High-Performance 3D Stacked Micro All-Solid-State Thin-Film Lithium-Ion Batteries Based on the Stress-Compensation Effect.

A novel all-solid-state thin-film lithium-ion battery (LIB) is presented to address the trade-off issue between the specific capacity and stabilities in a conventional LIB. Different from the conventional one, this LIB device consists of two same LIB components located at the front and back surfaces of the substrate, respectively. These two LIB components form parallel connection by using the conductive through vias distributed in the substrate. Compared with the conventional one, this LIB device doubles the areal specific capacity. More importantly, due to the stress-compensation effect, this device effectively suppresses the stress induced by its volume changes resulting from the lithiation/delithiation processes and thermal expansion. Consequently, this device shows good cycling and thermal stabilities even when working at an industrial-grade high temperature of 125 °C. To further improve the specific capacity without sacrificing the stabilities, a 3D stacked LIB is successfully realized by using this LIB device as the cell, in which each cell is parallelly connected by using the above-mentioned conductive through vias. This 3D stacked LIB is experimentally demonstrated to obtain high specific capacity (79.9 µAh cm-2) and good stabilities (69.3% of retained capacity after 100 cycles at 125 °C) simultaneously.

Cross-linked enzyme aggregates immobilization: preparation, characterization, and applications.

Enzymes are commonly used as biocatalysts for various biological and chemical processes. However, some major drawbacks of free enzymes (e.g. poor reusability and instability) significantly restrict their industrial practices. How to overcome these weaknesses remain considerable challenges. Enzyme immobilization is one of the most effective ways to improve the reusability and stability of enzymes. Cross-linked enzyme aggregates (CLEAs) has been known as a novel and versatile carrier-free immobilization method. CLEAs is attractive due to its simplicity and robustness, without purification. It generally shows: high catalytic specificity and selectivity, good operational and storage stabilities, and good reusability. Moreover, co-immobilization of different kinds of enzymes can be acquired. These CLEAs advantages provide opportunities for further industrial applications. Herein, the preparation parameters of CLEAs were first summarized. Next, characterization of structural and catalytic properties, stability and reusability are also proposed. Finally, some important applications of this technique in: environmental protection, industrial chemistry, food industry, and pharmaceutical synthesis and delivery are introduced. Potential challenges and future research directions, such as improving cross-linking efficiency and internal mass transfer efficiency, are also presented. This implies that CLEAs provide an efficient and feasible technique to improve the properties of enzymes for use in the industry.

Reversible Thermochromism and Stable Resistance Switching Behaviors Based on a Co(III)-Complex-Linked Polyoxoniobate.

A 3D Co(III)-complex hybrid polyoxoniobate framework Na10(H2O)36[Co2(phen)2(4,4'-bipy)(Nb6O19)2]·19H2O (1) has been constructed from [Co2(phen)2(4,4'-bipy)(Nb6O19)2]10- dimer units and 2D inorganic Na-O cluster layers. The Co(III) centers are coordinated with {Nb6O19}, 4,4'-bipy and phen simultaneously. The [Co2(phen)2(4,4'-bipy)(Nb6O19)2]10- fragments link the Na-O cluster layers to generate a 3D metal complex-modified hybrid polyoxoniobate framework with π-π interactions between phenanthroline rings. Compound 1 shows reversible thermochromic behavior resulting from electron transfer from {Nb6O19} to 4,4'-bipy and subsequent formation of radical products, which is first observed in polyoxoniobates. Furthermore, the compound exhibits stable nonvolatile storage behavior and rewritable resistive switching with a low switching voltage (1.12 V) and high current on/off ratio (1.18 × 103) along with stable cyclic performance during stability test for 200 cycles. Charge-transfer mechanism has been studied by analyzing the relationship between current and voltage in the process of resistance switching.

Effects of Capsaicin on Glucose Uptake and Consumption in Hepatocytes.

Obesity represents a major health challenge because it substantially increases the risk of metabolic diseases. Capsaicin, the major active ingredient of Capsicum spp., has been reported to possess anti-obesity activity. Hereon, the effect of capsaicin on glucose uptake and consumption in hepatocytes was extensively studied. Capsaicin was shown to accelerate the glucose uptake/consumption and the ATP production of hepatocytes. The elevation of intracellular Ca2+ was thought to be a potential mechanism. By transcriptome analysis, 78, 146 and 507 differentially expressed genes (DEGs) were identified between capsaicin and the control group for 4 h, 12 h and 24 h treatments. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that most of the DEGs were involved in canonical pathways, like MAPK and PI3K-AKT signaling pathways. Clustering analysis showed that many DEGs were associated with glucose and amino acid metabolism. The variation trend in genes related to glucose and amino acid metabolism (like CTH, VEGFA, PCK2 and IGFBP3) in the quantitative PCR (q-PCR) assay was consistent with the transcriptome data. These results demonstrated that capsaicin efficiently accelerated the glucose uptake and consumption of hepatocytes.

miR-767-3p suppresses melanoma progression by inhibiting ASF1B expression.

BACKGROUND: Melanoma, the type of skin cancer considered as most malignant, and known to be linked with a high incidence as well as high mortality rate. Although the dysregulation of ASF1B and miR-767-3p expression is involved in the progression of various cancers, their biological function in melanoma remains unclear. METHODS: Real-time qPCR was the primary source for determining the levels of ASF1B and miR-767-3p in melanoma. For the validation of association among miR-767-3p and ASF1B, luciferase activity assay was used. Quantification of cell apoptosis, proliferation, migration and viability in melanoma cells were carried out by flow cytometry, BrdU, transwell assays, and CCK-8, respectively. Further evaluation of tumor growth was achieved by xenograft in vivo. RESULTS: Results showed an increased expression of ASF1B while declined expression of miR-767-3p in melanoma. ASF1B knockdown repressed cell migration, viability, proliferation, and tumor growth whereas boosted apoptosis in A375 as well as in A875 melanoma cells. Moreover, miR-767-3p attenuated the migration and proliferation of melanoma cells and encouraged cell apoptosis by reducing ASF1B levels. CONCLUSION: In this study, miR-767-3p was shown to inhibit ASF1B which will attenuate melanoma tumorigenesis, and by this it can be a potential new effective biomarker for the treatment of melanoma.

Current Sample Preparation Methodologies for Determination of Catecholamines and Their Metabolites.

Catecholamines (CAs) and their metabolites play significant roles in many physiological processes. Changes in CAs concentration in vivo can serve as potential indicators for the diagnosis of several diseases such as pheochromocytoma and paraganglioma. Thus, the accurate quantification of CAs and their metabolites in biological samples is quite important and has attracted great research interest. However, due to their extremely low concentrations and numerous co-existing biological interferences, direct analysis of these endogenous compounds often suffers from severe difficulties. Employing suitable sample preparation techniques before instrument detection to enrich the target analytes and remove the interferences is a practicable and straightforward approach. To date, many sample preparation techniques such as solid-phase extraction (SPE), and liquid-liquid extraction (LLE) have been utilized to extract CAs and their metabolites from various biological samples. More recently, several modern techniques such as solid-phase microextraction (SPME), liquid-liquid microextraction (LLME), dispersive solid-phase extraction (DSPE), and chemical derivatizations have also been used with certain advanced features of automation and miniaturization. There are no review articles with the emphasis on sample preparations for the determination of catecholamine neurotransmitters in biological samples. Thus, this review aims to summarize recent progress and advances from 2015 to 2021, with emphasis on the sample preparation techniques combined with separation-based detection methods such capillary electrophoresis (CE) or liquid chromatography (LC) with various detectors. The current review manuscript would be helpful for the researchers with their research interests in diagnostic analysis and biological systems to choose suitable sample pretreatment and detection methods.

Estrogen can promote the expression of genes related to precocious puberty in GT1-7 mouse hypothalamic GnRH neuronal cell line via activating G protein-coupled estrogen receptor.

The G protein-coupled estrogen receptor (GPER) was proved to be a new type of estrogen receptor (ER). It is unknown that whether estrogen can regulate the secretion of gonadotrophin releasing hormone (GnRH) in GT1-7 cells through the mechanism with the involvement of GPER. The GnRH, estradiol (17ß-estradiol, E2) and GPER in peripheral blood of precocious puberty children were detected by ELISA and RT-qPCR assays. After E2 treatment, the levels of GPER and GnRH in GT1-7 cells were detected. Following G1 treatment, cell proliferation was examined using a CCK-8 assay. The levels of GnRH, KISS1, GPR54, nNOS, c-FOS in GT1-7 cells were assessed following GT1-7 cells were induced by E2 combined with G1 or G15. GnRH, E2 and GPER were significantly increased in precocious puberty children. After E2 treatment, GT1-7 cells expressed more GnRH and GPER was markedly elevated and reached a peak at 8 h. The KISS1, GPR54 and nNOS in GT1-7 cells were significantly increased with G1 induction, but were significantly decreased with G15 induction compared with E2 induction alone. Collectively, GPER cannot promote the release of GnRH via affecting the proliferation of GT1-7 cells, but it may regulate GnRH through KISS1/GPR54 pathway, which provides novel ideas for precocious puberty children treatment.

Synthesis and Evaluation of the Antitumor Activity of Novel 1-(4-Substituted phenyl)-2-ethyl Imidazole Apoptosis Inducers In Vitro.

Novel imidazole derivatives were designed, prepared, and evaluated in vitro for antitumor activity. The majority of the tested derivatives showed improved antiproliferative activity compared to the positive control drugs 5-FU and MTX. Among them, compound 4f exhibited outstanding antiproliferative activity against three cancer cell lines and was considerably more potent than both 5-FU and MTX. In particular, the selectivity index indicated that the tolerance of normal L-02 cells to 4f was 23-46-fold higher than that of tumor cells. This selectivity was significantly higher than that exhibited by the positive control drugs. Furthermore, compound 4f induced cell apoptosis by increasing the protein expression levels of Bax and decreasing those of Bcl-2 in a time-dependent manner. Therefore, 4f could be a potential candidate for the development of a novel antitumor agent.

MAPKs and NF-κB-mediated acrylamide-induced neuropathy in rat striatum and human neuroblastoma cells SY5Y.

Acrylamide (ACR) is a potent neurotoxin that can be produced during high-temperature food processing, but the underlying toxicological mechanism remains unclear. In this study, the detrimental effects of ACR on the striatal dopaminergic neurons and the roles of mitogen-activated protein kinases (MAPKs) and nuclear factor κB (NF-κB) in ACR-induced neuronal apoptosis were investigated. Acute ACR exposure caused dopaminergic neurons loss and apoptosis as revealed by decreased tyrosine hydroxylase (TH)-positive cells and TH protein level and increased terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells in the striatum. ACR-decreased glutathione content, increased levels of malondialdehyde, proinflammatory cytokines tumor necrosis factor α, and interleukin 6. In addition, nuclear NF-κB and MAPKs signaling pathway with c-Jun N-terminal kinase (JNK) and p38 were activated by ACR. Specific inhibitors were used to explore the roles of MAPKs and NF-κB pathways in ACR-induced apoptosis in SH-SY5Y cells. Pretreatment with JNK-specific inhibitors SP600125 markedly upregulated the reduced B-cell lymphoma 2 (Bcl-2) content and downregulated the increased Bcl-2-associated X protein (Bax) level and thereby eventually reduced the proportions of early and late apoptotic cells induced by ACR, while p38 suppression by SB202190 only reversed the decrease in Bcl-2 expression. Inhibition of NF-κB by BAY 11-7082 markedly upregulated Bax level and decreased Bcl-2 expression, and eventually increasing the proportions of neuronal apoptosis compared with that in ACR alone. These results suggested that JNK contributed to ACR-induced apoptosis, while NF-κB acted as a protective regulator in response to ACR-induced neuropathy. This study helps to offer a deeper insight into the mechanism of ACR-induced neuropathy.

Growth-promoting effects of low-level butyl benzyl phthalate exposure on human neuroblastoma SH-SY5Y cells.

The purpose of present study was to investigate the impact of butyl benzyl phthalate (BBP) on SH-SY5Y neuroblastoma cells in vitro. The cell counting kit-8 was used to measure cell proliferation and flow cytometry was utilized to study cell cycle phases and apoptosis. Western blotting and quantitative real-time polymerase chain reaction were used to detect levels of aromatase, estrogen receptors (ERs) and some apoptosis and cell cycle-related genes. Results showed BBP-stimulated SH-SY5Y cells in a dose-dependent manner and produced a reverted U-shaped dose-response curve. BBP at lower concentrations (0.01 and 0.1 µm) significantly induced cell proliferation while inhibited cell growth at 300 µm. The promoting effect of estradiol could be entirely blocked by administration of ICI182 780, a pure antagonist of ERs, while the effect of BBP could be partly blocked. Additionally, we confirmed 0.1 µm BBP-induced cell proliferation caused the arrest of cells in S phase and inhibited apoptosis, which might be partially explained by the decreased expression of p53, the increased expression of proliferating cell nuclear antigen, Bcl-2 and cell cycle regulator cyclin-D1, and the activation of aromatase. The addition of ICI182 780 had no effect on BBP-induced ERß mRNA expression, whereas ICI182 780 could effectively counteract the effect of estradiol. Moreover, pretreatment with ICI182 780 could block the induction of aromatase protein expression and activity by BBP, showing an involvement of ERs. Except for the ER pathway, these results showed there might be other pathways involved in promoting the effects of low-level BBP on SH-SY5Y cells, which require further investigation.

Improving the Retention Rate of Fat Grafts in Recipient Areas via Botulinum Toxin A Treatment.

BACKGROUND: Improving the retention rate of transplanted fat is, currently, of great concern. Partial immobilization, angiogenesis, and adipose tissue-derived stem cells, all proven to be influenced by botulinum toxin A (BTX-A), are significant in fat graft retention. OBJECTIVES: The authors sought to determine the impact of BTX-A on fat grafts. METHODS: Our study included 12 Sprague Dawley rats and each rat's hind limbs were randomly designated as the BTX-A side and control side. We injected 0.2 mL of BTX-A-treated fat into the quadriceps femoris and subcutaneous space of the BTX-A sides. This was also done for the control sides but with untreated fat. We performed electroneuromyography of recipient muscles at 1 week post-operation. The rats were euthanized at 12 weeks post-operation and we observed the fat retention rate, the fat's histologic characteristics, and the density of vessels and mature adipocytes. RESULTS: The amplitudes of electroneuromyography were smaller for the BTX-A sides than the control sides. For intramuscularly injected fat, the BTX-A sides had better retention rates and histologic characteristics and a higher density of vessels and mature adipocytes than the control sides. For subcutaneously injected fat, the BTX-A sides had better histologic characteristics and a higher density of vessels and mature adipocytes than the control sides, but the retention rates were not significantly different between the 2 sides. CONCLUSIONS: Injecting BTX-A-treated fat grafts can immobilize the surrounding muscles. BTX-A can improve the density of vessels and mature adipocytes, histologic characteristics of fat grafts, and retention rate of fat grafts transplanted into muscles.

Tau hyperphosphorylation and P-CREB reduction are involved in acrylamide-induced spatial memory impairment: Suppression by curcumin.

Acrylamide (ACR) is an axonal toxicant that produces peripheral neuropathy in laboratory animals and humans. Epidemiological study found that diet ACR exposure was associated with a mild cognitive decline in men. However, limited information is available as regards its potential and underlying mechanism to cause memory alterations. Curcumin is a polyphenol with neuroprotective and cognitive-enhancing properties. In this study, we aimed to investigate the mechanism of ACR-induced spatial memory impairment and the beneficial effect of curcumin. ACR exposure at 10 mg/kg/d for 7 weeks caused slight gait abnormality and spatial memory deficits, which was associated with an activation of glial cells, a reduction of phosphorylated cAMP response elements binding protein (P-CREB) and an aggregation of hyperphosphorylated tau including p-tau (Ser262), AT8 (p-tau Ser202/Thr205) and PHF1 (p-tau Ser396/404) in the hippocampus and cortex. ACR markedly regulate the expression of glycogen synthase kinase-3ß (GSK-3ß) and cyclin-dependent kinase-5 (cdk5) to accelerate tau hyperphosphorylation. ACR inhibited the protein phosphatase 2A (PP2A) and lysosomal protease cathepsin D to decrease the p-tau dephosphorylation and degradation. The P-CREB and brain derived neurotrophic factor (BDNF) were significantly decreased by ACR. The upstream signalings of P-CREB, extracellular signal-related kinase (ERK) and Akt were markedly inhibited. The protein kinase RNA-like endoplasmic reticulum kinase (PERK) -eukaryotic initiation factor-2α (eIF2α) - activating transcription factor 4 (ATF4) signaling which negatively regulate memory processes by suppressing CREB was activated by ACR. Curcumin alleviated ACR-induced spatial memory impairment through reversing tau abnormalities and P-CREB reduction in the hippocampus. These results offered deeper insight into the mechanisms of and presented a potential new treatment for ACR-induced neurotoxicity.

Pesticide exposure and risk of Parkinson's disease: Dose-response meta-analysis of observational studies.

The cause of late onset Parkinson's disease (PD) remains unknown. Evidence suggested that lifelong exposure to pesticides might contribute to the development of neurodegenerative diseases, but the results were controversial. Relevant studies were identified by searching PubMed and Web of Science through September 2017. We included cohort and case-control studies reporting relative risks (RRs) or odds ratios (ORs) with 95% confidence intervals (CIs) of three or more categories of pesticide exposure and PD. Ten articles with 13 reports (3 for cumulative exposure, 10 for duration exposure) were included. A nonlinearity association was seen between duration exposure and PD risk (P = 0.01 for nonlinearity). The summary ORs of developing PD for 5 and 10 years of duration exposure were 1.05 (95% CI: 1.02-1.09) and 1.11 (95% CI: 1.05-1.18), respectively. Sensitivity analyses with different effect models yielded similar results, and omission of any single study did not change the results. The 5 and 10 years of duration pesticide exposure were associated with a 5% and 11% augment in the risk of PD. Further high-quality cohort studies were required to validate a causal relationship.

On the inherent properties of Soluplus and its application in ibuprofen solid dispersions generated by microwave-quench cooling technology.

Polyvinyl caprolactam-polyvinyl acetate-polyethylene glycol graft copolymer, or Soluplus®, is a relatively new copolymer and a promising carrier of amorphous solid dispersions. Knowledge on the inherent properties of Soluplus® (e.g. cloud points, critical micelle concentrations, and viscosity) in different conditions is relatively inadequate, and the application characteristics of Soluplus®-based solid dispersions made by microwave methods still need to be clarified. In the present investigation, the inherent properties of a Soluplus® carrier, including cloud points, critical micelle concentrations, and viscosity, were explored in different media and in altered conditions. Ibuprofen, a BCS class II non-steroidal anti-inflammatory drug, was selected to develop Soluplus®-based amorphous solid dispersions using the microwave-quench cooling (MQC) method. Scanning electronic microscopy (SEM), differential scanning calorimetry (DSC), powder X-ray diffraction (PXRD), Raman spectroscopy (RS), and Fourier transform infrared spectroscopy (FT-IR) were adopted to analyze amorphous properties and molecular interactions in ibuprofen/Soluplus® amorphous solid dispersions generated by MQC. Dissolution, dissolution extension, phase solubility, equilibrium solubility, and supersaturated crystallization inhibiting experiments were performed to elucidate the effects of Soluplus® on ibuprofen in solid dispersions. This research provides valuable information on the inherent properties of Soluplus® and presents a basic understanding of Soluplus® as a carrier of amorphous solid dispersions.

The Influence of Cellulosic Polymer's Variables on Dissolution/Solubility of Amorphous Felodipine and Crystallization Inhibition from a Supersaturated State.

The collective impact of cellulosic polymers on the dissolution, solubility, and crystallization inhibition of amorphous active pharmaceutical ingredients (APIs) is still far from being adequately understood. The goal of this research was to explore the influence of cellulosic polymers and incubation conditions on enhancement of solubility and dissolution of amorphous felodipine, while inhibiting crystallization of the drug from a supersaturated state. Variables, including cellulosic polymer type, amount, ionic strength, and viscosity, were evaluated for effects on API dissolution/solubility and crystallization processes. Water-soluble cellulosic polymers, including HPMC E15, HPMC E5, HPMC K100-LV, L-HPC, and MC, were studied. All cellulosic polymers could extend API dissolution and solubility to various extents by delaying crystallization and prolonging supersaturation duration, with their effectiveness ranked from greatest to least as HPMC E15 > HPMC E5 > HPMC K100-LV > L-HPC > MC. Decreased polymer amount, lower ionic strength, or higher polymer viscosity tended to decrease dissolution/solubility and promote crystal growth to accelerate crystallization. HPMC E15 achieved greatest extended API dissolution and maintenance of supersaturation from a supersaturated state; this polymer thus had the greatest potential for maintaining sustainable API absorption within biologically relevant time frames.

Improvement in the Retention Rate of Transplanted Fat in Muscle by Denervation.

BACKGROUND: Improvement in the retention rate of transplanted fat is currently a topic of interest. The retention of transplanted fat relies heavily on the reestablishment of blood supply and the function of the adipose-derived stem cells (ADSCs), which may both be impeded by mechanical force. However, the effect of mechanical force on the retention of adipose implants remains unclear. OBJECTIVES: This study aimed to evaluate the effectiveness of immobilization on fat retention rate. METHODS: Immobilization was carried out by denervation of the hind limb of rats to reduce the mechanical force. Sprague-Dawley (SD) rats were used, and the two hind limbs were assigned at random to the immobilization side and the control side. On average, 0.4 mL of fat was injected into the bilateral muscle and subcutaneous space of the hind limb, and 6 rats were sacrificed at each time point. The outcome measures included the retention rate, the histologic evaluation, and the density of new vessels and proliferative ADSCs. RESULTS: For the muscle fat, the retention rate improved, and more proliferative ADSCs and new vessels were found in the immobilization group. The histologic evaluation between the two sides was of no statistical significance. For the fat in the subcutaneous space, no statistical difference was observed in all the outcome measures between the two sides. CONCLUSIONS: Regional immobilization of the recipient site by denervation can improve the retention of the fat graft in muscles owing to improved density of the new vessels and proliferative ADSCs.

Sub-chronic 90-day toxicity of neamine in SD rats and its anti-liver cancer activity in vitro and in vivo.

Neamine, an inhibitor of angiogenin (ANG), is a new investigative anticancer drug currently in preclinical stage. Here we report the 90-day sub-chronic toxicity of neamine in SD rats and its anti-liver cancer activity in vitro and in vivo. Neamine has a No Observed Adverse Effect Level (NOAEL) of 12 and 16mg·kg-1·d-1 for female and male rats, respectively. No mortality was found. The adverse effects included increased organ coefficients of spleen and kidney, increased BUN in both female and male rats at high dose, increased CR and decreased organ coefficients of heart and liver in male rats at high dose. All of which, except the kidney coefficient and BUN in males, returned to normal levels after 28-day recovery. Histopathological examination revealed vacuolar degeneration of glomerulus, degeneration of renal tubules and cast in the kidneys, which were also recovered except in males of high-dosing group. These results indicate that kidney is the most susceptible organ for neamine toxicity. Tissue microarray analysis validated that ANG is up-regulated in hepatocellular carcinoma accompanied by increased nuclear translocation, suggesting that ANG is a possible target for drug development in liver cancer treatment. Neamine blocked nuclear translocation of ANG in HUVEC and HepG2 cells, and inhibited ANG-stimulated cell proliferation without affecting basal level cell proliferation. Neamine also inhibited progression of HepG2 xenografts in athymic mice accompanied by decreased angiogenesis and cancer cell proliferation. These results suggest that neamine is a specific ANG inhibitor with low toxicity and high anti-liver cancer efficacy.

Effects of Combined General/Epidural Anesthesia on Hemodynamics, Respiratory Function, and Stress Hormone Levels in Patients with Ovarian Neoplasm Undergoing Laparoscopy.

BACKGROUND The aim of this study was to evaluate the influence of combined general/epidural anesthesia (GEA) on hemodynamics, respiratory function and stress hormone levels in patients with ovarian neoplasm undergoing laparoscopy. MATERIAL AND METHODS A total of 177 patients with ovarian neoplasm (screened by inclusion/exclusion criteria) receiving laparoscopy were divided into groups G (general anesthesia alone), L1.0 (GEA with 1.0% lidocaine), and L1.5 (GEA with 1.5% lidocaine). Hemodynamics, respiratory parameters and stress hormone levels in the 3 groups were recorded and analyzed. RESULTS Hemodynamic indexes and PaO2/PaCO2 in group L1.0 showed no differences at each time point (all P>0.05). At the end of anesthesia tracheal intubation (T1), 10 min after pneumoperitoneum (T2) and the end of anesthesia tracheal extubation (T3), there were significant differences in hemodynamic indexes, respiratory parameters, epinephrine (E), and noradrenalin (NE) of group G/L1.5, compared with before anesthesia induction (T0) (all P<0.05). Compared with group G, there were big differences in dosage of anesthetics (sufentanil, vecuronium, and propofol) and pharmaceutic adjuvants (ephedrine, atropine, and nitroglycerin), postoperative recovery time, extubation time, and incidence of agitation in group L1.0/L1.5 (all P<0.05). CONCLUSIONS GEA can improve the quality and efficiency in laparoscopy for ovarian neoplasm, with the advantages of reduced anesthetics dosage, satisfactory postoperative analgesia, maintained hemodynamic stability, excellent uterine relaxation, and reduced time of anesthesia induction, surgery, recovery, and extubation. In addition, compared with group L1.5, group L1.0 was more secure and worthy of clinical promotion in laparoscopy.

[Rules and characteristics of crystallization inhibition of cellulose polymers against drugs in supersaturated states].

This study aims to explore the characteristics of crystallization inhibition by cellulose polymers at the supersaturated states of drugs. The study was performed by simulating supersaturated process and preparing supersaturated drug solid, and was carried out by measuring the content of drugs at different time points using dissolution apparatus. The types, amounts, ionic intensity and viscosity of cellulose polymers were examined to assess the crystallization inhibition effect on BCS II class drug indomethacin. HPMC E15 exhibited the strongest crystallization inhibition effect. The more added, more obvious crystallization suppression was observed against indomethacin. The decrease in viscosity and increase in ionic intensity led to an enhanced inhibition. The research provides a scientific guide for the crystallization inhibition of supersaturated drug by cellulose polymers.

Abcc9 is required for the transition to oxidative metabolism in the newborn heart.

The newborn heart adapts to postnatal life by shifting from a fetal glycolytic metabolism to a mitochondrial oxidative metabolism. Abcc9, an ATP-binding cassette family member, increases expression concomitant with this metabolic shift. Abcc9 encodes a membrane-associated receptor that partners with a potassium channel to become the major potassium-sensitive ATP channel in the heart. Abcc9 also encodes a smaller protein enriched in the mitochondria. We now deleted exon 5 of Abcc9 to ablate expression of both plasma membrane and mitochondria-associated Abcc9-encoded proteins, and found that the myocardium failed to acquire normal mature metabolism, resulting in neonatal cardiomyopathy. Unlike wild-type neonatal cardiomyocytes, mitochondria from Ex5 cardiomyocytes were unresponsive to the KATP agonist diazoxide, consistent with loss of KATP activity. When exposed to hydrogen peroxide to induce cell stress, Ex5 neonatal cardiomyocytes displayed a rapid collapse of mitochondria membrane potential, distinct from wild-type cardiomyocytes. Ex5 cardiomyocytes had reduced fatty acid oxidation, reduced oxygen consumption and reserve. Morphologically, Ex5 cardiac mitochondria exhibited an immature pattern with reduced cross-sectional area and intermitochondrial contacts. In the absence of Abcc9, the newborn heart fails to transition normally from fetal to mature myocardial metabolism.-Fahrenbach, J. P., Stoller, D., Kim, G., Aggarwal, N., Yerokun, B., Earley, J. U., Hadhazy, M., Shi, N.-Q., Makielski, J. C., McNally, E. M. Abcc9 is required for the transition to oxidative metabolism in the newborn heart.