Knee osteoarthritis (OA) is one of the most prevalent disorders in elderly population. Among various therapeutic alternatives, we employed stromal vascular fraction (SVF), a heterogeneous cell population, to regenerate damaged knee cartilage. OA patients were classified on the basis of age, gender, body mass index (BMI), and x-ray-derived Kellgren–Lawrence (KL) grade. They were treated with SVF and followed-up for 24 months. Visual analogue scale (VAS) and Western Ontario and McMaster Universities Osteoarthritis (WOMAC) Index were used to determine treatment efficacy. Cartilage healing was assessed using the MRI-based Outerbridge score (OS) and evaluation of bone marrow edema (BME) lesions, while a placebo group was used as a control. Time- and KL-dependent changes were also monitored. We observed a decreasing trend in VAS score and WOMAC index in the SVF-treated group up to 24 months, as compared with the placebo group. Besides, a significant increase and decrease in Lysholm and OS, respectively, were observed in the treatment group. Compared with the values before treatment, the greatly reduced WOMAC scores of KL3 than KL2 groups at 24 months, indicate more improvement in the KL3 group. Highly decreased BME in the treated group was also noted. In conclusion, the SVF therapy is effective in the recovery of OA patients of KL3 grade in 24 months.

Recent years have witnessed an increased prevalence of knee osteoarthritis (KOA) among diabetes mellitus (DM) patients—conditions which might share common risk factors such as obesity and advanced aging. Therefore, we conducted dry-to-wet lab research approaches to assess the correlation of type 1 DM (T1DM) and type 2 DM (T2DM) with KOA among all age and genders of Taiwanese population. The strength of association (odds ratio: OR) was analyzed using a phenome-wide association study portal. Populations of 37,353 T1DM and 1,218,254 T2DM were included. We observed a significant association of KOA with T1DM (OR: 1.40 (1.33–1.47), p< 0.0001) and T2DM (OR: 2.75 (2.72–2.78), p< 0.0001). The association between T1DM and KOA among the obese (OR: 0.99 (0.54–1.67), p = 0.0477) was insignificant compared to the non-obese (OR: 1.40 (1.33–1.48), p < 0.0001). Interestingly, a higher association between T2DM and KOA among non-obese persons (OR: 2.75, (2.72–2.79), p < 0.0001) compared to the obese (OR: 1.71 (1.55–1.89), p < 0.0001) was noted. Further, histopathologic and Western blot studies of diabetic mice knee joints revealed enhanced carboxymethyl lysine (advanced glycation end product), matrix metalloproteinase-1, and reduced cartilage-specific proteins, including type II collagen (Col II), SOX9, and aggrecan (AGN), indicating deteriorated articular cartilage and proteoglycans. Results indicate that DM is strongly associated with KOA, and obesity may not be a confounding factor.

Cancer pathogenesis results from genetic alteration-induced high or low transcriptional programs, which become highly dependent on regulators of gene expression. However, their role in progressive regulation of non-small-cell lung cancer (NSCLC) and how these dependencies may offer opportunities for novel therapeutic options remain to be understood. Previously, we identified forkhead box F1 (FOXF1) as a reprogramming mediator which leads to stemnesss when mesenchymal stem cells fuse with lung cancer cells, and we now examine its effect on lung cancer through establishing lowly and highly expressing FOXF1 NSCLC engineered cell lines. Higher expression of FOXF1 was enabled in cell lines through lentiviral transduction, and their viability, proliferation, and anchorage-dependent growth was assessed. Flow cytometry and Western blot were used to analyze cellular percentage in cell-cycle phases and levels of cellular cyclins, respectively. In mice, tumorigenic behavior of FOXF1 was investigated. We found that FOXF1 was downregulated in lung cancer tissues and cancer cell lines. Cell proliferation and ability of migration, anchorage-independent growth, and transformation were inhibited in H441-FOXF1^H and H1299-FOXF1^H, with upregulated tumor suppressor p21 and suppressed cellular cyclins, leading to cell-cycle arrest at the gap 1 (G1) phase. H441-FOXF1^H and H1299-FOXF1^H injected mice showed reduced tumor size. Conclusively, highly expressing FOXF1 inhibited NSCLC growth via activating tumor suppressor p21 and G1 cell-cycle arrest, thus offering a potentially novel therapeutic strategy for lung cancer.

Schwannomas are benign and slow-growing peripheral nerve sheath neoplasms of Schwann cells. These are generally encountered in the neck, head, and flexor areas of the extremities. Even though many schwannomas are easily diagnosable, their variable morphology can occasionally create difficulty in diagnosis. In this study, we present a rare case of melanotic schwannoma of the sacrum, emphasizing the need for routine biopsy to understand the etiology. A 46-year-old man presented to the Department of Neurosurgery, Taipei Medical University Hospital, with buttock pain in the sacrum area for 1 year, which worsened in the last 1–2 months. The patient had no known history of trauma or malignancy. We evidenced an intradural extramedullary neurogenic tumor at the caudal end from S1 to S3. Histologic analysis revealed melanin deposition in the tumor cells. Round to oval tumor cells were positive for HMB-45 and S-100 proteins, suggestive of melanotic Schwannoma, which were removed by laminectomy. After 1 month, the tumor recurred and was further removed surgically. Conclusively, we observed the sacrum as an unusual anatomic site for the possible occurrence of melanotic schwannoma, especially in patients with no known history of trauma and malignancy. The possibility of melanotic schwannoma is very high. We hypothesize that melanotic schwannoma was possible because it occurred in the intradural and extramedullary regions of the spine. Hence, a routine biopsy should be performed to corroborate the exact cause and prevent incorrect presumptions.