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To explore the relationship between insulin-like growth factor (IGF)-1R expression and the pathological progression of Kashin-Beck disease (KBD).
KBD cartilage samples were collected from 5 patients. Additionally, T-2 toxin was administered to rats fed a selenium (Se)-deficient diet, and their knee joints were collected. Human C28/I2 chondrocytes and mouse hypertrophic ATDC5 chondrocytes were cultured
and treated with T-2 toxin and Se supplementation. Subsequently, the cultured human and mouse chondrocytes were treated with the IGF-1R inhibitor, picropodophyllin. Chondrocyte death and caspase-3 activity were analyzed using flow cytometry and a specific kit, respectively. Protein and mRNA expression levels of IGF-1R and matrix molecules were measured using immunohistochemistry, western blotting, and quantitative real-time reverse transcription-polymerase chain reaction analyses.
The cartilages from patients with KBD and T-2 toxin-treated rats on a Se-deficient diet showed significantly decreased expression of IGF-1R compared to cartilages from controls. find more T-2 toxin decreased IGF-1R mRNA and protein levels in both C28/I2 and hypertrophic ATDC5 chondrocytes in a dose-dependent manner; however, Se supplementation reduced the decrease of IGF-1R induced by T-2 toxin. Furthermore, inhibition of IGF-1R resulted in chondrocyte death of C28/I2 and hypertrophic ATDC5 chondrocytes, as well as decreased type II collagen expression and increased MMP-13 expression at the mRNA and protein levels.
Downregulation of IGF-1R was associated with KBD cartilage destruction. Therefore, inhibition of IGF-1R may mediate chondrocyte death and extracellular matrix degeneration related to the pathological progression of KBD.
Downregulation of IGF-1R was associated with KBD cartilage destruction. Therefore, inhibition of IGF-1R may mediate chondrocyte death and extracellular matrix degeneration related to the pathological progression of KBD.Chondromas are benign cartilaginous tumors that frequently occur in the long bones, pelvis, sternum, ribs, and scapula. They seldom develop in the head and neck region, and there have been rare reports of them arising in the nasal septum. Although the mainstay of management is surgery, surgical treatment strategies vary depending on the size, location, and extent of the disease. Herein, we describe a case of huge chondroma originated from the anterior nasal septum, which was completely removed by endoscopic septoplasty approach thorough modified Killian incision.
In this paper, we studied several serum clinical chemistry tests of cardiovascular disease (CVD), iron deficiency anemia, liver and kidney disorders in migraine.
We first explored the association of 22 clinical chemistry tests with migraine risk in 697 migraine patients and 2722 controls. To validate and interpret association findings, cross-trait genetic analyses were conducted utilising genome-wide association study (GWAS) data comprising 23,986 to 452,264 individuals.
Significant associations with migraine risk were identified for biomarkers of CVD risk, iron deficiency and liver dysfunction (odds ratios = 0.86-1.21; 1 × 10
<
< 3 × 10
). Results from cross-trait genetic analyses corroborate the significant biomarker associations and indicate their relationship with migraine is more consistent with biological pleiotropy than causality. For example, association and genetic overlap between a lower level of HDL-C and increased migraine risk are due to shared biology rather than a causal relationship. Furthermore, additional genetic analyses revealed shared genetics among migraine, the clinical chemistry tests, and heart problems and iron deficiency anemia, but not liver disease.
These findings highlight common biological mechanisms underlying migraine, heart problems and iron deficiency anemia and provide support for their investigation in the development of novel therapeutic and dietary interventions.
These findings highlight common biological mechanisms underlying migraine, heart problems and iron deficiency anemia and provide support for their investigation in the development of novel therapeutic and dietary interventions.Gastrointestinal ischemia may be presented as a complication associated with late shock detection in patients in critical condition. Prolonged ischemia can cause mucosal integrity to lose its barrier function, triggering alterations that can induce organ dysfunction and lead to death. Electrical impedance spectroscopy has been proposed to identify early alteration in ischemia-induced gastric mucosa in this type of patients. This work analyzed changes in impedance parameters, and tissue and molecular alterations that allow us to identify the time of ischemia in which the gastric mucosa still maintains its barrier function. The animals were randomly distributed in four groups Control, Ischemia 60, 90, and 120 min. Impedance parameters were measured and predictive values were determined to categorize the degree of injury using a receiver operating characteristic curve. Markers of inflammatory process and apoptosis (iNOS, TNFα, COX-2, and Caspase-3) were analyzed. The largest increase in impedance parameters occurred in the ischemia 90 and 120 min groups, with resistance at low frequencies (RL) and reactance at high frequencies (XH) being the most related to damage, allowing prediction of the occurrence of reversible and irreversible tissue damage. Histological analysis and apoptosis assay showed progressive mucosal deterioration with irreversible damage (p less then 0.001) starting from 90 min of ischemia. Furthermore, a significant increase in the expression of iNOS, TNFα, and COX-2 was identified in addition to apoptosis in the gastric mucosa starting from 90 min of ischemia. Tissue damage generated by an ischemia time greater than 60 min induces loss of barrier function in the gastric mucosa.
The impact of body mass index (BMI) on trauma severity after ground-level falls (GLF) is currently unclear. This study aimed to examine the associations between BMI, injuries, and outcomes after GLF.
All patients ≥16years of age injured by GLF were queried from the TQIP database (2013-2017). Exclusions were transfers, emergency department death, AIS 6 in any region, and missing data. Body mass index defined study groups Underweight (BMI<18.5), Normal (BMI 18.5-24.9), Overweight (25.0-29.9), and Obese (≥30).
After exclusions, 131570 patients remained for analysis. Most patients had a normal BMI (n = 58503, 44%). Median ISS was 9 [IQR 9-10] in all groups. The Obese group had significantly lower rates of fractures than the Normal group, particularly femur fractures (53% vs. 64%,
< .001), but required orthopedic surgical intervention more frequently (45% vs. 41%,
< .001). On multivariate analysis, being overweight was protective against mortality (OR .881,
= .005), while obesity was not associated with mortality (OR 1.