Efficacy and safety of intraperitoneal dexamethasone on postoperative nausea and vomiting following laparoscopy: study protocol for a systematic review and meta-analysis.

INTRODUCTION: Intraperitoneal dexamethasone has been reported to be effective to reduce the incidence of postoperative nausea and vomiting (PONV). Therefore, this meta-analysis will analyse the efficacy and safety of intraperitoneal dexamethasone on PONV following laparoscopy. METHODS AND ANALYSIS: Electronic databases (eg, Cochrane Library, PubMed, Excerpta Medica Database, Web of Science, National Institute of Informatics, Oriental Medicine Advanced Searching Integrated System and China National Knowledge Infrastructure) and clinical trial registries will be systematically searched from their inception to 1 October 2022. After the study and data collection processes, we will identify randomised controlled trials that reported details of intraperitoneal dexamethasone on PONV following laparoscopy to conduct a meta-analysis. We will perform the study process and data collection separately. The collected data will be statistically analysed using Review Manager 5.4 software. The risk of bias will be assessed using the Cochrane risk-of-bias tool 2. The Grading of Recommendations Assessment, Development and Evaluation certainty assessment, and a trial sequential analysis will be conducted to ensure the accuracy of this meta-analysis. ETHICS AND DISSEMINATION: Ethical approval and patient consent are not required since this study is a systematic review and meta-analysis. The findings of this meta-analysis will be submitted to a peer-reviewed journal for publication. PROSPERO REGISTRATION NUMBER: CRD42022362924.

Diagnosis and prognosis of serum Fut8 for epilepsy and refractory epilepsy in children.

With adequate serum concentration of antiepileptic drugs, the epilepsy symptoms in many patients still cannot be controlled well. The alteration of glycosyltransferase has obvious influence on the pathogenesis of epilepsy. In this study, we focus on the diagnostic and prognostic value of fucosyltransferase 8 (Fut8) on epilepsy and refractory epilepsy. Serum samples of 199 patients with epilepsy, 59 patients with refractory epilepsy and 22 healthy controls who were diagnosed in Shenzhen Children's hospital from August 2018 to August 2019 were collected. The level of lectins was further analyzed by lectin chip and enzyme linked immunosorbent assay (ELISA). The diagnostic value of serum Fut8 for epilepsy and refractory epilepsy was evaluated by receiver operating characteristic curve. Finally, the difference in the recurrence rate of convulsion in patients with epilepsy or refractory epilepsy within 2 years were observed in different Fut8 expression patients. The concentration of valproic acid (VPA) were significant different between epilepsy and refractory epilepsy group. The expression of α1, 6-fucosylation and Fut8 was significantly increased in the refractory epilepsy group compared with healthy controls. The area under the curve of Fut8 as a biomarker for predicting epilepsy or refractory epilepsy was 0.620 and 0.856, respectively. There was a significant difference in the recurrence rate of convulsion within 2 years in the children with refractory epilepsy (p = 0.0493) not epilepsy (p = 0.1865) between the high and low Fut8 expression groups. Fut8 was one of the effective indicators for the diagnosis and prognosis of refractory epilepsy.

Hypofucosylation of Unc5b regulated by Fut8 enhances macrophage emigration and prevents atherosclerosis.

BACKGROUND: Atherosclerosis (AS) is the leading underlying cause of the majority of clinical cardiovascular events. Retention of foamy macrophages in plaques is the main factor initiating and promoting the atherosclerotic process. Our previous work showed that ox-LDL induced macrophage retention in plaques and that the guidance receptor Uncoordinated-5 homolog B (Unc5b) was involved in this process. However, little is known about the role of Unc5b in regulating macrophage accumulation within plaques. RESULTS: In the present study, we found that Unc5b controls macrophage migration and thus promotes plaque progression in ApoE-/- mice. The immunofluorescence colocalization assay results first suggested that fucosyltransferase 8 (Fut8) might participate in the exacerbation of atherosclerosis. Animals with Unc5b overexpression showed elevated levels of Fut8 and numbers of macrophages and an increased lesion size and intimal thickness. However, these effects were reversed in ApoE-/- mice with Unc5b knockdown. Furthermore, Raw264.7 macrophages with siRNA-mediated silencing of Unc5b or overexpression of Unc5b were used to confirm the regulatory mechanisms of Unc5b and Fut8 in vitro. In response to ox-LDL exposure, Unc5b and Fut8 were both upregulated, and macrophages showed reduced pseudopod formation and migratory capacities. However, these capacities were restored by blocking Unc5b or Fut8. Furthermore, the IP assay indicated that Fut8 regulated the level of α-1,6 fucosylation of Unc5b, which mainly occurs in the endoplasmic reticulum (ER), and genetic deletion of the main fucosylation sites or Fut8 resulted in hypofucosylation of Unc5b. Moreover, the macrophage migration mediated by Unc5b depended on inactivation of the p-CDC42/p-PAK pathway. Conversely, macrophages with Unc5b overexpression displayed activation of the p-CDC42/p-PAK pathway and decreased migration both in vivo and in vitro. CONCLUSION: These results demonstrated that hypofucosylation of Unc5b regulated by Fut8 is positively associated with the delay of the atherosclerotic process by promoting the migration of foamy macrophages. These findings identify a promising therapeutic target for atherosclerosis.

Dexmedetomidine versus remifentanil for controlled hypotension under general anesthesia: A systematic review and meta-analysis.

This meta-analysis aimed to analyze and compare the efficacy and safety of remifentanil and dexmedetomidine applied respectively for controlled hypotension under general anesthesia. We searched the Cochrane Library, PubMed, EMBASE, Web of Science, CNKI, SinoMed, Wanfang, and VIP databases, as well as dissertations and conference papers, to obtain randomized controlled trials comparing remifentanil and dexmedetomidine applied respectively for controlled hypotension before August 23, 2021. The primary outcomes included hemodynamic profiles, surgical field score, and blood loss. Extubation time, sedation and pain score at the PACU, and perioperative adverse events were the secondary outcomes. Nine randomized controlled trials with 543 patients (272 in the dexmedetomidine group and 271 in the remifentanil group) were eventually included. This meta-analysis indicated no significant difference between dexmedetomidine and remifentanil in terms of surgical field score, blood loss, minimum values of mean arterial pressure (MD 0.24 with 95% CI [-1.65, 2.13], P = 0.80, I2 = 66%) and heart rate (MD 0.42 [-1.33, 2.17], P = 0.64, I2 = 40%), sedation scores at the PACU (MD -0.09 [-0.69, 0.50], P = 0.76, I2 = 92%), and incidence of bradycardia (OR 2.24 [0.70, 7.15], P = 0.17, I2 = 0%). Compared with remifentanil, dexmedetomidine as the controlled hypotensive agent showed a lower visual analogue score at the PACU (MD -1.01 [-1.25, -0.77], P<0.00001, I2 = 0%) and incidence of shivering (OR 0.22 [0.08, 0.60], P = 0.003, I2 = 0%), nausea, and vomiting (OR 0.34 [0.13, 0.89], P = 0.03, I2 = 0%). However, extubation time was shorter in the remifentanil group (MD 3.34 [0.75, 5.93], P = 0.01, I2 = 90%). In conclusion, dexmedetomidine and remifentanil are both effective in providing satisfactory controlled hypotension and surgical conditions. Dexmedetomidine is better in easing postoperative pain at the PACU and reducing the occurrence of shivering, nausea, and vomiting. Meanwhile, remifentanil is a fast-track anesthesia with a shorter extubation time. Given the limitations of this meta-analysis, further studies are needed for a more definitive comparison of the efficacy and safety of dexmedetomidine and remifentanil.

High expression of lncRNA PELATON serves as a risk factor for the incidence and prognosis of acute coronary syndrome.

Atherosclerosis is the primary origin of acute coronary syndrome (ACS) diseases. Previous studies have shown that lncRNA plaque-enriched long noncoding RNA in atherosclerotic macrophage regulation (lncRNA PELATON) is a specific lncRNA in macrophage nuclei. This study aims to identify serum lncRNA PELATON as a biomarker for assessing the incidence and prognosis of ACS. Levels of serum lncRNA PELATON were detected by real-time polymerase chain reaction (RT-PCR) in patients with ACS and healthy individuals. The clinical significance of lncRNA PELATON in patients with ACS was assessed by analyzing receiver operating characteristic and survival curves. The serum levels of lncRNA PELATON in patients with ACS were significantly higher than those in healthy individuals. LncRNA PELATON expression was positively correlated with the expression levels of high sensitivity C-reactive protein (hs-CRP), cardiac troponin T (cTnT) and creatine kinase MB (CK-MB) (p < 0.05). LncRNA PELATON can be used as a potential diagnostic index with an AUC of 0.706 for unstable angina pectoris (UA), 0.782 for acute non-ST-segment elevation myocardial infarction (NSTEMI) and 0.900 for acute ST-segment elevation myocardial infarction (STEMI). The incidence of major cardiovascular events in patients with ACS with high lncRNA PELATON expression was higher than that in those with low lncRNA PELATON expression. However, the mortality between patients in the high and low lncRNA PELATON groups was not significantly different. This study showed that higher levels of lncRNA PELATON were negatively correlated with the prognosis of ACS, revealing the potential of this measurement to serve as an index to assess the incidence and prognosis of ACS.

High Expression of PKM2 Was Associated with the Poor Prognosis of Acute Leukemia.

PURPOSE: To explore the clinical significance of plasma pyruvate kinase M2 (PKM2) in assessing the incidence and prognosis of acute leukemia. METHODS: Plasma samples from 56 acute myeloid leukemia (AML) patients, 40 acute lymphoblastic leukemia (ALL) patients, and 66 plasma samples from healthy individuals were collected. The level of plasma PKM2 was detected by enzyme-linked immunosorbent assay. The clinical significance of PKM2 in acute leukemia was assessed by analyzing receiver operating characteristic and survival curves. RESULTS: The plasma levels of PKM2 in AML or ALL patients were significantly higher than those in healthy individuals, respectively. PKM2 can be used as a potential diagnostic index with the AUC of 0.827 for AML and 0.837 for ALL. The level of plasma PKM2 in ALL patients with a BCR/ABL-positive genotype was significantly higher than that in patients with a BCR/ABL-negative genotype (p<0.05). The event-free survival and the overall survival of acute leukemia patients with higher PKM2 expression was worse than those with lower PKM2 expression. CONCLUSION: This study showed that higher levels of PKM2 was negatively correlated with the prognosis of acute leukemia. Therefore, PKM2 can be used as a potential index to assess the incidence and prognosis of acute leukemia.

Evaluation of systemic lupus erythematosus disease activity using anti-α-enolase antibody and RDW.

The objective of the study was to investigate the value of anti-α-enolase antibody (Ab) combined with RDW in evaluating the activity of systemic lupus erythematosus (SLE). Levels of serum anti-α-enolase Ab and RDW were detected in 193 SLE patients and 98 healthy controls by ELISA and automatic blood cell counter (XN9000), respectively. Furthermore, the correlation between anti-α-enolase Ab and RDW in evaluating the activity of SLE was evaluated by correlation analysis. The level of anti-α-enolase Ab (9.16 ± 0.44 ng/mL in stable group and 10.26 ± 0.36 ng/mL in activity group) was significantly higher than that in the healthy control (7.05 ± 0.27 ng/mL). The level of RDW (12.92% ± 1.23% in stable group and 13.57% ± 2.12% in activity group) was significantly higher than that in the healthy control (12.46% ± 0.61%). The levels of anti-α-enolase Ab or RDW in SLE patients were positively correlated with SLEDAI-2 K score (r= 0.75, r = 0.73), respectively. Compared with the anti-α-enolase Ab (AUC: 78.0%) or RDW (AUC:80.0%) alone, anti-α-enolase Ab combined with RDW (AUC: 81.0%) had the best of the effectiveness of evaluating activity of SLE. These data suggested that combined anti-α-enolase Ab with RDW might be good biomarker to predict the activity of SLE in clinical.

Neuroprotective effects of vitamin D and 17ß-estradiol against ovariectomy-induced neuroinflammation and depressive-like state: Role of the AMPK/NF-κB pathway.

Estrogen replacement therapy (ERT) has been proven to relieve menopausal-related mental disorders including depression in postmenopausal women. However, the unsafety of ERT hinders its clinical use. In this study, we would evaluate whether vitamin D (VD), a hormone with optimal safety profile, could relieve the depressive-like symptom in ovariectomized (OVX) rats. Furthermore, we would determine whether vitamin D and 17ß-estradiol (E2) exert neurological function through their immunomodulatory effect in OVX rats. Middle-aged female SD rats were randomly divided into four groups, namely, control (SHAM), OVX, OVX + VD, and OVX + E2. Vitamin D (calcitriol, 100 ng/kg) and 17ß-estradiol (30 µg/kg) had been daily gavaged in the OVX + VD and OVX + E2 group, respectively. After 10-week administration, vitamin D and 17ß-estradiol both showed anti-depressive-like activity in the OVX rats. Using the method of immunofluorescent staining and western blot, vitamin D and 17ß-estradiol were demonstrated to upregulate each other's receptors, including VDR, ERα, and ERß in the hippocampus of OVX rats. Additionally, the upregulation of VDR, calbindin-D28k, and calbindin-D9k suggested that the vitamin D signaling system was amplified by vitamin D and 17ß-estradiol. Vitamin D and 17ß-estradiol showed neuroprotective effects by decreasing OVX-induced apoptosis and neuronal damage, regulating the AMPK/NF-κB signaling pathway, and reducing the proinflammatory cytokines (IL-1ß, IL-6, and TNFα), as well as iNOS and COX-2 in the hippocampus of OVX rats. Collectively, the present study demonstrated that vitamin D and 17ß-estradiol could upregulate each other's receptors and regulate the AMPK/NF-κB pathway to relieve the OVX-induced depressive-like state. The results could stimulate translational research towards the vitamin D potential for prevention or treatment of menopause-related depression.

Exercise-induced Nitric Oxide Contributes to Spatial Memory and Hippocampal Capillaries in Rats.

Exercise has been argued to improve cognitive function in both humans and rodents. Angiogenesis significantly contributes to brain health, including cognition. The hippocampus is a crucial brain region for cognitive function. However, studies quantifying the capillary changes in the hippocampus after running exercise are lacking. Moreover, the molecular details underlying the effects of running exercise remain poorly understood. We show that endogenous nitric oxide contributes to the beneficial effects of running exercise on cognition and hippocampal capillaries. Four weeks of running exercise significantly improved spatial memory ability and increased the number of capillaries in the cornu ammonis 1 subfield and dentate gyrus of Sprague-Dawley rats. Running exercise also significantly increased nitric oxide synthase activity and nitric oxide content in the rat hippocampus. After blocking the synthesis of endogenous nitric oxide by lateral ventricular injection of NG-nitro-L-arginine methyl ester, a nonspecific nitric oxide synthase inhibitor, the protective effect of running exercise on spatial memory was eliminated. The protective effect of running exercise on angiogenesis in the cornu ammonis 1 subfield and dentate gyrus of rats was also absent after nitric oxide synthase inhibition. Therefore, during running excise, endogenous nitric oxide may contribute to regulating spatial memory ability and angiogenesis in cornu ammonis 1 subfield and dentate gyrus of the hippocampus.

Expression of Bace1 is positive with the progress of atherosclerosis and formation of foam cell.

Previous studies have shown that the occurrence of atherosclerosis is closely related to changes of α2, 6-sialic acid transferase I (ST6Gal-I). Bace1 has been identified as a protease responsible for the cleavage and secretion of Golgi-resident ST6Gal-I. There have been only a few attempts to clarify the direct connection between Bace1 and atherosclerosis. The purpose of this study was to investigate the relationship between Bace1 gene and atherosclerosis. Expressions of Bace1 protein and mRNA in ApoE-/- mice fed on high-fat diet were evaluated and the development of atherosclerosis was assessed in Bace1-/- mice fed on high-fat diet. In vitro, the expression of Bace1 gene was detected in foam cell model and the formation of foam cells was examined after knocking down Bace1 by siRNA. We observed a significant increase in Bace1 expression in the aortic root in the model of atherosclerosis in ApoE-/-mice. The expression of Bace1 protein and mRNA levels had a remarkable increase in high-fat group. After knocking out the Bace1 gene, serum lipid levels were significantly lower and intimal thickness was obvious thinner than those in wild-type mice with high-fat diet. Expression of Bace1 protein and mRNA levels were significantly elevated in foam cell. The formation of foam cells was blocked when Bace1 was knocked down by siRNA interferes. Our results suggested that elevated Bace1 gene had a positive role in the progression of atherosclerosis. Affecting the glycosyltransferase may be one of its mechanisms.

Chloride and amino acids are associated with K+-alleviated drought stress in tea (Camellia sinesis).

Drought is one of the main limiting factors affecting tea plant yield and quality. Previous studies have reported that K+ (potassium) application significantly alleviated drought-induced damage in tea plants. However, the intrinsic mechanisms underlying K+-alleviated drought stress are still obscure. In our study, two contrasting varieties, Taicha12 (drought tolerant) and Fuyun6 (drought sensitive), were used to investigate the intrinsic mechanisms behind K+-alleviated drought stress in tea plants. In the present study, we compared with the case of tea plants under drought: higher water and chlorophyll contents were found in drought-stressed tea plants with an external K+ supply, confirming the role of externally supplied K+ in mitigating drought stress. We also found that an adequate K+ supply promoted Cl- accumulation in the mesophyll of Taicha12 (drought tolerant) over that of in Fuyun6 (drought sensitive). Moreover, Gly, Cys, Lys and Arg were not detected in Fuyun6 under 'Drought' or 'Drought + K+' conditions. Results showed that an exogenous supply of Arg and Val significantly alleviated drought-induced damage in Fuyun6, suggesting their role in K+-alleviated drought stress in tea plants. Collectively, our results show that chloride and amino acids are important components associated with K+-alleviated drought stress in tea plants.

Running exercise protects oligodendrocytes in the medial prefrontal cortex in chronic unpredictable stress rat model.

Previous postmortem and animal studies have shown decreases in the prefrontal cortex (PFC) volume and the number of glial cells in the PFC of depression. Running exercise has been shown to alleviate depressive symptoms. However, the effects of running exercise on the medial prefrontal cortex (mPFC) volume and oligodendrocytes in the mPFC of depressed patients and animals have not been investigated. To address these issues, adult male rats were subjected to chronic unpredictable stress (CUS) for 5 weeks, followed by treadmill running for 6 weeks. Then, the mPFC volume and the mPFC oligodendrocytes were investigated using stereology, immunohistochemistry, immunofluorescence and western blotting. Using a CUS paradigm that allowed for the analysis of anhedonia, we found that running exercise alleviated the deficits in sucrose preference, as well as the decrease in the mPFC volume. Meanwhile, we found that running exercise significantly increased the number of CNPase+ oligodendrocytes and Olig2+ oligodendrocytes, reduced the ratio between Olig2+/NG2+ oligodendrocytes and Olig2+ oligodendrocytes and increased myelin basic protein (MBP), CNPase and Olig2 protein expression in the mPFC of the CUS rat model. However, running exercise did not change NG2+ oligodendrocyte number in the mPFC in these rats. These results indicated that running exercise promoted the differentiation of oligodendrocytes and myelin-forming ability in the mPFC in the context of depression. These findings suggest that the beneficial effects of running exercise on mPFC volume and oligodendrocytes in mPFC might be an important structural basis for the antidepressant effects of running exercise.

Lysophosphatidic acid decreased macrophage foam cell migration correlated with downregulation of fucosyltransferase 8 via HNF1α.

BACKGROUND AND AIMS: Aberrant fucosylation, such as α-1,6 fucosylation catalyzed by fucosyltransferase 8 (Fut8), is associated with reduced cell migration and is responsible for cholesterol-enriched foam cell accumulation in the intima in the early stage of atherosclerosis. The current study evaluated the impact of glycosyltransferases on foam cell migration induced by lysophosphatidic acid (LPA) and its potential mechanism. METHODS: The mobility of foam cells was evaluated via transwell and scratch assays. The expression of Fut8 and α-1,6 fucosylation of proteins were assessed by RT-PCR, Western blotting, etc. Overexpression of Fut8 was used to explore the direct relationship between Fut8 and foam cell migration. Dual luciferase reporter assay was performed to determine whether the regulation of Fut8 by LPA occurred at the transcriptional level. Binding of hepatocyte nuclear factor 1-alpha (HNF1α) to the Fut8 promoter was assessed by electrophoretic mobility shift assay and chromatin immunoprecipitation assay. RESULTS: We found that the migration capacity of foam cells induced by LPA was significantly decreased. Fut8 and α-1,6 fucosylation showed the most obvious decline after treatment with 200 µM LPA for 24 h. Overexpression of Fut8 was able to restore the foam cell migration capacity. Another important finding was that the LPA1 and LPA3 (LPA1,3) receptors were involved in the regulation of Fut8. It is interesting to note that LPA led to a decrease in Fut8 gene transcription activity, and HNF1α transcription factor played a positive role in downregulation of Fut8 promoter activity. CONCLUSIONS: Our results strongly indicated that the LPA-LPA1, 3 receptor-HNF1α pathway is involved in the downregulation of Fut8, leading to diminished foam cell migration.

Exercise improves depressive symptoms by increasing the number of excitatory synapses in the hippocampus of CUS-Induced depression model rats.

Exercise has been considered for the treatment of depression, but the mechanism by which exercise improves depression is still unclear. To clarify the mechanism, rats were randomly divided into the control, chronic unpredictable stress (CUS)/standard and CUS/running groups. The rats in the CUS/running group ran for four weeks. In this study, a sucrose preference test (SPT) was used to evaluate the depression-like symptoms in the rats, and western blot, immunohistochemical and stereological analyses were performed to study the expression of synaptic-related proteins in the hippocampus and the changes in excitatory synapses in each sub-region. The results show that sucrose preference in the CUS/standard group was significantly lower than that in the control group, but in the CUS/running group, sucrose preference was higher than that in the CUS/standard group. Surprisingly, there was no difference in the synaptic-related proteins in the hippocampus among groups. The CUS/standard group exhibited fewer spinophilin+ (Sp+) dendritic spines representing excitatory synapses in CA1, CA3 and dentate gyrus (DG) of the hippocampus than the control group, whereas the CUS/running group exhibited significantly more Sp+ dendritic spines in these regions than the CUS/standard group, indicating that excitatory synapses were reduced in depressed rats and that running exercises could reverse this change. We hypothesize that the changes in the number of excitatory synapses better reflect the changes in depressive symptoms than the level of synaptic proteins and that the effect of exercise on excitatory synapses in the sub-regions of the hippocampus may be an important structural indicator of the improvement of depressive symptoms.

The effects of running exercise on oligodendrocytes in the hippocampus of rats with depression induced by chronic unpredictable stress.

Running exercise has been shown to be associated with decreased symptoms of depression. However, the mechanisms underlying these antidepressant effects of running exercise remain relatively unclear. In the current study, we investigated the relationship between depressive symptoms in chronic unpredictable stress (CUS) model rats treated with running exercise and changes in oligodendrocytes in the hippocampus. After 4 weeks of CUS, the model group was randomly divided into a CUS standard group (18 rats) and a CUS running group (15 rats). Then, a 4-week treadmill running trial was performed with the CUS running group. In addition, the behavioral effects of exercise were investigated by means of a sucrose preference test (SPT) and an at the end of the 8th week. Immunohistochemical methods and modern stereological methods were used to precisely quantify the total number of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase)-positive (CNPase+) oligodendrocytes in each hippocampal subregion. At the behavioral level, after four weeks of running, the CUS running group displayed significantly higher consumption of sucrose water in the SPT than the CUS standard group. Unbiased stereological analyses revealed significantly higher total numbers of CNPase+ cells in the hippocampal CA3 and dentate gyrus regions in the CUS running group than in the CUS standard group, whereas there was no significant difference between the groups in the number of CNPase+ cells in the hippocampal CA1 region. The present results further confirm that exercise can alleviate symptoms and protect hippocampal oligodendrocytes in depressed rats.

Quantitative study of the capillaries within the white matter of the Tg2576 mouse model of Alzheimer's disease.

INTRODUCTION: To quantitatively investigate the capillaries within the white matter of Tg2576 Alzheimer's disease (AD) transgenic mice during the early stage. METHODS: In the current study, 10-month-old male Tg2576 AD mice were used as the early-stage AD group and age-matched nontransgenic littermate mice were used as the wild-type group. Then, the Morris water maze was used to examine the spatial learning and memory abilities of the mice in both groups, and unbiased stereological methods were used to accurately quantify the volume of white matter and the parameters of the capillaries within the white matter, such as the total length, total volume, and total surface area of capillaries. RESULTS: The Morris water maze performance of the Tg2576 group was worse than that of the wild-type group, while the white matter volume did not significantly differ between the wild-type group and the Tg2576 group. The total length, total volume, and total surface area of the capillaries within the white matter of the Tg2576 group were significantly decreased compared to those of the wild-type group. CONCLUSIONS: The current study provide structural basis for understanding the pathological changes of the early stage of AD and cognitive decline in AD might be associated with changes in the white matter capillaries. Capillaries within the white matter might, thus, serve as a valid target for the prevention and treatment of early-stage AD.

Mesophyll cells' ability to maintain potassium is correlated with drought tolerance in tea (Camellia sinensis).

Tea plant is an important economic crop and is vulnerable to drought. A good understanding of tea drought tolerance mechanisms is required for breeding robust drought tolerant tea varieties. Previous studies showed mesophyll cells' ability to maintain K+ is associated with its stress tolerance. Here, in this study, 12 tea varieties were used to investigate the role of mesophyll K+ retention ability towards tea drought stress tolerance. A strong and negative correlation (R2 = 0.8239, P < 0.001) was found between PEG (mimic drought stress)-induced K+ efflux from tea mesophyll cells and overall drought tolerance in 12 tea varieties. In agreement with this, a significantly higher retained leaf K+ content was found in drought tolerant than the sensitive tea varieties. Furthermore, exogenous applied K+ (5 mM) significantly alleviated drought-induced symptom in tea plants, further supporting our finding that mesophyll K+ retention is an important component for drought tolerance mechanisms in tea plants. Moreover, pharmacological experiments showed that the contribution of K+ outward rectifying channels and non-selective cation channels in controlling PEG-induced K+ efflux from mesophylls cells are varied between drought tolerant and sensitive tea varieties.

Changes in white matter and the effects of fluoxetine on such changes in the CUS rat model of depression.

OBJECTIVE: To explore the pathogenesis of depression and the possible mechanism of the effects of selective serotonin reuptake inhibitors (SSRIs) on the myelinated fibers and myelin sheaths in the white matter during the antidepressant action of fluoxetine. METHODS: In this study, Sprague Dawley (SD) rats were divided into a Control group, a group treated with CUS and no drugs (CUS/Standard group) and a group treated with CUS and fluoxetine (CUS/FLX group). The CUS/FLX group was treated with fluoxetine at dose of 5 mg/kg for 21 days. The white matter volume, the myelinated fiber parameters and the myelin sheath volume in the white matter were calculated from transmission electron microscope images through unbiased stereological methods. RESULTS: The total volume and total length of myelinated fibers;and mean volume of white matter of the CUS/Standard group were significantly decreased compared to values from the control group (p = 0.025, p = 0.007, p = 0.000), whereas no significant differences in these stereological parameters were found between the CUS/Standard and CUS/FLX groups (p > 0.05). CONCLUSIONS: Fluoxetine successfully treated depression-like behavior but had no effects on the white matter or its component myelinated fibers in the CUS rat model of depression.