Controlled synthesis of Fe3O4/MnO2 (3 1 0)/ZIF-67 composite with enhanced synergetic effects for the highly selective and efficient adsorption of Cu (II) from simulated copperplating effluents.

This study designed a composite material with internal synergistic effects among multiple components to achieve highly selective adsorption of Cu (II). Through controlled synthesis, the Fe3O4/MnO2(3 1 0)/ZIF-67 composite was successfully fabricated, leading to significant improvement in adsorption selectivity, capacity, and adsorption rate. The experimental results showed that the composite is of outstanding selectivity in the adsorption of Cu (II), with a partition coefficient K of Cu (II) that was 2.2-5.3 times higher than that of other coexisting ions. Moreover, the composite exhibited a remarkable adsorption capacity of 1261.0 mg g-1 and a fast adsorption rate of 840.7 mg g-1 h-1 at 298 K. Additionally, its magnetic property facilitated easy separation from wastewater, thereby enhancing its potential for commercial applications. The synergetic effect mechanism was analyzed through characterizations and DFT calculations. Furthermore, the recyclability of the composite was investigated, which showed that after seven cycles, the adsorption efficiency remained at 85% of its initial efficiency. It can be concluded that Fe3O4/MnO2(3 1 0)/ZIF-67 has potential to address challenges posed by heavy metal pollution in copperplating effluents.

Screening of MnO2 with desired facet and its behavior in highly selective adsorption of aqueous Pb (II): Theoretical and experimental studies.

In this study, Density Functional Theory (DFT) calculations and experimental methods were adopted to evaluate MnO2 with 5 different facets for their selective adsorption of Pb (II) from wastewater containing Cd (II), Cu (II), Pb (II), and Zn (II). The DFT calculations were performed to screen the selective adsorption capability of the facets and demonstrated that the MnO2 (3 1 0) facet has an excellent performance in selective adsorption of Pb (II) among all facets. The validity of DFT calculations was verified by comparing with the experimental results. MnO2 with different facets was prepared in a controlled manner and the characterizations confirmed that the lattice indices of the fabricated MnO2 have the desired facets. Adsorption performance experiments illustrated a high adsorption capacity (320.0 mg/g) on the (3 1 0) facet MnO2. The selectivity of adsorption of Pb (II) was 3-32 times greater than that of the other coexisting ions, i.e., Cd (II), Cu (II), and Zn (II)), which is consistent with results of the DFT calculations. Furthermore, results of DFT calculations on adsorption energy, charge density difference, and projected density of states (PDOS) showed that the adsorption of Pb (II) on the MnO2 (3 1 0) facet is non-activated chemisorption. This study shows that it is feasible to use DFT calculations to quickly screen suitable adsorbents for environmental applications.

Non-Linear Association between Folate/Vitamin B12 Status and Cognitive Function in Older Adults.

Although folate and vitamin B12 status have long been implicated in cognitive function, there is no consensus on the threshold of folate and vitamin B12 for assessing their impacts on cognition. The goal of this study was to detail the association between folate and vitamin B12 with cognitive performance. We analyzed cross-sectional data of older adults (≥60 y; n = 2204) from the NHANES (National Health and Nutrition Examination Surveys) cohort from 2011-2014. The restricted cubic spline model was used for describing the associations between serum total folate, RBC folate, 5-methyltetrahydrofolate, and vitamin B12 and the Consortium to Establish a Registry for Alzheimer's Disease Word Learning (CERAD-WL) and Delayed Recall (CERAD-DR) tests, the Animal Fluency (AF) test, and the Digit Symbol Substitution Test (DSST), respectively. Older adults with a different folate and vitamin B12 status were clustered by artificial intelligence unsupervised learning. The statistically significant non-linear relationships between the markers of folate or vitamin B12 status and cognitive function were found after adjustments for potential confounders. Inverse U-shaped associations between folate/vitamin B12 status and cognitive function were observed, and the estimated breakpoint was described. No statistically significant interaction between vitamin B12 and folate status on cognitive function was observed in the current models. In addition, based on the biochemical examination of these four markers, older adults could be assigned into three clusters representing relatively low, medium, and high folate/vitamin B12 status with significantly different scores on the CERAD-DR and DSST. Low or high folate and vitamin B12 status affected selective domains of cognition, and was associated with suboptimal cognitive test outcomes.

Role of lipocalin-2 in surgery-induced cognitive decline in mice: a signal from neuron to microglia.

BACKGROUND: Perioperative neurocognitive disorders (PNDs) are common complications observed among surgical patients. Accumulating evidence suggests that neuroinflammation is one of the major contributors to the development of PNDs, but the underlying mechanisms remain unclear. METHODS: qPCR and ELISA analysis were used for detecting LCN2 and cytokine levels. cx3cr1CreER/-:: R26iDTR/- crossed mouse line was used for microglia depletion; intracranial injection of recombinant LCN2 (rLCN2) and adeno-associated viruses (AAV)-mediated shRNA silencing approaches were used for gain and loss of function, respectively. Combing with in vitro microglia cell culture, we have studied the role of LCN2 in surgery-induced cognitive decline in mice. RESULTS: We revealed that Lcn2 mRNA and protein levels were greatly increased in mouse hippocampal neurons after surgery. This surgery-induced elevation of LCN2 was independent of the presence of microglia. Gain of function by intracranial injection of rLCN2 protein into hippocampus disrupted fear memory in naive mice without surgery. Conversely, silencing LCN2 in hippocampus by AAV-shRNA protected mice from surgery-induced microglia morphological changes, neuroinflammation and cognitive decline. In vitro, application of rLCN2 protein induced the expression of several pro-inflammatory cytokines in both BV-2 and primary microglia culture. CONCLUSIONS: These data suggest LCN2 acts as a signal from neuron to induce proinflammatory microglia, which contributes to surgery-induced neuroinflammation and cognitive decline in mice.

Emerging Roles of Microglia in Neuro-vascular Unit: Implications of Microglia-Neurons Interactions.

Microglia, which serve as the defensive interface of the nervous system, are activated in many neurological diseases. Their role as immune responding cells has been extensively studied in the past few years. Recent studies have demonstrated that neuronal feedback can be shaped by the molecular signals received and sent by microglia. Altered neuronal activity or synaptic plasticity leads to the release of various communication messages from neurons, which in turn exert effects on microglia. Research on microglia-neuron communication has thus expanded from focusing only on neurons to the neurovascular unit (NVU). This approach can be used to explore the potential mechanism of neurovascular coupling across sophisticated receptor systems and signaling cascades in health and disease. However, it remains unclear how microglia-neuron communication happens in the brain. Here, we discuss the functional contribution of microglia to synapses, neuroimmune communication, and neuronal activity. Moreover, the current state of knowledge of bidirectional control mechanisms regarding interactions between neurons and microglia are reviewed, with a focus on purinergic regulatory systems including ATP-P2RY12R signaling, ATP-adenosine-A1Rs/A2ARs, and the ATP-pannexin 1 hemichannel. This review aims to organize recent studies to highlight the multifunctional roles of microglia within the neural communication network in health and disease.

LncRNA-Fendrr protects against the ubiquitination and degradation of NLRC4 protein through HERC2 to regulate the pyroptosis of microglia.

OBJECTIVES: Targeted inhibition of inflammatory response can reduce diabetic cerebral ischemia-reperfusion (I/R) injure. Pyroptosis is characterized by caspase-1 dependence and the release of a large number of pro-inflammatory factors. LncRNA-Fendrr is associated with a variety of diseases, but Fendrr has not been studied in diabetic cerebral I/R. NLR-family CARD-containing protein 4 (NLRC4) regulate the pyroptosis of microglia cells. This study was designed to investigate whether Fendrr is involved in the effects of diabetic cerebral I/R injury. METHODS: The diabetic brain I/R model in mice was constructed. Mouse microglia cell line BV-2 cells were exposed to high glucose followed by hypoxia/reoxygenation (H/R). Fendrr and some pyroptosis-associated proteins were detected by qRT-PCR, western blot or ELISA. HE staining was used to detect pathological changes. Microglia pyroptosis was detected by TUNEL staining. RNA pull-down and RNA Immunoprecipitation were used to detect binding of Fendrr to HERC2 (E3 ubiquitin ligase), and CO-IP detected binding of HERC2 to NLRC4. The ubiquitination of NLRC4 was detected by ubiquitination experiments. RESULTS: Fendrr was significantly increased in the diabetic cerebral I/R model, and NLRC4 inflammatory complex and pyroptosis mediated inflammatory factors were increased. NLRC4 and inflammatory cytokines associated with pyroptosis were decreased in the high glucose-treated hypoxia/reoxygenation (H/R)-induced microglia after Fendrr knockdown. Fendrr bound to HERC2 protein, and HERC2 bound to NLRC4. Meanwhile, Fendrr could inhibit the ubiquitination of NLRC4, HERC2 promoted the ubiquitination of NLRC4 protein. Moreover, the effect of Fendrr overexpression in the diabetic cerebral I/R model of microglia can be reversed by HERC2 overexpression. CONCLUSION: Fendrr can protect against the ubiquitination and degradation of NLRC4 protein through E3 ubiquitin ligase HERC2, thereby accelerating the pyroptosis of microglia.

Airway Management of Retrosternal Goiters in 22 Cases in a Tertiary Referral Center.

BACKGROUND: The present study aimed to investigate the incidence and extent of difficult airway management in patients with massive retrosternal goiter. DESIGN: An 8-year retrospective analysis was performed to identify patients who underwent massive retrosternal thyroidectomy. A total of 22 cases were identified as giant retrosternal goiter, followed by a review of each patient's preoperative computerized tomography imaging. INTERVENTIONS: There were no cases of failed intubation. Twenty patients underwent uneventful tracheal intubation using direct laryngoscopy or Glidescope. Thirteen patients received a muscle relaxant intravenously, and two patients were induced with sevoflurane. Five patients underwent awake tracheal intubation, including awake fiberoptic intubation in three patients. Before entering the operating theatre, the remaining two patients underwent oral tracheal intubation with Glidescope in the emergency department. RESULTS: Two patients had tracheal intubation before they entered the operating theatre. Once entering vocal cords, tracheal intubation can pass beyond the site of the tracheal obstruction without difficulty. One patient died because of serious perioperative bleeding owing to the adhesion between the retrosternal goiter and large vessel within the thoracic cavity. One patient experienced dyspnea after extubation and was intubated again. CONCLUSION: Intravenous induction of muscle relaxant using laryngoscopy or Glidescope is feasible in patients with massive benign retrosternal goiter. The incidence of difficult intubation and postoperative tracheomalacia is likely too rare. Furthermore, perioperative bleeding and postoperative airway complication seem frequent.

Inhibiting Caspase-12 Mediated Inflammasome Activation protects against Oxygen-Glucose Deprivation Injury in Primary Astrocytes.

Stroke is one of the leading causes of death worldwide. Accumulating evidence suggests that NLRP3 inflammasome activation plays an important role in ischemic stroke injury. However, the existence of the NLRP3 inflammasome in astrocytes remains controversial. In this study, we demonstrated the presence of the NLRP3 inflammasome in primary mouse astrocytes and investigated the role of caspase-12 in NLRP3 inflammasome activation and cell injury in an in vitro astrocyte oxygen-glucose deprivation (OGD) model. Astrocytes exposed to 2, 3, and 4 h of OGD exhibited increased cell injury and apoptosis, and the protein levels of caspase-12, cleaved caspase-3, NLRP3 inflammasome components, and IL-1ß were also significantly elevated. Interestingly, pretreatment with the caspase-12-specific inhibitor Z-ATAD-FMK attenuated cell injury and apoptosis and decreased the levels of NLRP3, caspase-1, IL-1ß, and cleaved caspase-3 in the OGD group. In conclusion, Z-ATAD-FMK protected astrocytes against OGD-induced cell death and inhibited NLPR3-inflammasome activation. Our results indicate that caspase-12 and its potential regulation of NLRP3 inflammasome activation might be a promising target for treatment of ischemic stroke.

Preoperative assessment of cognitive function and risk assessment of cognitive impairment in elderly patients with orthopedics: a cross-sectional study.

BACKGROUND: Preexisting cognitive impairment is emerging as a predictor of poor postoperative outcomes in seniors. Nevertheless, cognitive impairment in a large proportion of geriatric patients has not been well identified and diagnosed. METHODS: This is a cross-sectional study. Mini-mental state examination scale was used to assess the cognitive function of elderly patients aged ≥65 years undergoing orthopedic surgery preoperatively. The baseline, living habits and laboratory examination results of two groups were compared, and a multivariable logistic regression model was used to identify independent predictors of preoperative cognitive impairment. RESULTS: A total of 374 elderly patients with orthopedic surgery indications met the inclusion criteria, and 28.61% of them had preoperative cognitive impairment. Multivariable logistic regression analysis showed that age (OR = 1.089, P < 0.001), subjective sleep disorders (OR = 1.996, P = 0.021), atherosclerosis (OR = 2.367, P = 0.017), and high cholesterol level (OR = 1.373, P = 0.028) were independent risk factors for preoperative cognitive impairment, while high education level performed as a protective factor (compared with the illiterate group, primary school group: OR = 0.413, P = 0.009; middle school or above group: OR = 0.120, P < 0.001). CONCLUSIONS: The prevalence of preoperative cognitive dysfunction in geriatric elective orthopedic surgical patients was high. Our study identified venerable age, low level of education, subjective sleep disorders, atherosclerosis, and high cholesterol level as risk factors for preoperative cognitive impairment in these patients. Understanding these risk factors contributes to assisting in prevention and directed interventions for the high-risk population.

[Anesthesia management in cesarean section for patient with COVID-19: a case report].

Since the coronavirus disease 2019 (COVID-19) affects the cardio-pulmonary function of pregnant women, the anesthetic management and protection of medical staff in the cesarean section is significantly different from that in ordinary surgical operation. This paper reports a case of cesarean section for a woman with COVID-19, which was successfully performed in the First Affiliated Hospital of Zhejiang University School of Medicine on February 8, 2020. Anesthetic management, protection of medical staff and psychological intervention for the pregnant woman during the operation were discussed. Importance has been attached to the preoperative evaluation of pregnant women with COVID-19 and the implementation of anesthesia plan. For moderate patients, intraspinal anesthesia is preferred in cesarean section, and try to reduce its influence in respiration and circulation in both maternal and infant; general anesthesia with endotracheal intubation should be adopted for severe or critically ill patients. Ensure the safety of medical environment, and anesthetists should carry out level-Ⅲ standard protection. Special attention and support should be paid to maternal psychology: fully explanation before operation to reduce anxiety; relieve the discomfort during operation, so as to reduce tension; avoid the bad mood due to pain after operation.

Novel Targets for Stroke Therapy: Special Focus on TRPC Channels and TRPC6.

Stroke remains a leading cause of death, disability, and medical care burden worldwide. However, transformation from laboratory findings toward effective pharmacological interventions for clinical stroke has been unsatisfactory. Novel evidence has been gained on the underlying mechanisms and therapeutic potential related to the transient receptor potential (TRP) channels in several disorders. The TRP superfamily consists of a diverse group of Ca2+ permeable non-selective cation channels. In particular, the members of TRP subfamilies, TRP canonical (TRPC) channels and TRPC6, have been found in different cell types in the whole body and have high levels of expression in the central nervous system (CNS). Notably, the TRPCs and TRPC6 channel have been implicated in neurite outgrowth and neuronal survival during normal development and in a range of CNS pathological conditions. Recent studies have shown that suppression of TRPC6 channel degradation prevents ischemic neuronal cell death in experimental stroke. Accumulating evidence supports the important functions of TRPC6 in brain ischemia. We have highlighted some crucial advancement that points toward an important involvement of TRPCs and TRPC6 in ischemic stroke. This review will make an overview of the TRP and TRPC channels due to their roles as targets for clinical trials and CNS disorders. Besides, the primary goal is to discuss and update the critical role of TRPC6 channels in stroke and provide a promising target for stroke prevention and therapy.

TRPC6 Attenuates Cortical Astrocytic Apoptosis and Inflammation in Cerebral Ischemic/Reperfusion Injury.

Transient receptor potential canonical 6 (TRPC6) channel is an important non-selective cation channel with a variety of physiological roles in the central nervous system. Evidence has shown that TRPC6 is involved in the process of experimental stroke; however, the underlying mechanisms remain unclear. In the present study, the role of astrocytic TRPC6 was investigated in an oxygen-glucose deprivation cell model and middle cerebral artery occlusion (MCAO) mouse model of stroke. HYP9 (a selective TRPC6 agonist) and SKF96365 (SKF; a TRPC antagonist) were used to clarify the exact functions of TRPC6 in astrocytes after ischemic stroke. TRPC6 was significantly downregulated during ischemia/reperfusion (IR) injury in cultured astrocytes and in cortices of MCAO mice. Application of HYP9 in vivo alleviated the brain infarct lesion, astrocytes population, apoptosis, and interleukin-6 (IL-6) and IL-1ß release in mouse cortices after ischemia. HYP9 dose-dependently inhibited the downregulation of TRPC6 and reduced astrocytic apoptosis, cytotoxicity and inflammatory responses in IR insult, whereas SKF aggravated the damage in vitro. In addition, modulation of TRPC6 channel diminished IR-induced Ca2+ entry in astrocytes. Furthermore, decreased Ca2+ entry due to TRPC6 contributed to reducing nuclear factor kappa light chain enhancer of activated B cells (NF-κB) nuclear translocation and phosphorylation. Overexpression of astrocytic TRPC6 also attenuated apoptosis, cytotoxicity, inflammatory responses, and NF-κB phosphorylation in modeled ischemia in astrocytes. The results of the present study indicate that the TRPC6 channel can act as a potential target to reduce both inflammatory responses and apoptosis in astrocytes during IR injury, subsequently attenuating ischemic brain damage. In addition, we provide a novel view of stroke therapy by targeting the astrocytic TRPC6 channel.

Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir-145 to up-regulate AQP4 expression.

Emerging studies have shown that long noncoding RNA (lncRNA) TUG1 (taurine-up-regulated gene 1) plays critical roles in multiple biological processes. However, the expression and function of lncRNA TUG1 in cerebral ischaemia/reperfusion injury have not been reported yet. In this study, we found that LncRNA TUG1 expression was significantly up-regulated in cultured MA-C cells exposed to OGD/R injury, while similar results were also observed in MCAO model. Mechanistically, knockdown of TUG1 decreased lactate dehydrogenase levels and the ratio of apoptotic cells and promoted cell survival in vitro. Moreover, knockdown of TUG1 decreased AQP4 (encoding aquaporin 4) expression to attenuate OGD/R injury. TUG1 could interact directly with miR-145, and down-regulation of miR-145 could efficiently reverse the function of TUG1 siRNA on AQP4 expression. Finally, the TUG1 shRNA reduced the infarction area and cell apoptosis in I/R mouse brains in vivo. In summary, our results suggested that lncRNA TUG1 may function as a competing endogenous RNA (ceRNA) for miR-145 to induce cell damage, possibly providing a new therapeutic target in cerebral ischaemia/reperfusion injury.

Correction to: Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.

Following publication of the original article [1], the authors reported that the given name of Liqing Wang was incorrectly published as Liqiang Wang. The original article has been updated.

Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.

BACKGROUND: The T cell Ig domain and mucin domain (TIM)-1 protein expressed on the surface of Th2 cells regulates the immune response by modulating cytokine production. The present study aimed to investigate the role and possible mechanism of TIM-1 in cerebral ischemia-reperfusion injury. METHODS: Western blot was used to detect TIM-1 and apoptosis-related protein expression, whereas TIM-1 mRNA was examined using quantitative real-time reverse transcription PCR. Flow cytometry and a TdT-mediated biotin-16-dUTP nick-end labeling (TUNEL) assay were used to detect the percentage of apoptotic cells and a pathological examination was performed. The migration of neutrophils and macrophages was analyzed by immunohistochemistry. RESULTS: Our results suggest that TIM-1 expression was transiently increased 24 h or 48 h following middle cerebral artery occlusion (MCAO)/reperfusion. The infarct size was markedly increased in MCAO, whereas treatment with a TIM-1-blocking mAb could reduce the infarct size. TIM-1 blocking mAb effectively reduced the number of neutrophils, macrophage functionality, cytokine (i.e., IL-6, IL-1ß, and TNF-α) and chemokine (i.e., CXCL-1 and CXCL-2) production in the brain tissue. The effect of in vitro T cell damage on neurons was significantly reduced following treatment with a TIM-1 blocking mAb or the knockdown of TIM-1 in co-cultured T cells and neurons. CONCLUSION: Take together, these results indicated that TIM-1 blockade ameliorated cerebral ischemia-reperfusion injury. Thus, TIM-1 disruption may serve as a novel target for therapy following MCAO.

Rare empty sella syndrome found after postoperative hypotension and respiratory failure: A case report.

BACKGROUND: Empty sella syndrome is a condition in which the pituitary gland shrinks or flattens. Patients with empty sella syndrome often present with headache, hypertension, obesity, visual disturbances, cerebrospinal fluid (CSF) rhinorrhoea, or endocrine dysfunction. Herein, we report a rare case of empty sella syndrome discovered after the patient experienced postoperative hypotension and respiratory failure. CASE SUMMARY: A 60-year-old man was admitted for further workup of left shoulder pain. He was assessed by the orthopaedics team and booked for internal fixation of the left clavicle. General anaesthesia with a nerve block was administered. His blood pressure continued to decrease post-operation. Endocrine tests were performed, with the results supporting a diagnosis of hypopituitarism with hypocortisolism and hypothyroidism. Brain magnetic resonance imaging demonstrated that the sella was enlarged and filled with CSF, confirming a diagnosis of empty sella syndrome. The patient was started on endocrine replacement therapy. The patient regained consciousness and spontaneous breath finally. CONCLUSION: This case highlights the importance of considering pituitary hormone insufficiency in the context of respiratory and hemodynamic failure during the perioperative period.

Transcriptome Profile in Hippocampus During Acute Inflammatory Response to Surgery: Toward Early Stage of PND.

Perioperative neurocognitive disorders (PND) are common complications observed in surgical patients, but there are no effective treatments and the detailed mechanisms remain largely unknown. In this study, transcriptome analysis was performed to investigate the hippocampal changes after surgery and underlying molecular mechanisms of PND. Tibial fracture surgery was performed in 3-4 months old C57BL/6J mice to mimic human orthopedic surgery. We demonstrated that memory consolidation of the hippocampal-dependent trace-fear conditioning task was significantly impaired. By using ELISA, a significant elevated IL-6 was observed both in circulating system and central nervous system and peaked at 6 h post-surgery, but transiently returned to baseline thereafter. Hippocampus were collected at 6 h post-surgery then processed for RNA-Seq. A total of 268 genes were screened differentially expressed between the Surgery and Control group, including 170 up-regulated genes and 98 down-regulated genes. By functional enrichment analysis of differently expressed genes, several KEGG pathways involved in inflammatory mediator regulation of TRP channels, neuroactive ligand-receptor interaction and cholinergic synapse were overrepresented. Quantitative real-time PCR confirmed 15 dysregulated genes of interest. These results provide a comprehensive insight into global gene expression changes during the acute presence of hippocampal inflammation and a better understanding on early stage of PND.

miR­29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4.

Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR­29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4 (AQP4). Real­time PCR and western blotting were used to assess miR­29a levels and AQP4 protein levels, respectively. Apoptosis was detected by flow cytometry, and lactate dehydrogenase (LDH) was determined by enzyme­linked immunosorbent assay (ELISA). Overexpression of miR­29a was significantly downregulated in OGD­induced primary astrocytes, and transfection with a miR­29a mimic decreased LDH release and apoptosis, and improved cell health in OGD­induced astrocytes. AQP4 was the target of miR­29a, which suppressed AQP4 expression, and knockdown of AQP4 mitigated OGD­induced astrocyte injury. Furthermore, miR­29a regulated AQP4 expression in OGD­induced astrocytes. AQP4 exacerbated astrocyte injury following ischemic stroke, and knockdown of AQP4 protected OGD/RX­induced primary cultured astrocytes against injury. The effect of miR­29a inhibitor on primary astrocytes was lost following AQP4 knockdown. These findings indicated that miR­29a prevented astrocyte injury in vitro by inhibiting AQP4. Thus, miR­29a may protect primary cultured astrocytes after OGD­induced injury by targeting AQP4, and may be a potential therapeutic target for ischemic injury of astrocytes.

Goal-directed fluid therapy does not reduce postoperative ileus in gastrointestinal surgery: A meta-analysis of randomized controlled trials.

BACKGROUND: Perioperative goal-directed fluid therapy (GDFT) aiming to maintain individual fluid balance based on sensitive parameters was prevalent in major surgery, especially in enhanced recovery after surgery (ERAS) pathway. This meta-analysis was conducted for the purpose of evaluating whether GDFT impacts on occurrence of postoperative ileus and whether its application is worthwhile in gastrointestinal surgery. METHODS: A systematic search of RCTs compared GDFT with other fluid management in patients undergoing gastrointestinal surgery from the PubMed, Web of Science, Embase, Cochrane Library databases was implemented. The primary outcome is incidence of postoperative ileus. Other outcome measures were length of hospital stay (LOS), postoperative morbidity and mortality. Subgroup analysis was planed a prior to verify the definite role of GDFT. RESULTS: 12 trials consisted of 1836 patients were included in the final analysis. GDFT did not influence the occurrence of postoperative ileus (relative risk, RR 0.71, 95% confidence interval, CI 0.47-1.07, P = .10), with moderate heterogeneity (I = 29%, P = .16). No difference was found between GDFT and control groups in LOS (mean difference -0.17 days, 95% CI -0.73 to 0.39, P = .55), total complication rate (RR 0.92, 95% CI 0.81-1.05, P = .23), and 30-day mortality (RR 0.91, 95% CI 0.47-1.75, P = .77). In other secondary outcomes, only wound infection rate was lower in the GDFT group (RR 0.68, 95% CI 0.50-0.93, P = .02). When performed subgroup analysis, GDFT was superior in reduction ileus only when compared with standard therapy or in those outside ERAS. CONCLUSIONS: It is possible that GDFT dose not affect the occurrence of postoperative ileus in gastrointestinal surgery. It scarcely influences postoperative morbidity and mortality as well. However, lower incidence of ileus is observed in GDFT group either outside ERAS or compared with standard fluid therapy. Probably, GDFT may not be necessary in the ERAS pathway or if a hybrid approach is adopted.

ZBTB16 Overexpression Enhances White Adipogenesis and Induces Brown-Like Adipocyte Formation of Bovine White Intramuscular Preadipocytes.

BACKGROUND/AIMS: Our study aims to characterize functions of ZBTB16 gene in the process of intramuscular fat (IMF) deposition and metabolism of bovine, thereby providing insights into mechanisms for the use of ZBTB16 in fat management. METHODS: Primary preadipocytes derived from bovine IMF tissue were isolated and used as the in vitro cell model. An adenovirus Ad-ZBTB16 was transfected into bovine preadipocytes to overexpress the ZBTB16 gene. By using real-time quantitative PCR (RT-qPCR), western blotting, Oil Red-O staining, glycerol-3-phosphate dehydrogenase (GPDH) activity assay, and cell counting kit-8 (CCK-8) test, adipogenic and proliferative signals in adipocytes were monitored to investigate effects of ZBTB16 on adipogenesis of bovine preadipocytes. RESULTS: After transfection, mRNA and protein levels of ZBTB16 gene were significantly increased. Enhanced ZBTB16 significantly promoted preadipocyte differentiation, as evidenced by accelerated lipid accumulation, enhanced GPDH activity, consistently increased mRNA expressions of adipogenic key transcription factors PPARγ, C/EBPα, FABP4, and ADIPOQ, and markedly increased protein expressions of PPARγ and FABP4. No difference was observed concerning proliferation of preadipocytes after treatment with Ad-ZBTB16. Furthermore, relative mRNA levels of brown adipocyte selective genes (PRDM16, UCP1, Cidea, Cox8b, and PGC-1α) and beige adipocyte selective genes (CD137, TMEM26, and Tbx1) as well as UCP1 protein expression were significantly increased by Ad-ZBTB16. Meanwhile, Ad-ZBTB16 treatment remarkably induced mitochondrial biogenesis and increased relative mitochondrial DNA (mtDNA) copy number in bovine adipocytes. CONCLUSION: These results suggest that ZBTB16 overexpression can promote white adipogenesis and induce brown-like adipocyte formation for bovine white intramuscular preadipocytes.