Search

To match the capacity of cut tobacco case filling system in tobacco store room with that of tobacco flavoring system, the capping/uncapping machine, case-sleeve and pressing mechanism in GARBUIO case filling system were modified on the premise of no addition to the number of silos. By simplifying case filling action, and synchronizing some auxiliary case filling actions, the waiting time for flavored cut tobacco to enter the silos was reduced. The case filling system in tobacco store room of Longyan Tobacco Industrial Limited Corporation was tested. The results showed that the average case filling capacity reached 11 134.6 kg/h, which was larger than the tobacco flavoring capacity (10 000 kg/h) ; and the average waiting time for flavored tobacco decreased by 0.23 h/batch. This technology provides a support for promoting the production efficiency of tobacco primary processing. [ABSTRACT FROM AUTHOR]

A recent report published in Nature Metabolism identified that glutamine synthetase (GS), the only enzyme in mammals to produce glutamine from glutamate, can directly control cancer cell mitosis by governing the APC/C complex via a metabolism-independent mechanism. It reported that GS can directly interact with the nuclear pore protein NUP88 to abolish its binging with CDC20, therefore licensing the activation of APC/CCDC20 to permit proper metaphase to anaphase transition of mitosis. These findings illustrated a dual-function mode of action of GS in cancer cells, in which GS's metabolic and non-metabolic functions coordinate with the concentration change of glutamine in the tumor microenvironment (TME) to ensure cell survival or proliferation, respectively. These findings revealed the multi-faceted roles of glutamine synthetase in tumor development and underscored the potential to target non-canonical functions of glutamine synthetase for cancer treatment. [ABSTRACT FROM AUTHOR]

The changes associated with malignancy are not only in cancer cells but also in environment in which cancer cells live. Metabolic reprogramming supports tumor cell high demand of biogenesis for their rapid proliferation, and helps tumor cell to survive under certain genetic or environmental stresses. Emerging evidence suggests that metabolic alteration is ultimately and tightly associated with genetic changes, in particular the dysregulation of key oncogenic and tumor suppressive signaling pathways. Cancer cells activate HIF signaling even in the presence of oxygen and in the absence of growth factor stimulation. This cancer metabolic phenotype, described firstly by German physiologist Otto Warburg, insures enhanced glycolytic metabolism for the biosynthesis of macromolecules. The conception of metabolite signaling, i.e., metabolites are regulators of cell signaling, provides novel insights into how reactive oxygen species (ROS) and other metabolites deregulation may regulate redox homeostasis, epigenetics, and proliferation of cancer cells. Moreover, the unveiling of noncanonical functions of metabolic enzymes, such as the moonlighting functions of phosphoglycerate kinase 1 (PGK1), reassures the importance of metabolism in cancer development. The metabolic, microRNAs, and ncRNAs alterations in cancer cells can be sorted and delivered either to intercellular matrix or to cancer adjacent cells to shape cancer microenvironment via media such as exosome. Among them, cancer microenvironmental cells are immune cells which exert profound effects on cancer cells. Understanding of all these processes is a prerequisite for the development of a more effective strategy to contain cancers. [ABSTRACT FROM AUTHOR]

B cell dysfunction and inflammatory cytokine over‐production participate in the pathogenesis of rheumatoid arthritis (RA). Here we compared peripheral B cell homeostasis and immune functions between RA patients and healthy controls (HC) and explored vital signaling pathways involved in altered RA B cells. We found that RA patients showed significantly decreased frequencies of peripheral CD19+CD27+CD24high regulatory B (Breg) cells but increased frequencies of CD19+CD27+CD38high plasmablasts and CD19+CD138+ plasma cells, and higher levels of serum immunoglobulin (Ig)M and IgG. Compared to HC peripheral B cells, RA peripheral B cells had more increased proliferation and higher expression of activation markers. Importantly, our results showed that RA peripheral B cells displayed the mTOR signaling pathway to be more activated, and inhibition of mTOR could restore RA B cell homeostasis and functions. RA serum‐treated B cells exhibited more increased expressions of mTOR, which could be restored with the addition of anti‐interleukin (IL)‐27 neutralizing antibody. Serum IL‐27 levels were significantly increased in RA patients and positively correlated with disease activity, the frequencies of plasma cells and the levels of autoantibodies. In vitro, IL‐27 notably promoted immune dysfunction of RA B cells, which were inhibited by anti‐IL‐27 neutralizing antibody. Also, the mTOR pathway was more activated in IL‐27‐treated RA B cells, and mTOR inhibition apparently reversed abnormalities of RA B cells mediated by IL‐27. These results suggest that increased serum IL‐27 levels could promote peripheral B cell dysfunction in RA patients via activating the mTOR signaling pathway. Thus, IL‐27 may play a pro‐pathogenic role in the development of RA, and antagonizing IL‐27 could be a novel therapy strategy for RA. [ABSTRACT FROM AUTHOR]

Background: Immune dysfunction is one of the mechanisms to promote polycystic ovary syndrome (PCOS). Various immune cells have been reported to be involved in the development of PCOS. Meanwhile, the disturbance of metabolism is closely related to PCOS. The aim of this study is to explore the association of mucosal-associated invariant T (MAIT) cells and myeloid-derived suppressor cells (MDSCs) with the metabolic dysfunction in PCOS. Methods: 68 PCOS patients and 40 controls were recruited in this study and we collected the peripheral blood of participants' during their follicular phase. The frequencies of MAIT cells and MDSCs were determined by flow cytometry after being stained with different monoclonal antibodies. And the concentrations of cytokines were determined by ELISA. Results: Compared to controls with normal metabolism, the frequency of MDSCs, CD8+MAIT cells and CD38+CD8+MAIT cells were significantly decreased in PCOS patients with normal metabolism, however, proportion of CD4+MAIT cells exhibited a noticeable increase. Similar results of CD8+MAIT, CD38+CD8+MAIT cells and reduced expression of IL-17 were observed in PCOS patients with metabolic dysfunction as compared to controls with metabolic disorders. PCOS patients with excessive testosterone levels displayed significantly decreased levels of CD8+MAIT, CD38+CD8+MAIT cells, MDSCs and Mo-MDSCs as compared to PCOS patients with normal testosterone concentrations. PCOS patients with abnormal weight showed a lower level and activation of CD8+MAIT cells. On the contrary, they displayed an enrichment of CD4+MAIT cells. PCOS patients with glucose metabolic disorder displayed a remarkable dysregulation of MDSCs and Mo-MDSCs. MDSCs were positively correlated with MAIT cells. Negative correlations between the frequency of CD8+MAIT cells, CD38+CD8+MAIT cells and body mass index were revealed. CD4+MAIT cells positively correlated with BMI. Mo-MDSCs were found to be negatively related to the levels of 2hour plasma glucose and HOMA-IR index. Conclusion: The impairment of CD8+MAIT cells and MDSCs is involved in the metabolic dysfunction of PCOS. [ABSTRACT FROM AUTHOR]

Second-hand smoke (SHS) has been shown to be associated with psychiatric distress in pregnant women spontaneously conceived (SC), but this has never been investigated in pregnant women with assisted reproductive technology (ART) treatment. This study aimed to investigate and compare the associations of SHS with psychiatric distress among SC and ART pregnant women. Participants (1467 SC and 857 ART women) were from the sub-study of Chinese National Birth Cohort (CNBC) in Anhui Province. SHS was assessed by the self-reported questionnaire. The symptoms of depression, anxiety, stress, and poor sleep quality were assessed using CES-D, SAS, CPSS, and PSQI questionnaire. Multivariable linear regression was used to determine the association between SHS and psychiatric distress in each trimester. In SC women, SHS (yes or no) was associated with depression and anxiety symptoms in the 3rd trimester (β = 0.90, 95% CI 0.07–1.73 for depression and β = 1.21, 95% CI 0.39–2.04 for anxiety) and stress symptom and poor sleep quality in both the 2nd and 3rd trimesters (β = 0.85, 95% CI 0.20–1.49 in the 2nd trimester and β = 0.69, 95% CI 0.07–1.32 in the 3rd trimester for stress, and β = 1.32, 95% CI 0.68–1.96 in the 2nd trimester and β = 1.38, 95% CI 0.64–2.11 in the 3rd trimester for poor sleep quality). By contrast, in ART women, SHS was associated with depression and stress symptoms in the 1st trimester (β = 1.97, 95% CI 0.59–3.35 for depression and β = 1.18, 95% CI 0.24–2.12 for stress) and poor sleep quality throughout the pregnancy (β = 0.64, 95% CI 0.22–1.06 in the 1st trimester, β = 0.77, 95% CI 0.35–1.18 in the 2nd trimester, and β = 0.99, 95% CI 0.50–1.48 in the 3rd trimester, respectively). Our findings indicate a universal and detrimental effect of SHS on psychiatric health among both SC and ART pregnant women. However, the SHS impact may be more substantial at the early stage of pregnancy for ART women and at later stages for SC women. This implies the importance of reducing SHS exposure during pregnancy and the necessary to be aware of the difference in the effect of SHS on psychiatric distress between SC and ART women. [ABSTRACT FROM AUTHOR]

The activation of phospholipase D (PLD) by v-Src is discussed in relation to the role of Ral GTPase. It had been earlier found out that PLD activity increases in response to tyrosine kinase activity in v-Src resulting in the production of such substances as diaglycerol and phosphatidic acid. Ral GTPase acted in a manner analogous to the activation by Ras of Ral-GDS.