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Type 1 diabetes mellitus (T1DM) is a long-term and chronic autoimmune disorder, in which the immune system attacks the pancreatic β-cells. Both adaptive and innate immune systems are involved in T1DM development. Both B-cells and T-cells, including CD4+ and CD8+ T-cells, as well as other T-cell subsets, could affect onset of autoimmunity. Furthermore, cells involved in innate immunity, including the macrophages, dendritic cells, and natural killer (NK) cells, could also accelerate or decelerate T1DM development. In this review, the crosstalk and function of immune cells in the pathogenesis of T1DM, as well as the corresponding therapeutic interventions, are discussed.

We studied the protective effect of stromal cell-derived factor-1β (SDF-1β) on cardiac cells from lipotoxicity in vitro and diabetes in vivo. Exposure of cardiac cells to palmitate increased apoptosis by activating NADPH oxidase (NOX)–associated nitrosative stress and endoplasmic reticulum (ER) stress, which was abolished by pretreatment with SDF-1β via upregulation of AMP-activated protein kinase (AMPK)–mediated p38 mitogen-activated protein kinase (MAPK) phosphorylation and interleukin-6 (IL-6) production. The SDF-1β cardiac protection could be abolished by inhibition of AMPK, p38 MAPK, or IL-6. Activation of AMPK or addition of recombinant IL-6 recaptured a similar cardiac protection. SDF-1β receptor C-X-C chemokine receptor type 4 (CXCR4) antagonist AMD3100 or CXCR4 small interfering RNA could not, but CXCR7 small interfering RNA completely abolished SDF-1β’s protection from palmitate-induced apoptosis and activation of AMPK and p38 MAPK. Administration of SDF-1β to diabetic rats, induced by feeding a high-fat diet, followed by a small dose of streptozotocin, could significantly reduce cardiac apoptosis and increase AMPK phosphorylation along with prevention of diabetes-induced cardiac oxidative damage, inflammation, hypertrophy, and remodeling. These results showed that SDF-1β protects against palmitate-induced cardiac apoptosis, which is mediated by NOX-activated nitrosative damage and ER stress, via CXCR7, to activate AMPK/p38 MAPK–mediated IL-6 generation. The cardiac protection by SDF-1β from diabetes-induced oxidative damage, cell death, and remodeling was also associated with AMPK activation.

ObjectivesWith the rapid development and spread of information technology, mobile healthcare (M-healthcare) is emerging as a feasible option for improved monitoring and treatment of patients with chronic diseases such as diabetes, particularly for those with limited access to medical institutions. Our study group has developed and evaluated an M-healthcare system that provides remote guidance for diabetic patients. This paper introduces the diabetic M-healthcare system and describes progress in implementation for remote and mobile healthcare in China. We provide evidence that this system improves diabetic patient management and can contribute to the establishment of a new model for patient-centered mobile healthcare.Target audienceThe main groups that this paper is aimed at are doctors, nurses, nutritionists, and sportspersons engaged in the design of mobile medical systems, and computer engineers involved in the construction of intelligent medical software systems.ScopeThe present article has as its scope designing the M-healthcare clinical follow-up system, identifying the advantages that the M-healthcare system has in comparison with traditional medical treatment, the clinical application effect of the M-healthcare system, and the development status of remote/mobile medical research in China and abroad.

Total aralosides of Aralia elata (Miq) Seem (TASAES) from Chinese traditional herb Longya Aralia chinensis L was found to improve cardiac function. The present study was to determine the protective effects of TASAES on diabetic cardiomyopathy, and the possible mechanisms. Therefore, a single dose of streptozotocin was used to induce diabetes in Wister rats. Diabetic rats were immediately treated with low, medium and high doses of TASAES at 4.9, 9.8 mg/kg and 19.6 mg/kg body weight by gavage, respectively, for eight weeks. Cardiac function was evaluated by in situ hemodynamic measurements, and patch clamp for the L-type Ca 2+ channel current ( I Ca 2+ -L) and transient outward K + channel current (I to ). Histopathological changes were observed under light and electron microscope. The expression of pro-fibrotic factor, connective tissue growth factor (CTGF) was monitored using immunohistochemistry staining. Compared with diabetic group, medium and high doses, but not low dose, of TASAES showed a significant protection against diabetes-induced cardiac dysfunction, shown by increased absolute value of left ventricular systolic pressure (LVSP) and maximum rates of pressure development (±dp/dt max ), and enhanced amplitude of I Ca 2+ -L ( P < 0.05). Histological staining indicated a significant inhibition of diabetes-caused pathological changes and up-regulation of CTGF expression ( P < 0.05). The results suggest that TASAES prevents diabetes-induced cardiac dysfunction and pathological damage through up-regulating I Ca 2+ -L in cardiac cells and decreasing CTGF expression.

Previous studies on telemedicine interventions have shown that older diabetic patients experience difficulty in using computers, which is a barrier to remote communication between medical teams and older diabetic patients. However, older people in China tend to find it easy to use mobile phones and personal messaging apps that have a user-friendly interface. Therefore, we designed a mobile health (mHealth) system for older people with diabetes that is based on mobile phones, has a streamlined operation interface, and incorporates maximum automation. The goal of the research was to investigate the use of mobile phone-based telemedicine apps for management of older Chinese patients with type 2 diabetes mellitus (T2DM). Variables of interest included efficacy and safety. A total of 91 older (aged over 65 years) patients with T2DM who presented to our department were randomly assigned to one of two groups. Patients in the intervention group (n=44) were provided glucometers capable of data transmission and received advice pertaining to medication, diet, and exercise via the mHealth telemedicine system. Patients assigned to the control group (n=47) received routine outpatient care with no additional intervention. Patients in both groups were followed up at regular 3-month intervals. After 3 months, patients in the intervention group showed significant (P<.05) improvement in postprandial plasma glucose level. After 6 months, patients in the intervention group exhibited a decreasing trend in postprandial plasma glucose and glycated hemoglobin levels compared with the baseline and those in the control group (P<.05). Mobile phone-based telemedicine apps help improve glycemic control in older Chinese patients with T2DM. China Clinical Trial Registration Center ChiCTR 1800015214; http://www.chictr.org.cn/showprojen.aspx?proj=25949 (Archived by WebCite at http://www.webcitation.org/73wKj1GMq).

Gingival overgrowth (GO) includes gingival enlargement and hyperplasia and may be induced by certain drugs, including calcium channel blockers (CCBs), particularly first-generation CCBs. However, to date, only few cases of GO induced by second- or third-generation CCBs have been reported. The present study reports on a case of a 48-year-old diabetic male who was admitted to the First Hospital of Jilin University (Changchun, China) due to poor blood glucose control. This patient was diagnosed with GO. Review of the patient's medical history revealed diagnoses of type 2 diabetes and hypertension, as well as the use of felodipine, a second-generation CCB, to control hypertension. The hypertensive drugs were replaced and the new drugs helped the patient control his blood glucose levels. Additionally, the patient was instructed on methods he could use to improve his oral hygiene, including rinsing of the teeth following each meal and increasing the frequency of tooth brushing per day. After 3 months, the clinical symptoms of GO were relieved. The relevant literature was also reviewed to gain an improved understanding of the correlation between GO and CCBs, as well as diabetes and poor oral hygiene.

We studied the protective effect of stromal cell-derived factor-1[beta] (SDF-1[beta]) on cardiac cells from lipotoxicity in vitro and diabetes in vivo. Exposure of cardiac cells to palmitate increased apoptosis by activating NADPH oxidase (NOX)--associated nitrosative stress and endoplasmic reticulum (ER) stress, which was abolished by pretreatment with SDF-1[beta] via upregulation of AMP-activated protein kinase (AMPK)--mediated p38 mitogen-activated protein kinase (MAPK) phosphorylation and interleuldn-6 (IL-6) production. The SDF-1[beta] cardiac protection could be abolished by inhibition of AMPK, p38 MAPK, or IL-6. Activation of AMPK or addition of recombinant IL-6 recaptured a similar cardiac protection. SDF-1[beta] receptor C-X-C chemokine receptor type 4 (CXCR4) antagonist AMD3100 or CXCR4 small interfering RNA could not, but CXCR7 small interfering RNA completely abolished SDF-1[beta]'s protection from palmitate-induced apoptosis and activation of AMPK and p38 MAPK. Administration of SDF-1[beta] to diabetic rats, induced by feeding a high-fat diet, followed by a small dose of streptozotocin, could significantly reduce cardiac apoptosis and increase AMPK phosphorylation along with prevention of diabetes-induced cardiac oxidative damage, inflammation, hypertrophy, and remodeling. These results showed that SDF-1[beta] protects against palmitate-induced cardiac apoptosis, which is mediated by NOX-activated nitrosative damage and ER stress, via CXCR7, to activate AMPK/p38 MAPK--mediated IL-6 generation. The cardiac protection by SDF-1[beta] from diabetes-induced oxidative damage, cell death, and remodeling was also associated with AMPK activation.

The signal sequence played a crucial role in the efficacy of mRNA vaccines against virus pandemic by influencing antigen translation. However, limited research had been conducted to compare and analyze the specific mechanisms involved. In this study, a novel approach was introduced by substituting the signal sequence of the mRNA antigen to enhance its immune response. Computational simulations demonstrated that various signal peptides differed in their binding capacities with the signal recognition particle (SRP) 54 M subunit, which positively correlated with antigen translation efficiency. Our data revealed that the signal sequences of tPA and IL-6-modified receptor binding domain (RBD) mRNA vaccines sequentially led to higher antigen expression and elicited more robust humoral and cellular immune protection against the SARS-CoV-2 compared to the original signal sequence. By highlighting the importance of the signal sequence, this research provided a foundational and safe approach for ongoing modifications in signal sequence-antigen design, aiming to optimize the efficacy of mRNA vaccines.

The major histocompatibility complex class I (MHCI) trafficking signal (MITD) plays a pivotal role in enhancing the efficacy of mRNA vaccines. However, there was a lack of research investigating its efficacy in enhancing immune responses to RNA virus infections. Here, we have developed an innovative strategy for the formulation of mRNA vaccines. This approach involved the integration of MITD into the mRNA sequence encoding the virus antigen. Mechanistically, MITD‐based mRNA vaccines can strengthen immune protection by mimicking the dynamic trafficking properties of MHCI molecule and thus expand the memory specific B and T cells. The model MITD‐based mRNA vaccines encoding binding receptor‐binding domain (RBD) of SARS‐CoV‐2 were indeed found to achieve protective duration, optimal storage stability, broad efficacy, and high safety.

Overburden strata fracture evolution is critical to dynamic disaster prevention and gas-relief drainage, so it is important to accurately determine the evolution relationships with mining disturbance. In this paper, experiments and numerical simulation were adopted jointly to characterize the time-varying fracture area of overlying strata. The experimental results showed that the roof strata gradually broke and collapsed with coal mining, which indicated the fractures of overburden strata developed in an upward direction. The fracture development causes were explained by numerical simulation, which showed that stress increase exceeded the strength of coal and rock strata, and fractures were formed and expanded. Both experiments and numerical simulation results showed the two sides and the top of fracture areas provided channels and spaces for gas migration and reservoir, respectively. In addition, the breaking angle of overburden strata and the height of fracture areas were analyzed quantitatively. Through microseismic monitoring at the mining site, the fracture scales and ranges of overburden strata were verified by the energy and frequency of microseismic events, which were consistent with the support of maximum resistance. The position of drainage boreholes was considered based on the results of overburden strata fracture evolution. Our study is aimed at promoting coal mining in safety and improving gas drainage with a sustainable approach.