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Objective To explore the associations of blood glucose fluctuation indexes with skeletal muscle content in different Chinese medicine syndromes of type 2 diabetes mellitus (T2DM). Methods A retrospective study was performed on 330 T2DM patients hospitalized in Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from September 2020 to September 2021. According to different Chinese medicine syndrome, the patients were divided into Qi and Yin deficiency syndrome (n=169), dryness-heat due to Yin deficiency syndrome (n=88) and damp-heat tapping spleen syndrome (n=73). For cenalying the relationship between blood glucose fluctuation and skeletal muscle content, the following indicators were observed and compared among the patients with different syndrome types, including time in range (TIR), standard deviation of blood glucose (SDBG), mean amplitude of glycemic excursion (MAGE), mean of daily difference (MODD), coefficient of variation (CV), glycosylated hemoglobin (HbA1c), relative appendicular skeletal muscle (RASM), appendicular skeletal muscle mass (ASM) and total lean mass (TLM). Compliance was based on TIR ≥ 70%. Results The TIR compliance rate of Qi and Yin deficiency syndrome group was 46.7%, dryness-heat due to Yin deficiency syndrome group was 30.7%, and damp-heat tapping spleen syndrome group was 47.9%. There was a significant difference in the TIR compliance rate among the three groups（χ2=7.145, P=0.028）, and the TIR compliance rate of Qi and Yin deficiency syndrome group and damp-heat tapping spleen syndrome group was significantly higher than that of dryness-heat due to Yin deficiency syndrome group (P

Objective To construct and identify Nrf2 knockout mouse model. Methods A pair of male and female heterozygous (Nrf2-/+) mice were introduced to breed F1 mice. Male and female Nrf2-/+ mice from F1 generation were bred to obtain F2 generation mice. DNA was extracted from the tail tissue of mice at 5 days of age and their genotype was determined by PCR and agarose gel electrophoresis. NRF2 protein was extracted and coding gene was knocked out from the lung tissues of mice. The expression of NRF2 protein was detected by Western blot, and the identification results were confirmed laterally. Results Homozygous (Nrf2-/-) mice continued to mate and obtain homozygous mice. Three genotypes were identified when F1 was mated with F2 generation heterozygous mice: wild type (Nrf2+/+), heterozygous (Nrf2+/-) and homozygous (Nrf2-/-). The genotypes of offspring mice were successfully identified by PCR. NRF2 protein expression in lung tissue of Nrf2 knockout mice was significantly lower than that of wild-type mice (P＜0.05). Conclusions The mouse model with Nrf2 knockout is successfully bred in this study, which provides a new experimental tool for further exploring the role and mechanism of NRF2.

White matter dysplasia (WMD) in preterm infants due to intrauterine inflammation is caused by excessive apoptosis of oligodendrocyte precursor cells (OPCs). In recent years, studies have found that excessive autophagy and apoptosis are highly interconnected and important in infection and inflammatory diseases in general. Therefore, in this study, we aimed to confirm whether regulation of autophagy by using the Akt phosphorylation agonist SC79 can inhibit abnormal apoptosis of OPCs and promote myelin maturation and white matter development in neonatal rats with WMD. We investigated the effect of inflammation on oligodendrocyte development in P0 neonatal rats by intracerebellar injection of LPS, and collected brain tissue at P2 and P5. Immunohistochemical and immunofluorescence staining were used to evaluate white matter damage, while immunofluorescence staining, terminal deoxynucleotidyl transferase dUTP nick end labeling analysis (TUNEL), and western blotting were used to evaluate autophagy and apoptosis. First, we observed that white matter development was arrested and white matter fiber maturation was impaired in LPS-inflicted pups compared with those in the sham-operated group. Second, treatment with SC79 reduced the levels of LC3II, caspase 3, caspase 9, and Bax/Bcl-2 and increased the levels of p62, p-Akt, and p-mTOR in the brain tissue of neonatal rats. Finally, SC79 treatment inhibited OPC apoptosis by increasing the binding of Beclin 1 to Bcl-2, which promoted OPC differentiation and maturation. However, the opposite results were observed after rapamycin administration. Taken together, our results suggest that SC79 can inhibit the abnormal apoptosis of OPCs caused by excessive autophagy through the Akt/mTOR pathway and that SC79 is a potential therapeutic agent for WMD in preterm infants. [ABSTRACT FROM AUTHOR]

Cyprinid herpesvirus 2 (CyHV-2) is a pathogen that causes significant losses to the global aquaculture industry due to mass mortality in crucian carp and goldfish. This study demonstrates that the ORF55/ORF57 deletion mutants CyHV-2-Δ55-CP and CyHV-2-Δ57-CP obtained through homologous recombination replicate effectively within the caudal fin of Carassius auratus gibelio (GiCF) cells and exhibit morphologies similar to the CyHV-2 wild-type strain. Both mutants demonstrated a decrease in virulence, with CyHV-2-Δ57-CP exhibiting a more significant reduction. This serves as a reference for the subsequent development of recombinant attenuated vaccines against CyHV-2. Additionally, both mutants expressed the inserted RGNNV-CP (capsid protein of Redspotted grouper nervous necrosis virus) fusion protein gene, and inoculation with CyHV-2-Δ57-CP-infected GiCF cell lysates elicited an antibody response in the grouper. These results indicate that, while ORF55 and ORF57 genes of CyHV-2 are not required for viral replication in vitro, they do play a role in virulence in vivo. Additionally, expression of foreign protein in CyHV-2 suggests that the fully attenuated mutant of CyHV-2 could potentially function as a viral vector for developing subunit vaccines or multivalent recombinant attenuated vaccines. [ABSTRACT FROM AUTHOR]

Cyprinid herpesvirus 3 (CyHV‐3) is the main pathogen of koi herpesvirus disease (KHVD), which has caused serious damage to the ornamental and food‐producing carp industry. Effective and rapid on‐site detection methods are needed for early diagnosis of CyHV‐3. A lateral flow immuno‐chromatographic assay (LFIA) using two specific anti‐CyHV‐3 monoclonal antibodies has been developed and validated for on‐site detection of CyHV‐3. MAb 3C9 was used to bio‐conjugate CyHV‐3 antigen with colloidal gold, and MAb 2A8 was used to capture antigen bound colloidal gold on the test line. The control line was lined with goat anti‐mouse IgG to capture unbound colloidal gold to validate performance. The test results can be viewed within 10 min after putting the strip into CyHV‐3 virus infection fluid. The lowest limit of detection for the LFIA test was found to be 1.5 × 104 copies/μL and it showed no cross‐reactivity with other fish viral pathogens. The specificity of the strip was 100% when spleen and kidney tissues of CyHV‐3‐infected and healthy koi were validated at the field level. The LFIA strip will be an effective device for the early detection of CyHV‐3 in the future. [ABSTRACT FROM AUTHOR]