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A study of the influence of membrane-bound protein serine/threonine phosphatase in determining K+ channel using patch-clamp method shows that OA-sensitive PP-2A and Mg2+-dependent phosphatase PP-2C help in dephosphorylation process. Dephosphorylation of phosphatase regulate K(sub ATP) channel. The K+ channel activity decreases due to elimination of ATP and absence of Mg2+ also suppresses the activity. The experimental procedure is discussed.

Abstract Background The provision of healthcare for asylum seekers is a global issue. Providing appropriate and culturally sensitive services requires us to understand the barriers facing asylum seekers and the facilitators that help them access health care. Here, we report on two linked studies exploring these issues, along with the health care needs and beliefs of asylum seekers living in the UK. Methods Two qualitative methods were employed: focus groups facilitated by members of the asylum seeking community and interviews, either one-to-one or in a group, conducted through an interpreter. Analysis was facilitated using the Framework method. Results Most asylum seekers were registered with a GP, facilitated for some by an Asylum Support nurse. Many experienced difficulty getting timely appointments with their doctor, especially for self-limiting symptoms that they felt could become more serious, especially in children. Most were positive about the health care they received, although some commented on the lack of continuity. However, there was surprise and disappointment at the length of waiting times both for hospital appointments and when attending accident and emergency departments. Most had attended a dentist, but usually only when there was a clinical need. The provision of interpreters in primary care was generally good, although there was a tension between interpreters translating verbatim and acting as patient advocates. Access to interpreters in other settings, e.g. in-patient hospital stays, was problematic. Barriers included the cost of over-the-counter medication, e.g. children's paracetamol; knowledge of out-of-hours medical care; and access to specialists in secondary care. Most respondents came from countries with no system of primary medical care, which impacted on their expectations of the UK system. Conclusion Most asylum seekers were positive about their experiences of health care. However, we have identified issues regarding their understanding of how the UK system works, in particular the role of general practitioners and referral to hospital specialists. The provision of an Asylum Support nurse was clearly a facilitator to accessing primary medical care. Initiatives to increase their awareness and understanding of the UK system would be beneficial. Interpreting services also need to be developed, in particular their role in secondary care and the development of the role of interpreter as patient advocate.

Nongenomic effects of aldosterone on Ca2+ in M-1 cortical collecting duct cells. Background. Aldosterone at physiological levels induces rapid (<5 min) increases in intracellular protein kinase C (PKC) activity and a rise in calcium and pH in mineralocorticoid hormone target epithelia, such as distal colon and sweat gland. The end targets of these rapid responses in epithelia are Na+/H+ exchange and K+ channels. Methods. The mouse cortical collecting duct (CCD) M-1 cell line was grown to confluency and loaded with Fura-2 for spectrofluorescence measurements of intracellular free calcium at 37°C bathed in Krebs solution. Results. Aldosterone (1 nmol/L) produced a rapid, transient peak increase in [Ca2+]i in M-1 cells. This effect was abolished upon removal of extracellular Ca2+, but was unaffected by pretreatment with spironolactone (10 μmol/L) or actinomycin D (10 μmol/L). However, pretreatment with the specific PKC inhibitor chelerythrine chloride (1 μmol/L) prevented the aldosterone-induced rise in [Ca2+]i. Dexamethasone, at a concentration 10,000-fold higher than aldosterone (10 μmol/L), also produced a transient increase in [Ca2+]i, but this response was significantly smaller than that of aldosterone. In contrast, hydrocortisone had no effect on [Ca2+]i at either nmol/L or μmol/L concentrations. Both of the sex steroids, 17β-estradiol (10 nmol/L) and progesterone (10 nmol/L), induced protein kinase C-dependent increases in [Ca2+]i. Conclusions. Aldosterone and sex steroid hormones activate intracellular calcium signaling in CCD cells via a nongenomic PKC-dependent pathway, which may have important implications for renal transport. [ABSTRACT FROM AUTHOR]