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1.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-989580

RESUMO

Objective:To analyze the global incidence and mortality of cancer from 1990 to 2019.Methods:The Global Burden of Disease Study 2019 (GBD2019) database was utilized to analyze the global incidence and mortality of cancer, the order of incidence and mortality of cancer, the incidence and mortality of different age groups, and the trend of incidence and mortality from 1990 to 2019. Standardized incidence and mortality rates were derived by utilizing the world standard population age structure.Results:In 1990, global cancer cases numbered 10.295 9 million with an incidence rate of 192.45/100 000, leading to 5.732 6 million deaths and a mortality rate of 107.16/100 000. While in 2019, global cancer cases escalated to 23.568 5 million with an incidence rate of 304.60/100 000, resulting in 10.022 8 million deaths and a mortality rate of 129.54/100 000, all higher than those in 1990. In 2019, lung cancer showed the highest incidence rate of both sexes combined in the world (29.21/100 000), followed by colorectal cancer, breast cancer, prostate cancer and gastric cancer. The incidence of lung cancer was highest among males (39.24/100 000), while the incidence of breast cancer was highest among females (51.27/100 000). Lung cancer also had the highest mortality rate worldwide in both sexes combined (26.40/100 000), followed by colorectal cancer, gastric cancer, breast cancer and pancreatic cancer. Lung cancer had the highest mortality among males (35.72/100 000), while breast cancer had the highest mortality among females (17.85/100 000). In 2019, the global cancer incidence rate showed an upward trend with age. The incidence rate was low before the age of 25, and increased rapidly after the age of 25. The incidence rates of both sexes combined, males and females all reached the peak in the age group of over 85 years old, which were 3 084.18/100 000, 4 434.81/100 000 and 2 353.07/100 000 respectively; The incidence rate of females in the age group of 20-50 years old was higher than that of males, but the incidence rate of males in the age group of over 55 years old was higher than that of females. Compared with 1990, the incidence rates of both sexes combined in the age group of over 20, of males over 55 years old, as well as of females over 15 years old, were all higher than those in 2019. In 2019, the global tumor mortality rate showed an upward trend with age. The mortality rate was relatively low before the age of 35, and increased rapidly after the age of 35. The mortality rates for both sexes combined, as well as for males and females, reached the peak in the age group of over 85 years old, which were 1 787.84/100 000, 2 509.87/100 000, and 1 369.99/100 000 respectively; The mortality rate of females in the age group of 20-40 years old was higher than that of males, and the mortality rate of males in the age group of over 45 years old was higher than that of females; For the age of 0-80 years old, the mortality rates for both sexes combined, males, and females were lower in 2019 than 1990, but higher in the age of 85 years old and above. The global standardized incidence rate of cancer showed an overall upward trend, with an average annual increase of 0.30% from 1990 to 2019. The global standardized mortality rate of cancer showed an overall downward trend, with an average annual decrease of 0.60% from 1990 to 2019.Conclusion:From 1990 to 2019, the global standardized incidence rate of cancers shows an overall upward trend, while the global standardized mortality rate of cancers has an overall downward trend, and the global incidence and mortality rate of cancers increases with age. The global burden of cancer disease is still heavy. Lung cancer is the cancer with the highest incidence and mortality rate in the world. The highest incidence rate is lung cancer among males, and breast cancer among females. Different countries or regions need to take corresponding cancer prevention and treatment strategies according to their actual conditions.

2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-871968

RESUMO

Objective:To evaluate the diagnostic value of the von Willebrand factor (vWF) GPIb activity to antigen ratio for thrombotic thrombocytopenic purpura (TTP) at acute phase.Methods:A cohort of 93 patients with suspected TTP and admited to our hospitalfrom January 2018 to December 2019 were prospectively enrolled, we analyzed the levels of vWF: GPIb activity and vWF antigen at acute phase, the diagnosis of acquired TTP was defined as ADAMTS13 activity<10%.The PLASMIC score and final diagnosis of included patients were recorded.Results:Twenty-twopatients were diagnosed as TTP, the median (interquartile range) of ADAMTS13 activity were 1.0% (0-7.4%), other diagnoses included hemolytic uremic syndrome (HUS, n=8), severe infection ( n=21), malignancy( n=3), connective tissue disease( n=8), et al. The vWF: GPIb activity, vWF antigen, and ratio of vWF: GPIb activity to antigen were all significantly lower in patients with TTP than in those without ( P<0.05). The ratio of vWF: GPIb activity to vWF antigen <0.75 could yield a sensitivityof 81.8% and a specificity of 95.2% respectively for TTP. In patients with PLASMIC score≥6, 88.9% patients with the ratio of vWF: GPIb activity to vWF antigen <0.75 were confirmed as TTP, and 15.4% patients with the ratio≥0.75 were confirmed as TTP. Conclusions:The ratio of vWF: GPIb activity to vWF antigen based on automaticassays might be useful for differential diagnosis and stratification of TTP at acute phase, especially when the ADAMTS13 assay is not available in time.

3.
Cell Physiol Biochem ; 49(5): 1747-1754, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30231246

RESUMO

BACKGROUND/AIMS: Diabetic nephropathy is the one of the most serious microvascular complications of diabetes mellitus, and "metabolic memory" plays a vital role in the development of diabetic complications. To investigate the effect of epigenetics on metabolic memory, we analyzed the impact of transient high-glucose stimulation on the secretion of inflammatory factors from rat glomerular mesangial cells. METHODS: Rat glomerular mesangial cells (HBZY-1) were divided into three groups: high-glucose group (25 mM glucose), hypertonic group (5.5 mM glucose+19.5 mM mannitol), and normal-glucose control group (5.5 mM glucose). Mesangial cells were cultured in high-glucose, hypertonic, and normal-glucose media for 24 h and transitioned to normal-glucose culture for 24, 48, and 72 h. Then, protein, mRNA, and supernatants were harvested. The expression of monomethylated H3K4 was determined by western blot analysis, and the expression of the NF-κB subunit p65 and histone methyltransferase set7/9 was determined by quantitative real-time PCR. The expression of monocyte chemoattractant protein 1 (MCP-1) and vascular cell adhesion molecule 1 (VCAM-1) was detected by an enzyme-linked immunosorbent assay. RESULTS: Compared with the control group, H3K4me1 expression was upregulated after transient high-glucose stimulation, gradually downregulated in the following 48 h (P < 0.05), and reached the level of the control group at 72 h (P > 0.05). The expression of set7/9 was increased after 24 h of high-glucose stimulation and the following 24 h and 48 h (P < 0.05); it then returned to the level of the control group at 72 h. Compared with the control group, the increased expression of p65, VCAM-1, and MCP-1 was sustained for at least 72 h in the high-glucose group. CONCLUSION: Transient high-glucose stimulation can induce the persistent secretion of inflammatory factors from rat glomerular mesangial cells via histone modification.


Assuntos
Epigênese Genética/efeitos dos fármacos , Glucose/farmacologia , Células Mesangiais/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos , Animais , Linhagem Celular , Quimiocina CCL2/metabolismo , Genes/genética , Histona Metiltransferases , Histona-Lisina N-Metiltransferase/genética , Histona-Lisina N-Metiltransferase/metabolismo , Histonas/metabolismo , Células Mesangiais/citologia , Células Mesangiais/metabolismo , Metilação/efeitos dos fármacos , Ratos , Fator de Transcrição RelA/genética , Fator de Transcrição RelA/metabolismo , Molécula 1 de Adesão de Célula Vascular/metabolismo
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