One endpoint of clinical islet cell transplantation for type 1 diabetic patients is the elimination or reduction of hypoglycemia. We previously developed a simple tool to evaluate islet graft function: the secretory unit of islet transplant objects (SUITO) index. The aim of this study is to clarify the association between the SUITO index and hypoglycemic episodes. Data from 310 clinical evaluations of 11 islet recipients were included in this study. Fasting plasma C-peptide and glucose levels were measured at every evaluation. The SUITO index was calculated according to the following formula: 1500 × C-peptide level (ng/ml)/[blood glucose level (mg/dl) - 63]. The number of hypoglycemic events (<3.8 mmol/L) and severe hypoglycemic events (<2.2 mmol/L or hypoglycemic unawareness) was assessed on the basis of interviews and self-monitoring of blood glucose (SMBG). Receiver operating characteristic (ROC) analysis was performed to determine the cut-off values of the SUITO index for hypoglycemic events. Based on the ROC study, follow-up data after transplantations were divided into the following three groups: low-SUITO (SUITO index <10, n = 91), middle-SUITO (10 ≤SUITO index <26, n = 83), high-SUITO (SUITO index ≤26, n = 125). The frequency of total hypoglycemia in the high-SUITO group was significantly decreased when compared to the other groups (value with Kruskal-Wallis test p < 0.001). The frequency of total severe hypoglycemia was significantly decreased in the low-SUITO group compared to pretransplant status and further decreased in the middle- and high-SUITO group. Spearman correlation coefficients were -0.663 (p < 0.001) between the number of total hypoglycemic events per one month and the SUITO index and -0.521 (p < 0.001) between that of severe events and the SUITO index. The SUITO index could predict the severity of hypoglycemic episodes in type 1 diabetic patients who received islet cell transplantations.

Getah virus (GETV) is a mosquito-borne virus that was first determined in Malaysia in 1955, and can infect humans and multiple other mammals. GETV infection in horses has been reported in Japan and India, and causes great economic losses. In China, GETV has been identified in mosquitoes, pigs, foxes, and cattle with a wide geographical distribution, but has not been detected in horses. In August 2018, a sudden onset of fever was observed in racehorse in an equestrian training center in Guangdong Province in southern China. Blood samples were collected from the sick horse, and PCR/RT-PCR analysis was performed to screen for equine viral pathogens associated with fever. The results indicated that the samples were GETV RNA positive. After RT-PCR, sequencing, and assembly, the genome of the first Chinese horse-derived GETV strain, GZ201808, was obtained. Compared with the genome sequences of other GETV strains, twelve unique nucleotide substitutions were observed in GZ201808. The genome of GZ201808 had the highest genetic identity (99.6%) with AH9192, which was detected in pigs in China in 2017. Phylogenetic analysis indicated that GZ201808 clustered in Group III, and was located in an independent branch distant from other horse-derived GETV strains, indicating a unique evolutionary pattern of GZ201808. This study first determined and described the disease course of horse infected with GETV in China, sequenced and characterized the genome of the field horse-derived GETV strain, and therefore presented an unequivocal report of GETV infection in horses in China.

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Dihydromyricetin (DHM) is a plant flavonoid and is the primary active ingredient isolated from the medicinal herb, Ampelopsis grossedentata. DHM has been shown to possess various pharmacological activities, including anti-inflammatory effects. However, the possible role of DHM in asthma treatment remains to be elucidated. The present study aimed to investigate its anti-inflammatory properties in mice with symptoms of allergic asthma. The C57BL/6 mice were sensitized and challenged with ovalbumin (OVA) to induce asthma. DHM or phosphate-buffered saline treatment was administered 1 h prior to the OVA challenge. The levels of interleukin (IL)-4, IL-5 and IL-13 in the bronchoalveolar lavage (BAL) fluid were measured by enzyme-linked immunosorbent assay (ELISA), and OVA-specific serum IgE and IgG1 levels were also determined by ELISA. Histopathological staining was performed to evaluate the infiltration of inflammatory cells into the BAL fluid, lung tissues and goblet cell hyperplasia. DHM treatment significantly reduced the total number of inflammatory cells, including eosinophils, neutrophils, lymphocytes and macrophages, in the BAL fluid. DHM also reduced the levels of IL-4, IL-5 and IL-13 in the BAL fluid, and reduced the secretion of OVA-specific IgE and IgG1 in the serum. The histological staining demonstrated that DHM treatment effectively suppressed the OVA-induced inflammatory cells in the lung tissues and in the mucus hypersecreted by goblet cells in the airway. These results showed that DHM had a potent anti-inflammatory effect in an OVA-induced mouse model of asthma, offering potential as an anti-inflammatory agent for the treatment of asthma.

Elevated serum tumor marker levels were found in PAP patients. The serum levels of CEA, NSE and SCC may reflect the severity of the disease and predict the therapeutic effect of whole lung lavage.

Newcastle disease virus (NDV) has been classified by the World Organization for Animal Health (OIE) as a notable disease-causing virus, and this virus has the ability to infect a wide range of birds. V protein is a non-structural protein of NDV. V protein has been reported to inhibit cell apoptosis (Park et al., 2003a) and promote viral replication (Huang et al., 2003), however, the mechanisms of action of V protein have not been elucidated. In the present study, a yeast two-hybrid screen was performed, and V protein was found to interact with the CacyBP/SIP protein. The results of co-immunoprecipitation and immuno-colocalization assays confirmed the interaction between V protein and CacyBP/SIP. The results of quantitative-PCR and viral plaque assays showed that overexpression of CacyBP/SIP inhibited viral replication in DF-1 cells. Overexpression of CacyBP/SIP in DF-1 cells induced caspase3-dependent apoptosis. The effect of knocking down CacyBP/SIP by siRNA was the opposite of that observed upon overexpression. Moreover, it is known that NDV induces cell apoptosis via multiple caspase-dependent pathways. Furthermore, V protein inhibited cell apoptosis and downregulated CacyBP/SIP expression in DF-1 cells. Taken together, the findings of the current study indicate that V protein interacts with CacyBP/SIP, thereby regulating cell apoptosis and viral replication.