Chronic obstructive pulmonary disease (COPD) is incurable chronic disease which kills 3.3 million each year worldwide. Number of global cases of COPD is steadily rising alongside with life expectancy, disproportionally hitting middle-income countries like Russia and China, in such conditions, new approaches to the COPD management are desperately needed. DNA microarray technology is a powerful genomic tool that has the potential to uncover underlying COPD biological alteration and brings up revolutionized treatment option to clinicians. We executed systematic review studies of studies published in last 10 years regarding DNA microarray application in COPD management, with complacence to PRISMA criteria and using PubMed and Medline data bases as data source. Out of 920 identified papers, 39 were included in the final analysis. We concluded that Genome-wide expression profiling using DNA microarray technology has great potential in enhancing COPD management. Current studied proofed this method is reliable and possesses many potential applications such as individual at risk of COPD development recognition, early diagnosis of disease, COPD phenotype identification, exacerbation prediction, personalized treatment optioning and prospect of oncogenesis evaluation in patients with COPD. Despite all the proofed benefits of this technology, researchers are still in the early stage of exploring it’s potential. Therefore, large clinical trials are still needed to set up standard for DNA microarray techniques usage implementation in COPD management guidelines, subsequently giving opportunity to clinicians for controlling or even eliminating COPD entirely.
The gut microflora is a combination of all microbes in intestine and their microenvironment, and its change can sensitively reflect the relevant response of the body to external environment and remarkably affect body's metabolism as well. Recent studies have found that cold exposure affects the body's gut microflora, which can lead to changes in the body's metabolism of glucose and lipid. This review summarizes recent research on the effects of cold exposure on gut microbes and metabolism of glucose and lipid, aiming to provide some new ideas on the approaches and measures for the prevention and treatment of diabetes and obesity.
Developmental disorders (DDs) are a kind of chronic maladies, which can cause serious irreversible detriment to children’s physical and mental health. It is predominantly regulated by the interaction of environment and heredity. Cold regions are mainly located in the high latitudes of China. Their living environment is characterized by frequent cold wave, huge temperature difference, severe air pollution, high calorie diet, less exercise, smoking, drinking, etc. In recent years, substantial advances have been made in studies of the correlation between the living environment features in cold regions and the DDs. Accordingly, this article reviews the impact of the peculiar living environment of cold regions on DDs, with a view to provide fresh prevention strategies for reducing the morbidity of DDs in China cold regions by ameliorating living environment.
Kashin-Beck disease (KBD) is an endemic osteoarthropathy. Its distribution region covers a long and narrow belt on the Pacific side and belongs to continental climate with short summer, long frost period, and large temperature differences between day and night. In particular, KBD patients are typically scattered in the rural areas with seasonal features such as cold winters and rainy autumns. Etiological studies have demonstrated that the carrier of pathogenic factors is the grains produced in endemic areas. Risk factors for KBD include fungal contamination of grains due to poor storage conditions associated with cold weather. The epidemiological characteristics of KBD include agricultural area, early age of onset, gender equality, family aggregation, regional differences, and annual fluctuations. A series of preventive measures have been successfully taken in the past decades. National surveillance data indicate that the annual incidence of KBD is gradually declining.
Objective: Clinical manifestation of the inflammatory process in its relation to biochemical markers (total cysteine [Cys], cysteine-glycine [CysGly], glutathione [GSH], glutamate-cysteine [Glu-Cys], homocysteine [Hcy], the ratio of reduced to oxidized glutathione [GSH/GSSG], the ratio of reduced to oxidized cysteine [CySH/CySS], malondialdehyde-oxidized low-density lipoproteins [MDA-oxLDL]) has been studied in patients with coronavirus disease 2019 (COVID-19). Material and methods: 48 patients with mild to severe COVID-19 and 20 healthy volunteers were included in our research. The participants were divided into 4 experimental groups according to inflammation intensity estimated based on the serum levels of interleukin 6 (IL-6). Results: All 4 groups showed the prevalence of male patients and elevated serum levels of IL-6 (by 54.6%). There was no comorbidity in patients with mild COVID-19 (nasopharyngitis symptoms) and in healthy control subjects. 50% of patients with lung damage had accompanying diseases. Alterations of aminoethyl metabolism were detected in COVID-19 patients: as reflected by the decreased levels of Cys, CysGly, and Glu-Cys and the increased levels of GSH as compared to the control group. Conclusion: Elevation of IL-6 over 7.5 pg/mL was associated with decreased GSH/GSSG and CySH/CySS ratios indicating enhanced oxidative stress and was followed by protein oxidation, specifically MDA-oxLDL.
Background: Taxus cuspidata S. et Z. is a precious species of frigid zone plant belonging to the Taxaceae family, which possesses anticancer, anti-inflammatory, hypoglycemic, and antibacterial pharmacological properties. While taxane extracted from Taxus chinensis has been reported to elicit antioxidant activities, whether Taxus cuspidata S. et Z. has skin-protective actions against injuries remained unknown. This study aims to explore the pharmacological effects of three Taxus extracts on skin melanin deposition, oxidation, inflammation, and allergy so as to provide new ideas for the prevention and treatment of various diseases related to skin damage. Methods: Skin melanin deposition was evaluated by measuring melanin content in the skin of guinea pigs by alkali lysis method. Antioxidant capacity was evaluated by measuring superoxide dismutase (SOD) concentration and glutathione (GSH) content in skin tissue homogenates of Kunming mice by SOD assay kit and micro reduced GSH assay kit. The quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to examine the levels of both SOD and recombinant glutathione peroxidase 4 (GPX4). Skin inflammation was evaluated by xylene-induced ear swelling test and egg-white-induced paw swelling test in mice. In a mouse model of skin allergy induced by 4-aminopyridine (4-AP), allergy was determined by licking body counts and histamine concentrations in tissue homogenates using enzyme-linked immunosorbent assay (ELISA) kits. Two proinflammatory factors tumor necrosis factor (TNF)-α and interleukin (IL)-1β were measured by qRT-PCR. Hematoxylin and eosin (HE) staining was conducted to assess the degree of skin lesion. Results: All three Taxus extracts including Taxus chinensis essential oil, Taxus chinensis extract and Taxus chinensis extract compound reduced the melanin deposits in the back skin relative to the non-treated control animals, of which Taxus chinensis essential oil produced the greatest effect. In contrast, the three Taxus extracts elevated SOD and GSH levels in the skin tissues, and the highest increase was seen with Taxus chinensis essential oil. Three Taxus extracts, especially Taxus chinensis essential oil, effectively reduce the rate of ear and paw swelling. All three Taxus extracts reduced the number of body licks, the levels of TNF-α and IL-1β, and the histamine content in tissue homogenates of mice and alleviated skin damage. Consistently, Taxus chinensis essential oil yielded the greatest magnitude of decreases. Conclusion: While all three Taxus extracts possessed the anti-skin melanin deposition, oxidation, and allergy properties, Taxus chinensis essential oil produced the superior effects.
Background: Myocardial infarctions (MI) is a major threat to human health especially in people exposed to cold environment. The polarization of macrophages towards different functional phenotypes (M1 macrophages and M2 macrophages) is closely related to MI repairment. The growth differentiation factor 11 (GDF11) has been reported to play a momentous role in inflammatory associated diseases. In this study, we examined the regulatory role of GDF11 in macrophage polarization and elucidated the underlying mechanisms in MI. Methods: In vivo, the mice model of MI was induced by permanent ligation of the left anterior descending coronary artery (LAD), and mice were randomly divided into the sham group, MI group, and MI+GDF11 group. The protective effect of GDF11 on myocardial infarction and its effect on macrophage polarization were verified by echocardiography, triphenyl tetrazolium chloride staining and immunofluorescence staining of heart tissue. In vitro, based on the RAW264.7 cell line, the effect of GDF11 in promoting macrophage polarization toward the M2 type by inhibiting the Notch1 Signaling pathway was validated by qRT-PCR, Western blot, and flow cytometry. Results: We found that GDF11 was significantly downregulated in the cardiac tissue of MI mice. And GDF11 supplementation can improve the cardiac function. Moreover, GDF11 could reduce the proportion of M1 macrophages and increase the accumulation of M2 macrophages in the heart tissue of MI mice. Furthermore, the cardioprotective effect of GDF11 on MI mice was weakened after macrophage clearance. At the cellular level, application of GDF11 could inhibit the expression of M1 macrophage (classically activated macrophage) markers iNOS, interleukin (IL)-1β, and IL-6 in a dose-dependent manner. In contrast, GDF11 significantly increased the level of M2 macrophage markers including IL-10, CD206, arginase 1 (Arg1), and vascular endothelial growth factor (VEGF). Interestingly, GDF11 could promote M1 macrophages polarizing to M2 macrophages. At the molecular level, GDF11 significantly down-regulated the Notch1 signaling pathway, the activation of which has been demonstrated to promote M1 polarization in macrophages. Conclusions: GDF11 promoted macrophage polarization towards M2 to attenuate myocardial infarction via inhibiting Notch1 signaling pathway.