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Background:Malnutrition is common in patients with cancer, whichadversely affectsthesurvival and quality of life ofcancer patients.However, there is no national data on the prevalence of malnutrition inChinese cancer patients. Thisstudy aims to evaluate the prevalenceof malnutrition and quality of life(QOL)ofChinese patients with localregional, recurrentor metastatic cancer,to address the prognostic value of nutritional status and QOLon the survival of cancer patients in China and to validate the patient-generated subjective global assessment (PG-SGA) questionnaire in Chinese cancer patients.Methods:Thisisanobservational,multi-centered,and hospital-based prospective cohort study.We aimed to recruit 50,000 cancer patients (age 18and above)overan 8-year period.Data collection will occur within 48hrafter patientsare admitted to hospital, 30-days after hospital admission, and the follow-up will be conducted1-8years after enrolment. The primary outcomeisoverall survival, and secondaryoutcomes arelength of hospital stay and hospital costs. Factors measured are demographic characteristics, tumor characteristics, anthropometry measurements,hematological measurement, body composition, PG-SGAscores,Karnofsky performance status scores,and QLQ C30 scores. This protocol wasapproved by local ethical committees of all the participant hospitals.Conclusions: This multi-centered, large-scale, long-time follow-up prospective study will help diagnose malnutrition in cancer patients in China, and identify the related risk factors associated with the negative outcomes. The anticipated results will highlight the need for a truly scientific appraisal of nutrition therapy, and help to improve outcomes among cancer patients in China.Trial Registration: The trial has been registered with the Chinese Clinical Trial Registry, ChiCTR1800020329. Registered on 19 December 2018
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Objective To investigate the effect of enteral nutrition tolerance assessment form on the early enteral nutrition tolerance in patients with gastric cancer after operation. Methods According to the admission sequence, 108 patients with gastric cancer were divided into the control group and the experiment group with 54 cases in each group. Enteral nutrition was used in the control group, while enteral nutrition tolerance assessment form was used to evaulate and care patients in experiment group. Finally, the two groups were compared in the anal exhaust time and the rate of complications. Result Anal exhaust in the experiment group was significantly earlier than that in the control group and the rate of complications was significantly smaller than that of the control group (P < 0.05). Conclusions The enteral nutrition tolerance assessment form for systemic evaluation and intervention is effective in improvement of the patients′tolerance to enteral nutrition in early postoperative enteral nutrition support to patients with gastric cancer. It can promote the recovery of patients.
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DNA damage response (DDR) in different cell cycle status of human peripheral blood lymphocytes (PBLs) and the role of H2AX in DDR were investigated. The PBLs were stimulated into cell cycle with phytohemagglutinin (PHA). The apoptotic ratio and the phosphorylation H2AX (S139) were flow cytometrically measured in resting and proliferating PBLs after treatment with camptothecin (CPT) or X-ray. The expressions of γH2AX, Bcl-2, caspase-3 and caspase-9 were detected by Western blotting. DDR in 293T cells was detected after H2AX was silenced by RNAi method. Our results showed that DNA double strand breaks (DSBs) were both induced in quiescent and proliferating PBLs after CPT or X-ray treatment. The phosphorylation of H2AX and apoptosis were more sensitive in proliferating PBLs compared with quiescent lymphocytes (P<0.05). The expression levels of anti-apoptotic proteins Bcl-2 were reduced and cleaved caspase-3 and caspase-9 were increased. No significant changes were observed in CPT-induced apoptosis in 293T cells between H2AX knocking down group and controls. It was concluded that proliferating PBLs were more vulnerable to DNA damage compared to non-stimulated lymphocytes and had higher apoptosis rates. γH2AX may only serve as a marker of DNA damage but exert no effect on apoptosis regulation.
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To examine the effects of ischemia and anoxia on cell activation and cell cycle of astrocytes in vitro, the cell cycles and the proliferation of astrocytes in different time points after ischemia and anoxia were studied by flow cytometry and BrdU labeling and the expression of GFAP and cyclin D1 was detected by the fluorescence immunochemistry. After ischemia and anoxia in vitro, the astrocytes in S phase were significantly increased as compared with those in the normal group and the proliferating ability of the astrocytes was highest 6 h after the treatment as revealed by BrdU pulse labeling, but the astrocytes in S phase and proliferating ability were decreased after 6 h. At the early stages of ischemia and anoxia, the positive staining intensity of GFAP was increased, peaked at 6th h, while 12 h after the ischemia and anoxia, the positive staining intensity of GFAP became weak, and the expression of cyclin D1 was gradually increased after the ischemic and anoxic damage. It is concluded that astrocytes are activated to proliferate and enter new cycle events by ischemia and anoxia, and cyclin D1 is implicated in the proliferation and repair of astrocytes. The cell cycle events are closely associated with the proliferation and activation of astrocytes.
Subject(s)
Animals, Newborn , Astrocytes/cytology , Cell Cycle , Cell Hypoxia , Cell Proliferation , Cells, Cultured , Cyclin D1/biosynthesis , Cyclin D1/genetics , Glial Fibrillary Acidic Protein/biosynthesis , Glial Fibrillary Acidic Protein/genetics , Rats, WistarABSTRACT
To examine the effects of ischemia and anoxia on cell activation and cell cycle of astrocytes in vitro, the cell cycles and the proliferation of astrocytes in different time points after ischemia and anoxia were studied by flow cytometry and BrdU labeling and the expression of GFAP and cyclin D1 was detected by the fluorescence immunochemistry. After ischemia and anoxia in vitro,the astrocytes in S phase were significantly increased as compared with those in the normal group and the proliferating ability of the astrocytes was highest 6 h after the treatment as revealed by BrdU pulse labeling, but the astrocytes in S phase and proliferating ability were decreased after 6 h.At the early stages of ischemia and anoxia, the positive staining intensity of GFAP was increased,peaked at 6th h, while 12 h after the ischemia and anoxia, the positive staining intensity of GFAP became weak, and the expression of cyclin D1 was gradually increased after the ischemic and anoxic damage. It is concluded that astrocytes are activated to proliferate and enter new cycle events by ischemia and anoxia, and cyclin D1 is implicated in the proliferation and repair of astrocytes. The cell cycle events are closely associated with the proliferation and activation of astrocytes.
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Summary: The threshold of cyclin E expression at G1/S boundary is a characteristic feature of cell cycle progressing. In this study, we tried to develop a quantitative approach to analyze cyclin E threshold by multiparameter flow cytometry. The expression of cyclin E in exponentially growing MOLT-4 cells was detected under different photomultiplier tube (PMT) voltages by cyclin E/DNA multiparameter flow cytometry. Additionally, cyclin E was detected in cells which were treated with caffeine and cycloheximide (CHX) under the same PMT voltage. Moreover, the expression of cyclin E in MOLT-4 cells was compared with that in JURKAT cells. Cyclin E threshold was quantified by formula B2/A×C (A, B, C indicates the minimum, threshold, and maximum of cyclin E fluorescence intensity, respectively). Results showed that in MOLT-4 cells, cyclin E threshold calculated by formula B2/A×C was invariable under different PMT settings. It was decreased in cells treated with caffeine and remained changeless in cells treated with cycloheximide. Cyclin E threshold in JURKAT cells was much lower than that in MOLT-4 cells. It was suggested that Formula B2/A×C we firstly set up could be used to analyze cyclin E expression threshold quantitatively.
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The threshold of cyclin E expression at G1/S boundary is a characteristic feature of cell cycle progressing. In this study, we tried to develop a quantitative approach to analyze cyclin E threshold by multiparameter flow cytometry. The expression of cyclin E in exponentially growing MOLT-4 cells was detected under different photomultiplier tube (PMT) voltages by cyclin E/DNA multiparameter flow cytometry. Additionally, cyclin E was detected in cells which were treated with caffeine and cycloheximide (CHX) under the same PMT voltage. Moreover, the expression of cyclin E in MOLT-4 cells was compared with that in JURKAT cells. Cyclin E threshold was quantified by formula B2/AxC (A, B, C indicates the minimum, threshold, and maximum of cyclin E fluorescence intensity, respectively). Results showed that in MOLT-4 cells, cyclin E threshold calculated by formula B2/AxC was invariable under different PMT settings. It was decreased in cells treated with caffeine and remained changeless in cells treated with cycloheximide. Cyclin E threshold in JURKAT cells was much lower than that in MOLT-4 cells. It was suggested that Formula B2/AxC we firstly set up could be used to analyze cyclin E expression threshold quantitatively.
Subject(s)
Caffeine/pharmacology , Cell Cycle/physiology , Cell Line, Tumor , Cyclin E/analysis , Cycloheximide/pharmacology , DNA, Neoplasm/analysis , Flow Cytometry/methods , Jurkat Cells , Leukemia, Lymphoid/pathologyABSTRACT
In order to explore the molecular mechanisms of sodium butyrate and trichostatin A on K562 cell proliferation/differentiation, K562 cells were grown in the absence or presence of sodium butyrate or trichostatin A. The percentage of viable cells was determined by trypan blue exclusion. Differentiation was determined by nitro-blue tetrazolium (NBT) reduction and cell surface adhesion molecules analyzed by FACS. Cell cycle distribution was studied after DNA staining by propidium iodide. Cell cycle regulatory proteins were detected by Western blot and reverse transcription-polymerase chain reaction. The results showed that sodium butyrate blocked cells mainly at the G0/G1 phase of the cell cycle, whereas trichostatin A arrested the cells at G2 phase. Sodium butyrate could down-regulate the mRNA expression of cyclin D1, but not affect its protein expression; down-regulate the protein expression of cyclin D3, but not affect its mRNA expression. Trichostatin A showed similar effects on cyclin D1 and D3 as sodium butyrate. Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels. It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins.
Subject(s)
Humans , Butyrates , Pharmacology , Cell Cycle , Cell Differentiation , Cell Division , Cyclin D , Cyclin-Dependent Kinase Inhibitor p21 , Cyclins , Genetics , Gene Expression , Histone Deacetylase Inhibitors , Hydroxamic Acids , Pharmacology , K562 CellsABSTRACT
<p><b>OBJECTIVE</b>To confirm the unscheduled in vivo and in vitro expression models of cyclin B1 in cancer cells so as to study the different profiles of cyclin B1 in G(1)-phase immortal cells under different culture states and culture conditions.</p><p><b>METHODS</b>Multiparameter flow cytometry (FCM) was used to correlate the expression of cyclin B1 with the position in cell cycle of immortal cells in vivo and in vitro using the MOLT-4 cell line as control. Cells which belonged to G(1)-phase were sorted by FCM according DNA diploidy, and then the expression of cyclin B1 was examined by confocal microscope to confirm the results. For further analysis, different subgroups in G(1) phase were sorted according to the fluorescent intensity of cyclin E, and then the exact period in G(1) phase when cyclin B1 was expressed, were assayed by Western blot.</p><p><b>RESULTS</b>Unscheduled expression of cyclin B1 expressed in G(1)-phase was found not only in synchronized leukemia cells MOLT-4 and in vivo transformed T-7 cells, but also in vivo tumor cells detached from clinical samples. In the synchronized growing cells, cyclin B1 was mainly detected in the early G(1) phase, while in transformed T7 cells, cyclin B1 was mainly detected in the late G(1) phase.</p><p><b>CONCLUSION</b>The limitation of detecting cyclin B1 is due to its unscheduled expression, rending cyclin B1 being detected at different time-spots in the G(1) phase. This phenomenon may be related to the adjustment between the loss of control in cell proliferation and cell apoptosis, thereby leading to tumorigenesis.</p>