Tetraspanin 1 regulates papillary thyroid tumor growth and metastasis through c-Myc-mediated glycolysis.

Papillary thyroid cancer (PTC) is the most common form of thyroid cancer and is characterized by its tendency for lymphatic metastasis, leading to a poor prognosis. Tetraspanin 1 (TSPAN1) is a member of the tetra-transmembrane protein superfamily and has been implicated in tumorigenesis and cancer metastasis in various studies. However, the role of TSPAN1 in PTC tumor development remains unclear. In this study, we aimed to investigate the impact of TSPAN1 on PTC cell behavior. Our results demonstrate that knockdown of TSPAN1 inhibits PTC cell proliferation, migration, and invasion, while overexpression of TSPAN1 has the opposite effect. These findings suggest that TSPAN1 might play a role in the tumorigenesis and invasiveness of PTC. Mechanistically, we found that TSPAN1 activates the ERK pathway by increasing its phosphorylation, subsequently leading to upregulated expression of c-Myc. Additionally, we observed that TSPAN1-ERK-c-Myc axis activation promotes glycolytic activity in PTC cells, as evidenced by the upregulation of glycolytic genes such as LDHA. Taken together, our findings indicate that TSPAN1 acts as an oncogene in PTC by regulating glycolytic metabolism. This discovery highlights the potential of TSPAN1 as a promising therapeutic target for PTC treatment. Further research in this area could provide valuable insights into the development of targeted therapies for PTC patients.

Preliminary Experience with Continuous Submucosal Anastomosis in Small-Diameter Hepaticojejunostomy during Single-Port Laparoscopic Choledochal Cyst Surgery in Children.

PURPOSE: Hepaticojejunostomy anastomosis (HJA) is the most challenging aspect in single-port laparoscopic choledochal cystectomy and Roux-en-Y hepaticojejunostomy (SPCH) in children, especially in small-diameter anastomoses (diameters less than 5 mm), which are more susceptible to anastomotic stricture. We developed the continuous submucosal technique for HJA (CS-HJA) to lessen postoperative complications. The purpose of this study is to introduce our preliminary experiences with CS-HJA. METHODS: We retrospectively analyzed all available clinical data of children who underwent SPCH surgery between March 2020 and October 2022. We operated with CS-HJA on 10 children who were diagnosed with small-diameter hepaticojejunostomy (diameter less than 5 mm). Data collection mainly included demographic information, imaging data, perioperative details, and postoperative outcomes. Ten patients were included in this study. The average patient age was 55.2 months; the age range was 3 to 120 months, and the average weight was 11.6 kg; male-female ratio was 1:9. The choledocho had fusiform dilatation in five cases and cystic dilatation in five cases. There was no dilatation of the left and right hepatic ducts or intrahepatic bile ducts in all patients. All patients had no dilatation of the left and right hepatic ducts or intrahepatic bile ducts. All patients underwent a single-port laparoscopic bile-intestinal anastomosis using a submucosal jejunal anastomosis technique. Analysis of the duration of the bile-intestinal anastomosis, the length of the child's stay in the hospital after surgery, the intraoperative complications, and the postoperative complications was performed. RESULTS: All the 10 patients underwent successful SPCH by CS-HJA technique. The average length of time for hepaticojejunostomy ranged from 22 to 40 minutes, and the postoperative hospital stay was 5.2 to 9.2 days. There were no instances of bile leakage following the operation. At 17 to 30 months of follow-up, there was no abdominal pain or jaundice, and the reexamination of transaminases, bilirubin, and amylase were normal. Ultrasonography showed no bile duct stricture or dilated bile ducts, and the incision is elegant, and the families of the patients were satisfied. CONCLUSION: In SPCH surgery in children, the CS-HJA technique is safe and feasible for small-diameter hepaticojejunostomy.

Developing a nomogram for predicting surgical intervention in pediatric intussusception after hydrostatic reduction.

Purpose: The aim of this study was to develop and validate a nomogram for predicting surgical intervention in pediatric intussusception after hydrostatic reduction. Methods: Children with intussusception who had treated with sonographically guided saline hydrostatic reduction as an initial treatment were enrolled in this study. The enrolled patients were randomly selected for training and validation sets, and the split ratio was 7:3. The medical records of enrolled patients were retrospectively reviewed. The patients were divided into a surgery and a non-surgery group according to the results of the nonsurgical reduction. A model for predicting the risk of surgical treatment was virtualized by the nomogram using logistic regression analysis. Results: The training set consisted of 139 patients and the validation set included 74. After logistic regression analysis using training set, duration of symptoms, bloody stools, white blood cells (WBCs), creatine kinase isoenzyme (CK-MB), long-axis diameter, poor prognostic signs by ultrasound and mental state were identified as the independent predictors of surgical intervention for intussusception. A model that incorporated the above independent predictors was developed and presented as a nomogram. The C-index of the nomogram in the validation set was 0.948 (95% CI, 0.888-1.000). The calibration curve demonstrated a good agreement between prediction and observation. The decision curve analysis (DCA) curve showed that the model achieved a net benefit across all threshold probabilities. Conclusion: Based on the predictors of duration of symptoms, bloody stools, WBCs, CK-MB, long-axis diameter, poor prognostic signs by ultrasound and mental state, we developed a nomogram for predicting surgical intervention after hydrostatic reduction. This nomogram could be applied directly to facilitate pre-surgery decision for pediatric intussusception.

A micro-chamber free digital bio-detection for multiplexed and ultrasensitive immunoassay based on encoded magnetic microbeads and tyramide signal amplification strategy.

Digital bio-detection has become one of the most appealing methods in recent years due to its excellent performance with ultra-sensitivity in detection of low-abundance targets. Traditional digital bio-detection needs the utilization of micro-chambers for physical isolation of targets, while the recently developed beads-based micro-chamber free one is attracting extensive attention, although there exist the disadvantages of overlaps between positive ("1") and negative ("0") signals as well as the decreased detection sensitivity in multiplexed mode. Here we propose a feasible and robust micro-chamber free digital bio-detection for multiplexed and ultrasensitive immunoassay based on encoded magnetic microbeads (EMMs) and tyramide signal amplification (TSA) strategy. An EMMs-based multiplexed platform is constructed by using a fluorescent encoding method, then a puissant signal amplification of positive events in TSA procedure is achieved via systematical revelation of key factors influences. For proof of concept, a three-plexed tumor markers detection is performed to evaluate our established platform. The detection sensitivity is comparable to the corresponding single-plexed assays and is also approximately 30-15,000 times improvement compared to the conventional suspension chip. Therefore, this multiplexed micro-chamber free digital bio-detection paves a promising way to be an ultrasensitive and powerful tool for clinical diagnosis.

Casein Hydrolysate Alleviates Adipose Chronic Inflammation in High Fat-Diet Induced Obese C57BL/6J Mice through MAPK Pathway.

Obesity-induced adipose chronic inflammation is closely related to the development of insulin resistance and T2DM. Tripeptides l-valyl-l-prolyl-l-proline (VPP) and l-isoleucyl-l-prolyl-L-proline (IPP) derived from bovine casein have been reported to prevent inflammatory changes and mitigate insulin resistance in adipocytes. In this study, we aimed to investigate the influence of casein hydrolysates (CH) containing VPP and IPP on a high fat diet (HFD)-induced obese mice and cytokine TNF-α-induced adipocytes. Our data showed that CH alleviated chronic inflammation both in vivo and in vitro. 4% CH suppressed HFD-induced systemic inflammatory factors, hypertrophic white adipocytes, and macrophage infiltration. More importantly, CH was able to improve adipocyte dysfunction induced by TNF-α by increasing the expression of CCAAT/enhancer binding protein α (C/EBP-α) rather than peroxisome proliferator-activated receptor γ (PPAR-γ). Furthermore, CH also dose-dependently suppressed mitogen-activated protein kinase (MAPK)-c-Jun N-terminal kinase (JNK) phosphorylation and enhanced the phosphorylation of Erk 1/2, but not nuclear factor-kappa B (NF-κB) p65 phosphorylation, in TNF-α-induced 3T3-L1 cells. These results indicated that CH could ameliorate adipose chronic inflammation through the MAPK pathway. Altogether, our findings suggested that 4% CH supplementation for 6 weeks exerted a protective role in preventing obesity-related inflammation and adipose dysfunction.

Convenient tumor 3D spheroid arrays manufacturing via acoustic excited bubbles for in situ drug screening.

The quick and convenient fabrication of in vitro tumor spheroids models has been pursued for clinical drug discovery and personalized therapy. Here, uniform three-dimensional (3D) tumor spheroids are quickly constructed by acoustically excited bubble arrays in a microfluidic chip and performed drug response testing in situ. In detail, bubble oscillation excited by acoustic waves induces second radiation force, resulting in the cells rotating and aggregating into tumor spheroids, which obtain controllable sizes ranging from 30 to 300 µm. These spherical tumor models are located in microfluidic networks, where drug solutions with gradient concentrations are generated from 0 to 18 mg mL-1, so that the cell spheroids response to drugs can be monitored conveniently and efficiently. This one-step tumor spheroids manufacturing method significantly reduces the model construction time to less than 15 s and increases efficiency by eliminating additional transfer processes. These significant advantages of convenience and high-throughput manufacturing make the tumor models promising for use in tumor treatment and point-of-care diagnosis.

[Corrigendum] Nogo­B promotes the epithelial­mesenchymal transition in HeLa cervical cancer cells via Fibulin­5.

Following the publication of the above article, an interested reader drew to the authors' attention that the 'NB­4' and 'NB­2' panels for the invasion and migration assays shown in Fig. 3B and C on p. 113 appeared to contain overlapping data, such that the data may have been derived from the same original source, even though the panels were intending to have shown results obtained under different experimental conditions. The authors have re­examined their raw data and realized that these data were inadvertently mixed up when Fig. 3B and C were assembled. A corrected version of Fig. 3, showing the data as they should have appeared for the 'NB­4' and 'NB­2' invasion and migration assay experiments in Fig. 3B and C, is shown on the next page. The authors sincerely apologize for the errors that were introduced into Fig. 3 of the published article, and thank the Editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum. All the authors agree to the publication of the authors, and they apologize to the readership for any inconvenience caused. [Oncology Reports 29: 109­116, 2013; DOI: 10.3892/or.2012.2069].

Development of multi-species biofilm formed by thermophilic bacteria on stainless steel immerged in skimmed milk.

Thermophilic bacteria, such as Bacillus licheniformis, Geobacillus stearothermophilus, Bacillus Subtilis and Anoxybacillus flavithermus, are detected frequently in milk powder products. Biofilms of those strains act as a major contamination to milk powder manufactures and pose potential risks in food safety. In this study, we explored the developing process of multi-species biofilm formed by the four thermophilic bacteria on stainless steel immerged in skimmed milk. The results showed that the thermophilic strains possessed strong capacities to decompose proteins and lactose in skimmed milk, and the spoilage effects were superimposed from multiple strains. B. licheniformis was the most predominant species in the mixed-species biofilm after 12-h incubation. From 24 h to 48 h, G. stearothermophilus occupied the highest proportion. Within the multi-species biofilm, competitive relation existed between B. licheniformis and G. stearothermophilus, while synergistic impacts were observed between B. licheniformis and A. flavithermus. The interspecies mutual influences on biofilm development provided important evidences for understanding colonization of the predominant thermophilic bacteria during milk powder processing.

TINCR inhibits the proliferation and invasion of laryngeal squamous cell carcinoma by regulating miR-210/BTG2.

BACKGROUND: Terminal differentiation-induced ncRNA (TINCR) plays an essential role in epidermal differentiation and is involved in the development of various cancers. METHODS: qPCR was used to detect the expression level of TINCR in tissues and cell lines of laryngeal squamous cell carcinoma (LSCC). The potential targets of TINCR were predicted by the bioinformation website. The expression of miR-210 and BTG2 genes were detected by qPCR, and the protein levels of BTG2 and Ki-67 were evaluated by western blot. CCK-8 assay, scratch test, and transwell chamber were used to evaluate the proliferation, invasion, and metastasis ability of LSCC cells. The relationships among TINCR, miR-210, and BTG2 were investigated by bioinformatics software and luciferase reporter assay. The in vivo function of TINCR was accessed on survival rate and tumor growth in nude mice. RESULTS: We used qRT-PCR to detect the expression of TINCR in laryngeal squamous cell carcinoma (LSCC) tissues and cells and found significantly lower levels in cancer tissues compared with adjacent tissues. Additionally, patients with high TINCR expression had a better prognosis. TINCR overexpression was observed to inhibit the proliferation and invasion of LSCC cells. TINCR was shown to exert its antiproliferation and invasion effects by adsorbing miR-210, which significantly promoted the proliferation and invasion of laryngeal squamous cells. Overexpression of miR-210 was determined to reverse the tumour-suppressive effects of TINCR. BTG2 (anti-proliferation factor 2) was identified as the target gene of miR-210, and BTG2 overexpression inhibited the proliferation and invasion of LSCC cells. BTG2 knockdown relieved the inhibitory effects of TINCR on the proliferation and invasion of LSCC. Finally, TINCR upregulation slowed xenograft tumour growth in nude mice and significantly increased survival compared with control mice. CONCLUSION: The results of this study suggest that TINCR inhibits the proliferation and invasion of LSCC by regulating the miR-210/BTG2 pathway, participates in cell cycle regulation, and may become a target for the treatment of LSCC.

Peptide Analogues of VPP and IPP with Improved Glucose Uptake Activity in L6 Myotubes can be Released from Cereal Proteins.

VPP (Val-Pro-Pro) and IPP (Ile-Pro-Pro) are two famous antihypertensive peptides with possible benefits for type 2 diabetes mellitus (T2DM). The study was aimed to investigate the effect of peptide analogues of VPP and IPP on glucose uptake activity in L6 myotubes. The analogues were designed by replacing the N-terminal, middle, or C-terminal amino acid residues of VPP and IPP with one amino acid at a time from five amino acid groups (polar, nonpolar, basic, acidic, and aromatic amino acids). Among 26 tripeptides tested, IQP, IPQ, VPE, and VEP showed significantly higher glucose uptake activity than their parent peptides, and all were successfully released from rice proteins at the contents of 5415.82 ± 63.34, 1586.77 ± 14.94, 354.07 ± 6.56, and 596.10 ± 2.32 ng/mg dry basis, respectively, and quantified by liquid chromatography-mass spectrometry (MS)/MS using multiple reaction monitoring. All four peptides were shown to promote glucose uptake via the adenosine monophosphate-activated protein kinase pathway accompanied by glucose transporter type 4 (Glut4) translocation rather than the insulin signaling pathway.

Naturally occurring low molecular peptides identified in egg white show antioxidant activity.

Egg white is a rich source of bioactive proteins that are essential to provide protection to the embryo in yolk. There is an ongoing interest in identifying novel egg white proteins; it is not known however if peptides are also present in egg white. The objectives of the study were to identify low molecular peptides occurring naturally in egg white using a peptidomics approach and to determine their potential antioxidant activity. A total of 45 peptides were identified but surprisingly all are originated from egg white minor proteins (except ovotransferrin); three most abundant peptides, STDVPRDPWVWGSAHPQAQHTR, GDPSAWSWGAEAHS, and ALGEDIVDLDSFSEQH are derived from ovocleidin, zona pellucida glycoprotein C (ZPC), and sulfhydryl oxidase 1, respectively. Neuropeptide Y was identified for the first time in egg whites. The concentrations of eight most abundant peptides in egg white ranged from 0.004 to 0.292 mg/g, determined by triple quadrupole mass spectrometer in multiple-reaction monitoring (MRM) mode. Six peptides were found to have antioxidant activities based on reduced formation of superoxide and increased levels of superoxide dismutase (SOD) and catalase (CAT) in cells. Our study provided evidence on the presence of naturally occurring antioxidant peptides in egg white.

Formation of bioactive peptides during simulated gastrointestinal digestion is affected by αs1-casein polymorphism in buffalo milk.

The polymorphism of buffalo αs1-casein has been reported, but little is known about their effect on the biological properties. The objective of this study was to investigate the effect of αs1-casein polymorphism on the digestive properties and bioactivities of buffalo milk protein in simulated gastrointestinal digestion. In this study, two variants of αs1-casein, with one amino acid substitution of Leu193 (AA) â†’ Ser193 (BB), were used. Under acidic gastric conditions, the particle size of αs1-casein variant BB was smaller and showed higher digestibility compared to variant AA. A total of 154 and 149 peptides were identified, respectively, from simulated gastrointestinal digestion of variants AA and BB; of three peptides have been previously reported to exert ACE-inhibition, anticancer, antioxidant, and anxiolytic activities. Our study demonstrated that αs1-casein polymorphism affects the digestive properties and the formation of bioactive peptides.

LncRNA MCM3AP-AS1 promotes proliferation and invasion through regulating miR-211-5p/SPARC axis in papillary thyroid cancer.

BACKGROUND: Long non-coding RNAs (lncRNAs) are an emerging class of regulators in cancer. A lncRNA, MCM3AP-AS1, has been demonstrated as a versatile mediator in many cancers, except papillary thyroid cancer. The aim of this study is to investigate the role and mechanism of MCM3AP-AS1 in papillary thyroid cancer. METHODS: Quantitative real-time PCR was used to assess the level of MCM3AP-AS1 and miR-211-5p in papillary thyroid cancer tissues and cells. Western blot was used to detect E-cadherin and secreted protein acidic and cysteine rich (SPARC) protein levels. CCK-8, scratch wound assay, and transwell assay were used to evaluate papillary thyroid cancer cell proliferation, migration, and invasion, respectively. BLAST alignment and luciferase assay were used to explore the interaction among MCM3AP-AS1, mi/r-211, and SPARC. RESULTS: In papillary thyroid cancer, MCM3AP-AS1 was upregulated, while miR-211 was downregulated. MCM3AP-AS1 overexpression promoted papillary thyroid cancer proliferation, migration, and invasion. Further, MCM3AP-AS1 was shown to be negatively correlated with miR-211-5p. We next validated that miR-211-5p overexpression could reverse the promoting role of MCM3AP-AS1 in papillary thyroid cancer, whereby SPARC plays an important regulating role. In vivo, we confirmed the anti-tumor role of MCM3AP-AS1 silencing and the close relation among MCM3AP-AS1, miR-211-5p, and SPARC. CONCLUSIONS: MCM3AP-AS1 promotes papillary thyroid cancer by regulating the MCM3AP-AS1/miR-211-5p/SPARC axis, which could potentially be a therapeutic target in papillary thyroid cancer.

miR-215 suppresses papillary thyroid cancer proliferation, migration, and invasion through the AKT/GSK-3ß/Snail signaling by targeting ARFGEF1.

The incidence of papillary thyroid cancer (PTC) has been rapidly increasing in recent years. PTC is prone to lymph node metastasization, which further increases the recurrence rate and mortality of thyroid cancer. However, the underlying mechanisms of this process remain elusive. Several reports have shown that the microRNA miR-215 plays an important role in cancer metastasis. Here, we investigated, for the first time, the potential association between miR-215 and metastasis in PTC. The results of qPCR analysis demonstrated that miR-215 was downregulated in PTC cell lines and tissues, and lower levels of miR-215 correlated with lymph node metastasis of PTC. In vitro and in vivo assays revealed that restoration of miR-215 dramatically inhibited PTC cell proliferation and metastasis. We identified ADP ribosylation factor guanine nucleotide-exchange factor 1 (ARFGEF1) as the target, which mediated the function of miR-215. The expression of ARFGEF1 was inhibited by miR-215, and the effects of miR-215 were abrogated by re-expression of ARFGEF1. Moreover, we found that miR-215 suppressed PTC metastasis by modulating the epithelial-mesenchymal transition via the AKT/GSK-3ß/Snail signaling. In summary, our study proves that miR-215 inhibits PTC proliferation and metastasis by targeting ARFGEF1 and indicates miR-215 as a biomarker for PTC prognosis.

CircRNA circRNA_102171 promotes papillary thyroid cancer progression through modulating CTNNBIP1-dependent activation of ß-catenin pathway.

BACKGROUND: As a type of recently discovered noncoding RNA, circular RNAs (circRNAs) exert pivot biological functions in diverse cancers. However, the role of circRNA_102171 in papillary thyroid cancer (PTC) has not been investigated. Our study was focused on the functional investigation toward circRNA_102171 in PTC progression. And we also aimed to reveal its potential molecular mechanism. METHODS: The expression pattern of circRNA_102171 was determined using quantitative polymerase chain reaction (qPCR) in PTC samples and cell lines. Cell proliferation was examined utilizing CCK8, colony formation and EdU incorporation assays. Apoptosis was analyzed by Annexin V/PI staining and FACS detection. Cell migration and invasion was measured using Transwell assay. Tumor growth in vivo was determined through a xenograft assay. RNA-pulldown, RNA-IP (RIP) and RNA-EMSA were used to analyze the interaction between circRNA_102171 and CTNNBIP1. RESULTS: CircRNA_102171 expression was upregulated in tumor tissues and cell lines. CircRNA_102171 silencing suppressed PTC cell proliferation, migration and invasion while promoting apoptosis. CircRNA_102171 knockdown inhibited PTC growth in vivo. CircRNA_102171 interacted with CTNNBIP1 to block its interaction with the ß-catenin/TCF3/TCF4/LEF1 complex, leading to activation of Wnt/ß-catenin pathway. CONCLUSIONS: CircRNA_102171 overexpression promotes PTC progression through activating Wnt/ß-catenin pathway in a CTNNBIP1-dependent way.

Molecular targets and mechanisms of bioactive peptides against metabolic syndromes.

Bioactive peptides are present in all living organisms and have critical roles ranging from protection against infection as the key element of innate immunity, regulating blood pressure and glucose levels, to reducing signs of ageing by killing senescent cells. Bioactive peptides are also encrypted within food protein sequences that can be released during proteolysis or food processing. These specific food protein fragments are reported to have potential for improving human health and preventing metabolic diseases through their impact on inflammation, blood pressure, obesity, and type-2 diabetes. This review mainly focuses on the molecular targets and the underlying mechanisms of bioactive peptides against various metabolic syndromes including inflammation, high blood pressure, obesity, and type-2 diabetes, to provide new insights and perspectives on the potential of bioactive peptides for management of metabolic syndromes.

Apoptosis induction of colorectal cancer cells HTL-9 in vitro by the transformed products of soybean isoflavones by Ganoderma lucidum.

Soybean isoflavones have been one of the potential preventive candidates for antitumor research in recent years. In this paper, we first studied the transformation of soybean isoflavones with the homogenized slurry of Ganoderma lucidum. The resultant transformed products (TSI) contained (703.21±4.35) mg/g of genistein, with transformed rates of 96.63% and 87.82% of daidzein and genistein, respectively, and TSI also could enrich the bioactive metabolites of G. lucidum. The antitumor effects of TSI on human colorectal cancer cell line HTL-9, human breast cancer cell line MCF-7, and human immortalized gastric epithelial cell line GES-1 were also studied. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay showed that TSI could dramatically reduce the viability rates of HTL-9 cells and MCF-7 cells without detectable cytotoxicity on GES-1 normal cells when the TSI concentration was lower than 100 µg/ml. With 100 µg/ml of TSI, HTL-9 cells were arrested in the G1 phase, and late-apoptosis was primarily induced, accompanied with partial early-apoptosis. TSI could induce primarily early-apoptosis by arresting cells in the G1 phase of MCF-7 cells. For HTL-9 cells, Western-blot and reverse-transcriptase polymerase chain reaction (RT-PCR) analysis showed that TSI (100 µg/ml) can up-regulate the expression of Bax, Caspase-3, Caspase-8, and cytochrome c (Cyto-c), indicating that TSI could induce cell apoptosis mainly through the mitochondrial pathway. In addition, the expression of p53 was up-regulated, while the expression of Survivin and nuclear factor κB (NF-κB) was down-regulated. All these results showed that TSI could induce apoptosis of HTL-9 cells by the regulation of multiple apoptosis-related genes.

New mechanistic insights into the motile-to-sessile switch in various bacteria with particular emphasis on Bacillus subtilis and Pseudomonas aeruginosa: a review.

A biofilm is a complex assemblage of microbial communities adhered to a biotic or an abiotic surface which is embedded within a self-produced matrix of extracellular polymeric substances. Many transcriptional regulators play a role in triggering a motile-sessile switch and in consequently producing the biofilm matrix. This review is aimed at highlighting the role of two nucleotide signaling molecules (c-di-GMP and c-di-AMP), toxin antitoxin modules and a novel transcriptional regulator BolA in biofilm formation in various bacteria. In addition, it highlights the common themes that have appeared in recent research regarding the key regulatory components and signal transduction pathways that help Bacillus subtilis and Pseudomonas aeruginosa to acquire the biofilm mode of life.

Comparison of Single-Incision and Conventional Laparoscopic Cyst Excision and Roux-en-Y Hepaticojejunostomy for Children with Choledochal Cysts.

The purpose of this study was to elucidate the potential benefits of single-incision laparoscopic Roux-en-Y hepaticojejunostomy comparing the conventional laparoscopic procedures. From January 2013 to July 2013, 17 consecutive children with choledochal cysts received single-incision laparoscopic Roux-en-Y hepaticojejunostomies by a single surgeon at our institution. Seventeen standard laparoscopic hepaticojejunostomies of consecutive children with choledochal cysts from July 2012 to December 2012 were employed as control. Demographic and perioperative information was identified retrospectively using clinic and hospital records including gender, age, total operating time, estimated blood loss, time to oral intake, drainage removal time, postoperative complications, and postoperative hospital stay. One patient was converted to open surgery and another 8-year-old boy conversed to conventional four-port laparoscopic procedure. There were no significant differences between the conventional laparoscopic group and the single-incision laparoscopic group with regard to preoperative variables including age (P = 0.697) and sex distribution (P = 1.000). For mean operative time (209.9 ± 7.5 vs 204.1 ± 6.9 min, P = 0.951), estimated blood loss (10.7 ± 1.1 vs 13.4 ± 1.7 ml, P = 0.103), time to oral intake (3.73 ± 0.21 vs 3.77 ± 0.20 days, P = 0.889), drainage removal time (4.20 ± 0.45 vs 4.06 ± 0.23 days, P = 0.067), and postoperative hospital stay (7.60 ± 0.25 vs 7.41 ± 0.21 days, P = 0.627), the differences were also nonsignificant. Nevertheless, this technique demonstrated improved cosmetic outcomes comparing with the conventional laparoscopic group. The results showed better cosmetic results and comparable postoperative outcomes. However, well-designed prospective studies are warranted to better address this issue.

Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis.

Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer. The regulation of LSCC progression by long non-coding RNA (lncRNA) was not well understood. In this study, we reported that the lncRNA H19 was upregulated in LSCC. The expression levels of H19 were inversely correlated with the survival rate of LSCC patients. Knockdown of H19 expression inhibited LSCC cell migration, invasion and proliferation. We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown. In summary, our study demonstrated that the lncRNA H19 promoted LSCC progression via miR-148a-3p and DNMT1.