Effect of glaucoma drainage implant surgery on corneal topography: a prospective study.

Purpose: To study the effect of glaucoma drainage implant (GDI) surgery on corneal topography during the first postoperative year.

Methods: Twenty-one adult glaucoma patients were implanted with a Molteno3 or a Baerveldt 250 GDI. Corneal topography measurements were taken preoperatively and at 6 and 12 months after surgery.

Intravenous hypertonic saline to reduce intraocular pressure.

Purpose: To quantitate the effect of intravenous hypertonic saline (IVHTS) injection on elevated intraocular pressure (IOP).

Methods:   Nineteen patients (median age, 65 years; range, 41-84 years) with glaucoma and an IOP 30 mmHg or higher were recruited. A bolus of IVHTS (sodium chloride concentration 23.

Activation of p53 in cervical cancer cells by human papillomavirus E6 RNA interference is transient, but can be sustained by inhibiting endogenous nuclear export-dependent p53 antagonists.

p53 is degraded in cervical cancer cells by the human papillomavirus E6 and can be stabilized with short interfering RNA (siRNA) molecules targeting E6 mRNA. In this in vitro study, we show that E6 siRNA-induced p53 activation is transient in HeLa cervical cancer cells despite continuous suppression of E6 mRNA; activation can be sustained if the endogenous p53 antagonists COP1, MDM2, Pirh2, and c-Jun-NH(2)-kinase are also targeted by siRNAs or by inhibiting the nuclear export of p53 with leptomycin B. The direct targeting of any one of these four cellular p53 antagonists had no effect on p53 activity when E6 was intact, but inhibited the fading off of E6 siRNA-induced p53 activation in nonstress conditions.

DNA topoisomerase I is a cofactor for c-Jun in the regulation of epidermal growth factor receptor expression and cancer cell proliferation.

DNA topoisomerase I (Topo I) is a molecular target for the anticancer agent topotecan in the treatment of small cell lung cancer and ovarian carcinomas. However, the molecular mechanisms by which topotecan treatment inhibits cancer cell proliferation are unclear. We describe here the identification of Topo I as a novel endogenous interaction partner for transcription factor c-Jun.

Chemotherapy compounds in cervical cancer cells primed by reconstitution of p53 function after short interfering RNA-mediated degradation of human papillomavirus 18 E6 mRNA: opposite effect of siRNA in combination with different drugs.

Constant expression of E6 and E7 mRNA by high-risk human papillomaviruses (HPV) abrogates p53 and retinoblastoma protein function, respectively, and is essential for the development of cervical cancer. Despite E6, some chemotherapy drugs can stabilize p53 in cervical cancer cells. It is not known how chemotherapy-induced p53 activation and cytotoxicity are affected when the amount of E6 mRNA is decreased before the drug treatment.

The cytotoxicity of chemotherapy drugs varies in cervical cancer cells depending on the p53 status.

Metastatic cervical cancer remains a clinical problem. The development of more efficient treatment modalities and the optimal use of chemo- and radiotherapy require better understanding of their impact on regulation of cell survival and apoptosis, but the issue is insufficiently explored. Human papillomavirus (HPV) E6 protein is present in nearly all cervical cancers, targeting the p53 tumor suppressor protein for degradation.

Chemoradiation of cervical cancer cells: targeting human papillomavirus E6 and p53 leads to either augmented or attenuated apoptosis depending on the platinum carrier ligand.

Recent clinical trials comparing concurrent chemotherapy and radiation with radiation alone in cervical cancer have shown that chemoradiation reduces the risk of death by 30-50%. Despite the clinical success, treatment responses at the cellular level are still inadequately explored. A key event in cervical carcinogenesis is the disruption of p53 tumor suppressor pathway by human papillomavirus (HPV) E6 oncogene.