Effective separation of dyes/salts by sulfonated covalent organic framework membranes based on phenolamine network conditioning.

This study developed a modified polyacrylonitrile (PAN) membrane controlled by a phenol-amine network and enhanced with a sulfonated covalent organic framework (SCOF), aimed at improving the efficiency of textile wastewater treatment. Utilizing a phenol-amine network control strategy allows for precise manipulation of interfacial reactions in the synthesis of SCOF, achieving highly uniform modification on the surface of the PAN membrane. This modified membrane demonstrated high rejection of over 98% for various water-soluble dyes, including Alcian blue 8GX, Coomassie Brilliant Blue G250, methyl blue, congo red, and rose bengal, and also exhibited specific selectivity in processing salt-containing wastewater. By adjusting the deposition time of the phenol-amine and the concentration of SCOF monomers, optimal retention performance and permeate flux were achieved, effectively separating dyes and salts. This research provides a new and effective solution for treating textile wastewater, especially in separating and recovering dyes and salts, offering broad application prospects in environmental management and water resource management, and highlighting its significant practical implications.

A high-protein retained PES hemodialysis membrane with tannic acid as a multifunctional modifier.

A high protein retention polyethersulfone (PES) membrane was prepared by nonsolvent-induced phase separation and surface coating, which exhibited enhanced hemocompatibility and antioxidant stress performance. The cross-linked network was constructed by tannic acid (TA) and alpha-lipoic acid (α-LA) on the surface of the membrane, which controlled the pores to a reasonable size. The enrichment of heparin-like groups on the membrane surface, implemented by "hydrophobic interaction" and "click reaction", confers anticoagulant properties; the presence of a large number of phenolic hydroxyl groups from TA and the introduction of α-LA allows the modified membranes to intervene in oxidative stress. The hemocompatibility characterizations included plasma recalcification time (PRT), activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT) and hemolysis rate (HR). Additionally, the DPPH ABTS radical scavenging capacity was tested to evaluate the antioxidant performance. The results show that the modified membrane presents an outstanding protein retention rate (99.3%) along with permeability. In addition, the PRT is prolonged to 341.7 s, and the DPPH• scavenging ability reaches 0.74 µmol•cm-2. The membranes can be easily prepared and present excellent comprehensive performance. This work provides a simple and facile strategy for the fabrication of hemodialysis membranes with controllable pore sizes.

Novel mutation in optineurin causing aggressive ALS+/-frontotemporal dementia.

OBJECTIVE: Mutations in optineurin (OPTN) have been identified in familial and sporadic amyotrophic lateral sclerosis (ALS). We screened a cohort of Chinese patients for mutations in optineurin. We also performed an extensive literatures review of all mutations in optineurin identified previously to detect genotype-phenotype associations. METHODS: All 16 exons of the OPTN gene in a cohort of 15 familial ALS indexes and 275 sporadic ALS patients of Chinese origin were sequenced by targeted next generation sequencing. RESULTS: Two known heterozygous missense mutations in the OPTN, c.1481T> G (p.L494W), and c.1546G> C (p.E516Q), as well as one novel heterozygous missense mutation c.1690G> C (p.D564H) were each detected in one sporadic ALS patient. The patient carrying the p.E516Q mutation developed clinical features of ALS-frontotemporal dementia (FTD) and the patient carrying the p.D564H mutation showed a phenotype of ALS. They both had an aggressive course, with a survival of 18 and 14 months respectively. Literature review showed that the clinical phenotypes in OPTN mutated ALS were not homogeneous, although some individuals showed a relatively slow progression and a long duration, some mutations carriers developed an aggressive progression and a short survival. INTERPRETATION: OPTN mutations contribute to ALS in Chinese population and account for 0.8% of sporadic ALS patients and 1.5% of familial ALS in the pooled Chinese ALS cohorts. Mutations in optineurin can cause aggressive ALS+/-FTD.

A novel VRK1 mutation associated with recessive distal hereditary motor neuropathy.

Vaccinia-related kinase 1 (VRK1) mutations can cause motor phenotypes including axonal sensorimotor neuropathy, distal hereditary motor neuropathy (dHMN), spinal muscular atrophy, and amyotrophic lateral sclerosis. Here, we identify a novel homozygous VRK1 p.W375X mutation causing recessive dHMN. The proband presented with juvenile onset of weakness in the distal lower extremities, slowly progressing to the distal upper limbs, with bilateral pes cavus and no upper motor or sensory neuron involvement. Nerve conduction studies showed a pure motor axonal neuropathy. Our findings extend the ethnic distribution of VRK1 mutations, indicating that these mutations should be included in genetic diagnostic testing for dHMN.

Superoleophobic micro-nanostructure surface formation of PVDF membranes by tannin and a condensed silane coupling agent.

A tannin-based hybrid coating was coated on the PVDF membrane surface through a simple one-step co-deposition of tannin and KH550. A micro/nano hierarchical structure was formed on the PVDF membrane surface through hydrolysis/condensation of KH550 and Michael addition reaction between oxidized tannin and an amino group revealed by the field-emission scanning electron microscopy, atomic force microscopy and Fourier transform infrared spectroscopy, which established a harsh surface. Abundant hydrophilic groups and high surface roughness endowed the modified membranes with high hydrophilicity and underwater superoleophobicity. The modified PVDF membranes possess excellent oil/water separation and antifouling performance due to the underwater superoleophobicity. Moreover, the modified membrane exhibited outstanding stability.

Valproate Attenuates 25-kDa C-Terminal Fragment of TDP-43-Induced Neuronal Toxicity via Suppressing Endoplasmic Reticulum Stress and Activating Autophagy.

Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disease. To date, there is no any effective pharmacological treatment for improving patients' symptoms and quality of life. Rapidly emerging evidence suggests that C-terminal fragments (CTFs) of TAR DNA-binding protein of 43 kDa (TDP-43), including TDP-35 and TDP-25, may play an important role in ALS pathogenesis. Valproate (VPA), a widely used antiepileptic drug, has neuroprotective effects on neurodegenerative disorders. As for ALS, preclinical studies also provide encouraging evidence for multiple beneficial effects in ALS mouse models. However, the potential molecular mechanisms have not been explored. Here, we show protective effects of VPA against TDP-43 CTFs-mediated neuronal toxicity and its underlying mechanisms in vitro. Remarkably, TDP-43 CTFs induced neuronal damage via endoplastic reticulum (ER) stress-mediated apoptosis. Furthermore, autophagic self-defense system was activated to reduce TDP-43 CTFs-induced neuronal death. Finally, VPA attenuated TDP-25-induced neuronal toxicity via suppressing ER stress-mediated apoptosis and enhancing autophagy. Taken together, these results demonstrate that VPA exerts neuroprotective effects against TDP-43 CTFs-induced neuronal damage. Thus, we provide new molecular evidence for VPA treatment in patients with ALS and other TDP-43 proteinopathies.

An adult case of multiphasic disseminated encephalomyelitis manifesting with optic neuritis.

A 25-year-old woman presented with a fever, headache, vomiting and somnolence. Cranial magnetic resonance imaging (MRI) showed multiple lesions in the cerebellum, brainstem, cerebral cortex and subcortex. Oligoclonal bands were positive in the cerebral spinal fluid (CSF). She experienced a good recovery after steroid treatment. Four months later, she developed right vision loss. Repeated MRI showed multiple cranial lesions different from those involved in the first attack in both size and distribution. An abnormal high signal was also observed in the front and intraorbital regions of the right optic nerve. The patient's vision progressively improved, and she obtained a full recovery following the administration of steroids. A diagnosis of multiphasic disseminated encephalomyelitis manifesting with optic neuritis was made.

Neuroprotective effects of new protein kinase C activator TPPB against Aß25₋35 induced neurotoxicity in PC12 cells.

Alzheimer's disease (AD) is pathologically characterized by presence of senile plaques in the hippocampus, which are composed mainly of extracellular deposition of a polypeptide known as the beta amyloid, the Aß. It has been demonstrated on numerous occasions that it was the deposition and aggregation of this Aß peptide that cause neuronal dysfunction and even finally, the dementia. Lowering the deposition of Aß or decreasing its neurotoxicity has long been one of the purposes of AD therapy. In previous study, we reported that protein kinase C (PKC) activator TPPB could regulate APP processing by increasing α-secretase activity. In this study we further investigated the potential neuroprotective effect of TPPB against Aß(25-35)-induced neurotoxicity in PC12 cells. The results indicated that TPPB at concentration of 1 µM could antagonize Aß(25-35) induced cell damage as evidenced by MTT assays, LDH release and by morphological changes. Furthermore, the neuroprotection in cell viability can be blocked by inhibitors of PKC, Akt and MAPK. The experiment also indicated that TPPB could increase the phosphorylation of Akt, PKC, MARCKS and MAPK, which were inhibited by Aß(25-35) treatment. Finally, TPPB inhibited the activation of caspase-3 induced by Aß(25-35). Taken together, the experiment here implies that TPPB has a role against Aß(25-35)-induced neurotoxicity in PC12 cells and may suggest its therapeutic potential in AD.