Concentration properties of biopolymers via dead-end forward osmosis.

Extracellular polymeric substances (EPSs) in excess sludge of wastewater treatment plants are valuable biopolymers that can act as recovery materials. However, effectively concentrating EPSs consumes a significant amount of energy. This study employed novel energy-saving pressure-free dead-end forward osmosis (DEFO) technology to concentrate various biopolymers, including EPSs and model biopolymers [sodium alginate (SA), bovine serum albumin (BSA), and a mixture of both (denoted as BSA-SA)]. The feasibility of the DEFO technology was proven and the largest concentration ratios for these biopolymers were 94.8 % for EPSs, 97.1 % for SA, 97.8 % for BSA, and 98.4 % for BSA-SA solutions. An evaluation model was proposed, incorporating the FO membrane's water permeability coefficient and the concentrated substances' osmotic resistance, to describe biopolymers' concentration properties. Irrespective of biopolymer type, the water permeability coefficient decreased with increasing osmotic pressure, remained constant with increasing feed solution (FS) concentration, increased with increasing crossing velocity in the draw side, and showed little dependence on draw salt type. In the EPS DEFO concentration process, osmotic resistance was minimally impacted by osmotic pressure, FS concentration, and crossing velocity, and monovalent metal salts were proposed as draw solutes. The interaction between reverse diffusion metal cations and EPSs affected the structure of the concentrated substances on the FO membrane, thus changing the osmotic resistance in the DEFO process. These findings offer insights into the efficient concentration of biopolymers using DEFO.

Risk factors for poor progression of addictive internet use across different COVID-19 periods in China.

BACKGROUND AND OBJECTIVES: Addictive behaviors are serious factors for mental health and usually increase during public crises. We identified the vulnerable characteristics for bad prognosis of addictive internet use across different periods of the coronavirus disease 2019 (COVID-19) pandemic. METHODS: Self-reported questionnaires were delivered in three waves through jdh.com during the outbreak (n = 17,960), remission (n = 15,666), and dynamic zero (n = 12,158) periods of COVID-19 pandemic in China. Internet addiction degree was assessed using the Internet Addiction Test. The different progression groups were divided using a latent class growth model among 1679 longitudinal participants. Risk factors for bad progression were identified by two-step logistic regression. RESULTS: A total of 40.16% of participants reported an increase in the addictive degree of internet use compared with prepandemic. Across different COVID-19 periods, the overall trend of addictive internet use was downward among general Chinese study participants (Mslope = -1.56). Childhood traumatic experiences, deterioration of physical health, depression, and anxiety during remission and dynamic periods were the main risk factors for the bad progression of pandemic-induced addictive internet use. DISCUSSION AND CONCLUSIONS: Addictive internet use was remitted following relaxed control policies during the COVID-19 pandemic. Negative childhood experiences and bad mental status during the recovery period were harmful to coping with pandemic-related addictive internet use. SCIENTIFIC SIGNIFICANCE: Our findings profiled the general trend of addictive internet use and the vulnerable characteristics of its bad progression across different periods of the first wave of COVID-19 pandemic in China. Our findings provide valuable insights for preventing the long-term adverse effects of negative public events on Internet addiction.

A collaborative secret sharing scheme based on the Chinese Remainder Theorem.

Secret sharing (SS) can be used as an important group key management technique for distributed cloud storage and cloud computing. In a traditional threshold SS scheme, a secret is shared among a number of participants and each participant receives one share. In many real-world applications, some participants are involved in multiple SS schemes with group collaboration supports thus have more privileges than the others. To address this issue, we could assign multiple shares to such participants. However, this is not a bandwidth efficient solution. Therefore, a more sophisticated mechanism is required. In this paper, we propose an efficient collaborative secret sharing (CSS) scheme specially tailored for multi-privilege participants in group collaboration. The CSS scheme between two or among more SS schemes is constructed by rearranging multi-privilege participants in each participant set and then formulated into several independent SS schemes with multi-privilege shares that precludes information leakage. Our scheme is based on the Chinese Remainder Theorem with lower recovery complexity and it allows each multi-privilege participant to keep only one share. It can be formally proved that our scheme achieves asymptotically perfect security. The experimental results demonstrate that it is efficient to achieve group collaboration, and it has computational advantages, compared with the existing works in the literature.

Dissociating nNOS (Neuronal NO Synthase)-CAPON (Carboxy-Terminal Postsynaptic Density-95/Discs Large/Zona Occludens-1 Ligand of nNOS) Interaction Promotes Functional Recovery After Stroke via Enhanced Structural Neuroplasticity.

Background and Purpose- Stroke is a major public health concern worldwide. Although clinical treatments have improved in the acute period after stroke, long-term therapeutics remain limited to physical rehabilitation in the delayed phase. This study is aimed to determine whether nNOS (neuronal NO synthase)-CAPON (carboxy-terminal postsynaptic density-95/discs large/zona occludens-1 ligand of nNOS) interaction may serve as a new therapeutic target in the delayed phase for stroke recovery. Methods- Photothrombotic stroke and transient middle cerebral artery occlusion were induced in mice. Adeno-associated virus (AAV)-cytomegalovirus (CMV)-CAPON-125C-GFP (green fluorescent protein)-3Flag and the other 2 drugs (Tat-CAPON-12C and ZLc-002) were microinjected into the peri-infarct cortex immediately and 4 to 10 days after photothrombotic stroke, respectively. ZLc-002 was also systemically injected 4 to 10 days after transient middle cerebral artery occlusion. Grid-walking task and cylinder task were conducted to assess motor function. Western blotting, immunohistochemistry, Golgi staining, and electrophysiology recordings were performed to uncover the mechanisms. Results- Stroke increased nNOS-CAPON association in the peri-infarct cortex in the delayed period. Inhibiting the ischemia-induced nNOS-CAPON association substantially decreased the number of foot faults in the grid-walking task and forelimb asymmetry in the cylinder task, suggesting the promotion of functional recovery from stroke. Moreover, dissociating nNOS-CAPON significantly facilitated dendritic remodeling and synaptic transmission, indicated by increased dendritic spine density, dendritic branching, and length and miniature excitatory postsynaptic current frequency but did not affect stroke-elicited neuronal loss, infarct size, or cerebral edema, suggesting that nNOS-CAPON interaction may function via regulating structural neuroplasticity, rather than neuroprotection. Furthermore, ZLc-002 reversed the transient middle cerebral artery occlusion-induced impairment of motor function. Conclusions- Our results reveal that nNOS-CAPON coupling can serve as a novel pharmacological target for functional restoration after stroke.

2-Methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine, an edaravone analog, exerts neuroprotective effects against acute ischemic injury via inhibiting oxidative stress.

Oxidative stress plays an indispensable role in the pathogenesis of cerebral ischemia. Inhibiting oxidative stress has been considered as an effective approach for stroke treatment. Edaravone, a free radical scavenger, has been shown to prevent cerebral ischemic injury. However, the clinical efficacy of edaravone is limited because it has a low scavenging activity for superoxide anions (O2·-). Here, we report that 2-methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine, a novel small-molecule compound structurally related to edaravone, showed a stronger inhibitory effect on oxidative stress in vitro. In vivo, 2-methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine reversed transient middle cerebral artery occlusion-induced dysfunctions of superoxide dismutases and malondialdehyde, two proteins crucial for oxidative stress, suggesting a strengthened antioxidant system. Moreover, 2-methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine decreased blood brain barrier permeability. Then, we found that 2-methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine had a stronger neuroprotective effect than edaravone. More importantly, 2-methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine decreased not only infarct size and neurological deficits in the acute phase but also modified neurological severity score and escape latency in Morris water maze task in the delayed period, indicating enhanced neuroprotection, sensorimotor function and spatial memory. Together, these findings suggest that 2-methyl-5H-benzo[d]pyrazolo[5,1-b][1,3]oxazin-5-imine could be a preferable option for stroke treatment.

[Pathologic changes of the cardiac conduction system in 12 patients with abnormal ECG].

OBJECTIVE: To investigate the relationship between abnormal ECG and pathologic changes in the cardiac conduction system (CCS). METHOD: Pathological changes of the CCS in 12 cases with abnormal ECG out of 16 pre-death ECG were observed. RESULTS: (1) Among 7 cases of sudden cardiac death, ECG monitoring recorded bradyarrhythmia in 6 cases, tachyarrhythmia 6 cases, bradycardia-tachycardia syndrome 2 cases, conduction block 6 cases, atrial premature beats 6 cases, ventricular premature beats 6 cases, and ST-T changes 4 cases. (2) The histopathological findings in the CCS were noted in all cases. Of these 12 cases, three had signs of fatty infiltration, and/or fibrous 4 cases, three of amyloidosis, one of chronic inflammatory changes, two of acute inflammatory changes, two of developmental anomalies, two of hemorrhages and one of LAD stenosis. (3) Acute inflammation changes in the CCS corresponded to tachyarrhythmia and multiple ventricular premature beats, whereas chronic inflammation and degenerative changes in the CCS were often related to bradyarrhythmia, bradycardia-tachycardia syndrome and conduction block. (4) The CCS changes alone could lead to ST-T changes in ECG. CONCLUSION: The pathological changes in the CCS are related to ECG changes, and attributed to the pathological bases of arrhythmia.

[Traumatic cerebral infarction: a histopathological study of 17 cases].

OBJECTIVE: To assess the morphologic changes in traumatic cerebral infarction and to discuss its mechanism. METHODS: Specimens from seventeen cases of cerebral infarction were selected from 81 patients with severe brain injury, and subject to routine gross and histological examinations. RESULTS: (1) The cerebral infarction in all cases was hemorrhagic in nature with a wedged or irregular shape upon gross inspection. The lesions were found in occipital gyrus (8 cases), occipital lobes (3 cases), basal nuclei (3 cases), cingulate gyrus (2 cases), and lateral occipitotemporal gyrus (1 case). Histologically, the lesions were located at the junction between the cortex and medulla, showing congestion, edema, hemorrhage, necrotic nerve tissue and blood vessels. In severe cases, the lesion extended into the entire cortex and subarachnoid spaces. (2) Swelling of the brain and cerebral hernia were found in all cases, 8 of which demonstrated that the posterior cerebral artery was compressed and stenotic within the space between the crus cerebri and uncus. CONCLUSION: Brain tissue necrosis in traumatic cerebral infarction is the result of brain swelling and cerebral hernia formation, following congestion, bleeding and ischemia due to vasculature compression.