Epidemiological,Clinical and Serological Characteristics of Children with Coronavirus Disease 2019 in Wuhan: A Single-centered,Retrospective Study

In December 2019, SARS-CoV-2 was first detected in the samples obtained from three adult patients who suffered from an unknown viral pneumonia in Wuhan (Li et al. 2020). This unknown viral pneumonia is further named as coronavirus disease 2019 (COVID-19) by the World Health Organization. To date, the number of new COVID-19 cases has continued to skyrocket and the impact of SARS-CoV-2 on humans is far greater than any pathogen of this century in both breadth and depth. Previous studies have shown that adults with COVID-19 have symptoms of fever, dry cough, dyspnea, fatigue and lymphocytopenia. Moreover, COVID-19 is more likely to cause death in the elderly, especially those with chronic comorbidities (Huang et al. 2020). In Wuhan, more than 50, 000 COVID-19 cases have been confirmed, including over 780 pediatric patients, and only one child death case (Lu et al. 2020). Although the number of children cases was far fewer than that of adults, COVID-19 might endanger children's health and the information on children remains limited, especially in serological study. In the retrospective study, the investigators analyzed the epidemiological, clinical and serological characteristics of children with COVID-19 in Wuhan in the early stages of the outbreak, which might provide theoretical and practical help in controlling COVID-19 and similar emerging infectious diseases in the future.     

Novel Antiviral Agents Targeting HIV Entry and Transmission

Studies of the mechanism of HIV entry and transmission have identified multiple new targets for drug development. A range of inhibitors have demonstrated potent antiretroviral activity by interfering with CD4-gp120 interaction,coreceptor binding or viral-cell fusion in preclinical and clinical studies. One of these agents,fusion inhibitor enfuvirtide,is already in clinical use. Here we review the progress in the development of specific entry inhibitors as novel therapeutics. The potential of entry inhibitors as topical microbicides to block HIV transmission is also discussed.     

Proteome analysis of up-regulated proteins in the rat spinal cord induced by transection injury

The inability of the CNS to regenerate in adult mammals propels us to reveal associated proteins involved in the injured CNS. In this paper, either thoracic laminectomy (as sham control) or thoracic spinal cord transection was performed on male adult rats. Five days after surgery, the whole spinal cord tissue was dissected and fractionated into water-soluble (dissolved in Tris buffer) and water-insoluble (dissolved in a solution containing chaotropes and surfactants) portions for 2-DE. Protein identification was performed by MS and further confirmed by Western blot. As a result, over 30 protein spots in the injured spinal cord were shown to be up-regulated no less than 1.5-fold. These identified proteins possibly play various roles during the injury and repair process and may be functionally categorized as several different groups, such as stress-responsive and metabolic changes, lipid and protein degeneration, neural survival and regeneration. In particular, over-expression of 11-zinc finger protein and glypican may be responsible for the inhibition of axonal growth and regeneration. Moreover, three unknown proteins with novel sequences were found to be up-regulated by spinal cord injury. Further characterization of these molecules may help us come closer to understanding the mechanisms that underlie the inability of the adult CNS to regenerate.     

Simultaneous removal of carbon and nitrogen from municipal-type synthetic wastewater using net-like rotating biological contactor (NRBC)

The treatment of municipal-type synthetic wastewater was carried out using a three stages net-like rotating biological contactor (NRBC). The results indicated that, compared with conventional rotating biological contactor (RBC), NRBC have several advantages, such as quick start-up, high biomass concentration and can handle high organic loading rates. The COD and total nitrogen removal rates achieved were 78.8–89.7% and 40.2–61.4%, respectively, in aerobic treatment of low COD municipal-type wastewater at hydraulic retention times (HRT) from 5 to 9 h. The COD removal rate achieved 80–95% when organic loading varied between 16 and 40 gCOD/m² d. A large amount of nematodes were found in the NRBC system, which made the NRBC system produce relatively low amounts of waste sludge, due to their grazing.     

生物素肼化学标记和DIG标记cDNA探针检测柑桔裂皮病类病毒

分别用生物素肼化学标记和ＤＩＧ标记我国柑桔裂皮病类病毒（ＣＥＶｄ）全长克隆ｃＤＮＡ,用以上探讨对不同来源的的核酸样品进行斑点杂交。两种探针可检出病柑桔总核酸的最低含量久为４００ｎｇ／斑点和８０ｎｇ／斑点;生物素肼标记ＣＥＶｄ－ＤＮＡ探讨针,可检出ＣＥＶｄ－ｃＤＮＡ的最低含量约为１０ｐｇ／斑点,研制的ＣＥＶｄ检测试剂盒能检测出发病和隐性带毒苗木中的ＣＥＶｄ,灵敏、特异、简便、快速。试剂盒已使用于检测     

XBP1 depletion precedes ubiquitin aggregation and Golgi fragmentation in TDP‐43 transgenic rats

Protein inclusion is a prominent feature of neurodegenerative diseases including frontotemporal lobar degeneration (FTLD) that is characterized by the presence of ubiquitinated TDP‐43 inclusion. Presence of protein inclusions indicates an interruption to protein degradation machinery or the overload of misfolded proteins. In response to the increase in misfolded proteins, cells usually initiate a mechanism called unfolded protein response (UPR) to reduce misfolded proteins in the lumen of endoplasmic reticules. Here, we examined the effects of mutant TDP‐43 on the UPR in transgenic rats that express mutant human TDP‐43 restrictedly in the neurons of the forebrain. Over‐expression of mutant TDP‐43 in rats caused prominent aggregation of ubiquitin and remarkable fragmentation of Golgi complexes prior to neuronal loss. While ubiquitin aggregates and Golgi fragments were accumulating, neurons expressing mutant TDP‐43 failed to up‐regulate chaperones residing in the endoplasmic reticules and failed to initiate the UPR. Prior to ubiquitin aggregation and Golgi fragmentation, neurons were depleted of X‐box‐binding protein 1 (XBP1), a key player of UPR machinery. Although it remains to determine how mutation of TDP‐43 leads to the failure of the UPR, our data demonstrate that failure of the UPR is implicated in TDP‐43 pathogenesis.     

Binding of HIV-1 virions to α4β7 expressing cells and impact of antagonizing α4β7 on HIV-1 infection of primary CD4+ T cells

HIV-1 envelope glycoprotein is reported to interact with α4β7, an integrin mediating the homing of lymphocytes to gut-associated lymphoid tissue, but the significance of α4β7 in HIV-1 infection remains controversial. Here, using HIV-1 strain Ba L, the gp120 of which was previously shown to be capable of interacting with α4β7, we demonstrated that α4β7 can mediate the binding of whole HIV-1 virions to α4β7-expressing transfectants. We further constructed a cell line stably expressing α4β7 and confirmed the α4β7-mediated HIV-1 binding. In primary lymphocytes with activated α4β7 expression, we also observed significant virus binding which can be inhibited by an anti-α4β7 antibody. Moreover, we investigated the impact of antagonizing α4β7 on HIV-1 infection of primary CD4+ T cells. In α4β7-activated CD4+ T cells, both anti-α4β7 antibodies and introduction of shorthairpin RNAs specifically targeting α4β7 resulted in a decreased HIV-1 infection. Our findings indicate that α4β7 may serve as an attachment factor at least for some HIV-1 strains. The established approach provides a promising means for the investigation of other viral strains to understand the potential roles of α4β7 in HIV-1 infection.     

Comparison of quantum dot immunofluorescence histochemistry with conventional immunohistochemistry in detecting Helicobacter pylori infection in paraffin-embedded tissues of gastric biopsy

Quantum dots (QDs) are a new type of fluorescent label, which has been widely used in many biological and biomedical imaging applications. In this study, we used QDs-based immunofluorescence histochemistry (QDs-IHC) and conventional immunohistochemistry (IHC) techniques to perform a retrospective analysis on paraffin-embedded tissues of gastric biopsies in 203 patients (112 of which were HP positive and 91 were negative). The ability of QDs-IHC to detect Helicobacter pylori (HP) in gastric biopsies compared to IHC technology was evaluated. In our study, both methods showed consistent HP morphology and localization. The positive detection rate of HP for QDs-IHC in formalin-fixed and paraffin-embedded (FFPE) tissue was 54.7% (111/203), and the sensitivity and specificity reached 99.11% and 100%, respectively. However the positive detection rate of HP for IHC was 53.7% (109/203), with a sensitivity and specificity of 97.32% and 100%, respectively. Weak positives (1+) were detected in 2 case of QDs-IHC with negative in IHC, and moderate positives (2+) were detected in 3 case of QDs-IHC with weak positives (1+) in IHC. The consistency test showed that the two methods showed good agreement (κ?=?0.980, P?=?0.014), but the sensitivity of QDs-IHC was slightly higher than that of conventional IHC. Our results show that QDs-IHC has strong sensitivity and high specificity. It is superior to conventional IHC in detecting HP infection in FFPE tissues of gastric biopsy, especially in tissues with low HP content.

     

Expression of ALS‐linked TDP‐43 mutant in astrocytes causes non‐cell‐autonomous motor neuron death in rats

Mutation of Tar DNA‐binding protein 43 (TDP‐43) is linked to amyotrophic lateral sclerosis. Although astrocytes have important roles in neuron function and survival, their potential contribution to TDP‐43 pathogenesis is unclear. Here, we created novel lines of transgenic rats that express a mutant form of human TDP‐43 (M337V substitution) restricted to astrocytes. Selective expression of mutant TDP‐43 in astrocytes caused a progressive loss of motor neurons and the denervation atrophy of skeletal muscles, resulting in progressive paralysis. The spinal cord of transgenic rats also exhibited a progressive depletion of the astroglial glutamate transporters GLT‐1 and GLAST. Astrocytic expression of mutant TDP‐43 led to activation of astrocytes and microglia, with an induction of the neurotoxic factor Lcn2 in reactive astrocytes that was independent of TDP‐43 expression. These results indicate that mutant TDP‐43 in astrocytes is sufficient to cause non‐cell‐autonomous death of motor neurons. This motor neuron death likely involves deficiency in neuroprotective genes and induction of neurotoxic genes in astrocytes.