We present a case of 50 year old male patient with coexistence of Pneumothorax and Chilaiditi sign. Chilaiditi sign is an incidental radiographic finding of a usually asymptomatic condition in which a part of intestine is located between the liver and diaphragm; however, the term "Chilaiditi syndrome" is used for symptomatic hepatodiaphragmatic interposition. The patient had no symptoms of abdominal pain, constipation, diarrhea, or emesis. Incidentally, Chilaiditi sign was diagnosed on chest radiography. Pneumothorax is defined as air in the pleural space. Pneumothoraces are classified as spontaneous or traumatic. Spontaneous pneumothorax is labelled as primary when no underlying lung disease is present, or secondary, when it is associated with pre-existing lung disease. Our case is the rare in the literature indicating the coexistence of Chilaiditi sign and pneumothorax.
Chest Pain ; Chilaiditi Syndrome ; complications ; diagnosis ; Dyspnea ; Humans ; Male ; Middle Aged ; Pneumothorax ; complications ; diagnosis

OBJECTIVE: The BCL2 family proteins are critical mediators of cellular apoptosis and, as such, have been implicated as determinants of cancer cell chemo-sensitivity. Recently, it has been demonstrated that the phosphorylation status of the BCL2 antagonist of cell death (BAD) protein may influence ovarian cancer (OVCA) cell sensitivity to cisplatin. Here, we sought to evaluate how kinase and phosphatase components of the BAD apoptosis pathway influence OVCA chemo-sensitivity. METHODS: Protein levels of cyclin-dependent kinase 1 (CDK1) and protein phosphatase 2C (PP2C) were measured by immunofluorescence in a series of 64 primary advanced-stage serous OVCA patient samples. In parallel, levels of cAMP-dependent protein kinase (PKA), AKT, and PP2C were quantified by Western blot analysis in paired mother/daughter platinum-sensitive/resistant OVCA cell lines (A2008/C13, A2780S/A2780CP, Chi/ChiR). BAD pathway kinase CDK1 was depleted using siRNA transfection, and the influence on BAD phosphorylation and cisplatin-induced apoptosis was evaluated. RESULTS: OVCA patient samples that demonstrated complete responses to primary platinum-based therapy demonstrated 4-fold higher CDK1 (p<0.0001) and 2-fold lower PP2C (p=0.14) protein levels than samples that demonstrated incomplete responses. Protein levels of PP2C were lower in the platinum-resistant versus that shown in the platinum-sensitive OVCA cell line sub-clones. Levels of PKA were higher in all platinum-resistant than in platinum-sensitive OVCA cell line sub-clones. Selective siRNA depletion of CDK1 increased sensitivity to cisplatin-induced apoptosis (p<0.002). CONCLUSION: BAD pathway kinases and phosphatases, including CDK1 and PP2C, are associated with OVCA sensitivity to platinum and may represent therapeutic opportunities to enhance cytotoxic efficacy.
Apoptosis ; Blotting, Western ; CDC2 Protein Kinase ; Cell Death ; Cell Line ; Cisplatin ; Cyclic AMP-Dependent Protein Kinases ; Fluorescent Antibody Technique ; Humans ; Ovarian Neoplasms ; Phosphoprotein Phosphatases ; Phosphoric Monoester Hydrolases ; Phosphorylation ; Phosphotransferases ; Platinum ; Proteins ; RNA, Small Interfering ; Transfection