Comparison of one-year outcomes and quality of life between endovenous microwave ablation and high ligation and stripping of the great saphenous vein.

INTRODUCTION: The objective of this study is to evaluate and compare the effectiveness of endovenous microwave ablation (EMA) and high ligation and strippingn (HLS) of the great saphenous vein (GSV) in the treatment of varicose veins. METHODS: We included 182 patients in each EMA and HLS groups. Follow-up outcomes included AVVQ, VCSS, chronic venous insufficiency questionnaire-14 (CIVIQ14) score, clinical recurrence rate of varicose vein treatment, and patient satisfaction during the 1-year follow-up period. RESULTS: At the 1-year follow-up, no significant difference was found in the clinical recurrence rate of varicose veins between the EMA and HLS groups (p = .75). The duration of the operation and the length of hospital stay for patients in the EMA group was shorter than that for the HLS group (p < .01). The Aberdeen Varicose Vein Questionnaire (AVVQ), Venous Clinical Severity Score (VCSS) score, and ecchymosis were lower for patients who underwent EMA surgery (p < .01). CONCLUSION: Our research results confirm that EMA improves patients' quality of life with lower limb varicose veins, with EMA showing higher patient satisfaction.

Isthmin: A multifunctional secretion protein.

Isthmin is a polypeptide secreted by adipocytes that was first detected in Xenopus gastrula embryos. Recent studies have focused on the biological functions of isthmin in growth and development, angiogenesis, and metabolism. Distinct spatiotemporal expression of isthmin-1 (ISM-1) was observed during growth and development. ISM-1 plays an important role in the occurrence and development of cancer by regulating cell proliferation, migration, angiogenesis, and immune microenvironments. Moreover, ISM-1, as a newly identified insulin-like adipokine, increases adipocyte glucose uptake and inhibits hepatic lipid synthesis. However, the biological function of ISM-1 remains largely unknown. In this review, we highlight the structure and physiological functions of isthmin and explore its application potential, contributing to a better understanding of its function and providing prevention and treatment strategies for various diseases.

Formaldehyde induces ferritinophagy to damage hippocampal neuronal cells.

Formaldehyde (FA) causes neurotoxicity and contributes to the occurrence of neurodegenerative diseases. However, the mechanism of FA-induced neurotoxicity has not been fully elucidated. Ferritinophagy, an autophagy process of ferritin mediated by the nuclear receptor coactivator 4 (NCOA4), is a potential mechanism of neurotoxicity. In this study, we explored whether ferritinophagy is associated with the neurotoxicity of FA. Our results showed that FA (50, 100, 200 µM; 24 h) exposure upregulated ferritinophagy in the mouse hippocampal neuronal HT22 cells, which was evidenced by the upregulated autophagic flux, the increased colocalizations of NCOA4 with ferritin heavy chain (FTH1) and NCOA4 with microtubule-associated protein 1 light chain-3B (LC3B), the augmented expression of NCOA4, and the reduced content of FTH1. We also found that FA (0.1, 1, and 10 µmol, i.c.v., 7d) administration boosted ferritinophagy in the hippocampus of Sprague-Dawley (SD) rats, which was demonstrated by the accumulated autophagosomes, the increased expressions of LC3II/I and NCOA4, and the decreased contents of p62 and FTH1 in the hippocampus. Further, we confirmed that inhibition of ferritinophagy by silencing the expression of NCOA4 decreased FA-induced toxic damage in HT22 cells. These results indicated that FA induces neurotoxicity by promoting ferritinophagy. Our findings suggest a potential mechanism insight into the FA-induced neurotoxicity, which in turn provides a new thought for the treatment of FA-related neurodegenerative diseases.

Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment.

Background and Aim: Sleep deprivation (SD) causes deficit of cognition, but the mechanisms remain to be fully established. Hydrogen sulfide (H2S) plays an important role in the formation of cognition, while excessive and prolonged autophagy in hippocampus triggers cognitive disorder. In this work, we proposed that disturbances in hippocampal endogenous H2S generation and autophagy might be involved in SD-induced cognitive impairment. Methods: After treatment of adult male wistar rats with 72-h SD, the Y-maze test, object location test (OLT), novel object recognition test (NORT) and the Morris water maze (MWM) test were performed to determine the cognitive function. The autophagosome formation was observed with electron microscope. Generation of endogenous H2S in the hippocampus of rats was detected using unisense H2S microsensor method. The expressions of cystathionine-ß-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), beclin-1, light chain LC3 II/LC3 I, and p62 in the hippocampus were assessed by western blotting. Results: The Y-maze, OLT, NORT, and MWM test demonstrated that SD-exposed rats exhibited cognitive dysfunction. SD triggered the elevation of hippocampal autophagy as evidenced by enhancement of autophagosome, up-regulations of beclin-1 and LC3 II/LC3 I, and down-regulation of p62. Meanwhile, the generation of endogenous H2S and the expressions of CBS and 3-MST (H2S producing enzyme) in the hippocampus of SD-treated rats were reduced. Conclusion: These results suggested that inhibition of endogenous H2S generation and excessiveness of autophagy in hippocampus are involved in SD-induced cognitive impairment.

Hydrogen sulfide prevents homocysteine­induced endoplasmic reticulum stress in PC12 cells by upregulating SIRT­1.

It was previously confirmed that hydrogen sulfide (H2S) has a neuroprotective effect, preventing homocysteine­induced neurotoxicity. However, the exact molecular mechanisms underlying this protective effect remain to be fully elucidated. Endoplasmic reticulum (ER) stress contributes to homocysteine­induced neurotoxicity. Silent mating type information regulator 2 homolog 1 (SIRT­1) can attenuate ER stress, exerting its neuroprotective effect. Therefore, the present study aimed to investigate whether H2S protects PC12 cells against homocysteine­induced ER stress and whether SIRT­1 mediates this protective effect of H2S. Western blotting was used to detect the expression of SIRT­1, glucose­regulated protein 78 (GRP78), and cleaved caspase­12 in PC12 cells. It was observed that sodium hydrosulfide (NaHS), an exogenous H2S donor, significantly attenuated the homocysteine­induced ER stress responses, including increases in the protein expression levels of GRP78 and cleaved caspase­12. Simultaneously, NaHS upregulated the expression of SIRT­1 and reversed the homocysteine­induced downregulation of SIRT­1 in PC12 cells. Sirtinol, a specific inhibitor of SIRT­1, eliminated the protective effects of H2S in homocysteine­induced ER stress. These data indicated that H2S prevented homocysteine­induced ER stress via enhancing the expression of SIRT­1. These findings offer novel insight into the protective mechanisms of H2S against homocysteine­induced neurotoxicity.

Hydrogen Sulfide Ameliorates Homocysteine-Induced Cognitive Dysfunction by Inhibition of Reactive Aldehydes Involving Upregulation of ALDH2.

Background: Homocysteine, a risk factor for Alzheimer's disease, induces cognitive dysfunction. Reactive aldehydes play an important role in cognitive dysfunction. Aldehyde-dehydrogenase 2 detoxifies reactive aldehydes. Hydrogen sulfide, a novel neuromodulator, has neuroprotective effects and regulates learning and memory. Our previous work confirmed that the disturbance of hydrogen sulfide synthesis is invovled in homocysteine-induced defects in learning and memory. Therefore, the present work was to explore whether hydrogen sulfide ameliorates homocysteine-generated cognitive dysfunction and to investigate whether its underlying mechanism is related to attenuating accumulation of reactive aldehydes by upregulation of aldehyde-dehydrogenase 2. Methods: The cognitive function of rats was assessed by the Morris water maze test and the novel object recognition test. The levels of malondialdehyde, 4-hydroxynonenal, and glutathione as well as the activity of aldehyde-dehydrogenase 2 were determined by enzyme linked immunosorbent assay; the expression of aldehyde-dehydrogenase 2 was detected by western blot. Results: The behavior experiments, Morris water maze test and novel objects recognition test, showed that homocysteine induced deficiency in learning and memory in rats, and this deficiency was reversed by treatment of NaHS (a donor of hydrogen sulfide). We demonstrated that NaHS inhibited homocysteine-induced increases in generations of MDA and 4-HNE in the hippocampus of rats and that hydrogen sulfide reversed homocysteine-induced decreases in the level of glutathione as well as the activity and expression of aldehyde-dehydrogenase 2 in the hippocampus of rats. Conclusion: Hydrogen sulfide ameliorates homocysteine-induced impairment in cognitive function by decreasing accumulation of reactive aldehydes as a result of upregulations of glutathione and aldehyde-dehydrogenase 2.

Antidepressant-like and anxiolytic-like effects of hydrogen sulfide in streptozotocin-induced diabetic rats through inhibition of hippocampal oxidative stress.

Depression is highly prevalent in individuals with diabetes, and depressive symptoms are less responsive to current antidepressant therapies. Oxidative stress plays a major role both in the pathogenesis of diabetes and in major depression and anxiety disorders. Hydrogen sulfide (H2S), the third gaseous mediator, is a novel signaling molecule in the brain that has both antioxidative activity and antidepressant-like and anxiolytic-like effects. We hypothesized that H2S could produce antidepressant-like and anxiolytic-like effects in diabetic patients through its antioxidative effect. To test this hypothesis, we generated streptozotocin (STZ)-induced diabetic rats. We found that H2S alleviated depressive-like behaviors of STZ-induced diabetic rats in the forced swimming and tail suspension tests and reduced their anxiety-like behaviors in the elevated plus maze test. We also found that H2S significantly reduced levels of malondialdehyde and 4-hydroxynonenal and elevated levels of superoxide dismutase and reduced glutathione in the hippocampus of STZ-induced diabetic rats. The results provide evidence for antidepressant-like and anxiolytic-like effects of H2S in STZ-induced diabetic rats and suggest that the therapeutic effects may result from inhibition of hippocampal oxidative stress. These findings suggest that elevating H2S signaling is a potential target for treatment of depressive and anxiety disorders related to diabetes.

Disturbance of endogenous hydrogen sulfide generation and endoplasmic reticulum stress in hippocampus are involved in homocysteine-induced defect in learning and memory of rats.

Homocysteine (Hcy) is a risk factor for Alzheimer's disease (AD). Hydrogen sulfide (H2S) acts as an endogenous neuromodulator and neuroprotectant. It has been shown that endoplasmic reticulum (ER) stress is involved in the pathological mechanisms of the learning and memory dysfunctions and that H2S exerts its neuroprotective role via suppressing ER stress. In the present work, we explored the effects of intracerebroventricular injection of Hcy on the formation of learning and memory, the generation of endogenous H2S, and the expression of ER stress in the hippocampus of rats. We found that intracerebroventricular injection of Hcy in rats leads to learning and memory dysfunctions in the Morris water maze and novel of object recognition test and decreases in the expression of cystathionine-ß-synthase, the major enzyme responsible for endogenous H2S generation, and the generation of endogenous H2S in the hippocampus of rats. We also showed that exposure of Hcy could up-regulate the expressions of glucose-regulated protein 78 (GRP78), CHOP, and cleaved caspase-12, which are the major mark proteins of ER stress, in the hippocampus of rats. Taken together, these results suggest that the disturbance of hippocampal endogenous H2S generation and the increase in ER stress in the hippocampus are related to Hcy-induced defect in learning and memory.

[Study on determination of sodium, vanadium and aluminum contents in fuel oil by ICP-AES].

The present paper considers synthetically all kinds of factors affecting excitation spectrum under traditional measurement conditions of fluorescence matter in liquor using plasma atomic emission spectra. The input power, carrier gas flow and assistant gas flow for BEC of Na, V, Al were optimized by testing. The input power, carrier gas flow and assistant gas flow for Na are 950 W, 0.6 L x min(-1) and 1.0 L x min(-1), respectively. The input power, carrier gas flow and assistant gas flow for V are 1 150 W, 0.5 and 1.1 L x min(-1), respectively. The input power, carrier gas flow and assistant gas flow for Al are 1 150 W, 0.6 and 1.0 L x min(-1), respectively. The result shows that the method is sensitive, accurate, linear in a wide range and highly precise. The precision is between 1.7%-2.2%, the linear ranges are between 0-100 mg x L(-1) and recoveries are between 96%-105%.

[MOA spectral analysis of additive element contents in lube oil].

The determination of the additive contents of marine lubrication oil by using atomic emission spectrometry is described. A new measuring method is suggested in accordance with the working principle of MOA atomic emission spectral instrument. The additive element contents, if not within the precision limits of MOA atomic emission spectra, are to be measured by being diluted with a standard oil. Error analysis is conducted and the calibration curve method is used. The testing result indicates that the RSD of Ca, P and Zn is 1.6%, 4.8% and 4.6% respectively, and the error result of oil sample before and after diluting is 4.21%, 6.99% and 5.09% respectively.

[Study on the characteristic parameter of oil spectrometric analysis].

This paper establishes a new mathematics model of fault diagnosis basis of oil spectrometric analysis by means of long time following up the mechanical equipment's lubrication oil. The characteristic parameter of oil spectrometric analysis has been confirmed using a new way that the laboratory experiment study and the mechanical equipment's lubrication oil spectrometric analysis are combined in order to confirm the time of fault and avoid serious fault. It will provide the academic and actual basis for RCM and enhance the dependability. The result of examples proves that the characteristic parameter of oil spectrometric analysis has very high stability and veracity. This method has been proved that it was effective in fault diagnosis basis of oil spectrometric analysis.