CEA was the first indicator of recurrent disease in 58 percent of all patients and in 80 percent of patients with liver metastases. The diagnosis of recurrent disease may be made several months earlier by investigating the first abnormal CEA level, although any benefit in terms of survival remains to be proven.

Obtaining proximal CCA control by inflating the POC does not sufficiently prevent embolization. However, reversal of flow in the ICA can always be created with the external shunt, which effectively prevents embolization. Thus, POC may markedly lower procedural stroke rates during carotid artery stenting. The ability of POC to prevent embolization before crossing the lesion with a guidewire may be an important advantage over other distal protection devices.

The modulation of large conductance Ca2+‐activated K+ (BKCa) channels by the nitric oxide (NO) donors S‐nitroso‐L‐cysteine (NOCys) and sodium nitroprusside (SNP) and agents which oxidize or reduce reactive thiol groups were compared in excised inside‐out membrane patches of the guinea‐pig taenia caeci. When the cytosolic side of excised patches was bathed in a physiological salt solution (PSS) containing 130 mm K+ and 15 nm Ca2+, few BKCa channel openings were recorded at potentials negative to 0 mV. However, the current amplitude and open probability (NPo) of these BKCa channels increased with patch depolarization. A plot of ln(NPo) against the membrane potential (V) fitted with a straight line revealed a voltage at half‐maximal activation (V0.5) of 9.4 mV and a slope (K) indicating an e‐fold increase in NPo with 12.9 mV depolarization. As the cytosolic Ca2+ was raised to 150 nm, V0.5 shifted 11.5 mV in the negative direction, with little change in K (13.1 mV). NOCys (10 μm) and SNP (100 μm) transiently increased NPo 16‐ and 3.7‐fold, respectively, after a delay of 2–5 min. This increase in NPo was associated with an increase in the number of BKCa channel openings evoked at positive potentials by ramped depolarizations (between −60 and +60 mV). Moreover, this NOCys‐induced increase in NPo was still evident in the presence of 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ; 10 μm), the specific blocker of soluble guanylyl cyclase. The sulfhydryl reducing agents dithiothreitol (DTT; 10 and 100 μm) and reduced glutathione (GSH; 1 mm) also significantly increased NPo (at 0 mV) 7‐ to 9‐fold, as well as increasing the number of BKCa channel openings evoked during ramped depolarizations. Sulfhydryl oxidizing agents thimerosal (10 μm) and 4,4′‐dithiodipyridine (4,4DTDP; 10 μm) and the thiol‐specific alkylating agent N‐ethylmaleimide (NEM; 1 mm) significantly decreased NPo (at 0 mV) to 40–50 % of control values after 5–10 min. Ramped depolarizations to +100 mV evoked relatively few BKCa channel openings. The effects of thimerosal on NPo were readily reversed by DTT, while the effects of NOCys were prevented by NEM. It was concluded that both redox modulation and nitrothiosylation of cysteine groups on the cytosolic surface of the α subunit of the BKCa channel protein can alter channel gating.

The patch‐clamp technique was used to record from intact ganglia of the guinea‐pig duodenum in order to characterize the K+ channels that underlie the slow afterhyperpolarization (slow AHP) of myenteric neurons. Cell‐attached patch recordings from slow AHP‐generating (AH) neurons revealed an increased open probability (Po) of TEA‐resistant K+ channels following action potentials. The Po increased from < 0.06 before action potentials to 0.33 in the 2 s following action potential firing. The ensemble averaged current had a similar time course to the current underlying the slow AHP. TEA‐ and apamin‐resistant Ca2+‐activated K+ (KCa) channels were present in inside‐out patches excised from AH neurons. The Po of these channels increased from < 0.03 to approximately 0.5 upon increasing cytoplasmic [Ca2+] from < 10 nm to either 500 nm or 10 μm. Po was insensitive to changes in transpatch potential. The unitary conductance of these TEA‐ and apamin‐resistant KCa channels measured approximately 60 pS under symmetric K+ concentrations between −60 mV and +60 mV, but decreased outside this range. Under asymmetrical [K+], the open channel current showed outward rectification and had a limiting slope conductance of about 40 pS. Activation of the TEA‐ and apamin‐resistant KCa channels by internal Ca2+ in excised patches was not reversed by washing out the Ca2+‐containing solution and replacing it with nominally Ca2+‐free physiological solution. Kinetic analysis of the single channel recordings of the TEA‐ and apamin‐resistant KCa channels was consistent with their having a single open state of about 2 ms (open dwell time distribution was fitted with a single exponential) and at least two closed states (two exponential functions were required to adequately fit the closed dwell time distribution). The Ca2+ dependence of the activation of TEA‐ and apamin‐resistant KCa channels resides in the long‐lived closed state which decreased from > 100 ms in the absence of Ca2+ to about 7 ms in the presence of submicromolar cytoplasmic Ca2+. The Ca2+‐insensitive closed dwell time had a time constant of about 1 ms. We propose that these small‐to‐intermediate conductance TEA‐ and apamin‐resistant Ca2+‐activated K+ channels are the channels that are primarily responsible for the slow AHP in myenteric AH neurons.

1. Peristalsis in the mammalian upper urinary tract (UUT) is mostly myogenic in origin, originating predominately in the proximal pelvicalyceal regions of the renal pelvis, an area that is enriched with specialized smooth muscle cells termed 'atypical' smooth muscle cells. Propagating peristaltic contractions are little affected by blockers of either autonomic nerve function or nerve impulse propagation; however, blockers of sensory nerve function or prostaglandin synthesis reduce both the frequency and the strength of the spontaneous contractions underlying peristalsis. 2. The electrical drive for these peristaltic contractions has long been considered to involve mechanisms analogous to the heart, such that 'atypical' smooth muscle cells generate spontaneous 'pacemaker' action potentials. These pacemaker potentials trigger the firing of action potentials and contraction in the muscular regions of the renal pelvis, which propagate distally to the ureter, propelling urine towards the bladder. 3. Recent intracellular microelectrode and single cell/channel patch-clamp studies have revealed that the ionic conductances underlying the action potentials recorded in the UUT are likely to involve the opening and slow closure of voltage-activated 'L-type' Ca2+ channels, offset by the time-dependent opening and closure of both voltage- and Ca(2+)-activated K+ channels. 4. In the present review we summarize the current knowledge of the ionic mechanisms underlying action potential discharge in the UUT, as well as present our view on how this electrical activity supports the initiation and conduction of UUT peristalsis.