Objective: To quantify the burden of cardiovascular disease (CVD) deaths that attributed to metabolic disorders in population aged ≥25 years in Jiangsu province. Methods: The data we used were from the following three sources: 1) 2015 Jiangsu Chronic Disease Risk Factor and Nutrition Survey, 2) death surveillance, 3) results of the 2016 Global Burden of Disease Study, based on population attributable fractions (PAF), to analyze related parameters as mortality, years of life lost (YLL), life expectancy (LE) and premature mortality. Results: Most people died from ischemic stroke (IS) showed the standard mortality as 87.48/100 000. High SBP appeared as the major cause on CVD deaths. PAF with high cholesterol and high BMI decreased along with the increase of age while high fasting plasma glucose increased. Deaths due to ischemic heart diseases, IS or hemorrhagic stroke that attributed to metabolism disorders would reduce the LE by 1.08, 1.07 or 0.55 years, respectively. Males appeared to have higher YLL than females and were more likely to die from premature CVD, as the consequence of having metabolism disorders. Conclusions: Blood pressure control should be considered an important approach to reduce the burden of CVD. According to the characteristics of gender-related risks and the distinct impact of age-related metabolism disorders on different CVD diseases, stratified strategies should be strengthened for comprehensive prevention and control of CVD, in Jiangsu province.
Adult ; Blood Pressure ; Cardiovascular Diseases/epidemiology* ; Chronic Disease ; Cost of Illness ; Female ; Humans ; Life Expectancy ; Male ; Metabolic Diseases/epidemiology* ; Mortality/trends* ; Mortality, Premature ; Risk Factors

Objective: To investigate the clinicopathological, immunophenotypic, and genetic features of malignant peripheral nerve sheath tumor (MPNST). Methods: Twenty-three cases of MPNST were diagnosed at the Jiangsu Province Hospital (the First Affiliated Hospital of Nanjing Medical University), China, between January 2012 and December 2022 and thus included in the study. EnVision immunostaining and next-generation sequencing (NGS) were used to examine their immunophenotypical characteristics and genomic aberrations, respectively. Results: There were 10 males and 13 females, with an age range of 11 to 79 years (median 36 years), including 14 cases of neurofibromatosis type I-associated MPNST and 9 cases of sporadic MPNST. The tumors were located in extremities (7 cases), trunk (4 cases), neck and shoulder (3 cases), chest cavity (3 cases), paraspinal area (2 cases), abdominal cavity (2 cases), retroperitoneum (1 case), and pelvic cavity (1 case). Morphologically, the tumors were composed of dense spindle cells arranged in fascicles. Periphery neurofibroma-like pattern was found in 73.9% (17/23) of the cases. Under low magnification, alternating hypercellular and hypocellular areas resembled marbled appearance. Under high power, the tumor cell nuclei were irregular, presenting with oval, conical, comma-like, bullet-like or wavy contour. In 7 cases, the tumor cells demonstrated marked cytological pleomorphism and rare giant tumor cells. The mitotic figures were commonly not less than 3/10 HPF, and geographic necrosis was often noted. Immunohistochemically, tumor cells were positive for S-100 (14/23, 60.9%) and SOX10 (11/23, 47.8%). The loss of the CD34-positive fibroblastic network encountered in neurofibromas was observed in 14/17 of the MPNST cases. The loss of H3K27me3 expression was observed in 82.6% (19/23) of the cases. Moreover, SDHA and SDHB losses were presented in one case. NGS revealed that NF1 gene loss of function (germline or somatic) were found in all 5 cases tested. Furthermore, four cases accompanied with somatic mutations of SUZ12 gene and half of them had somatic mutations of TP53 gene, while one case with germline mutation in SDHA gene and somatic mutations in FAT1, BRAF, and KRAS genes. Available clinical follow-up was obtained in 19 cases and ranged from 1 to 67 months. Four patients died of the disease, all of whom had the clinical history of neurofibromatosis type Ⅰ. Conclusions: MPNST is difficult to be differentiated from a variety of spindle cell tumors due to its wide spectrum of histological morphology and complex genetic changes. H3K27me3 is a useful diagnostic marker, while the loss of CD34 positive fibroblastic network can also be a diagnostic feature of MPNST. NF1 gene inactivation mutations and complete loss of PRC2 activity are the common molecular diagnostic features, but other less commonly recurred genomic aberrations might also contribute to the MPNST pathogenesis.
Female ; Male ; Humans ; Child ; Adolescent ; Young Adult ; Adult ; Middle Aged ; Aged ; Neurofibrosarcoma ; Neurofibromatosis 1 ; Histones ; Genes, p53 ; Nerve Sheath Neoplasms

Humans ; Goblet Cells ; Stomach Neoplasms ; Carcinoma

Humans ; Thyroid Cancer, Papillary ; Neck/pathology* ; Lymph Nodes/pathology* ; Thyroid Neoplasms/pathology* ; Lymphoma, T-Cell/pathology*