[Endoscopic totally visceral sac separation for ventral hernias repair: anatomy notes and technical considerations].

The abdominal wall can be treated as a whole physiological and functional entity which is composed of multiple anatomical structures and planes. Surgical approaches and technical details that required are diverse in different area. Indeed, the abdominal wall is confined by several anatomical boundaries which make these surgical planes separated. If one could dissect these boundaries, then separated spaces could be connected, establishing an ample retromuscular/preperitoneal space to accommodate the mesh of ventral hernia repair. The concept of totally visceral sac separation (TVS) is achieved. The TVS concept is a summary of diverse ventral hernia repair techniques. Since its initiation and spread, this technique has been widely accepted and implemented by domestic surgeons due to its outstanding performance. This treatise will review the relevant anatomy as well assurgical tricks by the authors that aid in performing TVS. Some of the details are more tricky and harder to understand, thus this in-depth description of the technique.

LncRNA AB073614 promotes the proliferation and inhibits apoptosis of cervical cancer cells by repressing RBM5.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "LncRNA AB073614 promotes the proliferation and inhibits apoptosis of cervical cancer cells by repressing RBM5, by L.-Y. Guo, C.-F. Qin, H.-X. Zou, M.-Y. Song, M.-L. Gong, C. Chen, published in Eur Rev Med Pharmacol Sci 2019; 23 (6): 2374-2379-DOI: 10.26355/eurrev_201903_17382-PMID: 30964162" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17382.

LncRNA AB073614 promotes the proliferation and inhibits apoptosis of cervical cancer cells by repressing RBM5.

OBJECTIVE: Recent studies have determined the crucial role of long noncoding RNAs (lncRNAs) in cancer development. Cervical cancer (CC) is a common type of fatal gynecological cancer worldwide. This study aims to identify the role of lncRNA AB073614 in the progression of CC. PATIENTS AND METHODS: Relative level of AB073614 in 3 CC cell lines and 48 paired CC samples was determined by the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The potential regulatory effects of AB073614 on the cellular behaviors of CC cells were explored through apoptosis assay, colony formation assay, and proliferation assay in vitro. The underlying mechanism of AB073614 in mediating the progression of CC was also conducted. RESULTS: The AB073614 expression was remarkably higher in CC tissues than that in adjacent tissues. The knockdown of AB073614 inhibited proliferation but induced apoptosis of CC cells. In addition, RBM5 (RNA binding motif 5) was upregulated in CC cells after knockdown of AB073614 in vitro. Furthermore, a negative correlation was seen between the expressions of RBM5 and AB073614 in CC tissues. CONCLUSIONS: AB073614 could promote proliferation and inhibit apoptosis of CC cells through downregulating RBM5, which may offer a new therapeutic intervention for CC patients.

EGF promotes HIF-1α expression in colorectal cancer cells and tumor metastasis by regulating phosphorylation of STAT3.

OBJECTIVE: Hypoxia-inducible factor 1α (HIF-1α) functions importantly in the development of colorectal cancer. HIF-1α is induced by some cytokines and growth factors and is also regulated by another kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathways. Meanwhile, inhibiting HIF-1α expression can inhibit the development of colorectal cancer. The aim of this study was to explore the effect of epidermal growth factor (EGF) on the activation of signal transducer and activator of transcription 3 (STAT3) in human colorectal cancer cells SW480. In addition, the underlying mechanism of the STAT3 signaling pathway in regulating HIF-1α and further affecting tumorigenesis and metastasis was investigated. MATERIALS AND METHODS: Immunofluorescence and Western blotting were used to detect the activation of STAT3 by EGF in human colorectal cancer cells SW480. SW480 cells were transfected with STAT3 siRNA or treated with STAT3 inhibitor Niclosamide, and then stimulated with EGF to change the expressions of STAT3 and p-STAT3. The expression level of HIF-1α mRNA in SW480 cells was detected by Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR). In addition, transwell assay and tumor formation experiments were performed to validate whether STAT3 and HIF-1α affected SW480 through EGF. RESULTS: STAT3 was not activated in SW480 cells in vitro. EGF induced STAT3 activation and enhanced its phosphorylation level, so that it shuttled into the nucleus. Phosphorylated activation of STAT3 was a necessary condition for EGF to induce HIF-1α up-regulation. Both HIF-1α and EGF-induced phosphorylation of STAT3 could significantly promote the proliferation and metastasis of SW480, and enhance tumorigenesis. CONCLUSIONS: In SW480 cells, EGF regulated HIF-1α through the STAT3 phosphorylation pathway, eventually promoting the occurrence and metastasis of colorectal cancer.

[Totally endoscopic sublay repair (TES)--a novel approach to repair midline ventral hernia].

Objective: Investigating a novel approach to treat a midline ventral hernia--totally endoscopic sublay repair (TES). The procedure will be described in detail and the safety and efficacy evaluated. Methods: During July and December 2017, eleven consecutive cases of primary and secondary epigastric midline ventral hernias were repaired using the TES procedure. A large mesh should be placed in the retrorectus position using this minimally invasive procedure. The indications for this procedure include umbilical, epigastric and incisional hernia equal in length to the rectus diastasis. Results: All operations were successful without open conversion. The mean operation time was 120 mins(80-205 min), postoperative pain was mild and the mean VAS was 2.5 on first postoperative day. The average postoperative stay in hospital was 3.3 days (2-5 days). 2 cases experienced postoperative seroma but without adverse effect on the final outcome and no recurrences during the follow-up period of 1 to 6 months. Conclusions: TES procedure is safe, practical and minimally invasive requiring no specific device and highly reproducible. Besides there is no need for expensive anti-adhesion mesh and fixation tacker which make it more cost effective. TES is a good technique for the surgical treatment of midline ventral hernia.

[Guidelines for diagnosis and treatment of dengue in China].

Dengue is the most prevalent and rapidly spreading mosquito-borne viral disease. As a dengue non-endemic country, China has experienced several dengue outbreaks in recent years. However, dengue patients in China displayed distinct clinical characteristics compared to patients in endemic countries. To standardize the diagnosis and treatment of dengue fever, the experts of the Society of Infectious Diseases, Society of Tropical Medicine and Parasitology of Chinese Medical Association, and the Society of Emergency Medicine, China Association of Chinese Medicine have reached this guideline based on guidelines for diagnosis, treatment, prevention and control of dengue (World Health Organization, 2009); guidelines for diagnosis and treatment of dengue (National Health and Family Planning Commission of the People's Republic of China, 2014, Edition 2), health industry standard of the People's Republic of China "diagnosis for dengue fever (WS216-2018)" and systemic reports on dengue. The guideline includes 8 aspects: introduction, terminology, epidemiology and prevention, etiology and pathogenesis, clinical features, diagnosis, treatment and problems to be solved.

MicroRNA-217 functions as a prognosis predictor and inhibits pancreatic cancer cell proliferation and invasion via targeting E2F3.

OBJECTIVE: Pancreatic cancer (PC) is the most malignant tumor among all the tumors in the digestive system. MiR-217 has been reported to take a critical part in various malignant tumors. The aim of this study was to explore the function of MiR-217 in pancreatic cancer and its target genes. PATIENTS AND METHODS: Twenty pairs of PC tissues and matched normal adjacent pancreatic tissues were collected. The expression of miR-217 in PC tissues and normal pancreatic tissues was detected by Real-time polymerase chain reaction (PCR). PC cells were transfected with miR-217 mimics, inhibitors and negative control, respectively. Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Cell apoptosis was checked via Annexin V-FITC/PI apoptosis kit. The protein expression of E2F3 was detected by Western blot. To detect repression by miR-217, HEK293T cells were co-transfected with the indicated E2F3 3'-UTR luciferase reporter. RESULTS: The expression of miR-217 was reduced in PC tissues comparing to normal pancreatic tissues. Meantime, the in-vitro study revealed that miR-217 suppressed PC cell growth, invasion but promoted apoptosis. Next, we proved that E2F3 was the target of miR-217 on PC cell function. CONCLUSIONS: miR-217 suppresses PC cell growth, invasion but promotes apoptosis in vitro through targeting E2F3. The miR-217-E2F3 axis may be used for PC therapy.

Long non-coding RNA TUG1 can promote proliferation and migration of pancreatic cancer via EMT pathway.

OBJECTIVE: This paper aimed to investigate the effect of long non-coding RNA TUG1 (lncRNA TUG1) on cell proliferation, as well as cell migration in pancreatic cancer. PATIENTS AND METHODS: The mRNA levels of Taurine-up-regulated gene 1 (TUG1) in three kinds of pancreatic cancer cells BxPC3, PaTu8988 and SW1990 was detected by RT-qPCR. Meantime, RT-qPCR was used to examine the mRNA levels of TUG1 in 20 cases of human pancreatic cancer tissues and its para-carcinoma tissues. pCDH-TUG1 plasmid and its empty plasmid pCDH were transfected into BxPC3 and PaTu8988 cells to up-regulate TUG1 expression. siRNA targeting TUG1 and the control siRNA were transfected into SW1990 cells to down-regulate TUG1 expression. Cell clone formation and CCK-8 assay were used to detect the cell proliferation capacity. Transwell assay was used to evaluate cell migration capacity. Western blot was applied to examine the protein expressions of MMP2, MMP9, E-cadherin, Smad 2, Smad 3, p-Smad 2, p-Smad 3, TGF-ß and TGF-ßR. RT-qPCR was used to detect the levels of MMP2 and MMP9. RESULTS: The results showed that TUG1 was differentially expressed in the three kinds of pancreatic cancer cells, among which the expression level of SW1990 was relatively high, and the expression levels of BxPC3 and PaTu8988 were relatively low. TUG1 had more expression in pancreatic cancer tissues than that in para-carcinoma tissues. After the up-regulation of TUG1, cell proliferation and migration capacities were increased, protein levels of MMP2 and MMP9 were increased and protein level of E-cadherin was declined. Conversely, after down-regulation of TUG1 expression, cell proliferation and migration capacities were weakened, protein levels of MMP2 and MMP9 were decreased and protein level of E-cadherin was increased. In addition, over-expressed TUG1 could promote Smad2 and Smad3 phosphorylation, but Smad2 and Smad3 phosphorylation were weakened after down-regulated expression of TUG1. The protein expression of TGF-ß and TGF-ß receptor were more in the TUG1 overexpression group than that in the control group, while the result was just opposite after TUG1 expression was down-regulated. CONCLUSIONS: These data suggest that lncRNA TUG1 may enhance the proliferation and migration of pancreatic cancer cells through EMT pathway.

Identification of a recombinant dengue virus type 1 with 3 recombination regions in natural populations in Guangdong province, China.

Using recombination analysis, we identified a recombinant dengue virus type 1 strain, namely, GD23/95, with three recombination regions, located within the sequences of the prM/E junction, NS1, and NS3, respectively. The recombinant dengue virus was further confirmed by phylogenetic analysis based on its recombination and non-recombination regions. This appears to be the first study to confirm the existence of three recombination regions in a single dengue virus isolate and to report recombination between parent virus strains isolated from the same geographic area (Guangdong province, China). It is also the first to report breakpoints within the NS3 gene of dengue viruses.

Capsid-targeted viral inactivation can destroy dengue 2 virus from within in vitro.

Capsid-targeted viral inactivation (CTVI) has emerged as a conceptually powerful antiviral strategy that exploits viral structural proteins to target a destructive enzyme specifically into progeny virions. We have recently demonstrated the principle of CTVI against dengue virus infection and observed a modest therapeutic effect in vitro (Arch Virol 2005, 150: 659-669). Here we tested a prophylactic model of CTVI, in which mammalian cells stably expressing the dengue 2 virus capsid protein fused to a nuclease were infected with dengue virus and determined the effects on progeny virion infectivity. CTVI efficiently destroyed dengue 2 virus from within and decreased the infectious titers by 10(3)- to 10(4)-fold, suggesting that CTVI has potential in the prophylactic application for dengue virus infection.

Therapeutic effects of dengue 2 virus capsid protein and staphylococcal nuclease fusion protein on dengue-infected cell cultures.

Dengue infection poses a serious public health problem in most tropical and subtropical areas. No effective antiviral drugs or vaccines are currently available against dengue infection. To explore the feasibility of using capsid-targeted viral inactivation (CTVI) as an antiviral strategy against dengue infection, we constructed a plasmid expressing a fusion protein consisting of staphylococcal nuclease (SN) fused to dengue 2 virus capsid protein (D2C), and investigated its effects on the production of infectious virions when introduced into BHK cells infected with dengue virus. The results indicated that D2C-SN can be expressed and tolerated in this mammalian cell culture. The enzymatically active SN moiety was incorporated into nascent virions during the process of viral assembly. By comparing the effects of incorporated SN and SN*, an enzymatically inactive missense mutant form of wild-type SN, on the infectivity of progeny virions, we clearly demonstrated that nucleolytic activity was the major antiviral mechanism. Expression of D2C-SN fusion protein as a therapeutic agent resulted in a reduction in infectious titers of 12- to 60-fold. Therefore, dengue virus may be particularly vulnerable to a CTVI therapeutic approach.