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1.
Preprint in English | bioRxiv | ID: ppbiorxiv-431722

ABSTRACT

The increasing numbers of infected cases of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses serious threats to public health and the global economy. Most SARS-CoV-2 neutralizing antibodies target the receptor binding domain (RBD) and some the N-terminal domain (NTD) of the spike protein, which is the major antigen of SARS-CoV-2. While the antibody response to RBD has been extensively characterized, the antigenicity and immunogenicity of the NTD protein are less well studied. Using 227 plasma samples from COVID-19 patients, we showed that SARS-CoV-2 NTD-specific antibodies could be induced during infection. As compared to the serological response to SARS-CoV-2 RBD, the SARS-CoV-2 NTD response is less cross-reactive with SARS-CoV. Furthermore, neutralizing antibodies are rarely elicited in a mice model when NTD is used as an immunogen. We subsequently demonstrate that NTD has an altered antigenicity when expressed alone. Overall, our results suggest that while NTD offers an alternative strategy for serology testing, it may not be suitable as an immunogen for vaccine development.

2.
Preprint in English | medRxiv | ID: ppmedrxiv-20091355

ABSTRACT

COVID-19, caused by SARS-CoV-2, is an acute self-resolving disease in most of the patients, but some patients can develop a severe illness or even death. To characterize the host responses and identify potential biomarkers during disease progression, we performed a longitudinal transcriptome analysis for peripheral blood mononuclear cells (PBMCs) collected from 4 COVID-19 patients at 4 different time points from symptom onset to recovery. We found that PBMCs at different COVID-19 disease stages exhibited unique transcriptome characteristics. SARS-CoV-2 infection dysregulated innate immunity especially type I interferon response as well as the disturbed release of inflammatory cytokines and lipid mediators, and an aberrant increase of low-density neutrophils may cause tissue damage. Activation of cell death, exhaustion and migratory pathways may lead to the reduction of lymphocytes and dysfunction of adaptive immunity. COVID-19 induced hypoxia may exacerbate disorders in blood coagulation. Based on our analysis, we proposed a set of potential biomarkers for monitoring disease progression and predicting the risk of severity.

3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-289755

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the cause of misdiagnosis of occupational chronic n-hexane poisoning and to investigate the diagnosis and differential diagnosis of this disease.</p><p><b>METHODS</b>The clinical data of 16 patients with occupational chronic n-hexane poisoning who had been misdiagnosed with other diseases were collected. The hospital they first visited, cause of misdiagnosis, clinical features, and the misdiagnosis rate among inpatients during the same period were retrospectively analyzed.</p><p><b>RESULTS</b>Sixteen of 62 patients hospitalized during the same period were misdiagnosed at the first visit; 11 cases were in the upper first-class hospitals, and 5 cases in the upper second-class hospitals; 5 cases were misdiagnosed as Green Barry syndrome, 2 cases as motor neuron disease, 2 cases as drug-induced peripheral neuropathy, 3 cases as periodic paralysis, and 4 cases had uncertain diagnosis.</p><p><b>CONCLUSION</b>Most doctors who work in ordinary hospitals do not know occupational chronic n-hexane poisoning, which is often misdiagnosed as general neuropathies or difficult diseases. The key to correct diagnosis is to know the patient's occupational history and clinical features.</p>


Subject(s)
Humans , Chronic Disease , Diagnosis, Differential , Diagnostic Errors , Hexanes , Poisoning , Hospitals , Peripheral Nervous System Diseases , Retrospective Studies
4.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-533087

ABSTRACT

Objective The purpose of this investigation was to observe the effects of the glutamate/aspartate transporter(GLAST) antibody to auditory brainstem response(ABR) and the pathologic morphology of hair cells in the guinea pig's cochlea. Methods 20 guinea pigs were randomly divided into the experimental group and control group. By perfusing the antibody to GLAST into tympanic canal in the cochlea of guinea pigs in experimental group and artificial perilymph into the guinea's cochlea in control group,the results of ABR ,basilar membrane stretched preparation and transmission electron microscope were observed. Results After antibody perfusion,the ABR was not induced from the third day to the ninth day.In control group,the ABR was nearly absent on the third day,but could be evolved,on the sixth day and the ninth day in all guinea pigs with the average threshold of 62.50?5.25 dB SPL and 47.50?6.18 dB SPL,respectively. The ABR thresholds at different time in control group were significantly different(P

5.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-581286

ABSTRACT

AIM: To study effects of hypericin associated with light emitting diode irradiation on nasopharyngeal carcinoma cell line of human in vitro. METHODS: CNE-2 cells were exposed respectively to different concentration of hypericin,and compared with hematoporphyrin as positive control group,and incubated for 6 h in the dark, then accumulative radiated energe of yellow and red light irradiation equivalent to 5. 67 J/cm2 were given throughout 90 min,killing effect and apoptosis of CNE-2 cells were detected by MTT assay after incubation of 24 h and flow cytometry. RESULTS: MTT assay showed that cytotoxicity of hypericin and hematoporphyrin with light irradiation presented in dose-dependent way,their IC50 values were 0. 049 and 0. 650 ?g/mL,respectively. Flow cytometry showed that hypericin with light irradiation could block cell growth at S phase and G2 phase,when CNE-2 cells were exposed to hypericin at 0. 20 ?g/mL for 18,28 and 48 h,the apoptosis rate reached at 9. 97% ,72. 19% and 92. 24% . CONCLUSION: Hypericin with light irradiation could obviously inhibit the growth of CNE-2 cells and induce apoptosis.

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