MTM1 gene is essential for SOD2 activity and normal mitochondrial function. MTM1 deletion results in decreased SOD2 activity, impaired mitochondrial function and growth defect on nonfermentable carbon source. A yeast genomic library was transformed into mtm1 deletion mutant to screen for suppressor genes of MTM1. The damage caused by MTM1 deletion is irreversible and even overexpression of MTM1 can not rescue the growth defect of mtm1 deletion mutant. Another screening strategy was adopted: a plasmid overexpressing MTM1 was transformed into wild type before the MTM1 gene on chromosome was deleted. The resulting strain, designated YES2MTM1, was transformed with a yeast genomic library. Transformants lost the plasmid overexpressing MTM1 after 5-FOA treatment. Yeast strains able to grow on nonfermentable carbon source with MTM1 deletion and overexpression of some DNA fragments were picked up and candidate suppressor genes were identified. Overexpression of five genes were identified to be able to rescue the growth defect on nonfermentable carbon source. The study will provide reference for MTM1 gene function and screening for suppressor of genes whose deletion result in irreversible damage.

Nutritional support therapy includes three main components:nutritional screening,nutritional assessment,and nutritional intervention.It is important to emphasize that nutritional screening and nutritional assessment are two different concepts and definitions,which are often confusing for many physicians,nurses,and dietitians.In this review,we present an overview on the main concepts about nutritional screening and nutritional assessment,highlight their features and complementarity,and discuss the future perspectives in the clinical practice.

Objective: To investigate the roles of N-acetyl-L-cysteine (NAC) against binge drinking-induced fatty liver in mice. Methods: SPF male C57BL/6 mice were randomly divided into 3 groups, i.e. control group, model group, and NAC/ethanol group (n=10). Mice in model and NAC/ethanol groups were exposed to 3 doses of ethanol (6 g/kg bw) to induced fatty liver, while mice in control group received equal volume and equal energy of maltodextrin solution. NAC was administered to mice at 1 h before ethanol exposure (100 mg/kg bw, i.p.). The mice were sacrificed at 6 h after the last ethanol exposure. The liver and epididymal adipose tissues were collected. Histopathological examination and biochemical assay kit were used to evaluate the fat accumulation, while Western-blot was performed to detect the protein levels of some key factors involved in fat metabolism in liver and adipose tissues. Results: Compored with control group mice, the liver index and liver weight were significantly increased compared with model group, the liver index and TG level in NAC/ethanol group mice were all significantly decreased (P<0.05). Histological examination showed NAC effectively suppressed binge drinking-induced fat accumulation in mice liver. In addition, NAC had no significant effects on the protein levels of peroxisome proliferator-activated receptor-α (PPAR-α), Acy-CoA oxidase (ACOX), sterol regulatory element binding protein 1 c (SREBP-1c) and fatty acid synthase (FAS). Furthermore, the protein levels of hormone sensitive lipase (HSL) did not significantly differ among 3 groups, whereas NAC prevented binge drinking-induced increase of HSL phosphorylation at ser563 and ser660. Conclusion NAC could effectively attenuate binge drinking-induced fatty liver, which might be associated with the inhibition of lipid mobilization by suppressing the phosphorylation of HSL.

Objective To establish the chronic low flow myocardial hibernation animal model in pigs, and to assess the diagnostic value for myocardial hibernation by using various imaging methods. Methods A total of 13 miniswine (30-40 kg) were used. All animals underwent general anesthesia and orotracheal intubation while the animals were mechanically ventilated. Under sterile conditions, left ventriculography and coronary angiography were performed by introduction of catheter into the right femoral artery. Further, a left anterolateral thoracotomy was performed in the third intercostal space. The proximal LCX was dissected free to allow placement of an ameroid constrictor. More than 1 month later, left ventriculography and coronary angiography were performed again, followed by cine MRI at rest and during stress with low dose of dobutamine (5 ?g?kg -1 ?min -1 ), respectively. Traditional and/or breath hold cine MRI were used to evaluate regional left ventricular wall motion, corresponding to basal, midventricular and apical short axis tomograms. Regional wall motion score index (WMSI) was calculated. At the same time 99m Tc MIBI myocardial SPECT was performed at rest and during nitroglycerin administration, respectively. All animals were finally sacrificed for pathological examination. Triphenyl tetrazolium chloride (TTC) staining was used to assess the myocardial infarction. Electron microscopy was used to identify myocardial cellular changes characteristic of hibernating myocardium. Results Three pigs died during surgery or within two weeks after surgery. One pig died of anesthesia during SPECT examination, 1 pig suffered from aneurysm, and another one pig showed negative findings. The other 7 pigs were found with hypokinetic ( n =4) or akinetic ( n =3) myocardial regions related to stenosed LCX (70%-99%). Resting cine MRI demonstrated decreased regional motion of the lateral and posteroinferior walls (ischemic regions) of the left ventricle ( n =7), compared with the nonischemic anteroseptal regions; but the low dose dobutamine (5 ?g?kg -1 ?min -1 ) could recover those hypokinetic or akinetic myocardial regions, characteristic of hibernating myocardium. Resting 99m Tc MIBI myocardial SPECT ( n =6) showed a fixed perfusion defect on the corresponding ischemic areas, which became reversible on the nitrate augmented myocardial perfusion imaging. It also indicated myocardial viability presented at the ischemic areas. TTC staining revealed patchy infarction of the area at risk localized to the endocardial surface ( n =3), and no myocardial infarction ( n =4). Electron microscopy of sections from the hibernating regions revealed loss of contractile materials, increased numbers of small mitochondria, and glycogen accumulation within viable cardiomyocytes, which had been described as hallmarks of hibernating myocardium. Conclusion Chronic low flow myocardial hibernation can be reproduced in an animal model during progressive coronary stenosis caused by ameroid constrictor.

Objective:To investigate the nutritional risk and prevalence of malnutrition in patients with terminal stage gastrointestinal malignant tumors in a tertiary hospital in Changsha.Methods:Cluster sampling was used to conduct a cross-sectional survey of inpatients from Departments of Gastroenterology, Gastrointestinal Surgery, Hepatobiliary Surgery and Oncology in Hunan Provincial People's Hospital from January 2019 to July 2020. Nutritional Risk Screening 2002 (NRS 2002) was used to assess the prevalence of nutritional risk with malnutrition defined as concurrent presence of BMI < 18.5 kg/m 2, poor general condition and NRS 2002 nutritional impairment score of 3. Step 2 of Global Leadership Initiative on Malnutrition (GLIM) diagnostic criteria (without whole body muscle mass) was adopted to diagnose malnutrition. Step 3 of GLIM criteria was used to evaluate the prevalence of severe malnutrition. Results:A total of 802 patients registered in the 4 departments were selected for screening via cluster sampling and 514 were enrolled according to the inclusion/exclusion criteria. The prevalence of nutritional risk in patients with terminal stage gastrointestinal cancer was 49.8% (256/514). The prevalence of malnutrition and severe malnutrition per GLIM criteria were 41.6% (214/514) and 18.3% (94/514), respectively.Conclusions:Although nutritional support therapy is not recommended for patients with end-stage cancer. This paper suggests that the prevalence of nutritional risk and malnutrition in patients with end-stage gastrointestinal cancer is not as high as described in some articles.

Objective To investigate the feasibility and clinical experience of kidney transplantation from donors with Marfan syndrome (MFS). Methods Clinical data of 2 recipients undergoing kidney transplantation from the same MFS patient were retrospectively analyzed and literature review of 2 cases was conducted. Characteristics and clinical diagnosis and treatment of kidney transplantation from MFS patients were summarized. Results The Remuzzi scores of the left and right donor kidneys of the MFS patient during time-zero biopsy were 1 and 2. No significant difference was observed in the renal arteriole wall compared with other donors of brain death and cardiac death. Two recipients who received kidney transplantation from the MFS patient suffered from postoperative delayed graft function. After short-term hemodialysis, the graft function of the recipients received the left and right kidney began to gradually recover at postoperative 10 d and 20 d. After discharge, serum creatinine level of the recipient received the left kidney was ranged from 80 to 90 μmol/L, whereas that of the recipient received the right kidney kept declining, and the lowest serum creatinine level was 232 μmol/L before the submission date (at postoperative 43 d). Through literature review, two cases successfully undergoing kidney transplantation from the same MFS donor were reported. Both two recipients experienced delayed graft function, and then renal function was restored to normal. Until the publication date, 1 recipient has survived for 6 years, and the other recipient died of de novo cerebrovascular disease at postoperative 2 years. Conclusions MFS patients may serve as an acceptable source of kidney donors. However, the willingness and general conditions of the recipients should be carefully evaluated before kidney transplantation. Intraoperatively, potential risk of tear of renal arterial media should be properly treated. Extensive attention should be paid to the incidence of postoperative complications.