Objective To investigate the influence of pain on liver function recovery after hepatectomy Methods Clinical data of 257 patients with primary hepatocellular carcinoma were analyzed retrospectively. The patients were divided into effective analgesia group(NRS ≤ 3 points)and ineffective analgesia group(NRS > 3 points)according to the digital hierarchy(NRS). The serum liver function indexes including ALT,AST,TBiL, ALB and PT were compared in 2 groups. Results There was no significant difference in preoperative liver function between 2 groups but the levels of ALT ,AST ,PT and TBIL at 1st ,3rd ,5th and 7th days postoperatively were lower in effective analgesia group than those in ineffective analgesic group after surgery(P<0.05). The incidence of the delay of liver function was lower in effective analgesia group than that in ineffective analgesic group. Conclusion Effective analgesic treatment can reduce liver damage and accelerate liver function recovery.

BACKGROUND: There are no effective treatments for spinal cord injury. Transplantation of olfactory ensheathing cells (OECs) has achieved great progress in repairing spinal cord injury. OBJECTIVE: To observe the effect of OECs transplantation on pathological and ultrastructural alterations of spinal cord, and the role in spinal cord injury developing.METHODS: A total of 60 SD rats were randomly divided into blank, model, transplantation and DF12 groups, with 15 animals in each group. The entire vertebral plate of T_(10), and partial vertebral plate of T_9 and T_(11) of blank group were cut open, and gelatin sponge was used for hemostasis. In the model group, the spinal cord was excised. In the transplantation and DF12 groups, OECs and DF12 culture solution were injected following spinal cord excision. The incision was sutured. Two rats from each group were anesthetized 1, 3, 7, 14, 28, 42, and 56 days following injury, and injured areas were observed by light microscopy and electron microscopy. RESULTS AND CONCLUSION: Following spinal cord injury, pathological and ultrastructural changes occurred, such as hemorrhage, edema, degeneration, necrosis, cavitation, gliacyte proliferation and nerve fiber regeneration. OECs transplantation attenuated neuronal and nerve fiber necrosis, relieved degree of pathological reaction, protected injured neurons, prevented gliacyte proliferation and increased nerve fiber regeneration. Results show that OECs transplantation ameliorated pathological reactions and promoted spinal cord injury repair.

Objective:To explore the effectiveness of humanism concept in the management of patients with spi-nal cord injury care.Methods:Choose between January 2011 and February 2011 hospitalized in our hospital 112 cases of spinal cord injury patients, randomly divided into control group and observation group ( 56 cases) , com-pared two groups of nursing effect.Control group routine nursing management, observation group will humanistic nursing management idea runs through in the routine nursing management.Results:Aware of knowledge about health education group is significantly higher than the control group, patients satisfaction survey in nursing, be-tween the two groups statistically significant depression levels lower than the control group.Conclusions:In the nursing management of patients with spinal cord injury in the application of humanistic nursing concept effect is good, not only improve the effect of the nursing, and obviously improve the patient′s satisfaction, promote the pa-tient′s psychological adaptability.

To describe the electroclinical features of epilepsy and neck myoclonus.Methods We searched the EEG database using the terms “epilepsy” and “neck myoclonus” over a 2-year period from January 2018 to January 2020 in the Xijing Hospital，Xi’an，China. The clinical and electrophysiological characteristics were studied. Results Four patients with epilepsy and neck myoclonus were male.They were diagnosed with genetic generalized epilepsy，of which 3 patients were epilepsy of generalized tonic-clonic seizures alone，1 patient was epilepsy of eyelid myoclonia with absences.The mean age at epilepsy onset was 9～27 years. Epilepsy and valproate treatment preceded neck myoclonus in two patients，and the neck myoclonus disappeared after discontinuation of valproate in one of them. A total of 254 neck myoclonus were recorded，92.5% of the events occurred during Rapid eye movement sleep，and then non-rapid eye movement 1 sleep. Conclusion Neck myoclonus may be more common in genetic generalized epilepsy. Video electroencephalography monitoring may be helpful to confirm the type of the myoclonus. The electroclinical features and mechanisms of the coexistence of epilepsy and neck myoclonus need further study.

Adolescent ; Adult ; Child ; Child, Preschool ; Early Diagnosis ; Female ; Hepatolenticular Degeneration ; diagnosis ; Humans ; Male ; Young Adult

Atherosclerosis is a chronic, inflammatory disorder characterized by the deposition of excess lipids in the arterial intima. The formation of macrophage-derived foam cells in a plaque is a hallmark of the development of atherosclerosis. Lipid homeostasis, especially cholesterol homeostasis, plays a crucial role during the formation of foam cells. Recently, lipid droplet-associated proteins, including PAT and CIDE family proteins, have been shown to control the development of atherosclerosis by regulating the formation, growth, stabilization and functions of lipid droplets in macrophage-derived foam cells. This review focuses on the potential mechanisms of formation of macrophage-derived foam cells in atherosclerosis with particular emphasis on the role of lipid homeostasis and lipid droplet-associated proteins. Understanding the process of foam cell formation will aid in the future discovery of novel therapeutic interventions for atherosclerosis.
Acyltransferases ; metabolism ; Apoptosis Regulatory Proteins ; metabolism ; Atherosclerosis ; metabolism ; pathology ; Cholesterol ; metabolism ; Foam Cells ; cytology ; metabolism ; Humans ; Lipid Metabolism ; physiology ; Macrophages ; cytology ; immunology ; Membrane Proteins ; metabolism ; Perilipin-2 ; Peroxisome Proliferator-Activated Receptors ; metabolism ; Sterol Regulatory Element Binding Proteins ; metabolism

Acute hypobaric hypoxic brain damage is a potentially fatal high-altitude sickness. Autophagy plays a critical role in ischemic brain injury, but its role in hypobaric hypoxia (HH) remains unknown. Here we used an HH chamber to demonstrate that acute HH exposure impairs autophagic activity in both the early and late stages of the mouse brain, and is partially responsible for HH-induced oxidative stress, neuronal loss, and brain damage. The autophagic agonist rapamycin only promotes the initiation of autophagy. By proteome analysis, a screen showed that protein dynamin2 (DNM2) potentially regulates autophagic flux. Overexpression of DNM2 significantly increased the formation of autolysosomes, thus maintaining autophagic flux in combination with rapamycin. Furthermore, the enhancement of autophagic activity attenuated oxidative stress and neurological deficits after HH exposure. These results contribute to evidence supporting the conclusion that DNM2-mediated autophagic flux represents a new therapeutic target in HH-induced brain damage.
Mice ; Animals ; Hypoxia ; Oxidative Stress ; Autophagy ; Cognition ; Sirolimus/therapeutic use*

Malignant mesothelioma of the tunica vaginalis testis (MMTVT) is a rare tumor. At present, there are still many disputes in its epidemiology, pathogenesis, selection of diagnostic methods, treatment and prognosis. Asbestos exposure, ionizing radiation and chromosome abnormalities are the risk factors of MMTVT. Immunohistochemistry, ultrasonography and electron microscope can be used for the diagnosis and aggressive surgery is the main treatment method. The development of endoscopic surgery, multi-disciplinary treatment (MDT), tumor targeted therapy and immunotherapy will bring more benefits to MMTVT patients.

Contraindications ; Humans ; Portasystemic Shunt, Transjugular Intrahepatic

AIM: To investigate the regulation of autophagy on high glucose-induced epithelial-mesenchymal transition(EMT)in human lens epithelial cells.

METHODS: In order to investigate the changes of EMT and autophagy induced by high glucose, HLE-B3 cells were divided into two groups. In NC group, cells were cultured in DMEM with 5.5mmol/L glucose, and in HG group, cells were treated with DMEM in addition with 30mmol/L glucose for 12h, 24h, and 48h. Western blot was used to detect the expression of EMT-marker proteins(E-cadherin and α-SMA)and autophagy-marker proteins(LC3, Beclin 1 and SQSTM1/p62). Wound healing assay was conducted to observe the migration ability. To investigate the regulation of autophagy on EMT, we employed rapamycin, an agonist of autophagy. HLE-B3 cells were divided into 4 groups. Two of them were mentioned as above, and the other two groups were treated with high glucose combined with DMSO(DMSO)and high glucose combined with 200nmol/L rapamycin(RAPA), respectively. Migration ability of cells was evaluated by Transwell assay. Expressions of proteins, such as EMT marker proteins, molecules in TGF-β signaling pathway(TGF-β2, Smad2/3, p-Smad2/3, Snail), and autophagy markers were detected by Western blot. The intracellular co-localization of SQSTM1/p62 and Smad2/3 was observed by immunofluorescence staining, and their interaction was confirmed by co-immunoprecipitation assay.

RESULTS: The expression of E-cadherin, LC3 Ⅱ/Ⅰ, and Beclin 1 in HLE-B3 cells of HG group gradually decreased(F=67.52, 163, 206; all P<0.0001), the expressions of α-SMA, SQSTM1/p62 increased with time(F=53.37, 302.1; all P<0.0001), and cell migration also increased compared with the cells in NC group(all P<0.001), indicating that high glucose stimulated EMT and suppressed autophagy. After treatment with rapamycin, the expressions of LC3 Ⅱ/Ⅰ and E-cadherin increased, the expressions of α-SMA, p-Smad2/Smad2, p-Smad3/Smad3 and Snail decreased(all P<0.05), and the expressions of TGF-β2 did not change(all P>0.05)in RAPA group compared with HG group and DMSO group, cell migration was also suppressed(all P<0.001), indicating that Rapamycin down regulated the expressions of molecules in TGF-βsignaling pathway after activation of autophagy, which resulted in inhibiting EMT. Immunofluorescence staining showed co-localization of SQSTM1/p62 and Smad2/3 in cytoplasm. Co-immunoprecipitation confirmed the combination between SQSTM1/p62 and Smad2/3.

CONCLUSION: High glucose stimulates the process of EMT and suppresses the autophagy in HLE-B3 cells. Autophagy regulates EMT by interacting with Smad2/3 via SQSTM1/p62, altering the amount of Smad2/3 which works in the TGF-β signaling pathway.