Flexible Sensors Based on Conductive Polymer Composites.

Elastic polymer-based conductive composites (EPCCs) are of great potential in the field of flexible sensors due to the advantages of designable functionality and thermal and chemical stability. As one of the popular choices for sensor electrodes and sensitive materials, considerable progress in EPCCs used in sensors has been made in recent years. In this review, we introduce the types and the conductive mechanisms of EPCCs. Furthermore, the recent advances in the application of EPCCs to sensors are also summarized. This review will provide guidance for the design and optimization of EPCCs and offer more possibilities for the development and application of flexible sensors.

CircRNF121 knockdown suppresses the progression of cervical cancer by regulating miR-153-3p/ATF2 axis and wnt/ß-catenin pathway.

Cervical cancer (CC) is a common malignancy in gynecology. Emerging evidence has demonstrated that circular RNAs (circRNAs) act as vital mediators in CC. However, the roles of circRNA ring finger protein 121 (circRNF121) in CC are largely unknown. Herein, we focused on the exact function and underlying mechanism of circRNF121 in CC development. Our results showed that circRNF121 was highly expressed in CC tissues and cells. Knockdown of circRNF121 suppressed cell growth, metastasis, epithelial-mesenchymal transition (EMT), autophagy, and wnt/ß-catenin pathway in CC cells in vitro and blocked tumor formation in vivo. For mechanism investigation, circRNF121 could affect activating transcription factor 2 (ATF2) expression by decoying miR-153-3p, thereby accelerating CC cell development. In conclusion, circRNF121 exerted the tumor-suppressive role in CC progression by altering miR-153-3p/ATF2 axis. These results suggested that circRNF121 might be a possible circ-targeted therapy for patients with CC.

Randomized comparison of sevoflurane versus propofol-remifentanil on the cardioprotective effects in elderly patients with coronary heart disease.

BACKGROUND: It is skeptical about cardioprotective property of sevoflurane in patients undergoing noncardiac surgery, especially in the elderly patients with coronary heart disease. We hypothesized that long duration of sevoflurane inhalation in noncardiac surgery could ameliorate myocardial damage in such patients. METHODS: This was a randomized, prospective study. One hundred twenty-one elderly patients with coronary heart disease were randomly allocated into two groups. Maintenance of anesthesia was achieved by sevoflurane inhalation (Group S) or propofol-remifentanil respectively (Group PR). Serum cardiac troponin I (cTnI) and brain natriuretic peptide (BNP) were measured before anesthesia induction (T0), 8 h (T1) and 24 h (T2) after anesthesia respectively. The perioperative cardiac output, complications and postoperative 3-month follow-up from end of surgery were recorded. RESULTS: Between the two groups, there were no statistical differences in the values of cTnI and BNP during the study. However, The area under the curve of cTnI values over 24 h after operation was less in Group S. Group PR had lower cardiac output and consumed more amount of phenylephrine during the study (P < 0.05). CONCLUSIONS: Compared with the group PR, sevoflurane had no benefit in the myocardial protection for the elderly patients with CHD. However, Sevoflurane showed advantage in maintaining hemodynamic stability during the operative period. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-IPR-16008871 , 21 July 2016.

A comparison of intrathecal magnesium and ketamine in attenuating remifentanil-induced hyperalgesia in rats.

BACKGROUND: Activation of NMDA receptors play an important role in the development of remifentanil-induced hyperalgesia. We hypothesized that in addition to ketamine, intrathecal MgSO4 could also relieve thermal and mechanical hyperalgesia in rats. METHODS: Initially, 24 Sprague-Dawley rats were divided into control group, remifentanil group, surgical incision group and remifentanil combined with surgical incision group to create an experimental model. Subsequently, 40 rats were divided into control group, model group, model group plus 100 µg MgSO4, 300 µg MgSO4 and 10 µg ketamine respectively. Paw withdrawal mechanical thresholds and paw withdrawal thermal latency tests were performed at -24 h, 2 h, 6 h, 24 h, 48 h, 72 h and 7 day after the surgical procedure. After behavior assessment on the 7th day, remifentanil was given again to ascertain whether or not NMDA antagonists could suppress the re-exposure of remifentanil-induced hyperalgesia. RESULTS: Remifentanil administration plus surgical incision induced significant postoperative hyperalgesia, as indicated by decreased paw withdrawal mechanical thresholds and paw withdrawal thermal latency to mechanical and thermal stimulation. In addition to ketamine, intrathecal MgSO4 (100, 300 µg) dose-dependently reduced remifentanil-induced mechanical and thermal hyperalgesia. Ketamine had less mechanical hyperalgesia in 6 h (p = 0.018), 24 h (p = 0.014) and 48 h (p = 0.011) than 300 µg MgSO4. There was no difference in inhibiting thermal hyperalgesia between the group ketamine and group MgSO4 (300 µg). The rats were given remifentanil again 7 days later after the first exposure of remifentanil. The hyperalgesic effect induced by re-exposure of remifentanil was not reversed in any groups of MgSO4 or ketamine. CONCLUSIONS: In addition to ketamine, intrathecal administration of MgSO4 dose-dependently reduced remifentanil-induced hyperalgesia in a surgical incision mode. Re-exposure to remifentanil 1 week later again produced hyperalgesia, and this was not altered by the prior intrathecal treatments in any 4 groups treated with MgSO4 or ketamine.

The single-cell transcriptomic atlas iPain identifies senescence of nociceptors as a therapeutical target for chronic pain treatment.

Chronic pain remains a significant medical challenge with complex underlying mechanisms, and an urgent need for new treatments. Our research built and utilized the iPain single-cell atlas to study chronic pain progression in dorsal root and trigeminal ganglia. We discovered that senescence of a small subset of pain-sensing neurons may be a driver of chronic pain. This mechanism was observed in animal models after nerve injury and in human patients diagnosed with chronic pain or diabetic painful neuropathy. Notably, treatment with senolytics, drugs that remove senescent cells, reversed pain symptoms in mice post-injury. These findings highlight the role of cellular senescence in chronic pain development, demonstrate the therapeutic potential of senolytic treatments, and underscore the value of the iPain atlas for future pain research.

Overexpressed microRNA (miR)-382-3p promoted vascular remodeling via suppressing autophagy-related protein 7 (ATG7) in chronic thromboembolic pulmonary hypertension.

BACKGROUND: This research has investigated the role of miR-382-3p in chronic thromboembolic pulmonary hypertension (CTEPH). METHODS: Human pulmonary artery smooth muscle cells (hPASMCs) were treated with PDGF-BB to induce proliferation, and then transfected with miR-382-3p mimic, miR-382-3p inhibitor, ATG7 overexpression plasmid, and siATG7. MiR-382-3p, ATG7, VEGF, PCNA, p62, and LC3-Ⅱ/LC3-I levels were detected by qRT-PCR and Western blotting. Cell viability and migration were tested through CCK-8 and wound healing assays, respectively. Target genes of miR-382-3p were predicted by Targetscan and starBase, and pathway analysis was implemented through WebGestalt. The binding relationship between miR-382-3p and ATG7 was analyzed by the dual-luciferase reporter and RIP assays. A CTEPH model was constructed in rats with the treatment of miR-382-3p antagomir or agomir, and mean pulmonary artery pressure (mPAP) was measured. Lung tissue was observed through the HE staining assay. RESULTS: MiR-382-3p level in hPASMCs was obviously upregulated with the increasing dose of PDGF-BB. MiR-382-3p mimic promoted yet miR-382-3p inhibitor suppressed hPASMC proliferation. MiR-382-3p directly targeted ATG7. ATG7 overexpression repressed hPASMC proliferation and migration, whereas siATG7 exerted the opposite effects. ATG7 overexpression partly neutralized the effects of miR-382-3p mimic on proliferation, migration, and autophagy-related proteins (ATG7, p62, and LC3-Ⅱ/LC3-I) in hPASMCs, whereas siATG7 partly offset the impacts of miR-382-3p inhibitor. MiR-382-3p antagomir reversed CTEPH-induced mPAP elevation, miR-382-3p upregulation, thickening of the pulmonary artery wall, and increased expressions of VEGF, PCNA, and autophagy-related proteins in rats, while miR-382-3p agomir potentiated these effects induced by CTEPH. CONCLUSION: Overexpressed miR-382-3p promotes vascular remodeling via ATG7 inhibition in CTEPH.

LncRNA-GAS5/miR-382-3p axis inhibits pulmonary artery remodeling and promotes autophagy in chronic thromboembolic pulmonary hypertension.

BACKGROUND: We have clarified the role of miR-382-3p in chronic thromboembolic pulmonary hypertension (CTEPH), but what is less clear lies in its upstream regulatory mechanism. OBJECTIVE: To explore the regulation mechanism of GAS5/miR-382-3p axis on CTEPH. METHODS: In vitro, we constructed cell models by treating Pulmonary Artery Smooth Muscle Cells (PASMCs) with platelet-derived growth factor-BB (PDGF-BB). The effects of different concentrations of PDGF-BB on the activity of PASMCs were tested by cell counting kit-8 (CCK-8). The upstream lncRNA of miR-382-3p was screened and confirmed through bioinformatics analysis, RNA pull-down, quantitative reverse transcription polymerase chain reaction (qRT-PCR), dual luciferase reporter gene and RNA immunoprecipitation assays. The effects of GAS5/miR-382-3p axis on the viability, migration, and expressions of autophagy- and angiogenesis-related proteins were confirmed by rescue experiments (CCK-8, wound healing and western blot). In vivo, animal models by perfusing autologous blood vessels, the effects of GAS5 overexpression or silencing on the expressions of miR-382-3p, angiogenesis- and autophagy-related genes, mean pulmonary arterial pressure (mPAP) and pulmonary artery wall were determined by biological signal acquisition system, hematoxylin-eosin staining, qRT-PCR and western blot. RESULTS: PDGF-BB dose-dependently promoted PASMCs viability. XIST and GAS5 expressions in PASMCs were affected by the concentration of PDGF-BB, but only GAS5 can be pulled down by miR-382-3p probe. GAS5 targeted miR-382-3p to inhibit the viability and migration of PAMSCs, mPAP in CTEPH rats, pulmonary artery wall thickening and angiogenesis, and promote autophagy. CONCLUSIONS: GAS5/miR-382-3p axis is involved in the regulation of pulmonary artery remodeling and autophagy in CTEPH.

A Birth Cohort Study of Neurodevelopmental Outcomes from Birth to 2 Years of Age in Preterm Infants under 34 Weeks of Gestation.

Background: The tissues and organs of premature infants are immature and easily damaged by external adverse factors, leading to functional development disorders and abnormalities. Besides, the incidence of premature babies in various countries has an increasing trend, with the incidence rate exceeding 10%. Objective: This study aims to investigate the neurodevelopment and the incidence of various developmental delays, cerebral palsy, autism spectrum disorder, and audio-visual impairment in premature infants under 34 weeks of gestation from birth to 2 years of age, so as to provide the basis for early intervention of premature infants in the clinic. Methods: A cohort of premature infants was established using 263 premature infants with a gestational age of 28-33 + 6 weeks who were born alive from March 1, 2018, to February 28, 2019, in four tertiary hospitals in Shenzhen. In addition, 263 full-term infants of the same sex who were born in the same period in the four hospitals were randomly selected and paired in a ratio of 1 : 1 as the control group. The subjects were assessed for neurodevelopment using the Gesell test scale at 6, 12, 18, and 24 months after birth (premature infants were corrected for months). We calculated the neurodevelopmental indicators of children in each month of age and the incidence of various developmental delays, cerebral palsy, autism spectrum disorder, and audio-visual impairment in the two groups. Results: The results of this study showed that the cohort of premature infants with birth gestational age less than 34 weeks had higher adaptive, fine motor, and personal-social energy domain development quotient (DQ) values from the corrected gestational age of 6 months to the corrected gestational age of 24 months after birth compared with the full-term cohort. And it also achieved catch-up growth in neurological development, but the detection rates of neurodevelopmental abnormalities at the corrected gestational age of 12 and 24 months were higher than those in the full-term cohort. Conclusion: It is important to reduce the disability rate and degree of premature infants by strengthening the systematic management, early promotion and supervision, as well as early intervention for preterm infants with developmental abnormalities who were born at gestational age less than 34 weeks after birth.

Direct Inhibition of Microglia Activation by Pretreatment With Botulinum Neurotoxin A for the Prevention of Neuropathic Pain.

Peripheral injection of botulinum neurotoxin A (BoNT/A) has been demonstrated to have a long-term analgesic effect in treating neuropathic pain. Around peripheral nerves, BoNT/A is taken up by primary afferent neurons and inhibits neuropeptide release. Moreover, BoNT/A could also be retrogradely transported to the spinal cord. Recent studies have suggested that BoNT/A could attenuates neuropathic pain by inhibiting the activation of spinal glial cells. However, it remains unclear whether BoNT/A directly interacts with these glial cells or via their interaction with neurons. Our aim here is to determine the direct effect of BoNT/A on primary microglia and astrocytes. We show that BoNT/A pretreatment significantly inhibits lipopolysaccharide (LPS) -induced activation and pro-inflammatory cytokine release in primary microglia (1 U/mL BoNT/A in medium), while it has no effect on the activation of astrocytes (2 U/mL BoNT/A in medium). Moreover, a single intrathecal pre-administration of a low dose of BoNT/A (1 U/kg) significantly prohibited the partial sciatic nerve ligation (PSNL)- induced upregulation of pro-inflammatory cytokines in both the spinal cord dorsal horn and dorsal root ganglions (DRGs), which in turn prevented the PSNL-induced mechanical allodynia and thermal hyperalgesia. In conclusion, our results indicate that BoNT/A pretreatment prevents PSNL-induced neuropathic pain by direct inhibition of spinal microglia activation.

Increased TRPV4 expression in non-myelinating Schwann cells is associated with demyelination after sciatic nerve injury.

Transient receptor potential vanilloid 4 (TRPV4) is a non-selective calcium-permeable cation channel that is widely expressed and activated in various neurons and glial cells in the nervous system. Schwann cells (SCs) are primary glia cells that wrap around axons to form the myelin sheath in the peripheral nervous system. However, whether TRPV4 is expressed and functions in SCs is unclear. Here, we demonstrate functional expression of TRPV4 in mouse SCs and investigated its physiological significance. Deletion of TRPV4 did not affect normal myelin development for SCs in sciatic nerves in mice. However, after sciatic nerve cut injury, TRPV4 expression levels were remarkably increased in SCs following nerve demyelination. Ablation of TRPV4 expression impaired the demyelinating process after nerve injury, resulting in delayed remyelination and functional recovery of sciatic nerves. These results suggest that local activation of TRPV4 could be an attractive pharmacological target for therapeutic intervention after peripheral nerve injury.

Z-Guggulsterone alleviated oxidative stress and inflammation through inhibiting the TXNIP/NLRP3 axis in ischemic stroke.

Ischemic stroke is a serious and life-threatening cerebrovascular thrombotic disease; however, the therapeutic strategy is limited for the complicated mechanism and narrow therapeutic window. Our previous study suggested that Z-Guggulsterone (Z-GS), an active component derived from myrrh, is a good candidate for cerebral injury. The object of this study is to investigate the exact mechanisms of Z-GS in cerebral ischemic stroke. Rats were used to conduct middle cerebral artery occlusion (MCAO) model and were treated with different dosage of Z-GS. Morphological results showed that Z-GS significantly alleviated neurological deficits, infarct volume and histopathological damage in MCAO rats. A total of 8276 differentially expressed genes were identified based on microarray analysis. Oxidation-reduction process and inflammatory response were enriched as the significant gene ontology items. TXNIP and NLRP3 were screened as the potential target genes by Series Test of Cluster (STC) analysis. The results were validated by immunohistochemistry and immunofluorescence staining. Besides, Z-GS successfully inhibited oxidative stress and inflammatory response in oxygen-glucose deprivation (OGD) treated neurons. Knockdown of TXNIP significantly decreased the expression of NLRP3 in OGD-induced neurons. In addition, Z-GS treatment scarcely changed the expressions of NLRP3 in siRNA-TXNIP pretreated cells compared with the siRNA-TXNIP alone treatment group, suggesting that the neuroprotective effect of Z-GS was dependent on TXNIP-NLRP3 axis. Taken together, this study revealed that Z-GS exerted neuroprotective property through alleviated oxidative stress and inflammation via inhibiting the TXNIP/NLRP3 axis. Z-GS could be considered as a promising candidate for the treatment of ischemic stroke.

Efficacy of weekly paclitaxel for the treatment of advanced ovarian cancer: A protocol for systematic review and meta-analysis.

BACKGROUND: This study aims to assess the efficacy and safety of weekly paclitaxel (WP) for the treatment of advanced ovarian cancer (AOC). METHODS: This study will systematically search bibliographic databases (MEDLINE, EMBASE, Cochrane Library, Web of Science, CINAHL, PSYCINFO, Allied and Complementary Medicine Database, CNKI, WANGFANG, and Chinese Biomedical Literature Database) and other literature sources from inception to the March 1, 2020 without language and publication time limitations. Two authors will independently complete all literature selection, data collection, and study quality evaluation. Any disagreements will be solved by a third author through discussion. We will analyze data by RevMan V.5.3 software. RESULTS: This study will systematically generate a comprehensive summary on the efficacy and safety of WP for the treatment of AOC. CONCLUSION: This study may provide beneficial evidence of WP for the treatment of AOC. SYSTEMATIC REVIEW REGISTRATION: INPLASY202040193.

Secondary Grain Growth in Organic-Inorganic Perovskite Films with Ethylamine Hydrochloride Additives for Highly Efficient Solar Cells.

The grain boundaries of perovskite polycrystalline are regarded as a defect region that not only provides carrier recombination sites but also introduces device degradation pathways. Efforts to enlarging the grain size of a perovskite film and reducing its grain boundary are crucial for highly efficient and stable perovskite solar cells (PSCs). Some effective methods that facilitate grain growth are postdeposition thermal annealing and solvent vapor annealing. However, a detailed understanding of grain growth mechanisms in perovskite films is lacking. In this study, perovskite films were prepared by adding ethylamine hydrochloride (EACl) to the precursor solution. This additive strategy promotes a new grain growth mode, secondary grain growth, in perovskite films. Secondary grain growth leads to much larger grains with a high crystallographic orientation. These excellent properties lead to reduced grain boundaries and the densities of boundary defects. The improved film quality results in a prolonged charge-carrier lifetime and a significantly enhanced power conversion efficiency (PCE). Compared with the 18.42% PCE of the control device, the PCE of the device with EACl additives reaches 21.07%.

circRNA/lncRNA-miRNA-mRNA Network in Oxidized, Low-Density, Lipoprotein-Induced Foam Cells.

Although long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) have been suggested to play important roles in the pathogenesis of diseases, atherosclerosis-related lncRNAs and circRNAs remain rarely reported. This study aimed to explore the underlying molecular mechanisms of atherosclerosis based on the competing endogenous RNA (ceRNA) regulatory hypothesis of lncRNAs and circRNAs. The expression profiles of circRNAs, lncRNAs, and mRNAs in human THP-1 macrophages treated with oxidized low-density lipoprotein (an in vitro atherosclerosis model), or not, were obtained from the Gene Expression Omnibus database under accession numbers GSE107522, GSE54666, and GSE54039, respectively. The present study identified 29 differentially expressed circRNAs in GSE107522, 544 differentially expressed genes (DEGs) in GSE54666, and 502 DEGs and 231 differentially expressed lncRNAs in GSE54039 datasets by using the Linear Models for Microarray Data method. Eight DEGs were found to be shared and expressed with the consistent trend in GSE54666 and GSE54039 datasets. Two of them (ASPH, aspartate beta-hydroxylase; and PDE3B, phosphodiesterase 3B) were suggested to be crucial based on functional enrichment, protein-protein interaction, and ceRNA network analyses. ASPH, through interaction with CACNA2D4 (calcium voltage-gated channel auxiliary subunit alpha2delta 4), may be associated with atherosclerosis by regulating the cellular response to calcium ion; and PDE3B may exert roles in negative regulation of angiogenesis through cross talk with ELMO1 (engulfment and cell motility 1). Furthermore, the expression of ASPH and PDE3B may be regulated by hsa_circ_0028198/hsa_circ_0092317/XIST-miR-543; PDE3B expression may be also modulated by hsa_circ_0092317/hsa_circ_0003546/H19/XIST-miR-326. In conclusion, our identified ceRNA interaction axes may possibly be important targets for treatment of atherosclerosis.

ω-3 fish oil fat emulsion preconditioning mitigates myocardial oxidative damage in rats through aldehydes stress.

ω-3 fish oil fat emulsions contain a considerable quantity of unsaturated carbon-carbon double bonds, which undergo lipid peroxidation to yield low-dose aldehydes. These aldehydes may stimulate the production of antioxidant enzymes, thereby mitigating myocardial oxidative damage. This study aims to (1) verify the cardioprotective effect of ω-3 fish oil fat emulsion in vivo and in vitro, and (2) determine whether aldehyde stress is a protective mechanism. For modeling purposes, we pretreated rats with 2 ml/kg of a 10% ω-3 fish oil fat emulsion for 5 days in order to generate a sufficient aldehyde stress response to trigger the production of antioxidant enzymes, and we obtained similar response with H9C2 cells that were pretreated with a 0.5% ω-3 fish oil fat emulsion for 24 h. ω-3 fish oil fat emulsion pretreatment in vivo reduced the myocardial infarct size, decreased the incidence of arrhythmias, and promoted the recovery of cardiac function after myocardial ischemia/reperfusion injury. Once the expression of nuclear factor E2-related factor 2 (Nrf2) was silenced in H9C2 cells, aldehydes no longer produced enough antioxidant enzymes to reverse the oxidative damage caused by tert-butyl hydroperoxide (TBHP). Our results demonstrated that ω-3 fish oil fat emulsion enhanced the inhibition of oxidation and production of free radicals, and alleviated myocardial oxidative injury via activation of the Nrf2 signaling pathway.

CXCL5, the upregulated chemokine in patients with uterine cervix cancer, in vivo and in vitro contributes to oncogenic potential of Hela uterine cervix cancer cells.

CXCL5 is showed a surprisingly elevated profile and implicated in tumorigenesis in several tumors. However, the expression and function of CXCL5 in uterine cervix cancer (UCC) remain largely unknown. The current study aimed to elucidate the expression pattern of CXCL5 in human UCC tissues and Hela cervix cancer cell, as well as its functions in Hela cells. Our data showed that CXCL5 and its receptor CXCR2 were expressed by Hela uterine cervix cancer cells. CXCL5 was upregulated in UCC tissues, and its overexpression was positively correlated with age, but did not correlate with clinical stages and tumor infiltration. Exogenous administration of CXCL5 and CXCL5 overexpression contributed to proliferation and migration activities of Hela cells in vitro, consistent with this, CXCL5 overexpression also promoted growth of Hela cells in a nude mouse xenograft model. At the gene level, CXCL5 overexpression regulated the expression of tumor-related genes including ERK, p-ERK, AKT, p-AKT, DIABOL, NUMB, NDRG3 and CXCR2. Taken together, CXCL5 may contribute to a dominant role in UCC progression and sever as a potential molecular therapeutic target for UCC.

Analgesic effect of perineural magnesium sulphate for sciatic nerve block for diabetic toe amputation: A randomized trial.

BACKGROUND AND OBJECTIVES: High concentrations of local anesthetics may be neurotoxic for diabetic patients. Additive perineural administration of magnesium was reported to decrease the consumption of local anesthetics for nerve block. It was hypothesized that MgSO4 added to dilute ropivacaine was equianalgesic to more concentrated ropivacaine for toe amputations in diabetic patients. METHODS: Seventy diabetic patients were allocated into 3 groups: 1) perineural 200 mg MgSO4 added to 0.25% ropivacaine, 2) 0.25% ropivacaine alone, and 3) 0.375% ropivacaine alone. All patients underwent popliteal sciatic nerve block that was guided by ultrasonography using the respective regimens. Time of onset, duration of motor and sensory block were recorded. Spontaneous and evoked pain score, worst pain score, additional analgesic consumption, satisfaction score and initial time of analgesic requirement of each patient were documented up to 48 hours postoperatively. RESULTS: In comparison with 0.25% ropivacaine alone, magnesium supplement prolonged the duration of sensory block (p = 0.001), as well as better evoked pain score at 6 hour postoperatively (p = 0.001). In comparison with evoked pain score (1.6/10) in group of 0.375% ropivacaine, magnesium plus 0.25% ropivacaine presented a little higher score (2.5/10) at 6 hour postoperatively (p = 0.001), while lower worst pain score (p = 0.001) and less postoperative total analgesic consumption (p = 0.002). CONCLUSIONS: The regimen of adding 200mg MgSO4 to 0.25% ropivacaine for sciatic nerve block yields equal analgesic effect in comparison with 0.375% ropivacaine. These findings have suggested that supplemental MgSO4 could not improve analgesic quality except reducing the total amount of local anesthetics requirement in diabetic toe amputations with sciatic nerve blocks.

Synergistic neuroprotective effects of Danshensu and hydroxysafflor yellow A on cerebral ischemia-reperfusion injury in rats.

Ischemic stroke is a common cerebrovascular disease with substantial morbidity and mortality worldwide. However, therapeutic options to minimize the cerebral ischemia-reperfusion (I/R) injury are limited. In China, combination of herb Danshen (Salvia miltiorrhiza Bge) and Honghua (Carthamus tinctorius L.) is effective for stroke treatment in patients but its underlying mechanism requires further investigation. Our study was conducted to evaluate and explore the synergistic effects of two herb ingredients Danshensu and hydroxysafflor yellow A (HSYA) on cerebral ischemia-reperfusion (I/R) injury in rats. Rats were randomly assigned to the following five groups: sham group, model group, Danshensu group, HSYA group, and Danshensu+HSYA group. Under our experimental conditions in vitro, oxygen-glucose deprivation (OGD) model was established to determine the synergistic neuroprotective effects of Danshensu and HSYA. With such methods as neurological deficits scoring, TTC, HE and TUNEL staining, and ELISA detection, the results demonstrated that administration of either Danshensu or HSYA improved neurological defects and alleviated pro-inflammatory and oxidative stress reactions. Notably, combination of Danshensu and HSYA exerted more effective results than that used alone. Furthermore, western blot analysis results showed that Danshensu and HSYA combination displayed synergistic regulation on TLR4/NF-κB and Nrf2/HO-1 pathways. Consistently, Danshensu +HSYA group exhibits better neuroprotection in primary neurons with OGD model compared with Danshensu or HSYA group. Taken together, we found for the first time that Danshensu plus HSYA could achieve remarkable synergistic neuroprotective effects on I/R injury, which is related to the anti-inflammatory and antioxidant pathways.

Giving Priority to Lipid Administration Can Reduce Lung Injury Caused by Epinephrine in Bupivacaine-Induced Cardiac Depression.

BACKGROUND AND OBJECTIVES: Epinephrine is usually administered in concert with a lipid emulsion during local anesthetic toxicity. However, the timing and role of epinephrine administration in combination with a lipid emulsion remain unclear. Specifically, the temporal association of epinephrine and lipid emulsion administration with related changes in pulmonary vascular pressures that may lead to pulmonary edema and hemorrhage needs to be determined. METHODS: This study consisted of 2 parts, experiments A and B. In experiment A, 24 adult male Sprague-Dawley rats were randomly divided into 3 groups (n = 8) to receive 1 of 3 treatments. All rats were anesthetized with an intraperitoneal injection of chloral hydrate, and anesthesia was maintained by sevoflurane. Each treatment group was initially given an infusion of bupivacaine (15 mg/kg) in order to produce cardiac depression. Group 1 (A-LEN) received a 30% lipid infusion (3 mL/kg) followed by a rapid epinephrine bolus (10 µg/kg), which was then followed by a normal saline infusion (3 mL/kg). Group 2 (A-NEL) first received a normal saline infusion (3 mL/kg) followed by a rapid epinephrine bolus, which was then followed by a 30% lipid emulsion. Group 3 (A-NEN, considered a control group) first received a normal saline infusion (3 mL/kg) followed by a rapid epinephrine bolus (10 µg/kg), which was then followed by another normal saline infusion (3 mL/kg). Lipid and normal saline infusions were administered over 1 minute, whereas epinephrine was injected rapidly. The continuous monitoring of blood pressure, heart rate, pulmonary arterial pressure, and pulmonary venous pressure occurred for 30 minutes. After the 30-minute monitoring period, lung tissue was sampled, and bronchoalveolar lavage fluid was collected. In experiment B, the experimental model and resuscitation protocol were similar to experiment A (B-LEN and B-NEL groups). In this arm of the experiment, bupivacaine concentrations of cardiac tissue were determined after the second minute of normal saline infusion. RESULTS: The A-LEN group produced the best rate pressure product when compared with the A-NEL or A-NEN group (P = 0.045, P = 0.011, respectively). In regard to pulmonary venous pressure, the A-LEN group was lower than the A-NEL or A-NEN group (P = 0.031, P = 0.006, respectively). Animals in the A-NEL and A-NEN groups rapidly developed pulmonary edema after infusion of epinephrine. The wet-to-dry ratio of the lungs in the A-LEN group was lower than that of the lungs in the A-NEL group (P = 0.024).The lung permeability index of the A-LEN group was lower than that of the A-NEL group (P = 0.011). In experiment B, concentrations of bupivacaine in cardiac tissue and plasma of the B-LEN group were lower than those of the B-NEL group (P = 0.001, P = 0.03, respectively). CONCLUSIONS: Giving priority to the administration of a lipid emulsion before the administration of epinephrine can reduce lung injury in bupivacaine-induced cardiac depression in rats.

Application of lariat lock catch knot suture in the achilles tendon rupture.

The aim of this study was to summarize the clinical experience of repairing the Achilles tendon rupture by lariat lock catch knot suture. Between January 2011 and February, 2014, 32 cases of the Achilles tendon rupture were treated by lariat lock catch knot suture. There were 26 males and 6 females, with the average age of 39 years (range 17-53 years), including 13 left knees and 19 right knees. 29 wounds healed by first intention, and 3 cases who were performed local flap transfer due to necrosis of skin were healed by second intention. Thirty-two cases were followed up 10-25 months (13 months on average). No re-rupture of Achilles tendon or deep infection occurred during follow-up period. According to Arner-Lindholm assessment standard, the results were excellent in 19 cases and good in 13 cases, the excellent and good rate was 100%. Lariat lock catch knot suture is a safe and effective method for repairing Achilles tendon.