Background: According to classical sources of Traditional Mongolian Medicine, the Mana-4 decoction clears internal heat and fever, alleviates febrile and infectious diseases, resolves pale-brown Badgan disorders, and alleviates severe pneumonia. Chimedragchaa.Ch. et al. (2002) demonstrated that Mana-4 possesses heat-clearing, anti-inflammatory, and immunomodulatory effects. Chronic Fatigue Syndrome (CFS) is a disorder characterized by clinical manifestations including physical exhaustion, low-grade fever, headache, mood fluctuations, cognitive impairment, and sleep disturbances. In recent years, as the pace of modern life and workload have increased, physical, psychological, and mental stress have intensified, leading to dysregulation of the nervous and endocrine systems, impaired immune function, and a rising global prevalence of CFS—a trend that has attracted increasing attention from researchers worldwide. However, the etiology and pathogenesis of CFS remain incompletely understood, and effective, evidence-based treatments continue to be sought. Therefore, we developed Immunoflu soluble granules, derived from the constituents of Mana-4, and this study aimed to investigate its anti-fatigue effects, as no such investigation had previously been conducted. Aim: To evaluate the anti-fatigue effect of Immunoflu, a formulation derived from the traditional Mana-4 decoction widely used in Traditional Mongolian Medicine. Materials and Methods: A chronic-fatigue rat model was established by forced-swimming induction, following the method of Jia Wang et al. (2013). The behavioral effects of Immunoflu were assessed using the open-field test (locomotor activity) and the elevated plus-maze test (anxiety-related behavior). Result: Immunoflu was administered at 100, 200, and 400 mg/kg to evaluate its effects in a chronic-fatigue model. In the open-field test, no significant difference (p>0.05) in central-zone entries was observed between Immunoflu and the model control. However, vertical locomotor activity increased significantly: Immunal 50 mg/kg +80.4% (p=0.024), Immunoflu 100 mg/kg +82.6% (p=0.003), and 200 mg/kg +77.4% (p=0.035). From these findings, Immunoflu at 100 and 200 mg/kg clearly enhanced locomotor activity in rats with chronic fatigue. In the elevated plus-maze test, Immunal 50 mg/kg increased the time spent in the central zone (10×10cm) by 53.3% (p=0.021) and in open arms by 61.4% (p=0.032) compared with the model control. Although Immunoflu produced no significant changes (p>0.05) in central-zone entries or time spent in the central zone, the time spent in the open arms increased by 60.6% at 200 mg/kg (p=0.026), indicating a reduction in anxiety and improved behavioral response to stress. Conclusion In a forced-swimming–induced chronic-fatigue model, Immunoflu increased locomotor activity by 77.4–82.6% at 100 and 200 mg/kg, reduced anxiety by 60.6% at 200 mg/kg, and reduced behavioral despair and fatigue by 35.3% at 100 mg/kg.

Background: Chronic Fatigue Syndrome (CFS) is a poorly understood disorder of unknown etiology, characterized by clinical manifestations including physical exhaustion, low-grade fever, myalgia, dizziness, mood fluctuations, cognitive impairment, and sleep disturbances. CFS is highly prevalent and frequently comorbid with psychiatric conditions, particularly depression and anxiety. Symptoms exacerbate during physical or mental exertion and do not completely resolve with rest. Currently, there is a lack of proven, effective pharmacological treatments for CFS. Therefore, this study aimed to investigate the anti-fatigue effects of Immunoflu. Aim: To evaluate the anti-fatigue effects of Immunoflu, a technologically modernized formulation derived from the traditional Mana-4 decoction. Materials and Methods: A chronic fatigue rat model was established using the forced-swim protocol described by Jia Wang and Chengxin Sun (2013). The pharmacological effects of Immunoflu were evaluated by quantifying serum levels of cytokines (IL-1β, IL-2, IL-5, IL-10, and IL-17a) by ELISA and assessing behavioral despair using the forced swim test (FST). Results: We evaluated how Immunoflu affects the chronic fatigue model at doses of 100, 200, and 400 mg/kg by measuring serum levels of IL-1β, IL-2, IL-5, IL-10, and IL-17a and assessing despair using the “Forced swim test”. In the forced-swimming-induced chronic fatigue model in rats, Immunoflu at a dose of 100 mg/kg increased the serum IL-2 indicator by 23.8%, and Immunal at a dose of 50 mg/kg increased it by 23.3% compared to the model control group, a statistically significant difference (p < 0.05). Furthermore, Immunoflu at 200 mg/kg reduced IL-17a cytokine levels by 23.7% compared with the model control group. When evaluating the swimming state of the animals with the Forced swim test, the group given Immunal 50 mg/kg (52.03±9.3 sec) decreased by 31.6% (*p=0.038), and the group given Immunoflu 100 mg/kg (49.19±8.54 sec) decreased by 35.3% (*p=0.01) respectively compared to the model control group, while no statistically significant difference was observed in other groups. Conclusions 1. Immunoflu at 100 mg/kg demonstrates immunostimulatory effects in a chronic fatigue model by increasing serum IL-2 levels by 23.8%. Additionally, at 200 mg/kg, it exhibits anti-inflammatory properties, reducing IL-17a levels by 23.7%. 2. In the forced-swimming model, Immunoflu at 100 mg/kg effectively reduced behavioral despair and physical fatigue by 35.3%.

: Childhood obesity is, according to the WHO, one of the most serious challenges of the 21st century. More than 100 million children have obesity today. Globally, the prevalence of obesity and overweight tripled in the child and youth populations from the mid-1970s (about 4%) to 2016 (greater than 18%). In 2016, more than 330 million children and adolescents were affected by overweight or obesity globally. It is estimated that by 2030 nearly 30% of all children will be affected by overweight or obesity. For this reason, childhood obesity is a major public health problem worldwide.
This study summarizes and reviewed research findings related to childhood obesity and health risks. Overweight and obesity are defined as an abnormal or excessive accumulation of fat that can harm health. Obesity has a multifactorial origin that involves both genetic and environmental factors. Several studies showed that excess body fat increased the risk of multiple comorbidities, such as high blood pressure, coronary heart disease, type 2 diabetes, insulin resistance, and cancer. According to the results of the research, the mother's nutritional status and obesogenic environments have a great influence on childhood obesity. A summary of the results of many studies concluded that childhood obesity is more likely to develop non-communicable diseases in adulthood. The global prevalence of overweight in children aged 5 years or under has increased modestly, but with heterogeneous trends in low and middle-income regions, while the prevalence of obesity in children aged 2–4 years has increased moderately. Overweight or obesity during childhood has important short-term and long-term consequences. Conclusion In recent decades, the prevalence of obesity in children has increased dramatically. For the successful implementation of activities to prevent overweight and obesity in children, it is necessary to create a supportive environment and to promote health.

Tissue fibrosis, characterized by excessive accumulation of aberrant extracellular matrix (ECM) produced by myofibroblasts, is a growing cause of mortality worldwide. Understanding the factors that induce myofibroblastic differentiation is paramount to prevent or reverse the fibrogenic process. Integrin-mediated interaction between the ECM and cytoskeleton promotes myofibroblast differentiation. In the present study, we explored the significance of integrin alpha 11 (ITGA11), the integrin alpha subunit that selectively binds to type I collagen during tissue fibrosis in the liver, lungs and kidneys. We showed that ITGA11 was co-localized with α-smooth muscle actin-positive myofibroblasts and was correlatively induced with increasing fibrogenesis in mouse models and human fibrotic organs. Furthermore, transcriptome and protein expression analysis revealed that ITGA11 knockdown in hepatic stellate cells (liver-specific myofibroblasts) markedly reduced transforming growth factor β-induced differentiation and fibrotic parameters. Moreover, ITGA11 knockdown dramatically altered the myofibroblast phenotype, as indicated by the loss of protrusions, attenuated adhesion and migration, and impaired contractility of collagen I matrices. Furthermore, we demonstrated that ITGA11 was regulated by the hedgehog signaling pathway, and inhibition of the hedgehog pathway reduced ITGA11 expression and fibrotic parameters in human hepatic stellate cells in vitro, in liver fibrosis mouse model in vivo and in human liver slices ex vivo. Therefore, we speculated that ITGA11 might be involved in fibrogenic signaling and might act downstream of the hedgehog signaling pathway. These findings highlight the significance of the ITGA11 receptor as a highly promising therapeutic target in organ fibrosis.
Animals ; Collagen ; Collagen Type I ; Cytoskeleton ; Extracellular Matrix ; Fibrosis ; Hedgehogs ; Hepatic Stellate Cells ; Humans ; In Vitro Techniques ; Kidney ; Liver ; Liver Cirrhosis ; Lung ; Mice ; Mortality ; Myofibroblasts* ; Phenotype* ; Transcriptome ; Transforming Growth Factors