Background: Anti-SARS-CoV-2 virus antibody levels in convalescent plasma (CP), which may be useful in severe Anti-SARS-CoV-2 virus infections, have been rarely reported. Results: A total of eight donors were considered for enrollment; two of them were excluded because of ineligible routine check. Of the six remaining participants, five samples were tested weakly positive by the IgM ELISA. Meanwhile, high titers of IgG were observed in five samples. The patient treated with CP did not require mechanical ventilation 11 days after plasma transfusion, and was then transferred to a general ward. Conclusions: Our serological findings in convalescent plasma from recovered patients may help facilitate understanding of the SARS-CoV-2 infection and establish CP donor screening protocol in COVID-19 outbreak. Methods: Anti-SARS-CoV-2 antibodies including IgM and IgG were measured by two enzyme-linked immunosorbent assays (ELISA) in convalescent plasma from six donors who have recovered from coronavirus disease 2019 (COVID-19) in Nanjing, China. CP was also utilized for the treatment of one severe COVID-19 patient.

Background: The pandemic coronavirus disease 2019 (COVID-19) has threaten the global health. The characteristics of laboratory findings of coronavirus are of great significance for clinical diagnosis and treatment. We found indicators that may most effectively predict a non-severe COVID-19 patient develop into a severe patient. Methods: We conducted a meta-analysis to compare the laboratory findings of severe patients with non-severe patients with COVID-19 from searched articles. Results: Through the analysis of laboratory examination information of patients with COVID-19 from 35 articles (5912 patients), we demonstrated that severe cases possessed higher levels of leukocyte (1.20-fold), neutrophil (1.33-fold), CRP (3.04-fold), PCT (2.00-fold), ESR (1.44-fold), AST (1.40-fold), ALT (1.34-fold), LDH (1.54-fold), CK (1.44-fold), CK-MB (1.39-fold), total bilirubin (1.14-fold), urea (1.28-fold), creatine (1.09-fold), PT (1.03fold) and D-dimer (2.74-fold), as well as lower levels of lymphocytes (1.44-fold), eosinophil (2.00-fold), monocyte (1.08-fold), Hemoglobin (1.53-fold), PLT (1.15-fold), albumin (1.15-fold), and APTT (1.02-fold). Lymphocyte subsets and series of inflammatory cytokines were also different in severe cases with the non-severe ones, including lower levels of CD4 T cells (2.10-fold) and CD8 T cells (2.00-fold), higher levels of IL-1β (1.02fold), IL-6 (1.93-fold) and IL-10 (1.55-fold). Conclusions: Some certain laboratory inspections could predict the progress of the COVID-19 changes, especially lymphocytes, CRP, PCT, ALT, AST, LDH, D-dimer, CD4 T cells and IL6, which provide valuable signals for preventing the deterioration of the disease.

Background: Previous studies of insomnia focused mainly on the improvement of sleep condition and ignored the effects of sleep-related psychological activity and daytime function after pharmacological and behavioral treatments. We compared the clinical effects of both therapies on sleep condition, sleep-related psychological activity and daytime function in chronic insomnia. Methods: Seventy-one patients with chronic insomnia were randomly divided into 4 groups and either received cognitive-behavior therapy (CBT, n = 19), pharmacological therapy (PCT, n = 17), CBT plus medication (Combined, n = 18) or placebo (n = 17). The treatments lasted for 8 weeks with follow-ups conducted at 3 and 8 months. On the day after treatment ended, all patients were assessed using a polysomnogram (PSG), a sleep diary and a psychological assessment. Results: The three active treatments were more effective than placebo at the time the treatments were completed. Subjective sleep-onset latency, sleep efficacy and total sleep time were better in the PCT group than in the CBT group. At the 3-month follow-up, subjective and objective sleep-onset latency, sleep efficacy and total sleep time were better in the CBT group than in both the PCT and the Combined group. At the 8-month follow-up, the CBT group showed a steady comfortable sleep state, while the PCT and Combined groups were gradually returning to the pre-treatment condition. The Combined group showed a variable long-term effect. On the other hand, pre-sleep arousal at nighttime, dysfunctional beliefs about sleep as well as daytime functioning in the CBT group not only improved, but was better than in the other active treatment groups. Conclusion: Medication and Combined therapy produced a short-term effect on chronic insomnia while CBT had a long-term effect of improved sleep-related psychological activity and daytime functioning.

Repetitive administration of phencyclidine (PCP) in the perinatal period results in cortical apoptosis and a long-lasting deficit in sensorimotor gating. Because these changes are olanzapinesensitive, we have suggested that the effects of perinatal PCP could be used to model certain aspects of schizophrenia. Studies of PCP and N-methyl-D-aspartate-induced cell death suggested that superoxide could play a role in the pathway leading to death after PCP administration. The purpose of the current study was to determine whether the in vivo administration of M40403, a superoxide dismutase mimetic, could prevent PCPinduced cortical apoptosis and/or deficits in prepulse inhibition. Perinatal rat pups were administered 10 mg/kg PCP on postnatal (PN) days 7, 9, and 11 with or without treatment with 10 mg/kg M40403. Pups were either killed on PN 12 for analysis of various apoptotic markers or they were assessed for prepulse inhibition on PN 24 to 26. Treatment with M40403 2 and 24 h after each PCP treatment prevented PCP-induced increases in two measures of apoptosis in the dorsolateral frontal cortex and in the olfactory cortex. PCP-induced proapoptotic changes in Bax and Bcl-X L were also prevented by M40403 treatment. This regimen did not prevent the deficit in prepulse inhibition caused by PCP treatment, but when the treatment regimen was extended through PN 23, M40403 completely prevented the PCP-induced deficit in prepulse inhibition. These data suggest that perinatal PCP treatment leads to long-lasting changes in the pathway(s), leading to cell death and behavioral deficits, and that the superoxide radical plays a critical role in the underlying mechanism.

Porcine reproductive and respiratory syndrome virus (PRRSV) continues to be a major problem in the pork industry worldwide. The limitations of current PRRSV vaccines require the development of a new generation of vaccines. One of the key steps in future vaccine development is to include markers for diagnostic differentiation of vaccinated animals from those naturally infected with wild-type virus. Using a cDNA infectious clone of type 1 PRRSV, this study constructed a recombinant green fluorescent protein (GFP)-tagged PRRSV containing a deletion of an immunogenic epitope, ES4, in the nsp2 region. In a nursery pig disease model, the recombinant virus was attenuated with a lower level of viraemia in comparison with that of the parental virus. To complement the marker identification, GFP and ES4 epitope-based ELISAs were developed. Pigs immunized with the recombinant virus lacked antibodies directed against the corresponding deleted epitope, but generated a high-level antibody response to GFP by 14 days post-infection. These results demonstrated that this recombinant marker virus, in conjunction with the diagnostic tests, enables serological differentiation between marker virus-infected animals and those infected with the wild-type virus. This rationally designed marker virus will provide a basis for further development of PRRSV marker vaccines to assist with the control of PRRS. INTRODUCTIONPorcine reproductive and respiratory syndrome (PRRS) is the most economically significant disease of swine worldwide. It is characterized by late-term reproductive failure in sows and severe pneumonia in neonatal pigs. Since its emergence in domestic swine in the 1980s, PRRS has resulted in immense economic losses to the swine industry, with recent costs in the USA of at least US$600 million annually (Neumann et al., 2005). The aetiological agent of PRRS is a small, enveloped virus (PRRSV) containing a single, positive-stranded RNA genome. PRRSV belongs to the family Arteriviridae, which includes equine arteritis virus (EAV), lactate dehydrogenase-elevating virus and simian hemorrhagic fever virus (Snijder & Meulenberg, 1998). Nucleotide sequence comparisons have shown that PRRSV can be divided into distinct European (type 1) and North American (type 2) genotypes (Allende et al., 1999;Nelsen et al., 1999).The PRRSV genome is about 15 kb in length and contains nine open reading frames (ORFs). The 39 end of the genome encodes four membrane-associated glycoproteins (GP2, GP3, GP4 and GP5, encoded by subgenomic mRNAs 2a, 3, 4 and 5), two unglycosylated membrane proteins (E and M; encoded by subgenomic mRNAs 2b and 6) and a nucleocapsid protein (N; encoded by subgenomic mRNA 7) Mounir et al., 1995;Bautista et al., 1996;Mardassi et al., 1996;Meng et al., 1996;Meulenberg & Petersen-den Besten, 1996;Wu et al., 2001Wu et al., , 2005. The replicase-associated genes, ORF1a and ORF1b, situated at the 59 end of the genome, represent almost 75 % of the viral genome. The ORF1ab-encoded polyprotein pp1ab is predicted to be cleaved at 12 sites ...