The properties of small magnetic flux ropes inside the solar wind come from coronal holes, active regions, and quiet Sun

The origination and generation mechanisms of small magnetic flux ropes (SFRs), which are important structures in solar wind, are not clearly known. In present study, 1993 SFRs immersed in coronal holes, active regions, and quiet Sun solar wind are analyzed and compared. We find that the properties of SFRs immersed in three types of solar wind are signicantly different. The SFRs are further classifed into hot-SFRs, cold-SFRs, and normal-SFRs, according to whether the O7+/O6+ is 30% elevated or dropped inside SFRs as compared with background solar wind. Our studies show that the parameters of normal-SFRs are similar to background in all three types of solar wind. The properties of hot-SFRs and cold-SFRs seem to be lying in two extremes. Statistically, the hot-SFRs (cold-SFRs) are associated with longer (shorter) duration, lower (higher) speeds and proton temperatures, higher (lower) charge states, helium abundance, and FIP bias as compared with normal-SFRs and background solar wind. The anti-correlations between speed and O7+/O6+ inside hot-SFRs (normal-SFRs) are different from (similar to) those in background solar wind. Most of hot-SFRs and cold-SFRs should come from the Sun. Hot-SFRs may come from streamers associated with plasma blobs and/or small-scale activities on the Sun. Cold-SFRs may be accompanied by small-scale eruptions with lower-temperature materials. Both hot-SFRs and cold-SFRs could also be formed by magnetic erosions of ICMEs that do not contain or contain cold-filament materials. The characteristics of normal-SFRs can be explained reasonably by the two originations, from the Sun and generated in the heliosphere both.Comment: 19 pages, 5 figure

Effects of knee loading on obesity‐related nonalcoholic fatty liver disease in an ovariectomized mouse model with high fat diet

Aim Hormonal and nutritional disorders are the main causes of obesity and nonalcoholic fatty liver disease, especially in the elderly and postmenopausal women. Although physical activity may alleviate these disorders, the elderly may often have difficulty in conducting physical exercise. The purpose of this study was to investigate the therapeutic effect of knee loading, a new form of physical stimulation, on the symptom of obesity and fatty liver. Methods Using ovariectomized mice with high fat diet, we evaluated the effect of knee loading that applies gentle cyclic loads to the knee. Female C57BL/6 mice were divided into five groups: control (SCD), high fat diet (HF), HF with loading (HF+L), HF with ovariectomy (HF+OVX), and HF+OVX with loading (HF+OVX+L). Except for SCD, mice underwent sham operation or ovariectomy and maintained on high fat diet. After 6 weeks, the mice in HF+L and HF+OVX+L were treated with 6‐week knee loading. Results Compared to the obesity groups (HF and HF+OVX), knee loading significantly decreased a gain in body weight, liver weight, and white adipose tissue (all P<0.01). It also reduced the lipid level in the serum (P<0.01) and histological severity of hepatic steatosis (P<0.01). Furthermore, knee loading downregulated biomarkers related to the endoplasmic reticulum stress (GRP78, p‐eIF2α and ATF4) and altered biomarkers in autophagy (LC3 and p62). Conclusions Knee loading suppressed obesity‐associated metabolic alterations and hepatic steatosis, the effect with knee loading might be associated with suppression of the ER stress and promotion of autophagy

Age and tissue specific differences in the development of acute insulin resistance following injury.

Injuries, hemorrhage, sepsis, burn, and critical illnesses all induce insulin resistance, and insulin resistance is strongly associated with advancing age. However, the effect of age on injury induced insulin resistance is not well studied. We performed surgical trauma in male rats of three different ages (3-, 6-, and 10-weeks old). Rats were either hemorrhaged to a mean arterial pressure of 35-40 mmHg and subsequently maintained at that pressure for up to 90 min, or maintained without hemorrhage as controls. Results indicate that insulin-induced intracellular signaling was diminished in liver and skeletal muscle of 6- and 10-week old rats following trauma and hemorrhage. In even younger rats, immediately post-weaning ( approximately 3 weeks of age), insulin signaling was lost in liver, but not in skeletal muscle. Glucocorticoids can play a role in the chronic development of insulin resistance. Our results demonstrate that corticosterone levels were increased in 6- and 10-week old animals following hemorrhage, but little change was measured in 3-week old animals. Blockade of glucocorticoid synthesis prevented the development of insulin resistance in skeletal muscle, but not in liver of 6- and 10-week old rats. Moreover, skeletal muscle glucocorticoid receptor levels increased dramatically between 3 and 6 weeks of age. These results indicate that trauma and hemorrhage-induced hepatic insulin resistance occurs at all ages tested. However, there is no development of insulin resistance following trauma and hemorrhage in skeletal muscle of post-weaning rats. In skeletal muscle of 6- and 10-week old rats, inhibition of glucocorticoid levels prevents the development of insulin resistance.http://deepblue.lib.umich.edu/bitstream/2027.42/192884/2/Zhai 2009 J Endocrinol.pdfPublished versionDescription of Zhai 2009 J Endocrinol.pdf : Published versio

High-Methionine Diet Attenuates Severity of Arthritis and Modulates IGF-I Related Gene Expressions in an Adjuvant Arthritis Rats Model

Rheumatoid arthritis, a synthesized form of adjuvant arthritis exhibited throughout many animal species, inhibits liver function and circulation of IGF-I and contributes to the degradation of skeletal muscle mass. One of the primary goals of the present study is determining whether a high-Methionine (high-Met) diet is capable of reducing the adverse effects of arthritis, namely, loss of body mass. Following adjuvant injection, forty arthritic rats were randomly assigned to either a control group with a basal diet or a high-Met group with the same basal diet + 0.5% Methionine. After 14 days all rats were terminated. The high-Met group exhibited an increase in body weight and food intake in comparison with the control group (P<0.05). High-Met diet debilitated arthritis-induced surges in the gastrocnemius in both atrogin-1 and the MuRF1 expressions; however, it was observed to have little to no effect on atrogin-1 and MuRF1 gene expression in soleus. At the same time, high-Met diet rats experienced a rise in IGF-I, with lowering of IGFBP-3 gene expression in the gastrocnemius and the soleus. These data suggest that arthritis severity can be partly attenuated by high-Met diet

Effect of Methionine Restriction on Bone Density and NK Cell Activity

Methionine restriction (MR) is proven to increase the lifespan; and it also affects the bone density and the innate immune system. The aim of this study is to explore the effect of methionine restriction on bone density and natural killer (NK) cells. C57BL/6J mice were subjected to either basal diet (BD, containing 0.80% methionine) or methionine-restricted diet (containing 0.14% methionine). Mice with MR diet displayed reduced bone mass and decrease in the cytotoxicity of NK from the spleen, compared to BD animals. Also, mice with MR diet had an inferior body weight (P<0.05) and higher plasma levels of adiponectin and FGF21 (P<0.05) but lower concentrations of leptin and IGF-1 (P<0.05). Overall, the investigation shows that methionine affects bone density and NK cell cytotoxicity

Role of Reactive Oxygen Species in Injury-Induced Insulin Resistance

AbstractAcute insulin resistance is common after injury, infection, and critical illness. To investigate the role of reactive oxygen species (ROS) in critical illness diabetes, we measured hepatic ROS, which rapidly increased in mouse liver. Overexpression of superoxide dismutase 2, which decreased mitochondrial ROS levels, protected mice from the development of acute hepatic insulin resistance. Insulin-induced intracellular signaling was dramatically decreased, and cellular stress signaling was rapidly increased after injury, resulting in the hyperglycemia of critical illness diabetes. Insulin-induced intracellular signaling, activation of stress (c-Jun N-terminal kinase) signaling, and glucose metabolism were all normalized by superoxide dismutase 2 overexpression or by pretreatment with antioxidants. Thus, ROS play an important role in the development of acute hepatic insulin resistance and activation of stress signaling after injury.http://deepblue.lib.umich.edu/bitstream/2027.42/192885/2/Zhai 2011 Mol Endocrinol.pdfPublished versionDescription of Zhai 2011 Mol Endocrinol.pdf : Published versio

A Challenging Correlation between Tumor Cellularity and Somatic Variant Allele Fraction in Lung and Colorectal Cancers—Specimens of Low Tumor Percentage Should Be Analyzed with Caution

Background and aims: The percentage of tumor cells (tumor cellularity) in a cancerous tissue has been assumed to correlate with the variant allele fraction (VAF) of an identified pathogenic variant. Many laboratories use the tumor cellularity as part of a quality criteria for specimen processing and clinical reporting. However, a systematic study of such correlation has yet to be shown. We performed a relatively large-scale study to determine whether pathologist-estimated tumor cellularity is correlated with next-generation sequencing (NGS)-derived VAF. Materials and Methods: A total of 1511 non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) specimens, including formalin-fixed paraffin-embedded (FFPE) and fine needle aspirated (FNA) tissues, were analyzed by cancer hotspot NGS. For a given specimen, pathogenic variants of BRAF, EGFR, KRAS, and NRAS were identified and the determined VAFs were correlated with the corresponding tissue tumor cellularity. Results: The coefficient of determination R-squared (R2) values were calculated for each correlation. All R2 values were lower than 0.25, indicating poor correlations. Pathogenic variants were found, not uncommonly, in tumor specimens that carried 10% or lower tumor cellularity. There were no apparent differences of R2 values between the FFPE and FNA specimens. Conclusion: In both NSCLC and CRC, the lack of linear relationship between tumor cellularity and VAF was found across a wide range of tumor cell percentages. Caution should be used when using tumor cellularity to triage specimens for NGS testing. The tumor cellularity should be considered in relation to the limit of detection of the specific assay for the proper interpretation of a negative test result