Clinical outcomes and prognostic risk factors of Langerhans cell histiocytosis in children: Results from the BCH-LCH 2014 protocol study.

Langerhans cell histiocytosis (LCH) is a rare myeloid neoplasm mainly affecting young children. This study aimed to evaluate the outcomes of 449 pediatric patients enrolled in the BCH-LCH 2014 study. 52.6% of patients were classified with single-system (SS) LCH, 28.1% with multisystem (MS) risk organ negative (RO-) LCH, and 19.4% with MS RO+ LCH. Three hundred ninety-six patients (88.2%) were initially treated with first-line therapy based on the vindesine-prednisone combination. One hundred thirty-nine patients who lacked a response to initial treatment were shifted to second-line therapy, 72 to intensive treatment Arm S1 (a combination of cytarabine, cladribine, vindesine, and dexamethasone), and 67 to Arm S2 (without cladribine). The 5-year overall survival (OS), progression-free survival (PFS), and relapse rates were 98.2% (median: 97.6 months), 54.6% (median: 58.3 months), and 29.9%, respectively. MS RO+ patients had the worst prognosis among the three clinical subtypes. For the patients initially treated with first-line therapy, the 5-year OS, PFS, and relapse rates were 99.2%, 54.5%, and 29.3%, respectively. Patients in Arm S1 had a significantly better prognosis than patients in Arm S2 (5-year PFS: 69.2% vs. 46.5%, p = .042; relapse rate: 23.4% vs. 44.2%, p = .031). Multivariate analysis revealed that early treatment response, the involvement of RO, skin, and oral mucosa, as well as laboratory parameters, including CRP and γ-GT, were independent risk factors for the PFS of LCH. Thus, the prognosis of LCH in children has been improved significantly with stratified chemotherapy, and progression and relapse remained the challenges, especially for RO+ patients.

Lipid Droplets in Lung Cancers Are Crucial for the Cell Growth and Starvation Survival.

For rapid and unlimited cell growth and proliferation, cancer cells require large quantities of nutrients. Many metabolic pathways and nutrient uptake systems are frequently reprogrammed and upregulated to meet the demand from cancer cells, including the demand for lipids. The lipids for most adult normal cells are mainly acquired from the circulatory system. Whether different cancer cells adopt identical mechanisms to ensure sufficient lipid supply, and whether the lipid demand and supply meet each other, remains unclear, and was investigated in lung cancer cells. Results showed that, despite frequent upregulation in de novo lipogenesis and the lipid transporter system, different lung cancer cells adopt different proteins to acquire sufficient lipids, and the lipid supply frequently exceeds the demand, as significant amounts of lipids stored in the lipid droplets could be found within lung cancer cells. Lipid droplet surface protein, PLIN3, was found frequently overexpressed since the early stage in lung cancer tissues. Although the expression is not significantly associated with a specific gender, age, histology type, disease stage, and smoking habit, the frequently elevated expression of PLIN3 protein indicates the importance of lipid droplets for lung cancer. These lipid droplets are not only for nutrient storage, but are also crucial for tumor growth and proliferation, as well as survival in starvation. These results suggest that manipulation of lipid droplet formation or TG storage in lung cancer cells could potentially decrease the progression of lung cancer. Further exploration of lipid biology in lung cancer could help design novel treatment strategies.

ATG16L1 autophagy pathway regulates BAX protein levels and programmed cell death.

Previously we reported that adipocyte SNAP23 (synaptosome-associated protein of 23 kDa) deficiency blocks the activation of macroautophagy, leading to an increased abundance of BAX, a pro-death Bcl-2 family member, and activation and adipocyte cell death both in vitro and in vivo Here, we found that knockdown of SNAP23 inhibited the association of the autophagosome regulators ATG16L1 and ATG9 compartments by nutrient depletion and reduced the formation of ATG16L1 membrane puncta. ATG16L1 knockdown inhibited autophagy flux and increased BAX protein levels by suppressing BAX degradation. The elevation in BAX protein had no effect on BAX activation or cell death in the nutrient-replete state. However, following nutrient depletion, BAX was activated with a concomitant induction of cell death. Co-immunoprecipitation analyses demonstrated that SNAP23 and ATG16L1 proteins form a stable complex independent of nutrient condition, whereas in the nutrient-depleted state, BAX binds to SNAP23 to form a ternary BAX-SNAP23-ATG16L1 protein complex. Taken together, these data support a model in which SNAP23 plays a crucial function as a scaffold for ATG16L1 necessary for the suppression of BAX activation and induction of the intrinsic cell death program.

Knock-down Sox5 suppresses porcine adipogenesis through BMP R-Smads signal pathway.

Adipogenesis, a differentiation process that transitions preadipocytes to adipocytes, is key to understanding the biology of fat accumulation and obesity. During this process, there many crucial transcription factors, such as PPARγ and the C/EBP family. Here we show a transcription factor in preadipocytes --- Sox5, that has a function in porcine adipogenesis. In our porcine subcutaneous-derived preadipocyte differentiation model, we found Sox5 expression displayed a significant upregulation after initial induction and decreased afterwards, which resembles the PPARγ expression pattern. siRNA knockdown of Sox5 in porcine preadipocytes significantly promoted cell growth and accelerated cell cycle progression. After inducing differentiation, knockdown of Sox5 notably down-regulated the expression of adipogenic marker genes: PPARγ, aP2, FAS and impaired lipid accumulation. Mechanistically, the deletion of Sox5 down-regulated the BMP R-Smads signal pathway, a crucial signal pathway for controlling preadipocyte fate commitment and adipogenesis. After using BMP4 recombinant protein to activate the BMP R-Smads signal, Sox5 function was partially rescued. In conclusion, our findings uncovered a function of Sox5 in porcine adipogenesis and reveal an interaction between Sox5 and BMP signaling.

MiR-127 attenuates adipogenesis by targeting MAPK4 and HOXC6 in porcine adipocytes.

MicroRNAs (miRNAs) have critical roles during adipogenesis; however, their precise functions are not completely understood. Porcine miRNA expression profiles show that miR-127 is dramatically downregulated with age in adipose tissue. We aimed to identify the precise functions and mechanisms of miR-127 in proliferation and adipogenesis. Preadipocytes were cultured under conditions to induce proliferation or differentiation and the effect of miR-127 overexpression on these processes, and the associated bioinformatically predicted target genes, were assessed using luciferase assays, quantitative real-time PCR, western blot analysis, and cell staining techniques. miR-127 increased proliferation by promoting cell cycling, whereas it suppressed differentiation, which was accompanied by reduced lipid accumulation. miR-127 targeted mitogen-activated protein kinase 4 and homeobox C6 (HOXC6) to activate preadipocyte proliferation. During differentiation, miR-127 targeted HOXC6 to attenuate adipogenesis. These findings identify miR-127 as an inhibitor of porcine adipogenesis, which may inform future strategies to reduce porcine fat deposition and treat human obesity.

Acute effects of the translocator protein drug ligand FGIN-1-27 on serum testosterone and luteinizing hormone levels in male Sprague-Dawley rats†.

We reported that FGIN-1-27 (N,N-dihexyl-2-(4-fluorophenyl)indole-3-acetamide, FGIN), a synthetic ligand for translocator protein (TSPO, 18 kDa), increased serum testosterone levels in young and aged Brown Norway rats after its administration daily for 10 days. It is not known, however, how soon after treatment with FGIN serum testosterone rises, how long levels remain elevated after cessation of treatment, or whether the drug acts solely through TSPO. Adult Sprague-Dawley male rats received a single ip dose of FGIN (1 mg/kg BW). Serial blood samples were collected, and serum testosterone and luteinizing hormone (LH) were assessed hourly throughout 24 h. Testosterone concentration was maximal by 3 h, remained significantly higher than the controls at 10 h, and returned to the control level by 24 h. Consistent with the in vivo study, culturing isolated Leydig cells with either FGIN (40 µM) or LH (0.1 ng/ml) resulted in significantly increased testosterone production by 30 min, and the stimulatory effects persisted through 48 h. At a very early (15 min) treatment time, however, FGIN significantly increased testosterone production but LH had not yet done so. Surprisingly, in vivo treatment with FGIN not only increased serum testosterone but also serum LH concentration, raising the possibility that FGIN may increase serum testosterone concentration by dual mechanisms.

Steroidogenesis in Leydig cells: effects of aging and environmental factors.

Serum testosterone (TS) levels decrease with aging in both humans and rodents. Using the rat as a model system, it was found that age-related reductions in serum TS were not due to loss of Leydig cells, but rather to the reduced ability of the Leydig cells to produce TS in response to luteinizing hormone (LH). Detailed analyses of the steroidogenic pathway have suggested that two defects along the pathway, LH-stimulated cAMP production and cholesterol transport to and into the mitochondria, are of particular importance in age-related reductions in TS production. Although the mechanisms involved in these defects are far from certain, increasing oxidative stress appears to play a particularly important role. Interestingly, increased oxidative stress also appears to be involved in the suppressive effects of endocrine disruptors on Leydig cell TS production.

A highly enantioselective Friedel-Crafts reaction of 3,5-dimethoxylphenol with nitroolefins mediated by a bifunctional quinine derived thiourea catalyst.

A useful enantioselective Friedel-Crafts reaction of 3,5-dimethoxylphenol with nitroolefins catalyzed by a bifunctional quinine derived thiourea catalyst 9 was developed. The Michael addition products could be obtained in good to high yields (68-92%) and with excellent enantioselectivities (89-98% ee). Such a reaction is exceptionally attractive in virtue of its simple protocol, ready availability of the starting materials, and practical applications of the products.

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway.

Skeletal muscle is the dominant executant in locomotion and regulator in energy metabolism. Embryonic myogenesis and postnatal muscle growth are controlled by a cascade of transcription factors and epigenetic regulatory mechanisms. MicroRNAs (miRNAs), a family of non-coding RNA of 22 nucleotides in length, post-transcriptionally regulates expression of mRNA by pairing the seed sequence to 3' UTR of target mRNA. Increasing evidence has demonstrated that miRNAs are important regulators in diverse myogenic processes. The profiling of miRNA expression revealed that miR-432 is more enriched in the longissimus dorsi of 35-day-old piglets than that of adult pigs. Our gain of function study showed that miR-432 can negatively regulate both myoblast proliferation and differentiation. Mechanically, we found that miR-432 is able to down-regulate E2F transcription factor 3 (E2F3) to inactivate the expression of cell cycle and myogenic genes. We also identified that phosphatidylinositol 3-kinase regulatory subunit (P55PIK) is another target gene of miR-432 in muscle cells. downregulation of P55PIK by miR-432 leads to inhibition of P55PIK-mediated PI3K/AKT/mTOR signaling pathway during differentiation. The blocking effect of miR-432 on this pathway can be rescued by insulin treatment. Taken together, our findings identified microRNA-432 as a potent inhibitor of myogenesis which functions by targeting E2F3 and P55PIK in muscle cells.

miR-425-5p Inhibits Differentiation and Proliferation in Porcine Intramuscular Preadipocytes.

Intramuscular fat (IMF) content affects the tenderness, juiciness, and flavor of pork. An increasing number of studies are focusing on the functions of microRNAs (miRs) during porcine intramuscular preadipocyte development. Previous studies have proved that miR-425-5p was enriched in porcine skeletal muscles and played important roles in multiple physiological processes; however, its functions during intramuscular adipogenesis remain unclear. To explore the role of miR-425-5p in porcine intramuscular adipogenesis, miR-425-5p agomir and inhibitor were used to perform miR-425-5p overexpression and knockdown in intramuscular preadipocytes, respectively. Our results showed that the agomir of miR-425-5p dramatically inhibited intramuscular adipogenic differentiation and downregulated the expression levels of adipogenic marker genes PPARγ, FABP4, and FASN, whereas its inhibitor promoted adipogenesis. Interestingly, the agomir repressed proliferation of porcine intramuscular preadipocytes by downregulation of cyclin B and cyclin E. Furthermore, we demonstrated that miR-425-5p inhibited adipogenesis via targeting and repressing the translation of KLF13. Taken together, our findings identified that miR-425-5p is a novel inhibitor of porcine intramuscular adipogenesis possibly through targeting KLF13 and subsequently downregulating PPARγ.

miR-429 Inhibits Differentiation and Promotes Proliferation in Porcine Preadipocytes.

MicroRNAs (miRNAs) are crucial regulatory molecules for adipogenesis. They contribute to the controlling of proliferation and differentiation of preadipocytes. Previous studies revealed an important role of miR-429 in cell invasion, migration, and apoptosis. Our previous work has shown that the expression of miR-429 in subcutaneous fat can be observed in newly born (3-day-old) Rongchang piglets rather than their adult counterparts (180-day-old). This expression pattern suggests that miR-429 might be functionally related to postnatal adipogenesis. However, we currently lack a mechanistic understanding of miR-429 within the context of preadipocyte differentiation. In this study, we investigated the function of miR-429 in porcine subcutaneous and intramuscular preadipocyte proliferation and differentiation. In our porcine preadipocyte differentiation model, miR-429 expression decreased remarkably upon adipogenic induction. Overexpression of miR-429 notably down-regulated the expression of adipogenic marker genes: PPARγ, aP2, FAS and impaired the triglyceride accumulation, while the expression of lipolytic gene ATGL was not affected. In addition, we observed that miR-429 significantly promoted the proliferation of porcine preadipocytes. We also found that miR-429 could directly bind to the 3'-UTRs of KLF9 and p27, which have been well documented to promote preadipocyte differentiation and repress cell cycle progression. Taken together, our data support a novel role of miR-429 in regulating porcine preadipocyte differentiation and proliferation, and KLF9 and p27 are potent targets of miR-429 during these processes.

Effect of Anterior Ankle-Foot Orthoses on Weight Shift in Persons With Stroke.

OBJECTIVE: To examine the effects of an anterior ankle-foot orthosis (AAFO) on the speed and accuracy of weight shift in persons with stroke. DESIGN: Cross sectional, repeated measures. SETTING: Neurologic rehabilitation department. PARTICIPANTS: People with stroke (N=24) who were unable to voluntarily dorsiflex the foot against gravity. INTERVENTION: The weight-shift performance was measured with and without the AAFO. MAIN OUTCOME MEASURES: The speed and accuracy of sustained and cyclic bilateral weight shift were measured using the computerized dynamic posturography. The movement velocity, maximum excursion, and directional control of sustained weight shift were calculated using the limits of stability test. The on-axis velocity gap, directional control, and stability of cyclic bilateral weight shift were calculated using the rhythmic weight shift test. RESULTS: For sustained weight shift, the maximum excursion of weight shift to the affected side was greater with the AAFO (P=.002). For cyclic bilateral weight shift, the on-axis velocity gap in the mediolateral (ML) direction was smaller at a fast speed (P=.004). The stability of the ML and anteroposterior weight shift was higher at slow (P=.002 and P<.001, respectively) and fast (P=.001 and P<.001, respectively) speeds when wearing the AAFO. CONCLUSIONS: The findings demonstrated that persons with stroke who wear an AAFO might improve the excursion of the sustained weight shift to the affected side and the speed and stability of cyclic bilateral weight shift in the ML direction.

Effects of an anterior ankle-foot orthosis on walking mobility in stroke patients: get up and go and stair walking.

OBJECTIVE: To examine the effects of an anterior ankle-foot orthosis (AAFO) on walking mobility in stroke patients. DESIGN: Cross-sectional and repeated-measures study design. SETTING: A university's neurologic rehabilitation department. PARTICIPANTS: Ambulant stroke patients (N=21). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Walking mobility was measured by the Timed Up and Go (TUG) test and the Timed Up and Down Stairs (TUDS) test. The paired t test was used to determine the difference between the mobility performances measured with and without the AAFO. RESULTS: There were significant differences between mobility performances with and without an AAFO in the TUG test (P=.038) and the TUDS test (P=.000). CONCLUSIONS: This study supports the effect of an AAFO on walking mobility in stroke patients. The findings demonstrate that stroke patients wearing an AAFO may ambulate with greater speed and safety on level surfaces and stairs.

Effects of Supercritical CO2 Treatment on Color, Lipid Oxidation, Heme Iron, Non-Heme Iron and Metmyoglobin Contents in Ground Pork.

The color, lipid oxidation, heme iron (HI) and non-heme iron (NHI) contents, metmyoglobin content and Soret band of myoglobin of ground pork subjected to supercritical CO2 treatment under different conditions, or to heat treatment (40°C, 2 h) and subsequent storage at 4°C were evaluated during 9-day period. Supercritical CO2 treatment significantly increased CIE L* and CIE b* values of ground pork during subsequent storage, while the HI content was slightly affected. In general, CIE a* value and metmyoglobin content were decreased. Supercritical CO2 treatment for 2 h could increase the thiobarbituric acid-reactive substances (TBARS) value, while treatment for 1 h or less had no effect. The NHI content could be increased only after treatment at above 40°C or 17.2 MPa for 2 h. The Soret band of myoglobin was shifted to longer wavelength. Increasing treatment temperature from 35°C to 45°C could increase CIE L*, CIE a*, CIE b* and TBARS values, HI and NHI contents of the ground pork, while decreasing metmyoglobin content. As the treatment pressure increased from 13.8 MPa to 20.7 MPa, CIE b* and TBARS values were decreased, while the NHI and metmyoglobin contents were increased. However, the other parameters were unchanged. Extending exposure time from 0.5 h to 2 h could increase CIE L*, CIE b* and TBARS values, HI contents, while decreasing CIE a* value and metmyoglobin content. Correlation analysis showed that the TBARS value was significantly and negatively correlated with the HI content or metmyoglobin content in samples treated at 40°C or above for 2 h.

Dietary patterns, metabolomics and frailty in a large cohort of 120 000 participants.

Objective: To examine the associations of dietary patterns with frailty and whether metabolic signatures (MSs) mediate these associations. Methods: We used UK Biobank data to examine (1) the associations of four dietary patterns (i.e., alternate Mediterranean diet [aMED], Recommended Food Score [RFS], Dietary Approaches to Stop Hypertension [DASH] and Mediterranean-DASH Intervention for Neurodegenerative Delay [MIND] diet) with frailty (measured by the frailty phenotype and the frailty index) using multivariable logistic regression (analytic sample 1: N = 124 261; mean age = 57.7 years), and (2) the mediating role of MSs (weighted sums of the metabolites selected from 168 plasma metabolites using the LASSO algorithm) in the above associations via mediation analysis (analytic sample 2: N = 26 270; mean age = 57.7 years). Results: Four dietary patterns were independently associated with frailty (all P < 0.001). For instance, compared to participants in the lowest tertile for RFS, those in the intermediate (odds ratio [OR]: 0.81; 95% confidence interval [CI]: 0.74, 0.89) and highest (OR: 0.62; 95% CI: 0.56, 0.68) tertiles had a lower risk of frailty. We found that 98, 68, 123 and 75 metabolites were associated with aMED, RFS, DASH and MIND, respectively, including 16 common metabolites (e.g., fatty acids, lipoproteins, acetate and glycoprotein acetyls). The MSs based on these metabolites partially mediated the association of the four dietary patterns with frailty, with the mediation proportion ranging from 26.52% to 45.83%. The results were robust when using another frailty measure, the frailty index. Conclusions: The four dietary patterns were associated with frailty, and these associations were partially mediated by MSs. Adherence to healthy dietary patterns may potentially reduce frailty development by modulating metabolites.

Age, sex, and APOE gene-specific associations between dynapenic obesity and dementia in a large cohort.

OBJECTIVE: To investigate the associations between dynapenic obesity and the risk of dementia, and the modifying effects of age, sex, and the APOE gene, using a large population-based cohort. METHODS: 279,884 participants aged 55 and above from the UK Biobank were included. The participants were classified into four categories based on body mass index and hand grip strength: healthy, obesity, dynapenia, and dynapenic obesity. The incident dementia was identified based on linked hospital records and death register data. Cox proportional hazards regression models were used to estimate the associations, followed by age-, sex-, and apolipoprotein E (APOE) gene-stratified analyses. RESULTS: During the median follow-up of 12.4 years, 5,170 (1.8%) participants developed dementia. Compared with the healthy group, participants with dynapenic obesity had 67% higher dementia risk (hazard ratio [HR]: 1.67, 95% confidence interval [CI]: 1.44-1.94). Compared with the healthy group, higher risks of dementia in participants with dynapenic obesity were respectively observed in male (HR: 2.03, 95% CI: 1.65-2.50), younger (<65 years, HR: 1.97, 95% CI: 1.55-2.50), and non-ε4-carrier (HR: 1.97, 95% CI: 1.60-2.44) (all P for interaction <0.05). In participants under 65 years and non-ε4-carrier, those with dynapenic obesity had the highest risk of dementia (HR: 2.63, 95% CI: 1.91-3.62), compared with the healthy group (P for second order interaction = 0.026). CONCLUSIONS: Dynapenic obesity is associated with increased risks of dementia, especially in participants under 65 years and non-ε4-carrier, suggesting the importance of managing dynapenic obesity in the prevention of cognition-related disorders.

Involution of brown adipose tissue through a Syntaxin 4 dependent pyroptosis pathway.

Aging, chronic high-fat diet feeding, or housing at thermoneutrality induces brown adipose tissue (BAT) involution, a process characterized by reduction of BAT mass and function with increased lipid droplet size. Single nuclei RNA sequencing of aged mice identifies a specific brown adipocyte population of Ucp1-low cells that are pyroptotic and display a reduction in the longevity gene syntaxin 4 (Stx4a). Similar to aged brown adipocytes, Ucp1-STX4KO mice display loss of brown adipose tissue mass and thermogenic dysfunction concomitant with increased pyroptosis. Restoration of STX4 expression or suppression of pyroptosis activation protects against the decline in both mass and thermogenic activity in the aged and Ucp1-STX4KO mice. Mechanistically, STX4 deficiency reduces oxidative phosphorylation, glucose uptake, and glycolysis leading to reduced ATP levels, a known triggering signal for pyroptosis. Together, these data demonstrate an understanding of rapid brown adipocyte involution and that physiologic aging and thermogenic dysfunction result from pyroptotic signaling activation.

Research progress on the regulation of production traits by gastrointestinal microbiota in dairy cows.

The composition and abundance of microorganisms in the gastrointestinal tract of cows are complex and extensive, and they play a crucial role in regulating nutrient digestion, absorption, maintaining digestive tract stability, and promoting the production and health of the host. The fermentation carried out by these microorganisms in the gastrointestinal tract is fundamental to the health and productivity of cows. Rumen microorganisms produce the majority of enzymes required to break down feed substrates, such as cellulose, protein, lipids, and other plant materials, through fermentation. This process provides energy metabolism substrates that satisfy approximately 70% of the host's energy requirements for physiological activities. Gut microorganisms primarily decompose cellulose that is difficult to digest in the rumen, thereby providing heat and energy to the hosts. Additionally, they have an impact on host health and productivity through their role in immune function. Understanding the composition and function of the cow gut microbiota can help regulate dairy cattle breeding traits and improve their health status. As a result, it has become a popular research topic in dairy cattle breeding. This article provides a review of the composition, structure, physiological characteristics, and physiological effects of the cow gut microbiota, serving as a theoretical foundation for future studies that aim to utilize the gut microbiota for dairy cattle breeding or improving production traits. It may also serve as a reference for research on gut microbiota of other ruminants.

Cognitive Function and Upper Limb Rehabilitation Training Post-Stroke Using a Digital Occupational Training System.

Stroke rehabilitation often requires frequent and intensive therapy to improve functional recovery. Virtual reality (VR) technology has shown the potential to meet these demands by providing engaging and motivating therapy options. The digital occupational training system is a VR application that utilizes cutting-edge technologies, including multi-touch screens, virtual reality, and human-computer interaction, to offer diverse training techniques for advanced cognitive capacity and hand-eye coordination abilities. The objective of this study was to assess the effectiveness of this program in enhancing cognitive function and upper extremity rehabilitation in stroke patients. The training and assessment consist of five cognitive modules covering perception, attention, memory, logical reasoning, and calculation, along with hand-eye coordination training. This research indicates that after eight weeks of training, the digital occupational training system can significantly improve cognitive function, daily living skills, attention, and self-care abilities in stroke patients. This software can be employed as a time-saving and clinically effective rehabilitation aid to complement traditional one-on-one occupational therapy sessions. In summary, the digital occupational training system shows promise and offers potential financial benefits as a tool to support the functional recovery of stroke patients.

Comparison of microstructure, mechanical property, and degradation rate of Mg-1Li-1Ca and Mg-4Li-1Ca alloys.

Mg-1 wt.% Li-1 wt.% Ca (LX11) and Mg-4 wt.% Li-1 wt.% Ca (LX41) alloys share the same hexagonal closed-packed crystalline structure. However, the differences in microstructure, mechanical properties, and degradation rates between the two alloys are not well understood. Hereby, the above three aspects of LX11 and LX41 alloys were studied via optical microscopy, tensile tests, and electrochemical polarization and electrochemical impedance spectroscopy, together with hydrogen evolution. The concentration of the released Mg2+, Ca2+, and Li+ ions was analyzed using a flame atomic absorption spectrophotometer. Results demonstrated that the LX11 alloy was composed of finer α-Mg grains, fewer twins, and smaller volume fractions of the intermetallic phases Mg2Ca than the LX41 alloy. The increasing Li concentration generated a weak decrease in the yield strength of the Mg-Li-Ca alloys, a remarkable increase in elongation to failure, and a stable ultimate tensile strength. The LX11 alloy had better corrosion resistance than the LX41 alloy. The release rate of the cations (Mg2+, Ca2+, and Li+) varied significantly with time. The release rate of metallic ions in Hank's solution cannot reflect the true corrosion rate of Mg-Li-Ca alloys due to the formation of the precipitated corrosion products and their difference in solubility. The dealloying corrosion mechanism of the Mg2Ca phase in Mg-Li-Ca alloys was proposed.