current treatments available for bromhidrosis, such as subdermal excision of the apocrine glands, liposuction-curettage, and laser therapy, have certain drawbacks, for example, requirement of repeated treatments, high recurrence rate, and induration, pain, and scarring in the armpits. In this study we aimed to investigate the clinical efficacy and complications of endoscopic surgery for treatment of bromhidrosis. PATIENTS AND METHODS: From August 2010 to June 2013, 18 patients (15 women and 3 men; mean age, 31 years old; age range, 19-40 years) with axillary bromhidrosis underwent endoscopic resection of the apocrine glands. The clinical efficiency and patient satisfaction were investigated by the Dermatology Quality Life Index scoring system, and complications of the surgery were assessed. RESULTS: The mean operative time was 128 minutes (range, 92-164 minutes). Subcutaneous fluid drainage occurred in 5 of the 18 patients. Skin necrosis, upper limb edema, and bleeding did not occur in any patient. In 2 patients, subcutaneous fluid accumulation recurred after discharge. Numbness of the inside of the upper arm occurred in 3 patients. After approximately 0.5-2 years of follow-up, all patients had considerably reduced axillary sweating. The Dermatology Quality Life Index assessment indicated that the influence of bromhidrosis on the patients' life quality was greatly reduced. CONCLUSIONS: Our endoscopic surgical technique for the treatment of axillary bromhidrosis causes minimal tissue damage, allows full exposure, and is associated with few complications and a low recurrence rate.

[A meta-analysis of clinical outcomes after laparoscopic operation for rectal cancer].

OBJECTIVE: To evaluate the clinical outcomes after laparoscopic surgery for rectal cancer. METHODS: A systematic literature search (Medline, Embase, Cochrane Library) as of March 2010 was performed to identify all eligible studies. Two reviewers independently screened and extracted the data. Differences in short-term and long-term clinical outcomes after laparoscopic resection (LR) and open resection (OR) were analyzed using RevMan 5. RESULTS: A total of 1042 abstracts were retrieved and 16 clinical controlled studies finally included. The total number of patients was 2850. There were 1145 patients received LR and 1705 received OR. The analyses showed that LR had longer operative time (WMD=42.50, 95%CI: 29.27 to 55.74, P<0.05), less harvested lymph nodes (WMD=-0.94, 95%CI: -1.47 to -0.41, P<0.05), and less blood loss (WMD=-158.46, 95%CI: -221.08 to -95.84, P<0.05) as compared to OR. LR was superior to OR in terms of surgical mortality (OR=0.40, 95%CI: 0.18 to 0.92, P=0.03), postoperative complications (OR=0.73, 95%CI: 0.61 to 0.87, P<0.05), and 5-year overall survival rate (OR=1.56, 95%CI: 1.21 to 2.02, P<0.05). There was no significant difference in positive rate of circumferential resection margin between the two groups (OR=1.00, 95%CI: 0.45 to 2.20, P=1.00). CONCLUSION: Compared to open surgery, short-term and long-term clinical outcomes after laparoscopic surgery are favorable.