Factors influencing stone-free rate of Extracorporeal Shock Wave Lithotripsy (ESWL); a cohort study.

Objective: To evaluate the success rate of Extracorporeal Shock Wave Lithotripsy (ESWL) therapy and identify relevant treatment-specific factors affecting stone-free rate (SFR) after ESWL.

Materials And Methods: All ESWL treatments in the years 2016-2019, in Ängelholm Hospital, Skåne, Sweden were analysed retrospectively. Primary outcome was stone-free rate (SFR) at 3 months.

Cancer cells with defective RB and CDKN2A are resistant to the apoptotic effects of rapamycin.

Inhibition of mammalian target of rapamycin complex 1 (mTORC1) with rapamycin in the absence of transforming growth factor-β (TGFβ) signaling induces apoptosis in many cancer cell lines. In the presence of TGFβ, rapamycin induces G cell cycle arrest; however, in the absence of TGFβ, cells do not arrest in G and progress into S-phase where rapamycin is cytotoxic rather than cytostatic. However, we observed that DU145 prostate and NCI-H2228 lung cancer cells were resistant to the cytotoxic effect of rapamycin.

Phosphatidic acid drives mTORC1 lysosomal translocation in the absence of amino acids.

Mammalian target of rapamycin complex 1 (mTORC1) promotes cell growth and proliferation in response to nutrients and growth factors. Amino acids induce lysosomal translocation of mTORC1 via the Rag GTPases. Growth factors activate Ras homolog enriched in brain (Rheb), which in turn activates mTORC1 at the lysosome.

Elevated phospholipase D activity in androgen-insensitive prostate cancer cells promotes both survival and metastatic phenotypes.

Prostate cells are hormonally driven to grow and divide. Typical treatments for prostate cancer involve blocking activation of the androgen receptor by androgens. Androgen deprivation therapy can lead to the selection of cancer cells that grow and divide independently of androgen receptor activation.

Knockout of p21-activated kinase-1 attenuates exercise-induced cardiac remodelling through altered calcineurin signalling.

Aims: Despite its known cardiovascular benefits, the intracellular signalling mechanisms underlying physiological cardiac growth remain poorly understood. Therefore, the purpose of this study was to investigate a novel role of p21-activated kinase-1 (Pak1) in the regulation of exercise-induced cardiac hypertrophy.

Methods And Results: Wild-type (WT) and Pak1 KO mice were subjected to 6 weeks of treadmill endurance exercise training (ex-training).