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Mutations F1764A and Y1771A Reduce the Affinity of Inactivated Channels for Lidocaine and Phenytoin. Since lidocaine Fig. 2 ; and phenytoin see below ; bound to depolarized channels without requiring them to open, whereas quinidine and flecainide required channel opening, different protocols were used to assess effects of mutations on block by the two types of drugs. In this section, we address effects of mutations on lidocaine and phenytoin block of resting and depolarized channels. Resting and inactivated channels are in dynamic equilibrium, with hyperpolarized membrane potentials favoring the resting states, and depolarized potentials favoring the inactivated states. Only resting channels are available to open during depolarizations. Thus, the proportion of available Na + channels as a function membrane potential can be determined by assessing the amplitudes of Na + currents elicited by stimulus pulses applied from varying holding potentials. For WT channels, inactivation was observed for holding potentials more positive than -70 mV, and the midpoint of the holding potential versus availability relationship was -53 mV Fig. 3A ; . After application of lidocaine, the midpoint of the relationship was shifted 12 mV negative Fig. 3A ; . This negative shift in channel availability AlVK2 ; can be explained by preferential drug binding to inactivated channels compared with resting channels, causing a shift in the equilibrium between these two sets of functional states favoring inactivation 8, 9, 15 ; . The magnitude of AV, 12 increased with increasing lidocaine concentration up to at least 2 mM Fig. 3C ; . Phenytoin also shifted VK 2 to more negative potentials in a concentration-dependent manner Fig. 3D ; . The F1764A and Y1771A mutations substantially reduced AV, 2 for both lidocaine and phenytoin over the entire range of drug concentrations Fig. 3 B-D ; , indicating that these mutations reduced preferential drug binding to inactivated states. In contrast, quinidine and flecainide did not shift availability curves for WT or mutant channels not shown ; , as expected for drugs that require channels to open in order to bind. To quantify effects of F1764A and Y1771A on lidocaine and phenytoin binding to inactivated Na + channels more accurately, we determined concentration-effect relationships by.
Nificant late INa, which could have been blocked by flecainide. Liu et al. 14 ; , using several Na channel disease mutations with distinct flecainide sensitivities, concluded that channel opening is necessary but flecainide binds tightly to "an inactivated state." They estimated mean open times 0.50 0.02 ms for WT and 0.42 0.03 ms for DG ; . However, they did not consider the possibility of a change in flecainide affinity to the open-state between WT and DG [calculated open-state Kd koff kon ; were 5.38 M for WT-ICM and 2.61 M for DGICM], which is the main finding in our study. Slowed recovery from flecainide block in the above studies and our current study ; may also represent differential voltage- and state-dependent "trapping" of the drug 20 ; and not necessarily an increased affinity to an inactivated state. A neutral form of flecainide, which does not depend on the pore access path for block, has been shown to shift the steady-state availability inactivation ; curve 13 ; . However, it is not clear whether the behavior of the neutral drug truly represents that of flecainide. We used a holding potential of 140 mV, sufficiently hyperpolarized to deactivate sodium channels fully. Our choice of such a hyperpolarized holding potential may have lessened the contribution from an inactivated state toward flecainide UDB. At 140 mV, all channels are uniformly in the closed state; it is approximately 35 mV more negative than halfavailable voltage V1 2 ; of the steady-state availability SSA ; curves of DG channels not shown ; , similar to the conditions in the study by Abriel et al. 1 ; . UDB recovery was nearly complete Fig. 3A ; within 200 s and was accurately estimated with a two-exponential function. Even at 140 mV, the difference in UDB recovery between WT-ICM and DG-ICM channels persisted, similar to the results by Abriel et al. 1 ; at 100 mV. In our study, we found two significant differences in flecainide UDB between the WT and DG channels, increased openchannel affinity to flecainide and slowed recovery from UDB. The fast-inactivated state appeared to have little influence on flecainide block because the lack of it did not decrease UDB or prolong UDB recovery. Direct involvement of a slow-inactivated state seems unlikely because the time constants for the open-channel block ranged from 1 to 30 Table 2 ; , while slow-inactivated states have been associated with longer time constants when fast inactivation is disabled. We used the guarded-receptor model 25, 26 ; to mathematically model the flecainide UDB so that the observed differences in open-channel affinities and UDB recovery accounts for the differing flecainide UDB in the WT-ICM and DG-ICM channels. The model predicted flecainide UDB accurately by using open-channel flecainide affinities and kinetic constants for UDB recovery during the interpulse intervals without contribution from any inactivated states. We believe that the difference in open-channel affinity for flecainide is the predominant factor in the increased UDB in DG channels because the recovery from UDB during each interpulse interval is relatively small. Consistent with this is the observation that, in physiological conditions, flecainide slows conduction but does not prolong refractoriness significantly 22 ; . In fact, when the faster component of UDB recovery see RESULTS and Table 3 ; was omitted in the mathematical modeling, was completely dominated by the open-channel parameters d ; . Prediction of UDB was still very accurate, and ssUDB levels were overestimated i.e., the model predicts higher flecainide UDB than.

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W grupie ciarnych z prawidowym przyrostem masy ciaa BMI 5 ; znalazo si 107 pacjentek, natomiast w grupie nadmiernym przyrostem masy ciaa BMI 5 ; 105 kobiet ciarnych. Wiek badanych w obydwu grupach nie rni si istotnie statystycznie i wynosi odpowiednio 27, 24, 2 lata w grupie z prawidowym i 27, 64, 6 lat w grupie z nadmiernym przyrostem masy ciaa. Z grupy wyczono ciarne z cukrzyc, nadcinieniem ttniczym i innymi chorobami sercowo-naczyniowymi. Do badania kwalifikowano pacjentki w ciy pojedynczej, rasy biaej, ktre byy mieszkankami regionu Wielkopolski. Ponadto u kadej ciarnej porwnywano obwd talii i bioder przed ci, co wykorzystano do obliczania wskanika talia-biodro WHR waist-hip ratio ; . W obydwu badanych grupach porwnywano take mas urodzeniow dziecka, mas oyska, cinienie skurczowe i rozkurczowe tabela I ; . Na przeprowadzenie bada uzyskano zgod Komisji Bioetycznej UM w Poznaniu. Genomowy DNA izolowano z leukocytw krwi wykorzystujc zestaw do izolacji DNA-QIAamp DNA Blood Mini Kit QIAGEN, Niemcy ; . W celu oznaczenia polimorfizmu insercyjno-delecyjnego genu ACE przeprowadzano reakcj acuchow polimerazy PCR polymerase chain reaction ; pozwalajc amplifikowa pojedynczy fragment intronu 16 genu konwertazy angiotensynowej. Do reakcji uyto swoistych starterw oligonukleotydowych, opisanych po raz pierwszy przez Rigat i wsp. 1992 ; o nastpujcych sekwencjach: ACEF 5'CTg gAg ACC ACT CCC ATC CTT TCT 3' oraz ACER 5'gAT gTG gCC ATC ACA TTC gTC AgA T3' [19]. Dla wszystkich prb przygotowano mieszanin reakcyjn zawierajc: 1x Taq-Bufor Fermentas, Litwa 2, 5mM MgCL2 Fermentas, Litwa 7, 5nmoli dNTPs GeneCraft, Niemcy ; , 10pmoli kadego startera Tib MolBiol, Polska ; i 1 jedn. polimerazy Taq Fermentas, Litwa ; , ktr nastpnie rozdzielono do probwek zawierajcych badane DNA. Reakcj PCR prowadzono w termocyklerze PTC-200 MJ Research, USA ; w nastpujcych warunkach: denaturacja wstpna w 94C przez 5 min., 30 cykli denaturacja w 95C 0, 5min., hybrydyzacja w 62C 1min., elongacja w 72C 1min. oraz kocowe wyduanie w 72C przez 10min. Schodzon do okoo 4C mieszanin produktu reakcji PCR rozdzielono elektroforetycznie na 1, 5% elu agarozowym 80V, 120min. ; . W przypadku delecji obserwowano obecno fragmentw o dugoci 193 par zasad homozygota DD ; , przy obecnoci insercji fragmenty miay dugo 480 par zasad homozygota II ; . Pojawienie si prkw o dugoci 193 oraz 480 par zasad wiadczyo o obecnoci genotypu heterozygotycznego ID. W metodzie opisanej przez Rigat i wsp. krtszy allel D niekiedy amplifikuje si bardziej efektywnie ni duszy allel I, co moe by przyczyn mylnego odczytania genotypw ID oraz DD po ich rozdziale elektroforetycznym. Jako pierwszy na ten fakt zwrci uwag Shanmuagam i wsp. w 1993 roku [20]. Prawdopodobiestwo takiej pomyki jest szacowane na okoo 5-10% [21, 22]. Dlatego w powyej pracy celem weryfikacji wynikw uyto dodatkowego startera proponowanego przez Ueda i wsp. 1996 ; , specyficznego dla insercji, o nastpujcej sekwencji: 5` Tgg gAT TAC Agg CgT gAT ACA g 3`. Zastosowanie tego startera razem ze starterem sensownym ACE-F ; w kolejnej reakcji PCR pozwolio na otrzymanie prka wielkoci 160 par zasad w przypadku allela I, natomiast w przy.

TABLE 1. Effects of Flecainide on Exit Conduction From Atrial Ectopic Foci and flucytosine. Hospital CUF Descobertas, Department of Oncology, Lisbon, Portugal 2 Hospital CUF Descobertas, Chaplaincy, Lisbon, Portugal 3 Hospital de Santa Maria, Psychiatry Department, Palliative Care Center of the Faculty of Medicine of Lisbon, Lisbon, Portugal Objective: We aim to understand the features that oncologic patients with advanced disease recognize and value in their experience of spiritual suffering using a conceptual framework of authors from Christian and Budist thougt. Methods and patients: A qualitative study was undertaken using Collaizi methodology. The knowledge of the phenomena came from the experience of a patient with advanced disease, interviewed in a semi-structured profound way in order to know and understand the experiences of the patient in it's spiritual dimension. Results: Relevant data showed that the patient with spiritual suffering facing his oncologic reality, is focused in the qualification of his spiritual pathway, assuring a strong link to earthly things; for that, he recognizes and values: 1- There is a spiritual implication in the organic disease. The disease emerges in a circle of silence and reclusion. 2- Disease has a place in the spiritual dimension of human being. Emerging feelings of compassion, courage authenticity, hope-sense of life, sharing-fraternity. 3- Genesis of the feeling of inner peace, that encloses meditation, miracle and grace, sense of eternity and faith. 4- The disease might be explored in a spiritual way, through self knowledge and prayer. Conclusions: We discuss the repercussion of our praxis, being aware of the real distance from what would ideally be recommended for Palliative Care in order to have a "Quality Sense of Life". 504. DIIFICULTIES IN ADDRESSING SPIRITUAL CARE OF THE PATIENTS: A QUALITATIVE STUDY Syed Qamar Abbas 1, Simon Dein 2.

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