Serotonin modulates insect gut bacterial community homeostasis.

BACKGROUND: Metazoan guts are in permanent contact with microbial communities. However, the host mechanisms that have developed to manage the dynamic changes of these microorganisms and maintain homeostasis remain largely unknown. RESULTS: Serotonin (5-hydroxytryptamine [5-HT]) was found to modulate gut microbiome homeostasis via regulation of a dual oxidase (Duox) gene expression in both Bactrocera dorsalis and Aedes aegypti. The knockdown of the peripheral 5-HT biosynthetic gene phenylalanine hydroxylase (TPH) increased the expression of Duox and the activity of reactive oxygen species, leading to a decrease in the gut microbiome load. Moreover, the TPH knockdown reduced the relative abundance of the bacterial genera Serratia and Providencia, including the opportunistic pathogens, S. marcescens and P. alcalifaciens in B. dorsalis. Treatment with 5-hydroxytryptophan, a precursor of 5-HT synthesis, fully rescued the TPH knockdown-induced phenotype. CONCLUSIONS: The findings reveal the important contribution of 5-HT in regulating gut homeostasis, providing new insights into gut-microbe interactions in metazoans.

Co-Administration of Simvastatin Does Not Potentiate the Benefit of Gene Therapy in the mdx Mouse Model for Duchenne Muscular Dystrophy.

Duchenne muscular dystrophy (DMD) is the most common and cureless muscle pediatric genetic disease, which is caused by the lack or the drastically reduced expression of dystrophin. Experimental therapeutic approaches for DMD have been mainly focused in recent years on attempts to restore the expression of dystrophin. While significant progress was achieved, the therapeutic benefit of treated patients is still unsatisfactory. Efficiency in gene therapy for DMD is hampered not only by incompletely resolved technical issues, but likely also due to the progressive nature of DMD. It is indeed suspected that some of the secondary pathologies, which are evolving over time in DMD patients, are not fully corrected by the restoration of dystrophin expression. We recently identified perturbations of the mevalonate pathway and of cholesterol metabolism in DMD patients. Taking advantage of the mdx model for DMD, we then demonstrated that some of these perturbations are improved by treatment with the cholesterol-lowering drug, simvastatin. In the present investigation, we tested whether the combination of the restoration of dystrophin expression with simvastatin treatment could have an additive beneficial effect in the mdx model. We confirmed the positive effects of microdystrophin, and of simvastatin, when administrated separately, but detected no additive effect by their combination. Thus, the present study does not support an additive beneficial effect by combining dystrophin restoration with a metabolic normalization by simvastatin.

Associations between the 1438A/G, 102T/C, and rs7997012G/A polymorphisms of HTR2A and the safety and efficacy of antidepressants in depression: a meta-analysis.

The correlations between hydroxytryptamine receptor 2A (HTR2A) gene polymorphisms (1438A/G, 102T/C, and rs7997012G/A) and the safety and efficacy of antidepressants in depression patients were constantly reported, but conclusions are debatable. This meta-analysis ascertained forty-two studies on the efficacy (including response and remission) and side-effect issued before February 2020. Pooled analyses indicated significant associations of 1438A/G polymorphism (16 studies, 1931 subjects) and higher response within dominant model (OR: 1.40, 95% CI: 1.12-1.76); rs7997012G/A polymorphism (nine studies, 1434 subjects) and higher remission in overall models (dominant model: OR: 1.30, 95% CI: 1.01-1.66; recessive model: OR: 2.20, 95% CI: 1.53-3.16; homozygote model: OR: 2.73, 95% CI: 1.78-4.17); 102T/C polymorphism (eight studies, 804 subjects) and reduced risk of side-effect within recessive (OR: 0.57, 95% CI: 0.4-0.83) and homozygote models (OR: 0.54, 95% CI: 0.29-0.99). For depression patients, genotyping of HTR2A polymorphisms is a promising tool for estimating the outcome and side-effect of antidepressants.

Elastography for the diagnosis of high-suspicion thyroid nodules based on the 2015 American Thyroid Association guidelines: a multicenter study.

BACKGROUND: An accurate diagnosis for high-suspicion nodules based on the 2015 American Thyroid Association (ATA) guidelines would reduce unnecessary invasive examinations. Elastography is a useful tool for discriminating benign and malignant thyroid nodules. The aim of this study is to investigate the diagnostic efficiency of elastography for high-suspicion thyroid nodules based on the 2015 ATA guidelines in the Chinese population. METHODS: Thyroid nodules with high-suspicion characteristics based on the 2015 ATA guidelines were subjected to conventional ultrasound (US) and ultrasound strain elastography (USE) examinations at 12 hospitals from 4 geographic regions across China. Cytology/histology of thyroid nodules was used as a reference method. Receiver operating characteristic (ROC) curves were plotted to evaluate the diagnostic performance of the elasticity score (ES) and strain ratio (SR). Logistic regression analysis was used to determine the predictors of malignancy. RESULTS: Overall, a total of 1445 thyroid nodules (834 malignant, 611 benign) from 12 centers were included in the final analysis. The areas under the curve of the ES and SR were 0.828 and 0.732, respectively. The sensitivity, specificity, accuracy, positive predictive value (PPV) and negative predictive value (NPV) of the ES were 92.4, 60.7, 79.0, 76.3 and 85.5%, respectively, and those of the SR were 81.1, 50.1, 68.9, 65.9 and 67.9%, respectively. The combination of the Thyroid Imaging Reporting and Data System (TI-RADS) and ES led to a significant increase in the sensitivity and NPV (97.1 and 91.9%, respectively) compared with the TI-RADS alone. Logistic regression analysis showed that microcalcifications (OR = 5.290), taller than wide (OR = 12.710), irregular margins (OR = 10.117), extrathyroidal extension (ETE; OR = 6.412), the ES (OR = 3.741) and the SR (OR = 1.083) were independent predictors of malignant thyroid nodules. The sensitivity, specificity, accuracy, PPV and NPV of the ES were all superior in nodules ≥1 cm than in those < 1 cm (95.0% vs 90.4, 68.8% vs 56.8, 85.9% vs 74.4, 85.2% vs 69.9, and 87.8% vs 84.2%, respectively). CONCLUSIONS: Elastography combined with the ES is a valuable tool for the assessment of high-suspicion thyroid nodules based on the 2015 ATA guidelines, especially in nodules ≥1 cm.

LncRNA NEAT1 mediates progression of oral squamous cell carcinoma via VEGF-A and Notch signaling pathway.

BACKGROUND: lncRNAs and VEGF have been shown to have close connections with oral squamous cell carcinoma (OSCC). We explored the interaction between lncRNA NEAT1 and VEGF-A in OSCC. METHODS: RT-qPCR was implemented to measure levels of lncRNA NEAT1 and VEGF-A in OSCC cell lines and normal cell lines. Cell functions then were checked after regulating the expressions of lncRNA NEAT1 and VEGF-A separately. Cell viabilities were examined with CCK-8 and apoptosis rate was checked with flow cytometry. Meanwhile, EMT-related genes E-cadherin, N-cadherin, Vimentin, and Snail and Notch signaling genes Notch1, Notch2, and Jagged were evaluated by RT-qPCR. IMR-1 was applied for impeding Notch signaling pathway. Later, cell viabilities, apoptosis, and EMT were assessed. RESULTS: Expressions of lncRNA NEAT1 and VEGF-A were both increased significantly in OSCC cell lines especially in TSCC1 cell line. Suppression of lncNRA NEAT1 was associated with lower cell viabilities and EMT and higher apoptosis rate in the TSCC1 cell line. Meanwhile, knockdown of VEGF-A significantly repressed cell viabilities and EMT in the TSCC1 cell line. Magnifying functions of inhibited lncRNA NEAT1 Notch signaling pathway was obviously activated with overexpressions of lncRNA NEAT1 and VEGF-A. Adding IMR-1 significantly downregulated cell viabilities and EMT and sharply increased apoptosis in the context of lncRNA NEAT1 and VEGF-A overexpression. CONCLUSION: LncRNA NEAT1 may upregulate proliferation and EMT and repress apoptosis through activating VEGF-A and Notch signaling pathway in vitro, suggesting an underlying regulatory factor in OSCC. Nevertheless, further research is necessary to gain a greater understanding of lncRNA NEAT1 and connections with VEGF-A in vivo and in clinical study.

Correction to: LncRNA NEAT1 mediates progression of oral squamous cell carcinoma via VEGF-A and Notch signaling pathway.

An amendment to this paper has been published and can be accessed via the original article.

Identification, characterization and expression analysis of transient receptor potential channel genes in the oriental fruit fly, Bactrocera dorsalis.

BACKGROUND: Members of the transient receptor potential (TRP) superfamily are proteins that are critical for insects to detect changes in environmental stimuli and also play key roles in their sensory physiology. Moreover, this family provides potential targets for the design of insecticides. In contrast to a large number of studies conducted on Drosophila melanogaster, molecular studies to characterize TRP channels in agricultural pests are lacking. RESULTS: In this study, we identified 15 TRP channel genes in the genome of a notorious agricultural pest, the oriental fruit fly (Bactrocera dorsalis). Comparative analysis of the TRP channels (TRPs) in B. dorsalis with those in D. melanogaster, Glossina morsitans, Musca domestica and the closely related Ceratitis capitata, and TRPs from mosquitoes, Hymenoptera, Lepidoptera, Coleoptera and Hemiptera reveals that members of TRPA and TRPP subfamily are most diverse among insects. The results also suggest that Tephritidae family have two TRP-Polycystin 2 members even though most insects either possess just one or none. The highest expression levels of these two genes are in the testes of B. dorsalis, implying a role in regulating sperm function. We analyzed the expression profiles of the TRP channels identified in this study at different life stages using quantitative real time PCR. The results of this study demonstrate that all TRP channels are mainly expressed in adults, especially at mature stages. The one exception to this trend is BdTRPM, which is more highly expressed in the eggs of B. dorsalis, implying an important role in early development. We also detected the spatial expression of TRP channels in mature adult fruit flies by investigating expression levels within various tissues including those involved in sensory function, such as antennae, compound eyes, mouthparts, legs, and wings, as well as tissues critical for homeostasis and physiology (i.e., Malpighian tubules, the brain and gut as well as fat bodies, ovaries, and testes). CONCLUSION: The results of this study establish a solid foundation for future functional characterization of B. dorsalis TRP channels as well as those of other insects and will help future insecticide design targeting these channels.

Electrospun LiFePO4/C Composite Fiber Membrane as a Binder-Free, Self-Standing Cathode for Power Lithium-Ion Battery.

A LiFePO4/C composite fiber membrane was fabricated by the electrospinning method and subsequent thermal treatment. The thermal decomposition process was analyzed by TG/DSC, the morphology, microstructure and composition were studied using SEM, TEM, XRD, Raman, respectively. The results indicated that the prepared LiFePO4/C composite fibers were composed of nanosized LiFePO4 crystals and amorphous carbon coatings, which formed a three dimensional (3D) long-range networks, greatly enhanced the electronic conductivity of LiFePO4 electrode up to 3.59× 10-2 S · cm-2. The 3D LiFePO4/C fiber membrane could be directly used as a binder-free, self-standing cathode for lithium-ion battery, and exhibited an improved capacity and rate performance. The LiFePO4/C composite electrode delivered a discharge capacity of 116 mAh·g-1, 109 mAh·g-1, 103 mAh·g-1, 91 mAh·g-1, 80 mAh·g-1 at 0.1 C, 0.5 C, 1 C, 3 C, 5 C, respectively. And a stable cycling performance was also achieved that the specific capacity could retain 75 mA·g-1 after 500 cycles at 5 C. Therefore, this LiFePO4/C composite fiber membrane was promising to be used as a cathode for power lithium ion battery.

AMPKα1 overexpression alleviates the hepatocyte model of nonalcoholic fatty liver disease via inactivating p38MAPK pathway.

Nonalcoholic fatty liver disease (NAFLD) has a wide spectrum of liver damage with a worldwide prevalence of almost 20%. AMP-activated protein kinase α1 (AMPKα1) is an energy sensor that plays a key role in regulating lipid metabolism of the liver. This study explores the role of AMPKα1 overexpression in a steatotic hepatocyte model. The results displayed that the AMPKα1 overexpression suppressed lipid accumulation in the cytoplasm, decreased triglyceride levels, maintained the survival of steatotic hepatocyte model with decreased cell apoptosis and increased survival rate. Besides, AMPKα1 overexpression promoted the expression of lipid catabolism-related genes, reduced the level of anabolism-related genes, alleviated the inflammatory response by reducing pro-inflammatory cytokines and increasing anti-inflammatory cytokines. Moreover, AMPKα1 overexpression could inhibit the activation of p38 mitogen-activated protein kinase (p38MAPK). Finally, Anisomycin, a frequently-used activator of p38MAPK, reversed the inhibitory effect of pc-AMPKα1 on the expression of p-p38MAPK, suggesting that AMPKα1 overexpression alleviates inflammatory response through the inactivation of p38MAPK. These results indicated that AMPKα1 may serve as a novel target for treatment of NAFLD.

Dlk1-Dio3 cluster miRNAs regulate mitochondrial functions in the dystrophic muscle in Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is a severe muscle disease caused by impaired expression of dystrophin. Whereas mitochondrial dysfunction is thought to play an important role in DMD, the mechanism of this dysfunction remains to be clarified. Here we demonstrate that in DMD and other muscular dystrophies, a large number of Dlk1-Dio3 clustered miRNAs (DD-miRNAs) are coordinately up-regulated in regenerating myofibers and in the serum. To characterize the biological effect of this dysregulation, 14 DD-miRNAs were simultaneously overexpressed in vivo in mouse muscle. Transcriptomic analysis revealed highly similar changes between the muscle ectopically overexpressing 14 DD-miRNAs and the mdx diaphragm, with naturally up-regulated DD-miRNAs. Among the commonly dysregulated pathway we found repressed mitochondrial metabolism, and oxidative phosphorylation (OxPhos) in particular. Knocking down the DD-miRNAs in iPS-derived skeletal myotubes resulted in increased OxPhos activities. The data suggest that (1) DD-miRNAs are important mediators of dystrophic changes in DMD muscle, (2) mitochondrial metabolism and OxPhos in particular are targeted in DMD by coordinately up-regulated DD-miRNAs. These findings provide insight into the mechanism of mitochondrial dysfunction in muscular dystrophy.

Anti-HCMV and KSHV effect of a trapping ligand antagonist for herpesvirus-encoded GPCR.

We have found and synthesized a trapping ligand peptide H22-LP (the conservative sequence is NAHCALL) from a random phage library according to the broad-spectrum trapping receptor H22, which derived from the residue 14-35 near the N-terminal region of receptor US28 on HCMV. In this study, we will evaluate its potential as an efficient antagonist of US28 and the anti-virus activity, acting as a broad spectrum chemokine receptors antagonist. Stable expression of US28 and ORF74 in NIH/3T3 cells were successfully constructed in vitro. Flow cytomety was used to determine the concentration of Ca2+ induced by H22-LP, and the binding of H22-LP and US28 was confirmed by enzyme-linked immunosorbent assay (ELISA). Antivirus activity of H22-LP on HCMV and KSHV was evaluated by anti-virus experiments. Our data suggest that H22-LP is an effectual antagonist of receptor US28 of HCMV and ORF74 of KSHV in the transfection assay, and it has potential to inhibit infection of HCMV and KSHV. These results provide support for the development of anti-virus strategies based on targeted inhibiting the infection of herpesvirus.

[Chemical constituents of Berchemia lineate].

OBJECTIVE: To investigate the chemical constituents of the roots of Berchemia lineate as a medicinal plant of Yao nationality in China. METHODS: Compounds were isolated by various column chromatography and elucidated by physicochemical and spectral analysis. RESULTS: Nine compounds were isolated from the 95% ethanol extract of the roots of Berchemia lineate and their structures were identified as palmitic acid (1), octadecanoic acid (2), beta-sitosterol (3), stigmasterol (4), fernenol (5), chrysophanol (6), physcion (7), floribundiquinone D (8), 2-acetylphyscion(9) respectively. CONCLUSION: Compounds 1-4,7-9 are isolated from this plant for the first time,and compounds land 2 are firstly isolated from this genus.

Deciphering the Molecular Mechanism of Incurable Muscle Disease by a Novel Method for the Interpretation of miRNA Dysregulation.

It is now well-established that microRNA dysregulation is a hallmark of human diseases, and that aberrant expression of miRNA is not randomly associated with human pathologies but plays a causal role in the pathological process. Investigations of the molecular mechanism that links miRNA dysregulation to pathophysiology can therefore further the understanding of human diseases. The biological effect of miRNA is thought to be mediated principally by miRNA target genes. Consequently, the target genes of dysregulated miRNA serve as a proxy for the biological interpretation of miRNA dysregulation, which is performed by target gene pathway enrichment analysis. However, this method unfortunately often fails to provide testable hypotheses concerning disease mechanisms. In this paper, we describe a method for the interpretation of miRNA dysregulation, which is based on miRNA host genes rather than target genes. Using this approach, we have recently identified the perturbations of lipid metabolism, and cholesterol in particular, in Duchenne muscular dystrophy (DMD). The host gene-based interpretation of miRNA dysregulation therefore represents an attractive alternative method for the biological interpretation of miRNA dysregulation.

Serum vitamin D status among healthy children in Hainan, South China: a multi-center analysis of 10,262 children.

Background: There are limited data regarding the prevalence and risk factors relating to vitamin D deficiency (VDD) in children of Hainan, a tropical city with abundant sunlight in China. To gather and analyze the serum VD levels of healthy children in Hainan, so as to understand their VD nutritional status and improve the representative data of VD nutritional status in south China. Methods: Children who presented to the outpatient clinic for physical examination at 4 hospitals in the Hainan Province from 2012 to 2020 were enrolled in this study. The serum 25-hydroxyvitamin D (25-OHD) levels was analyzed. 25-OHD levels <50 nmol/L is considered VDD, 50-75 nmol/L is vitamin D insufficiency (VDI), and ≥75 nmol/L is VD sufficient (VDS). Results: The average serum 25-OHD level was 94.63±49.99 nmol/L [95% confidence interval (CI): 93.67-95.60]. VDD was detected in 13.98% of participants (1,435 cases), VDI was detected in 30.60% of participants (3,140 cases), and 55.42% presented with VDS (5,687 cases). The average 25-OHD level of boys was significantly higher than that of girls (t=3.67, P<0.001). The average serum 25-OHD levels in the following age groups 0-1, 1-3, 3-7, 7-14, and 14-18 years were 105.92±57.39, 100.55±53.22, 86.35±39.19, 73.61±34.21, and 54.97±19.19 nmol/L, respectively. These results suggested that with an increase in age, the 25-OHD levels decreased. The average 25-OHD levels of children with a body mass index (BMI) <85th percentile were significantly higher than that of children in the overweight and obese group (F=7.393, P=0.001). Conclusions: A certain proportion of all age groups showed vitamin D deficiency and insufficiency in Hainan. A formal recommendation for vitamin D supplementation should be considered, especially in autumn and winter seasons for children over 7 years old, and in those with BMI ≥85th percentile or BMI ≥95th percentile.

A new pregnane glycoside and oligosaccharide from Parabarium huaitingii.

Two new compounds, along with two known compounds, were isolated from the barks of Parabarium huaitingii, and their structures were determined as 5α-pregn-6-ene-3ß,17α,20(S)-triol-20-O-ß-d-digitoxopyranoside (1), cymaropyranurolactone 4-O-ß-d-digitalopyranosyl-(1 â†’ 4)-O-ß-d-cymaropyranosyl-(1 â†’ 4)-O-ß-d-oleandropyranosyl-(1 â†’ 4)-O-ß-d-cymaropyranoside (2), 3ß,17α,20(S)-trihydroxy-5α-pregn-6-ene (3), and 5α-pregn-6-ene-3ß,17α,20(S)-triol-3-O-ß-d-digitalopyranoside (4) by spectroscopic methods.

A revised model for mitochondrial dysfunction in Duchenne muscular dystrophy.

We recently identified a signaling pathway that links the upregulation of miR-379 with a mitochondrial response in dystrophic muscle. In the present commentary, we explain the significance that this pathway may have in mitochondrial dysfunction in Duchenne muscular dystrophy (DMD). We identified the upregulation of miR-379 in the serum and muscles of DMD animal models and patients. We found that miR-379 is one of very few miRNAs whose expression was normalized in DMD patients treated with glucocorticoid. We identified EIF4G2 as a miR-379 target, which may promote mitochondrial oxidative phosphorylation (OxPhos) in the skeletal muscle. We found enriched EIF4G2 expression in oxidative fibers, and identified the mitochondrial ATP synthase subunit DAPIT as a translational target of EIF4G2. The identified signaling cascade, which comprises miR-379, EIF4G2 and DAPIT, may link the glucocorticoid treatment in DMD to a recovered mitochondrial ATP synthesis rate. We propose an updated model of mitochondrial dysfunction in DMD.

Cholesterol metabolism is a potential therapeutic target in Duchenne muscular dystrophy.

BACKGROUND: Duchenne muscular dystrophy (DMD) is a lethal muscle disease detected in approximately 1:5000 male births. DMD is caused by mutations in the DMD gene, encoding a critical protein that links the cytoskeleton and the extracellular matrix in skeletal and cardiac muscles. The primary consequence of the disrupted link between the extracellular matrix and the myofibre actin cytoskeleton is thought to involve sarcolemma destabilization, perturbation of Ca2+ homeostasis, activation of proteases, mitochondrial damage, and tissue degeneration. A recently emphasized secondary aspect of the dystrophic process is a progressive metabolic change of the dystrophic tissue; however, the mechanism and nature of the metabolic dysregulation are yet poorly understood. In this study, we characterized a molecular mechanism of metabolic perturbation in DMD. METHODS: We sequenced plasma miRNA in a DMD cohort, comprising 54 DMD patients treated or not by glucocorticoid, compared with 27 healthy controls, in three groups of the ages of 4-8, 8-12, and 12-20 years. We developed an original approach for the biological interpretation of miRNA dysregulation and produced a novel hypothesis concerning metabolic perturbation in DMD. We used the mdx mouse model for DMD for the investigation of this hypothesis. RESULTS: We identified 96 dysregulated miRNAs (adjusted P-value <0.1), of which 74 were up-regulated and 22 were down-regulated in DMD. We confirmed the dysregulation in DMD of Dystro-miRs, Cardio-miRs, and a large number of the DLK1-DIO3 miRNAs. We also identified numerous dysregulated miRNAs yet unreported in DMD. Bioinformatics analysis of both target and host genes for dysregulated miRNAs predicted that lipid metabolism might be a critical metabolic perturbation in DMD. Investigation of skeletal muscles of the mdx mouse uncovered dysregulation of transcription factors of cholesterol and fatty acid metabolism (SREBP-1 and SREBP-2), perturbation of the mevalonate pathway, and the accumulation of cholesterol in the dystrophic muscles. Elevated cholesterol level was also found in muscle biopsies of DMD patients. Treatment of mdx mice with Simvastatin, a cholesterol-reducing agent, normalized these perturbations and partially restored the dystrophic parameters. CONCLUSIONS: This investigation supports that cholesterol metabolism and the mevalonate pathway are potential therapeutic targets in DMD.

Identification of putative muscarinic acetylcholine receptor genes in Bactrocera dorsalis and functional analysis of Bdor-mAChR-B.

Muscarinic acetylcholine receptors (mAChRs) play important roles in the insect nervous system. These receptors are G protein-coupled receptors, which are potential targets for insecticide development. While the investigation of pharmacological properties of insect mAChRs is growing, the physiological roles of the receptor subtype remain largely indeterminate. Here, we identified three mAChR genes in an important agricultural pest Bactrocera dorsalis. Phylogenetic analysis defined these genes as mAChR-A, -B, and -C. Transcripts of the three mAChRs are most prevalent in 1-d-old larvae and are more abundant in the brain than other body parts in adults. Functional assay of Bdor-mAChR-B transiently expressed in Chinese hamster ovary cells showed that it was activated by acetylcholine (EC50, 205.11 nM) and the mAChR agonist oxotremorine M (EC50, 2.39 µM) in a dose-dependent manner. Using the CRISPR/Cas9 technique, we successfully obtained a Bdor-mAChR-B knockout strain based on wild-type (WT) strain. When compared with WT, the hatching and eclosion rate of Bdor-mAChR-B mutants are significantly lower. Moreover, the crawl speed of Bdor-mAChR-B knockout larvae was lower than that of WT, while climbing performance was enhanced in the mutant adults. Adults with loss of function of Bdor-mAChR-B showed declined copulation rates and egg numbers (by mated females). Our results indicate that Bdor-mAChR-B plays a key role in the development, locomotion, and mating behavior of B. dorsalis.

Epidemiological investigation of a COVID-19 family cluster outbreak transmitted by a 3-month-old infant.

OBJECTIVE: To investigate the clinical characteristics, epidemiological characteristics, and transmissibility of coronavirus disease 2019 (COVID-19) in a family cluster outbreak transmitted by a 3-month-old confirmed positive infant. METHODS: Field-based epidemiological methods were used to investigate cases and their close contacts. Real-time fluorescent reverse transcription polymerase chain reaction (RT-PCR) was used to detect Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) for all collected specimens. Serum SARS-CoV-2 IgM and IgG antibodies were detected by Chemiluminescence and Gold immnnochromatography (GICA). RESULTS: The outbreak was a family cluster with an attack rate of 80% (4/5). The first case in this family was a 3-month-old infant. The transmission chain was confirmed from infant to adults (her father, mother and grandmother). Fecal tests for SARS-CoV-2 RNA remained positive for 37 days after the infant was discharged. The infant's grandmother was confirmed to be positive 2 days after the infant was discharged from hospital. Patients A (3-month-old female), B (patient A's father), C (patient A's grandmother), and D (patient A's mother) had positive serum IgG and negative IgM, but patients A's grandfather serum IgG and IgM were negative. CONCLUSION: SARS-CoV-2 has strong transmissibility within family settings and presence of viral RNA in stool raises concern for possible fecal-oral transmission. Hospital follow-up and close contact tracing are necessary for those diagnosed with COVID-19.

Poly[bis-[µ-1,4-bis-(1,2,4-triazol-1-ylmeth-yl)benzene-κN:N]dichloridomanganese(II)].

The Mn(II) atom in the title coordination polymer, [MnCl(2)(C(12)H(12)N(6))(2)](n), lies on a center of inversion in a six-coordinate octa-hedral environment comprising four N-atom donors from four N-heterocyclic ligands and two chloride atoms. Bridging by the ligands results in a layer structure of a 14.79 (5) × 14.79 (5) Š(4,4) rhombic net topology, with the Mn(II) atoms all lying on a plane. The parallel layers stack in an ABCABC… manner through inter-layer C-H⋯N and C-H⋯Cl hydrogen bonds.