Smaller bladder capacity and stronger bladder contractility in patients with ketamine cystitis are associated with elevated TRPV1 and TRPV4.

Stronger contractility and smaller bladder capacity are common symptoms in ketamine cystitis (KC). This study investigates the association between expression levels of transient receptor potential cation channel subfamily V (TRPV) proteins and the clinical characteristics of KC. Bladder tissues were obtained from 24 patients with KC and four asymptomatic control subjects.

The putative involvement of actin-binding proteins and cytoskeleton proteins in pathological mechanisms of ketamine cystitis-Revealed by a prospective pilot study using proteomic approaches.

Purpose: Ketamine-induced cystitis (KC) among chronic ketamine young abusers has increased dramatically and it has brought attention for Urologists. The underlying pathophysiological mechanism(s) of KC is still unclear. Therefore, the purpose of this study is to elucidate the possible pathophysiological mechanism(s) of KC through proteomic techniques.

Proteomic-based identification of multiple pathways underlying n-butylidenephthalide-induced apoptosis in LNCaP human prostate cancer cells.

Although numerous studies have shown the cancer-preventive properties of butylidenephthalide (BP), there is little report of BP affecting human prostate cancer cells. In the present study, proteomic-based approaches were used to elucidate the anticancer mechanism of BP in LNCaP human prostate cancer cells. BP treatment decreased the viability of LNCaP human prostate cancer cells in a concentration- and time-dependent manner, which was correlated with G0/G1 phase cell cycle arrest.

Depletion of albumin and immunoglobulin G from human serum using epitope-imprinted polymers as artificial antibodies.

Serum is a readily available source for noninvasive studies in clinical research, but it contains abundant proteins such as albumin and immunoglobulin G that can hinder the presence of low-abundant proteins as well as decrease sample loading capacity of analytical methods. Therefore, depletion of these two proteins is required to observe low-abundance serum proteins. Molecularly imprinted polymers are template-induced artificial antibodies with the ability to recognize and selectively bind the target molecule.

The C-terminus of PARK2 is required for its self-interaction, solubility and role in the spindle assembly checkpoint.

PARK2, an ubiquitin ligase closely correlated with Parkinson's disease and cancer, has been shown to accumulate at centrosomes to ubiquitinate misfolded proteins accumulated during interphase. In the present study, we demonstrated that PARK2 can also localize to centrosomes in mitosis and that the protein does not fluctuate through the S- to M-phase. A C-terminal truncation of PARK2 resulted in a spindle assembly checkpoint defect, characterized by HeLa cells able to bypass mitotic arrest induced by nocodazole and form multinucleated cells when overexpressing the C-terminal truncated PARK2 protein.