Antibacterial potential and mechanism of action of dithiocyano-methane as a bactericidal agent for farm disinfection.

AIMS: This study aimed to investigate the antibacterial ability and action mechanism of dithiocyano-methane against Aeromonas hydrophila, so as to provide a reference for its application in farm disinfection. METHODS AND RESULTS: After exposing the bacteria to dithiocyano-methane, the minimum inhibitory concentration (MIC), minimum bactericide concentration (MBC), activities of alkaline phosphatase, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase and electric conductivity in bacterial suspensions were determined, transmission electron microscope images on cellular structure and SDS-PAGE profile of bacterial proteins were analysed and the expression of genes related to the above experimental observations was confirmed by real-time quantitative PCR. The MIC and MBC of dithiocyano-methane against three tested strains was 1·46 and 2·93 mg l-1 respectively. The results showed that dithiocyano-methane significantly damaged bacterial cell structure, inhibited the biosynthesis of bacterial proteins and changed the integrity and permeability of bacterial cell wall and cell membrane. CONCLUSIONS: Dithiocyano-methane showed remarkable antibacterial ability against three tested strains, indicating it is a potential effective bactericidal agent for preventing animal diseases resulted from Aer. hydrophila. SIGNIFICANCE AND IMPACT OF THE STUDY: To our best knowledge, this is the first report to examine the antibacterial ability and action mechanism of dithiocyano-methane against bacteria. The results demonstrate the great potential of dithiocyano-methane as a disinfectant against Aer. hydrophila in settings such as aquaculture ponds and livestock farms.

Effect of imatinib on DOCA-induced myocardial fibrosis in rats through P38 MAPK signaling pathway.

OBJECTIVE: To explore the role of imatinib in desoxycorticosterone acetate (DOCA)-induced myocardial fibrosis in rats by the p38 mitogen-activated protein kinase (MAPK) signaling pathway. MATERIALS AND METHODS: Normal group (n=20), DOCA induction group (n=20), and imatinib treatment group (treatment group, n=20) were set up. Then, the cardiac function was examined via magnetic resonance imaging (MRI) and echocardiography (ECG) on the 21st d after modeling. Alkaline phosphatase (ALP) and myocardial function index creatine kinase-MB (CK-MB) were detected. The enzyme-linked immunosorbent assay (ELISA) was performed to measure tumor necrosis factor-gamma (TNF-γ) and interleukin-6 (IL-6). Hematoxylin-eosin (HE) staining assay was carried out to observe the pathological changes in myocardial tissues. Quantitative Polymerase Chain Reaction (qPCR) and Western blotting were employed to measure the expression levels of important myocardial fibrosis-related genes [checkpoint kinase 1 (Chek1) and alpha-smooth muscle actin (α-SMA)], as well as genes and proteins of the p38 MAPK signaling pathway. RESULTS: In comparison with the normal group, DOCA induction group had significantly lowered fractional shortening (FS, %) and ejection fraction (EF, %), but overtly increased left ventricular end-diastolic dimension (LVEDd) and left ventricular end-systolic dimension (LVESd), as well as levels of serum ALP, alanine aminotransferase (ALT), and CK-MB. Besides, the levels of TNF-γ, IL-6, and IL-1ß were notably raised in the DOCA induction group. HE staining results showed that myocardial injury was more severe in DOCA induction group. The results of the gene detection revealed that the expression levels of Chek1, α-SMA, p38 MAPK, and JNK were evidently higher in DOCA induction group than those in the imatinib treatment group (p<0.05), and the expression of p38 MAPK protein in the rat myocardial tissues was remarkably lower in the treatment group than that in the DOCA induction group (p<0.05). CONCLUSIONS: Imatinib can regulate the repair of myocardial injury caused by DOCA-induced myocardial fibrosis in rats by repressing the p38 MAPK signaling pathway.

[Repair of pressure ulcers in ischial tuberosity of 15 patients by partially de-epithelialized posterior femoral bilobed flaps].

Fifteen patients with sinus-type pressure ulcer in ischial tuberosity were admitted to our unit from April 2013 to April 2017, including 12 patients of unilateral pressure ulcer and 3 patients of bilateral pressure ulcer. The wounds were with infection of different degrees. The outer wound area of pressure ulcer before debridement ranged from 1.5 cm×1.0 cm to 6.0 cm×5.0 cm. Fifteen patients with 15 pressure ulcers were treated with vacuum sealing drainage for 3 to 13 days after debridement and sinus wall resection. Unilateral pressure ulcer was repaired with posterior femoral bilobed flap. One side of bilateral pressure ulcer was repaired with posterior femoral bilobed flap, and the other side was repaired with gluteus maximus muscle flap combined with local flap. The size of flaps ranged from 11.0 cm×7.5 cm to 15.0 cm×10.0 cm. Epidermis of the distal part and edge of the main flap was removed to make complex dermal tissue flap to fill the deep cavity. The other part of the main flap was applied to cover wound, and another flap of the bilobed flap was applied to cover the donor site where main flap was resected. The donor sites were sutured directly. The posterior femoral bilobed flaps in 15 patients survived after operation. Pressure ulcers of 12 patients were healed well. Incision of 2 patients ruptured and healed 15 days after second sewing. One pressure ulcer with infection under the flap healed on 16 days post second completely debridement. During follow-up of 3 to 18 months, flaps were with soft texture, good appearance, and no recurrence.