Microstate-based brain network dynamics distinguishing temporal lobe epilepsy patients: A machine learning approach.

Temporal lobe epilepsy (TLE) stands as the predominant adult focal epilepsy syndrome, characterized by dysfunctional intrinsic brain dynamics. However, the precise mechanisms underlying seizures in these patients remain elusive. Our study encompassed 116 TLE patients compared with 51 healthy controls. Employing microstate analysis, we assessed brain dynamic disparities between TLE patients and healthy controls, as well as between drug-resistant epilepsy (DRE) and drug-sensitive epilepsy (DSE) patients. We constructed dynamic functional connectivity networks based on microstates and quantified their spatial and temporal variability. Utilizing these brain network features, we developed machine learning models to discriminate between TLE patients and healthy controls, and between DRE and DSE patients. Temporal dynamics in TLE patients exhibited significant acceleration compared to healthy controls, along with heightened synchronization and instability in brain networks. Moreover, DRE patients displayed notably lower spatial variability in certain parts of microstate B, E and F dynamic functional connectivity networks, while temporal variability in certain parts of microstate E and G dynamic functional connectivity networks was markedly higher in DRE patients compared to DSE patients. The machine learning model based on these spatiotemporal metrics effectively differentiated TLE patients from healthy controls and discerned DRE from DSE patients. The accelerated microstate dynamics and disrupted microstate sequences observed in TLE patients mirror highly unstable intrinsic brain dynamics, potentially underlying abnormal discharges. Additionally, the presence of highly synchronized and unstable activities in brain networks of DRE patients signifies the establishment of stable epileptogenic networks, contributing to the poor responsiveness to antiseizure medications. The model based on spatiotemporal metrics demonstrated robust predictive performance, accurately distinguishing both TLE patients from healthy controls and DRE patients from DSE patients.

o-Semiquinone Radical and o-Benzoquinone Selectively Degrade Aniline Contaminants in the Periodate-Mediated Advanced Oxidation Process.

Advanced oxidation processes (AOPs) often employ strong oxidizing inorganic radicals (e.g., hydroxyl and sulfate radicals) to oxidize contaminants in water treatment. However, the water matrix could scavenge the strong oxidizing radicals, significantly deteriorating the treatment efficiency. Here, we report a periodate/catechol process in which reactive quinone species (RQS) including the o-semiquinone radical (o-SQ•-) and o-benzoquinone (o-Q) were dominant to effectively degrade anilines within 60 s. The second-order reaction rate constants of o-SQ•- and o-Q with aniline were determined to be 1.0 × 108 and 4.0 × 103 M-1 s-1, respectively, at pH 7.0, which accounted for 21% and 79% of the degradation of aniline with a periodate-to-catechol molar ratio of 1:1. The major byproducts were generated via addition or polymerization. The RQS-based process exhibited excellent anti-interference performance in the degradation of aniline-containing contaminants in real water samples in the presence of diverse inorganic ions and organics. Subsequently, we extended the RQS-based process by employing tea extract and dissolved organic matter as catechol replacements as well as metal ions [e.g., Fe(III) or Cu(II)] as periodate replacements, which also exhibited good performance in aniline degradation. This study provides a novel strategy to develop RQS-based AOPs for the highly selective degradation of aniline-containing emerging contaminants.

Recovery and genetic characterization of black queen cell virus.

Black queen cell virus (BQCV) is a severe threat to the honeybee (Apis mellifera) worldwide. Although several BQCV strains have been reported in China, the molecular basis for BQCV pathogenicity has not been well understood. Thus, a reverse genetic system of BQCV is required for studying viral replication and its pathogenic mechanism. Here, the complete genome sequence of BQCV was obtained from honeybees using reverse transcription PCR (RT-PCR), namely a BQCV China-GS1 strain (KY741959). Then, a phylogenetic tree was built to analyse the genetic relationships among BQCV strains from different regions. Our results showed that the BQCV China-GS1 contained two ORFs, consistent with the known reference strains, except for the BQCV China-JL1 strain (KP119603). Furthermore, the infectious clone of BQCV was constructed based on BQCV China-GS1 using a low copy vector pACYC177 and gene recombination. Due to the lack of culture cells for bee viruses, we infected the healthy bees with infectious clone of BQCV, and the rescued BQCV resulted in the recovery of recombinant virus, which induced higher mortality than those of the control group. Immune response after inoculated with BQCV further confirmed that the infectious clone of BQCV caused the cellular and humoral immune response of honeybee (A. mellifera). In conclusion, the full nucleotide sequence of BQCV China-GS1 strain was determined, and the infectious clone of BQCV was constructed in this study. These data will improve the understanding of pathogenesis and the host immune responses to viral infection.

[Analysis of three patients with KBG syndrome and epileptic seizures due to variants of ANKRD11 gene].

OBJECTIVE: To summarize the clinical phenotype and genotypic characteristics of 3 patients with KBG syndrome and epileptic seizure. METHODS: Clinical data of the patients were collected. Family-trio whole exon sequencing (WES) was carried out. Candidate variants were verified by Sanger sequencing. RESULTS: Patients 1 and 2 were boys, and patient 3 was an adult woman. All patients had epileptic seizures and mental deficiency. Their facial features included triangular face, low hair line, hypertelorism, large forward leaning auricles, broad nasal bridge, upturned nostrils, long philtrum, arched upper lip, and macrodontia. The two boys also had bilateral Simian creases. WES revealed that the three patients all harbored heterozygous de novo frameshift variants in exon 9 of the ANKRD11 gene including c.2948delG (p.Ser983Metfs*335), c.5397_c.5398insC (p.Glu1800Argfs*150) and c.1180_c.1184delAATAA (p.Asn394Hisfs*42). So far 291 patients with ANKRD11 gene variants or 16q24.3 microdeletions were reported, with over 75% being de novo mutations. CONCLUSION: Above findings have enriched the spectrum of ANKRD11 gene mutations underlying KBG syndrome. WES is helpful for the early diagnosis of KBG, and provided reference for genetic counseling of this disease.

CELSR1 variants are associated with partial epilepsy of childhood.

CELSR1 gene, encoding cadherin EGF LAG seven-pass G-type receptor 1, is mainly expressed in neural stem cells during the embryonic period. It plays an important role in neurodevelopment. However, the relationship between CELSR1 and disease of the central nervous system has not been defined. In this study, we performed trios-based whole-exome sequencing in a cohort of 356 unrelated cases with partial epilepsy without acquired causes and identified CELSR1 variants in six unrelated cases. The variants included one de novo heterozygous nonsense variant, one de novo heterozygous missense variant, and four compound heterozygous missense variants that had one variant was located in the extracellular region and the other in the cytoplasm. The patients with biallelic variants presented severe epileptic phenotypes, whereas those with heterozygous variants were associated with a mild epileptic phenotype of benign epilepsy with centrotemporal spikes (BECTS). These variants had no or low allele frequency in the gnomAD database. The frequencies of the CELSR1 variants in this cohort were significantly higher than those in the control populations. The evidence from ClinGen Clinical-Validity Framework suggested a strong association between CELSR1 variants and epilepsy. These findings provide evidence that CELSR1 is potentially a candidate pathogenic gene of partial epilepsy of childhood.

Identification of a robust signature for clinical outcomes and immunotherapy response in gastric cancer: based on N6-methyladenosine related long noncoding RNAs.

BACKGROUND: Gastric cancer (GC) is a globally prevalent cancer, ranking fifth for incidence and fourth for mortality worldwide. The N6-methyladenosine (m6A) related long noncoding RNAs (lncRNAs) were widely investigated in recent studies. Nevertheless, the underlying prognostic implication and tumor immune mechanism of m6A-related lncRNA in GC remain unknown. METHODS: We systematically assessed the m6A modification expression of 407 GC clinical samples based on 23 m6A regulators and comprehensively associated these genes with lncRNAs. Then, we constructed a m6A-related lncRNA prognostic signature (m6A-LPS) to evaluate both status and prognosis of the disease. Immune-related mechanisms were explored via dissecting tumor-infiltrating cells as well as applying tumor immune dysfunction and the exclusion algorithm. Furthermore, we validated the latent regulative mechanism of m6A-related lncRNA in GC cell lines. RESULTS: The m6A-LPS containing nine hub lncRNAs was built, which possessed a superior capability to predict the outcomes of GC patients. Meanwhile, we found an intimate correlation between the m6A-LPS and tumor infiltrating cells, and that the low-risk group had a higher expression of immune checkpoints and responsed more to immunotherapy than the high-risk group. Clinically, these crucial lncRNAs expression levels were verified in ten pairs of GC samples. In in vitro experiments, the abilities of migration and proliferation were significantly enhanced via downregulating the lncRNA AC026691.1. Both migrative and proliferative capabilities of tumor cells were significantly enhanced via downregulating the lncRNA AC026691.1. in vitro. CONCLUSIONS: Collectively, the m6A-LPS could provide a novel prediction insight into the prognosis of GC patients and serve as an independent clinical factor for GC. These m6A-related lncRNAs might remodel the tumor microenvironment and affect the anti-cancer ability of immune checkpoint blockers. Importantly, lncRNA AC026691.1 could inhibit both migration and proliferation of GC by means of FTO regulation.

Epilepsy centers in China: Current status and ways forward.

OBJECTIVE: China has the largest population of patients with epilepsy worldwide, which imposes a heavy burden on the public and health care systems. Several epidemiological surveys on epilepsy have been performed in China. Although these surveys grossly describe the prevalence and gap in treatment of epilepsy, the status of epilepsy centers is unclear. The number of epilepsy centers has increased substantially in recent decades. Therefore, a nationwide investigation of the scale and distribution, personnel, equipment, and epilepsy care capacity of each epilepsy center is of great value. METHODS: In 2017-2018, a multicenter cross-sectional survey was performed by the Commission on Standardized Development of Epilepsy Centers, China Association Against Epilepsy in 31 provinces, autonomous regions, and municipalities. The survey consisted of 74 questions divided into four sections: (1) overview, (2) personnel, (3) essential equipment and facilities, and (4) epilepsy care service capacity. The questions ranged from January 1, 2016 to December 31, 2016. The data were analyzed using descriptive statistics. RESULTS: There were 358 epilepsy centers for the 1.38 billion national population in 2016. Three quarters were in the eastern and western regions, and >90% were in tertiary hospitals. There were 9688 doctors engaged in epilepsy care, and 4.8% of doctors and electrophysiological physicians/technicians passed the national test for electroencephalography technical accreditation. A total of 9667 patients underwent resective surgeries in 2016. There were 888 vagus nerve stimulation procedures and 275 deep brain stimulation procedures. SIGNIFICANCE: This study is the first unique survey of epilepsy centers in China. Despite their rapid development, epilepsy centers cannot meet patients' needs at this stage. The results provide data-based evidence for the formulation of policies related to epilepsy service planning.

Microplastic Polystyrene Ingestion Promotes the Susceptibility of Honeybee to Viral Infection.

Microplastics (MPs) are an emerging threat to ecological conservation and biodiversity; however, little is known of the types and possible impacts of MPs in pollinators. To examine whether MPs were present in honeybees, we analyzed the honeybee samples collected in fields from six provinces in China. Four types MPs were identified in honeybee including polystyrene (PS) by Raman spectroscopic analysis, and these plastic polymers were detected in 66.7% bee samples. Then, we assessed the physical and biological impacts of PS of three sizes (0.5, 5, and 50 µm) on bees for 21 days. Next, we measured how the presence of PS affected the Israeli acute paralysis virus proliferation, a small RNA virus associated with bee colony decline. Experimental evidence showed that a large mass of PS was ingested and accumulated within the midgut and enhanced the susceptibility of bees to viral infection. Not only histological analysis showed that PS, especially 0.5 µm PS, damaged the midgut tissue and was subsequently transferred to the hemolymph, trachea, and Malpighian tubules, but also qPCR and transcriptomic results indicated that genes correlated with membrane lipid metabolism, immune response, detoxification, and the respiratory system were significantly regulated after PS ingestion. Our results highlight neglected MP contamination to the bees, a pollination ecosystem stressed by the anthropogenic pollution, and have implications for human health via ingestion of bee products.

IAPV-Induced Paralytic Symptoms Associated with Tachypnea via Impaired Tracheal System Function.

Although it had been reported that Israeli acute paralysis virus (IAPV) can cause systemic infection in honey bees, little is known about how it establishes this infection and results in the typical symptoms, paralysis and trembling. Here, we used our previously constructed IAPV infectious clone to investigate viral loads in different tissues of honey bees and further identify the relation between tissue tropism and paralytic symptoms. Our results showed that tracheae showed a greater concentration of viral abundance than other tissues. The abundance of viral protein in the tracheae was positively associated with viral titers, and was further confirmed by immunological and ultrastructural evidence. Furthermore, higher viral loads in tracheae induced remarkable down-regulation of succinate dehydrogenase and cytochrome c oxidase genes, and progressed to causing respiratory failure of honey bees, resulting in the appearance of typical symptoms, paralysis and body trembling. Our results showed that paralysis symptoms or trembling was actually to mitigate tachypnea induced by IAPV infection due to the impairment of honey bee tracheae, and revealed a direct causal link between paralysis symptoms and tissue tropism. These findings provide new insights into the understanding of the underlying mechanism of paralysis symptoms of honey bees after viral infection and have implications for viral disease prevention and specific therapeutics in practice.

[New variants in FLNA gene cause periventricular nodular heterotopia and epileptic seizure in three cases].

OBJECTIVE: To explore the genetic bases of 3 patients with periventricular nodular heterotopia and epileptic seizure. METHODS: The clinical data of three patients presenting with periventricular nodular ectopic with epileptic seizure were analyzed. Whole exome sequencing (WES) was performed on the patients, and Sanger sequencing was used to validate the suspected variants. RESULTS: In three female patients, head MRI showed nodular gray matter ectopic in the bilateral ventricle. WES identified the heterozygous c.2720del T(p.Leu907Argfs*39) variant of FLNA gene in case 1 and her mother (case 2), and heterozygous c.1387_1390del GTGC(p.Val463Profs*34) of FLNA gene in case 3. According to the American College of Medical Genetics and Genomics standards and guidelines, the c.2720delT(p.Leu907Argfs*39) and c.1387_1390del GTGC (p.Val463Profs*34) variants of FLNA gene were predicted to be pathogenic (PVS1+PM2+PP1) and likely pathogenic(PVS1+PM2), respectively. CONCLUSION: The c.2720delT(p.Leu907Argfs*39) and c.1387_1390del GTGC(p.Val463Profs*34) variants of FLNA gene may be the genetic cause of the three patients.

A Reverse Genetics System for the Israeli Acute Paralysis Virus and Chronic Bee Paralysis Virus.

Honey bee viruses are associated with honey bee colony decline. Israeli acute paralysis virus (IAPV) is considered to have a strong impact on honey bee survival. Phylogenetic analysis of the viral genomes from several regions of the world showed that various IAPV lineages had substantial differences in virulence. Chronic bee paralysis virus (CBPV), another important honey bee virus, can induce two significantly different symptoms. However, the infection characteristics and pathogenesis of IAPV and CBPV have not been completely elucidated. Here, we constructed infectious clones of IAPV and CBPV using a universal vector to provide a basis for studying their replication and pathogenesis. Infectious IAPV and CBPV were rescued from molecular clones of IAPV and CBPV genomes, respectively, that induced typical paralysis symptoms. The replication levels and expression proteins of IAPV and CBPV in progeny virus production were confirmed by qPCR and Western blot. Our results will allow further dissection of the role of each gene in the context of viral infection while helping to study viral pathogenesis and develop antiviral drugs using reverse genetics systems.

Brilliant red X-3B uptake by a novel polycyclodextrin-modified magnetic cationic hydrogel: Performance, kinetics and mechanism.

A novel polycyclodextrin-modified magnetic cationic hydrogel (PCD-MCH) was developed and its performance, kinetics and mechanism for the removal of reactive brilliant red X-3B (X-3B) were studied. The results showed that the zeta-potential of PCD-MCH was 32.8 to 16.7mV at pH3.0-10.5. The maximum X-3B adsorption capacity of PCD-MCH was 2792.3mg/g. The adsorption kinetics could be well-described by the Weber-Morris model and the homogeneous surface diffusion model (HSDM). Diffusion stages corresponding to surface or film diffusion, intra-particle or wide mesopore diffusion, and narrow mesopore/micropore diffusion occurred at 0-120, 120-480 and 480-1200min, respectively. The latter two diffusion stages were rate-controlling for X-3B adsorption kinetics. At the initial X-3B concentration of 600mg/L, the diffusion coefficient (Ds) and external mass transfer coefficient in the liquid phase (kF) were 3×10-11cm2/min and 4.68×10-6cm/min, respectively. X-3B approaching the center of PCD-MCH particles could be observed at 360min. At the end of the third diffusion stage, the Cp at q/qe=0 was 45.20mg/L, which was close to the homogeneous Cp value of 46mg/L along the radius of PCD-MCH particles. At pH3.0-10.0, PCD-MCH showed stable X-3B adsorption capacities. After five regeneration-reuse cycles, the residual adsorption capacity of regenerated PCD-MCH was higher than 892.7mg/g. The corresponding adsorption mechanism was identified as involving electrostatic interactions, cyclodextrin cavities and hydrogen bonds, of which cyclodextrin cavities showed prominent capture performance towards dye molecules through the formation of inclusion complexes.

Carbamazepine removal from water by carbon dot-modified magnetic carbon nanotubes.

Carbon dot- and magnetite-modified magnetic carbon nanotubes (CMNTs) were synthesized and evaluated for carbamazepine removal from water. The adsorbent was characterized by multiple modern surface and microstructure analyzing techniques. CMNTs were composed of three components including carbon dots (CDs), carbon nanotubes (CNTs) and magnetite. CDs and CNTs introduce abundant carboxyl groups onto CMNTs and magnetite allows rapid magnetic separation of the adsorbent realizable after batch adsorption. This adsorbent has a moderately high adsorption capacity of 65 mg-carbamazepine/g-adsorbent at pH 7.0 ±â€¯0.2, which is superior to many reported adsorbents. Carbamazepine was uptaken well in a wide pH range, regardless of the surface charging of CMNTs. Its adsorption on CMNTs was quite fast and reached 80% of removal during the initial 3 h. The mass transfer within CMNTs and the time-dependent utilization, exhaustion and depletion of the adsorption capacity were successfully described using a simplified homogeneous surface diffusion model (HSDM). The surface diffusion coefficients (Ds) rose with increasing initial carbamazepine concentrations. After six regeneration and recycle experiments, the capacity loss of CMNTs was less than 2.2% at the conditions tested. FTIR spectra showed the characteristics of the components. Raman spectra implied a π-π electron donor-acceptor (EDA) interaction during adsorption. This work proposed a method of combining π-bond-rich materials (CNTs and CDs) and magnetite to make separable composite adsorbents with high affinity interactions between carbamazepine and carbon materials. The prepared adsorbent is attractive for carbamazepine removal due to its good performance, moderate cost, ease of separation, and ability to regenerate.

Electroclinical aspects and therapy of Han patients with juvenile myoclonic epilepsy in northern China.

OBJECTIVE: The objective of this study was to assess the electroclinical aspects and treatment of Han patients with juvenile myoclonic epilepsy (JME) in northern China. METHODS: One hundred fifty-six outpatients with JME from six epilepsy centers, between January 2011 and June 2012, were followed up for at least two years. They underwent twenty-four-hour video-EEG recording. Brain imaging was performed using magnetic resonance imaging (MRI). Clinical aspects, electroencephalographic (EEG) features, and antiepileptic drugs (AEDs) received were reviewed. RESULTS: Generalized tonic-clonic seizures (GTCS) were found in 150/156 patients. Delay of diagnosis was 4.60±9.92years. Photosensitivity was more common in eye closure condition during IPS in patients with JME; in addition, patients with JME with myoclonic seizures (MS) and GTCS as seizure types were likely to present photoparoxysmal responses (PPRs). The 82 nontreated patients showed a median latency to first interictal or ictal generalized spike-wave discharge (GSWD) of 50min (IQR: 22-102min). The first GSWDs were recorded in 63%, 76%, 90%, and 98% patients within one, two, three, and 4h, respectively; only 2% of patients had first GSWDs after 4h. One hundred eleven patients (111/156) chose extended-release valproate (VPA) at daily doses ≤1000mg. The percentages of seizure-free patients among MS, GTCS, and absence seizure (AS) groups were 88.3%, 99.0%, and 94.9%, respectively. CONCLUSION: Photoparoxysmal responses were more common in patients with JME with MS and GTCS and rare in patients with JME with MS and AS in northern Chinese Han patients. Most patients with JME in northern China chose VPA as first therapeutic choice, and low dose (500 to 1000mg daily) of extended-release VPA may be an optimal choice for them. Video-EEG monitoring for at least 4h may be helpful in detecting the first interictal or ictal GSWD in patients with potential JME. Moreover, video-EEG monitoring performed at about 9 o'clock in the morning with patients in the awake state might be useful to find the first GSWD. For JME diagnosis, Class II criteria are more helpful than Class I counterparts, the latter yielding more missed diagnoses.

Jeavons syndrome in China.

OBJECTIVES: Jeavons syndrome (JS) is one of the underreported epileptic syndromes and is characterized by eyelid myoclonia (EM), eye closure-induced seizures or electroencephalography (EEG) paroxysms, and photosensitivity. In the Western populations, it has been reported to be characterized by focal posterior, occipital predominant epileptiform discharges (OPEDs) or frontal predominant epileptiform discharges (FPEDs) followed by generalized EDs in both interictal and ictal EEG recordings. However, it is not clear if there are different clinical manifestations between OPEDs and FPEDs. The clinical and electrographic presentations in the Chinese population are largely unknown. Here, we report the clinical and electroencephalographic features of 50 Chinese patients with JS and evaluate for the presence of different clinical features between patients with OPEDs and patients with FPEDs. METHODS: We identified 50 cases who met the Jeavons syndrome criteria from 4230 patients with epilepsy at Xijing Hospital, Xi'an, China from the period of January 2010 to November 2011. These patients underwent long-term 24-hour video-EEG recording. Brain imaging was performed using magnetic resonance imaging (MRI) or computerized tomography (CT). Webster IQ testing was performed to determine intellectual development. We reviewed and described the interictal abnormalities, ictal EEG pattern, and demographic, clinical, and neuroimaging findings of these 50 Chinese patients in Xi'an. We divided the 50 patients into two groups according to the predominance of EDs and analyzed their clinical features. RESULTS: Twenty-five of these 50 patients were male. Twenty-two out of 32 patients in the group with FPEDs were male, and 3/18 patients in the group with OPEDs were male. The median age of EMA-EM onset in FPEDs was 8years and that in OPEDs was 5.8years. Eyelid myoclonia occurred in all the 50 patients. Twenty-one out of 32 patients in the group with FPEDs had EM with absences, and 14/32 of them had EM with eyeball rolling up. Two out of 18 patients in the group with OPEDs had EM with absences, and only 1 of 18 had EM with eyeball rolling up. CONCLUSION: Eyelid myoclonia with or without absences or JS diagnosis is easily missed and underreported in China. As an IGE, either the frontal or the occipital lobe may initiate generalized spike-and-wave discharges (GSWDs) and generalized seizures (GSs). There may be two subtypes of JS with distinctive clinical and electroencephalogrphic features: a predominantly male group with frontal predominant epileptiform discharges, eyelid myoclonia, and eyes rolling up and a predominantly female group with occipital predominant epileptiform discharges with eyelid myoclonia alone.

Chronic bee paralysis virus exploits host antimicrobial peptides and alters gut microbiota composition to facilitate viral infection.

The significance of gut microbiota in regulating animal immune response to viral infection is increasingly recognized. However, how chronic bee paralysis virus (CBPV) exploits host immune to disturb microbiota for its proliferation remains elusive. Through histopathological examination, we discovered that the hindgut harbored the highest level of CBPV, and displayed visible signs of damages. The metagenomic analysis showed that a notable reduction in the levels of Snodgrassella alvi and Lactobacillus apis, and a significant increase in the abundance of the opportunistic pathogens such as Enterobacter hormaechei and Enterobacter cloacae following CBPV infection. Subsequent co-inoculation experiments showed that these opportunistic pathogens facilitated the CBPV proliferation, leading to accelerated mortality in bees and exacerbation of bloated abdomen symptoms after CBPV infection. The expression level of antimicrobial peptide (AMP) was found to be significantly up-regulated by over 1000 times in response to CBPV infection, as demonstrated by subsequent transcriptome and quantitative real-time PCR investigations. In particular, through correlation analysis and a bacteriostatic test revealed that the AMPs did not exhibit any inhibitory effect against the two opportunistic pathogens. However, they did demonstrate inhibitory activity against S. alvi and L. apis. Our findings provide different evidence that the virus infection may stimulate and utilize the host's AMPs to eradicate probiotic species and facilitate the proliferation of opportunistic bacteria. This process weakens the intestinal barrier and ultimately resulting in the typical bloated abdomen.

Photochemical Transformation of Monochloramine Induced by Triplet State Dissolved Organic Matter.

The photoexcited dissolved organic matter (DOM) could produce reactive intermediates, affecting chemical oxidant transformation in UV based advanced oxidation processes (AOPs). This study confirmed the critical role of triplet state DOM (3DOM*), generated from DOM photoexcitation, in the transformation of monochloramine (NH2Cl), a commonly used chemical oxidant and disinfectant in water treatment. NH2Cl (42.25 µM, as Cl2) was decayed by 17.4-73.4 % within 60 min, primarily due to 3DOM* , in DOM (2-30 mgC L-1) solutions irradiated by 365 nm, where NH2Cl has no absorption. The second-order quenching rate constants of triplet state model photosensitizers by NH2Cl were determined to be 0.95(± 0.04)-4.49(± 0.04)× 108 M-1 s-1 by using laser flash photolysis. As a reductant, 3DOM* reacted with NH2Cl through one-transfer mechanism, leading to amino radical (NH2•) generation, which then transferred to ammonia (NH4+, pKa 9.25) through H-abstraction by the phenolic moieties in DOM. Additionally, the intermediate product of 3DOM* oxidized by NH2Cl or those triplet state quinones can hydrolyze to form phenolic moieties, elevating NH4+ yield to higher than 99% upon 365 nm irradiation. These findings suggest that the widespread DOM can be applied to convert NH2Cl via 3DOM* with minimal toxic risks.

A chromosome-scale genome provides new insights into the typical carotenoid biosynthesis in the important red yeast Rhodotorula glutinis QYH-2023 with anti-inflammatory effects.

Rhodotorula spp. has been studied as one powerful source for a novel cell factory with fast growth and its high added-value biomolecules. However, its inadequate genome and genomic annotation have hindered its widespread use in cosmetics and food industries. Rhodotorula glutinis QYH-2023, was isolated from rice rhizosphere soil, and the highest quality of the genome of the strain was obtained at chromosome level (18 chromosomes) than ever before in red yeast in this study. Comparative genomics analysis revealed that there are more key gene copies of carotenoids biosynthesis in R. glutinis QYH-2023 than other species of Rhodotorula spp. Integrated transcriptome and metabolome analysis revealed that lipids and carotenoids biosynthesis was significantly enriched during fermentation. Subsequent investigation revealed that the over-expression of the strain three genes related to carotenoids biosynthesis in Komagataella phaffii significantly promoted the carotenoid production. Furthermore, in vitro tests initially confirmed that the longer the fermentation period, the synthesized metabolites controlled by R. glutinis QYH-2023 genome had the stronger anti-inflammatory properties. All of the findings revealed a high-quality reference genome which highlight the potential of R. glutinis strains to be employed as chassis cells for biosynthesizing carotenoids and other active chemicals.

A clinical study of the effects of lead poisoning on the intelligence and neurobehavioral abilities of children.

BACKGROUND: Lead is a heavy metal and important environmental toxicant and nerve poison that can destruction many functions of the nervous system. Lead poisoning is a medical condition caused by increased levels of lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and issues, including the central nervous system. It interferes with the development of the nervous system, and is therefore particularly toxic to children, causing potentially permanent neural and cognitive impairments. In this study, we investigated the relationship between lead poisoning and the intellectual and neurobehavioral capabilities of children. METHODS: The background characteristics of the research subjects were collected by questionnaire survey. Blood lead levels were detected by differential potentiometric stripping analysis (DPSA). Intelligence was assessed using the Gesell Developmental Scale. The Achenbach Child Behavior Checklist (CBCL) was used to evaluate each child's behavior. RESULTS: Blood lead levels were significantly negatively correlated with the developmental quotients of adaptive behavior, gross motor performance, fine motor performance, language development, and individual social behavior (P < 0.01). Compared with healthy children, more children with lead poisoning had abnormal behaviors, especially social withdrawal, depression, and atypical body movements, aggressions and destruction. CONCLUSION: Lead poisoning has adverse effects on the behavior and mental development of 2-4-year-old children, prescribing positive and effective precautionary measures.

Ginsenoside Rd blocks AIF mitochondrio-nuclear translocation and NF-κB nuclear accumulation by inhibiting poly(ADP-ribose) polymerase-1 after focal cerebral ischemia in rats.

Our previous clinical and basic studies have demonstrated that ginsenoside Rd (GS-Rd) has remarkable neuroprotective effects after cerebral ischemia but the underlying mechanisms are still unknown. In our latest studies, we revealed that GS-Rd could prevent mitochondrial release of apoptosis-inducing factor (AIF) and reduce inflammatory response following transient focal ischemia in rats. Poly(ADP-ribose) polymerase-1 (PARP-1) is required for both AIF release from mitochondria and NF-κB-mediated inflammation. Here, we investigated whether GS-Rd could act on PARP-1 and subsequently affect AIF translocation and NF-κB activation. Sprague-Dawley rats were treated with GS-Rd (10 mg/kg) 30 min before surgery with the right middle cerebral artery occlusion, and at different time points following cerebral ischemia, brain tissues were collected for western blotting analysis. Our results showed that GS-Rd significantly attenuated ischemia-triggered increased levels of Poly(ADP-ribose), an enzymatic product catalyzed by PARP-1, but not altered the expression of PARP-1 per se. Meanwhile, GS-Rd pretreatment reduced AIF mitochondrio-nuclear translocation and inhibited NF-κB p65 subunit nuclear accumulation after cerebral ischemia. Therefore, our findings provide the first evidence that GS-Rd can inhibit PARP-1 activity and sequential AIF translocation and NF-κB nuclear accumulation, which may be responsible for GS-Rd's neuroprotection against both neuronal cell death and inflammation after ischemic stroke.