Search

Postbiotics are a preparation of inanimate microorganisms and/or their components are beneficial to the health of the host, with multiple advantages such as safety, stability, easy storage and production, and clear chemical structure. This article reviews the major bioactive ingredients, probiotic functions and current application status of postbiotics; elaborates the health benefits of inactivated bacterial cells, bacterial components and bacterial metabolites to the host; summarizes recent progress in understanding the health benefits of postbiotics such as enhancing immunity, regulating gastrointestinal function, alleviating obesity, maintaining oral health, and preventing osteoporosis; outlines commercially available postbiotic products in Japan, the United States, Germany and China; and proposes the challenges and new research directions of postbiotics.

The impact of prebiotics on the structural characteristics of yogurt is an important aspect of evaluating its functional properties. This study aimed to evaluate and compare the effects of several commonly used prebiotics, including fructooligosaccharide (FOS), galactooligosaccharide (GOS), inulin (INU), polydextrose (PDX), and xylooligosaccharide (XOS), on the gel properties of milk protein and the structural features, with respect to the texture and rheology, of stirred yogurt during and after fermentation. The results revealed that the supplementation of INU, PDX, and XOS was involved in the construction of protein networks during fermentation, promoting a viscous and more elastic gel structure, due to the enhanced protein–water interactions. This resulted in a significant increase (p < 0.05) in structural stability (higher critical strain (γc) and greater thixotropy), firmness, cohesiveness, and rheology (G′ and G″) and a significant decrease (p < 0.05) in the loss of yogurt during centrifugation. Conversely, the supplementation of GOS and FOS did not appear to be involved in the construction of the protein network and barely affected the rheological properties of the gel during fermentation. However, a significant increase (p < 0.05) in viscosity and firmness, and a slight decrease (p > 0.05) in loss during centrifugation were still observed in the yogurt. These findings could be useful for a comprehensive assessment of the application potential of these prebiotics in yogurt, when combined with their respective prebiotic properties. [ABSTRACT FROM AUTHOR]

Many probiotic bacteria have been proven to prevent allergic airway responses through immunomodulation. This study was conducted to evaluate the effects of heat-killed Bifidobacterium longum BBMN68 (BBMN68) in pasteurized yogurt on the alleviation of mugwort pollen (MP)-induced allergic inflammation. BALB/c mice aged 5–6 weeks were randomly assigned and fed pasteurized yogurt containing heat-killed BBMN68 for 27 days, followed by allergic sensitization and challenge with MP extract. The allergic mice that received pasteurized yogurt containing heat-killed BBMN68 had improved immune status, including a lower serum IgE level, decreased serum interleukin (IL)-4, IL-5, and IL-13 concentrations, and alleviated airway inflammation manifested by increased macrophage and decreased eosinophil and neutrophil counts in BALF, as well as airway remodeling and suppressed peribronchial cellular infiltration. Moreover, oral administration of pasteurized yogurt containing heat-killed BBMN68 significantly modulated gut microbiota composition by influencing the proportion of beneficial genera associated with inflammation and immunity, such as Lactobacillus, Candidatus_Saccharimonas, Odoribacter, and Parabacteroides, which also negatively correlated with serum IgE and Th2 cytokine levels. These results demonstrated that pasteurized yogurt containing heat-killed BBMN68 had mitigative effects on allergic airway inflammation, likely through maintaining the systemic Th1/Th2 immune balance by altering the structure and function of the gut microbiota. [ABSTRACT FROM AUTHOR]

Sevoflurane is identified as an effective candidate drug for acute lung injury (ALI) treatment, but its curing effects and detailed mechanisms have not been fully disclosed. The present study was designed to resolve this academic issue. The ALI mice models were established, and Hematoxylin-eosin staining assay was performed to examine tissue morphologies. Cell viability was determined by CCK-8 assay, and Annexin V-FITC/PI double staining assay was used to examine cell apoptosis. The expression levels of proteins were determined by performing Western Blot analysis and immunofluorescence staining assay. ROS levels were examined by using DCFH-DA staining assay. In this study, we investigated this issue and the ALI models were respectively established by treating the BALB/c mice and the murine macrophage cell line RAW264.7 with different concentrations of lipopolysaccharide (LPS) in vivo and in vitro, which were subsequently subjected to sevoflurane co-treatment. The results showed that sevoflurane reduced LPS-induced ALI in mice and suppressed LPS-triggered oxidative stress and apoptotic cell death in the RAW264.7 cells. Interestingly, we evidenced that the elimination of reactive oxygen species (ROS) by N-acetyl-L-cysteine (NAC) reversed LPS-induced cell apoptosis in RAW264.7 cells. Then, we verified that sevoflurane suppressed oxidative damages to restrain LPS-induced apoptotic cell death in the RAW264.7 cells through activating the anti-oxidant Keap1/Nrf2 pathway. Mechanistically, sevoflurane down-regulated Keap1 and upregulated Nrf2 in nucleus to activate the downstream anti-oxidant signaling cascades, which further ameliorated LPS-induced cell apoptosis and lung injury by eliminating oxidative damages. Taken together, our study illustrated that the sevoflurane attenuates LPS-induced ALI by inhibiting oxidative stress-mediated apoptotic cell death and inflammation, and the Keap1/Nrf2 pathway played an important role in this process. [ABSTRACT FROM AUTHOR]

Traditional methods only consider topic information in English vocabulary information extraction, lose the statistical feature information of the keywords themselves, and easily ignore the semantic information of the words. In order to improve the extraction efficiency of English keyword information, based on the CAD mesh model, this paper adds constraint factors such as vertex neighborhood flatness, vertex degree, side length, and flatness on both sides of the side on the basis of the original QEM quadratic error simplification algorithm, and it incorporates a smoothing effect into the edge folding cost function. Moreover, based on the proposed normal vector-based QEM mesh simplification algorithm, the point selection after the edge folding operation is fixed as the vertices of the original edge, and it is applied to the mesh parameterization. In addition, the algorithm solves the local parameterization problem of partially deleted vertices after the simplification operation of each layer is completed. After the model is constructed, the performance of the model is verified through experiments. The research shows that the English keyword information extraction model constructed in this paper is effective. [ABSTRACT FROM AUTHOR]

In order to explore students' boredom in English learning, a recognition algorithm based on fuzzy neural network is proposed. The algorithm selects Gaussian membership function and initializes the clustering center obtained by fuzzy c-means algorithm to the center of Gaussian function, and the width of Gaussian function is obtained by the membership and center of fuzzy c-means clustering algorithm. In the construction of base classifier, diversity strategy is adopted to increase its diversity and complementarity. In the selection of base classifiers, the combination of contour coefficient and clustering algorithm is used to determine the number of classifiers to be fused, and the inconsistency measurement method is used to evaluate their differences. In the combination strategy, we learn from the Bayesian thought and dynamically adapt the weight of learning base classifier based on its a priori probability and class conditional probability. The experimental results show that 10 times of cross-validation are carried out, respectively, and the accuracy of each algorithm is given. The algorithm based on tree structure obviously has better performance, followed by the rule-based algorithm, and finally the fuzzy neural network algorithm based on neural network, while the accuracy of SVM and logistic regression algorithm LR is lower. It is proved that the fuzzy neural network can effectively identify students' boredom in English learning. [ABSTRACT FROM AUTHOR]

We aimed to explore the effects of hypercholesterolemia on sevoflurane‐induced cognitive impairment in aged rats and the underlying mechanism(s). Aged rats were administrated with high‐fat diet, sevoflurane, or both. Thereafter, the plasma levels of total cholesterol (TC), triglyceride (TG), low‐density lipoprotein (LDL), and high‐density lipoprotein (HDL) were evaluated. The Morris water maze task was performed to evaluate the spatial learning and memory ability of rats. Moreover, Nissl and Evans blue staining were conducted to test nerve damage and detect the blood–brain barrier permeability, respectively. The percentage of apoptotic cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The messenger RNA expression of inflammatory factors and protein expression of microglial activation markers and apoptosis‐related proteins were tested by real‐time polymerase chain reaction, enzyme‐linked immunosorbent assay, or western blot analysis, respectively. High‐fat diet induced high levels of TC, TG, and LDL but decreased levels of HDL. However, sevoflurane had no effects on these levels. In contrast, sevoflurane significantly induced the impairment of learning and memory, nerve damage, neuroinflammatory damage, and neuronal apoptosis. Hypercholesterolemia exacerbated the sevoflurane‑induced impairment in aged rats. These results suggested that hypercholesterolemia aggravates sevoflurane‑induced cognitive impairment in aged rats, possibly by inducing neurological inflammation and apoptosis. [ABSTRACT FROM AUTHOR]

To investigate the MRI features and clinical outcomes of unexpected uterine sarcomas in patients after high-intensity focused ultrasound (HIFU) ablation for presumed uterine fibroids. 15,759 consecutive patients who came for HIFU treatment, from November 2008 to September 2019, for presumed uterine fibroids were retrospectively reviewed. All the patients had completed a pre-HIFU MRI. All MRI images were independently analyzed and interpreted by two radiologists in every center. According to the T2WI MRI features of hyperintensity, accompanied by irregular margins, necrosis or cystic degeneration, multi-lobulated lesion with internal septation, 46 patients were suspected to be uterine sarcomas before HIFU. Eleven patients were histologically diagnosed as uterine sarcomas after laparotomy. Among the 15713 patients who received HIFU treatment for presumed uterine fibroids, 8 patients were found to have occult recurrence during the follow-up period, and 6 were confirmed histologically as uterine sarcomas after laparotomy. The incidence rate of uterine sarcomas was 0.108% (17/15759). Among them, 12 cases were low-grade endometrial stromal sarcoma (LG-ESS) and 5 cases were uterine leiomyosarcoma (LMS). No histological dissemination of the sarcoma was detected in patients with unexpected uterine sarcomas. Although some MRI features of uterine sarcomas and uterine fibroids overlapped, MRI is valuable in distinguishing between uterine fibroids and uterine sarcomas. HIFU does not seem to cause histological dissemination of the sarcoma, but follow-up visits should be strictly adhered to in order to detect unexpected uterine sarcomas at an early stage and to treat them in a timely manner. [ABSTRACT FROM AUTHOR]

The ability to perceive students’ emotions in real time is related to whether the description of the student’s state is accurate, and it is also related to whether the goal of achieving the students’ individual learning needs can be achieved. This paper studies the students’ boring emotion in English learning, and builds the recognition system of students’ boring emotion in English learning based on fuzzy neural network. Moreover, this paper combines the actual needs to construct the system function modules, and carries out the algorithm analysis and framework construction, and uses the mathematical modeling method to add the emotional factor to the English learner state modeling. In addition, according to the actual needs of the system constructed in this paper, the boring emotion of English learners is recognized. In addition, this paper designs experiments to verify the performance of the model, and analyze the system reliability from the theoretical perspective and the practical perspective. The experimental research results show that the model constructed in this paper meets the expected goals. [ABSTRACT FROM AUTHOR]

The study of nonconventional luminescence is important for revealing the luminescence of natural systems and has gradually drawn the attention of researchers in recent years. However, the underlying mechanism is still inexplicable. Herein, the luminescence behavior of two series of simple, heteroatom‐containing small molecules without aromatic rings, i.e., maleimide and succinimide derivatives, are studied to gain further mechanistic insight into the nonconventional luminescence process. It has been unveiled that all the molecules exhibit bright and visible luminescence in concentrated solution and solid state and the formation of clusters is the root cause for such behaviors, which can effectively increase the possibility of both the nonradiative n–π* and favorable π–π* transitions and stabilize the excitons formed in the excited state. The distinctive luminescent phenomena and intriguing mechanism presented in this work will be significant for understanding the mechanism of clusteroluminescence and provide new strategies for the rational design of novel luminescent materials. [ABSTRACT FROM AUTHOR]

Multicomponent polymerizations (MCPs) are a group of fascinating polymer synthesis approaches that are developed rapidly in the recent decade. As a popular alkyne‐based MCP, the A3‐polycouplings of alkynes, aldehydes, and amines are developed for the synthesis of poly(propargylamine)s under the catalysis of metal catalysts. In this work, through the design of carboxylic acid group‐activated alkyne monomers, a catalyst‐free, four‐component polymerization of propiolic acids, benzylamines, organoboronic acids, and formaldehyde is reported under mild condition at 45 °C in dichloroethane. This four‐component polymerization is applicable to different monomer structures, which can afford seven poly(propargylamine)s with up to 94% yields and molecular weights of up to 13 900 g mol−1. Moreover, the poly(propargylamine)s demonstrate good solubility and processibility, high thermal stability and light refractivity, unique photophysical property, and so on. The simple monomers, mild condition, low cost, high efficiency, and procedure simplicity of this catalyst‐free four‐component polymerization demonstrates an elegant example of functional polymer synthesis. [ABSTRACT FROM AUTHOR]

Background: Exploring the effective therapy for neonatal hypoxic-ischemic brain injury is an important goal. This study was designed to investigate how dexmedetomidine (DEX) contribute to hypoxic brain injury. Methods: Developing Sprague-Dawley rat models of hypoxia/reoxygenation (H/R) injury were constructed to simulate neonatal hypoxic brain injury for DEX treatment. Immunohistochemistry and western blot were performed to measure neuroglobin (Ngb) protein expression in hippocampal tissues. Hippocampal neuron injury and apoptosis were detected by Nissl staining and TUNEL assay, respectively. A Morris water maze (MWM) test was performed to evaluate the long-term learning and memory function. Results: The expression of Ngb was increased following H/R model establishment and up-regulated by medium and high doses of DEX, but not up-regulated by low doses of DEX. Medium and high doses of DEX alleviated the H/R injury as well as induced the reduction of Nissl bodies and apoptosis. Besides, medium and high doses of DEX down-regulated cytosolic Cyt-c, Apaf-1, and caspase-3 in H/R injury model. MWM test showed that medium and high doses of DEX significantly shortened the escape latency and enhanced the number of platform crossings. However, low doses of DEX have no effect on Nissl bodies, mitochondrial apoptosis, expression of apoptosis-related proteins and long-term learning functions. Conclusions: DEX induced Ngb expression in H/R rat models. The neuroprotection of DEX-mediated Ngb up-regulation may be achieved by inhibiting neuronal apoptosis through the mitochondrial pathway. Findings indicated that DEX may be useful as an effective therapy for neonatal hypoxic brain injury. [ABSTRACT FROM AUTHOR]

To investigate the mechanism dexmedetomidine in relieving the neurotoxicity of a developing brain induced by sevoflurane. Sprague-Dawley rats, 6 days old, were randomly divided into three groups. Rats in the control group were inhaled with air after injection of normal saline; rats in the sevoflurane group were injected with normal saline and inhaled with 3% sevoflurane for 2 h in three consecutive day; rats in the dexmedetomidine group were inhaled with 3% sevoflurane after intraperitoneal injection of dexmedetomidine 25 μg/kg. WB results showed that mBDNF, pTrkB/TrkB, and CREB were significantly decreased in the hippocampus of the sevoflurane group, which are significantly upregulated in the dexmedetomidine group. In the sevoflurane group, proBDNF, P75NRT, and RhoA were significantly increased, which were significantly lower than those in the dexmedetomidine group than those in the sevoflurane group. The expression BDNF was downregulated in the sevoflurane group, while the proBDNF was upregulated in the sevoflurane group. In the Morris water maze test, the escape latency of the sevoflurane group was significantly prolonged. In sevoflurane groups, the number of crossing platform was significantly reduced, the synaptic protein decreased significantly, and this effect was reversed in rats of the dexmedetomidine group. Dexmedetomidine could reduce synaptic plasticity decline in developing rats induced by sevoflurane, through downregulating the proBDNF-p75NTR-RhoA pathway and upregulating BDNF-TrkB-CREB. [ABSTRACT FROM AUTHOR]

Background. Hydrogen-rich saline (HRS) has strong anti-inflammatory, antioxidative stress, and antiapoptotic properties. The study focused on the protection of HRS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rat models and the relationship with autophagic regulation and mTOR/TFEB signaling pathway. Material and Methods. The LPS-induced ALI rats' model was established. Pathohistological change in lung tissue was detected by hematoxylin-eosin staining. The inflammatory cytokines were examined by enzyme-linked immunosorbent assay (ELISA). The key apoptosis proteins and autophagy-relevant proteins were analyzed by western blotting. In vitro, HPMEC models of ALI were treated with LPS. The inflammatory cytokines were detected. Apoptosis rate was determined by flow cytometry. The autophagy and mTOR/TFEB signaling pathway-related proteins were detected by western blot and immunohistochemical staining. Results. HRS attenuated LPS-induced ALI and apoptosis both in vivo and in vitro. HRS attenuated inflammatory response, inhibited apoptosis, induced and activated autophagy in LPS-induced ALI model, and downregulated mTOR/TFEB signaling pathway. The protection of HRS can be blocked by autophagy inhibitor. Moreover, mTOR activator reversed HRS protection and mTOR inhibitor enhanced HRS protection in LPS-induced model and HRS activated autophagy via mTOR/TFEB signaling pathway. Conclusion. The results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Many studies have reported that sevoflurane can increase neuronal apoptosis and result in cognitive deficits in rodents. Although neurotoxicity may be associated with mitochondrial dysfunction and oxidative stress, the exact mechanism remains unclear. In order to evaluate potential treatment therapies, we studied the effects of hemin on neurotoxicity of neonatal rat sevoflurane exposure. Methods: Postnatal day (P) seven rats were assigned randomly to four groups; (1) group C: non-anesthesia, (2) group H: intraperitoneal hemin (50 mg kg−1) treatment on days 5 and 6, (3) group S: 3% sevoflurane exposure for 4 h, and (4) group SH: hemin treatment + sevoflurane exposure. The expression of neuroglobin in neonatal hippocampus was determined by western blot and immunohistochemistry. Neuroglobin was localized by immunofluorescence. Western blot for the expression of cleaved caspase-3 and TUNEL were used to detect neonatal hippocampal apoptosis, and cytochrome c was used to evaluate mitochondrial function. Drp-1 and Mfn-2 immunoblotting were used to assess mitochondrial dynamics. The Morris water maze test was performed to detect cognitive function in the rats on P30. Results: Exposure to sevoflurane increased the expression of cleaved caspase-3, cytochrome c , and Drp1 in the neonatal hippocampus and resulted in cognitive deficiency but decreased expression of Mfn2. Hemin reduced apoptosis, improved mitochondrial dynamics and ameliorated the cognitive impairment caused by sevoflurane exposure. Conclusion: Hemin reduced neuronal apoptosis, improved mitochondrial dynamics and protected against cognitive deficits induced by sevoflurane in neonatal rats. This neuroprotective effect may be achieved by increasing the expression of neuroglobin. [ABSTRACT FROM AUTHOR]

Background/Aims: Cardiopulmonary bypass (CPB) is prone to inducing brain injury during open heart surgery. A hydrogen-rich solution (HRS) can prevent oxidation and apoptosis, and inhibit inflammation. This study investigated effects of HRS on brain injury induced by CPB and regulatory mechanisms of the PI3K/Akt/GSK3ß signaling pathway. Methods: A rat CPB model and an in vitro cell hypoxia model were established. After HRS treatment, Rat behavior was measured using neurological deficit score; Evans blue (EB) was used to assess permeability of the blood-brain barrier (BBB); HE staining was used to observe pathological changes; Inflammatory factors and brain injury markers were detected by ELISA; the PI3K/Akt/GSK3ß pathway-related proteins and apoptosis were assessed by western blot, immunohistochemistry and qRT -PCR analyses of brain tissue and neurons. Results: After CPB, brain tissue anatomy was disordered, and cell structure was abnormal. Brain tissue EB content increased. There was an increase in the number of apoptotic cells, an increase in expression of Bax and caspase-3, a decrease in expression of Bcl2, and increases in levels of Akt, GSK3ß, P-Akt, and P-GSK3ß in brain tissue. HRS treatment attenuated the inflammatory reaction, brain tissue EB content was significantly reduced and significantly decreased expression levels of Bax, caspase-3, Akt, GSK3ß, P-Akt, and P-GSK3ß in the brain. After adding the PI3K signaling pathway inhibitor, LY294002, to rat cerebral microvascular endothelial cells (CMECs), HRS could reduce activated Akt expression and downstream regulatory gene phosphorylation of GSK3ß expression, and inhibit CMEC apoptosis. Conclusion: The PI3K/Akt/GSK3ß signaling pathway plays an important role in the mechanism of CPB-induced brain injury. HRS can reduce CPB-induced brain injury and inhibit CMEC apoptosis through the PI3K/Akt/GSK3ß signaling pathway. [ABSTRACT FROM AUTHOR]

[Display omitted] • Sevoflurane alleviates LPS-induced ALI by activating cell protective autophagy. • Sevoflurane triggers protective autophagy by activating AMPK/ULK1/PIKFYVE pathway. • Sevoflurane restrains LPS-induced ALI via AMPK/ULK1 pathway. Sevoflurane anesthesia is deemed as potential therapeutic drug for lipopolysaccharide (LPS)-induced acute lung injury (ALI), but the molecular mechanisms have not been fully delineated. The present study explored the specific molecular mechanism of sevoflurane regulating autophagy to reduce LPS induced ALI. Male C57BL/6J mice and mouse pulmonary microvascular endothelial cells (MPVECs) were treated with LPS to construct ALI models, and the levels of inflammation, apoptosis and autophagy were detected after treatment with sevoflurane. Meanwhile, cells were treated with autophagy inhibitor or AMP-activated protein kinase (AMPK)/unc-51 like autophagy activating kinase 1 (ULK1) pathway inhibitor in vitro to detect their effects on cell survival. Sevoflurane reduced inflammation, recovered cell division so as to suppress cell apoptosis and maintain cell survival, and activated autophagic flux in LPS-induced ALI models in vivo and in vitro. Of note, the suppressing effects of sevoflurane on LPS-induced cell death were abrogated by inhibiting autophagy. Moreover, we evidenced that sevoflurane promoted activation of the AMPK/ULK1 pathway in LPS-induced ALI models. Blockage of this pathway abrogated the promoting effects of sevoflurane on cell autophagy and cell viability in LPS-treated cells. Collectively, sevoflurane suppresses apoptosis and inflammation via activating protective autophagy, thereby ameliorating LPS-induced ALI, and the AMPK/ULK1/ PIKFYVE pathway is responsible for the process. [ABSTRACT FROM AUTHOR]

Sevoflurane, a commonly used inhaled anesthetic, causes endogenous apoptosis in fetal rats. Microglia polarization is associated with inflammation, and the IL-10/STAT3/SOCS3 pathway is involved in this process. Neuroglobin (Ngb) is a neuroprotective protein which exhibits an anti-inflammatory effect. The purpose of this study was to investigate whether neurotoxicity induced by sevoflurane exposure in prenatal rats correlates with neuroinflammation and microglia polarization and whether Ngb can moderate this response. We found that exposure to sevoflurane on the 20th day of gestation (G20) induced discernable inflammation in postnatal day 0 (P0) rats, promoted M1 polarization of microglia, and inhibited M2 polarization. Hemin-mediated Ngb elevation inhibited sevoflurane-induced neuroinflammation. Additionally, elevated Ngb inhibited M1 polarization and promoted M2 polarization of microglia. We also found that elevated Ngb could alleviate the effect of sevoflurane on the expression of Interleukin-10 (IL-10), phosphorylated-signal transduction and activators of transcription 3 (P-STAT3), and suppressor of cytokine signaling 3 (SOCS3). Furthermore, we found that elevated Ngb ameliorated the effects of sevoflurane on long-term exploratory behavior and learning and memory in the offspring. Our results show that Ngb alleviates the neurotoxicity of sevoflurane to fetal rats by inhibiting neuroinflammation and affecting microglial polarization, a process which may involve the IL-10/STAT3/SOCS3 pathway. • Exposure to sevoflurane in prenatal rats can cause neuroinflammation in offspring rats. • Hemin-mediated Ngb elevation can inhibit neuroinflammation caused by sevoflurane. • Elevated Ngb affects microglia polarization phenotype. • Elevated Ngb can alleviate the long-term neurotoxicity induced by sevoflurane. [ABSTRACT FROM AUTHOR]

The global pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its threat to humans have drawn worldwide attention. The acute and long-term effects of SARS-CoV-2 on the nervous system pose major public health challenges. Patients with SARS-CoV-2 present diverse symptoms of the central nervous system. Exploring the mechanism of coronavirus damage to the nervous system is essential for reducing the long-term neurological complications of COVID-19. Despite rapid progress in characterizing SARS-CoV-2, the long-term effects of COVID-19 on the brain remain unclear. The possible mechanisms of SARS-CoV-2 injury to the central nervous system include: 1) direct injury of nerve cells, 2) activation of the immune system and inflammatory cytokines caused by systemic infection, 3) a high affinity of the SARS-CoV-2 spike glycoprotein for the angiotensin-converting enzyme ACE2, 4) cerebrovascular disease caused by hypoxia and coagulation dysfunction, and 5) a systemic inflammatory response that promotes cognitive impairment and neurodegenerative diseases. Although we do not fully understand the mechanism by which SARS-CoV-2 causes nerve injury, we hope to provide a framework by reviewing the clinical manifestations, complications, and possible mechanisms of neurological damage caused by SARS-CoV-2. With hope, this will facilitate the early identification, diagnosis, and treatment of possible neurological sequelae, which could contribute toward improving patient prognosis and preventing transmission. [ABSTRACT FROM AUTHOR]

• Anesthetics can cause neurotoxicity and cognitive dysfunction in animals. • Whether anesthetics can cause cognitive impairment in humans is still uncertain. • Studies have shown that anesthetics can cause neuronal damage in multiple ways. • Drugs and exercise are effective in reducing neurotoxicity of anesthetics. Every year, a large number of infants and young children worldwide are administered general anesthesia. Whether general anesthesia adversely affects the intellectual development and cognitive function of children at a later date remains controversial. Many animal experiments have shown that general anesthetics can cause nerve damage during development, affect synaptic plasticity, and induce apoptosis, and finally affect learning and memory function in adulthood. The neurotoxicity of pediatric anesthetics (PAN) has received extensive attention in the field of anesthesia, which has been listed as a potential problem affecting public health by NFDA of the United States. Previous studies on rodents and non-human primates indicate that inhalation of anesthetics early after birth can induce long-term and sustained impairment of learning and memory function, as well as changes in brain function. Many anti-oxidant drugs, dexmedetomidine, as well as a rich living environment and exercise have been proven to reduce the neurotoxicity of anesthetics. In this paper, we summarize the research progress, molecular mechanisms and current intervention measures of anesthetic neurotoxicity. [ABSTRACT FROM AUTHOR]

Highlights • Sevoflurane could increase the expression of connexin 43 and induce apoptosis in developing rat hippocampus. • The JNK/c-Jun pathway was activated after sevoflurane exposure in hippocampus and inhibited by JNK inhibitor SP600125. • SP600125 reversed upregulation of connexin 43 and neuroapoptosis, and improved learning and memory abilities in adolescent rats. Abstract As one of the most popular anesthetics, sevoflurane is widely used in pediatric anesthesia. Unfortunately, an increasing number of studies have demonstrated that sevoflurane has potential neurotoxic effects on the developing brain and cognition, even in adolescence. Connexin 43 (Cx43) has been documented to contribute to cognitive dysfunction. The present study hypothesized that Cx43 may participate in sevoflurane-induced neuroinjury and investigated the underlying mechanisms in young Sprague Dawley (SD) rats. Seven-day-old SD rats (P7) were exposed to 3% sevoflurane for 4 h. The levels of Cx43,mitogen-activated protein kinase (MAPK) signaling pathway components(including total and phosphorylated p38, extracellular signal-regulated kinase (ERK), and c-Jun n-terminal kinase (JNK) and activator protein 1(AP-1) transcription factors (including total and phosphorylated c-Fos, and c-Jun) were assessed by Western blot analysis. Neuronal apoptosis was detected using immunohistochemistry (IHC). The Morris water maze (MWM) was performed to evaluate cognitive function from P28 to P33. The results showed that anesthesia with 3% sevoflurane for 4 h increased Cx43 levels in the rat hippocampus from 6 h to 3 d, and compared with sevoflurane exposure in the control group rats, exposure in P7 SD rats also increased the ratios of phosphorylated JNK to JNK and, phosphorylated c-Jun to c-Jun in the hippocampus from 6 h to 3 d. All these effects could be alleviated by pretreatment with the JNK inhibitor SP600125 (10 mg/kg). Neuroapoptosis was similarly increased from 6 h to 1 d after inhaled sevoflurane exposure. Finally, the MWM indicated that sevoflurane could increase the escape latency and, decrease the number of platform crossings from P28 to P33. Overall, our findings suggested that sevoflurane increased Cx43 expression and induced to apoptosis by activating the JNK/c-Jun signaling pathway in the hippocampus of P7 rats. This finding may reveal a new strategy for preventing sevoflurane-induced neuronal dysfunction. [ABSTRACT FROM AUTHOR]

Escherichia coli ( E. coli ) commonly reside in human intestine and most E. coli strains are harmless, but some serotypes cause serious food poisoning. This study identified and molecularly characterized bla SHV genes from 490 E. coli strains with multi-drug resistance in a hospital population. PCR and molecular cloning and southern blot were performed to assess functions and localizations of this resistant E. coli gene and the pulsed-field gel electrophoresis (PFGE) was utilized to demonstrate the clonal relatedness of the positive E. coli strains. The data showed that 4 of these 490 E. coli strains (4/499, 0.8%) carried bla SHV genes that included EC D2485 ( bla SHV-5 ), EC D2487 ( bla SHV-5 ), EC D2684 ( bla SHV-11 ) and EC D2616 ( bla SHV-195, a novel bla SHV ). Analysis of bla SHV open-reading frame showed that bla SHV-5 had a high hydrolysis activity to the broad-spectrum penicillin (ampicillin or piperacillin), ceftazidime, ceftriaxone, cefotaxime and aztreonam. bla SHV-195 and bla SHV-11 had similar resistant characteristics with high hydrolysis activities to ampicillin and piperacillin, but low activities to cephalosporins. Moreover, the two bla SHV-5 genes were located on a transferable plasmid (23 kb), whereas the other two bla SHV variants ( bla SHV-11 and bla SHV-195 ) seemed to be located in the chromosomal material. Both EC D2485 and EC D2487 clones isolated in 2010 had the same DNA finger printing profile and they might be the siblings of clonal dissemination. The data from the current study suggest that the novel bla SHV and clonal dissemination may be developed, although bla SHV genes were infrequently identified in this hospital population. The results of the work demonstrate the necessity for molecular surveillance in tracking bla SHV -producing strains in large teaching hospital settings and emphasize the need for epidemiological monitoring. [ABSTRACT FROM AUTHOR]

Exposure to general anesthesia in early childhood may lead to adverse effects on adolescent neurocognition. This study investigated the effects of multiple inhalations of sevoflurane on long-term learning and memory in developing rats, and explored the mechanistic role of the tissue plasminogen activator (tPA)/plasminogen activator inhibitor-1 (PAI-1) fibrinolysis system and its regulatory relationship with the brain derived neurotrophic factor (BDNF) by activation of tropomysin related kinase B (TrkB). After rats were inhaled with sevoflurane for 2 h/d for three days, the expression levels of tPA, PAI-1, BDNF, its precursor(proBDNF), TrkB and phosphorylation of TrkB (p-TrkB) were detected at different time points. After 28 d, Morris water maze was used to examine learning and memory function; Golgi staining was used to investigate synaptic plasticity and synaptic-related proteins, such as Synapsin I(SYN1), growth associated protein 43(GAP-43), and postsynaptic density protein 95(PSD-95). Rats were given exogenous tPA and an inhibitor of PAI-1, TM5275. The results showed multiple inhalation of sevoflurane led to learning and memory dysfunction, downregulated the expression of the synaptic-related proteins, decreased dendritic spine density in the hippocampus, increased the expression level of proBDNF and PAI-1, and reduced expression of BDNF, tPA, and p-TrkB. Interestingly, tPA or TM5275 partially reversed the learning and memory dysfunction and the reduction of synaptic plasticity induced by sevoflurane exposure. Furthermore, they blocked the upregulation of proBDNF and PAI-1 protein expression and increased the expression of BDNF, tPA, and p-TrkB. The protective effect of tPA or TM5275 on rats following multiple sevoflurane inhalation was blocked by a TrkB inhibitor. Multiple inhalation of sevoflurane in rats inhibited the cleavage of proBDNF by disrupting the balance of the tPA/PAI-1 fibrinolysis system. This blocked the activation of the downstream TrkB signaling pathway and reduced hippocampal synaptic plasticity, leading to long-term learning and memory dysfunction. Therefore, Sevoflurane exposure could lead to learning and memory dysfunction by inhibiting BDNF cleavage via breaking the balance of tPA/PAI-1. • Learning and memory dysfunction after multiple sevoflurane exposure was caused by decreased tPA activity in hippocampus. • Sevoflurane can elevate PAI-1 expression. • Sevoflurane can inhibite the conversion of proBDNF to mature BDNF as well as the activation of TrkB. • TM5275 and tPA can be used to treat the brain injury caused by sevoflurane. [ABSTRACT FROM AUTHOR]

To observe the effect of dexmedetomidine (DEX) on mitochondrial apoptosis of hippocampal neurons in hypoxia/reoxygenation (H/R) brain injury in developing rats, and to investigate its regulatory mechanism on HIF-1α/p53 signaling pathway. Hypoxia/reoxygenation model was used in this study. TUNEL assay was performed to detect cell apoptosis. Immunohistochemical analysis and Western-blotting analysis were conducted to detect Cytochrome-C (Cyt-c), APAF-1, Caspase-3, Neuroglobin (Ngb), HIF-1α and p53 expression. After 28 days, Morris water maze (MWM) was performed. 50 μg/kg DEX improved H/R-induced brain injury and inhibited mitochondrial apoptosis in rats. Western-blotting and Immunohistochemical results demonstrated that DEX could up-regulate Ngb through α 2 receptor to inhibit H/R-induced mitochondrial apoptosis. In addition, by adding inhibitors yohimbine and 2-methoxyestradiol (2ME2), we found that DEX could activate HIF-1α/p53 signaling pathway. MWM test showed that DEX could enhance long-term learning and memory of H/R brain injury rats. DEX alleviates H/R-induced brain injury and mitochondrial apoptosis in developing rats through α 2 receptor, which may be related to activation of HIF-1α/p53 signaling pathway to up-regulate the expression of Ngb. [ABSTRACT FROM AUTHOR]

Sulfur-containing polymers with unique structures and fascinating properties have attracted much attention recently, the efficient and economic synthetic approaches for various sulfur-containing polymers have rapidly developed. Herein, the multicomponent reaction of elemental sulfur, isocyanide, and alcohol was designed at mild condition with the assistance of NaOH, and the corresponding NaOH-assisted multicomponent polymerization of elemental sulfur, diisocyanides, and diols were developed at room temperature or 40 oC in air, to produce poly(O-thiocarbamate)s with well-defined structures, high molecular weights (Mws up to 32 500 g/mol) and high yields (up to 99%). The facilely available monomers, mild condition, and high efficiency of this MCP enabled scale-up synthesis of poly(O-thiocarbamate)s, and 7.34 g polymer was obtained in 98% yield. These functional poly(O-thiocarbamate)s could enrich Au3+ from aqueous solution with high enrichment capacity (983 mg·Au3+/g) and high efficiency (>99.99%) in 1 min, demonstrating superior gold enrichment performance and their potential industrial and economic values., (© 2024 Wiley‐VCH GmbH.)

Introduction: Obesity, a pervasive global epidemic, has heightened susceptibility to chronic ailments and diminished the overall life expectancy on a global scale. Probiotics and inulin (IN) have been documented to mitigate obesity by exerting an influence on the composition of the gut microbiota. Whether heat-killed Bifidobacterium longum BBMN68 (MN68) and IN have an anti-obesity effect remains to be investigated., Methods: In this study, Wistar rats were fed a high-fat diet (HFD), and orally administered heat-killed MN68 (2 × 10 11 CFU/kg) and/or inulin (0.25 kg/kg) for 12 weeks. Histological analysis, serology analysis and 16S rRNA gene sequencing were performed., Results: Heat-killed MN68 + IN treatment showed an enhanced effect on preventing weight gain, diminishing fat accumulation, and regulating lipid metabolism, compared to either heat-killed MN68 treatment or inulin treatment. Gut microbiota results showed that heat-killed MN68 + IN treatment significantly increased the relative abundance of Bacteroidota , Oscillospira , Intestinimonas , Christensenella , and Candidatus&#95;Stoquefichus , and reduced the relative abundance of Enterococcus . Furthermore, heat-killed MN68 + IN significantly increased the SCFA levels, which were correlated with changes in the gut microbiota., Discussion: This research provides support for the application of heat-killed MN68 and IN in the treatment of obesity, and highlights the combination of heat-killed BBMN68 and IN as functional food ingredients., Competing Interests: DL and HL were employed by Inner Mongolia Mengniu Dairy (Group) Co., Ltd., China. HL, HM and XW were employed by Mengniu Hi-Tech Dairy (Beijing) Co., Ltd., China. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Sun, Zhang, Li, Li, Ma, Wu, Li, Wang, Liu, Feng, Zhang, Sang, Fang and Wang.)

Background: Several observational studies have proposed a potential link between gut microbiota and the onset and progression of sepsis. Nevertheless, the causality of gut microbiota and sepsis remains debatable and warrants more comprehensive exploration., Methods: We conducted a two-sample Mendelian randomization (MR) analysis to test the causality between gut microbiota and the onset and progression of sepsis. The genome-wide association study (GWAS) summary statistics for 196 bacterial traits were extracted from the MiBioGen consortium, whereas the GWAS summary statistics for sepsis and sepsis-related outcomes came from the UK Biobank. The inverse-variance weighted (IVW) approach was the primary method used to examine the causal association. To complement the IVW method, we utilized four additional MR methods. We performed a series of sensitivity analyses to examine the robustness of the causal estimates., Results: We assessed the causality of 196 bacterial traits on sepsis and sepsis-related outcomes. Genus Coprococcus2 [odds ratio (OR) 0.81, 95% confidence interval (CI) (0.69-0.94), p = 0.007] and genus Dialister (OR 0.85, 95% CI 0.74-0.97, p = 0.016) had a protective effect on sepsis, whereas genus Ruminococcaceae UCG011 (OR 1.10, 95% CI 1.01-1.20, p = 0.024) increased the risk of sepsis. When it came to sepsis requiring critical care, genus Anaerostipes (OR 0.49, 95% CI 0.31-0.76, p = 0.002), genus Coprococcus1 (OR 0.65, 95% CI 0.43-1.00, p = 0.049), and genus Lachnospiraceae UCG004 (OR 0.51, 95% CI 0.34-0.77, p = 0.001) emerged as protective factors. Concerning 28-day mortality of sepsis, genus Coprococcus1 (OR 0.67, 95% CI 0.48-0.94, p = 0.020), genus Coprococcus2 (OR 0.48, 95% CI 0.27-0.86, p = 0.013), genus Lachnospiraceae FCS020 (OR 0.70, 95% CI 0.52-0.95, p = 0.023), and genus Victivallis (OR 0.82, 95% CI 0.68-0.99, p = 0.042) presented a protective effect, whereas genus Ruminococcus torques group (OR 1.53, 95% CI 1.00-2.35, p = 0.049), genus Sellimonas (OR 1.25, 95% CI 1.04-1.50, p = 0.019), and genus Terrisporobacter (OR 1.43, 95% CI 1.02-2.02, p = 0.040) presented a harmful effect. Furthermore, genus Coprococcus1 (OR 0.42, 95% CI 0.19-0.92, p = 0.031), genus Coprococcus2 (OR 0.34, 95% CI 0.14-0.83, p = 0.018), and genus Ruminiclostridium6 (OR 0.43, 95% CI 0.22-0.83, p = 0.012) were associated with a lower 28-day mortality of sepsis requiring critical care., Conclusion: This MR analysis unveiled a causality between the 21 bacterial traits and sepsis and sepsis-related outcomes. Our findings may help the development of novel microbiota-based therapeutics to decrease the morbidity and mortality of sepsis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Gao, Liu, Cui, Zhang and Wu.)

Objective: The purpose of this systematic review and meta-analysis was to assess the clinical efficacy and safety of ultrasound (US)-guided high intensity focused ultrasound (HIFU) in the treatment of breast fibroadenoma in different studies., Methods: Studies evaluating the efficacy and safety of US-guided HIFU in the treatment of histologically-proven FA with follow-up outcomes of more than 3 months were searched through MEDLINE/PubMed databases. Volume reduction rate (VRR) and side effects were extracted and compared for further analysis., Results: Of 29 identified articles, 10 studies involving 385 women and more than 545 FAs met the inclusion criteria. The mean VRR at 6 months and 12 months after HIFU was 52.00% and 72.00%. In terms of intraoperative safety, nine studies reported mild to moderate pain, with an average visual analogue scale (VAS) score ranging from 1.60 to 7.10. The most common postoperative side effect associated with HIFU was subcutaneous ecchymosis and less frequent were pain, erythema, and skin pigmentation, most of which disappeared within weeks. No serious side effects were observed., Conclusion: S-guided HIFU is an effective and safe noninvasive treatment for breast FA that does not cause serious side effects. Further studies are needed to explore crucial influencing factors of VRR.

Background: Tear trough deformity is one of the most common complaints in clinical settings. The correction of this groove is challenging in facial rejuvenation. The lower eyelid blepharoplasty varies with different conditions. A novel approach of using orbital fat in the lower eyelid to increase the volume of the infraorbital rim with granule fat injection has been applied in our institution for more than 5 years., Objectives: This article aims to describe the detailed steps of our technique and verify its effectiveness by a cadaveric head dissection after surgical simulation., Methods: In this study, a total of 172 patients with tear trough deformity underwent lower eyelid orbital rim augmentation with fat filling in the sub-periosteum pocket. According to Barton's grades, 152 patients underwent lower eyelid orbital rim augmentation with orbital fat filling, 12 patients had it combined with autologous granule fat from other body parts, and 8 patients received only transconjunctival fat removal to correct tear trough., Results: The modified Goldberg score system was used to compare preoperative and postoperative photographs. Patients were satisfied with the cosmetic results. Excessive protruding fat was released, and the tear trough groove was flattened by using autologous orbital fat transplantation. The lower eyelid sulcus deformities were well-corrected. To further illustrate the anatomical structure of the lower eyelid area and injection layers, six cadaveric heads were used for surgical simulation and demonstrated the effectiveness of our technique., Conclusions: This study indicated that the infraorbital rim could be increased by transplanting orbital fat to the pocket, which was dissected under the periosteum, and the procedure has been verified as reliable and effective., Evidence-Based Medicine Ebm Level: Level II., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Liu, Wang, Cai, Wu and Wang.)

Selenium-containing polymers are a group of fascinating functional polymers with unique structures, properties, and applications, which have been developed recently but only with limited examples. The challenges of developing selenium-containing polymers with structural and functional diversity include the lack of economic and safe monomers, lack of efficient and convenient synthetic approaches, and poor stability of selenium-involving covalent bonds. In this work, room-temperature metal-free multicomponent polymerizations (MCPs) of elemental selenium, diisocyanides, and dipropargyl alcohols were developed, and polymers with a selenium-containing aliphatic heterocycle, 1,3-oxaselenolane, were synthesized through these MCPs directly from elemental selenium. The alicyclic poly(oxaselenolane)s enjoyed high yields (up to 93%), high molecular weights (up to 15 600 g/mol), high thermal and chemical stability, good solubility and processability. With the structural design of the poly(oxaselenolane)s and their high selenium contents of up to 33.7 wt %, the refractive indices of their spin-coated thin films could reach 1.8026 at 633 nm and maintain 1.7770 at 1700 nm. It is anticipated that these efficient, convenient, mild, and economic multicomponent polymerizations of elemental selenium can promote the selenium-related polymer chemistry and accelerate the exploration of diversified selenium-containing functional polymer materials.

Objective: To assess the long-term outcomes and the factors affecting local recurrence of uterine fibroids after ultrasound-guided high-intensity focused ultrasound (USgHIFU) ablation., Materials and Methods: 629 patients with a solitary uterine fibroid smaller than 10 cm in diameter treated with USgHIFU at our institutes between January 2011 and December 2016 were retrospectively analyzed. The patients were requested to take pre-HIFU and one day post-HIFU MRI. The patients were asked to return to the hospital every 3 months until January 2020, for imaging evaluation and to check on improvement in symptoms., Results: Five hundred and thirty-six patients completed follow-up according to our protocol. The median follow-up time was 69 (interquartile range: 48 to 89) months. Among them, local recurrence was detected in 110 patients. 18 (16.4%) patients required additional treatment between 12 and 24 months after USgHIFU treatment, 59 (53.6%) patients required additional treatment 24 months after USgHIFU. Therefore, in total, 77 patients required additional treatment, of which 32 received USgHIFU and 45 underwent myomectomy. The median non-perfused volume (NPV) ratio in patients with recurrence was 73%, compared to 89% among patients without recurrence. Multivariate analysis showed that NPV ratio, maximum fibroid diameter and fibroid enhancement type were the independent factors affecting the recurrence of fibroids after USgHIFU treatment., Conclusions: Achievement of NPV ratio higher than 70% has led to acceptable re-intervention rate during the follow-up period after USgHIFU. NPV ratio, maximum fibroid diameter, and fibroid enhancement type were the independent factors affecting the recurrence of fibroids after USgHIFU treatment.

Background: In recent decades, long non-coding RNAs (lncRNAs) have been reported as crucial functional regulators involved in ovarian cancer. In the present study, we explored how lncRNA RHPN1-AS1 influences the progression of epithelial ovarian cancer (EOC) through tumor cell-dependent mechanisms., Results: The expression of RHPN1-AS1 in EOC tissues was higher than that in para-cancerous control tissues. High expression of RHPN1-AS1 was closely associated with poor prognosis in EOC patients. N6-methyladenosine (m6A) improved the stability of RHPN1-AS1 methylation transcript by reducing RNA degradation, which resulted in upregulation of RHPN1-AS1 in EOC. In vitro and in vivo functional experiments showed that RHPN1-AS1 promoted EOC cell proliferation and metastasis. RHPN1-AS1 acted as a ceRNA to sponge miR-596, consequently increasing LETM1 expression and activating the FAK/PI3K/Akt signaling pathway., Conclusion: RHPN1-AS1-miR-596-LETM1 axis plays a crucial role in EOC progression. Our findings may provide promising drug targets for EOC treatment., Methods: We determined the aberrantly expressed lncRNAs in EOC via microarray analysis and validated RHPN1-AS1 expression by qRT-PCR. The RHPN1-AS1-miR-596-LETM1 axis was examined by dual-luciferase reporter assay and RIP assay. The mechanism of RHPN1-AS1 was investigated through gain- and loss-of-function studies both in vivo and in vitro.

Minocycline has been demonstrated to exert neuroprotective effects in various experimental models. In the present study, we investigated the mechanisms underlying the protective effects of minocycline on cell injury induced by the inhalation of the anesthetic, sevoflurane. In our in vivo experiments using rats, minocycline attenuated sevoflurane-induced neuronal degeneration and apoptosis in the rat hippocampus, and this effect was associated with the minocycline-mediated suppression of oxidative stress in the hippocampus. In in vitro experiments, minocycline inhibited sevoflurane-induced apoptosis and the production of reactive oxygen species (ROS) in H4 human neuroglioma cells. In addition, minocycline suppressed the sevoflurane-induced upregulation of interleukin (IL)-6 and the activation of the nuclear factor-κB (NF-κB) signaling pathway in H4 cells. Furthermore, we found that nuclear factor E2-related factor 2 (Nrf2), an activator of the stress response, was upregulated and activated upon sevoflurane treatment both in the rat hippocampus and in H4 cells. In addition, minocycline further augmented the upregulation and activation of Nrf2 when used in conjunction with sevoflurane. Moreover, the knockdown of Nrf2 in H4 cells by small interfering RNA (siRNA) diminished the cytoprotective effect of minocycline, and attenuated the inhibitory effect of minocycline on ROS production, IL-6 upregulation and the activation of the NF-κB signaling pathway. On the whole, our findings indicate that minocycline may exert protective effects against sevoflurane-induced cell injury via the Nrf2-modulated antioxidant response and the inhibition of the activation of the NF-κB signaling pathway.