Explore the vast range of titles available.

Chinese are reported to have a higher percent body fat (%BF) and a higher percent trunk fat (%TF) than whites for a given body mass index (BMI). However, the associations of these ethnic differences in body composition with metabolic risks remain unknown. A total of 1 029 Chinese from Hangzhou, China, and 207 whites from New York, NY, USA, were recruited in the present study. Body composition was measured using dual-energy X-ray absorptiometry (DXA). Analysis of covariance was used to assess the ethnic differences in fat, fat distribution, and metabolic risk factors. After adjusting for BMI, age, and height, Chinese men had an average of 3.9% more %BF and 12.1% more %TF than white men; Chinese women had an average of 2.3% more %BF and 11.8% more %TF than white women. Compared with whites, higher metabolic risks were detected in Chinese for a given BMI after adjusting for age and height. Further adjustment for %BF did not change these ethnic disparities. However, after adjusting for %TF, the ethnic differences decreased and become insignificant in triglyceride, high-density lipoprotein cholesterol, and blood pressure (except for systolic blood pressure in men). For fasting plasma glucose, the ethnic differences persisted after adjustment for %BF, but decreased significantly from 0.910 to 0.686 mmol/L among men, and from 0.629 to 0.355 mmol/L among women, when the analyses were further controlled for %TF. Chinese have both higher %BF and %TF than white people for a given BMI. However, only %TF could in part account for the higher metabolic risk observed in Chinese men and women.

Gao, F.X. and Song, A.H., 2020. Fund management method of ocean shipping enterprises based on cost control theory. In: Al-Tarawneh, O. and Megahed, A. (eds.), Recent Developments of Port, Marine, and Ocean Engineering. Journal of Coastal Research, Special Issue No. 110, pp. 291–294. Coconut Creek (Florida), ISSN 0749-0208. This article starts from the perspective of the cost control theory of ocean shipping companies, and deeply explores the cost management of ocean shipping companies under the new economic situation. This article introduces in detail the research significance of the maritime cost management structure, and through the ABC analysis method (operation cost method), specifically analyzes the ocean shipping company's transportation cost budget analysis and calculation method. Through the study of the ocean shipping cost budget and dynamic targets, the source of actual value, the five major items of ocean shipping cost: terminal cargo fee, station cargo fee, transit fee, port fee, canal fee, are specifically defined, and the planning cost occurs The process analysis chart and corresponding formation of a mathematical analysis model to initially establish a cost management evaluation index system for liner transportation enterprises. From the enterprise's strategic point of view, the cost control methods at multiple levels are discussed, and the concept of improving liner transportation cost control is proposed.

Studies on the relationship between television (TV) viewing and bone mineral density (BMD) in adults are limited. The purpose of this study was to examine whether longer duration of TV viewing increased the risk of lower BMD in Chinese women. A total of 626 female adults were voluntarily recruited into the study. Anthropometric measurements were obtained using standard procedures. Body composition including total body and regional BMD was estimated using dual-energy X-ray absorptiometry. The duration of TV viewing was categorized into 4 groups: <1 h, 1 to <2 h, 2 to <3 h, and ≥3 h. Multiple linear regression models were applied to analyze the associations between duration of TV viewing and total and regional BMD in all subjects and in subjects stratified by age of 45 years, respectively. After adjusting for age, BMI, alcohol use, smoking, education, income, urbanicity, leisure time physical activity, occupational physical activity, and menopause, the significant trend of pelvic BMD across categories of TV viewing was observed in all subjects ( p  < 0.05). Further analysis revealed that women aged <45 years, the 1 to <2 h group, the 2 to <3 h group, and the ≥3 h group were significantly associated with lower total body and regional BMD compared to women aged <45 years in the <1 h group. We concluded that the duration of TV viewing was negatively associated with BMD in Chinese women, especially in those aged 18–44 years. It might be sensible to reduce TV viewing time to prevent bone loss in young women.

Autoimmune target tissues in type 1 diabetes include pancreatic β-cells and peri-islet Schwann cells (pSC)--the latter active participants or passive bystanders in pre-diabetic autoimmune progression. To distinguish between these alternatives, we sought to suppress pSC autoimmunity by transgenic expression of the negative costimulatory molecule B7-H1 in NOD pSC. A B7-H1 transgene was placed under control of the glial fibrillary acidic protein (GFAP) promoter. Transgenic and wild-type NOD mice were compared for transgene PD-1 affinities, diabetes development, insulitis, and pSC survival. Mechanistic studies included adoptive type 1 diabetes transfer, B7-H1 blockade, and T-cell autoreactivity and sublineage distribution. Transgenic and endogenous B7-H1 bound PD-1 with equal affinities. Unexpectedly, the transgene generated islet-selective CD8(+) bias with accelerated rather than suppressed diabetes progression. T-cells of diabetic transgenics transferred type 1 diabetes faster. There were no earlier pSC losses due to conceivable transgene toxicity, but transgenic pSC loss was enhanced by 8 weeks, preceded by elevated GFAP autoreactivity, with high-affinity T-cells targeting the major NOD K(d)-GFAP epitope, p253-261. FoxP3(+) regulatory T- and CD11c(+) dendritic cell pools were unaffected. In contrast with transgenic B7-H1 in NOD mouse β-cells, transgenic B7-H1 in pSC promotes rather than protects from type 1 diabetes. Here, ectopic B7-H1 enhanced the pathogenicity of effector T-cells, demonstrating that pSC can actively impact diabetes progression-likely through modification of intraislet T-cell selection. Although pSC cells emerge as a new candidate for therapeutic targets, caution is warranted with regard to the B7-H1-PD1 axis, where B7-H1 overexpression can lead to accelerated autoimmune disease.

Sjögren's syndrome is a common (about 1% of the population) autoimmune disease of salivary and lacrimal glands. Its cause and pathogenesis are poorly understood, and treatments are mostly for symptoms of the disease. ICA69 is a self-antigen expressed in brain, pancreas, salivary, and lacrimal glands. NOD-strain mice are an animal model of spontaneous Sjögren's syndrome. We aimed to assess the role of ICA69 in autoimmunity against Sjögren's syndrome. We inactivated the genomic ICA69 locus, generated NOD congenic mice that were deficient in ICA69, and assessed development of Sjögren's syndrome. ICA69 autoimmunity was investigated in controls and in patients with primary Sjögren's syndrome or systemic lupus erythematosus, and in various NOD mice, some of which were given an ICA69-directed prototype peptide vaccine. Disruption of the ICA69 locus prevented lacrimal gland disease and greatly reduced salivary gland disease in NOD mice. In healthy NOD mice, ICA69-specific T cells accumulated in lymph nodes that drain salivary tissue. T-cell and B-cell autoreactivity against ICA69 was much the same in patients with primary Sjögren's syndrome, but not in those with systemic lupus erythematosus or in healthy controls. Immunotherapy with a high-affinity mimicry peptide targeting ICA69-specific T-cells reduced established Sjögren's syndrome in wild-type NOD mice in the long term. ICA69 is a new autoantigen in primary Sjögren's syndrome that has an important role in progression of disease and could be of diagnostic value. Immunotherapy of primary Sjögren's syndrome is promising, since autoimmunity in NOD mice with Sjögren's syndrome seems to be uniquely susceptible to such treatment even late in disease.

To investigate the association of regional fat depots with metabolic risk factors in Chinese women. Total and regional fat depots including android fat and gynoid fat were measured by dual-energy X-ray absorptiometry. Central fat distribution was defined as android:gynoid fat ratio. Metabolic risk factors were defined as elevated TAG, reduced HDL-cholesterol, elevated blood pressure and elevated fasting plasma glucose. Logistic regression analyses were performed to examine the associations of regional fat depots with metabolic risk factors. The odds ratios of metabolic risks were further calculated according to tertiles of android fat and gynoid fat. Participants were recruited from a community-based cross-sectional study. Face-to-face questionnaires, anthropometric and dual-energy X-ray absorptiometry measures were conducted. Chinese women (n 609) aged 18-79 years. Android fat and android:gynoid fat ratio were associated with significantly increased odds (OR = 1·4-3·7; P < 0·01) for almost all risk factors, whereas gynoid fat was independently associated with significantly decreased odds (OR = 0·3-0·6; P < 0·01). The inverse associations of gynoid fat with metabolic risk factors remained after adjusting for android fat. Even if their android fat level was in high, women in the highest tertile of gynoid fat had lower odds of having at least two metabolic risk factors compared with women in the lowest gynoid fat tertile (P for trend < 0·01). There were opposite associations of android and gynoid fat with metabolic risks in Chinese women. Gynoid fat rather than android fat might be a more important inclusion in metabolic disease risk evaluation in female Asians.

Objective to explore lead pollution and its health impact on workers in a lead zinc smelter. Methods By convenient sampling method, 142 workers exposed to lead in the smelting workshop of a lead zinc smelter in Inner Mongolia were chosen as test group, 88 administrative and logistic personnel without occupational lead exposure as control group. Occupational health field survey, detection and evaluation of lead smoke and lead dust in the air of workplace were conducted, and occupational health examination was carried out for the two groups of people. Results From 2015 to 2017, the TWA level of lead and lead dust decreased year by year. The detection rates of blood lead, blood routine abnormality, urine routine abnormality, liver function abnormality, electrocardiogram abnormality and blood pressure abnormality in exposed workers were higher than those in control group (P<0.05). Conclusion The level of blood lead is closely related to the level of lead in the workplace. Blood lead is a reliable indicator for lead exposure bio-monitoring and lead poisoning assessment. Reasonable and effective engineering protection measures can effectively inhibit lead hazards in workplace.

Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100β. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable β-cell death. Humans with probable prediabetes generate similar autoreactivities, and autoantibodies in islet-cell autoantibody (lCA) –positive sera co-localize to pSC. Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100β prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip–LCMV) glycoprotein/CD8 + T-cell receptor gp double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and β-cell destruction. However, pSC were deleted in spontaneously diabetic NOD mice carrying the CD8 + /8.3 T-cell receptor transgene, a T cell receptor commonly expressed in earliest islet infiltrates. Autoimmune targeting of pancreatic nervous system tissue elements seems to be an integral, early part of natural type 1 diabetes.

Type I diabetes (T1D) in human and rodents is an autoimmune disease, selectively targeting pancreatic β cells in islets of Langerhans. Disease development is determined by polygenic and multiple environmental factors. In NOD mice, the disease initiates at 4–5 weeks of age with periinsulitis, and transforms into aggressively invasive insulitis by 8–10 weeks of age. In our colony, the first overtly diabetic animals are about 16 weeks old, but disease can take as much as 36 weeks in some animals. Prediabetes is thus a slow process, involving multiple immune cells and molecules, and its progression is determined by finely tuned balance and shifting bias among multiple players. It remains unknown what drives the loss of self-tolerance to islets, and what precipitates and/or halts prediabetes progression in NOD mice. Autoantigens are core elements in T cell mediated islet β cell damage, thus serving as excellent tools to study these issues. Conscious of the fact that expression of major autoantigens in T1D, including (pro)insulin, GAD65/67, ICA69, HSP and IA-2, is not islet restricted, we generated transgenic NOD mice expressing an ICA69-EGFP fusion protein under control of a β-actin promoter. Transgenics showed significant disease protection, associated with a dramatic absence of CD8+ T cells in the enhanced IFNγ-rich insulitis lesion. There was no infiltration of other ‘green’ tissues. Islet and heart transplantation as well as alloxan experiments demonstrated that transgene-specific T cells were primed and maintained only by islets. In this model, prediabetes appears to reflect strictly local events, initiated and maintained by islet-exclusive tissue factors. Autoantigen expression in the thymus is critical for the induction of tolerance and formation of T cell repertoire. We generated one tet07-ICA69 transgenic line with a promoter-independent ICA69 overexpression exclusively in thymus and spleen. These transgenic mice showed persistent tolerance to the dominant epitope of ICA69, Tep69, and disease protection. With adoptive transfer and thymus transplant experiments, it was clear that the transgene modified T cell repertoire was important for disease protection, and that re-selection of such a T cell pool in the thymus or by immunotherapy could arrest prediabetes progression even in models of late NOD prediabetes.

The development of phrenic motoneurons and descending bulbospinal projections to the cervical spinal cord have been examined in prenatal and early postnatal rats with the aid of the carbocyanine dyes DiI and DiA. Phrenic motoneurons could be identified by retrograde labelling as early as E13, while aggregation of phrenic motoneurons into a column and the formation of dendritic bundles became apparent from E16. The initial phrenic motoneuron dendritic bundles were oriented in the dorsolateral and ventromedial directions, while ventrolaterally directed bundles entering the marginal zone appeared by E16, and rostrocaudal bundles were clearly visible by E21. The column of phrenic motoneurons extended rostrocaudally from C2 to C6 at E13 and E14, but this became confined to the C3-5 segments by E21. Two-way tracing of connections between putative brainstem respiratory centres and cervical spinal cord with the carbocyanine dyes, DiI and DiA, indicated that brainstem bulbospinal neurons in the position of the adult ventral respiratory group (VRG) and medial parabrachial (MPB) nuclei appeared to project to the cervical cord white matter as early as E15 and may contribute axons to the grey matter of the cervical cord as early as E17 These findings are consistent with electrophysiological studies of respiratory function development in the fetal rat, which found relatively regular rhythmic phrenic discharge by E20 to 21. In summary, our findings indicate that the structural differentiation of phrenic motoneurons is well-advanced prior to birth and that the descending pathways involved in the control of respiratory function are in place several days before birth.