Sleep restriction promotes brain oxidative stress and inflammation, and aggravates cognitive impairment in insulin-resistant mice.

Sleep deprivation and insulin resistance (IR) are two risk factors for Alzheimer's disease. As the population of people with IR increases and sleep restriction (SR) due to staying up late becomes the "new normal", it is necessary to investigate the effects and molecular pathogenesis of chronic SR on cognitive function in insulin resistance. In this study, 4-week-old mice were fed a high-fat diet (HFD) for 8 weeks to establish IR model, and then the mice were subjected to SR for 21 days, and related indicators were assessed, including cognitive capacity, apoptosis, oxidative stress, glial cell activation, inflammation, blood-brain barrier (BBB) permeability and adiponectin levels, for exploring the potential regulatory mechanisms. Compared with control group, IR mice showed impaired cognitive capacity, meanwhile, SR not only promoted Bax/Bcl2-induced hippocampal neuronal cell apoptosis and Nrf2/HO1- induced oxidative stress, but also increased microglia activation and inflammatory factor levels and BBB permeability, thus aggravating the cognitive impairment in IR mice. Consequently, changing bad living habits and ensuring sufficient sleep are important intervention strategies to moderate the aggravation of IR-induced cognitive impairment.

Efficacy of virtual reality training on motor performance, activity of daily living, and quality of life in patients with Parkinson's disease: an umbrella review comprising meta-analyses of randomized controlled trials.

OBJECTIVE: There are several meta-analyses of randomized controlled trials (RCTs) demonstrating the benefits of virtual reality (VR) training as an intervention for motor performance, activity of daily living (ADL) and quality of life (QoL) outcomes in patients with Parkinson's disease (PD). However, the aggregate evidence collected to date has not been thoroughly evaluated for strength, quality, and reproducibility. An umbrella review from published meta-analyses of RCTs was conducted to evaluate the strength and quality of existing evidence regarding the efficacy of VR training in improving the motor performance, ADL and QoL outcomes of patients with PD. METHODS: PubMed, PsychInfo, Web of Science, and Scopus were searched to identify relevant meta-analysis of RCTs examining the effects of VR training on motor performance and quality of life outcomes in PD patients. We recalculated the effect sizes (Hedges'g) for VR training using DerSimonian and Laird (DL) random effects models. We further assessed between-study heterogeneity, prediction interval (PI), publication bias, small-size studies, and whether the results of the observed positive studies were better than would be expected by chance. Based on these calculations, the quality of evidence for each outcome was assessed by using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) criteria. RESULTS: Four meta-analysis with eight outcomes included in the umbrella review was recalculated effect size. Pooled results found VR training can large improve the basic balance ability, moderate improve the overall balance capacity and moderate improve the stride length in PD patients. For ADL and QoL, the effect sizes were pooled that suggested VR training can moderate improve ADL and QoL for PD patients. However, no statistically clear evidence was found in walking speed, motor function and gait function during VR training. The analyzed meta-analyses showed low-to-moderate methodological quality (AMSTAR2) as well as presented evidence of moderate-to-very low quality (GRADE). Tow adverse reactions were reported in the included meta-analyses. CONCLUSIONS: In this umbrella review, a beneficial correlation between VR and balance ability, stride length, ADL and QoL in PD patients was discovered, especially for the very positive effect of VR on balance because of two of the eight outcomes related to balance ability showed large effect size. The observations were accompanied by moderate- to very low-quality rating evidence, supporting VR training as a practical approach to rehabilitation.

Neurotropin alleviates cognitive impairment by inhibiting TLR4/MyD88/NF-κB inflammation signaling pathway in mice with vascular dementia.

Vascular dementia (VD) is the second most common cause of dementia after Alzheimer's disease. Neuroinflammation contributes to pathogenesis of VD. Neurotropin (NTP) is an analgesic that has been shown to suppress inflammation and neural repair. But its effects on VD are still unclear. Therefore, this study aimed to investigate the therapeutic effects and potential mechanisms of NTP in the VD model mice established by bilateral common carotid artery stenosis method. In VD mice, we found that NTP treatment increased cerebral blood flow by Laser speckle imaging, reduced neuron loss by Nissl, HE and immunochemistry staining, attenuated white matter damage by magnetic resonance imaging and ultrastructural damage by transmission electron microscope, improved cognitive functions by new object recognition test and three-chamber test, Y maze test and Morris water maze test, inhibited significantly glial activation by immunofluorescence methods, reduced the expression of TLR4, down-regulated expression of MyD88 and phosphorylation of NF-κB P65, decreased the levels of pro-inflammatory cytokines IL-1ß, IL-6 and TNFα. Further, we showed that administration of a TLR4 inhibitor TAK242 had a similar effect to NTP, while the TLR4 agonist CRX-527 attenuated the effect of NTP in the VD mice. Collectively, our study suggested that NTP alleviates cognitive impairment by inhibiting TLR4/MyD88/NF-κB inflammation signaling pathway in the VD mice. Thus, NTP may be a promising therapeutic approach and a potential TLR4 inhibitor for VD.

Inhibiting Polyamide Intrusion of Thin Film Composite Membranes: Strategies and Environmental Implications.

Thin film composite polyamide (TFC) nanofiltration (NF) membranes represent extensive applications at the water-energy-environment nexus, which motivates unremitting efforts to explore membranes with higher performance. Intrusion of polyamide into substrate pores greatly restricts the overall membrane permeance because of the excessive hydraulic resistance, while the effective inhibition of intrusion remains technically challenging. Herein, we propose a synergetic regulation strategy of pore size and surface chemical composition of the substrate to optimize selective layer structure, achieving the inhibition of polyamide intrusion effective for the membrane separation performance enhancement. Although reducing the pore size of the substrate prevented polyamide intrusion at the intrapore, the membrane permeance was adversely affected due to the exacerbated "funnel effect". Optimizing the polyamide structure via surface chemical modification of the substrate, where reactive amino sites were in situ introduced by the ammonolysis of polyethersulfone substrate, allowed for maximum membrane permeance without reducing the substrate pore size. The optimal membrane exhibited excellent water permeance, ion selectivity, and emerging contaminants removal capability. The accurate optimization of selective layer is anticipated to provide a new avenue for the state-of-the-art membrane fabrication, which opens opportunities for promoting more efficient membrane-based water treatment applications.

Methamphetamine induces cardiomyopathy through GATA4/NF-κB/SASP axis-mediated cellular senescence.

With the world pandemic of methamphetamine (METH), METH-associated cardiomyopathy (MAC) has become a widespread epidemic and is also recognized as a cause of heart failure in young people. The mechanism of occurrence and development of MAC is not clear. In this study, firstly, the animal model was evaluated by echocardiography and myocardial pathological staining. The results revealed that the animal model exhibited cardiac injury consistent with clinical alterations of MAC, and the mice developed cardiac hypertrophy and fibrosis remodeling, which led to systolic dysfunction and left ventricular ejection fraction (%LVEF) < 40%. The expression of cellular senescence marker proteins (p16 and p21) and senescence-associated secretory phenotype (SASP) was significantly increased in mouse myocardial tissue. Secondly, mRNA sequencing analysis of cardiac tissues revealed the key molecule GATA4, and Western blot, qPCR and immunofluorescence results showed that the expression level of GATA4 was significantly increased after METH exposure. Finally, knockdown of GATA4 expression in H9C2 cells in vitro significantly attenuated METH-induced cardiomyocyte senescence. Consequently, METH causes cardiomyopathy through cellular senescence mediated by the GATA4/NF-κB/SASP axis, which is a feasible target for the treatment of MAC.

Clinical Characteristics of Chlamydia psittaci Pneumonia Confirmed by Metagenomic Next-Generation Sequencing.

BACKGROUND: Chlamydia psittaci pneumonia has atypical clinical manifestations and the diagnosis may be missed by traditional methods of microbiological diagnosis. METHODS: Twelve cases of Chlamydia psittaci pneumonia diagnosed by metagenomic next-generation sequencing (mNGS) in Huizhou Central People's Hospital in China between January 2020 and August 2021 were reviewed and analyzed, retrospectively, using hospital records, the clinical characteristics, treatment, and prognosis. RESULTS: Ten of the 12 cases (83%) were associated with a definite history of bird/poultry contact. Common symptoms included high fever, cough, fatigue, anorexia (12/12, 100%), dyspnea (11/12, 92%), and changes in the level of consciousness and headache (5/12, 42%). There was a marked increase in C-reactive protein and D-dimer levels, but white blood cells and neutrophils were normal or slightly increased. Nine patients (75%) had liver enzyme abnormalities, and six (50%) had cardiac insufficiency and myocardial injury. There was no correlation between the mNGS sequence number of Chlamydia psittaci and the pneumonia severity. The chest imaging manifestations were mainly large areas of consolidation, predominantly in the lower lung lobes. Monotherapies or combinations of doxycycline, moxifloxacin/levofloxacin, and azithromycin were effective for treating Chlamydia psittaci pneumonia. CONCLUSIONS: The use of mNGS increases the probability of diagnosing Chlamydia psittaci pneumonia, and good prognosis can be achieved with timely use of appropriate antibiotics.

New insight into methamphetamine-associated heart failure revealed by transcriptomic analyses: Circadian rhythm disorder.

Methamphetamine (METH) abuse is a significant public health concern globally. Cardiac toxicity is one of the important characteristics of METH, in addition to its effects on the nervous system. However, to date, research on the cardiotoxic injury induced by METH consumption has been insufficient. To systematically analyze the potential molecular mechanism of cardiac toxicity in METH-associated heart failure (HF), a rat model was constructed with a dose of 10 mg/kg of METH consumption. Cardiac function was evaluated by echocardiography, and HE staining was used to clarify the myocardial histopathological changes. Integrated analyses, including mRNA, miRNA and lncRNA, was performed to analyze the RNA expression profile and the potential molecular mechanisms involved in METH-associated HF. The results showed that METH caused decreased myocardial contractility, with a decreased percent ejection fraction (%EF). Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses of the RNAs with expression changes revealed abnormal circadian rhythm regulation in the METH groups, with circadian rhythm-related genes and their downstream effectors expressed differentially, especially the aryl hydrocarbon receptor nuclear translocator-like (Arntl). Competing endogenous RNA (ceRNA) networks associated with circadian rhythm, including Arntl, was also observed. Therefore, this study revealed that long-term METH consumption was associated with the HF in a rat model by decreasing the %EF, and that the abnormal circadian rhythm could provide new directions for investigating the METH-associated HF, and that the differentially expressed genes in this model could provide candidate genes for the identification and assessment of cardiac toxicity in METH-associated HF, which is fundamental for further understanding of the disease.

Methamphetamine exposure induces neuronal programmed necrosis by activating the receptor-interacting protein kinase 3 -related signalling pathway.

Methamphetamine (METH) is a synthetic drug with severe neurotoxicity, however, the regulation of METH-induced neuronal programmed necrosis remains poorly understood. The aim of this study was to identify the molecular mechanisms of METH-induced neuronal programmed necrosis. We found that neuronal programmed necrosis occurred in the striatum of brain samples from human and mice that were exposed to METH. The receptor-interacting protein kinase 3 (RIP3) was highly expressed in the neurons of human and mice exposed to METH, and RIP3-silenced or RIP1-inhibited protected neurons developed neuronal programmed necrosis in vitro and in vivo following METH exposure. Moreover, the RIP1-RIP3 complex causes cell programmed necrosis by regulating mixed lineage kinase domain-like protein (MLKL)-mediated cell membrane rupture and dynamin-related protein 1 (Drp1)-mediated mitochondrial fission. Together, these data indicate that RIP3 plays an indispensable role in the mechanism of METH-induced neuronal programmed necrosis, which may represent a potential therapeutic target for METH-induced neurotoxicity.

MiR-328-3p inhibits lung adenocarcinoma-genesis by downregulation PYCR1.

BACKGROUND: A vast majority of patients with NSCLC (non-small cell lung cancer) have lung adenocarcinoma (LA), and the survival rate of LA varies from 5% to 75% depending on the severity of this adenocarcinoma. PYCR1 (abnormal pyrroline-5-carboxylate reductase 1) gene and miR-328-3p have been found to be associated with cancer development. However, the underlying mechanism of interaction between miR-328-3p and PYCR1 in LA needs further investigation. METHODS: The expressions of miR-328-3p and PYCR1 in samples with LA were identified by RT-qPCR. Next, we investigated the targeting relationship between these two biological factors using luciferase assay. CCK-8, BrdU, transwell-migration, and flow cytometry assays were performed to detect cell viability, cell proliferation, cell migration and cell apoptosis in LA cells. RESULTS: We noticed that miR-328-3p expression was downregulated in LA samples. MiR-328-3p mimic restricted cell proliferation and cell migration, while it enhanced cell apoptosis. Furthermore, the overexpression of PYCR1 promoted the proliferation and migration of LA cells, but it repressed cell apoptosis. Moreover, PYCR1 directly interacted with miR-328-3p in the LA cells, and miR-328-3p restrained the expression of PYCR1, thus suppressing LA tumorigenesis. CONCLUSION: In summary, our study revealed that miR-328-3p targeting to PYCR1 suppressed the malignancy of LA cells by impeding cell proliferation and migration, while effectively promoting cell apoptosis.

Circ_0020123 Increases ZFX Expression to Facilitate Non-Small Cell Lung Cancer Progression by Sponging miR-142-3p.

BACKGROUND: Circular RNA (circRNA) is involved in the progression of various cancers and has been shown to be an important potential target for cancer therapy. Circ_0020123 has been found to act as oncogene to participate in the malignant progression of non-small cell lung cancer (NSCLC). Therefore, exploring new mechanisms of circ_0020123 regulating NSCLC progression will help us better understand its role in NSCLC. METHODS: Relative expression levels of circ_0020123, microRNA (miR)-142-3p, and zinc-finger protein X-linked (ZFX) in tissues and cells were determined by quantitative real-time PCR (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were assessed using cell counting kit 8 (CCK8) assay, colony formation assay, flow cytometry and transwell assay. Western blot (WB) analysis was used to detect relative protein level. Besides, the interaction between miR-142-3p and circ_0020123 or ZFX was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Our results showed that circ_0020123 was upregulated in NSCLC, and its knockdown could suppress NSCLC cell proliferation, migration, invasion, and promote apoptosis. Circ_0020123 was found to interact with miR-142-3p. The inhibition effect of circ_0020123 silencing on NSCLC progression could be reversed by miR-142-3p inhibitor. ZFX could be targeted by miR-142-3p. The silencing of ZFX could hinder the progression of NSCLC and abolish the promotion effect of miR-142-3p inhibitor on NSCLC progression. In addition, circ_0020123 silencing inhibited NSCLC tumorigenesis by the miR-142-3p/ZFX axis. CONCLUSION: These findings suggested that circ_0020123 might be a potential therapy target for NSCLC, which could promote NSCLC progression through regulating the miR-142-3p/ZFX axis.

[Analysis of clinical features of 16 cases with Chlamydia psittaci pneumonia].

OBJECTIVE: To analyze the clinical characteristics of Chlamydia psittaci pneumonia and to investigate the correlation between serum inflammatory biomarkers and severity of the disease. METHODS: Sixteen patients with Chlamydia psittaci pneumonia admitted to the Huizhou Municipal Central Hospital from January 2020 to July 2021 were selected as the study subjects, including 10 severe cases and 6 mild cases. Clinical data were collected and analyzed, such as baseline characteristics, clinical symptoms, laboratory inspection and chest imaging manifestations. RESULTS: (1) Thirteen Chlamydia psittaci pneumonia were associated with a definite bird or poultry contact history. Common symptoms included high fever, chill, cough, fatigue, and anorexia (16 cases), dyspnoea (12 cases), and other systemic symptoms. (2) Laboratory test results showed normal white blood cell count (WBC, 10 cases), decreased lymphocyte count (LYM, 13 cases), increased high sensitive C-reactive protein (hs-CRP, 16 cases), D-dimer (15 cases), lactate dehydrogenase (LDH, 13 cases), aspartate aminotransferase (AST, 16 cases) and alanine aminotransferase (ALT, 12 cases) levels, however, the albumin (Alb, 15 cases) lever was decreased. The numbers of CD3+ T cells and CD4+ T cells decreased in 10 patients. (3) The levels of D-dimer, interleukins (IL-2, IL-6, IL-10) in severe Chlamydia psittaci pneumonia were significantly higher than those in mild Chlamydia psittaci pneumonia [D-dimer (µg/L): 10 257±4 203 vs. 1 085±642, IL-2 (ng/L): 1.1 (0.8, 1.7) vs. 0.3 (0.1, 0.7), IL-6 (ng/L): 315 (182, 505) vs. 75 (18, 131), IL-10 (ng/L): 7.0±4.1 vs. 2.3±0.7], but the LYM was lower (×109/L: 0.4±0.1 vs. 1.1±0.4), with significant differences (all P < 0.05). (4) Chest imaging manifestations were exudative lesions and large consolidation of lungs. Large consolidation of both lungs can occur in some critically ill patients. CONCLUSIONS: Chlamydia psittaci pneumonia is mainly associated with a bird or poultry contact history. The clinical manifestations usually present high fever, dyspnea, normal or slightly increased leucocytes, and lung consolidation. The levels of LYM, D-dimer, IL-2, IL-6 and IL-10 in serum are expected to predict the severity of the Chlamydia psittaci pneumonia.

Astrocyte-Derived Lipocalin-2 Is Involved in Mitochondrion-Related Neuronal Apoptosis Induced by Methamphetamine.

Methamphetamine (METH) is a widely abused and highly addictive psychoactive stimulant that can induce neuronal apoptosis. Lipocalin-2 (LCN2) is a member of the lipocalin family, and its upregulation is involved in cell death in the adult brain. However, the role of LCN2 in METH-induced neurotoxicity has not been reported. In this study, we found that LCN2 was predominantly expressed in hippocampal astrocytes after METH exposure and that recombinant LCN2 (Re LCN2) can induce neuronal apoptosis in vitro and in vivo. The inhibition of LCN2 and LCN2R, a cell surface receptor for LCN2, reduced METH- and Re LCN2-induced mitochondrion-related neuronal apoptosis in cultures of primary rat neurons and animal models. Our study supports the role of reactive oxygen species (ROS) generation and the PRKR-like ER kinase (PERK)-mediated signaling pathway in the upregulation of astrocyte-derived LCN2 after METH exposure. Additionally, the serum and cerebrospinal fluid (CSF) levels of LCN2 were significantly upregulated after METH exposure. These results indicate that upregulation of astrocyte-derived LCN2 binding to LCN2R is involved in METH-induced mitochondrion-related neuronal apoptosis.

Role of C/EBP-ß in Methamphetamine-Mediated Microglial Apoptosis.

Methamphetamine (MA) is a widely abused psychoactive drug that primarily damages the nervous system. However, the involvement of MA in the survival of microglia remains poorly understood. CCAAT-enhancer binding protein (C/EBP-ß) is a transcription factor and an important regulator of cell apoptosis. Lipocalin2 (lcn2) is a known apoptosis inducer and is involved in many cell death processes. We hypothesized that C/EBP-ß is involved in MA-induced lcn2-mediated microglial apoptosis. To test this hypothesis, we measured the protein expression of C/EBP-ß after MA treatment and evaluated the effects of silencing C/EBP-ß or lcn2 on MA-induced apoptosis in BV-2 cells and the mouse striatum after intrastriatal MA injection. MA exposure increased the expression of C/EBP-ß and stimulated the lcn2-mediated modulation of apoptosis. Moreover, silencing the C/EBP-ß-dependent lcn2 upregulation reversed the MA-induced microglial apoptosis. The in vivo relevance of these findings was confirmed in mouse models, which demonstrated that the microinjection of anti-C/EBP-ß into the striatum ameliorated the MA-induced decrease survival of microglia. These findings provide a new insight regarding the specific contributions of C/EBP-ß-lcn2 to microglial survival in the context of MA abuse.

Correction to: A multimodal imaging features of the brain in adult-onset neuronal intranuclear inclusion disease.

In the original article, Zaiqiang Zhang was affiliated to Department of Neurology, Beijing Hospital, National Center of Gerontology, Beijing, China. The corrected affiliation should be: Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Is hyperhomocysteinemia associated with the structural changes of the substantia nigra in Parkinson's disease? A two-year follow-up study.

OBJECTIVE: It was recently found that structural changes in the substantia nigra (SN) and motor symptoms become more prominent in Parkinson's disease (PD) patients with striatal silent lacunar infarction (SSLI) than in those without SSLI. Hyperhomocysteinemia (HHCY) was an independent risk factor for SSLI in PD patients. In this follow-up study, we investigated the relationship between HHCY and structural changes of the SN in PD patients. METHODS: A total of 72 untreated early PD patients without SSLI, divided into control and HHCY groups, were enrolled in this study. All participants underwent conventional MRI and diffusion kurtosis imaging (DKI) twice; at baseline and at the 2-year visit. The differences of the following variables between the two groups were analyzed: mean kurtosis (MK) values of the SN, the severity of disease, daily dosage of levodopa, and the variation of these indexes from baseline to 2-year visit. Logistic regression analysis was used to identify the relationship between HHCY and structural changes of the SN in PD patients. RESULTS: 1.All variables mentioned above showed significant differences between the two groups. 2. The variation in MK values of the SN were positively correlated with the variation in the severity of disease. 3. HHCY was an independent risk factor for the variation in MK values of the SN in PD patients. CONCLUSION: HHCY is associated with the structural changes of the SN in PD patients. As PD progresses, motor symptoms become aggravated with increased structural changes to the SN, especially in patients with HHCY.

The effects of striatal silent lacunar infarction on the substantia nigra and movement disorders in Parkinson's disease: A follow-up study.

OBJECTIVE: Striatal silent lacunar infarction (SSLI) is associated with structural changes to the substantia nigra (SN), detectable by diffusion kurtosis imaging (DKI). In this follow-up study, we investigated the effects of SSLI on the SN and movement disorders in patients with Parkinson's disease (PD). METHODS: A total of 60 untreated patients with early-stage PD, divided into control and SSLI groups, were enrolled in this study. All participants underwent conventional MRI and DKI twice; at baseline and after a 1-year period. We analyzed the differences of the following variables between the two groups: mean kurtosis (MK) values of the SN, the severity of disease, daily dosage of levodopa, and the variation of these indexes from baseline to 1-year visit. Logistic regression analysis was used to identify the major risk factors for SSLI in PD patients. RESULTS: 1. All variables showed significant differences between the two groups. 2. The variation in MK values of the SN had a positive correlation with the variation in the severity of disease. 3. Hypertension and hyperhomocysteinemia were independent factors for SSLI in patients with PD. CONCLUSION: As PD progresses, movement disorders become more prominent, with increased structural changes to the SN, especially in patients with SSLI. Furthermore, PD patients with hypertension and hyperhomocysteinemia are more likely to have SSLI.

Elevated Plasma Homocysteine Level Increased the Risk of Early Renal Impairment in Acute Ischemic Stroke Patients.

Renal insufficiency is associated with the prognosis of acute ischemic stroke (AIS) and homocysteine (Hcy) levels. This study investigated the association between plasma Hcy levels and renal insufficiency in patients with AIS. A total of 987 patients with AIS who had been treated at the First People's Hospital of Foshan between 2011 and 2014 were retrospectively studied. Based on their cystatin C (Cys C) levels, the patients were divided into the normal renal function group (Cys C ≤ 1.25 mg/L) or the renal impairment group (Cys C > 1.25 mg/L). Multivariate regression analysis was applied to reveal the association between hyperhomocysteinemia (HHcy) and renal impairment. The renal impairment group showed more advanced age of onset, higher percentage of prior stroke and hypertension, higher baseline National Institute of Health Stroke Scale score, lower high-density lipoprotein cholesterol levels, and higher Hcy levels compared with the normal renal function group. A multivariate analysis revealed a relationship between early renal impairment and Hcy levels: an increase of Hcy by 1 µmol/L was associated with an increase of 12-18% of the risk of renal impairment among patients with AIS and HHcy. Patients with AIS and HHcy had a 2.42-3.51 fold increase of the risk of renal impairment compared with patients with normal Hcy level (P < 0.001). In conclusion, patients with stroke and HHcy could be more prone to renal impairment.

Simultaneous energy recovery and autotrophic nitrogen removal from sewage at moderately low temperatures.

This study assessed the technical feasibility of treating sewage with a combination of direct anaerobic treatment and autotrophic nitrogen removal, while simultaneously achieving energy recovery and nitrogen removal under moderately low temperatures. The concentrations of ammonia, nitrite, and COD in effluent were below 1, 0.1, and 30 mg/L, respectively. In the up-flow, anaerobic sludge fixed-bed, there was no obvious change observed in the total methane production at temperatures of 35 ± 1 °C, 28 ± 1 °C, 24 ± 3 °C, and 17 ± 3 °C, with the accumulation of volatile fatty acids occurring with decreasing temperatures. The control strategy employed in this study achieved a stable effluent with equimolar concentrations of nitrite and ammonium, coupled with high nitrite accumulation (>97 %) in the partial nitrification sequencing batch reactor system at moderately low temperatures. In the anaerobic ammonium oxidation (anammox) reactor, a short hydraulic retention time of 0.96 h, with a nitrogen removal rate of 0.83 kgN/(m(3)/day) was achieved at 12-15 °C. At low temperatures, the corresponding fluorescence in situ hybridization image revealed a high amount of anammox bacteria. This study demonstrates that efficient nitrogen removal and energy recovery from sewage at moderately low temperatures can be achieved by utilizing a combined system. Additionally, this system has the potential to become energy-neutral or even energy-producing.

[Influence of different recovery methods on the activity of nitrification granular sludge].

Aerobic nitrifying granule sludge cultivated in sequential batch reactor (SBR) was used to investigate the critical activity point of granules and the effect of different ammonia concentration and aeration time on reactivation after storage. The results showed that there was big difference in the activity (SOUR, 02/VSS) of nitrifying bacteria after different storage time. The specific oxygen utilization rate (SOUR) of granules before storage was 13. 15 mg.(g h)-1. After a storage period of 20 days, the SOUR decreased by 1.26 mg.(g.h)-1 , after 5 cycles of reactivation, the ammonia removal efficiency was already increased to 95% while the SOUR was recovered to 13.87 mg.(g.h)-1. But after a storage period of 30 days, the SOUR decreased by 11.63 mg.(g.h)-1, after 51 cycles of reactivation, the ammonia removal efficiecny only eached 92. 64% while the SOUR was recovered to 14.92 mg.(g.h)-1. Meanwhile, this storage method required a longer recovery time. Therefore, we put forward that the critical activity of denitrifying granular sludge should be the activity when activity recovery starts and the nitrifying bacteria SOUR begins to decline. On the basis of the critical activity, we began to restore the activity when the activity of the denitrifying bacteria was reduced to critical activity, and then started a new storage cycle. This storage method was named dynamic storage. Different influent ammonia concentrations of 20, 30 and40 mg.L-1 were applied to reactivate the aerobic granules. Highest SOUR could be achieved when fed with an ammonia concentration of 40 mg.L-1 after reactivation. After three times of dynamic storage, the SOUR remained stable. Different aeration time of 1, 2 and 3 h was applied to reactivate the aerobic granules. Highest SOUR could be obtained when aeration time of 1 h was applied after reactivation and remained stable along with dynamic storage.