Zinc regulation of chlorophyll fluorescence and carbohydrate metabolism in saline-sodic stressed rice seedlings.

Saline-sodic stress can limit the absorption of available zinc in rice, subsequently impacting the normal photosynthesis and carbohydrate metabolism of rice plants. To investigate the impact of exogenous zinc application on photosynthesis and carbohydrate metabolism in rice grown in saline-sodic soil, this study simulated saline-sodic stress conditions using two rice varieties, 'Changbai 9' and 'Tonghe 899', as experimental materials. Rice seedlings at 4 weeks of age underwent various treatments including control (CT), 2 µmol·L-1 zinc treatment alone (Z), 50 mmol·L-1 saline-sodic treatment (S), and 50 mmol·L-1 saline-sodic treatment with 2 µmol·L-1 zinc (Z + S). We utilized JIP-test to analyze the variations in excitation fluorescence and MR820 signal in rice leaves resulting from zinc supplementation under saline-sodic stress, and examined the impact of zinc supplementation on carbohydrate metabolism in both rice leaves and roots under saline-sodic stress. Research shows that zinc increased the chloroplast pigment content, specific energy flow, quantum yield, and performance of active PSII reaction centers (PIABS), as well as the oxidation (VOX) and reduction rate (Vred) of PSI in rice leaves under saline-sodic stress. Additionally, it decreased the relative variable fluorescence (WK and VJ) and quantum energy dissipation yield (φDO) of the rice. Meanwhile, zinc application can reduce the content of soluble sugars and starch in rice leaves and increasing the starch content in the roots. Therefore, the addition of zinc promotes electron and energy transfer in the rice photosystem under saline-sodic stress. It enhances rice carbohydrate metabolism, improving the rice plants' ability to withstand saline-sodic stress and ultimately promoting rice growth and development.

Chronic Alcohol Exposure Alters the Levels and Assembly of the Actin Cytoskeleton and Microtubules in the Adult Mouse Hippocampus.

BACKGROUND: Alcohol abuse, a prevalent global health issue, is associated with the onset of cognitive impairment and neurodegeneration. Actin filaments (F-actin) and microtubules (MTs) polymerized from monomeric globular actin (G-actin) and tubulin form the structural basis of the neuronal cytoskeleton. Precise regulation of the assembly and disassembly of these cytoskeletal proteins, and their dynamic balance, play a pivotal role in regulating neuronal morphology and function. Nevertheless, the effect of prolonged alcohol exposure on cytoskeleton dynamics is not fully understood. This study investigates the chronic effects of alcohol on cognitive ability, neuronal morphology and cytoskeleton dynamics in the mouse hippocampus. METHODS: Mice were provided ad libitum access to 5% (v/v) alcohol in drinking water and were intragastrically administered 30% (v/v, 6.0 g/kg/day) alcohol for six weeks during adulthood. Cognitive functions were then evaluated using the Y maze, novel object recognition and Morris water maze tests. Hippocampal histomorphology was assessed through hematoxylin-eosin (HE) and Nissl staining. The polymerized and depolymerized states of actin cytoskeleton and microtubules were separated using two commercial assay kits and quantified by Western blot analysis. RESULTS: Mice chronically exposed to alcohol exhibited significant deficits in spatial and recognition memory as evidenced by behavioral tests. Histological analysis revealed notable hippocampal damage and neuronal loss. Decreased ratios of F-actin/G-actin and MT/tubulin, along with reduced levels of polymerized F-actin and MTs, were found in the hippocampus of alcohol-treated mice. CONCLUSIONS: Our findings suggest that chronic alcohol consumption disrupted the assembly of the actin cytoskeleton and MTs in the hippocampus, potentially contributing to the cognitive deficits and pathological injury induced by chronic alcohol intoxication.

Intestinal Flora Dysbiosis Aggravates Cognitive Dysfunction Associated With Neuroinflammation in Heart Failure.

BACKGROUND: Cognitive dysfunction after heart failure (HF) is characterized by neuroinflammation, which plays an important role in the occurrence and development of cognitive dysfunction. Recent studies have shown that an intestinal flora imbalance may also trigger neuroinflammation in Alzheimer's disease. The present study was designed to reveal that intestinal flora dysbiosis caused by HF aggravates neuroinflammation-associated cognitive impairment. METHODS AND RESULTS: Adult male Sprague-Dawley rats were fed daily for 2 weeks with probiotics or placebo until the day of surgery. HF was then triggered by 8 weeks of sustained coronary artery occlusion. 16S rDNA sequencing was used to confirm intestinal flora dysbiosis after HF and demonstrate that the changes paralleled intestinal pathology scores. The permeability of the blood-brain barrier was increased after HF, and such an increase in permeability may increase the levels of inflammatory cytokines caused by intestinal flora disorders. The changes in the intestinal flora caused by probiotics significantly reduced the level of neuroinflammation. In addition, probiotic administration considerably improved the impaired spatial memory in HF rats. CONCLUSIONS: We conclude that intestinal flora dysbiosis plays a potential role in aggravating the impaired cognition associated with neuroinflammation and that these effects may be attenuated by probiotics.

Neural network disturbance in the medial prefrontal cortex might contribute to cognitive impairments induced by neuroinflammation.

Neuroinflammation plays a key role in the progression of many neurodegenerative diseases, yet the underlying mechanism remains largely unexplored. Using an animal model of neuroinflammation induced by repeated lipopolysaccharide (LPS) injections, we found selectively reduced expression of parvalbumin (PV) but not somatostatin (SST) in the medial prefrontal cortex (mPFC). The reduced PV expression resulted in decreased intensities of vesicular GABA transporter and PV buttons, suggesting disinhibition in the mPFC. These further induced abnormal mPFC neural activities and consequently contributed to cognitive impairments. In addition, gamma oscillations supported by PV interneuron function were positively associated with time spent with the novel object in the novel object recognition test. Notably, down-regulation of neuroinflammation by microglia inhibitor minocycline or boosting gamma oscillations by dopamine 4 receptor agonist RO-10-5824 improved cognitive performance. In conclusion, our study proposes neural network disturbance as a likely mechanistic linker between neuroinflammation and cognitive impairments in neurodegeneration and possibly other psychiatric disorders.

Trained Innate Immunity by Repeated Low-Dose Lipopolysaccharide Injections Displays Long-Term Neuroprotective Effects.

Disrupted immune response is an important feature of many neurodegenerative conditions, including sepsis-associated cognitive impairment. Accumulating evidence has demonstrated that immune memory occurs in microglia, which has a significant impact on pathological hallmarks of neurological diseases. However, it remains unclear whether immune memory can cause subsequent alterations in the brain immune response and affect neurobehavioral outcomes in sepsis survivors. In the present study, mice received daily intraperitoneal injection of low-dose lipopolysaccharide (LPS, 0.1 mg/kg) for three consecutive days to induce immune memory (immune tolerance) and then were subjected to sham operation or cecal ligation and puncture (CLP) 9 months later, followed by a battery of neurobehavioral and biochemical studies. Here, we showed that repeated low-dose LPS injection-induced immune memory protected mice from sepsis-induced cognitive and affective impairments, which were accompanied by significantly decreased brain proinflammatory cytokines and immune response. In conclusion, our study suggests that modulation of brain immune responses by repeated LPS injections confers neuroprotective effects by preventing overactivated immune response in response to subsequent septic insult.

Propofol Prevents Oxidative Stress by Decreasing the Ischemic Accumulation of Succinate in Focal Cerebral Ischemia-Reperfusion Injury.

Oxidative stress caused by mitochondrial dysfunction during reperfusion is a key pathogenic mechanism in cerebral ischemia-reperfusion (IR) injury. Propofol (2,6-diisopropylphenol) has been proven to attenuate mitochondrial dysfunction and reperfusion injury. The current study reveals that propofol decreases oxidative stress injury by preventing succinate accumulation in focal cerebral IR injury. We evaluated whether propofol could attenuate ischemic accumulation of succinate in transient middle cerebral artery occlusion in vivo. By isolating mitochondria from cortical tissue, we also examined the in vitro effects of propofol on succinate dehydrogenase (SDH) activity and various mitochondrial bioenergetic parameters related to oxidative stress injury, such as the production of reactive oxidative species, membrane potential, Ca2+-induced mitochondrial swelling, and morphology via electron microscopy. Propofol significantly decreased the ischemic accumulation of succinate by inhibiting SDH activity and inhibited the oxidation of succinate in mitochondria. Propofol can decrease membrane potential in normal mitochondria but not in ischemic mitochondria. Propofol prevents Ca2+-induced mitochondrial swelling and ultrastructural changes to mitochondria. The protective effect of propofol appears to act, at least in part, by limiting oxidative stress injury by preventing the ischemic accumulation of succinate.

A method for addressing right upper lobe obstruction with right-sided double-lumen endobronchial tubes during surgery: a randomized controlled trial.

BACKGROUND: A right-sided double-lumen tube (R-DLT) tends to obstruct the right upper lobe intraoperatively due to anatomical distortion during surgery. If the R-DLT is poorly matched with the patient's airway anatomy, it will not be possible to correctly replace the tube with a fiberoptic bronchoscope (FOB). In our study, we aimed to explore an efficient method for difficult repositioning caused by right upper lobe occlusion during surgery: repositioning the R-DLT from the right main bronchus into the left main bronchus. The current study was designed to assess the efficacy and safety of this method. METHODS: Sixty adult patients scheduled to undergo left-sided thoracic surgery were randomly assigned to two groups. With the patient in the right lateral position during surgery, the R-DLT was pulled back to the trachea while being rotated 90° clockwise; it was then either rotated 90° clockwise for placement into the left main bronchus (Group L) or rotated 90° anticlockwise and returned to the right main bronchus (Group R) using FOB guidance. The primary outcomes included clinical performance, which was measured by intubation time, and the quality of lung collapse. A secondary outcome was safety, which was determined according to bronchial injury and vocal cord injury. RESULTS: The median intubation time (IQR [range]) required for placement of a R-DLT into the left main bronchus was shorter than the time required for placement into the right main bronchus (15.0 s [IQR, 12.0 to 20.0 s]) vs 23.5 s [IQR, 14.5 to 65.8 s], P = 0.005). The groups showed comparable overall results for the quality of lung collapse during the total period of one-lung ventilation (P = 1.000). The numbers of patients with bronchial injuries or vocal cord injuries were also comparable between groups (Group R, 11/30 vs. Group L 8/30, P = 0.580 for bronchus injuries; Group R, 15/30 vs. Group L 13/30, P = 0.796 for vocal cord injuries). CONCLUSIONS: Repositioning a R-DLT from the right main bronchus into the left main bronchus had good clinical performance without causing additional injury. This may be an efficient method for the difficult repositioning of a R-DLT due to right upper lobe occlusion during surgery. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-IPR-15006933 , registered on 15 August 2015.

Optimal control analysis of a tuberculosis model.

In this paper, we extend the model of Liu and Zhang (Math Comput Model 54:836-845, 2011) by incorporating three control terms and apply optimal control theory to the resulting model. Optimal control strategies are proposed to minimize both the disease burden and the intervention cost. We prove the existence and uniqueness of optimal control paths and obtain these optimal paths analytically using Pontryagin's Maximum Principle. We analyse our results numerically to compare various strategies of proposed controls. It is observed that implementation of three controls is most effective and less expensive among all the strategies. Thus, we conclude that in order to reduce tuberculosis threat all the three controls must be taken into consideration concurrently.

Fasudil alleviates alcohol-induced cognitive deficits and hippocampal morphology injury partly by altering the assembly of the actin cytoskeleton and microtubules.

Alcohol-Related Brain Damage (ARBD) manifests predominantly as cognitive impairment and brain atrophy with the hippocampus showing particular vulnerability. Fasudil, a Rho kinase (ROCK) inhibitor, has established neuroprotective properties; however, its impact on alcohol-induced cognitive dysfunction and hippocampal structural damage remains unelucidated. This study probes Fasudil's neuroprotective potential and identifies its mechanism of action in an in vivo context. Male C57BL/6 J mice were exposed to 30% (v/v, 6.0 g/kg) ethanol by intragastric administration for four weeks. Concurrently, these mice received a co-treatment with Fasudil through intraperitoneal injections at a dosage of 10 mg/kg/day. Fasudil was found to mitigate alcohol-induced spatial and recognition memory deficits, which were quantified using Y maze, Morris water maze, and novel object recognition tests. Concurrently, Fasudil attenuated hippocampal structural damage prompted by chronic alcohol exposure. Notably, Fasudil moderated alcohol-induced disassembly of the actin cytoskeleton and microtubules-mechanisms central to the maintenance of hippocampal synaptic integrity. Collectively, our findings indicate that Fasudil partially reverses alcohol-induced cognitive and morphological detriments by modulating cytoskeletal dynamics, offering insights into potential therapeutic strategies for ARBD.

Memantine alleviates cognitive impairment and hippocampal morphology injury in a mouse model of chronic alcohol exposure.

Alcohol-related cognitive impairment (ARCI) is highly prevalent among patients with alcohol abuse and dependence. The pathophysiology of ARCI, pivotal for refined therapeutic approaches, is not fully elucidated, posing a risk of progression to severe neurological sequelae such as Korsakoff's syndrome (KS) and Alcohol-Related Dementia (ARD). This study ventures into the underlying mechanisms of chronic alcohol-induced neurotoxicity, notably glutamate excitotoxicity and cytoskeletal disruption, and explores the therapeutic potential of Memantine, a non-competitive antagonist of the N-methyl-d-aspartate (NMDA) receptor known for its neuroprotective effect against excitotoxicity. Our investigation centers on the efficacy of Memantine in mitigating chronic alcohol-induced cognitive and hippocampal damages in vivo. Male C57BL/6J mice were subjected to 30 % (v/v, 6.0 g/kg) ethanol via intragastric administration alongside Memantine co-treatment (10 mg/kg/day, intraperitoneally) for six weeks. The assessment involved Y maze, Morris water maze, and novel object recognition tests to evaluate spatial and recognition memory deficits. Histopathological evaluations of the hippocampus were conducted to examine the extent of alcohol-induced morphological changes and the potential protective effect of Memantine. The findings reveal that Memantine significantly improves chronic alcohol-compromised cognitive functions and mitigates hippocampal pathological changes, implicating a moderating effect on the disassembly of actin cytoskeleton and microtubules in the hippocampus, induced by chronic alcohol exposure. Our results underscore Memantine's capability to attenuate chronic alcohol-induced cognitive and hippocampal morphological harm may partly through regulating cytoskeleton dynamics, offering valuable insights into innovative therapeutic strategies for ARCI.

Experimental study on a new radioactive probe for the treatment of lacrimal duct stenosis.

Our aim was to study the treatment effect of a radioactive probe on lacrimal duct stenosis. We applied experimentally in 30 inbred white rabbits a lacrimal duct stenosis model and the rabbits were randomly divided into 3 groups: the stenosis group, the surgery group and the radioactive probe group. We also separated a blank control group of 5 rabbits. Rabbits in the surgery group and the radioactive probe group were examined by digital subtraction angiography (DSA) 10 min and 30 d after treatment before being sacrificed. Rabbits in the stenosis group and the control group were examined by DSA 60 min before they were sacrificed. Specimens of the lacrimal ducts at the stenosis site were collected immediately after the rabbits were sacrificed. Morphological changes were observed through haematoxyline-eosin staining, while lumen areas of lacrimal duct were observed through computer based photo analysis. For the surgery and the radioactive probe group, stenosis cure rates were 100% 10 min after treatment. Thirty days after treatment, the rates of stenosis were 40% and 5% for the above groups, respectively. Morphological observations showed that each layer of the lacrimal duct wall in the stenosis group became thicker with higher proliferation of cells. Each layer of the lacrimal duct wall in the surgery group was thinner than in the stenosis group; however, the extent of cell profileration was similar. In the radiation treatment group, the interstitial layers of the lacrimal duct epithelium, elastin and collagen fibers and other connective tissue components were thinner than in the surgery group. Cells proliferation was significantly weakened in the radiation treatment than in the stenosis and in the surgery groups. The average areas of lacrimal duct in the control, stenosis, surgery and the radioactive probe groups of the examined sites, were: 0.84±0.28 mm2, 0.26±0.13 mm2, 0.55±0.31 mm2 and 0.80±0.36 mm2, respectively. In conclusion, the radioactive lacrimal duct probe showed distinct therapeutic effects in curing lacrimal duct stenosis and in preventing restenosis after the operation.

Sevoflurane Preconditioning Alleviates Posttraumatic Stress Disorder-Induced Apoptosis in the Hippocampus via the EZH2-Regulated Akt/mTOR Axis and Improves Synaptic Plasticity.

Posttraumatic stress disorder (PTSD) is a persistent and severe psychological and mental disorder resulting from experiences of serious trauma or stress and is suffered by many individuals. Previous studies have shown that pretreatment with sevoflurane is efficient in reducing the incidence of PTSD. However, we require a more comprehensive understanding of the specific mechanisms by which sevoflurane works. Enhancer of zeste homolog 2 (EZH2) has been reported to be regulated by sevoflurane, and to improve patient cognition. In this study, we aimed to explore the mechanisms of sevoflurane and the role of EZH2 in PTSD cases. We explored the effects of sevoflurane and EPZ-6438 (inhibitor of EZH2) on rat behavior, followed by an investigation of EZH2 mRNA and protein expression. The effects of sevoflurane and EZH2 on neuronal survival were assessed by western blotting and TUNEL staining, while western blotting was used to examine the expression of PSD95 and the AKT/mTOR proteins. Sevoflurane preconditioning restored EZH2 expression and significantly inhibited apoptosis by regulating phosphorylation of the AKT/mTOR pathway. Synaptic plasticity was also significantly improved. These results suggest that pretreatment with sevoflurane could play an important role in PTSD prevention by regulating EZH2 expression.

Intraoperative Low-Dose S-Ketamine Reduces Depressive Symptoms in Patients with Crohn's Disease Undergoing Bowel Resection: A Randomized Controlled Trial.

Background: Patients with Crohn's disease (CD) undergoing bowel resection often suffer from depression and acute pain, which severely impairs their recovery. We aimed to investigate the effects of S-ketamine preconditioning on postoperative depression in patients with CD undergoing a bowel resection with mild to moderate depression and to observe whether it can relieve postoperative pain and anti-inflammation. Methods: A total of 124 adult patients were randomized into one of the two groups. Patients in the S-ketamine group received a 0.25 mg/kg S-ketamine intravenous drip under general anesthesia induction, followed by a continuous infusion of S-ketamine with 0.12 mg/kg/h for more than 30 min through target-controlled infusion. Patients in the placebo group received 0.9% saline at an identical volume and rate. The primary outcome measure was the 17-item Hamilton depression Scale (HAMD-17). The secondary outcomes were scores on the following questionnaires: a nine-item patient health questionnaire (PHQ-9); a quality of recovery (QoR-15) form; and a numeric rating scale (NRS). Additional secondary outcomes included the levels of C-reactive protein (CRP) and interleukin 6 (IL-6) on postoperative days (PODs) 1, 3, and 5, the length of hospital stay, and opioid use throughout the hospital stay. Results: The scores of PHQ-9 and HAMD-17 in the S-ketamine group were lower than those in the placebo group on postoperative days (PODs) 1, 2, and 7 (p < 0.05). The scores of QoR-15 in the S-ketamine group were higher than those in the placebo group on postoperative days (PODs) 3 and 5 (p < 0.05). The NRS scores of PACU, postoperative days 1 and 2 in the S-ketamine group were lower than those in the placebo group (p < 0.05). There was no significant difference in the CRP and IL-6 levels on postoperative days (PODs) 1, 3, and 5, postoperative complications, and hospital stay between the two groups (p > 0.05). Conclusions: The trial indicated that the intraoperative administration of low-dose S-ketamine could alleviate mild-to-moderate depressive symptoms and postoperative pain in patients with Crohn's disease undergoing bowel resection without worsening their safety.

[Effects of dexmedetomidine combined with fentanyl in patients undergoing anesthesia induction by sevoflurane].

OBJECTIVE: To investigate the effects of dexmedetomidine combined with fentanyl in patients undergoing anesthesia induction by sevoflurane. METHOD: Eighty patients for elective endotracheal intubation under general anesthesia operations were randomly and double-blindly divided into Dex combined with fentanyl group (Group DF) and the fentanyl group (Group F) from April 2011 to September 2011 at the Fourth Affiliated Hospital of Harbin Medical University, and there were 40 cases in each group. The investigation was approved by all the patients and by the Ethics Committee of the hospital. In group DF, each patient was pumped in the 0.5 µg/kg Dex by vein before 10 minutes of anesthesia induction and group F were given the same amount of normal saline, and tidal volume method was used to induce anesthesia of sevoflurane. All the patients were given 2 µg/kg fentanyl and 0.1 mg/kg vecuronium by tracheal intubation and the MAP and HR and adverse reactions were observed before anesthesia induction (T(0)), before endotracheal intubation (T(1)), at the moment of tracheal intubation (T(2)), after 1 minutes of tracheal intubation (T(3)), after 3 minutes of tracheal intubation (T(4)) and after 5 minutes of tracheal intubation (T(5)). RESULT: The loss of eyelash reflex time of group DF is shorter (P < 0.05), adverse reaction is less (P < 0.05) and the number of adding atropine case is higher than that of group F (P < 0.05), the MAP of the two groups after induction of other moments are lower than that of T(0) (P < 0.05); MAP of group F at T(1) is lower than that of T(0), T(2), T(3) and group DF (P < 0.05); T(1) of group DF is lower than that of T(0) (P < 0.05), the HR after induction of group DF is lower than that of T(0) and F group (P < 0.05), and that of T(2) and T(4) are higher than that of T(1) (P < 0.05); HR of group F at T(1) is lower than that of T(2) and T(3) (P < 0.05). CONCLUSION: Dexmedetomidine in combination with fentanyl can inhibit stress response of tracheal intubation of sevoflurane induction efficiently and stabilize hemodynamics.

Effect of different concentrations of foliar iron fertilizer on chlorophyll fluorescence characteristics of iron-deficient rice seedlings under saline sodic conditions.

The effectiveness of iron is reduced in saline conditions, which can easily lead to iron deficiency and inhibit photosynthesis in rice. In this study, 4-week-old Fe-deficient rice seedlings were treated under saline sodic stress (50 mM) to different concentrations (0, 0.2%, 0.4%, 0.8%, 1.6%, and 3.2%) of foliar iron fertilizer (FeEDDHA). Differences in prompting fluorescence and the MR820 signal of rice leaves after 7 days of treatment were probed using the JIP-test. The results show that the performances of the two rice varieties were in general agreement. Under iron deficiency and soda salinity stress conditions, rice growth was inhibited, and the pigment content, specific energy flux, quantum yield, performance of the active PSII reaction center (PIABS) and the oxidation (Vox) and reduction rates (Vred) of PSI were reduced. These indicators first increase and then decrease with increasing iron fertiliser concentrations. The best results were obtained with the Fe3 treatment (0.8%). Fluorescence parameters such as the relative variable fluorescence (WK and VJ) and the quantum yield of energy dissipation (φDo) showed opposite trends. This suggests that iron deficiency/excess and soda saline stress disrupt the electron and energy transport in the photosystem. Appropriate iron fertilization concentration can repair the photosynthetic electron transport chain, improve electron transport efficiency and promote balanced energy distribution. Therefore, we suggest that moderate amounts of Fe are beneficial for improving the electron and energy transport properties of the photosystem, while spraying high concentrations of Fe fertilizer has a negative effect on improving salt tolerance in rice.

Pharmacophore-based design, synthesis, and biological evaluation of novel chloro-pyridazine piperazines as human rhinovirus (HRV-3) inhibitors.

A series of chloro-pyridazine piperazines were developed based on the structure of human rhinovirus (HRV) capsid-binding inhibitors with proven activity using a pharmacophore model. A preliminary evaluation demonstrated potent activity against HRV-3 with low cytotoxicity. A docking analysis indicated that 8a could fit into, and form tight interactions (e.g., H-bonds, σ-π effect) with the active site in VP1.

Existence of traveling wave solutions for a delayed nonlocal dispersal SIR epidemic model with the critical wave speed.

This paper is about the existence of traveling wave solutions for a delayed nonlocal dispersal SIR epidemic model with the critical wave speed. Because of the introduction of nonlocal dispersal and the generality of incidence function, it is difficult to investigate the existence of critical traveling waves. To this end, we construct an auxiliary system and show the existence of traveling waves for the auxiliary system. Employing the results for the auxiliary system, we obtain the existence of traveling waves for the delayed nonlocal dispersal SIR epidemic model with the critical wave speed under mild conditions.

Probiotics alleviate cognitive dysfunction associated with neuroinflammation in cardiac surgery.

Neuroinflammation plays a key role in the progression and pathogenesis of postoperative cognitive dysfunction, but it does not always occur in the local response to primary injury. In this study, we revealed that probiotics alleviate cognitive dysfunction associated with neuroinflammation in cardiac surgery. Rats were administered a probiotic or placebo once a day by gavage for 2 weeks until the day of surgery. Cardiac surgery was induced by ischemia/reperfusion of the left coronary artery. Key factors, such as the gut microbiome, the gut barrier and the blood-brain barrier (BBB), were systematically investigated to determine whether changes in the gut microbiome lead to neuroinflammation. We used 16S rDNA sequencing to confirm that cardiac surgery induced intestinal flora dysbiosis by altering the number of organisms rather than the structure in the cecum microbiome, which occurs at the same time as damage to the gut barrier. Cardiac surgery also increased BBB permeability, suggesting that disruption of the microbiome may increase the likelihood of neuroinflammation. Probiotics-induced alterations in the intestinal flora significantly reduced the level of inflammatory cytokines (IL-6 and IL-1ß). Importantly, we found that the administration of probiotics significantly improved spatial memory impairment in rats after cardiac surgery, as measured by the Morris water maze. Overall, dysbiosis of the gut flora may aggravate cognitive impairment associated with neuroinflammation after cardiac surgery, and probiotics may attenuate this effect.

Global stability analysis of an SVEIR epidemic model with general incidence rate.

In this paper, a susceptible-vaccinated-exposed-infectious-recovered (SVEIR) epidemic model for an infectious disease that spreads in the host population through horizontal transmission is investigated, assuming that the horizontal transmission is governed by an unspecified function f ( S , I ) . The role that temporary immunity (vaccinated-induced) and treatment of infected people play in the spread of disease, is incorporated in the model. The basic reproduction number R 0 is found, under certain conditions on the incidence rate and treatment function. It is shown that the model exhibits two equilibria, namely, the disease-free equilibrium and the endemic equilibrium. By constructing a suitable Lyapunov function, it is observed that the global asymptotic stability of the disease-free equilibrium depends on R 0 as well as on the treatment rate. If R 0 > 1 , then the endemic equilibrium is globally asymptotically stable with the help of the Li and Muldowney geometric approach applied to four dimensional systems. Numerical simulations are also presented to illustrate our main results.

The effect of melatonin on early postoperative cognitive decline in elderly patients undergoing hip arthroplasty: A randomized controlled trial.

STUDY OBJECTIVE: The purpose of the present study was to investigate whether exogenous melatonin supplementation could ameliorate early postoperative cognitive decline (POCD) in aged patients undergoing hip arthroplasty with spinal anesthesia. DESIGN: Prospective cohort study. SETTING: Department of Anesthesiology, Jinling Hospital, Nanjing University, Nanjing, China. PATIENTS: One hundred and thirty-nine patients with ASA I-III, older than 65yr of age (mean age: 74.5±5.5; gender: male 53 and female 86), scheduled for hip arthroplasty were included in the present study. INTERVENTIONS: Patients were randomized to receive 1mg oral melatonin or placebo daily 1h before bedtime one day before surgery and for another 5 consecutive days postoperatively. MEASUREMENTS: The subject assessment, including Mini-Mental State Examination (MMSE) score, subjective sleep quality, general well-being, postoperative fatigue, and visual analogue scale for pain were evaluated pre-operatively and at days 1, 3, 5, and 7 after surgery. MAIN RESULTS: The MMSE score in the control group decreased significantly after surgery when compared with its own preoperative value or the melatonin group at days 1, 3, and 5. However, the MMSE score in the melatonin group remained unchanged during the 7days of monitoring. In addition, significant postoperative impairments of subjective sleep quality, general well-being, and fatigue were found in the control group when compared with the melatonin group. CONCLUSION: Peroperative melatonin supplementation might improve early POCD, suggesting restoration of normal circadian function with good sleep quality may be one of the key factors in preventing or treating POCD.