With increasing aging population, osteoporosis has emerged as a public health problem worldwide. Epidemiological data reveal that the prevalence of osteoporosis in cold regions is high, and low temperatures may crucially affect bone mass. Recent studies have found that the transient receptor potential melastatin-8 (TRPM8) channel, a cold-sensitive ion channel, can sense cold environment, and can be activated in cold environment. It may play an antagonistic role in low temperature-induced bone mass reduction. Mechanistically, this function may be ascribed to the activation of TRPM8 channel proteins in human bone marrow mesenchymal stem cells (hBM-MSCs), which causes osteoblast differentiation and mineralization in the bone. TRPM8 channel on the surface of brown adipocytes participates in the thermogenesis in brown adipose tissue (BAT) and the regulation of whole-body energy balance to maintain bone homeostasis. TRPM8 may be involved in bone remodeling throughout life. This paper reviews recent research on the possible antagonistic mechanism of TRPM8 in signaling pathways related to low temperature-induced bone mass loss and assesses the possibility of TRPM8 as a molecular target for the prevention and treatment of low temperature-induced osteoporosis in cold regions.
Cold stimulation has been linked to acute myocardial infarction and other cardiovascular diseases. Residents in the frigid zones, such Heilongjiang Province, experience a higher incidence of adverse cardiovascular events during winter, posing a significant health threat and increasing the overall medical burden. Cold stimulation serves as an detrimental stressor, inducing inflammation in the body. Therefore, understanding the role of inflammatory responses induced by cold stimulation in the occurrence and development of cardiovascular diseases is of paramount importance. Given the impact of cold on inflammation in cardiovascular diseases and the expanding array of anti-inflammatory methods for the treatment of cardiovascular diseases, delving into the inflammatory responses mediated by can significantly complement cardiovascular disease management. This review explorest the synergistic relationship between cold stimulation and inflammation induction, elucidating how this interplay influences the occurrence and progression of cardiovascular diseases.
Objective: Cold exposure has been suggested to be advantageous for the spread and infection of the coronavirus, and the gut microbiota influences the severity of the infection by modulating host inflammatory and immune responses. However, it remains unclear whether the promotion of viral infection through cold exposure is linked to the gut microbiota. Methods: In this study, we performed an unbiased analysis of gut microbiota, serum, and lung tissue metabolome changes in cold-exposed and virus-infected mice, alongside the assessment of immune-inflammatory indicators in serum and lung tissue. Results: The results revealed that both cold exposure and viral infection significantly decreased the percentage of peripheral blood lymphocytes (CD4+ T cells, CD8+ T cells, and B cell) and increased the expression of inflammatory factors (IL-6, IL-1β, TNF-α, and IFN-γ). Meanwhile, cold exposure disrupted the homeostasis of gut microbiota, elevating the abundance of pathogenic bacteria (Staphylococcus) and diminishing the abundance of beneficial bacteria (Alistipes). Notably, in virus-infected mice exposed to a cold environment, the reduction in the abundance of beneficial bacteria Alistipes was more pronounced than in cases of single virus infection and cold exposure. Analysis of altered serum and lung tissue metabolites highlighted glycerophospholipids, fatty acids, and eicosanoids as the most affected metabolites by cold exposure. These metabolites, closely associated with virus infection, exhibited a significant correlation with immune-inflammatory indicators. Conclusion: These findings establish a mechanistic connection between cold exposure and virus infection, suggesting that cold exposure-induced dysregulation of gut microbiota and lipid metabolism diminishes host immunity, promoting virus infection.
Background: Previous studies have established a link between fluctuations in climate and increased mortality due to coronary artery disease (CAD). However, there remains a need to explore and clarify the evidence for associations between meteorological changes and hospitalization incidences related to CAD and its subtypes, especially in cold regions. This study aimed to systematically investigate the relationship between exposure to meteorological changes, air pollutants, and hospitalization for CAD in cold regions. Methods: We conducted a cross-sectional study using hospitalization records of 86,483 CAD patients between January 1, 2009, and December 31, 2019. Poisson regression analysis, based on generalized additive models, was applied to estimating the influence of hospitalization for CAD. Results: Significant associations were found between low ambient temperature [-10°C, RR = 1.65; 95% CI: (1.28-2.13)] and the incidence of hospitalization for CAD within a lag of 0-14 days. Furthermore, O3 [95.50 μg/m3, RR = 12; 95% CI: (1.03-1.21)] and NO2 [48.70 μg/m3, RR = 1.0895% CI: (1.01-1.15)] levels were identified as primary air pollutants affecting the incidence of CAD, ST-segment-elevation myocardial infarction (STEMI), and non-STEMI (NSTEMI) within the same lag period. Furthermore, O3 [95.50 μg/m3, RR = 1.12; 95% CI: (1.03-1.21)] and NO2 [48.70 μg/m3, RR = 1.0895% CI: (1.01-1.15)] levels were identified as primary air pollutants affecting the incidence of CAD, ST-segment-elevation myocardial infarction (STEMI), and non-STEMI (NSTEMI) within the same lag period. The effect curve of CAD hospitalization incidence significantly increased at lag days 2 and 4 when NO2 and O3 concentrations were higher, with a pronounced effect at 7 days, dissipating by lag 14 days. No significant associations were observed between exposure to PM, SO2, air pressure, humidity, or wind speed and hospitalization incidences due to CAD and its subtypes. Conclusion: Our findings suggest a positive correlation between short-term exposure to low ambient temperatures or air pollutants (O3 and NO2) and hospitalizations for CAD, STEMI, and NSTEMI. These results could aid the development of effective preparedness strategies for frequent extreme weather events and support clinical and public health practices aimed at reducing the disease burden associated with current and future abnormal weather events.
Background and Objective: Self-monitoring of blood glucose (SMBG) is crucial for achieving a glycemic target and upholding blood glucose stability, both of which are the primary purpose of anti-diabetic treatments. However, the association between time in range (TIR), as assessed by SMBG, and β-cell insulin secretion as well as insulin sensitivity remains unexplored. Therefore, this study aims to investigate the connections between TIR, derived from SMBG, and indices representing β-cell functionality and insulin sensitivity. The primary objective of this study was to elucidate the relationship between short-term glycemic control (measured as points in range [PIR] ) and both β-cell function and insulin sensitivity. Methods: This cross-sectional study enrolled 472 hospitalized patients with type 2 diabetes mellitus (T2DM). To assess β-cell secretion capacity, we employed the insulin secretion-sensitivity index-2 (ISSI-2) and (ΔC-peptide0-120/Δglucose0-120) × Matsuda index, while insulin sensitivity was evaluated using the Matsuda index and HOMA-IR. Since SMBG offers glucose data at specific point-in-time, we substituted TIR with PIR. According to clinical guidelines, values falling within the range of 3.9-10 mmol were considered "in range, " and the corresponding percentage was calculated as PIR. Results: We observed significant associations between higher PIR quartiles and increased ISSI-2, (ΔC-peptide0-120/Δglucose0-120) × Matsuda index, Matsuda index (increased) and HOMA-IR (decreased) (all P < 0.001). PIR exhibited positive correlations with log ISSI-2 (r = 0.361, P < 0.001), log (ΔC-peptide0-120/Δglucose0-120) × Matsuda index (r = 0.482, P < 0.001), and log Matsuda index (r = 0.178, P < 0.001) and negative correlations with log HOMA-IR (r = -0.288, P < 0.001). Furthermore, PIR emerged as an independent risk factor for log ISSI-2, log (ΔC-peptide0-120/Δglucose0-120) × Matsuda index, log Matsuda index, and log HOMA-IR. Conclusion: PIR can serve as a valuable tool for assessing β-cell function and insulin sensitivity.
In recent years, cryotherapy has gained increasing acceptance as a treatment for prostate cancer, offering complementary therapeutic benefits when combined with radical surgery and radiotherapy. Despite the potential for surgical complications, it stands as a safe and viable therapeutic modality. Cryotherapy provides an efficient approach for elderly patients, especially those with compromised physical conditions and individuals experiencing recurrence after initial treatment. It has shown promise in extending survival periods and improving the overall quality of life for these patients. This article aims to comprehensively examine the developmental trajectory, surgical techniques, indications, therapeutic outcomes, and potential complications associated within prostate cancer treatment.