Characteristics associated with effectiveness in postoperative delirium research: a systematic review of randomised controlled trials with meta-regression and meta-analysis.

BACKGROUND: Postoperative delirium remains prevalent despite extensive research through randomised trials aimed at reducing its incidence. Understanding trial characteristics associated with interventions' effectiveness facilitates data interpretation. METHODS: Trial characteristics were extracted from eligible trials identified through two systematic literature searches. Multivariable meta-regression was used to investigate trial characteristics associated with effectiveness estimated using odds ratios. Meta-analysis was used to investigate pooled effectiveness. RESULTS: We identified 201 eligible trials. Compared with China, trials from the USA/Canada (ratio of odds ratio, 1.89; 95% confidence interval, 1.45-2.45) and Europe/Australia/New Zealand (1.67; 1.29-2.18) had an 89% and 67% higher odds ratio, respectively, suggesting reduced effectiveness. The effectiveness was enhanced when the incidence of postoperative delirium increased (0.85; 0.79-0.92, per 10% increase). Trials with concerns related to deviations from intended interventions reported increased effectiveness compared with those at low risk (0.69; 0.53-0.90). Compared with usual care, certain interventions appeared to have reduced the incidence of postoperative delirium in low-risk trials with low-to-moderate certainty of evidence. However, these findings should be considered inconclusive because of challenges in grouping heterogeneous interventions, the limited number of eligible trials, the prevalence of small-scale studies, and potential publication bias. CONCLUSIONS: The effectiveness of postoperative delirium trials varied based on the region of trial origin, the incidence of delirium, and the risk of bias. The limitations caution against drawing definitive conclusions from different bodies of evidence. These findings highlight the imperative need to improve the quality of research on a global scale. SYSTEMATIC REVIEW PROTOCOL: PROSPERO (CRD42023413984).

Evaluation of preoperative difficult airway prediction methods for adult patients without obvious airway abnormalities: a systematic review and meta-analysis.

BACKGROUND: This systematic review aims to assist clinical decision-making in selecting appropriate preoperative prediction methods for difficult tracheal intubation by identifying and synthesizing literature on these methods in adult patients undergoing all types of surgery. METHODS: A systematic review and meta-analysis were conducted following PRISMA guidelines. Comprehensive electronic searches across multiple databases were completed on March 28, 2023. Two researchers independently screened, selected studies, and extracted data. A total of 227 articles representing 526 studies were included and evaluated for bias using the QUADAS-2 tool. Meta-Disc software computed pooled sensitivity (SEN), specificity (SPC), positive likelihood ratio (PLR), negative likelihood ratio (NLR), and diagnostic odds ratio (DOR). Heterogeneity was assessed using the Spearman correlation coefficient, Cochran's-Q, and I2 index, with meta-regression exploring sources of heterogeneity. Publication bias was evaluated using Deeks' funnel plot. RESULTS: Out of 2906 articles retrieved, 227 met the inclusion criteria, encompassing a total of 686,089 patients. The review examined 11 methods for predicting difficult tracheal intubation, categorized into physical examination, multivariate scoring system, and imaging test. The modified Mallampati test (MMT) showed a SEN of 0.39 and SPC of 0.86, while the thyromental distance (TMD) had a SEN of 0.38 and SPC of 0.83. The upper lip bite test (ULBT) presented a SEN of 0.52 and SPC of 0.84. Multivariate scoring systems like LEMON and Wilson's risk score demonstrated moderate sensitivity and specificity. Imaging tests, particularly ultrasound-based methods such as the distance from the skin to the epiglottis (US-DSE), exhibited higher sensitivity (0.80) and specificity (0.77). Significant heterogeneity was identified across studies, influenced by factors such as sample size and study design. CONCLUSION: No single preoperative prediction method shows clear superiority for predicting difficult tracheal intubation. The evidence supports a combined approach using multiple methods tailored to specific patient demographics and clinical contexts. Future research should focus on integrating advanced technologies like artificial intelligence and deep learning to improve predictive models. Standardizing testing procedures and establishing clear cut-off values are essential for enhancing prediction reliability and accuracy. Implementing a multi-modal predictive approach may reduce unanticipated difficult intubations, improving patient safety and outcomes.

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.

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.

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.

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.

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.

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.

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.

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.

[Progress on perioperative monitoring of cerebral blood flow autoregulation].

Cerebral blood flow autoregulation is physiologically protective mechanism to maintain the stability of cerebral blood flow. Once autoregulation is impaired, the cerebral blood flow fluctuates with blood pressure, leading to the risk of brain ischemia or cerebral hyperemia. Multiple research results indicate that cerebral blood flow can be monitored indirectly and continuously with transcranial Doppler, near infrared spectroscopy or ICP. The correlation coefficient calculated by the surrogate for cerebral blood flow and blood pressure is used to judge cerebral blood flow autoregulation. When the correlation coefficient is close to 1, cerebral blood flow will be passively fluctuated by blood pressure, indicating autoregulation is impaired. When the coefficient is less than 0, cerebral blood flow will not be changed with blood pressure, indicating autoregulaiton is intact. The status of autoregualtion is closely associated with mortality or poor neurological outcomes in patients with cardiac surgery underwent cardiopulmonary bypass, liver transplantation patients or patients with deep trendelenburg position for long time or beach chair position. Continuous monitoring of cerebral blood flow autoregulation can identify the lower or the upper limit of autoregulation, and provide information to individualize the perioperative management of blood pressure.

Probenecid protects against transient focal cerebral ischemic injury by inhibiting HMGB1 release and attenuating AQP4 expression in mice.

Stroke results in inflammation, brain edema, and neuronal death. However, effective neuroprotectants are not available. Recent studies have shown that high mobility group box-1 (HMGB1), a proinflammatory cytokine, contributes to ischemic brain injury. Aquaporin 4 (AQP4), a water channel protein, is considered to play a pivotal role in ischemia-induced brain edema. More recently, studies have shown that pannexin 1 channels are involved in cerebral ischemic injury and the cellular inflammatory response. Here, we examined whether the pannexin 1 channel inhibitor probenecid could reduce focal ischemic brain injury by inhibiting cerebral inflammation and edema. Transient focal ischemia was induced in C57BL/6J mice by middle cerebral artery occlusion (MCAO) for 1 h. Infarct volume, neurological score and cerebral water content were evaluated 48 h after MCAO. Immunostaining, western blot analysis and ELISA were used to assess the effects of probenecid on the cellular inflammatory response, HMGB1 release and AQP4 expression. Administration of probenecid reduced infarct size, decreased cerebral water content, inhibited neuronal death, and reduced inflammation in the brain 48 h after stroke. In addition, HMGB1 release from neurons was significantly diminished and serum HMGB1 levels were substantially reduced following probenecid treatment. Moreover, AQP4 protein expression was downregulated in the cortical penumbra following post-stroke treatment with probenecid. These results suggest that probenecid, a powerful pannexin 1 channel inhibitor, protects against ischemic brain injury by inhibiting cerebral inflammation and edema.

Blood pressure excursions below the cerebral autoregulation threshold during cardiac surgery are associated with acute kidney injury.

OBJECTIVES: To determine whether mean arterial blood pressure excursions below the lower limit of cerebral blood flow autoregulation during cardiopulmonary bypass are associated with acute kidney injury after surgery. SETTING: Tertiary care medical center. PATIENTS: Four hundred ten patients undergoing cardiac surgery with cardiopulmonary bypass. DESIGN: Prospective observational study. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Autoregulation was monitored during cardiopulmonary bypass by calculating a continuous, moving Pearson's correlation coefficient between mean arterial blood pressure and processed near-infrared spectroscopy signals to generate the variable cerebral oximetry index. When mean arterial blood pressure is below the lower limit of autoregulation, cerebral oximetry index approaches 1, because cerebral blood flow is pressure passive. An identifiable lower limit of autoregulation was ascertained in 348 patients. Based on the RIFLE criteria (Risk, Injury, Failure, Loss of kidney function, End-stage renal disease), acute kidney injury developed within 7 days of surgery in 121 (34.8%) of these patients. Although the average mean arterial blood pressure during cardiopulmonary bypass did not differ, the mean arterial blood pressure at the limit of autoregulation and the duration and degree to which mean arterial blood pressure was below the autoregulation threshold (mm Hg × min/hr of cardiopulmonary bypass) were both higher in patients with acute kidney injury than in those without acute kidney injury. Excursions of mean arterial blood pressure below the lower limit of autoregulation (relative risk 1.02; 95% confidence interval 1.01 to 1.03; p < 0.0001) and diabetes (relative risk 1.78; 95% confidence interval 1.27 to 2.50; p = 0.001) were independently associated with for acute kidney injury. CONCLUSIONS: Excursions of mean arterial blood pressure below the limit of autoregulation and not absolute mean arterial blood pressure are independently associated with for acute kidney injury. Monitoring cerebral oximetry index may provide a novel method for precisely guiding mean arterial blood pressure targets during cardiopulmonary bypass.

Validation of a stand-alone near-infrared spectroscopy system for monitoring cerebral autoregulation during cardiac surgery.

BACKGROUND: Individualizing arterial blood pressure (ABP) targets during cardiopulmonary bypass (CPB) based on cerebral blood flow (CBF) autoregulation monitoring may provide a more effective means for preventing cerebral hypoperfusion than the current standard of care. Autoregulation can be monitored in real time with transcranial Doppler (TCD). We have previously demonstrated that near-infrared spectroscopy (NIRS)-derived regional cerebral oxygen saturation (rS(c)O(2)) provides a clinically suitable surrogate of CBF for autoregulation monitoring. The purpose of this study was to determine the accuracy of a stand-alone "plug-and-play" investigational system for autoregulation monitoring that uses a commercially available NIRS monitor with TCD methods. METHODS: TCD monitoring of middle cerebral artery CBF velocity and NIRS monitoring were performed in 70 patients during CPB. Indices of autoregulation were computed by both a personal computer-based system and an investigational prototype NIRS-based monitor. A moving linear correlation coefficient between slow waves of ABP and CBF velocity (mean velocity index [Mx]) and between ABP and rS(c)O(2) (cerebral oximetry index [COx]) were calculated. When CBF is autoregulated, there is no correlation between CBF and ABP; when CBF is dysregulated, Mx and COx approach 1 (i.e., CBF and ABP are correlated). Linear regression and bias analysis were performed between time-averaged values of Mx and COx derived from the personal computer-based system and from COx measured with the prototype monitor. Values for Mx and COx were categorized in 5 mm Hg bins of ABP for each patient. The lower limit of CBF autoregulation was defined as the ABP where Mx incrementally increased to ≥0.4. RESULTS: There was correlation and good agreement between COx derived from the prototype monitor and Mx (r = 0.510; 95% confidence interval, 0.414-0.595; P < 0.001; bias, -0.07 ± 0.19). The correlation and bias between the personal computer-based COx and the COx from the prototype NIRS monitor were r = 0.957 (95% confidence interval, 0.945-0.966; P < 0.001 and 0.06 ± 0.06, respectively). The average ABP at the lower limit of autoregulation was 63 ± 11 mm Hg (95% prediction interval, 52-74 mm Hg). Although the mean ABP at the COx-determined lower limit of autoregulation determined with the prototype monitor was statistically different from that determined by Mx (59 ± 9 mm Hg; 95% prediction interval, 50-68 mm Hg; P = 0.026), the difference was not likely clinically meaningful. CONCLUSIONS: Monitoring CBF autoregulation with an investigational stand-alone NIRS monitor is correlated and in good agreement with TCD-based methods. The availability of such a device would allow widespread autoregulation monitoring as a means of individualizing ABP targets during CPB.

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.

Continuous cerebral blood flow autoregulation monitoring in patients undergoing liver transplantation.

BACKGROUND: Clinical monitoring of cerebral blood flow (CBF) autoregulation in patients undergoing liver transplantation may provide a means for optimizing blood pressure to reduce the risk of brain injury. The purpose of this pilot project is to test the feasibility of autoregulation monitoring with transcranial Doppler (TCD) and near-infrared spectroscopy (NIRS) in patients undergoing liver transplantation and to assess changes that may occur perioperatively. METHODS: We performed a prospective observational study in 9 consecutive patients undergoing orthotopic liver transplantation. Patients were monitored with TCD and NIRS. A continuous Pearson's correlation coefficient was calculated between mean arterial pressure (MAP) and CBF velocity and between MAP and NIRS data, rendering the variables mean velocity index (Mx) and cerebral oximetry index (COx), respectively. Both Mx and COx were averaged and compared during the dissection phase, anhepatic phase, first 30 min of reperfusion, and remaining reperfusion phase. Impaired autoregulation was defined as Mx ≥ 0.4. RESULTS: Autoregulation was impaired in one patient during all phases of surgery, in two patients during the anhepatic phase, and in one patient during reperfusion. Impaired autoregulation was associated with a MELD score >15 (p = 0.015) and postoperative seizures or stroke (p < 0.0001). Analysis of Mx categorized in 5 mmHg bins revealed that MAP at the lower limit of autoregulation (MAP when Mx increased to ≥ 0.4) ranged between 40 and 85 mmHg. Average Mx and average COx were significantly correlated (p = 0.0029). The relationship between COx and Mx remained when only patients with bilirubin >1.2 mg/dL were evaluated (p = 0.0419). There was no correlation between COx and baseline bilirubin (p = 0.2562) but MELD score and COx were correlated (p = 0.0458). Average COx was higher for patients with a MELD score >15 (p = 0.073) and for patients with a neurologic complication than for patients without neurologic complications (p = 0.0245). CONCLUSIONS: These results suggest that autoregulation is impaired in patients undergoing liver transplantation, even in the absence of acute, fulminant liver failure. Identification of patients at risk for neurologic complications after surgery may allow for prompt neuroprotective interventions, including directed pressure management.

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.

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.