Hepatic myelopathy is one of special category changes of nervous system,which was secondary to the end-stage hepatic diseases and is a syndrome of myeleterosis.It usually occurred after portosystemic shunt surgery or collateral circulation of portosystemic vein.The prognosis of hepatic myelopathy is poor,and the progression of this disease is slow.Surgical approaches such as dissociation of colon and anastomosis of ileum and rectum aimed at reducing the absorption of toxic substance and thus to breakdown the blood ammonia and improve the symptoms of nervous system,but the effects are not satisfactory.The clinical data of 1 patient with hepatic myelopathy who received liver transplantation at the Second Affiliated Hospital of Dalian Medical University in April 2012 were retrospectively analyzed.The clinical symptoms and physical signs were improved,and muscle strength was effectively recovered in the patient.Liver transplantation might be an effective method for the treatment of hepatic myelopathy.

Objective To study the effects of survivin antisense oligodexynucleotide(ASODN) on the expression of survivin mRNA and its protein in human malignant melanoma cell line A375.Methods Survivin ASODN was synthesized and transfected into melanoma cell line A375 by the liposome-encapsulation.Survivin mRNA and protein were detected by in situ hybridization and immunohistochemistry,respectively. Results At 24h after the transfection,the expression of survivin mRNA was significantly lower in the ASODN group than in the control group(P

One hundred and ten patients with primary hepatocellular carcinoma underwent hepatectomy from 2005 to 2010.Different methods of hepatic exclusion were applied in the surgery,including 54 patients with total hepatic vascular exclusion,22 with half hepatic vascular exclusion and 34 with regional hepatic vascular exclusion.The recovery of postoperative liver function was retrospectively analyzed.The results showed that the postoperative liver function of regional hepatic vascular exclusion [ALT(311 ± 80) U/L,total bilirubin (TB) (22.2 ± 8.3) μmoL/L at 1 st day and ALT (58 ± 17) U/L,TB (11.3 ± 3.1)μmol/L at 7th day] was better than that of total hepatic vascular exclusion [ALT(874 ±299)U/L,TB (42.9± 19.1) μmol/L at 1st day (P＜0.05) and ALT (108-±52)U/L,TB (14.6±9.2) μmol/L at 7th day] (P ＜ 0.05,＞ 0.05),indicating that regional hepatic vascular exclusion can effectively reduce hepatic injury during the operation and promote recovery of liver function after operation.

Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN).AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.