An unusual case of urinothorax after percutaneous nephrostolithotomy.

We present here a case of severe dyspnea after a percutaneous nephrostolithotomy, which resulted from an urinothorax, an uncommon complication of posturological procedures. Chest X-ray indicated a significant left pleural effusion, and a diagnosis was confirmed by the pleural fluid analysis. Chest tube placement did not improve the patient's clinical status; retrograde pyelogram was performed, and a stent was placed in the left ureter orifice where a narrowing was discovered. Correcting the cause of the urinothorax is the key in such cases of severe pleural effusions as seen in our case.

Differential effects of hypoxia and acidosis on p53 expression, repair of UVC-damaged DNA and viability after UVC in normal and tumor-derived human cells.

Hypoxia and low pH are commonly associated with the tumor microenvironment. We have examined the effects of hypoxia alone (HA) and hypoxia coupled to low pH (HApH) on p53 expression, nucleotide excision repair (NER) and cellular sensitivity to UVC in normal human fibroblasts and human tumor cells. p53 expression was measured using Western blotting, NER using host cell reactivation (HCR) of a UV-damaged reporter gene and cell sensitivity using the MTT assay. HApH resulted in a transient increase in p53 expression in normal fibroblasts at 6h and in tumor cells at 6-18h. In normal fibroblasts HApH resulted in a transient increase in HCR at early times (12-24h) and a concomitant decrease in UVC sensitivity. In contrast, for the tumor-derived cells, the increased HCR of the UVC-treated reporter gene was delayed (36-40h) and UVC sensitivity increased or remained the same after HApH treatment. These results suggest that early upregulation of p53 and increased repair of UV-damaged DNA after HApH treatment is required for increased cell viability after UVC. HA treatment alone also resulted in a transient increase in HCR of the UVC-damaged reporter gene at early times (12-24h) in normal fibroblasts and a delayed increase (36-40h) in the tumor-derived cells. However, the enhanced p53 expression was less or even absent for treatment with HA alone, and HA had no significant affect on cell viability after UVC for any of the cell lines. These results indicate a different cellular response following HApH compared to HA alone.

Increased expression of p53 enhances transcription-coupled repair and global genomic repair of a UVC-damaged reporter gene in human cells.

Ultraviolet (UV) light-induced DNA damage is repaired by nucleotide excision repair, which is divided into two sub-pathways: global genome repair (GGR) and transcription-coupled repair (TCR). While it is well established that the GGR pathway is dependent on the p53 tumour suppressor protein in human cells, both p53-dependent and p53-independent pathways have been reported for TCR. In the present work, we investigated the role of p53 in both GGR and TCR of a UVC-damaged reporter gene in human fibroblasts. We employed a non-replicating recombinant human adenovirus, AdCA17lacZ, that can efficiently infect human fibroblasts and express the beta-galactosidase (beta-gal) reporter gene under the control of the human cytomegalovirus promoter. We examined host cell reactivation (HCR) of beta-gal expression for the UVC-treated reporter construct in normal fibroblasts and in xeroderma pigmentosum (XP) and Cockayne syndrome (CS) fibroblasts deficient in GGR, TCR, or both. HCR was examined in fibroblasts that had been pre-infected with Ad5p53wt, which expresses wild-type p53, or a control adenovirus, AdCA18luc, which expresses the luciferase gene. We show that increased expression of p53 results in enhanced HCR of the UVC-damaged reporter gene in both untreated and UVC-treated cells for normal, CS-B (TCR-deficient), and XP-C (GGR-deficient), but not XP-A (TCR- and GGR-deficient) fibroblasts. These results indicate an involvement of p53 in both TCR and GGR of the UV-damaged reporter gene in human cells.