Autophagy is an important homeostatic cellular recycling mechanism responsible for degrading injured or dysfunctional subcellular organelles and proteins in all living cells. The process of autophagy can be divided into three relatively independent steps: the initiation of phagophore, the formation of autophagosome and the maturation/degradation stage. Different morphological characteristics and molecular marker changes can be observed at these stages. Morphological approaches are useful to produce novel knowledge that would not be achieved through other experimental methods. Here we summarize the morphological methods in monitoring autophagy, the principles in data interpretation and the cautions that should be considered in the study of autophagy.

Autophagy is an important homeostatic cellular recycling mechanism responsible for degrading injured or dysfunctional subcellular organelles and proteins in all living cells. The process of autophagy can be divided into three relatively independent steps: the initiation of phagophore, the formation of autophagosome and the maturation/degradation stage. Different morphological characteristics and molecular marker changes can be observed at these stages. Morphological approaches are useful to produce novel knowledge that would not be achieved through other experimental methods. Here we summarize the morphological methods in monitoring autophagy, the principles in data interpretation and the cautions that should be considered in the study of autophagy.
Autophagy ; Homeostasis ; Humans ; Organelles ; Phagosomes

Colorectal cancer remains a major threat to people’s health around the world. Researchers have paid more and more attention to colorectal cancer epigenetics. From two main aspects of colorectal cancer epigenetics: DNA methylation and histone modiifcation, this article analyzes the similarities and differences between patients with colorectal cancer in Eastern and Western countries. This review brielfy introduces epigenetic modiifcation of genes that were used to be biomarkers and therapeutic targets. Although there are some common features of colorectal cancer in the world, analysis has showed that some obvious epigenetic differences do exist in different races. For example, it had been conifrmed in the studies that there are differences in speciifc gene methylation, histone modiifcation sites and the degree of methylation and acetylation among countries, which provide the basis for speciifc diagnosis, treatment and prognosis of colorectal cancer in different ethnic groups. With improved research methods and increased sample size, more and more special molecular targets of colorectal cancer tissues will be found, and then personalized therapy for colorectal cancer can be achieved.

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Study the infect of child anorexia granule on serum ghrelin and leptin of anorexia children and its clinical efficacy. Selected 81 cases of anorexia children aged 1-6 years old into treatment group (42 cases) and control group (39 cases), in addition, 30 case healthy children as healthy control group. The control group children were treated with domperidone suspension 0.3 mg x kg(-1) x d(-1), tid, orally 30 minutes before meals. Treatment group were treated with child anorexia granule, 1-3 years 1 package, bid; 4-6 years 1 package, tid; po, 4 weeks as a course of treatment. Study the change of serum ghrelin and leptin before and after therapy. The study demonstrates that before treatment, the serum ghrelin level of disease group was lower than healthy group (P < 0.01), and the serum leptin level was higher than healthy group (P < 0.01). After treatment, the serum ghrelin level both increase, and the serum leptin decline. And the change of treatment group was significantly different with control group (P < 0.01). And the clinical effective rate are 95.23% and 74.35% (P < 0.01). After 6 months of follow-up visit, the children weight significantly increase in treatment group (P < 0.01). Results indicate that child anorexia granule can facilitate secretion of ghrelin, and inhibit secretion of leptin, so as to work up an appetite. And the molecular mechanism is its infect on serum ghrelin, leptin.
Anorexia ; drug therapy ; metabolism ; physiopathology ; Appetite Regulation ; drug effects ; Body Weight ; drug effects ; Child ; Child, Preschool ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Ghrelin ; metabolism ; Humans ; Infant ; Leptin ; metabolism ; Male

Autophagy is an important homeostatic cellular recycling mechanism responsible for degrading injured or dysfunctional cellular organelles and proteins in all living cells. Aging is a universal phenomenon characterized by progressive deterioration of cells and organs due to accumulation of macromolecular and organelle damage. Growing evidences indicate that the rate of autophagosome formation and maturation and the efficiency of autophagosome/lysosome fusion decline with age. Dysfunctional autophagy has also been observed in age-related diseases. Autophagy disruption resulted accumulation of mutated or misfolded proteins is the essential feature of neurodegenerative disorders. However, in cancers, fibroproliferative diseases or cardiovascular diseases, autophagy can play either a protective or destructive role in different types of disease, and even in different stages of the same disease. The review will discuss the cellular and molecular mechanisms of autophagy and its important role in the pathogenesis of aging and age-related diseases, and the ongoing drug discovery strategies for therapeutic intervention.
Aging ; Autophagy ; Drug Discovery ; Humans ; Lysosomes ; metabolism ; Neurodegenerative Diseases ; Phagosomes ; metabolism ; Protein Folding

Objective To study the epidemiological and clinical characteristics of patients with severe acute respiratory syndrome(SARA). Methods Clinical data from 682 patients with SARS were retrospectively analyzed. Results The patients ranged from 13 to 76 years old, 387 male and 295 female. A total of 356 patients (52.2) had a history of close contact with diagnosed SARS patients, and 113 (25.1%) had been to hospital ever. The most common symptom was fever (99.3%), followed by cough (44.4%), shortness of breath (12.2% ), diarrhea (8.9%). 596 patients (87.4%) had normal or decreased white blood cell counts. Serum ALT and CPK levels were elevated in 112 patients (16.4%)and 17 patients (2.5%) respectively. Infiltrates on chest radiography were seen in all patients, with 69.8% involved both lungs. Six patients (0.9%) died of SARS. Conclusion SARS is infectious. Hospital is an important place where SARS transmits. Fever, cough and infiltrative changes on chest radiography are mainly symptoms and signs.

Objective To construct an Lentiviral expression vector of pLVX‐IRES‐ZsGreen1‐MIA2 targeting to MIA2 and in‐vestigate its effect on the expression of MIA2 and growth of HCC cell line HepG2 in vitro ,observe MIA2 changes and the influence on apotheosis ,thus to provide preliminary experimental fundament for successive researching on the role of MIA2 in the pathogene‐sis of HCC .Methods The sequence of pLVX‐IRES‐ZsGreen1‐MIA2 was designed and synthesized .The pLVX‐IRES‐ZsGreen1‐MIA2 Lentiviral expression vector was constructed and then transiently transfected into HepG2 HCC cells in vitro .The proportion of pLVX‐IRES‐ZsGreen1‐MIA2 positive cells was observed under the fluorescence microscope .Then ,the expression level of MIA2 was detected by real time PCR .Moreover ,the proliferation of HepG2 cells was observed by MTT assay and colony formation as‐say .Finally ,the migration of HepG2 cells in vitro was also determined by Scratch assay .Results pLVX‐IRES‐ZsGreen1‐MIA2 Lentiviral expression vector was successfully constructed .Compared with control group (NC) ,the expression level of MIA2 was significantly decreased in transfected groups(P<0 .05);MTT assay showed that the proliferation of HepG2 cells was dramatically reduced in pIRES2‐ZsGreen1‐MIA2transfected groups(P< 0 .05);furthermore ,the number of both colony forming and migrating cells were also remarkably reduced in transfected groups(P<0 .05) .Conclusion The pIRES2‐ZsGreen1‐MIA2 can significantly re‐duce the expression level of MIA2 and inhibit the proliferation and migration of the HepG2 HCC cells in vitro .

Objective To investigate the status of food intolerance of patients with ulcerative colitis,(UC),to provide the basis for directing UC patients diet related nursing.Methods Forty-seven UC patients were selected from September 2013 to August 2014 in General Hospital of Tianjin University.The Southerland Disease Activity Index (DAI) was used to divide the UC patients into remission,mild activity and moderate to severe activity groups.The food-specific IgG antibodies status were tested by enzyme-linked immunosorbent assay in UC patients and healthy people.Relevant clinical parameters were analyzed statistically.Results Food intolerance rate in UC patients was as high as 68.08％(32/47);the food species:egg,wheat and milk ranked the most frequently intolerance food.The food intolerance rates in remission,mild activity and moderate to severe activity groups were 9/16,11/18,12/13,there were significantly different,x2=7.418,P＜0.05.Extraintestinal manifestation group had significantly higher food intolerance rate compareed to non extraintestinal manifestation group:1 1/13 vs.55.88％(19/34),x2=2.234,P＜0.05.No significant difference of food intolerance rate were showed among groups categorized according to sex,age,body mass index,site of lesion,P＞0.05.Conclusions UC patients show higher food intolerance rate than healthy people.UC disease activity and extraintestinal manifestations are correlated to food intolerance,which is of great significance to guide diet related nursing of UC patient.

This study is to determine the preventive effect and mechanism of targeting IL-17A on pulmonary inflammation and fibrosis after acute lung injury. Mice were treated with anti-IL-17A antibody on the day 7 and sacrificed on the day 14 after bleomycin lung injury. The pulmonary inflammatory status and the deposition of collagen were measured by HE and Sirius stains staining. The contents of hydroxyproline and collagen were measured by using commercial kits. The survival rate of mice was calculated by Kaplan-Meier methods. The inflammatory cytokines in bronchoalveolar lavage fluid were measured by ELISA and the expressions of inflammation-related molecules were detected by Western blotting assay. Targeting of IL-17A could prevent the development of lung inflammation, decrease collagen deposition and the contents of hydroxyproline, and protect against the development of pulmonary fibrosis, which together led to an increase in the animal survival. Moreover, blocking IL-17A decreased the expression ofpro-fibrotic cytokines such as IL-17A, TGF-beta1 and IL-13; increased the expression of anti-fibrotic or anti-inflammatory factors such as IFN-gamma, COX-2, 5-LOX, 15-LOX. Indeed, IL-17A antagonism suppressed the activation of pro-inflammatory p65NF-kappaB but enhanced the activation of pro-resolving p50NF-kappaB. In conclusion, that blockade of IL-17A prevents the development of pulmonary fibrosis from acute lung injury, is because blocking IL-17A may prevent acute inflammation converting to chronic inflammation.