Skeletal metastasis is a frequent complication of cancer resulting in significant morbidity as well as mortality. We highlight a case of a 73-year old gentleman with metastatic squamous cell carcinoma of the sternum. He denied dysphagia, shortness of breath, goitre, and presence of chronic non-healing ulcer. He was anaemic and carcinoembryonic antigen (CEA) was 18.7. Chest radiograph on lateral view showed a suspicious cortical irregularity. Computed tomography (CT) scan of thorax revealed an aggressive sternal lesion with soft tissue component. Ultrasound guided biopsy was performed and the biopsy was consistent with metastatic squamous cell carcinoma. Squamous cell carcinoma has a predilection to metastasize via haematogenous spread, but direct extension of tumour into the bone is not frequently seen. Finding the primary cause is utmost importance either via imaging modalities or invasive procedures. Isolated secondary lesion is extremely rare but unfortunate among defaulters. We discuss its diagnostic work-up and treatment options conserved to manage this condition.
Developing experimental models to study ischemic heart disease is necessary for understanding of biological mechanisms to improve the therapeutic approaches for restoring cardiomyocytes function following injury. The aim of this study was to develop an in vitro hypoxic/re-oxygenation model of ischemia using primary human cardiomyocytes (HCM) and define subsequent cytotoxic effects. HCM were cultured in serum and glucose free medium in hypoxic condition with 1% O2 ranging from 30 min to 12 h. The optimal hypoxic exposure time was determined using Hypoxia Inducible Factor 1α (HIF-1α) as the hypoxic marker. Subsequently, the cells were moved to normoxic condition for 3, 6 and 9 h to replicate the re-oxygenation phase. Optimal period of hypoxic/re-oxygenation was determined based on 50% mitochondrial injury via 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide assay and cytotoxicity via lactate dehydrogenase (LDH) assay. It was found that the number of cells expressing HIF-1α increased with hypoxic time and 3 h was sufficient to stimulate the expression of this marker in all the cells. Upon re-oxygenation, mitochondrial activity reduced significantly whereas the cytotoxicity increased significantly with time. Six hours of re-oxygenation was optimal to induce reversible cell injury. The injury became irreversible after 9 h as indicated by > 60% LDH leakage compared to the control group cultured in normal condition. Under optimized hypoxic reoxygenation experimental conditions, mesenchymal stem cells formed nanotube with ischemic HCM and facilitated transfer of mitochondria suggesting the feasibility of using this as a model system to study molecular mechanisms of myocardial injury and rescue.