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A glossa pinguinalis (L.) is recorded from Nathia Gali, Pakistan and redescribed in detail with special reference to its head appendages, venation of fore and hind wings, sex genitalia and diversity. [ABSTRACT FROM AUTHOR]

Objective. Progesterone (P4) has been implicated as a protective factor for ovarian and endometrial cancers, yet little is known about its mechanism of action. We have shown apoptosis in ovarian and endometrial cancer cells with high doses of P4. Increased generation of reactive oxygen species (ROS) and an altered redox status have long been observed in cancer cells. The goal of this study was to assess the effect of P4 on cell growth, ROS generation, oxidative stress markers, and the expression of antioxidant proteins. Methods. All experiments were performed in vitro using cancer cell lines. Cell proliferation was determined using MTS proliferation assay. Production of ROS in cells was measured with the ROS indicator dye, aminophenyl fluorescein. Alterations in expression of antioxidant and apoptotic proteins were assessed by Western blotting. Results. The exposure of ovarian and endometrial cancer cell cultures to various doses of P4 caused a dose-dependent decrease in cell viability and the activation of caspase-3. Levels of ROS, markers of oxidative stress, and antioxidant proteins were elevated in cancer cells compared to normal cells and a marked decrease in their expression was seen following P4 treatment. In cancer cells, ROS was elevated while p-53 expression was low. P4 exposure of cells resulted in increased p-53 and BAX and decreased BCL-2 expression. Conclusions. The data indicates that P4 has antioxidant effects. It alleviates ROS stress and causes apoptosis by upregulating proapoptotic (p-53 and BAX) and decreasing antiapoptotic (BCL-2) gene expression in cancer cells. These findings could have potential therapeutic implications. [ABSTRACT FROM AUTHOR]

Background: Reproductive hormones are associated with risk for epithelial ovarian cancer. To determine the effect of such hormones on the activation of interleukin 6 (IL-6)/STAT3 (signal transducer and activator of transcription-3) signaling, which may be involved in ovarian cancer, we investigated the status of STAT3, IL-6, and its receptor in immortalized human ovarian surface epithelial (HOSE) and ovarian cancer (OVCA) cell lines.Methods: Two immortalized HOSE cell lines and two OVCA cell lines were cultured with gonadotropins, sex steroid hormones, and/or IL-6, alone or with specific inhibitors or IL-6-neutralizing antibodies. Expression of IL-6, the IL-6 receptor alpha chain (IL-6Ralpha), and phosphorylated and unphosphorylated STAT3 messenger RNAs (mRNAs) and proteins in all cells was determined. Cell proliferation and soft-agar colony formation were assessed. STAT3 activity was investigated in OVCA cells transfected with a dominant negative STAT3 (Dn-STAT3), wild-type STAT3, or an empty control vector. All statistical tests were two-sided.Results: Levels of IL-6 mRNA and protein increased in all cells treated with follicle-stimulating hormone (FSH), luteinizing hormone (LH), 17beta-estradiol, or estrone but increased only in OVCA cells treated with testosterone and 5alpha-dihydrotestosterone. For all lines, IL-6 antibodies partially inhibited hormone-stimulated cell proliferation but completely inhibited IL-6-enhanced cell proliferation. IL-6 induced STAT3 phosphorylation and activation in HOSE cells; STAT3 was constitutively activated in OVCA cells. Higher levels of IL-6Ralpha and STAT3 transcription factors were observed in OVCA cells than in HOSE cells. After transfection, Dn-STAT3 suppressed endogenous STAT3 and inhibited all forms of IL-6-stimulated OVCA cell proliferation (OVCA 429 cells, P<.001; OVCA 432 cells, P<.006), whereas wild-type STAT3 enhanced HOSE cell proliferation (wild-type STAT3 at 0.5 microg/mL in HOSE 306 cells, P<.002; STAT3 at 1.0 microg/mL in HOSE 306 or both concentrations of wild-type STAT3 in HOSE 642 cells, P<.001).Conclusions: The IL-6/STAT3 signaling pathway may mediate FSH-, LH-, and estrogen-stimulated HOSE cell proliferation. Increased IL-6Ralpha expression and constitutive STAT3 activation may be associated with ovarian cancer. [ABSTRACT FROM AUTHOR]

Hymenia recurvalis (Fabr.) is recorded from Thatta (Coastal belt of Sindh), Pakistan and redescribed in detail with special reference to its head appendages, venation of fore and hind wings and male genitalia. [ABSTRACT FROM AUTHOR]

Initially, patients that respond to cisplatin (DDP) treatment later relapse and develop chemoresistance. Agents that enhance DDP effectiveness will have a significant impact on cancer treatment. We have shown pronounced inhibitory effects of the progesterone-calcitriol combination on endometrial and ovarian cancer cell growth. Here, we examined whether and how progesterone-calcitriol combination potentiates DDP anti-tumor effects in cancer cells. Ovarian and endometrial cancer cells treated with various concentrations of DDP showed a concentration-dependent decrease in cell proliferation. Concurrent treatment of cells with DDP and progesterone-calcitriol ombination potentiated anticancer effects of DDP compared to DDP-calcitriol, or DDP-progesterone treated groups. The anticancer effects were mediated by increased caspase-3, BAX, and decreased BCL2 and PARP-1 expression in DDP and progesterone-calcitriol combination-treated cells. Stimulation of the PI3K/AKT and MAPK/ERK pathways seen in cancer cells was reduced in DDP-progesterone-calcitriol treated cells. Pretreatment of cells with specific inhibitors further diminished AKT and ERK expression. Furthermore, progesterone-calcitriol potentiated the anti-growth effects of DDP on cancer cells by attenuating the expression of SMAD2/3, multidrug resistance protein- 1 (MDR-1), and ABC transporters (ABCG1, and ABCG2), thereby impeding the efflux of chemo drugs from cancer cells. These results suggest a potential clinical benefit of progesterone-calcitriol combination therapy when used in combination with DDP. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) is implicated in several biological processes, including cancer progression. At low concentrations, it promotes cell survival and tumor progression, and at high concentrations it causes apoptosis and cell death. Until now, the impact of NO donors has not been investigated on human endometrial tumors. Four cancer cell lines were exposed to different concentrations of DETA/NO for 24 to 120 h. The effects of DETA/NO on cell proliferation and invasion were determined utilizing MTS and Boyden chamber assays, respectively. The DETA/NO induced a dose and time-dependent reduction in cell viability by the activation of caspase-3 and cell cycle arrest at the G0/G1 phase that was associated with the attenuated expression of cyclin-D1 and D3. Furthermore, the reduction in the amount of CD133-expressing cancer stem-like cell subpopulation was observed following DETA/NO treatment of cells, which was associated with a decreased expression of stem cell markers and attenuation of cell invasiveness. To understand the mechanisms by which DETA/NO elicits anti-cancer effects, RNA sequencing (RNA-seq) was used to ascertain alterations in the transcriptomes of human endometrial cancer cells. RNA-seq analysis revealed that 14 of the top 21 differentially expressed genes were upregulated and seven were downregulated in endometrial cancer cells with DETA/NO. The genes that were upregulated in all four cell lines with DETA/NO were the tumor suppressors Ras association domain family 1 isoform A (RASSF1) and Cyclin-dependent kinase inhibitor 1A (CDKN1A). The expression patterns of these genes were confirmed by Western blotting. Taken together, the results provide the first evidence in support of the anti-cancer effects of DETA/NO in endometrial cancer. [ABSTRACT FROM AUTHOR]

An 80-year-old male, who presented with a history of unprovoked collapse, was found to have a visible pulsation in the central upper abdomen, which disappeared on raising his arms above his shoulder ('head and shoulder' technique). There was no tenderness noted over the pulsation. He had a ventricular demand inhibited pacemaker inserted 3 weeks ago for a significant bradycardia with atrial fibrillation. His ECG showed heart rate of 32 bpm with underlying atrial fibrillation. No pacing spikes noted. His chest x-ray confirmed displacement of pacing lead into the right subclavian vein. It caused stimulation of phrenic nerve resulting in rhythmical diaphragmatic contraction. He later had his pacemaker re-inserted with no more collapses. [ABSTRACT FROM AUTHOR]

A 65-year-old female was admitted with an 8-week history of gradual onset headache. The headache was worse in the morning and on bending forwards. This was associated with 1 week history of vomiting and 1 day history of difficulty in walking. Medical history was unremarkable apart from treated hypothyroidism. There was no history of trauma. Observations and physical examination were entirely normal. Routine blood tests including the ESR and clotting profile were normal. Given the history had red flags for headache, a CT scan was ordered and this showed bilateral subdural haematomas. The patient was referred to the regional neurosurgical centre where the haematomas were evacuated with good recovery. A follow-up MRI brain and spine did not show any source of bleeding. [ABSTRACT FROM AUTHOR]

Abstract: Protein kinase D1 (PKD1), founding member of PKD protein family, is down-regulated in advanced prostate cancer (PCa). We demonstrate that PKD1 and androgen receptor (AR) are present as a protein complex in PCa cells. PKD1 is associated with a transcriptional complex which contains AR and promoter sequence of the Prostate Specific Antigen (PSA) gene. Ectopic expression of wild type PKD1 and the kinase dead mutant PKD1 (K628W) attenuated the ligand-dependent transcriptional activation of AR in prostate cancer cells and yeast cells indicating that PKD1 can affect AR transcription activity, whereas knocking down PKD1 enhanced the ligand-dependent transcriptional activation of AR. Co-expression of kinase dead mutant with AR significantly inhibited androgen-mediated cell proliferation in both LNCaP and DU145 PC cells. Our data demonstrate for the first time that PKD1 can influence AR function in PCa cells. [Copyright &y& Elsevier]

Epithelial ovarian cancer is the fourth leading cause of death from gynecologic malignancies in the United States. Most cases are diagnosed at late stages, with the solid tumor masses growing as peritoneal implants, or floating within the ascitic fluid (peritoneal ovarian carcinomatosis). Despite aggressive surgical "debulking," recurrence of recalcitrant disease is frequent with poor patient survival. Efforts to improve survival rates are hindered by lack of biomarkers that can detect and effectively treat ovarian cancer in its early stages. Urokinase plasminogen activator receptor (uPAR) is a multifunctional receptor involved in a myriad of tumor cell processes. However, the role of host uPAR in ovarian cancer is still elusive. To define the potential proinflammatory role of uPAR in ovarian cancer, first, using a syngeneic murine model in uPAR-/- mice, we found that ablation of uPAR restrained tumor take and peritoneal implants and prolonged the survival of uPAR-/- mice compared with their uPAR+/+ counterparts. Ascitic fluid accumulation was significantly decreased in uPAR-/- mice with decreased macrophage infiltration. Second, in vitro mechanistic studies revealed that host uPAR is involved in the multiple steps of peritoneal metastatic cascade. Third, we evaluated the prognostic utility of tumor and stromal uPAR in human ovarian cancer tissue microarray. In summary, our studies indicated that uPAR plays a significant role in ovarian cancer cell-stromal crosstalk and contributes to increased vascular permeability and inflammatory ovarian cancer microenvironment. This provides a rationale for targeting the uPAR with either specific neutralizing antibodies or targeting its downstream inflammatory effectors in patients with ovarian cancer. [ABSTRACT FROM AUTHOR]