Porcine Haptoglobin Related Protein ELISA Kit

Influence of salinity on acidogenic fermentation (AF) specific to the production of biohydrogen (H-2), volatile fatty acids (VFA) and biohythane from food waste (FW) was studied by varying salinity concentration [1 g L-1 (S-1), 5 g L-1 (S-5), 10 g L-1 (S-10), 20 g L-1 (S-20), 30 g L-1 (S-30), 40 g L-1 (S-40) and 50 g L-1 (S-50)]. Maximum H-2 production rate (HPR) of 0.044 L h(-1) and cumulative H-2 production (CHP) of 1.05 L was achieved at 40 g NaCl L-1 salinity. Hypersaline conditions (>10 g NaCl L-1) suppressed methanogenic activity and resulted in zero methane evolution. Benefits of salinity were also seen on VFA production with accumulation of more butyric acid (C4: 3.04 g L-1) and acetic acid (C2:1.17 g L-1) along with traces of valeric acid (C5:11 mg L-1) with good acidification potential (AP) of 65.38% at 40 g NaCl L-1. Dehydrogenase (DH) enzyme activity was well correlated with H-2 production, wherein S-40 showed the highest DH activity of 6.77 mu g mL(-1). Elevated NaCl concentration (50 g L-1) not only suppressed methanogenic activity but also reduced the acidogenic activity. Increased salinity conditions (30-40 g L-1) depicted good in situ buffering capacity during acidogenic fermentation and also aided in higher H-2/VFA production. Study illustrated the significance of salinity as a regulator parameter in aiding the bio-conversion of waste to bioenergy and platform chemicals.

Prostate stem cells (PSC) are characterized by their intrinsic resistance to androgen deprivation therapy (ADT), possibly due to the lack of androgen receptor (AR) expression. PSCs resistance to ADT and PSC expansion in castration resistant prostate cancer (CRPC) has sparked great interest in using differentiation therapy as an adjuvant to ADT. Understanding the mechanisms, by which PSCs maintain their undifferentiated phenotype, thus has important implications in differentiation therapy. In the prostate, the ATP binding cassette sub-family G member 2 (ABCG2) transporters, which enrich for AR-positive, ADT-resistant PSCs, play an important role in regulating the intracellular androgen levels by effluxing androgens. We hypothesized that the ABCG2-mediated androgen efflux is responsible for maintaining PSCs in an undifferentiated state. Using the HPr-1-AR (nontumorigenic) and CWR-R1 (tumorigenic) prostate cell lines, it was demonstrated that inhibiting the ABCG2-mediated androgen efflux, with Ko143 (ABCG2 inhibitor), increased the nuclear AR expression due to elevated intracellular androgen levels. Increased nuclear translocation of AR is followed by increased expression of AR regulated genes, a delayed cell growth response, and increased luminal differentiation. Furthermore, Ko143 reduced tumor growth rates in mice implanted with ABCG2-expressing CWR-R1 cells. In addition, Ko143-treated mice had more differentiated tumors as evidenced by an increased percentage of CK8(+)/AR(+) luminal cells and decreased percentage of ABCG2-expressing cells. Thus, inhibiting ABCG2-mediated androgen efflux forces the PSCs to undergo an AR-modulated differentiation to an ADT-sensitive luminal phenotype. (C) 2016 AACR.