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

Objective To study the effect of esomeprazole,clarithromycin,metronidazole triple therapy for helicobactor pylori(Hp) infection in children.Methods Ninty-eight cases of children,identified by ~ 13 C-urea breath test(~ 13 C-UBT) Hp infection,deparded into therapy group(66 cases) and control group(32 cases).Therapy group were given Esomeprazole[0.8 mg/(kg?d),1 time/d],clarithromycin[15 mg/(kg?d),2 times/d],metronidazole[30 mg/(kg?d),3 times/d]triple therapy.Control group were given the same treatment except ameprazole.The course was 1 week.They were followed up 4 weeks later after the course and re-tested by ~ 13 C-UBT.Results The recurrent abdominal pain of the two groups recovered in different degrees,and the efficacy rate was 100%.The eradication rate of Hp in therapy group and control group were separately 90.9%(60/66) and 87.5%(28/32).There was no significance difference of the eradication of Hp.Conclusions The trearment of esomeprazole,clarithromycin,metronidazole triple therapy on Hp infection in children is quite effective and safe.The side effect is moderate.

Objective To evaluate the effect of vacuum sealing drainage(VSD)ON the destroyed hand injuries.Methods From January 2006 to December 2008,forty pafients with destroyed hand injuries (surface of wound)were randomly divided into VSD group(20 cases)and control group(chlorhexidine wet compress)(20 cases)after debridement. The outcomes were retrospectively analysed by pain score,swelling score,bacterial positive rate and necrotic tissue.Results Three days after treatment,the pain score of VSD group was(2.62±1.54)degree,and that of control group was(3.39±1.64)degree.There wag significant difference between the two groups(P＜0.01).The swelling score of VSD group was(1.51±0.25)degree which was different from control group(2.29±1.26)degree(P＜0.05).The bacterial positive rate of control group was 20%(4/20),but that of VSD group was 5%(1/20).There was significant difference between the two groups(P＜0.05).The VSD group had no necrotic tissue occurrence,but the control group had 2 cases,one of which had serious necrosis and had escapology.Conclusion VSD Can inhibit bacterial infection,ease pain,exempt changing dressings and stimulate growing of granulation tissue also can maintain a good environment for tissue transplantation later.So VSD combining with tissue transplantation is an ideal therapy in destroyed hand injuries.

Autophagy is an active research area in the biomedical field as its role has been identified in many physiological and pathological processes. Accordingly, there is a growing demand to identify, quantify and manipulate the process accurately. Meanwhile, there is great interest in identifying compounds that modulate autophagy because they may have applications in the treatment of a variety of autophagy-related diseases. In this review, we summarize the current status of autophagy screening systems to facilitate identification of autophagy modulators.
Autophagy ; Humans

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 understand well this disease,8 children with familial periodic paralysis(FPP) were reported and the(rela)-ted literatures were reviewed.Methods The hereditary characters,clinical manifestations,auxiliary examination and managements were summarized retrospectively in 8 cases of FPP patients hospitalized from January 1996 to December 2005,and etiopathogenis and diagnosis were also analyzed.Results Six cases of FPP were diagnosed as hypokalemic periodic paralysis,and all occured as an autosomal dominant condition.During paralytic episodes,the patients showed obviously low serum potassium levels [1.9-2.8 mmol/L,(2.4?0.38) mmol/L)] and hypokalemic electrocardiogram findings,such as U-wave.The level of blood glucose was lower than normal range.Other 2 cases with normal serum potassium ion level at attack were diagnosed as normokalemic periodic paralysis with autosomal dominant pattern.One of the two cases,the level of blood glucose was lower.Thyroid functions,renal functions and electromyograms were all normal in 8 cases.Conclusions FPP is a group of relatively uncommon inherited disorders known as the skeletal muscle channelophathies.It can be diagnosed by hereditary characters,clinical manifestataions,auxiliary examinations.

Objective To study the impact of lymph node metastasis on prognosis of patients with pancreatic cancer and to evaluate predictors of postoperative survival of these patients.Methods The clinical data on patients with pancreatic cancer who underwent pancreatic cancer radical surgery in our hospital from January 2002 to December 2013 were reviewed and analyzed.Data on lymph node metastasis,number of lymph node dissection,number of positive lymph nodes and positive lymph ratio were analyzed.Results Of 101 patients,the 6-month,1-year and 2-year survival rates were 84.2％,56.6％ and 28.5％,respectively.The median survival was 13.8 months.Univariate and multivariate analyses showed lymph node metastasis,a positive lymph node ratio,number of lymph node dissection and positive lymph nodes were independent influential factors of prognosis.Results of subgroup analysis showed the number of lymph node dissection was a prognostic factor for pNO patients,while a positive lymph ratio had no impact on survival of pN1 patients.In the subgroup of patients with pancreatic head cancer,lymph node metastasis was associated with prognosis but not in the subgroup of patients with pancreatic body and tail carcinoma.Conclusions For patients with pancreatic head cancer,lymph node metastasis was closely correlated with prognosis.In addition,factors including lymph node metastasis,number of lymph node dissection,a positive lymph node ratio and number of positive lymph nodes were independent influential factors of prognosis for patients with pancreatic head cancer.However,for pN1 patients,a positive lymph node ratio has no influence on prognosis.

AIM To observe the protective effect of Ganduqing Granule(GDQ) on acute hepatic injury. METHODS Sixty male Wistar rats were divided into 6 groups, namely normal control group, model group, Ganduqing large (GDQ Ⅰ), middle(GDQ Ⅱ), small dose(GDQ Ⅲ) groups and Yiganning (YGN) positive group. Acute hepatic injury induced by thioacetamide. The changes of blood serum ALT, AST activity and plasma endotoxin (ET) level and TNF-?, IL-6 levels were measured and livers were taken for pathology examination. RESULTS Plasma ET level and blood serum ALT, AST levels and TNF-?, IL-6 levels were significantly lower than model group ( P

The nuclear transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) plays a crucial role in maintaining cellular redox homeostasis. The aberrant NRF2 signaling confers enhanced antioxidant capacity, which is linked to tumor progression and therapeutic resistance. The current study investigates the biological effects and molecular mechanism of tribbles homolog 3 (TRIB3), a stress-induced protein, in regulating cell survival and apoptosis in lung cancer. This study first performed the RNA sequencing data analysis with 576 lung adenocarcinoma patients from the cancer genome atlas (TCGA) database. The NRF2- antioxidant response element (ARE) signature was enriched in patients with high TRIB3 expression. Dual-luciferase reporter assay and real-time quantitative polymerase chain reaction (PCR) were used to confirm the effect of TRIB3 on the kelch-like ECH-associated protein-1 (KEAP1)-NRF2 pathway. Abrogation of TRIB3 impaired NRF2 transcriptional activity and reduced the expression of its target genes. Moreover, TRIB3 enhanced NRF2 stability via blocking KEAP1-NRF2 interaction. TRIB3-depletion promoted reactive oxygen species (ROS) production, restrained cell proliferation, and enhanced carboplatin-induced apoptosis. In addition, NRF2 overexpression recovered the tumor inhibition effect of TRIB3-depletion. Consistently, TRIB3 failed to modulate apoptosis in NRF2 depletion cells. In summary, this study shows that TRIB3 inhibits the KEAP1-NRF2 interaction and upregulates the transcriptional activity of NRF2, thereby promoting lung cancer cell proliferation and reducing the sensitivity to chemotherapy. Targeting the TRIB3-NRF2 signal axis may become a new strategy for ROS homeostasis and lung cancer treatment.

Objective To further investigated the effect of minocycline on the inhibition of microglial activation and subsequent protection of nigral DA neuron.Methods 20 rats injected with LPS in the substantia nigra (SN) were randomly divided into two groups (LPS group and LPS+Minocycline group).The behavior was observed on the 7~(th) d and 14~(th) d.The immunohistoehemistry,in situ hybridization and Western-blot were used to detect the levels of positive neuron,mRNA,protein of TH and OX-42. Results The slightly rotational behavior was observed in LPS+Minoeyeline group.The majority of mieroglias were activated in the two groups.Some microglia in the SNpc remained ramified in LPS+ Minocycline group.The numbers of hypertophie microglia in LPS+Minoeyeline group were less than that in LPS group.Western-blot showed that the protein of OX-42 in two LPS groups was higher than in normal group(P