Certification of stroke centers at primary hospitals and the improvement of thrombolysis n South China during 2020-2022.

INTRODUCTION: IVT use declined globally in 2020 due to the Corona Virus Disease 2019 (COVID-19) pandemic, but it increased in South China. This study was conducted to evaluate the association of establishing Stroke Prevention Centers (SPCs) at primary hospitals with IVT increase in South China. MATERIALS AND METHODS: We conducted a longitudinal observational study across 336 hospitals in 114 areas in South China during 2020-2022. Data regarding certified stroke centers, IVT volumes, and IVT rates were collected. Correlations between IVT rates and the number or density of stroke centers were accessed. IVT use was compared among areas with different levels of stroke centers or on different certification process. RESULTS: During 2020-2022, there were 83, 125, and 152 stroke centers, with 26, 65, and 92 SPCs, respectively. IVT therapies were 12,795, 17,266, and 20,411, representing a 29.8% increase/year (all p < 0.001). IVT rates increased from 7.2% in 2020 to 8.8% and 10.4% in 2021 and 2022, demonstrating a 22.2% increase/year (all p < 0.001). IVT rates correlated with the number and density of SPCs (all p < 0.05). IVT rates were higher in areas equipped with SPCs than in those without stroke centers (all p < 0.05). IVT rates consistently increased during the SPC certification process from 1 year before through the certification and subsequent maintenance (both p < 0.05). DISCUSSION AND CONCLUSION: Well-organised SPCs and IVT therapy demonstrated substantial increase during the 3-year period. Certification of SPCs at primary hospitals is associated with improved IVT therapy in South China even with city lockdown during COVID-19 pandemic.

Acoustic stimulation during sleep improves cognition and ameliorates Alzheimer's disease pathology in APP/PS1 mice.

Nonpharmacological therapies for Alzheimer's disease (AD) have become a popular research topic, and acoustic stimulation during sleep is one such promising strategy for the clinical treatment of AD. Some animal experiments have illustrated that acoustic stimulation at a specific frequency can ameliorate AD-related pathology or improve cognition in mice, but these studies did not explore the effective time window of auditory stimulation. Here, we explored the effects of acoustic stimulation during wakefulness and acoustic stimulation during sleep on cognition and AD-related pathology in APP/PS1 mice and the underlying mechanisms. In this study, forty APP/PS1 mice were equally divided into the following 4 groups and treated for 28 days: the chronic sleep deprivation (CSD) group (exposed to sleep deprivation from zeitgeber time [ZT] 0 to ZT 12 each day), the normal sleep and stress exposure (NSS) group (exposed to a stressor from ZT 0 to ZT 12 each day), the acoustic stimulation during wakefulness (ASW) group (exposed to sleep deprivation and 40 Hz acoustic stimulation from ZT 0 to ZT 12 each day) and the acoustic stimulation during sleep (ASS) group (exposed to sleep deprivation from ZT 0 to ZT 12 and 40 Hz acoustic stimulation from ZT 12 to ZT 24 each day). After the intervention, cognition was assessed by behavioural experiments. The amyloid-ß burden was analysed by Western blotting, immunofluorescence and enzyme-linked immunosorbent assay. Tau pathology was assessed by Western blotting. Mitochondrial function was evaluated by transmission electron microscopy, Western blotting and fluorescence intensity measurement. We found that the NSS and ASS groups had better cognitive functions than the CSD and ASW groups. The Aß burden and tau phosphorylation were lower in the NSS and ASS groups than in the CSD and ASW groups. Mitochondrial function was better in the NSS and ASS groups than in the CSD and ASW groups. However, the differences in these parameters between the NSS and ASS groups and between the CSD and ASW groups were not significant. Our findings suggest that acoustic stimulation at a specific frequency during sleep, but not during wakefulness, reduces the amyloid-ß burden by inhibiting amyloid beta precursor protein-binding protein 2, hinders tau phosphorylation by blocking glycogen synthase kinase 3 beta, and restores mitochondrial function by elevating mitophagy and promoting mitochondrial biogenesis.

Association between preoperative C-reactive protein to albumin ratio and late arteriovenous fistula dysfunction in hemodialysis patients: a cohort study.

Arteriovenous fistula (AVF) dysfunction is a critical complication in hemodialysis (HD) patients, with inflammation potentially contributing to its development. This retrospective cohort study aimed to investigate the association between preoperative C-reactive protein to albumin ratio (CAR) and AVF dysfunction in Chinese HD patients. A total of 726 adults with end-stage renal disease who underwent new AVF placement between 2011 and 2019 were included. Multivariable Cox regression and Fine and Gray competing risk models were employed to assess the relationship between CAR and AVF dysfunction, considering death and renal transplantation as competing risks. Among 726 HD patients, 29.2% experienced AVF dysfunction during a median follow-up of 36 months. Adjusted analyses revealed that higher CAR levels were associated with an increased risk of AVF dysfunction, with a 27% higher risk per one-unit increase in CAR. Furthermore, patients with CAR values ≥ 0.153 exhibited a 75% elevated risk compared to those with CAR values < 0.035 (P = 0.004). The relationship between CAR and AVF dysfunction varied by the site of internal jugular vein catheter placement (P for trend = 0.011). Notably, the Fine and Gray analysis confirmed the association between CAR and AVF dysfunction, with a 31% increased risk per one-unit increase in CAR. The highest CAR tertile remained an independent predictor of AVF dysfunction (HR = 1.77, 95% CI 1.21-2.58, P = 0.003). These findings highlight the potential of CAR as a prognostic marker for AVF dysfunction in Chinese HD patients. Clinicians should consider CAR levels and catheter placement site when assessing the risk of AVF dysfunction in this population.

Ginsenoside Rg1 ameliorates Alzheimer's disease pathology via restoring mitophagy.

Background: Alzheimer's disease (AD) is a common form of dementia, and impaired mitophagy is a hallmark of AD. Mitophagy is mitochondrial-specific autophagy. Ginsenosides from Ginseng involve in autophagy in cancer. Ginsenoside Rg1 (Rg1 hereafter), a single compound of Ginseng, has neuroprotective effects on AD. However, few studies have reported whether Rg1 can ameliorate AD pathology by regulating mitophagy. Methods: Human SH-SY5Y cell and a 5XFAD mouse model were used to investigate the effects of Rg1. Rg1 (1µM) was added to ß-amyloid oligomer (AßO)-induced or APPswe-overexpressed cell models for 24 hours. 5XFAD mouse models were intraperitoneally injected with Rg1 (10 mg/kg/d) for 30 days. Expression levels of mitophagy-related markers were analyzed by western blot and immunofluorescent staining. Cognitive function was assessed by Morris water maze. Mitophagic events were observed using transmission electron microscopy, western blot, and immunofluorescent staining from mouse hippocampus. The activation of the PINK1/Parkin pathway was examined using an immunoprecipitation assay. Results: Rg1 could restore mitophagy and ameliorate memory deficits in the AD cellular and/or mouse model through the PINK1-Parkin pathway. Moreover, Rg1 might induce microglial phagocytosis to reduce ß-amyloid (Aß) deposits in the hippocampus of AD mice. Conclusion: Our studies demonstrate the neuroprotective mechanism of ginsenoside Rg1 in AD models. Rg1 induces PINK-Parkin mediated mitophagy and ameliorates memory deficits in 5XFAD mouse models.

Disturbance of REM sleep exacerbates microglial activation in APP/PS1 mice.

Although both nonrapid eye movement (NREM) sleep loss and rapid eye movement (REM) sleep loss exacerbate Alzheimer's disease (AD) progression, they exert different effects. Microglial activation can be beneficial or detrimental to AD patients under different conditions. However, few studies have investigated which sleep stage is the main regulator of microglial activation or the downstream effects of this activation. We aimed to explore the roles of different sleep phases in microglial activation and to investigate the possible effect of microglial activation on AD pathology. In this study, thirty-six 6-month-old APP/PS1 mice were equally divided into 3 groups: the stress control (SC), total sleep deprivation (TSD), and REM deprivation (RD) groups. All mice underwent a 48-hour intervention before their spatial memory was assessed using a Morris water maze (MWM). Then, microglial morphology, activation- and synapse-related protein expression, and inflammatory cytokine and amyloid ß (Aß) levels in hippocampal tissues were measured. We found that the RD and TSD groups exhibited worse spatial memory in the MWM tests. In addition, the RD and TSD groups showed greater microglial activation, higher inflammatory cytokine levels, lower synapse-related protein expression and more severe Aß accumulation than the SC group, but there were no significant differences between the RD and TSD groups. This study demonstrates that disturbance of REM sleep may activate microglia in APP/PS1 mice. These activated microglia may promote neuroinflammation and engulf synapses but show a weakened ability to clear plaques.

NREM sleep loss increases neurofilament light chain levels in APP/PS1 and C57BL/6 J mice.

PURPOSE: Sleep disturbances exacerbate the progression of Alzheimer's disease (AD), but disturbances of non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep may have different effects. Neurofilament light chain (NfL), an axon-specific protein, is an indicator of the severity of neuronal apoptosis. To investigate whether or not NREM or REM sleep is crucial to neuronal survival, we examined the effects of induced NREM or REM sleep loss on NfL levels in APP/PS1 mice, a model of AD, and their wild-type (WT) C57BL/6 J littermates. METHODS: At 6 months of age, WT mice and AD mice were equally divided into six groups, namely, the WT-normal sleep (S), WT-total sleep deprivation (TSD), WT-REM deprivation (RD), AD-S, AD-TSD and AD-RD groups, according to the type of sleep intervention applied. All mice underwent 6 days of sleep intervention. Cerebrospinal fluid (CSF) and plasma NfL levels were measured at baseline and on days 2, 4 and 6, and spatial memory was assessed in the Morris water maze (MWM) test. RESULTS: Among the 18 WT and 18 AD mice, CSF and plasma NfL levels were higher in AD-TSD mice than in AD-S or AD-RD mice, while no significant difference was observed between the latter two groups. In AD-TSD mice, CSF and plasma NfL levels increased with the duration of sleep deprivation. A similar pattern of results was observed for the WT groups. CONCLUSIONS: NREM sleep loss may increase CSF and plasma NfL levels in both WT and AD mice.

Acoustic Stimulation Improves Memory and Reverses the Contribution of Chronic Sleep Deprivation to Pathology in 3xTgAD Mice.

Acoustic stimulation during sleep is believed to enhance slow waves, which are critical to memory consolidation. However, clinical trials of acoustic stimulation have yielded mixed results concerning its effectiveness in improving human memory. A few studies have implied that acoustic stimulation ameliorates the pathology of Alzheimer's disease (AD) in mice with normal sleep. Here, we explored the effect of acoustic stimulation on 3xTgAD mice suffering from chronic sleep deprivation, as these data may shed light on the potential use of acoustic stimulation in AD patients with insomnia. Methods: Twenty-four 8-month-old 3xTgAD mice were randomly and equally divided into three groups: the normal sleep group (S group), the sleep deprivation group (SD group), and the acoustic stimulation group (AS group). During a 14-day sleep intervention, the SD and AS groups received 6 h of sleep deprivation per day, and the AS group also received acoustic stimulation in the dark phase. Then, the mice underwent Morris water maze (MWM) tests and arterial spin labelling (ASL) magnetic resonance imaging (MRI) scans and were sacrificed for pathological evaluation. Results: The three groups showed similar stress levels. The S and AS groups exhibited better spatial memory, better brain perfusion, and milder amyloid ß (Aß) and tau pathology than the SD group, although no significant discrepancies were found between the S and AS groups. Conclusion: Acoustic stimulation may exert a protective effect in 3xTgAD mice by improving spatial memory, enhancing the blood supply of the brain, and reversing the contribution of chronic sleep deprivation to Aß and tau pathology to mimic the effect of normal sleep patterns.

Association between Preoperative Monocyte-to-Lymphocyte Ratio and Late Arteriovenous Fistula Dysfunction in Hemodialysis Patients: A Cohort Study.

BACKGROUND: Inflammation appears to be at the biological core of arteriovenous fistula (AVF) dysfunction, and the occurrence of AVF dysfunction is related to high death and disability in hemodialysis (HD) patients. Despite several studies on the correlations between AVF dysfunction and inflammatory indicators, how AVF dysfunction is related to the monocyte-to-lymphocyte ratio (MLR) is much unclear. We hypothesize that preoperative MLR is associated with AVF dysfunction in Chinese HD patients. METHODS: In this single-center retrospective cohort study, totally 769 adult HD patients with a new AVF created between 2011 and 2019 were included. Association of preoperative MLR with AVF dysfunction (thrombosis or decrease of normal vessel diameter by >50%, requiring either surgical revision or percutaneous transluminal angioplasty) was assessed by multivariable Cox proportional hazard regression. RESULTS: The patients were aged 55.8 ± 12.2 years and were mostly males (55%). During the average 32-month follow-up (maximum 119 months), 223 (29.0%) patients had permanent vascular access dysfunction. In adjusted multivariable Cox proportional hazard regression analyses, the risk of AVF dysfunction was 4.32 times higher with 1 unit increase in MLR (hazard ratio [HR]: 5.32; 95% confidence interval [CI]: 3.1-9.11). Compared with patients with MLR <0.28, HRs associated with an MLR of 0.28-0.41 and ≥0.41 are 1.54 (95% CI: 1.02-2.32) and 3.17 (2.18-4.62), respectively. CONCLUSIONS: A higher preoperative MLR is independently connected with a severer risk of AVF dysfunction in HD patients. Its clinical value should be determined in the future.

Alpha 1-antichymotrypsin may be a biomarker for the progression of amnestic mild cognitive impairment.

Alpha 1-antichymotrypsin (ACT), an acute-phase protein, has been reported to be increased in the brain and blood of Alzheimer's disease (AD) patients. However, few previous studies have focused on amnestic mild cognitive impairment (aMCI) patients. The aim of our study was to investigate the changing trend in ACT concentrations during the progression of aMCI. Hence, we measured the cerebrospinal fluid (CSF) and serum levels of ACT in aMCI subjects and normal controls (NC) at 2-year follow-up assessments using ELISA and Western blot. Forty-four NCs, 28 stable aMCI (sMCI) patients, and 20 progressive aMCI (pMCI) patients finished the follow-up assessments, and their data were used for analysis. We found that CSF and serum ACT levels of both sMCI and pMCI patients increased over time, while those of NCs remained stable; CSF and serum ACT levels were significantly higher in both sMCI and pMCI patients than in NCs, except for baseline serum ACT. In pMCI patients prior to developing AD, CSF and serum ACT levels were already significantly higher than those in sMCI patients. The ROC curve results demonstrated that combining CSF and serum ACT levels can distinguish aMCI patients from NCs with high specificity and sensitivity. Our data suggest that ACT may be a biomarker for diagnosing aMCI.

Identification of key genes and pathways in IgA nephropathy using bioinformatics analysis.

BACKGROUND: IgA nephropathy (IgAN) is the most frequent type of primary glomerulonephritis globally and the leading cause of end-stage renal disease in young adults. Its pathogenesis is not fully known, but is largely attributed to genetic factors. This study was aimed to explore the prognostic values of key genes in IgAN. METHODS: The gene expression profile GSE93798 of 20 IgAN samples and 22 normal samples using glomeruli from kidney biopsy was adopted. Totally 447 upregulated and 719 downregulated differentially expressed genes were found in IgAN patients on the R software. The Gene Ontology enrichment and the Kyoto Encyclopedia of Gene and Genomes pathway were investigated on DAVID, and the protein-protein interaction network and the top 13 hub genes of the differentially expressed genes were built via the plug-in molecular complex detection and cytoHubba of Cytoscape. RESULTS: From the protein-protein interaction network, of the top 13 hub genes, FOS, EGFR, SIRT1, ALB, TFRC, JUN, IGF1, HIF1A, and SOCS3 were upregulated, while CTTN, ACTR2, CREB1, and CTNNB1 were downregulated. The upregulated genes took part in the HIF-1 signaling pathway, Choline metabolism in cancer, Pathways in cancer, Amphetamine addiction, Estrogen, TNF, and FoxO signaling pathways, and Osteoclast differentiation, while the downregulated genes were involved in Pathogenic Escherichia coli infection, Bacterial invasion of epithelial cells, prostate cancer, and melanogenesis. CONCLUSION: This study based on the Gene Expression Omnibus database updates the knowledge about the mechanism of IgAN and may offer new treatment targets.

Plasma Neurofilament Light Chain May Be a Biomarker for the Inverse Association Between Cancers and Neurodegenerative Diseases.

An inverse association may exist between cancers and neurodegenerative diseases, although convenient biomarkers for verifying this inverse association are lacking. Plasma neurofilament light chain (NfL) is a novel biomarker for neurodegenerative diseases, such as Alzheimer's disease (AD), but it has not been measured in patients with cancers, such as gastric cancer (GC). We aimed to explore whether plasma NfL could be a biomarker for GC and AD and whether an inverse association of NfL exists between GC and AD. In this study, plasma NfL levels of 60 normal controls (NC), 91 GC subjects, and 74 AD subjects were measured by a highly sensitive single-molecule array assay. We found that GC subjects expressed lower plasma NfL levels but AD subjects expressed higher plasma NfL levels than NCs. After controlling for confounding factors, plasma NfL levels in the GC group were associated with serum tumor marker levels, and plasma NfL levels in the AD group were associated with cognitive performance and cerebrospinal fluid (CSF) pathological marker levels. Across the entire cohort, plasma NfL levels were associated with cognitive performance, CSF pathological marker levels and serum tumor marker levels. These results suggest thatplasma NfL may be a potential biomarker for GC and AD and may be convenient for evaluating the inverse association between cancers and neurodegenerative diseases.

Spontaneous K-Complexes may be biomarkers of the progression of amnestic mild cognitive impairment.

OBJECTIVE: Spontaneous K-complexes (SKCs), a hallmark of stage 2 sleep, have been reported to decrease in density in Alzheimer's disease (AD) patients. However, few former studies have explored the alterations in SKC characteristics in the pre-clinical phase of AD-amnestic mild cognitive impairment (aMCI). The aim of our prospective cohort study was to investigate the changing trend in SKC characteristics during the progression of aMCI. METHODS: SKC density, amplitude and duration were measured in aMCI subjects and normal controls (NC) at two-year follow-up assessments by polysomnography (PSG). In sum, 22 NCs, 25 stable aMCI (sMCI) subjects and 20 progressive aMCI (pMCI) subjects finished the four follow-up PSG assessments, and their data were used for analysis. RESULTS: SKC density and amplitude, but not duration, decreased during the follow-up assessments in both NCs and aMCI subjects, but the rate of decrease of these parameters was greater in aMCI subjects. With the progression of aMCI, significant differences in SKC density and amplitude among the three groups were observed, whereas SKC density showed no difference at the early stage of aMCI. The receiver operating characteristic (ROC) curve results demonstrated that SKC density and amplitude could distinguish aMCI subjects from NCs with high specificity and sensitivity. CONCLUSION: Our results suggest that SKCs decrease with ageing and the progression of aMCI, and SKC characteristics may be potential biomarkers for diagnosing aMCI.

Sleep spindles, K-complexes, limb movements and sleep stage proportions may be biomarkers for amnestic mild cognitive impairment and Alzheimer's disease.

PURPOSE: Sleep disturbances are common in Alzheimer's disease (AD) and mild cognitive impairment (MCI) patients. Non-rapid eye movement stage 3 (N3), rapid eye movement stage (REM), spindle density, and K-complex (KC) density are decreased in MCI and AD patients. Periodic limb movements in sleep (PLMS) are increased in other neurodegenerative diseases. We aimed to distinguish amnestic mild cognitive impairment (aMCI) patients from the overall population of MCI patients by comparing the N3 and REM proportions, the morphological characteristics of spindles and KCs and the periodic limb movement index (PLMI) among control, aMCI and AD subjects. METHODS: In 92 subjects (30 controls, 32 aMCI and 30 AD), sleep stages, spindles, KCs and PLMS were recorded during the second of two nights of polysomnography (PSG). We compared the above parameters among the three groups. RESULTS: AD and aMCI subjects had lower proportions of N3 and REM, poorer spindle and KC activities and more frequent PLMS than controls. These alterations were associated with decreased Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores. We determined cut-off values for distinguishing aMCI and AD using logistic regression and receiver operating characteristic (ROC) analyses. CONCLUSIONS: AD and aMCI patients have abnormal sleep stage proportions, spindles, KCs and PLMS. The combination of the above alterations may distinguish aMCI and AD patients from controls with high specificity and sensitivity.

Generation of an integration-free iPSC line(SYSUi001-A) from a sporadic Alzheimer's disease patient.

Human iPSC line, iPSC-ADM01(SYSUi001-A), was generated from a 70-year-old male patient with sporadic Alzheimer's disease, using non-integrative reprogramming method. This cell line shows pluripotency both in vitro and in vivo, and has a normal karyotype.

Increased Risk of Post-Thrombolysis Intracranial Hemorrhage in Acute Ischemic Stroke Patients with Leukoaraiosis: A Meta-Analysis.

BACKGROUND: Leukoaraiosis is common in patients with acute ischemic stroke. The results from many studies investigating the association between leukoaraiosis and intracranial hemorrhage after thrombolysis remain conflicting. METHODS: A meta-analysis was performed to compare the risk of post-thrombolytic intracranial hemorrhage in patients with and without leukoaraiosis. Relevant reports were identified by searching PubMed, EmBase, Cochrane Library, and ISI Web of Science through December 2015 using a combination of subjective and random terms. Eligible studies that were original articles with a clear definition of leukoaraiosis and intracranial hemorrhage were selected and analyzed. Funnel plots, Egger's test, and Begg's test were conducted to assess the publication bias. Sensitivity analysis was also performed to evaluate the influence of each individual study. RESULTS: Eleven trials that enrolled 6912 participants were included. There was a significantly increased risk for acute ischemic stroke patients with leukoaraiosis (odds ratio: 1.89, 95% confidence interval 1.51-2.37, P<0.001). Low heterogeneity and less publication bias was detected among these studies. The results of both computed tomography and magnetic resonance imaging performed on the subgroups of leukoaraiosis were significant. Furthermore, an association between leukoaraiosis and symptomatic intracranial hemorrhage was also confirmed. The odds ratios remained stable with no obvious variations on the sensitivity analysis. The limitations consisted of types of including trials and not matching some baseline variables. CONCLUSIONS: The results of this meta-analysis show that leukoaraiosis approximately doubles the incidence of intracranial hemorrhage after thrombolytic therapy. However, it does not critically affect decision making regarding thrombolysis for patients with acute ischemic stroke. Additional investigations are required.

PEG-PEI/siROCK2 Protects Against Aß42-Induced Neurotoxicity in Primary Neuron Cells for Alzheimer Disease.

Gene therapy that targets the ROCK2 gene has yielded promising results in the treatment of AD. Our previous study indicated that PEG-PEI/siROCK2 could effectively suppress ROCK2 mRNA expression and showed a promising prospect for the treatment of Alzheimer's disease. However, the ability of PEG-PEI/siROCK2 to reduce Aß-induced cytotoxicity is unknown. To investigate the effect of PEG-PEI/siROCK2 against Aß42-induced neurotoxicity, primary cultured cortical neurons were pretreated with PEG-PEI/siROCK2 for 24 h and then treated with 5 µM Aß42 for 24 h. We found that PEG-PEI/siROCK2 increased the cell viability and reduced the number of apoptotic cells induced by Aß42, as measured using an MTT assay and Annexin V/PI staining. A further study revealed that PEG-PEI/siROCK2 can activate p-Akt, and treatment with the PI3K inhibitor LY294002 attenuated the neuroprotective effects. These results suggest that PEG-PEI/siROCK2 prevents Aß42-induced neurotoxicity and that the activation of PI3K/Akt pathway is involved in neuroprotection. Taken together, these findings shed light on the role of PEG-PEI/siROCK2 as a potential therapeutic agent for AD.

Diagnostic value of phospholipase A2 receptor in idiopathic membranous nephropathy: a systematic review and meta-analysis.

BACKGROUND: Detection of M-type phospholipase A2 receptor (PLA2R) can be used in serologic diagnosis of idiopathic membranous nephropathy (IMN), but there are limited data about the sensitivity and specificity of its diagnostic values. METHODS AND RESULTS: Meta-analysis of diagnostic test studies assessing the values of PLA2R in diagnosis of IMN. MEDLINE, EMBASE, and CENTRAL databases and congress abstracts were searched for studies reporting the value of PLA2R to predict IMN. The quality of the studies was evaluated using the guidelines of the updated Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool. The results are summarized as sensitivity, specificity, and diagnostic odds ratio (OR). Data from 10 studies involving 1,550 participants were analyzed. Across all settings, the diagnostic OR for serum anti-PLA2R level to predict IMN at different stages was 247.41, with sensitivity of 0.69 and specificity of 0.99. The estimated sensitivity and specificity of serum anti-PLA2R level for diagnosis of IMN in the active stage were 74.0 and 95.0%, respectively, with diagnostic OR of 54.22. The estimated sensitivity and specificity of biopsy anti-PLA2R for diagnosis of IMN at different stages was 73.0 and 83.0%, respectively, with diagnostic OR of 13.75. CONCLUSIONS: This meta-analysis shows that serum anti-PLA2R level is of diagnostic value for IMN in the active stage. Future large-cohort prospective studies are required to reveal the diagnostic value of circulating anti-PLA2R antibodies versus PLA2R antigens in kidney biopsy for IMN at different stages.

The report of sustained low-efficiency dialysis (SLED) treatment in fifteen patients of severe snakebite.

To investigate the therapeutic efficacy of sustained low-efficiency dialysis (SLED) in severe snakebite patients. Fifteen patients of severe snakebite was treated with SLED from July 2005 to August 2009 were included in the study. Central venous access was established in all patients. SLED was administered using Dialog(+) dialyzer (B. Braun, Germany). SLED sessions were 6-12 h in duration at a blood flow rate of 200 ml/min and a dialysate flow rate of 300 ml/min. Heparin or low molecular weight heparin was used as anticoagulant. Biochemical indicators, APACHE II scores before and after SLED, and clinical outcomes were evaluated. The levels of serum creatinine, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, creatine kinase isozyme MB, and creatine kinase were significantly lower than the level before SLED (P < 0.05); the level of cholinesterase was significantly higher after SLED (P < 0.01); the APACHE II score before SLED was 14.1 ± 3.8, but decreased significantly to 7.9 ± 1.4, 6.2 ± 1.1, and 4.2 ± 0.8 on days 1, 2, and 7 after SLED, respectively (P < 0.01). Three patients died on days 1, 3, and 4 after SLED, respectively. The remaining twelve patients were either cured or showed improvement at the time of discharge. The survival rate was 80 % where as mortality was 20 %. SLED may be an effective treatment option in severe snakebite patients. It can reduce mortality, thereby, resulting in increased survival rates.

Therapeutic effectiveness of sustained low-efficiency hemodialysis plus hemoperfusion and continuous hemofiltration plus hemoperfusion for acute severe organophosphate poisoning.

There is no report on the effects of sustained low-efficiency dialysis (SLED) plus hemoperfusion (HP) (SLED + HP) in patients with acute severe organophosphate (OP) poisoning (ASOPP). This study was designed to compare the therapeutic effectiveness between SLED + HP and continuous hemofiltration (CHF) plus HP (CHF + HP) in patients with ASOPP. In order to assess the two treatment methods, 56 patients with ASOPP were divided into CHF + HP group and SLED + HP group. The biochemical indicators, in-hospital duration, hemodynamic parameters, Acute Physiology, and Chronic Health Evaluation (APACHE II) score, and survival and mortality rates were compared. In both groups after treatment, the levels of serum creatine kinase isozyme MB, creatine kinase, creatinine, glutamic-oxalacetic transaminease, and glutamate-pyruvate transaminase, and the APACHE II scores on the first, second, and seventh day decreased (P < 0.05), whereas the levels of serum acetylcholinesterase increased. The two groups showed no statistical differences in in-hospital duration, biochemical indicators, APACHE II score, hemodynamic parameters, survival rate, or the mortality rate (P > 0.05). In conclusion, SLED has similar hemodynamic stability to CHF and the two treatment methods have similar effects on ASOPP patients. More importantly, SLED plus HP is relatively economical and convenient for patients with ASOPP in clinical practice.

Comparison of the therapeutic effectiveness of sustained low-efficiency dialysis (SLED) with continuous blood purification (CBP) in critically ill patients.

The differences in therapeutic effectiveness between sustained low-efficiency dialysis (SLED) and continuous blood purification (CBP) were investigated. In order to assess the different treatment methods, 56 critically ill patients were divided into two groups, the CBP group and the SLED group. A comparison was made between all the biochemical indicators, in-hospital duration, hemodynamic parameters, acute physiology and chronic health evaluation (APACHE-II), the survival, and the mortality rates. After treatment, the levels of serum creatine kinase isozyme MB (CK-MB), creatine kinase, creatinine, glutamate-oxalacetate transaminase (AST), glutamate-pyruvate transaminase (ALT), APACHE II score on the 1st, 2nd, and 7th day in both the treatment groups were lower than that before the treatment (P < 0.05). There are no statistical differences in in-hospital duration, biochemical indicators, APACHE II score, hemodynamic parameters, the survival rate and the mortality rate between the two groups (P > 0.05). It was concluded that SLED has similar hemodynamic stability with CBP and the two methods have similar treatment effects in critically ill patients. However, we noticed that SLED can be relatively economical and convenient for critically ill patients in clinical practice.