Extremely Low-Frequency Electromagnetic Field Impairs the Development of Honeybee (Apis cerana).

Increasing ELF-EMF pollution in the surrounding environment could impair the cognition and learning ability of honeybees, posing a threat to the honeybee population and its pollination ability. In a social honeybee colony, the numbers of adult bees rely on the successful large-scale rearing of larvae and continuous eclosion of new adult bees. However, no studies exist on the influence of ELF-EMFs on honeybee larvae. Therefore, we investigated the survival rate, body weight, and developmental duration of first instar larvae continuously subjected to ELF-EMF exposure. Moreover, the transcriptome of fifth instar larvae were sequenced for analyzing the difference in expressed genes. The results showed that ELF-EMF exposure decreases the survival rate and body weight of both white-eye pupae and newly emerged adults, extends the duration of development time and seriously interferes with the process of metamorphosis and pupation. The transcriptome sequencing showed that ELF-EMF exposure decreases the nutrient and energy metabolism and impedes the degradation of larvae tissues and rebuilding of pupae tissues in the metamorphosis process. The results provide an experimental basis and a new perspective for the protection of honeybee populations from ELF-EMF pollution.

Trafficked Malayan pangolins contain viral pathogens of humans.

Pangolins are the most trafficked wild animal in the world according to the World Wildlife Fund. The discovery of SARS-CoV-2-related coronaviruses in Malayan pangolins has piqued interest in the viromes of these wild, scaly-skinned mammals. We sequenced the viromes of 161 pangolins that were smuggled into China and assembled 28 vertebrate-associated viruses, 21 of which have not been previously reported in vertebrates. We named 16 members of Hunnivirus, Pestivirus and Copiparvovirus pangolin-associated viruses. We report that the L-protein has been lost from all hunniviruses identified in pangolins. Sequences of four human-associated viruses were detected in pangolin viromes, including respiratory syncytial virus, Orthopneumovirus, Rotavirus A and Mammalian orthoreovirus. The genomic sequences of five mammal-associated and three tick-associated viruses were also present. Notably, a coronavirus related to HKU4-CoV, which was originally found in bats, was identified. The presence of these viruses in smuggled pangolins identifies these mammals as a potential source of emergent pathogenic viruses.

Human parainfluenza 3 and respiratory syncytial viruses detected in pangolins.

Pangolins have gained increasing global attention owing to their public health significance as potential zoonotic hosts since the identification of SARS-CoV-2-related viruses in them. Moreover, these animals could carry other respiratory viruses. In this study, we investigated the virome composition of 16 pangolins that died in 2018 with symptoms of pneumonia using metagenomic approaches. A total of eight whole virus sequences belonging to the Paramyxoviridae or Pneumoviridae families were identified, including one human parainfluenza virus 3, one human respiratory syncytial virus A, and six human respiratory syncytial virus B. All of these sequences showed more than 99% nucleotide identity with the virus isolated from humans at the whole-genome level and clustered with human viruses in the phylogenetic tree. Our findings provide evidence that pangolins are susceptible to HPIV3 and HRSV infection. Therefore, public awareness of the threat of pangolin-borne pathogens is essential to stop their human consumption and to prevent zoonotic viral transmission.

FAM134B-Mediated ER-Phagy in Mg2+-Free Solution-Induced Mitochondrial Calcium Homeostasis and Cell Death in Epileptic Hippocampal Neurons.

Mitochondrial-associated endoplasmic reticulum (ER) membranes (MAMs) regulate calcium (Ca2+) homeostasis via Ca2+ transport-related proteins such as inositol-1,4,5-triphosphate receptor (IP3R). FAM134B-mediated ER-phagy plays an important role in ER homeostasis. However, it remains unknown whether FAM134B-mediated ER-phagy affects mitochondrial Ca2+ homeostasis and cell death through MAMs. In this study, we demonstrated that colocalization degree of FAM134B with LC3 and the LC3-II/LC3-I ratio were elevated in the hippocampal neuronal culture (HNC) model of acquired epilepsy (AE), which indicate an increased level of autophagy. In this model, FAM134B overexpression enhanced ER-phagy, while FAM134B downregulation had the opposite effect. Additionally, FAM134B overexpression significantly reversed the increases in IP3R expression and mitochondrial Ca2+ concentration and the decrease in the ER Ca2+ concentration in this model. FAM134B overexpression also ameliorated the AE-induced ultrastructural damage in neuronal mitochondria, decrease in mitochondrial membrane potential (mMP), cytochrome c (CytC) release and caspase-3 activation, while FAM134B downregulation induced the opposite effects. Altogether, our data indicate that FAM134B-mediated ER-phagy can attenuate AE-induced neuronal apoptosis, possibly by modulating the IP3R in MAMs to alter Ca2+ exchange between ER and mitochondria and thus inhibit mitochondrial structural damage, a decrease in mMP, release of CytC and mitochondrial apoptosis.

The reference genome and transcriptome of the limestone langur, Trachypithecus leucocephalus, reveal expansion of genes related to alkali tolerance.

BACKGROUND: Trachypithecus leucocephalus, the white-headed langur, is a critically endangered primate that is endemic to the karst mountains in the southern Guangxi province of China. Studying the genomic and transcriptomic mechanisms underlying its local adaptation could help explain its persistence within a highly specialized ecological niche. RESULTS: In this study, we used PacBio sequencing and optical assembly and Hi-C analysis to create a high-quality de novo assembly of the T. leucocephalus genome. Annotation and functional enrichment revealed many genes involved in metabolism, transport, and homeostasis, and almost all of the positively selected genes were related to mineral ion binding. The transcriptomes of 12 tissues from three T. leucocephalus individuals showed that the great majority of genes involved in mineral absorption and calcium signaling were expressed, and their gene families were significantly expanded. For example, FTH1 primarily functions in iron storage and had 20 expanded copies. CONCLUSIONS: These results increase our understanding of the evolution of alkali tolerance and other traits necessary for the persistence of T. leucocephalus within an ecologically unique limestone karst environment.

Transcriptional identification of differentially expressed genes associated with division of labor in Apis cerana cerana.

Workers of Apis cerana cerana undergo an in-hive nursing to outdoor foraging transition, but the genes underlying this age-related transition remain largely unknown. Here, we sequenced the head transcriptomes of its 7-day-old normal nurses, 18- and 22-day-old normal foragers, 7-day-old precocious foragers and 22-day-old over-aged nurses to unravel the genes associated with this transition. Mapping of the sequence reads to Apis mellifera genome showed that the three types of foragers had a greater percentage of reads from annotated exons and intergenic regions, whereas the two types of nurses had a greater percentage of reads from introns. Pair- and group-wise comparisons of the five transcriptomes revealed 59 uniquely expressed genes (18 in nurses and 41 in foragers) and 14 nurse- and 15 forager-upregulated genes. The uniquely expressed genes are usually low-abundance long noncoding RNAs, transcription factors, transcription coactivators, RNA-binding proteins, kinases or phosphatases that are involved in signaling and/or regulation, whereas the nurse- or forager-upregulated genes are often high-abundance downstream genes that directly perform the tasks of nurses or foragers. Taken together, these results suggest that the nurse-forager transition is coordinated by a social signal-triggered epigenetic shift from introns to exons/intergenic regions and the resulting transcriptional shift between the nurse- and forager-associated genes.

Antimicrobial resistance of Escherichia coli isolated from retail foods in northern Xinjiang, China.

To determine antimicrobial resistance, 431 samples of retail foods purchased at different supermarkets in Northern Xinjiang were examined in this study. There were 112 Escherichia coli strains that were isolated, with approximately 26% of the samples contaminated by E. coli. The detection rate of E. coli isolated from pork was the highest (59.6%), followed by mutton (52.6%), retail fresh milk (52.4%), duck (36.4%), beef (35.3%), chicken (33.3%), and ready-to-eat food (12.9%); the E. coli detection rate for fish and vegetables was <11%. The result showed that the 112 isolates were mostly resistant to tetracycline (52%), followed by ampicillin (42%), compound trimethoprim/sulfamethoxazole (37%), amoxicillin (33%), and nalidixic acid (32%), imipenem resistance was not detected. One hundred isolates carried at least one antimicrobial resistance gene. The detection rate of resistance genes of our study was as follows: tetA (38%), tetB (27%), bla OXA (40%), bla TEM (20%), floR (20%), sul1 (16%), sul2 (27%), aad Ala (19%), aadB (11%), strA (28%), and strB (24%); tetC and bla PSE were not detected. Virulence genes fimC, agg, stx2, fimA, fyuA, papA, stx1, and eaeA were found in 52, 34, 21, 19, 6, 3, 2, and 2 isolates, respectively; papC was not detected. There was a statistically significant association between fimC and resistance to ciprofloxacin (p = .001), gentamicin (p = .001), amikacin (p = .001), levofloxacin (p = .001), and streptomycin (p = .001); between fimA and resistance to tetracycline (p = .001), ampicillin (p = .001), compound trimethoprim/sulfamethoxazole (p = .001), and amoxicillin (p = .003); between agg and resistance to gentamicin (p = .001), tetracycline (p = .001), ciprofloxacin (p = .017), and levofloxacin (p = .001); and between stx2 and resistance to ampicillin (p = .001), tetracycline (p = .001), compound trimethoprim/sulfamethoxazole (p = .002), and amoxicillin (p = .015).

FAM134B Attenuates Seizure-Induced Apoptosis and Endoplasmic Reticulum Stress in Hippocampal Neurons by Promoting Autophagy.

Autophagy plays a critical role in epileptic neuronal injury, and recent studies have demonstrated that FAM134B plays an important role in regulating autophagy. However, the effect of FAM134B on epileptic neuronal injury remains unclear. In this study, we investigated the role of FAM134B in neuronal apoptosis and endoplasmic reticulum (ER) stress using the hippocampal neuronal culture model of acquired epilepsy (AE) in vitro. We found that in this model, the level of autophagy significantly increased, indicated by an elevated LC3-II/LC3-I ratio. FAM134B overexpression using lentiviral vectors enhanced autophagy, whereas FAM134B downregulation using lentiviral vectors impaired this process. In addition, the ER Ca2+ concentration was decreased and the intracellular level of reactive oxygen species was increased in this model. FAM134B overexpression was sufficient to reverse these changes. Moreover, FAM134B overexpression attenuated ER stress as shown by a decrease in the expression of C/-EBP homologous protein and glucose-regulated protein 78, and neuronal apoptosis induced by seizure, while FAM134B downregulation caused the opposite effects. Further, pre-treatment with the selective autophagy inhibitor 3-methyladenine abolished the effects of FAM134B on ER stress and neuronal apoptosis. Altogether, we demonstrate that FAM134B is an important regulator of AE-induced ER stress and neuronal apoptosis by controlling autophagy function.

A new compound heterozygous mutation in adult-onset Krabbe disease.

Purpose: Krabbe disease (KD) or globoid cell leukodystrophy is an autosomal recessive lysosomal disorder caused by a lack of the lysosomal enzyme galactocerebrosidase (GALC) because of mutations in GALC. Patients with KD exhibit a wide spectrum of clinical symptoms; therefore, their diagnosis can be challenging. We report the clinical features and gene mutations in a 48-year-oldpatient with adult-onset KD.Methods: We collected and analyzed clinical data of the patientwith a diagnosis of KD. Gene mutations were identified by whole exome sequencing.Results: We describe a case of adult-onset KD caused by a novel compound heterozygous mutation; a missense mutation, c. 1901 T > C (p. L634S); and a novel nonsense mutation, c.1005C > G (p. Y335X), in GALC. The disease onset started when the patient was 40 years old, and manifested as typical paralytic paraplegia. Magnetic resonance imaging indicated demyelination of the white matter, which is consistent with the typical symptoms of adult-onset KD. Biochemical analysis revealed GALC activity to be 1.5 nmol/17 h/mg protein, confirming its deficiency and KD diagnosis.Conclusions: Our findings provide evidence of a novel mutation, providing additional information toward to the GALC mutation database.

Role of the mitochondrial calcium uniporter in Mg2+-free-induced epileptic hippocampal neuronal apoptosis.

PURPOSE: Mitochondrial Ca2+ overload is closely associated with seizure-induced neuronal damage. The mitochondrial calcium uniporter (MCU) plays a crucial role in regulating mitochondrial Ca2+ homeostasis. However, the role of the MCU in seizure-induced neuronal damage remains elusive. Materials and methods: In this study, the hippocampal neuronal culture (HNC) model of acquired epilepsy (AE) was used to investigate the role of the MCU in seizure-induced neuronal injury. Results: We found an increase in mitochondrial Ca2+ concentration in the HNC model of AE. The MCU inhibitor, Ru360, significantly reduced the rate of seizure-induced cell apoptosis and mitochondrial reactive oxygen species (ROS) production; whereas, the MCU agonist, spermine, exacerbated these processes. In addition, Ru360 significantly attenuated seizure-induced endoplasmic reticulum (ER) stress, which is characterized by the expression of glucose-regulated protein 78 (GRP78) and C/-EBP homologous protein (CHOP), while spermine had the opposite effect. We also found that pre-treatment with the mitochondria-targeted antioxidant, mitoquinone, decreased GRP78 and CHOP expression. Moreover, knockdown of CHOP using CHOP-specific small interfering RNA reduced neuronal seizure-induced apoptosis. Conclusions: Taken together, our data indicate that MCU inhibition has a neuroprotective effect against seizure-induced neuronal damage and that this mechanism may involve reduction of ROS-mediated ER stress.

Both left upper lobectomy and left pneumonectomy are risk factors for postoperative stroke.

Retrospective studies have found that left upper lobectomy (LUL) may be a new risk factor for stroke, and the potential mechanism is pulmonary vein thrombosis, which more likely develops in the left superior pulmonary vein (LSPV) stump. The LSPV remaining after left pneumonectomy is similar to that remaining after LUL. However, the association between left pneumonectomy, LUL, and postoperative stroke remains unclear. Thus, we sought to analyze whether both LUL and left pneumonectomy are risk factors for postoperative stroke. We prospectively included consecutive patients who underwent resection between November 2016 and March 2018 at our institution with 6 months of follow-up. Baseline demographic and clinical data were taken. A logistic regression model was used to determine independent predictors of postoperative stroke. In our study, 756 patients who underwent an isolated pulmonary lobectomy procedure were screened; of these, 637 patients who completed the 6-month follow-up were included in the analysis. Multivariable logistic regression analysis adjusted for common risk factors showed that the LUL and left pneumonectomy were independent predictors of stroke (odds ratio, 18.12; 95% confidence interval, 2.12-155.24; P = 0.008). Moreover, diabetes mellitus also was a predictor of postoperative stroke. In conclusion, both LUL and left pneumonectomy are significant risk factors for postoperative stroke.