Allulose mitigates chronic enteritis by reducing mitochondria dysfunction via regulating cathepsin B production.

Metabolic changes have been linked to the development of inflammatory bowel disease (IBD), which includes colitis. Allulose, an endogenous bioactive monosaccharide, is vital to the synthesis of numerous compounds and metabolic processes within living organisms. Nevertheless, the precise biochemical mechanism by which allulose inhibits colitis remains unknown. Allulose is an essential and intrinsic protector of the intestinal mucosal barrier, as it maintains the integrity of tight junctions in the intestines, according to the current research. It is also important to know that there is a link between the severity of inflammatory bowel disease (IBD) and colorectal cancer (CRC), chemically-induced colitis in rodents, and lower levels of allulose in the blood. Mice with colitis, either caused by dextran sodium sulphate (DSS) or naturally occurring colitis in IL-10-/- mice, had less damage to their intestinal mucosa after being given allulose. Giving allulose to a colitis model starts a chain of reactions because it stops cathepsin B from ejecting and helps lysosomes stick together. This system effectively stops the activity of myosin light chain kinase (MLCK) when intestinal epithelial damage happens. This stops the breakdown of tight junction integrity and the start of mitochondrial dysfunction. To summarise, the study's findings have presented data that supports the advantageous impact of allulose in reducing the advancement of colitis. Its ability to stop the disruption of the intestinal barrier enables this. Therefore, allulose has potential as a medicinal supplement for treating colitis.

Arabinose confers protection against intestinal injury by improving integrity of intestinal mucosal barrier.

There is a growing amount of research that highlights the significant involvement of metabolic imbalance and the inflammatory response in the advancement of colitis. Arabinose is a naturally occurring bioactive monosaccharide that plays a crucial role in the metabolic processes and synthesis of many compounds in living organisms. However, the more detailed molecular mechanism by which the administration of arabinose alleviates the progression of colitis and its associated carcinogenesis is still not fully understood. In the present study, arabinose is recognized as a significant and inherent protector of the intestinal mucosal barrier through its role in preserving the integrity of tight junctions within the intestines. Also, it is important to note that there is a positive correlation between the severity of inflammatory bowel disease (IBD) and colorectal cancer (CRC), as well as chemically-induced colitis in mice, and lower levels of arabinose in the bloodstream. In two mouse models of colitis, caused by dextran sodium sulfate (DSS) or by spontaneous colitis in IL-10-/- mice, damage to the intestinal mucosa was reduced by giving the mice arabinose. When arabinose is administrated to model with colitis, it sets off a chain of events that help keep the lysosomes together and stop cathepsin B from being released. During the progression of intestinal epithelial injury, this process blocks myosin light chain kinase (MLCK) from damaging tight junctions and causing mitochondrial dysfunction. In summary, the results of the study have provided evidence supporting the beneficial effects of arabinose in mitigating the progression of colitis. This is achieved through its ability to avoid dysregulation of the intestinal barrier. Consequently, arabinose may hold promise as a therapeutic supplementation for the management of colitis.

Corrigendum to "Basal cell carcinoma arising from the scrotum: An understated entity" [Urol Case Rep 33 (2020) 101332].

[This corrects the article DOI: 10.1016/j.eucr.2020.101332.].

[Retracted] Long non­coding RNA MCM3AP­AS1 drives ovarian cancer progression via the microRNA­143­3p/TAK1 axis.

Following the publication of this article, the authors' attention was drawn to the fact that Table I and Fig. 6 contained some errors: The former contained some incorrect data, whereas the latter contained some inappropriately selected tumor images. Following a further investigation in the Editorial Office, it has come to light that there were other possible anomalies associated with the presentation of the tumor images, and also that parts of the figure may have been published previously. Taking everything into consideration, the Editor has decided that the article should be retracted from the publication due to a lack of confidence in the data presented in this article. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not received any reply. The Editor regrets any inconvenience that the retraction of the paper will cause. [the original article was published in Oncology Reports 44: 1375­1384, 2020; DOI: 10.3892/or.2020.7694].

Estrogen and Preeclampsia: Potential of Estrogens as Therapeutic Agents in Preeclampsia.

There is a significant decline in the estrogen levels in preeclampsia, and exogenous administration of estradiol normalizes blood pressure and other associated symptoms of preeclampsia. The decrease in estrogen levels may be due to changes in enzyme activities of hydroxysteroid (17-ß) dehydrogenase 1, aromatase, and COMT. There is also a decrease in the novel, estrogenic G-protein-coupled receptor 30 (GPR30) in the placental trophoblast cells in preeclampsia. The activation of GPR30 protects the placenta from hypoxia-reoxygenation injury, decreases apoptosis and increases proliferation through eNOS and PI3K-Akt signaling pathways. Estrogens may also increase Ca2+-activated K+ channel function, decrease the release of inflammatory cytokines, and oxidative stress to improve placental perfusion. Both preclinical and clinical studies show the decrease in the 2-methoxyestradiol levels in preeclampsia, which may be due to a decrease in estradiol itself along with a decrease in the enzymatic actions of the COMT enzyme. 2-Methoxyestradiol activates HIF1α and vascular endothelial growth factor receptors (VEGFR-2) to maintain placental perfusion by increasing angiogenesis. The present review discusses the preclinical and clinical studies describing the role of estrogen in preeclampsia along with possible mechanisms.

Integrin ß1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling.

AIMS: Abnormal trophoblast invasion is one of the onsets of preeclampsia (PE). Studies found that integrin ß1 (ITGB1) is closely related to PE, but the role of ITGB1 in the progression of trophoblast remained unclear. Therefore, we studied the functional role of ITGB1 in PE and its effects on trophoblast. METHODS: ITGB1 expression in placenta tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of transfection on HTR-8/SVneo cells were analyzed by qRT-PCR and western blotting. After cell transfection, colony formation assay, flow cytometry, wound healing assay, and transwell assay were performed to detect cell proliferation, apoptosis, migration, and invasion. Western blotting assay was used for determining phosphoinositide 3 kinase (PI3K) and protein kinase B (Akt) signaling pathway. After inhibiting PI3K/Akt pathway, apoptosis-regulated proteins were detected by western blotting, and the effects of inhibitor on the migration and invasion changes were examined. RESULTS: ITGB1 was downregulated in placenta tissues from PE patients, as compared with normal. ITGB1 overexpression in HTR-8/SVneo cells enhanced cell proliferation, migration, and invasion, reduced cell apoptosis, and improved phosphorylation of PI3K and Akt. However, ITGB1 depletion resulted in an opposite effect to its overexpression. Inhibition of PI3K/Akt pathway completely blocked the effect of ITGB1 overexpression on cells, because we observed that apoptosis-regulated proteins were highly upregulated, and that cell migration and invasion were reduced. CONCLUSION: ITGB1 regulated HTR-8/SVneo cell progression by activation of the PI3K/Akt pathway.

Application and Prospects of Molecular Imaging in Immunotherapy.

Recently, immunotherapies that target the interactions of programmed cell death 1 (PD-1) with its major ligands, programmed death ligand 1 (PD-L1) and programmed death ligand 2 (PD-L2), have achieved significant success. To date, several immune checkpoint inhibitors targeting the PD-1/PD-L1 pathway have been developed to treat melanoma, non-small cell lung cancer, head and neck cancer, renal cell carcinoma, and urothelial carcinoma. Despite promising outcomes with immunotherapy, there are many limitations to several current immune biomarkers for predicting immune benefits and to traditional imaging for evaluating the efficacy and prognosis of immunotherapy and monitoring adverse reactions. In this review, we recommend a novel imaging method, molecular imaging. This paper reviews the application and prospects of molecular imaging in the context of current immunotherapies in regard to the following aspects: 1) detecting the expression of PD-1/PD-L1; 2) evaluating the efficacy of immunotherapy; 3) assessing patient prognosis with immunotherapy; 4) monitoring the toxicity of immunotherapy; and 5) other targets imaging.

Basal cell carcinoma arising from the scrotum: An understated entity.

Basal cell carcinoma (BCC) is the most commonly occurring carcinoma among humans. Reports of this lesion on nonexposed areas, such as the scrotum, soles, vulva, groin, pubic region, and axilla, are relatively uncommon. We present the case of a male patient with BCC located in the scrotum with a duration of 12 years who was successfully treated by local excision. Histopathology revealed infiltration by BCC. Our objective of this report is to remind specialists like urologists of the possibility of scrotal BCC when encountering scrotal lesions of unknown origin or not responding to topical treatments in a reasonable time frame.

Long non­coding RNA MCM3AP­AS1 drives ovarian cancer progression via the microRNA­143­3p/TAK1 axis.

The long non­coding RNA (lncRNA) MCM3AP antisense 1 (MCM3AP­AS1) has previously been shown to be a key regulator of multiple types of cancer; however whether it is important in the context of ovarian cancer (OC) is uncertain. The present study determined that MCM3AP­AS1 expression in samples from patients with OC was significantly increased, and was associated with tumor stage, presence of lymph node metastases and poorer overall survival. The role of this lncRNA was investigated in vitro, and it was observed that knockdown of MCM3AP­AS1 impaired OC cell proliferation, migration and colony formation. Similarly, it disrupted tumor growth in vivo. The present study further determined that MCM3AP­AS1 was able to directly interact with microRNA (miRNA or miR)­143­3p as a competing endogenous (ce)RNA for this miRNA, thereby regulating the expression of transforming growth factor­ß­activated kinase 1 (TAK1), a known target of miR­143­3p in OC. Consistent with this, inhibition of miR­143­3p was sufficient to partially reverse the effects of MCM3AP­AS1­knockdown, which inhibited the proliferation, migration and invasion of OC cells. Together, these results indicate that MCM3AP­AS1 serves as an oncogenic lncRNA in OC by binding to miR­143­3p and thereby promoting TAK1 expression, and suggest that this lncRNA may be a possible target for therapy in OC.

circ_KIAA1429 accelerates hepatocellular carcinoma advancement through the mechanism of m6A-YTHDF3-Zeb1.

AIMS: Hepatocellular carcinoma (HCC), one of the most common cancer, causes the fourth cancer-related deaths around the world. N6-methyladenosine (m6A) has been reported to mediate circRNA translation in cancer biology. However, the mechanisms by which m6A and circRNA in post-transcriptional in HCC progression remain poorly understood. This study aimed to explore the mechanisms by which m6A and circRNA in post-transcriptional in HCC progression. MAIN METHODS: circ_KIAA1429 (hsa_circ_0084922) expression profiles in matched normal and HCC tissues were detected using microarray analysis. The biological roles of circ_KIAA1429 in progression of HCCC were measured both in vitro and in vivo. KEY FINDINGS: In this study, we found hsa_circ_0084922, which came from KIAA1429, named circ_KIAA1429, was upregulated in HCC cells and tumor tissues. Overexpression of circ_KIAA1429 can facilitate HCC migration, invasion, and EMT process. However, knockdown of circ_KIAA1429 lead to the opposite results. Furthermore, it was demonstrated that Zeb1 was the downstream target of circ_KIAA1429. Up-regulation of Zeb1 led to HCC cells metastasis induced by circ_KIAA1429. In addition, YTHDF3 enhanced Zeb1 mRNA stability via an m6A dependent manner. SIGNIFICANCE: This study revealed that circ_KIAA1429 could accelerate HCC advancement, maintained the expression of Zeb1 through the mechanism of m6A-YTHDF3-Zeb1 in HCC. What's more, it might represent a potential therapeutic target in HCC.

Benign testicular cavernous hemangioma presenting with acute onset: A case report.

Cavernous hemangioma is a congenital, benign vascular tumor that occurs in the deep dermis and subcutaneous tissue. Testicular cavernous hemangioma is extremely rare, mostly occurring during childhood or adolescence. Testicular cavernous hemangioma is a benign tumor that appears as a slowly growing painless mass. In rare cases, it may be associated with acute testicular infarction or torsion with acute onset. We herein report the case of a patient with an atypical presentation of testicular cavernous hemangioma, characterized by acute painful testicular enlargement triggered by minor injury. The patient underwent right radical orchiectomy, and histopathological examination confirmed the diagnosis of testicular cavernous hemangioma. Although this is a rare tumor, it should be considered in the differential diagnosis of testicular tumors.

Depiction of Vaginal Microbiota in Women With High-Risk Human Papillomavirus Infection.

Persistent infection with the carcinogenic human papillomavirus (HPV) is a prerequisite for the progression of cervical lesions and cancer. A growing body of research has focused on the functional role of the vaginal microbiota in the persistence of HPV infection. Understanding the microbial composition and structure in women with high-risk (hr)-HPV infection may help reveal associations between the vaginal microbiota and HPV infection, and identify potential biomarkers. Our study investigated the vaginal microbial community in women with and without hr-HPV infection, by using 16s rRNA gene sequencing. We found that microbial perturbations occurred in the early phase of hr-HPV infection. Lactobacillus and Sporolactobacillus were decreased, while bacteria related to bacterial vaginosis (BV), such as Gardnerella, Prevotella, Dialister, Slackia, Actinomyces, Porphyromonas, Peptoniphilus, Anaerococcus, Peptostreptococcus, Streptococcus, Ureaplasma, Megasphaera, and Mycoplasma were increased. Our results could offer insights into the correlations between hr-HPV and the vaginal microbiota in the early infection period, and provide indications that the predominance of some BV-associated bacteria during hr-HPV infection may increase the risk for cervical neoplasia.

Chaperone-mediated autophagy regulates apoptosis and the proliferation of colon carcinoma cells.

Chaperone-mediated autophagy (CMA) is one of the three types of autophagy. In recent years, CMA has been shown to be associated with the pathogenesis of several types of cancer. However, whether CMA is involved in the pathogenesis of colorectal cancer (CRC) remains unclear. In this study, we investigated CMA activity in tissue specimens from CRC patients and mouse models of colitis-associated CRC (induced by administration of AOM plus DSS). In addition, we down-regulated CMA in CT26 colon carcinoma cells stably transfected with a vector expressing a siRNA targeting LAMP-2A, the limiting component in the CMA pathway, to explore the role of CMA in these cells. Apoptosis was detected using TUNEL assay, and the apoptosis-related proteins were detected using western blotting. Cell proliferation was assessed using MTT assay, Ki-67 labelling and western blotting for PCNA. We found that LAMP-2A expression was significantly increased in CRC patients and mouse models and varied according to the stage of the disease. Inhibition of CMA in CT26 cells facilitated apoptosis, as evidenced by increased TUNEL immunolabeling, increased expression of Bax and Bnip3, and decreased expression of Bcl-2. Cell proliferation assays showed that inhibition of CMA impeded the proliferation of CT26 cells. These data support the hypothesis that CMA is up-regulated in CRC, and inhibition of CMA may be a new therapeutic strategy for CRC patients.

Concurrent apatinib and docetaxel vs apatinib monotherapy as third- or subsequent-line therapy for advanced gastric adenocarcinoma: a retrospective study.

PURPOSE: The aim of this study was to assess the efficacy and safety of concurrent apatinib and docetaxel therapy vs apatinib monotherapy as third- or subsequent-line treatment for advanced gastric adenocarcinoma (GAC). METHODS: Patients, who had received apatinib with or without docetaxel as third or more line therapy for advanced GAC, were retrospectively reviewed. Propensity score matching (PSM) analysis was performed to minimize the potential confounding bias. Kaplan-Meier curve and log-rank test were used to analyze the survival. Prognostic factors were estimated by Cox regression. Adverse events (AEs) were evaluated using CTCAE 4.0. RESULTS: Thirty-four patients received concurrent therapy, whereas 31 received monotherapy. The median progression-free survival (PFS) and overall survival (OS) in monotherapy and con-therapy groups were 2.5 and 4 months (P=0.002), 3.3 and 6 months (P=0.004), respectively. After PSM, the median PFS and OS in the con-therapy group were also superior to the monotherapy group (P=0.004 and P=0.017). Cox regression suggested that Eastern Cooperative Oncology Group performance status (ECOG PS; HR =2.437, 95% CI: 1.349-4.404, P=0.003), CA199 (HR =1.001, 95% CI: 1.000-1.002, P=0.016), and treatment options (HR =0.388, 95% CI: 0.222-0.679, P=0.001) had significant effects on OS. Grade 3/4 toxicities in the monotherapy and con-therapy groups were as follows: leukopenia (0% vs 8.8%), neutropenia (3.2% vs 2.9%), anemia (9.8% vs 8.8%), thrombocytopenia (6.4% vs 2.9%), proteinuria (3.2% vs 2.9%), aminotransferase (0% vs 11.8%), hyperbilirubinemia (9.8% vs 5.9%), hypertension (9.8% vs5.9%), hand-foot syndrome (3.2% vs 8.8%), nausea and vomiting (0% vs 11.8%), diarrhea (0% vs 5.9%), and fatigue (6.5% vs 2.9%). CONCLUSION: Patients with advanced GAC benefit more from concurrent apatinib and docetaxel therapy than apatinib monotherapy.

Protective Role of TNIP2 in Myocardial Injury Induced by Acute Pancreatitis and Its Mechanism.

BACKGROUND Aberrant regulation of nuclear factor-κB (NF-κB) and the signaling pathways that regulate its activity have been found to be involved in various pathologies, particularly cancers, as well as inflammatory and autoimmune diseases. Acute pancreatitis (AP) is a complex pathological process, depending on autodigestion caused by premature activation of zymogens. This study aimed to investigate the effect of high expression of TNIP2 gene on AP and AP-induced myocardial injury. MATERIAL AND METHODS To investigate the effect of TNIP2 on AP and AP-induced myocardial injury, we established an AP cell model and rat model. HE staining was applied for histological examination. ELISA was used to determine the level of pro-inflammatory cytokines (TNF-α and IL-6) and myocardial injury markers (LDH and CK-MB). QRT-PCR and Western blot analysis were performed to determine the mRNA and protein level of related genes, respectively. RESULTS We found that the protein level of TNIP2 was relatively higher in the normal AR42J cells. At 4 h after stimulating with cerulein, the protein level of TNIP2 decreased, reached a minimum at 8 h, and then gradually increased. We also found that TNIP2 was correlated with the activation of NF-κB in cerulein-stimulated AR42J cells, and TNIP2 over-expression inhibited the inflammatory response caused by cerulein. Moreover, our results suggest that TNIP2 over-expression relieved the cerulein-triggered inflammatory response and AP-induced myocardial injury in mice. CONCLUSIONS TNIP2 was shown to exert a protective effect on AP and AP-induced myocardial injury.

Co-delivery of paclitaxel and TOS-cisplatin via TAT-targeted solid lipid nanoparticles with synergistic antitumor activity against cervical cancer.

BACKGROUND: Cervical cancer is a major world health problem for women. Currently, cancer research focuses on improving therapy for cervical cancer using various treatment options such as co-delivery of chemotherapeutic agents by nanocarriers. PURPOSE: The aim of this study was to develop trans-activating transcriptional activator (TAT)-modified solid lipid nanoparticles (SLNs) for co-delivery of paclitaxel (PTX) and α-tocopherol succinate-cisplatin prodrug (TOS-CDDP) (TAT PTX/TOS-CDDP SLNs) in order to achieve synergistic antitumor activity against cervical cancer. METHODS: Lipid prodrug of CDDP (TOS-CDDP) and TAT-containing polyethylene glycol-distearoyl-phosphatidylethanolamine (TAT-PEG-DSPE) were synthesized. TAT PTX/TOS-CDDP SLNs were prepared by emulsification and solvent evaporation method. Physicochemical characteristics of SLNs such as size, morphology, and release profiles were explored. In vitro and in vivo studies were carried out to assess the efficacy of their antitumor activity in target cells. RESULTS: TAT PTX/TOS-CDDP SLNs could be successfully internalized by HeLa cells and showed a synergistic effect in the suppression of cervical tumor cell growth. They exhibited high tumor tissue accumulation, superior antitumor efficiency, and much lower toxicity in vivo. CONCLUSION: The present study indicates that the co-delivery system provides a promising platform as a combination therapy for the treatment of cervical cancer, and possibly other types of cancer as well.

MicroRNA-497 downregulation contributes to cell proliferation, migration, and invasion of estrogen receptor alpha negative breast cancer by targeting estrogen-related receptor alpha.

Metastasis has become the main challenge for treatment of estrogen receptor alpha (ERα) negative breast cancer. Here, we found a negative correlation between miR-497 and estrogen-related receptor alpha (ERRα), a nuclear receptor overexpressed in ERα negative breast cancer. Targeted inhibition of ERRα by si-RNA increased miR-497 expression while overexpression of ERRα inhibited miR-497 expression. Further investigation showed that miR-497 targeted ERRα by binding to the 3'UTR region of ERRα. Luciferase assay and ChIP assay confirmed that ERα directly regulated the transcription of miR-497, suggesting that loss of ERα lowered miR-497 level in ERα negative breast cancer. Further, overexpression of miR-497 not only inhibited ERRα expression but also reduced MIF level and MMP9 activity, which led to significant decreases in cell proliferation, migration, and invasion of ERα negative breast cancer. Taken together, our findings suggested that, in ERα negative breast cancer, the low level of ERα reduced miR-497 expression, which promoted ERRα expression that enhanced cell proliferation, migration, and invasion by increasing MIF expression and MMP9 activity.

Gemcitabine Plus Vinorelbine as Second-Line Therapy in Patients With Metastatic Esophageal Cancer Previously Treated With Platinum-Based Chemotherapy.

We evaluated the efficacy and feasibility of the combination of gemcitabine plus vinorelbine in patients with platinum-based chemotherapy-refractory esophageal cancer. We enrolled 35 patients who received gemcitabine plus vinorelbine as second-line treatment after platinum-based chemotherapy failure between May 2009 and April 2012. Dosage: gemcitabine 1,000 mg/m(2) plus vinorelbine 25 mg/m(2); all drugs were administered on days 1 and 8 of a 21-day cycle, and this was continued until failure or unacceptable toxicity. A total of 125 cycles of treatment were administered, and all patients received at least two cycles of treatment (two to five cycles; median number of cycles: three). Thirty-two patients were evaluable for response. The response rate was 31.3%, and the disease control rate (partial response plus stable disease) was 62.5%. The progression-free survival (PFS) was 4.3 ± 0.2 months [95% confidence interval (CI), 4.0-4.6], and the median overall survival (OS) was 7.3 ± 0.3 months (95% CI, 6.7-7.8). In the subgroup analysis, median PFS was 4.0 ± 0.2 months (95% CI, 3.6-4.3) in patients with high expression of miRNA-214, while it was 4.6 ± 0.3 months (95% CI, 4.1-5.1) in patients with low expression of miRNA-214 (log rank = 0.023). Myelosuppression with neutropenia and thrombocytopenia was the most common side effect observed with this combination regimen, and higher than grade 3 neutropenia and thrombocytopenia were observed in 10 (31.3%) and 8 patients (25.0%), respectively. Grade 3 fatigue was the most common nonhematologic toxicity, which was observed in 2 (6.1%) patients. The combination of gemcitabine plus vinorelbine was well tolerated as second-line treatment for platinum-based chemotherapy-refractory esophageal cancer patients and appeared to provide enhanced clinical activity especially in patients with low expression of miRNA-214.

Isocentric C-arm three-dimensional navigation versus conventional C-arm assisted C1-C2 transarticular screw fixation for atlantoaxial instability.

OBJECTIVE: The Isocentric C-arm 3D navigation has been widely used in superior cervical surgeries in recent years. Several clinical researches reported that navigation system was an effective support device for treatment of atlantoaxial instability. But there were few studies about the advantages of navigation system compared to conventional C-arm fluoroscopy in C1-C2 transarticular screw fixation for atlantoaxial instability. The aim of the study was to evaluate the precision of computer-assisted C1-C2 transarticular screw fixation (Magerl's technique) for atlantoaxial instability and compare the clinical results with conventional C-arm fluoroscopy. METHODS: Forty-two patients diagnosed as atlantoaxial instability who underwent C1-C2 transarticular screw fixation under two different fluoroscopy methods were studied. The Iso-C 3D navigation group included 18 patients and the other 24 patients were in the conventional C-arm group. The clinical and radiographic results were recorded and compared between the two groups. Patients were followed up with clinical examination and radiographs at a mean of 18.4 months. RESULTS: There were no significant differences between two groups in the mean age, gender, and causes of atlantoaxial instability. The mean blood loss in the navigation group was 236.1 ± 28.5 mL versus 308.3 ± 21.2 mL in the conventional C-arm group. The radiation time was significantly reduced using 3D navigation (48.8 ± 1.05 s versus 60.3 ± 2.23 s). Overall, 97.2 % (35/36) of 3D navigated screws and 91.7 % (44/48) of fluoroscopy screws were placed into the C1-C2 transarticular passages. Thirty-nine of forty patients showed evidence of solid fusion after 12 months on cervical plain radiographies or CT scans. CONCLUSIONS: On comparing the two imaging techniques, it was found that using Iso-C 3D navigation can improve accuracy of the C1-C2 transarticular screws, decrease intra-operative fluoroscopic time and blood loss, and not prolong the operative time. This study demonstrates that Iso-C 3D navigation is a safe and effective means of guiding C1-C2 transarticular screw fixation for atlantoaxial instability.

Cervical cancer gene therapy by gene loaded PEG-PLA nanomedicine.

BACKGROUND AND AIMS: Advances in the treatment of cervical cancer over the last decade have predominantly involved the development of genes directed at molecular targets. Gene therapy is recognized to be a novel method for the treatment of cervical cancer. Genes can be administered into target cells via nanocarriers. This study aimed to develop systemically administrable nano-vectors. Floate (Fa) containing gene loaded nanoparticles (NPs) could target HeLa human cervical cancer cells through combination with receptors on the cells to increase the nuclear uptake of genetic materials. METHODS: Fa was linked onto Poly (ethylene glycol)-b-poly (D, L-lactide) (PEG-PLA) to form Fa-PEG-PLA, and the resulting material was used to load plasmids of enhanced green fluorescence protein (pEGFP) to obtain gene loaded nanoparticles (Fa-NPs/DNA). Physical-chemical characteristics, in vitro release and cytotoxicity of Fa-NPs/DNA were evaluated. The in vitro transfection efficiency of Fa-NPs/ DNA was evaluated in HeLa cells and human umbilical vein endothelial cells (HUVEC). PEG-PLA without Fa was used to load pEGFP from NPs/DNA as a control. RESULTS: Fa-NPs/DNA has a particle size of 183 nm and a gene loading quantity of 92%. After 72h of transfection, Fa-NPs/DNA displayed over 20% higher transfection efficiency than NPs/DNA and 40% higher than naked DNA in HeLa cells. However, in HUVECs, no significant difference appeared between Fa-NPs/DNA and NPs/DNA. CONCLUSIONS: Fa-PEG-PLA NPs could function as excellent materials for gene loading. This nano-approach could be used as tumor cell targeted medicine for the treatment of cervical cancer.