Long-Term Disinfection in Operating Rooms Affects Skin Microbiota and Metabolites of Medical Personnel.

INTRODUCTION: Disinfectants play a critical role in reducing healthcare-associated infections by eliminating microorganisms on surfaces. However, prolonged use of disinfectants may adversely affect the skin microflora, essential for skin health and infection prevention. This study investigates the impact of disinfection on the skin microbiota and metabolites of medical personnel in operating rooms, aiming to provide a scientific foundation for safeguarding their skin health. METHODS: We conducted 16S sequencing and metabolomic analysis to assess the effects of disinfection on the skin microbiota and metabolites of medical personnel. Samples were collected from operating room personnel after disinfectant exposure to identify changes in microbial communities and metabolite profiles. RESULTS: Our analysis revealed that prolonged use of disinfectants led to alterations in skin microbial communities and microbial metabolites. These alterations included the production of harmful metabolites that could potentially promote skin infections and other health issues among medical personnel. CONCLUSION: The findings underscore the importance of minimizing disruptions to skin microbiota and metabolites caused by long-term disinfectant use to preserve the overall health of medical personnel. This study provides valuable insights into the relationship between disinfectant use, skin microbiota, and metabolites, highlighting the necessity for further research in this area.

Hot Deformation Behavior and Mechanisms of SiC Particle Reinforced Al-Zn-Mg-Cu Alloy Matrix Composites.

A systematic and comprehensive analysis of the hot deformation and mechanisms of SiC particle-reinforced aluminum matrix composites is significant for optimizing the processing of the composites and obtaining the desired components. Based on this, related research on 11 vol% SiCp particle-reinforced 7050Al matrix composites was carried out. Hot compression experiments were carried out on the Gleeble-3500 thermal simulator to study the hot deformation behavior of composites at the temperature of 370-520 °C and strain rate of 0.001-10 s-1. The hyperbolic sine constitutive equation of the material was established, and the processing map was calculated. Combining the typical metallograph and misorientation angle distribution, the microstructure evolution mechanism of composites was analyzed, and the effect of particles on recrystallization behavior was investigated. Under certain process conditions, the dominant deformation mechanism of composites changed from dynamic recovery (DRV) to dynamic recrystallization (DRX), and the grain boundary sliding mechanism began to play a role. In addition, high temperature tensile and elongation at break were tested, and it was found that the dominant form of fracture failure changed from brittle fracture of the particles to ductile fracture of the matrix as the temperature increased.

Study on Fabrication and Properties of Graphite/Al Composites by Hot Isostatic Pressing-Rolling Process.

Graphite/Al composites have attracted much attrition due to their excellent thermal properties. However, the improvement of thermal conductivity (TC) is limited by the difficulty in controlling the orientation of graphite and the poor wettability between graphite and aluminum. In this study, a novel process for fabricating the Graphite/Al composites is proposed, which involves fabricating graphite film and aluminum foil into laminate material. Then, taking a rolling method, the fractured and well oriented graphite film can help the composite achieve high TC while maintaining a certain strength. The result reveals that both single and total reduction have a significant influence on the diameter and orientation of the graphite, and by adjusting the process parameters, composites with high TC can be acquired at a relatively low reinforcement volume. This near-net-forming process can directly meet the thickness requirements for electronic packaging and avoids the exposure of graphite to the surface during secondary processing, which is promising to promote the application for high TC Graphite/Al composites in thermal management.

Interfacial Structure of Carbide-Coated Graphite/Al Composites and Its Effect on Thermal Conductivity and Strength.

Graphite/Al composites had attracted significant attention for thermal management applications due to their excellent thermal properties. However, the improvement of thermal properties was restricted by the insufficient wettability between graphite and Al. In this study, silicon carbide and titanium carbide coatings have been uniformly coated on the graphite by the reactive sputtering method, and Graphite/Al laminate composites were fabricated by a hot isostatic pressing process to investigate the influence on thermal conductivity and mechanical properties. The results show that carbide coating can effectively improve the interfacial thermal conductance of SiC@Graphite/Al and TiC@Graphite/Al composites by 9.8 times and 3.4 times, respectively. After surface modification, the in-plane thermal conductivity (TC) of the composites with different volume fractions are all exceeding the 90% of the predictions. In comparison, SiC is more conducive to improving the thermal conductivity of composite materials, since the thermal conductivity of the 28.7 vol.% SiC@Graphite/Al reached the highest value of 499 W/m·K, while TiC is favorable for improving the mechanical properties. The finding is beneficial to the understanding of carbide coating engineering in the Graphite/Al composites.

Strengthening and Weakening Effects of Particles on Strength and Ductility of SiC Particle Reinforced Al-Cu-Mg Alloys Matrix Composites.

The strengthening and weakening effects of SiC particles on composite strength and ductility were studied. Al-Cu-Mg alloys matrices with three different mechanical properties were used. Their yield strength, ultimate strength, and elongation range from 90 to 379 MPa, 131 to 561 MPa, and 18% to 31%, respectively. SiC particles with sizes of 4, 8, 12, 15, 20, and 30 µm were used to reinforce these three matrices, separately, and the composites of eighteen combinations of the particle sizes and matrix strengths were manufactured. Yield strength, ultimate strength, elongation, and fracture morphology of these composites were characterized. Based on the analysis, the strengthening to weakening behavior on strength and ductility were comprehensively discussed. The critical particle size having the best ductility was obtained. The strengthening limit and match range of the particle and the matrix to achieve effective strengthening were defined as a function of the particle size and matrix strength. This work offers an important reference for optimization of mechanical properties of the particle-reinforced metal matrix composites.

Effect of the Particle Size and Matrix Strength on Strengthening and Damage Process of the Particle Reinforced Metal Matrix Composites.

Roles of the particle, strengthening, and weakening during deformation of the particle reinforced metal matrix composite, were studied using in situ technique. Composites with three different strengths Al-Cu-Mg alloy matrices reinforced by three sizes SiC particles were manufactured and subjected to in situ tensile testing. Based on in situ observation, damage process, fraction and size distribution of the cracked particles were collected to investigate the behavior of the particle during composite deformation. The presence of the particle strengthens the composite, while the particle cracking under high load weakens the composite. This strengthening to weakening transformation is controlled by the damage process of the particle and decided by the particle strength, size distribution, and the matrix flow behavior together. With a proper match of the particle and matrix, an effective strengthening can be obtained. Finally, the effective match range of the particle and the matrix was defined as a function of the particle size and the matrix strength.

Long-term low-dose ethanol intake improves healthspan and resists high-fat diet-induced obesity in mice.

Numerous epidemiological studies have reported that moderate alcohol drinking has beneficial effects. However, few studies have focused on the beneficial effects of ethanol, the common component in alcoholic beverages. Here we fed the C57BL/6 mice with 3.5% v/v ethanol as drinking water substitute to investigate the effects of long-term low-dose ethanol intake in vivo. We evaluated the metabolic rate and mitochondrial function of the long-term low-dose ethanol-intake (LLE) mice, assessed the exercise ability of LLE mice, and fed the LLE mice with a high-fat diet to investigate the potential impact of ethanol on it. The LLE mice showed improved thermogenic activity, physical performance, and mitochondrial function, as well as resistance against the high-fat diet-induced obesity with elevated insulin sensitivity and subdued inflammation. Our results suggest that long-term low-dose ethanol intake can improve healthspan and resist high-fat diet-induced obesity in mice. It may provide new insight into understanding the protective effects of moderate alcohol drinking.

Low-dose ethanol intake prevents high-fat diet-induced adverse cardiovascular events in mice.

A high-fat diet is recognized as an important factor in the development of cardiovascular diseases including cardiomyopathy. Besides high-fat diets, large quantities of ethanol also induce cardiomyopathy in both animals and humans. Emerging evidence suggests that low ethanol intake may have a protective effect on the cardiovascular system. This study aimed to clarify whether low-dose ethanol intake could prevent high-fat diet-induced adverse effects on cardiomyocytes in mice. After 6-8 weeks of feeding, the heart weight significantly decreased in ethanol + HFD mice compared to HFD mice. In addition, cardiac triglycerides and lipid droplets also decreased, but no statistically significant difference in cholesterol level was found between the two groups. Expression of the fatty acid transporters Cd36, Slc27a1 and Got2 was downregulated in the ethanol + HFD group. According to echocardiography, the mass and volume of the left ventricle were reduced, and the ejection fraction (EF) and fractional shortening (FS) were increased in mice fed with alcohol. Low doses of ethanol reduced the cardiomyocytes' cross-sectional area and the expression of the hypertrophic markers ANP and BNP. Moreover, Col1a1, the main collagen type expressed in the heart, was also reduced by low-dose ethanol consumption. Also, the expression of Rgs5, a crucial component of the signaling pathway involved in cardiac remodeling and heart failure, was upregulated in response to ethanol intake. The data suggest that low ethanol intake prevents adverse effects induced by a high-fat diet, such as lipid accumulation, cardiac dysfunction, hypertrophy and fibrosis. Furthermore, low ethanol intake upregulates Rgs5, which suggests it plays a role in cardiac remodeling and heart failure.

Effects of ethanol on the anticancer function of doxorubicin in JJ012 cells.

AIM: Chondrosarcoma is difficult to treat because of resistance to conventional chemotherapy and radiotherapy. This study evaluated the effects of ethanol in combination with doxorubicin in chondrosarcoma cells. MATERIALS & METHODS: JJ012, was treated with doxorubicin alone or in combination with ethanol. Effects on cellular proliferation, migration, invasion, apoptosis, and the cell cycle were evaluated. RESULTS: Treatment of JJ012 cells with 100 mM ethanol and doxorubicin resulted in reduced cell growth, invasion, and migration. In addition, doxorubicin uptake into the nucleus was enhanced and p53 mRNA expression was upregulated in JJ012 cells. CONCLUSION: Ethanol combined with doxorubicin increased doxorubicin uptake in the nucleus and enhanced the effects of doxorubicin in JJ012 cells.

SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice.

Cell death inducing DNA fragmentation factor-alpha-like A (Cidea) is a member of cell death-inducing DFF45-like effector (CIDE) protein. The initial function of CIDE is the promotion of cell death and DNA fragmentation in mammalian cells. Cidea was recently reported to play critical roles in the development of hepatic steatosis. The purpose of present study is to determine the effect of chronic alcohol intake on Cidea expression in the livers of mice with alcoholic fatty liver disease. Cidea expression was significantly increased in the liver of alcohol-induced fatty liver mice. While, knockdown of Cidea caused lipid droplets numbers reduction. Next, we detected the activity of ALDH2 reduction and the concentration of serum acetaldehyde accumulation in our alcohol-induced fatty liver mice. Cidea expression was elevated in AML12 cells exposed to 100uM acetaldehyde. Interestingly, Dual-luciferase reporter gene assay showed that 100 uM acetaldehyde led to the activation of Cidea reporter gene plasmid which containing SRE element. What's more, the knockdown of SREBP1c suppressed acetaldehyde-induced Cidea expression. Overall, our findings suggest that Cidea is highly associated with alcoholic fatty liver disease and Cidea expression is specifically induced by acetaldehyde, and this up-regulation is most likely mediated by SREBP1c.

Effect of iron on cholesterol 7α-hydroxylase expression in alcohol-induced hepatic steatosis in mice.

Both iron and lipids are involved in the progression of alcoholic fatty liver disease (AFLD), but the interaction between iron and lipids in AFLD is unclear. Here, we tested the hypothesis that iron regulates the expression of genes involved in lipid metabolism through iron regulatory proteins (IRPs), which interact with the iron-responsive elements (IREs) in the untranslated regions (UTRs) of genes, resulting in lipid accumulation. Using "RNA structure software", we predicted the mRNA secondary structures of more than 100 genes involved in lipid metabolism to investigate whether the IRE structure exists in novel mRNAs. Cholesterol 7α-hydroxylase (Cyp7a1) has an IRE-like stem-loop, a noncanonical IRE structure, in its 3'-UTR. Cyp7a1 expression can be regulated by in vivo and in vitro iron treatment. In addition, the noncanonical IRE motif can efficiently bind both to IRP1 and IRP2. The results indicate that hepatic iron overloading in AFLD mice decreased Cyp7a1 expression and resulted in cholesterol accumulation, providing a new mechanism of iron-regulated gene transcription and translation through the interaction between iron and a noncanonical IRE structure in Cyp7a1 mRNA. This finding has significant implications in studying a proposed mechanism for the regulation of cholesterol homeostasis by an Fe/IRP/noncanonical IRE axis.

Establishment of an alcoholic fatty liver disease model in mice.

BACKGROUND: Alcoholic fatty liver disease (AFLD) defines an important stage in the progression of alcoholic liver disease (ALD), which is a major cause of morbidity and mortality worldwide. OBJECTIVE: To establish a mouse model of AFLD. METHODS: Male C57BL/6 mice were divided into the following two groups: (i) a control group, which was allowed free access to food and water and (ii) an alcohol-treated group, which was administered a 15% (v/v) alcohol solution instead of water. After 8-9 months of treatment, serum biochemical indexes, histopathological changes, liver triglyceride content, iron storage, and ferritin light chain protein expression were measured using an automatic biochemical analyzer, hematoxylin-eosin (HE) staining, a commercially available kit, Prussian blue staining, and Western blot analysis, respectively. RESULTS: Compared with the control group, the alcohol-treated group displayed increased levels of serum LDH, ALT, and AST, decreased levels of ALB, and no significant change in levels of TP. Additionally, increased levels of serum TG, T-CHO, and LDL and decreased levels of serum GLU and HDL were observed in the alcohol-treated mice. HE staining showed that lipid vacuolization occurred in the livers of alcohol-treated mice. The alcohol-treated mice also exhibited increased liver triglyceride content. Moreover, Prussian blue staining and Western blot analysis demonstrated that chronic alcohol administration caused iron overloading of the liver. CONCLUSIONS: Chronic administration of 15% (v/v) alcohol in the drinking water over 8-9 months caused AFLD in mice. Our results establish an AFLD model that represents a promising tool for the future study of the progression of ALD.

Chronic Moderate Alcohol Intakes Accelerate SR-B1 Mediated Reverse Cholesterol Transport.

Cholesterol is essential for all animal life. However, a high level of cholesterol in the body is strongly associated with the progression of various severe diseases. In our study, the potential involvement of alcohol in the regulation of high density lipoprotein (HDL) receptor scavenger receptor class B and type I (SR-B1)-mediated reverse cholesterol transport was investigated. We separated male C57BL/6 mice into four diets: control, alcohol, Control + HC and alcohol + HC. The SR-B1 level and 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate- high- density lipoprotein (DiI-HDL) uptake were also measured in AML12 cells and HL7702 cells treated with alcohol. The control + HC diet led to increased hepatic triglyceride and cholesterol levels while alcohol + HC led no significant change. Compared with that of the control group, the SR-B1 mRNA level was elevated by 27.1% (P < 0.05), 123.8% (P < 0.001) and 343.6% (P < 0.001) in the alcohol, control + HC and alcohol + HC groups, respectively. In AML12 and HL7702 cells, SR-B1 level and DiI-HDL uptake were repressed by SR-B1 siRNA or GW9662. However, these effects were reversed through alcohol treatment. These data suggest that a moderate amount of alcohol plays a novel role in reverse cholesterol transport, mainly mediated by PPARγ and SR-B1.

Morphine acts via mu-opioid receptors to enhance spinal regeneration and synaptic reconstruction of primary afferent fibers injured by sciatic nerve crush.

The present study investigated whether morphine can promote regeneration and synaptic reconstruction of the terminals of injured primary afferent fibers in lamina II of the spinal cord in rats following sciatic nerve injury. Fluoride-resistant acid phosphatase (FRAP)-positive terminals in lamina II of the L4 spinal segment after sciatic nerve injury were assessed after treatment with vehicle, morphine, and naloxone plus morphine. Under the electron microscope, types I and II complex terminals of unmyelinated afferent fibers from the dorsal root, simple terminals of interneuronal axons, and terminals of descending axons at lamina II of the L4 spinal segment were documented in the different groups after injury. FRAP-positive terminals in lamina II were depleted after sciatic nerve injury in the vehicle group. Treatment with morphine increased the numbers of FRAP-positive terminals, and this was prevented by naloxone. The present study demonstrates that morphine may promote the regeneration and synaptic reconstruction of the terminals of injured primary unmyelinated afferent fibers in lamina II of spinal cord, by a process mediated by mu-opioid receptors.