Prediction of cervical lymph node metastasis in solitary papillary thyroid carcinoma based on ultrasound radiomics analysis.

Objective: To assess the utility of predictive models using ultrasound radiomic features to predict cervical lymph node metastasis (CLNM) in solitary papillary thyroid carcinoma (PTC) patients. Methods: A total of 570 PTC patients were included (456 patients in the training set and 114 in the testing set). Pyradiomics was employed to extract radiomic features from preoperative ultrasound images. After dimensionality reduction and meticulous selection, we developed radiomics models using various machine learning algorithms. Univariate and multivariate logistic regressions were conducted to identify independent risk factors for CLNM. We established clinical models using these risk factors. Finally, we integrated radiomic and clinical models to create a combined nomogram. We plotted ROC curves to assess diagnostic performance and used calibration curves to evaluate alignment between predicted and observed probabilities. Results: A total of 1561 radiomics features were extracted from preoperative ultrasound images. After dimensionality reduction and feature selection, 16 radiomics features were identified. Among radiomics models, the logistic regression (LR) model exhibited higher predictive efficiency. Univariate and multivariate logistic regression results revealed that patient age, tumor size, gender, suspicious cervical lymph node metastasis, and capsule contact were independent predictors of CLNM (all P < 0.05). By constructing a clinical model, the LR model demonstrated favorable diagnostic performance. The combined model showed superior diagnostic efficacy, with an AUC of 0.758 (95% CI: 0.712-0.803) in the training set and 0.759 (95% CI: 0.669-0.849) in the testing set. In the training dataset, the AUC value of the nomogram was higher than that of the clinical and radiomics models (P = 0.027 and 0.002, respectively). In the testing dataset, the AUC value of the nomogram model was also greater than that of the radiomics models (P = 0.012). However, there was no significant statistical difference between the nomogram and the clinical model (P = 0.928). The calibration curve indicated a good fit of the combined model. Conclusion: Ultrasound radiomics technology offers a quantitative and objective method for predicting CLNM in PTC patients. Nonetheless, the clinical indicators persists as irreplaceable.

All-Solid-State Photo-Assisted Li-CO2 Battery Working at an Ultra-Wide Operation Temperature.

At present, photoassisted Li-air batteries are considered to be an effective approach to overcome the sluggish reaction kinetics of the Li-air batteries. And, the organic liquid electrolyte is generally adopted by the current conventional photoassisted Li-air batteries. However, the superior catalytic activity of photoassisted cathode would in turn fasten the degradation of the organic liquid electrolyte, leading to limited battery cycling life. Herein, we tame the above limitation of the traditional liquid electrolyte system for Li-CO2 batteries by constructing a photoassisted all-solid-state Li-CO2 battery with an integrated bilayer Au@TiO2/Li1.5Al0.5Ge1.5(PO4)3 (LAGP)/LAGP (ATLL) framework, which can essentially improve battery stability. Taking advantage of photoelectric and photothermal effects, the Au@TiO2/LAGP layer enables the acceleration of the slow kinetics of the carbon dioxide reduction reaction and evolution reaction processes. The LAGP layer could resolve the problem of liquid electrolyte decomposition under illumination. The integrated double-layer LAGP framework endows the direct transportation of heat and Li+ in the entire system. The photoassisted all-solid-state Li-CO2 battery achieves an ultralow polarization of 0.25 V with illumination, as well as a high round-trip efficiency of 92.4%. Even at an extremely low temperature of -73 °C, the battery can still deliver a small polarization of 0.6 V by converting solar energy into heat to achieve self-heating. This study is not limited to the Li-air batteries but can also be applied to other battery systems, constituting a significant step toward the practical application of all-solid-state photoassisted Li-air batteries.

LncRNA NEAT1 alleviates ischemic stroke via transcriptional inhibition of NLRP3 mediated by the miR­10b­5p/BCL6 axis.

Cerebral ischemic stroke (CIS) is a significant cause of disability and death. Inflammation usually occurs after CIS and accelerates cellular damage. NLRP3 plays a key role in the formation of CIS­associated inflammasome. Understanding how NLRP3 is regulated bears great importance. We hypothesized that lncRNA NEAT1 can downregulate NLRP3 expression by regulating the miR­10b­5p/BCL6 axis, and thus regulate microglia­driven inflammation. The expression of NEAT1 was analyzed in CIS patients and an in vitro model of oxygen and glucose deprivation/re­oxygenation (OGD/R). We assessed the levels of pro­inflammatory cytokines IL­18 and IL­1ß with ELISA. Interactions between NEAT1/miR­10b­5p and miR­10b­5p/BCL6 were determined by luciferase assay. The interaction of BCL6 and NLRP3 was identified by ChIP; RNA, and protein levels were evaluated by qRT­PCR and western blot, respectively. We found that NEAT1 level was decreased in CIS patients and OGD/R treated cells. OGD/R exerted pro­inflammasome effects by increasing the expression of inflammasome­associated proteins and ROS and malondialdehyde (MDA) while inhibiting SOD production. This effect was partially antagonized by NEAT1. We bioinformatically identified interactions between NEAT1/miR­10b­5p, BCL6/miR­10b­5p, and NLRP3­promoter/BCL6, and validated them by luciferase assay, qRT­PCR, and ChIP. NEAT1 inhibited miR­10b­5p and upregulated BCL6 by ceRNA mechanism and alleviated OGD/R induced cell damage. We also proved that BCL6 was a repressive transcription factor in the regulation of NLRP3 expression. Thus, lncRNA NEAT1 inhibited inflammasome activation by NLRP3 in microglia via the NEAT1/ miR­10b­5p/BCL6/NLRP3 regulatory axis, which alleviated deleterious outcomes of ischemic stroke.

Aerobic exercise reverses the NF-κB/NLRP3 inflammasome/5-HT pathway by upregulating irisin to alleviate post-stroke depression.

Background: Post-stroke depression (PSD) is one of the most common and serious sequelae of stroke. The pathogenesis of PSD involves both psychosocial and biological mechanisms, and aerobic exercise is a potential therapeutic target. We conducted an in-depth exploration of the protective mechanisms of aerobic exercise in a PSD mouse model. Methods: In this study, C57BL/6 mice were used as the research objects, and a PSD mouse model was established by combining middle cerebral artery occlusion and chronic unpredictable mild stimulation. Real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assays, adeno-associated virus microinjection technology, co-immunoprecipitation, fluorescence in-situ hybridization, and western blotting were performed. A moderate-load treadmill exercise was used for aerobic exercise intervention. The moderate-intensity aerobic exercise training method adopted 0 slopes and treadmill adaptation training for 5 days. We verified the effects of aerobic exercise on the nuclear factor kappa B (NF-κB)/nucleotide-binding oligomerization domain--like receptor protein 3 (NLRP3) inflammasome/5-hydroxytryptamine (5-HT) pathway. Results: Aerobic exercise effectively alleviated the neurological damage caused by PSD (P<0.01). The results from the PSD mouse model in vivo were consistent with those of the cell experiments. Moreover, overexpression of irisin improves depression-like behavior in PSD mice. We confirmed that aerobic exercise is involved in PSD through 5-HT, which inhibits NF-κB/NLRP3 inflammasome initiation through irisin and alleviates mitochondrial damage under stress by reducing calcium overload, thereby inhibiting NLRP3 inflammasome activation. Conclusions: Aerobic exercise reversed the NF-κB/NLRP3 inflammasome/5-HT pathway by upregulating irisin expression to alleviate PSD.

Real-world data on the use of secukinumab as treatment for moderate-to-severe psoriasis in Chinese patients.

BACKGROUND: The efficacy and safety of secukinumab, an interleukin-17 inhibitor, as systemic treatment for patients with moderate-to-severe psoriasis have been demonstrated, but real-world data pertaining to this is limited in China. OBJECTIVE: To evaluate the efficacy and safety of secukinumab in clinical practice in Chinese psoriasis patients with or without psoriatic arthritis (PsA) and identify potential baseline factors that affect the response of patients to secukinumab treatment. MATERIALS & METHODS: Data from 81 patients treated with secukinumab for at least 16 weeks were analysed in a retrospective observational study. RESULTS: After 16 weeks of treatment with secukinumab, 91.1%, 73%, and 38.3% of patients achieved a PASI 75 (75% improvement based on the Psoriasis Area and Severity Index), PASI 90, and PASI 100, respectively. A significant improvement in the quality of life of patients was also observed. Notably, baseline factors, such as young age, lower BMI, no scalp involvement and absence of concomitant PsA, were associated with better clinical response to secukinumab. Approximately 42% of patients (34/81) experienced adverse events, of which the most common was pruritus. CONCLUSION: The results demonstrated that secukinumab appears to be an effective treatment alternative for the majority of Chinese plaque psoriasis patients. Baseline factors, including age, BMI, scalp involvement and concomitant presence of PsA, were associated with response to secukinumab.

Ozone alleviates ischemia/reperfusion injury by inhibiting mitochondrion-mediated apoptosis pathway in SH-SY5Y cells.

Cerebral ischemia/reperfusion (I/R) injuries are common and often cause severe complications. Ozone has been applied for protecting I/R injury in animal models of several organs including cerebra, but the detailed mechanism remains unclear. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase measurement were used to determine the influence of ozone on cell activity and damage of SH-SY5Y cells. Some redox items such as catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) were measured by enzyme-linked immunosorbent assay. The mitochondrial membrane potential (ΔΨm ) was determined by JC-1 assay. Cytochrome-c (cyt-c) level in the cytoplasm and mitochondrion was measured by western blotting. Apoptosis was determined by flow cytometry, and some apoptosis-related molecules were detected by quantitative real-time polymerase chain reaction and western blotting. Ozone alleviated oxidative damage by increasing GSH-Px, SOD, CAT, and decreasing MDA. Ozone decreased mitochondrial damage caused by I/R injury and inhibited the release of cyt-c from mitochondrion to cytoplasm in SH-SY5Y cells. The cell apoptosis caused by I/R was inhibited by ozone, and ozone could decrease apoptosis by increasing the ratio of Bcl-2/Bax and inhibiting caspase signaling pathway in SH-SY5Y cells. Ozone has the ability of maintaining redox homeostasis, decreasing mitochondrion damage, and inhibiting neurocytes apoptosis induced by I/R. Therefore, ozone may be a promising protective strategy against cerebral I/R injury.

Iatrogenic crystalline lens injury during intravitreal injection of triamcinolone acetonide: A report of two cases.

BACKGROUND: Intravitreal injection has become an efficient approach for delivering drugs at therapeutic levels to the posterior segment in retinal diseases. However, the increased frequency and number of intravitreal injections have raised concerns about their side effects. As manipulation during surgery is relatively simple, details of the procedure are easily overlooked. Iatrogenic crystalline lens injury is a rare complication caused by improper manipulation during surgical procedures. We report two cases of crystalline lens injury during intravitreal injection of triamcinolone acetonide (TA) with the hope of providing an insight into this treatment. CASE SUMMARY: Case 1 was a 62-year-old woman with macular edema caused by central retinal vein occlusion in her right eye, and Case 2 was a 65-year-old man with macular edema caused by branch retinal vein occlusion in his right eye. In view of the patients' condition and economic constraints, an intravitreal injection of TA was administered. Due to inappropriate manipulation during surgery, the lens was injured. The site of lens injury and clinical manifestations were different in the two cases. Symptomatic treatment and continuous follow-up were carried out. The therapeutic effect following phacoemulsification of the cataract was satisfactory. CONCLUSION: Well-defined surgical incision under proper anesthesia, sufficient patient information and proficient anatomical skills of the physician are mandatory to prevent this rare adverse event. Careful and meticulous phacoemulsification of the cataract is suggested.

Ginsenoside (Rg-1) promoted the wound closure of diabetic foot ulcer through iNOS elevation via miR-23a/IRF-1 axis.

BACKGROUND: Impaired wound healing in diabetes foot ulcers (DFUs) brings a great burden to diabetic patients. Pro-angiogenesis through elevating nitric oxide (NO) is beneficial to the wound healing process. Ginsenoside Rg1, the main active in Notoginseng, is reported to regulate the angiogenesis in endothelial cells through modulating miR-23a. However, the effect of Rg1 in diabetes remains elusive. METHODS: High fat diet combined with streptozotocin-induced diabetic rats were treated with Rg1. Then incision area and tissue NO level were measured to evaluate the wound closure efficacy of Rg1. Then high glucose cultured HUVECs were employed to mimic diabetic environment in vitro. Overexpression and knockdown plasmids of miR-23a or IRF-1 were constructed and transfected in HUVECs. qPCR and western blot were used to determine the mRNA and protein level, respectively. Dual-luciferase reporter assay was utilized to determine the interaction of IRF-1/miR-23a. RESULTS: Rg1 accelerated the wound closure speed in diabetic rats and increased NO level through elevating iNOS expression. Knockdown of iNOS reversed Rg1-induced VEGF expression, cell proliferation, anti-apoptotic efficacy and cell migration ability in high glucose cultured HUVECs. Further investigation revealed that Rg1 mediated iNOS through miR-23a. miR-23a inhibited the expression of IRF-1, a protein which could directly bind to the iNOS mRNA 3'UTR. CONCLUSION: Rg1 promoted angiogenesis in diabetic wound healing process through NO signaling via miR-23a, providing a novel candidate for DFUs treatment.

LncRNA NEAT1 facilitates survival and angiogenesis in oxygen-glucose deprivation (OGD)-induced brain microvascular endothelial cells (BMECs) via targeting miR-377 and upregulating SIRT1, VEGFA, and BCL-XL.

OBJECTIVE: The present study was designed to investigate the mechanism by which lncRNA NEAT1 regulates survival and angiogenesis in oxygen-glucose deprivation (OGD)-induced brain microvascular endothelial cells (BMECs). METHODS: OGD-treated BMECs were used to mimic cerebral ischaemia in vitro. The expression of lncRNA NEAT1 and miR-377 and proteins including VEGFA, SIRT1, and BCL-XL were measured by real-time quantitative PCR (qRT-PCR) and western blot, respectively. Cell viability and caspase 3 activity of BMECs under different conditions were determined using MTT and caspase activity assays, respectively. Matrigel-based angiogenesis assays were employed to evaluate the effect of lncRNA NEAT1 on angiogenesis. A dual-luciferase reporter assay was used to validate direct binding of miR-377 to putative targets. RESULTS: OGD exposure reduced the cell viability of BMECs. Upregulation of lncRNA NEAT1 and downregulation of miR-377 were also observed under OGD conditions. Knockdown of lncRNA NEAT1 inhibited angiogenesis and aggravated apoptosis in OGD-induced BMECs. Meanwhile, the expression level of miR-377 was upregulated while its downstream targets (VEGFA, SIRT1, and BCL-XL) were downregulated after lncRNA NEAT1 knockdown. Furthermore, miR-377 inhibited the angiogenesis and survival of OGD-induced BMECs. The expression of VEGFA, SIRT1, and BCL-XL were all attenuated by miR-377 overexpression. The dual-luciferase reporter assay proved miR-377 targeted the 3' UTR sequences of lncRNA NEAT1, VEGFA, SIRT1, and BCL-XL. CONCLUSION: lncRNA NEAT1 facilitated the survival and angiogenesis of OGD-induced BMECs via targeting miR-377 and promoting the expression of VEGFA, SIRT1, and BCL-XL, suggesting that lncRNA NEAT1 could be a promising target for cerebral ischaemia treatment.

The presence of EGFR mutations predicts the response in Chinese non-small cell lung cancer patients treated with erlotinib.

Non-small cell lung cancer (NSCLC) is a leading cause of death worldwide. The upregulation of the epidermal growth factor receptor (EGFR) due to mutations has been observed in a number of cancers, and tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, which specifically target EGFR signaling, have been used to treat NSCLC patients. The presence of EGFR mutations was previously shown to confer sensitivity to TKIs. In this study, we evaluated the correlation between EGFR mutations and response to erlotinib in Chinese NSCLC patients. We recruited 36 patients with stage IIIB/IV NSCLC who had failed first-line chemotherapy, and treated them with erlotinib. We used immunohistochemistry to determine EGFR expression, and we screened for mutations using PCR analysis. We used Cox regression analysis and Kaplan-Meier curves for survival analysis. We found that 8 patients had exon 19 mutations, while 3 patients had exon 21 mutations. An Eastern Cooperative Oncology Group (ECOG) grade of 2 was a significant negative predictor of overall survival (OS). Patients with EGFR mutations showed a significantly better OS compared to those without EGFR mutations. Additionally, multivariate analysis showed that erlotinib-treated stage IV patients had a significantly longer progression-free survival (PFS) compared to stage IIIB patients. Patients with EGFR mutations also had a significantly better PFS compared to those without EGFR mutations. The overall remission rate (22.2%) and disease control rate (75%) were significantly higher compared to the rates after second-line chemotherapy (<10%). In conclusion, the presence of EGFR mutations could be a marker to predict the therapeutic efficacy of erlotinib and the prognosis in Chinese NSCLC patients.

Effects of cigarette smoke on aerobic capacity and serum MDA content and SOD activity of animal.

OBJECTIVE: Study the effects of cigarette smoke on aerobic capacity, serum MDA content and SOD activity of animal. METHODS: 60 male mice are randomly divided into mild smoking group, heavy smoking group, and control group, and the exhausted swimming time, serum SOD activity and MDA content of the three groups of mice are respectively measured before and after the experiment. RESULTS: After the experiment, the exhausted swimming time for the control group, mild smoking and heavy smoking groups is respectively 276.57 min, 215.57 min and 176.54 min, and the serum SOD activities for the three objects are 216.46 U/mL, 169.16 U/mL and 154.91 U/mL, and the MDA contents are respectively 16.41 mol/mL, 22.31 mol/mL and 23.55 mol/mL. According to the comparison, it is found that compared with the control group and pre-intervention, the exhausted swimming time and serum SOD activity of the smoking group decreases obviously, and its MDA content rises sharply, and the difference has significance (P < 0.05), moreover, the heavy smoking group has more obvious changes than the mild group. CONCLUSION: Cigarette smoke can significantly weaken the aerobic capacity and fatigue resistance of mice, and the more the smoking time is longer, the more the harmful effect is more serious, this is related to the SOD activity drops and MDA content rises due to smoking.

Reconstruction after complete avulsion of the nipple caused by a human bite using an amputated tissue graft in situ.

Integrated avulsion of the nipple by human bite is not common. We treated a patient whose left nipple had been completely avulsed by modifing the nipple as a free skin graft and reconstructing a pillar-like fascia flap as the core to reshape the configuration of the nipple.

[Comparison of the effect of palonosetron versus tropisetron in prevention of vomiting in patients receiving high dose cisplatin-based chemotherapy].

OBJECTIVE: To evaluate the efficacy and toxicity of palonosetron for prevention of vomiting induced by high dose cisplatin-based chemotherapy. METHODS: One-hundred and twenty-eight patients received tropisetron 5 mg plus dexamethasone 10 mg at the first cycle or palonosetron 0.25 mg plus dexamethasone 10 mg, respectively, each administered 30 min before the initiation of high dose cisplatin-based chemotherapy. To observe the remission rate of acute emetic episodes and delayed emetic episodes, adverse effects and daily food-intake in the patients after the chemotherapy. RESULTS: The complete response (CR) rates for acute vomiting were not significantly different between the tropisetron and palonosetron cycles (75.8% vs. 79.7%, P>0.05). The complete control rate of delayed vomiting in the palonosetron cycle was significantly higher than that in the tropisetron cycle (70.3% vs. 50.8%, P<0.01). The food-intake decrease rate of palonosetron cycle was 18.8%, significantly lower than the 53.1% of the tropisetron cycle (P<0.05). The toxicity in the two cycles was similar and no grade 3-4 toxicity was observed. CONCLUSIONS: Palonosetron is superior to tropisetron with a lower remission rate of delayed emesis induced by high dose cisplatin-based chemotherapy and with tolerable toxicity. Moreover, the apparent emesis control of palonosetron treatment seems to provide an adequate food-intake in these patients.

Complications after polyacrylamide hydrogel injection for facial soft-tissue augmentation in China: twenty-four cases and their surgical management.

BACKGROUND: Polyacrylamide hydrogel has been used for soft-tissue augmentation for more than 10 years. Although it is considered a nontoxic, nonimmunogenic material, complications after polyacrylamide hydrogel injections during facial soft-tissue augmentation have been reported. METHODS: Between 2003 and 2009, 24 patients underwent surgical management of complications after facial soft-tissue augmentation. Histories, preoperative imaging, and photographs of operations were recorded. RESULTS: Complications included hematomas, infection, nodule formation, and migration. Ultimately, 23 of 24 cases underwent surgery to remove the gel; the remaining case underwent surgical drainage to remove it. CONCLUSIONS: As more complications have been reported, especially ones that are difficult to treat, the safety of polyacrylamide hydrogel needs to be reconsidered. The authors' experiences provide methods to remove polyacrylamide hydrogel if complications occur. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, V.