Gut microbiota is involved in leptin-induced thermoregulation in Mongolian gerbil (Meriones unguiculatus).

Leptin is a hormone that secreted by adipocytes and may promote energy expenditure by increasing thermogenesis. Our previous studies have shown that thermo-transient receptor potentials (thermo-TRPs) and gut microbiota are associated with thermoregulation in Mongolian gerbils, which are characterized by relative high serum leptin concentrations. Here, we test whether leptin can stimulate non-shivering thermogenesis (NST) in Mongolian gerbils, and whether thermo-TRPs and gut microbiota are involved in leptin-induced thermogenesis. First, gerbils were given acute leptin treatment (ALT) with different doses. Results showed that ALT significantly increased the body temperature of gerbils and change the composition of gut microbiota. Moreover, ALT groups showed a trend towards increased expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). Then, we investigated the effect of chronic leptin treatment (CLT) on gerbils. Surprisingly, CLT did not affect gerbils' food intake and body weight, but it significantly increased the body temperature at the end. Besides, CLT did not affect the expression of thermogenic markers in BAT, white adipose tissue (WAT) and skeletal muscle. However, CLT increased the expression of leptin receptors and TRPV2 in the small intestine and affected the composition of gut microbiota. Together, our data suggest leptin may increase body temperature by regulating gut microbiota. In conclusion, the Mongolian gerbils with serum hyperleptin is beneficial for adapting the cold living environments, and TRPV2 and gut microbiota are involved.

Sulfated fucans from algae Saccharina japonica promotes intestinal stem cell-mediated intestinal development in juvenile mouse by modulating the gut microbiota.

Intestinal development has a crucial role in the absorption of nutrients and the ability to resist infections in the early stages of life. This study utilized a 3-week-old C57BL/6 mice model to evaluate the beneficial impacts of sulfated fucans from Saccharina japonica (SJ-FUC) on the growth and development of the intestines. SJ-FUC enhanced the dimensions of the intestine, specifically the length, height of villi, and depth of the crypts. Additionally, it raised the mRNA expression of ZO-1 and Occludin, hence enhancing the structural integrity of the intestinal epithelium. SJ-FUC significantly increased mRNA expression of Lyz1, Muc2, and Math1, which resulted in the promotion of intestinal epithelial development. Furthermore, SJ-FUC augmented the mRNA levels of the ISC markers (Lgr5, Olfm4, and Ascl2). Our further research uncovered that SJ-FUC has a positive impact on the growth of beneficial bacteria, such as Akkermansia, Dubosiella, and Lactobacillus, which in turn promotes epithelial development of the intestine. In summary, our research indicates that SJ-FUC has a beneficial impact on the growth of the intestines in young mice. This is achieved by enhancing the stemness of intestinal stem cells (ISCs) and promoting the formation of the intestinal epithelium through the regulation of gut bacteria.

Sleep deprivation stimulates adaptive thermogenesis by activating AMPK pathway in mice.

Sleep deprivation (SD) can affect the adaptive thermogenesis in laboratory rodents, but the molecular mechanism and the crosstalk with other organs remain largely unknown. In order to investigate the effects and mechanisms of SD on thermoregulation and energy metabolism, here we measured the changes of body weight, body fat mass, body temperature, resting metabolic rate (RMR), and thermogenic gene expression in brown adipose tissue (BAT), white adipose tissue (WAT), skeleton muscle and liver in C57BL/6J mice during 7-day SD with rotating rod sleep deprivation device. Results showed that compared with the control group, the body weight and body fat mass of SD mice were decreased and RMR of SD mice increased. The gene expression of Ampk, Pgc1α and Ucp1 which related to thermogenesis in BAT and WAT were significantly increased, and the expression of Ampk, Serca1, Serca2 and Ucp3 which related to thermogenesis in skeletal muscle were significantly increased in SD mice. Taken together, these data demonstrated that 7-day SD enhanced the adaptive thermogenesis in mice by activating AMPK, including the upregulation of the AMPK - PGC1α - UCP1 pathway in BAT, and the AMPK - UCP3 and SLN - SERCA pathway in skeleton muscle. Our data provide the molecular evidence for SD-stimulated adaptive thermogenesis and energy metabolism in small mammals.

Personalized delayed anticoagulation therapy alleviates postoperative bleeding in total knee arthroplasty (TKA) patients.

Purpose: Ecchymosis is one of the most common complications following total knee arthroplasty (TKA), which is closely related to postoperative bleeding. However, it is still controversial whether anticoagulation treatment should be continued for postoperative ecchymosis patients. We suppose that personalized delayed anticoagulation therapy could be beneficial for decreasing postoperative bleeding. Methods: A total of 201 TKA patients were retrospectively included in this study, among whom ecchymosis patients received drug anticoagulation treatment 1-2 days later than usual, while nonecchymosis patients received regular drug anticoagulation treatment. The perioperative blood loss, coagulation state, fibrinolytic state and complications were collected and analyzed. Results: Eighty-nine patients (44.3%) developed ecchymosis within 3 days after TKA. There were no differences in baseline characteristics between the two groups. In the ecchymosis group, higher K values and lower calculated coagulation index values were observed in thromboelastography, along with greater total blood loss and a more significant decrease in haemoglobin levels on postoperative Day 1 (POD1) compared to the nonecchymosis group. Additionally, the ecchymosis patients exhibited higher levels of fibrinogen degradation products and D-dimer (D-D) on POD1, with no differences noted on POD3, indicating that patients with ecchymosis are in a relatively hypocoagulable and hyperfibrinolytic state compared to those without ecchymosis. Therefore, the delayed anticoagulation treatment proved beneficial for correcting these postoperative conditions. No statistically significant differences were found between the two groups in postoperative complications, demonstrating that delayed anticoagulation treatment is safe. Conclusion: Patients with ecchymosis exhibited a relatively hypocoagulable and hyperfibrinolytic state with a stronger tendency for postoperative bleeding. Delayed anticoagulation in ecchymosis patients could effectively prevent further exacerbation of postoperative bleeding by avoiding sustained hypocoagulable and hyperfibrinolysis states. Personalized delayed anticoagulation therapy could be beneficial for managing postoperative ecchymosis for TKA patients. Level of Evidence: Level IV.

Incidence of Gastric Foveolar Metaplasia in Duodenal Mucosa of the Pediatric Patients.

OBJECTIVE: The prevalence and the clinical significance of gastric foveolar metaplasia (GFM) of duodenal mucosa in pediatric patients are undetermined. The aim was to investigate the event of GFM in duodenal biopsies and its association with gastrointestinal tract disorders in pediatric patients. METHODS: We performed a chart review of the characteristics and pathologic findings in patients with GFM described in the pathology reports during 2020 to 2022. RESULTS: Sixty-five out of 3,857 patients (1.7%) had GFM observed in a total of 70/4,778 (1.5%) cases with duodenal biopsies. The ages ranged from 3 to 19 years. The duodenal bulb with GFM was identified in 65 out of 70 cases (92.9%). 17/70 (24.3%) biopsies had coexisting chronic duodenitis, and 52/70 (74.3%) had isolated GFM in duodenum. 48/70 (68.6%) cases had pathologic findings in other parts of the gastrointestinal tract, including 20 (28.6%) inflammatory bowel disease (IBD) and four (5.7%) H. pylori gastritis. Of all 4,778 cases, 136 (2.8%) and 92 (1.9%) cases were diagnosed as IBD and H. pylori gastritis, which had an odds ratio for GFM at 15.8 and 3.2 respectively (p<0.05). CONCLUSION: Both H. pylori gastritis and IBD are associated with GFM in pediatric patients, while isolated GFM itself in the duodenal bulb has limited clinical implications.

Time-restricted feeding modulates gene expression related with rhythm and inflammation in Mongolian gerbils.

Time-restricted feeding (TRF) has the potential to modulate circadian rhythm and widely studied in humans and laboratory mice. However, less is known about the physiological responses to TRF in wild mammals. Here, we used Mongolian gerbils, Meriones unguiculatus, to explore the effect of 6-week TRF on gene expression related with circadian rhythm and inflammation. The TRF gerbils had higher cumulative food intake than the ad libitum (AL) group, but body mass, feeding frequency/time and metabolic rate did not differ between groups. In the hypothalamus, downregulation of rhythm-related genes Per3, Cry1 and Dbp was detected in the daytime-restricted feeding (DRF) group and Cry1 was downregulated in the nighttime-restricted feeding (NRF) group. In the liver, the expression of Per1/3, Rev-erbα/ß and Dbp was lower, and Bmal1 was higher in the DRF than in AL group, while NRF gerbils showed no changes. In the colon, the expression of Bmal1 and Cry1 was higher but Per3, Rev-erbα/ß and Dbp were lower in the DRF than in AL group. Further, the expression of inflammation-related genes such as NF-κB, IL-1ß, IL-18 and Nlrp3 was lower in the liver of DRF gerbils, and IL-1ß was lower both in the hypothalamus and liver of NRF gerbils. Moreover, the genes related with inflammation such as NF-κB, Nlrp3, IL-10/18/1ß and Tnf-α were positively or negatively correlated with multiple rhythm-related genes in the central and peripheral organs. In conclusion, TRF, particularly DRF, could modulate rhythm-related genes in the central and peripheral tissues and reduce hepatic expression of inflammation-related genes in gerbils.

Enhancing total knee arthroplasty outcomes: the role of individualized femoral sagittal alignment in robotic-assisted surgery - A randomized controlled trial.

BACKGROUND: Optimal sagittal alignment of the femoral prosthesis is critical to the success of total knee arthroplasty (TKA). While robotic-assisted TKA can improve alignment accuracy, the efficacy of default femoral alignment versus individualized alignment remains under scrutiny. This study aimed to compare the differences in prosthetic alignment, anatomical restoration, and clinical outcomes between individualized femoral sagittal alignment and default sagittal alignment in robotic-assisted TKA. METHODS: In a prospective randomised controlled trial, 113 patients (120 knees) underwent robotic-assisted TKA were divided into two groups: 61 with individualized femoral flexion (individualized alignment group) and 59 with default 3-5° flexion (default alignment group). The individualized alignment was based on the distal femoral sagittal anteverted angle (DFSAA), defined as the angle between the mechanical and distal anatomical axes of the femur. The radiographic and clinical outcomes were compared. RESULTS: Despite similar postoperative femoral flexion angles between groups (P = 0.748), the individualized alignment group exhibited significantly lower incidences of femoral prosthesis extension and higher rates of optimal 0-3° prosthesis flexion (9.8% vs. 27.1%, P = 0.014,78.7% vs. 55.9%, p = 0.008, respectively). The individualized alignment group also demonstrated more favourable changes in sagittal anatomy, with higher maintenance of postoperative anterior femoral offset within 1 mm (54.1% vs. 33.9%, P = 0.026) and posterior condylar offset within 1 mm and 2 mm (44.3% vs. 25.4%, p = 0.031,73.8% vs. 50.8%, p = 0.010, respectively). Although slight improvement in the Hospital for Special Surgery Knee Score (HSS) at three months was observed (P = 0.045), it did not reach a minimal clinically important difference. CONCLUSION: Individualized tailoring of femoral sagittal alignment in robotic-assisted total knee arthroplasty (TKA) enhances prosthetic alignment and anatomical restoration, suggesting potential improvements in postoperative outcomes.

Involvement of the gut microbiota in the metabolic phenotypes of two sympatric gerbils.

Temporal niche partitioning is a crucial strategy for sympatric species to avoid predation and competition for habitat space and food resources. This study investigated the effect of the gut microbiota on the metabolic rhythms of two sympatric gerbil species (Meriones unguiculatus and Meriones meridianus) to test the hypothesis that the oscillatory patterns of microbiota may not fully mirror those of the host's metabolism. Experiment 1 compared the circadian metabolic and gut microbiota rhythms of M. unguiculatus (n = 12) and M. meridianus (n = 12) and measured the subjects' body temperatures and environmental temperature preferences. In Experiment 2.1, six M. meridianus gerbils were treated with antibiotics, and in Experiment 2.2, 21 M. unguiculatus gerbils (seven per treatment) were randomly gavaged with saline or a gut microbiota suspension from either M. unguiculatus or M. meridianus; their metabolic rhythms were subsequently measured. The results showed that the two gerbils had different metabolic phenotypes that determined activity heterogeneity and contributed to their coexistence. The relative abundances of Bacteroidetes, Actinobacteria, and Cyanobacteria in M. meridianus varied rhythmically in parallel with the daily metabolic rate, which was significantly higher at night than during the day. The rhythm of the metabolic rate was not noticeable in M. unguiculatus. However, in M.unguiculatus, the relative abundances of Firmicutes, Bacteroidetes, Proteobacteria, and Verrucomicrobia were significantly higher during the day than at night, while Cyanobacteria exhibited the opposite pattern. Antibiotic treatment significantly weakened the metabolic rhythms of M. meridianus, and the circadian rhythms slowly recovered after stopping antibiotic gavage. However, after transplanting M. meridianus' gut microbiota into M. unguiculatus, the metabolic rate of M. unguiculatus was not significantly different from that of the control groups. Our hypothesis was partly supported: the microbiota was only partially involved in regulating the metabolic rhythms of gerbils, and other factors could compensate for the effect of the gut microbiota on host metabolic rhythms. This finding underscores the complexity of host-microbiota interactions and highlights the need for further exploration into the multifaceted mechanisms governing host metabolic regulation.

Single-cell sequencing and multiple machine learning algorithms to identify key T-cell differentiation gene for progression of NAFLD cirrhosis to hepatocellular carcinoma.

Introduction: Hepatocellular carcinoma (HCC), which is closely associated with chronicinflammation, is the most common liver cancer and primarily involves dysregulated immune responses in the precancerous microenvironment. Currently, most studies have been limited to HCC incidence. However, the immunopathogenic mechanisms underlying precancerous lesions remain unknown. Methods: We obtained single-cell sequencing data (GSE136103) from two nonalcoholic fatty liver disease (NAFLD) cirrhosis samples and five healthy samples. Using pseudo-time analysis, we systematically identified five different T-cell differentiation states. Ten machine-learning algorithms were used in 81 combinations to integrate the frameworks and establish the best T-cell differentiation-related prognostic signature in a multi-cohort bulk transcriptome analysis. Results: LDHA was considered a core gene, and the results were validated using multiple external datasets. In addition, we validated LDHA expression using immunohistochemistry and flow cytometry. Conclusion: LDHA is a crucial marker gene in T cells for the progression of NAFLD cirrhosis to HCC.

A comprehensive meta-analysis on the association of SGLT2is and GLP-1RAs with vascular diseases, digestive diseases and fractures.

AIM: Sodium-glucose cotransporter-2 inhibitors (SGLT2is) and glucagon-like peptide 1 receptor agonists (GLP-1RAs) are two new classes of antidiabetic agents. We aimed to evaluate the association between these two drug classes and risk of various vascular diseases, digestive diseases and fractures. METHODS: Large randomized trials of SGLT2is and GLP-1RAs were included. Outcomes of interest were the various serious adverse events related to vascular diseases, digestive diseases and fractures. We performed meta-analyses using synthesize risk ratio (RR) and 95% confidence interval (CI) as effect size. RESULTS: We included 27 large trials. SGLT2is had significant association with less hypertension (RR 0.70, 95% CI 0.54-0.91), hypertensive crisis (RR 0.63, 95% CI 0.47-0.84), varicose vein (RR 0.34, 95% CI 0.13-0.92), and vomiting (RR 0.55, 95% CI 0.31-0.97); but more spinal compression fracture (RR 1.73, 95% CI 1.02-2.92) and tibia fracture. GLP-1RAs had significant association with more deep vein thrombosis (RR 1.92, 95% CI 1.23-3.00), pancreatitis (RR 1.54, 95% CI 1.07-2.22), and cholecystitis acute (RR 1.51, 95% CI 1.08-2.09); but less rib fracture (RR 0.59, 95% CI 0.35-0.97). Sensitivity analyses suggested that our findings were robust. CONCLUSIONS: SGLT2is may have protective effects against specific vascular and digestive diseases, whereas they may increase the incidence of site-specific fractures (e.g., spinal compression fracture). GLP-1RAs may have protective effects against site-specific fractures (i.e., rib fracture), whereas they may increase the incidence of specific vascular and digestive diseases. These findings may help to make a choice between SGLT2is and GLP-1RAs in clinical practice.

Coordination cages integrated into swelling poly(ionic liquid)s for guest encapsulation and separation.

Coordination cages have been widely reported to bind a variety of guests, which are useful for chemical separation. Although the use of cages in the solid state benefits the recycling, the flexibility, dynamicity, and metal-ligand bond reversibility of solid-state cages are poor, preventing efficient guest encapsulation. Here we report a type of coordination cage-integrated solid materials that can be swelled into gel in water. The material is prepared through incorporation of an anionic FeII4L6 cage as the counterion of a cationic poly(ionic liquid) (MOC@PIL). The immobilized cages within MOC@PILs have been found to greatly affect the swelling ability of MOC@PILs and thus the mechanical properties. Importantly, upon swelling, the uptake of water provides an ideal microenvironment within the gels for the immobilized cages to dynamically move and flex that leads to excellent solution-level guest binding performances. This concept has enabled the use of MOC@PILs as efficient adsorbents for the removal of pollutants from water and for the purification of toluene and cyclohexane. Importantly, MOC@PILs can be regenerated through a deswelling strategy along with the recycling of the extracted guests.

Dysregulated innate immune signaling cooperates with RUNX1 mutations to transform an MDS-like disease to AML.

Dysregulated innate immune signaling is linked to preleukemic conditions and myeloid malignancies. However, it is unknown whether sustained innate immune signaling contributes to malignant transformation. Here we show that cell-intrinsic innate immune signaling driven by miR-146a deletion (miR-146aKO), a commonly deleted gene in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), cooperates with mutant RUNX1 (RUNX1mut) to initially induce marrow failure and features of MDS. However, miR-146aKO hematopoietic stem and/or progenitor cells (HSPCs) expressing RUNX1mut eventually progress to a fatal AML. miR-146aKO HSPCs exhaust during serial transplantation, while expression of RUNX1mut restored their hematopoietic cell function. Thus, HSPCs exhibiting dysregulated innate immune signaling require a second hit to develop AML. Inhibiting the dysregulated innate immune pathways with a TRAF6-UBE2N inhibitor suppressed leukemic miR-146aKO/RUNX1mut HSPCs, highlighting the necessity of TRAF6-dependent cell-intrinsic innate immune signaling in initiating and maintaining AML. These findings underscore the critical role of dysregulated cell-intrinsic innate immune signaling in driving preleukemic cells toward AML progression.

The function of brown adipose tissue at different sites of the body in Brandt's voles during cold acclimation.

Ambient temperatures have great impacts on thermoregulation of small mammals. Brown adipose tissue (BAT), an obligative thermogenic tissue for small mammals, is localized not only in the interscapular depot (iBAT), but also in supraclavicular, infra/subscapular, cervical, paravertebral, and periaortic depots. The iBAT is known for its cold-induced thermogenesis, however, less has been paid attention to the function of BAT at other sites. Here, we investigated the function of BAT at different sites of the body during cold acclimation in a small rodent species. As expected, Brandt's voles (Lasiopodomys brandtii) consumed more food and reduced the body mass gain when they were exposed to cold. The voles increased resting metabolic rate and maintained a relatively lower body temperature in the cold (36.5 ± 0.27 °C) compared to those in the warm condition (37.1 ± 0.36 °C). During cold acclimation, the uncoupling protein 1 (UCP1) increased in aBAT (axillary), cBAT (anterior cervical), iBAT (interscapular), nBAT (supraclavicular), and sBAT (suprascapular). The levels of proliferating cell nuclear antigen (PCNA), a marker for cell proliferation, were higher in cBAT and iBAT in the cold than in the warm group. The pAMPK/AMPK and pCREB/CREB were increased in cBAT and iBAT during cold acclimation, respectively. These data indicate that these different sites of BAT play the cold-induced thermogenic function for small mammals.

Boldness suppresses hoarding behavior in food hoarding season and reduces over-wintering survival in a social rodent.

The "pace-of-life" syndrome (POLS) framework can encompass multiple personality axes that drive important functional behaviors (e.g., foraging behavior) and that co-vary with multiple life history traits. Food hoarding is an adaptive behavior important for an animal's ability to adapt to seasonal fluctuations in food availability. However, the empirical evidence for the relationships between animal personality and hoarding behavior remains unclear, including its fitness consequences in the POLS framework. In this study, the Mongolian gerbil (Meriones unguiculatus), a social rodent, was used as a model system to investigate how boldness or shyness is associated with food hoarding strategies during the food hoarding season and their impact on over-winter survival and reproduction at both individual and group levels. The results of this study showed that, compared with shy gerbils, bold gerbils had a lower effort foraging strategy during the food hoarding season and exhibited lower over-winter survival rates. However, bold-shy personality differences had no effect on over-winter reproduction. These findings suggest that the personality is a crucial factor influencing the foraging strategy during the food hoarding season in Mongolian gerbils. Personality may be related to energy states or the reaction to environmental changes (e.g., predation risk and food availability) in bold or shy social animals. These results reflect animal life history trade-offs between current versus future reproduction and reproduction versus self-maintenance, thereby helping Mongolian gerbils in adapting to seasonal fluctuations in their habitat.

Derlin-1 promotes diet-induced non-alcoholic fatty liver disease via increasing RIPK3-mediated necroptosis.

BACKGROUND & AIMS: Unrestricted endoplasmic reticulum (ER) stress and the continuous activation of ER associated protein degradation (ERAD) pathway might lead to the aggravation of non-alcoholic steatohepatitis (NASH). Derlin-1 has been considered to be an integral part of the ERAD pathway, which is involved in the regulation of the transport and excretion of protein degradation products within ER. However, the regulatory role and mechanism of Derlin-1 in NASH remains unclear. METHODS: The expression of Derlin-1 was firstly detected in the liver of normal and NASH animal model and patient. Then, western diet (WD)-induced NASH mice were administrated with the lentivirus-mediated Derlin-1 knockdown or overexpression. Finally, RIPK3 knockout mice were used to explore the mechanism. The liver injury, hepatic steatosis, inflammation, and fibrosis as well as ER stress signal pathway were evaluated. RESULTS: The levels of Derlin-1 were significantly elevated in the liver of WD-fed mice and NASH patients when compared to the control group. Furthermore, Derlin-1 knockdown attenuated WD-induced liver injury, lipid accumulation, inflammatory response, and fibrosis. Conversely, overexpression of Derlin-1 presented the completely opposite results. Mechanistically, Derlin-1 enhanced ER stress pathways and led to necroptosis, and RIPK3 knockout dramatically reduced Derlin-1 expression and reversed the progression of NASH aggravated by Derlin-1. CONCLUSIONS: Notably, Derlin-1 is a critical modulator in NASH. It may accelerate the progression of NASH by regulating the activation of the ERAD pathway and further aggravating the ER stress, which might be involved in RIPK3-mediated necroptosis. Therefore, targeting Derlin-1 as a novel intervention point holds the potential to delay or even reverse NASH.

Metal-organic cages for gas adsorption and separation.

The unique high surface area and tunable cavity size endow metal-organic cages (MOCs) with superior performance and broad application in gas adsorption and separation. Over the past three decades, for instance, numerous MOCs have been widely explored in adsorbing diverse types of gas including energy gases, greenhouse gases, toxic gases, noble gases, etc. To gain a better understanding of the structure-performance relationships, great endeavors have been devoted to ligand design, metal node regulation, active metal site construction, cavity size adjustment, and function-oriented ligand modification, thus opening up routes toward rationally designed MOCs with enhanced capabilities. Focusing on the unveiled structure-performance relationships of MOCs towards target gas molecules, this review consists of two parts, gas adsorption and gas separation, which are discussed separately. Each part discusses the cage assembly process, gas adsorption strategies, host-guest chemistry, and adsorption properties. Finally, we briefly overviewed the challenges and future directions in the rational development of MOC-based sorbents for application in challenging gas adsorption and separation, including the development of high adsorption capacity MOCs oriented by adsorbability and the development of highly selective adsorption MOCs oriented by separation performance.

Hypothalamic Neuromodulation of Hypothermia in Domestic Animals.

When an organism detects decreases in their core body temperature, the hypothalamus, the main thermoregulatory center, triggers compensatory responses. These responses include vasomotor changes to prevent heat loss and physiological mechanisms (e.g., shivering and non-shivering thermogenesis) for heat production. Both types of changes require the participation of peripheral thermoreceptors, afferent signaling to the spinal cord and hypothalamus, and efferent pathways to motor and/or sympathetic neurons. The present review aims to analyze the scientific evidence of the hypothalamic control of hypothermia and the central and peripheral changes that are triggered in domestic animals.

Increased knee torsional misalignment associated with femoral torsion is related to non-contact anterior cruciate ligament injury: a case-control study.

BACKGROUND: Altered axial biomechanics of the knee are recognized as a risk factor for non-contact anterior cruciate ligament (ACL) injury. However, the relationship of knee and segmental torsion to non-contact ACL and combined anterolateral ligament (ALL) injury is unclear. This study aims to determine the relationship of knee and segmental torsion to non-contact ACL injury and to explore their relationship with ALL injuries. METHODS: We divided 122 patients with arthroscopically confirmed non-contact ACL injuries into an ACL injury group (isolated ACL injury, 63 patients) and an ACL + ALL injury group (ACL combined with ALL injury,59 patients). Additionally, 90 normal patients with similar age, gender and body mass index (BMI) were matched as a control group. The tibial tubercle-trochlear groove (TT-TG) distance, distal femoral torsion (DFT), posterior femoral condylar torsion (PFCT) and proximal tibial torsion (PTT) were measured using magnetic resonance imaging (MRI). We assessed the differences between the groups using an independent samples t test and utilized receiver operating characteristic (ROC) curves to determine the cut-off value for the increased risk of ACL injury. RESULTS: In patients with ACL injury, the measurements of the TT-TG (11.8 ± 3.1 mm), DFT (7.7° ± 3.5°) and PFCT (3.6° ± 1.3°) were significantly higher compared to the control group (9.1 ± 2.4 mm, 6.3° ± 2.7° and 2.8° ± 1.3°, respectively; P < 0.05), but the PTT did not differ between the two groups. The TT-TG, DFT and PFCT were not significantly larger in patients combined with ALL injury. ROC curve analysis revealed ACL injury is associated with TT-TG, DFT and PFCT. CONCLUSIONS: Knee torsional alignment is associated with ACL injury, predominantly in the distal femur rather than the proximal tibia. However, its correlation with ALL injury remains unclear. These findings may help identify patients at high risk for non-contact ACL injury and inform the development of targeted prevention and treatment strategies.

Multi-parametric assessment of cardiac magnetic resonance images to distinguish myocardial infarctions: A tensor-based radiomics feature.

AIM: This study assessed the myocardial infarction (MI) using a novel fusion approach (multi-flavored or tensor-based) of multi-parametric cardiac magnetic resonance imaging (CMRI) at four sequences; T1-weighted (T1W) in the axial plane, sense-balanced turbo field echo (sBTFE) in the axial plane, late gadolinium enhancement of heart short axis (LGE-SA) in the sagittal plane, and four-chamber views of LGE (LGE-4CH) in the axial plane. METHODS: After considering the inclusion and exclusion criteria, 115 patients (83 with MI diagnosis and 32 as healthy control patients), were included in the present study. Radiomic features were extracted from the whole left ventricular myocardium (LVM). Feature selection methods were Least Absolute Shrinkage and Selection Operator (Lasso), Minimum Redundancy Maximum Relevance (MRMR), Chi-Square (Chi2), Analysis of Variance (Anova), Recursive Feature Elimination (RFE), and SelectPersentile. The classification methods were Support Vector Machine (SVM), Logistic Regression (LR), and Random Forest (RF). Different metrics, including receiver operating characteristic curve (AUC), accuracy, F1- score, precision, sensitivity, and specificity were calculated for radiomic features extracted from CMR images using stratified five-fold cross-validation. RESULTS: For the MI detection, Lasso (as the feature selection) and RF/LR (as the classifiers) in sBTFE sequences had the best performance (AUC: 0.97). All features and classifiers of T1 + sBTFE sequences with the weighted method (as the fused image), had a good performance (AUC: 0.97). In addition, the results of the evaluated metrics, especially mean AUC and accuracy for all models, determined that the T1 + sBTFE-weighted fused method had strong predictive performance (AUC: 0.93±0.05; accuracy: 0.93±0.04), followed by T1 + sBTFE-PCA fused method (AUC: 0.85±0.06; accuracy: 0.84±0.06). CONCLUSION: Our selected CMRI sequences demonstrated that radiomics analysis enables to detection of MI accurately. Among the investigated sequences, the T1 + sBTFE-weighted fused method with the highest AUC and accuracy values was chosen as the best technique for MI detection.

The function role of HIGD1A in nonalcoholic steatohepatitis from chronic hepatitis B.

BACKGROUND: Accompanied by the growing prevalence of nonalcoholic fatty liver disease (NAFLD), the coexistence of chronic hepatitis B (CHB) and NAFLD has increased. In the context of CHB, there is limited understanding of the factors that influence the development of NASH. METHODS: We enrolled CHB combined NAFLD patients who had liver biopsy and divided them to NASH vs. non-NASH groups. A whole transcriptome chip was used to examine the expression profiles of long noncoding RNAs (lncRNAs) and mRNA in biopsied liver tissues. The function analysis of HIGD1A were performed. We knocked down or overexpressed HIGD1A in HepG2.2.15 cells by transient transfection of siRNA-HIGD1A or pcDNA-HIGD1A. In vivo investigations were conducted using hepatitis B virus (HBV) transgenic mice. RESULTS: In 65 patients with CHB and NAFLD, 28 were patients with NASH, and 37 were those without NASH. After screening 582 differentially expressed mRNAs, GO analysis revealed differentially expressed mRNAs acting on nicotinamide adenine dinucleotide phosphate (NADPH), which influenced redox enzyme activity. KEGG analysis also shown that they were involved in the NAFLD signaling pathway. The function analysis revealed that HIGD1A was associated with the mitochondrion. Then, both in vivo and in vitro CHB model, HIGD1A was significantly higher in the NASH group than in the non-NASH group. HIGD1A knockdown impaired mitochondrial transmembrane potential and induced cell apoptosis in HepG2.2.15 cells added oleic acid and palmitate. On the contrary, hepatic HIGD1A overexpression ameliorated free fatty acids-induced apoptosis and oxidative stress. Furthermore, HIGD1A reduced reactive oxygen species (ROS) level by increasing glutathione (GSH) expression, but Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/Acetyl-CoA carboxylase (ACC) pathway was not involved. CONCLUSION: Both in vivo and in vitro CHB model, an upward trend of HIGD1A was observed in the NASH-related inflammatory response. HIGDIA played a protective role in cells against oxidative stress. Our data suggested that HIGD1A may be a positive regulator of NASH within the CHB context.