Early warning model for stroke recurrence in acute ischemic stroke patients based on traditional Chinese medicine syndrome theory.

OBJECTIVE: This study aimed to establish an early warning model for stroke recurrence in acute ischemic stroke patients based on Traditional Chinese Medicine (TCM) syndrome theory. METHODS: This retrospective study collected the data of 1741 patients with ischemic stroke from 7 clinical centers between July 2016 and November 2019. Distance correlation coefficient, mutual information entropy, and statistical correlation test were used for univariate analysis. Cox proportional hazards regression model was applied to construct and validate the stroke recurrence warning model at different time. The area under the ROC curve (AUC) was used to evaluate the early warning ability of the model. RESULTS: We successfully constructed the early warning model. The median follow-up time was 1.42 years (95% CI [1.37, 1.47]). Recurrence events occurred in 175 patients, with a cumulative recurrence rate of 10.05% (95% CI [8.64, 11.47]). The AUC of the model was 0.64±0.02 in the training set and 0.70±0.03 in the validation set. CONCLUSION: The TCM syndrome model can give an early warning for the recurrence of stroke and provide reference for the secondary prevention of ischemic stroke.

Revealing the Nature of Binary-Phase on Structural Stability of Sodium Layered Oxide Cathodes.

The emergence of layered sodium transition metal oxides featuring a multiphase structure presents a promising approach for cathode materials in sodium-ion batteries, showcasing notably improved energy storage capacity. However, the advancement of cathodes with multiphase structures faces obstacles due to the limited understanding of the integrated structural effects. Herein, the integrated structural effects by an in-depth structure-chemistry analysis in the developed layered cathode system NaxCu0.1Co0.1Ni0.25Mn0.4Ti0.15O2 with purposely designed P2/O3 phase integration, are comprehended. The results affirm that integrated phase ratio plays a pivotal role in electrochemical/structural stability, particularly at high voltage and with the incorporation of anionic redox. In contrast to previous reports advocating solely for the enhanced electrochemical performance in biphasic structures, it is demonstrated that an inappropriate composite structure is more destructive than a single-phase design. The in situ X-ray diffraction results, coupled with density functional theory computations further confirm that the biphasic structure with P2:O3 = 4:6 shows suppressed irreversible phase transition at high desodiated states and thus exhibits optimized electrochemical performance. These fundamental discoveries provide clues to the design of high-performance layered oxide cathodes for next-generation SIBs.

A novel machine learning prediction model for metastasis in breast cancer.

BACKGROUND: Breast cancer (BC) metastasis is the common cause of high mortality. Conventional prognostic criteria cannot accurately predict the BC metastasis risk. The machine learning technologies can overcome the disadvantage of conventional models. AIM: We developed a model to predict BC metastasis using the random survival forest (RSF) method. METHODS: Based on demographic data and routine clinical data, we used RSF-recursive feature elimination to identify the predictive variables and developed a model to predict metastasis using RSF method. The area under the receiver operating characteristic curve (AUROC) and Kaplan-Meier survival (KM) analyses were plotted to validate the predictive effect when C-index was plotted to assess the discrimination and Brier scores was plotted to assess the calibration of the predictive model. RESULTS: We developed a metastasis prediction model comprising three variables (pathological stage, aspartate aminotransferase, and neutrophil count) selected by RSF-recursive feature elimination. The model was reliable and stable when assessed by the AUROC (0.932 in training set and 0.905 in validation set) and KM survival analyses (p < .0001). The C-indexes (0.959) and Brier score (0.097) also validated the good predictive ability of this model. CONCLUSIONS: This model relies on routine data and examination indicators in real-time clinical practice and exhibits an accurate prediction performance without increasing the cost for patients. Using this model, clinicians can facilitate risk communication and provide precise and efficient individualized therapy to patients with breast cancer.

The new insights into autophagy in thyroid cancer progression.

In recent decades, the incidence of thyroid cancer keeps growing at a shocking rate, which has aroused increasing concerns worldwide. Autophagy is a fundamental and ubiquitous biological event conserved in mammals including humans. Basically, autophagy is a catabolic process that cellular components including small molecules and damaged organelles are degraded for recycle to meet the energy needs, especially under the extreme conditions. The dysregulated autophagy has indicated to be involved in thyroid cancer progression. The enhancement of autophagy can lead to autophagic cell death during the degradation while the produced energies can be utilized by the rest of the cancerous tissue, thus this influence could be bidirectional, which plays either a tumor-suppressive or oncogenic role. Accordingly, autophagy can be suppressed by therapeutic agents and is thus regarded as a drug target for thyroid cancer treatments. In the present review, a brief description of autophagy and roles of autophagy in tumor context are given. We have addressed summary of the mechanisms and functions of autophagy in thyroid cancer. Some potential autophagy-targeted treatments are also summarized. The aim of the review is linking autophagy to thyroid cancer, so as to develop novel approaches to better control cancer progression.

Molecular mechanism of engineered Zymomonas mobilis to furfural and acetic acid stress.

Acetic acid and furfural (AF) are two major inhibitors of microorganisms during lignocellulosic ethanol production. In our previous study, we successfully engineered Zymomonas mobilis 532 (ZM532) strain by genome shuffling, but the molecular mechanisms of tolerance to inhibitors were still unknown. Therefore, this study investigated the responses of ZM532 and its wild-type Z. mobilis (ZM4) to AF using multi-omics approaches (transcriptomics, genomics, and label free quantitative proteomics). Based on RNA-Seq data, two differentially expressed genes, ZMO_RS02740 (up-regulated) and ZMO_RS06525 (down-regulated) were knocked out and over-expressed through CRISPR-Cas technology to investigate their roles in AF tolerance. Overall, we identified 1865 and 14 novel DEGs in ZM532 and wild-type ZM4. In contrast, 1532 proteins were identified in ZM532 and wild-type ZM4. Among these, we found 96 important genes in ZM532 involving acid resistance mechanisms and survival rates against stressors. Furthermore, our knockout results demonstrated that growth activity and glucose consumption of mutant strains ZM532∆ZMO_RS02740 and ZM4∆ZMO_RS02740 decreased with increased fermentation time from 42 to 55 h and ethanol production up to 58% in ZM532 than that in ZM532∆ZMO_RS02740. Hence, these findings suggest ZMO_RS02740 as a protective strategy for ZM ethanol production under stressful conditions.

Revealing An Intercalation-Conversion-Heterogeneity Hybrid Lithium-Ion Storage Mechanism in Transition Metal Nitrides Electrodes with Jointly Fast Charging Capability and High Energy Output.

The performance of electrode materials depends intensively on the lithium (Li)-ion storage mechanisms correlating ultimately with the Coulombic efficiency, reversible capacity, and morphology variation of electrode material upon cycling. Transition metal nitrides anode materials have exhibited high-energy density and superior rate capability; however, the intrinsic mechanism is largely unexplored and still unclear. Here, a typical 3D porous Fe2 N micro-coral anode is prepared and, an intercalation-conversion-heterogeneity hybrid Li-ion storage mechanism that is beyond the conventional intercalation or conversion reaction is revealed through various characterization techniques and thermodynamic analysis. Interestingly, using advanced in situ magnetometry, the ratio (ca. 24.4%) of the part where conversion reaction occurs to the entire Fe2 N can further be quantified. By rationally constructing a Li-ion capacitor comprising 3D porous Fe2 N micro-corals anode and commercial AC cathode, the hybrid full device delivers a high energy-density (157 Wh kg-1 ) and high power-density (20 000 W kg-1 ), as well as outstanding cycling stability (93.5% capacitance retention after 5000 cycles). This research provides an original and insightful method to confirm the reaction mechanism of material related to transition metals and a fundamental basis for emerging fast charging electrode materials to be efficiently explored for a next-generation battery.

Development and Validation of a New Multiparametric Random Survival Forest Predictive Model for Breast Cancer Recurrence with a Potential Benefit to Individual Outcomes.

Purpose: Breast cancer (BC) is a multi-factorial disease. Its individual prognosis varies; thus, individualized patient profiling is instrumental to improving BC management and individual outcomes. An economical, multiparametric, and practical model to predict BC recurrence is needed. Patients and Methods: We retrospectively investigated the clinical data of BC patients treated at the Third Affiliated Hospital of Sun Yat-sen University and Liuzhou Women and Children's Medical Center from January 2013 to December 2020. Random forest-recursive feature elimination (run by R caret package) was used to determine the best variable set, and the random survival forest method was used to develop a predictive model for BC recurrence. Results: The training and validations sets included 623 and 151 patients, respectively. We selected 14 variables, the pathological (TNM) stage, gamma-glutamyl transpeptidase, total cholesterol, Ki-67, lymphocyte count, low-density lipoprotein, age, apolipoprotein B, high-density lipoprotein, globulin, neutrophil count to lymphocyte count ratio, alanine aminotransferase, triglyceride, and albumin to globulin ratio, using random survival forest (RSF)-recursive feature elimination. We developed a recurrence prediction model using RSF. Using area under the receiver operating characteristic curve and Kaplan-Meier survival analyses, the model performance was determined to be accurate. C-indexes were 0.997 and 0.936 for the training and validation sets, respectively. Conclusion: The model could accurately predict BC recurrence. It aids clinicians in identifying high-risk patients and making treatment decisions for Breast cancer patients in China. This new multiparametric RSF model is instrumental for breast cancer recurrence prediction and potentially improves individual outcomes.

Oxidative stress induced in rice suspension cells exposed to microcystin-LR at environmentally relevant concentrations.

Microcystins (MCs) are cyclic heptapeptide hepatotoxins that are highly soluble in water and can be transferred to farmland through irrigation with potentially substantial effects on crops, especially rice. In order to investigate the possible negative effects of microcystin-LR (MC-LR) on rice, the oxidative stress induced in rice suspension cells exposed to MC-LR at environmentally relevant concentrations (0.05, 0.5, 5.0, and 50.0 µg·L-1) was investigated. Results showed that the exposure to MC-LR at 0.5-50.0 µg·L-1 resulted in a significant decline in viability of rice suspension cells and an increase in malondialdehyde (MDA) contents. In the 50.0-µg·L-1 MC-LR treatment group, the content of MDA was as much as 5.39 times that of the control group after 6 days of exposure. The excess MDA production indicated that MC-LR exposure has caused lipid peroxidation damage in rice cells, whereas these negative effects could be recovered over time when suspension cells were exposed to low concentration of MC-LR (0.05 µg·L-1). When exposed to MC-LR for 3 days, the O2- content in all treatment groups increased significantly compared with the control group. Additionally, the antioxidant system of rice suspension cells initiated a positive stress response to MC-LR exposure. Indeed, peroxidase (POD) played an active role in the removal of reactive oxygen species (ROS) in rice suspension cells during the early period of exposure, while total superoxide dismutase (T-SOD) was induced after 6 days. Similarly, after 6 days of exposure, the anti-superoxide anion free radical activity (ASAFR), glutathione (GSH), and glutathione-S transferase (GST) in rice suspension cells were higher than that in the control group. These results provided a comprehensive understanding of the exposure time- and dose-dependent oxidative stress induced by the environmentally relevant concentrations of MC-LR in rice suspension cells.

Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo.

The oncolytic herpes simplex virus (HSV) G47Δ can selectively eliminate glioblastoma cells via viral replication and temozolomide (TMZ) has been clinically used to treat glioblastoma. However, the combined effect of G47Δ and TMZ on cancer cells, particularly on breast cancer cells, remains largely unknown. The objective of the present study was to investigate the role and underlying mechanism of G47Δ and TMZ, in combination, in breast cancer cell tumorigenesis. The human breast cancer cell lines SK-BR-3 and MDA-MB-468 were treated with G47Δ and TMZ individually or in combination. Cell viability, flow cytometry, reverse transcription quantitative-PCR and western blotting were performed to investigate the synergy between G47Δ and TMZ in regulating breast cancer cell behavior in vitro. The role of G47Δ and TMZ in suppressing tumorigenesis in vivo was investigated in a xenograft mouse model. G47Δ and TMZ served a synergistic role resulting in decreased breast cancer cell viability, induction of cell cycle arrest, promotion of tumor cell apoptosis and enhancement of DNA damage response in vitro. The combined administration of G47Δ and TMZ also effectively suppressed breast cancer cell-derived tumor growth in vivo, compared with the administration of G47Δ or TMZ alone. Synergy between G47Δ and TMZ was at least partially mediated via TMZ-induced acceleration of G47Δ replication, and such a synergy in breast cancer cells in vitro and in vivo provides novel insight into the future development of a therapeutic strategy against breast cancer.

Formononetin Activates the Nrf2/ARE Signaling Pathway Via Sirt1 to Improve Diabetic Renal Fibrosis.

Oxidative stress is the main factor responsible for the induction of diabetic renal fibrosis. Thus, improving the state of oxidative stress can effectively prevent the further deterioration of diabetic nephropathy (DN). Previous research has shown that formononetin (FMN), a flavonoid with significant antioxidant activity and Sirt1 activation effect, can improve diabetic renal fibrosis. However, the exact mechanisms underlying the effect of FMN on diabetic renal fibrosis have yet to be elucidated. In this study, we carried out in vivo experiments in a db/db (diabetic) mouse model and demonstrated that FMN activated the nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway and improved oxidative stress by increasing levels of sirtuin-1 (Sirt1) protein level in renal tissue. We also found that this process reversed the up-regulation of fibronectin (FN) and intercellular adhesion molecule 1 (ICAM-1) and led to an improvement in renal insufficiency. In vitro results further showed that FMN significantly reversed the upregulation of FN and ICAM-1 in glomerular mesangial cells (GMCs) exposed to high glucose. FMN also promoted the expression of Nrf2 and widened its nuclear distribution. Thus, our data indicated that FMN inhibited hyperglycemia-induced superoxide overproduction by activating the Nrf2/ARE signaling pathway. We also found that FMN up-regulated the expression of Sirt1 and that Sirt1 deficiency could block the activation of the Nrf2/ARE signaling pathway in GMCs induced by high glucose. Finally, we found that Sirt1 deficiency could reverse the down-regulation of FN and ICAM-1 induced by FMN. Collectively, our data demonstrated that FMN up-regulated the expression of Sirt1 to activate the Nrf2/ARE signaling pathway, improved oxidative stress in DN to prevent the progression of renal fibrosis. Therefore, FMN probably represents an efficient therapeutic option of patients with DN.

Gentiopicroside activates the bile acid receptor Gpbar1 (TGR5) to repress NF-kappaB pathway and ameliorate diabetic nephropathy.

Our previous studies indicated that the G-protein-coupled bile acid receptor, Gpbar1 (TGR5), inhibits inflammation by inhibiting the NF-κB signalling pathway, eventually attenuating diabetic nephropathy (DN). Gentiopicroside (GPS), the main active secoiridoid glycoside of Gentiana manshurica Kitagawa, has been demonstrated to inhibit inflammation in various diseases via inhibiting the inflammatory signalling pathways. However, whether GPS inhibits the NF-κB signalling pathway by activating TGR5 and regulates the pathological progression of diabetic renal fibrosis requires further investigation. In this study, we found that GPS significantly reversed the downregulation of TGR5 and inhibited the overproduction of fibronectin (FN), transforming growth factor ß1 (TGF-ß1), intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) in glomerular mesangial cells (GMCs) exposed to high glucose (HG). Additionally, GPS prevented the phosphorylation and degradation of IκBα, and subsequently inhibited the activation of the NF-κB signalling pathway. Further investigation found that GPS enhanced the stabilization of IκBα by promoting the interaction of ß-arrestin2 with IκBα via TGR5 activation, which contributed to the inhibition of NF-κB signalling pathway. Importantly, the depletion of TGR5 blocked the inhibition of the NF-κB signalling pathway and reversed the downregulation of FN, ICAM-1, VCAM-1 and TGF-ß1 by GPS in HG-induced GMCs. Moreover, GPS increased the TGR5 protein levels and promoted the interaction between IκBα and ß-arrestin2, thereby inhibiting the reduction of IκBα and blocked NF-κB p65 nuclear translocation in the kidneys of STZ-induced diabetic mice. Collectively, these data suggested that GPS regulates the TGR5-ß-arrestin2-NF-κB signalling pathway to prevent inflammation in the kidneys of diabetic mice, and ultimately ameliorates the pathological progression of diabetic renal fibrosis.

Paeonol Ameliorates Glucose and Lipid Metabolism in Experimental Diabetes by Activating Akt.

Our previous study proved that paeonol (Pae) could lower blood glucose levels of diabetic mice. There are also a few reports of its potential use for diabetes treatment. However, the role of Pae in regulating glucose and lipid metabolism in diabetes remains largely unknown. Considering the critical role of serine/threonine kinase B (Akt) in glucose and lipid metabolism, we explored whether Pae could improve glucose and lipid metabolism disorders via Akt. Here, we found that Pae attenuated fasting blood glucose, glycosylated serum protein, serum cholesterol and triglyceride (TG), hepatic glycogen, cholesterol and TG in diabetic mice. Moreover, Pae enhanced glucokinase (GCK) and low-density lipoprotein receptor (LDLR) protein expressions, and increased the phosphorylation of Akt. In insulin-resistant HepG2 cells, Pae increased glucose uptake and decreased lipid accumulation. What's more, Pae elevated LDLR and GCK expressions as well as Akt phosphorylation, which was consistent with the in vivo results. Knockdown and inhibition experiments of Akt revealed that Pae regulated LDLR and GCK expressions through activation of Akt. Finally, molecular docking assay indicated the steady hydrogen bond was formed between Pae and Akt2. Experiments above suggested that Pae ameliorated glucose and lipid metabolism disorders and the underlying mechanism was closely related to the activation of Akt.

The anticancer activity of genistein is increased in estrogen receptor beta 1-positive breast cancer cells.

BACKGROUND: Most breast cancers are estrogen dependent and were sensitive to endocrine therapy, and genistein (GEN) shows strong affinity with human oestrogen receptor beta (ERß). PURPOSE: The present study aimed to investigate the anticancer activity of GEN in breast cancer cell lines that constitutively expressing ERß1 in vitro and in vivo. METHODS: MCF-7/ERß1 and MDA-MB-231/ERß1 cell sub-lines were established through lentiviral infection. Then, cells were treated with increasing concentrations of GEN (10-6 mol/l, 10-5 mol/l and 10-4 mol/l) for 48 h, and cell proliferation, cell cycle analyses were performed to investigate different biological characteristics of ERß1-overexpressing cell lines. Studies in vivo were also performed to investigate the effects of dietary GEN on MCF-7/ERß1 and MDA-MB-231/ERß1 cells implanted mice. RESULTS: Results showed that compared to parental cells, GEN inhibited the proliferation ability of MCF-7/ERß1 cells to a greater extent, especially at high concentrations. MDA-MB-231 cells were also inhibited by high doses of GEN, but the overexpressed ERß1 did not enhance the anti-proliferative effect on MDA-MB-231 cells. ERß1 arrested cells in G2/M phase, and GEN arrested cells in G0/G1, which led to a combinatorial effect on cell cycle blockade. Furthermore, ERß1 increased the anti-tumour activity of dietary GEN in MCF-7/ERß1 subcutaneous tumour models. Our data indicated that ERß1 increased the anticancer efficacy of GEN in MCF-7 cells by affecting cell cycle transition. CONCLUSION: As a result, GEN could be a potential therapeutic agent for ERß1-positive cancer.

Scinderin-knockdown inhibits proliferation and promotes apoptosis in human breast carcinoma cells.

Previous studies have reported that scinderin (SCIN) affects multiple cellular processes, including proliferation, migration and differentiation in cancer. However, the specific role of SCIN in breast cancer (BC) cells is unknown. Immunohistochemistry was used to investigate SCIN expression in 46 BC and 21 mammary fibroadenoma or fibroadenomatoid hyperplasia tissue samples. SCIN expression was ablated in MDA-MB-231 and T-47D cells using lentivirus-mediated small interfering RNA technology. Cell proliferation was tested using Celigo and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. Cell apoptosis was analyzed by measuring Caspase 3/7 activity and annexin-V staining. The results of the present study demonstrated that SCIN expression was elevated in BC tissues compared with mammary fibroadenoma or fibroadenomatoid hyperplasia tissues. Specifically, higher SCIN expression was observed in Ki-67-positive BC tissues (78.6%) compared with Ki-67-negative BC tissues. Furthermore, knockdown of SCIN expression in the BC cell lines significantly suppressed cell proliferation and induced apoptosis. The data presented in the present study indicate that SCIN serves an important role in the development of breast cancer.

A novel oncolytic herpes simplex virus armed with the carboxyl-terminus of murine MyD116 has enhanced anti-tumour efficacy against human breast cancer cells.

Oncolytic herpes simplex virus-1 (oHSV-1) vectors are promising therapeutic agents for cancer. The deletion of the γ34.5 gene eliminates the neurovirulence but attenuates virus replication at the same time. The carboxyl-terminus of protein phosphatase 1 regulatory subunit 15A (also known as MyD116/GADD34) is homologous to that of γ34.5; hence, it may substitute for γ34.5 to enhance the replication and cytotoxicity of the virus. To investigate whether the C-terminus of MyD116 can enhance the anti-tumour efficacy of G47Δ on human breast cancer cells, a GD116 mutant was constructed by inserting a γ34.5-MyD116 chimaera into the G47Δ genome using a bacterial artificial chromosome and two recombinase systems (Cre/loxP and FLPE/FRT). A GD-empty mutant containing only the cytomegalovirus sequence was also created as a control using the same method. Next, the replication and cytotoxicity of these two virus vectors were evaluated in breast cancer cells. Compared with the GD-empty vector, GD116 possessed an enhanced replication capability and oncolytic activity in MCF-7 and MDA-MB-231 cells. On the fifth day after infection with GD116 at MOIs of 0.01 and 0.1, 49.2 and 82.8% of MCF-7 cells, respectively, were killed, with 35.0 and 50.2% of MDA-MB-231 cells, respectively, killed by GD116 at MOIs of 0.1 and 0.3. Additionally, the insertion of the γ34.5-MyD116 chimaera promoted virus replication in MDA-MB-468 at 48 h after infection, although no increased cytotoxic effect was observed. The findings of the present study indicate that the C terminus of the MyD116 gene can be substituted for the corresponding domain of the γ34.5 gene of oHSV-1 to promote the replication of the virus in infected cells. Furthermore, the novel virus mutant GD116 armed with a γ34.5-MyD116 chimaera has enhanced anti-tumour efficacy against human breast cancer cells in vitro.

MicroRNA­663b mediates TAM resistance in breast cancer by modulating TP73 expression.

Breast cancer is the second leading cause of cancer­associated mortalities in women. Tamoxifen (TAM) is an endocrine therapy commonly used in the treatment of patients with breast cancer expressing estrogen receptor α. However, treatment often ends in failure due to the emergence of drug resistance. MicroRNAs (miRNAs), a family of small non­coding RNAs, serve critical roles in the regulation of gene expression and cell events. To date, whether miRNA­663b could mediate TAM resistance in breast cancer remains unknown. Therefore, the aim of the present study was to investigate the role of miRNA­663b in TAM resistance in breast cancer. The results demonstrated that miRNA­663b was upregulated in breast cancer with TAM resistance. Tumor protein 73 (TP73) was a direct target of miRNA­663b, and was negatively regulated by miRNA­663b in MCF­7 cells. Furthermore, it was identified that downregulation of miRNA­663b inhibited cell proliferation ability and promoted cell apoptosis, resulting in enhanced TAM sensitivity. In addition, these findings suggested that TP73 silencing may have eliminated the effects of miRNA­663b inhibitor on breast cancer cells. In conclusion, the present study verified a novel molecular link between miRNA­663b and TP73, and indicated that miRNA­663b may be a critical therapeutic target in breast cancer.

Gastric acid secretion and gastrin release during continuous vagal neuromonitoring in thyroid surgery.

PURPOSE: The vagus nerve (VN) has essential regulatory roles in the gastric acid secretion and gastrin release. Continuous intraoperative neuromonitoring (CIONM) via VN stimulation is a promising technique in thyroid surgery because it potentially avoids injury to the recurrent laryngeal nerve. However, no studies have investigated changes in gastric acid secretion and gastrin release during CIONM. METHOD: This prospective study of 58 thyroid surgery patients compared gastric acid and serum gastrin at five time points: (1) before skin incision, (2) after baseline calibration of CIONM probe, (3) +20 min from baseline, (4) before probe removal, and (5) after extubation. Patients were excluded if they had any history of using tobacco, acid suppression medications, or drugs that affect gastric motility. Patients were also excluded if they had any history of gastroesophageal reflux symptoms, gastroesophageal reflux disease, peptic ulcer disease, helicobacter pylori infection, or chronic kidney disease. RESULTS: Non significant differences in mean gastric pH values were observed at all time points, i.e., (1) before skin incision (2.2 ± 0.2; p = 0.50), (2) after baseline calibration of CIONM probe (2.0 ± 0.8; p = 0.62), (3) +20 min from baseline (2.5 ± 0.5; p = 0.24), (4) before probe removal (2.9 ± 0.9; p = 0.52), and (5) after extubation (2.6 ± 1.0; p = 0.60). Comparisons of pH monitoring parameters revealed no significant differences in age, gender, side of CIONM (left vs. right), sequence of CIONM, or duration of CIONM. Gastrin values were normal in sequential determinations and did not significantly differ at any time points. CONCLUSIONS: CIONM performed via VN stimulation during total thyroidectomy in healthy patients does not influence gastrin secretion and gastric pH.

New endoscopic procedures for diabetes mellitus type 2 and obesity treatment.

BACKGROUND: Obesity continues to be a growing epidemic worldwide. Obese patients have severe comorbidities that make risky and technically demanding the execution of bariatric surgery from both surgical and anesthetic point of view; therefore, the focus of bariatric surgeons is increasingly moving towards minimally invasive, endoscopic techniques. METHODS: The present review presents and discusses recent endoscopic techniques employed in obesity treatment, their features and results. RESULTS: Endoscopic treatment can be primary or revisional; we can mainly divide the endoscopic devices into five categories: space-occupying devices, restrictive procedures, bypass liner, aspiration therapy and endoscopic revision of gastric bypass for dilated gastric pouch. CONCLUSIONS: Endoscopic treatments for obesity are promising techniques for selected patients but each procedure should be tailored on the patient in a multimodal approach.

Safety of energy based devices for hemostasis in thyroid surgery.

Energy based devices (EBD) have been developed, implemented and increasingly applied in thyroid surgery because they can provide a combined dissection and haemostatic effect. In particular, advantages of EBD have been described in terms of efficacious haemostasis, reduction of procedure-associated time, reduced incision length, less operative blood loss and transfusion need, decreased postoperative drain, pain and hospital stay. In addition, EBD are essential for endoscopic procedures. On the contrary, a potential drawback is the increased health care costs. This paper reviews relevant medical literature published on the safety of new devices for achieving hemostasis and dissection around the recurrent laryngeal nerve (RLN).

Indocyanine green-enhanced fluorescence for assessing parathyroid perfusion during thyroidectomy.

Identification of the parathyroid glands during thyroid surgery may prevent their inadvertent surgical removal and thus provide a better postoperative quality of life. Nevertheless, the most common "technique" for intraoperative evaluation of perfusion of parathyroid gland tissues during thyroid surgery is visual inspection of the physical condition of tissues, e.g., their color and bleeding edges. Another technique is measurement of intact parathyroid hormone. Recently, indocyanine green-enhanced fluorescence has been used in various surgical techniques, particularly laparoscopic surgery, to improve visualization and to provide detailed anatomical information. Fluorescent optical guidance helps surgeons to avoid inadvertent tissue injury while enhancing procedural efficiency. This technique has potential use for evaluating perfusion of the parathyroid gland in real-time intraoperative angiography.