Biomedical subjects
Publications and source records attributed to J M Russell.
Three hundred and thirty Black pregnant patients attending the Baragwanath Hospital antenatal clinic were treated for symptomatic vaginal discharge with econazole (Ecostatin; Squibb). Patients with positive Candida albicans cultures were treated for either 7 or 14 days. The results of treatment in both groups are presented.
Evidence has been presented and reviewed to show that chloride is often not in electrochemical equilibrium across neuronal cell membranes. An ATP- and sodium-dependent uptake mechanism has been described for the squid giant axon. Finally, the role of chloride in the maintenance of pH1 has been discussed. Present evidence favors a net chloride extrusion being involved in the acid extrusion process. Measurements of free, ionized chloride levels in several neuronal cells have suggested that the transmembrane distribution of chloride does not conform to thermodynamic equilibrium conditions. Net extrusion of Cl- against its electrochemical gradient has been measured in the giant neuron of the Aplysia abdominal ganglion. In the squid giant axon, cellular Cl- levels are higher than predicted from passive thermodynamic considerations. An ATP requirement as well as a dependence upon extracellular sodium has been demonstrated for chloride influx. Similarly, there is an ATP-, external Cl-dependent, Na+ influx. Thus, an ATP-requiring Na-Cl cotransport mechanism appears to account for the high cellular chloride content of the squid giant axon. Chloride efflux from several neurons appears to be involved in the regulation of intracellular pH (pHI). When pHi is made acidic, chloride efflux from the squid giant axon increases and this stimulation requires cellular ATP and external HCO3-. When pHi is measured following an acid load, it is found that pHi recovery toward normal values requires cellular Cl-, ATP and external HCO3-. Thus, an exchange process between cellular Cl- and extracellular HCO3- appears to play an important role in pH1 regulation. Such a process appears to be responsible for the lower-than-equilibrium levels of chloride found in certain neuronal cells.
Unidirectional chloride-36 fluxes were measured in internally dialyzed barnacle giant muscle fibers. About 50--60% of the Cl efflux was irreversibly blocked by the amino-group reactive agent, 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid (SITS), when it was applied either intra- or extracellularly. Similarly, Cl influx was also blocked by SITS. No significant effect on [Cl]i of SITS was noted in intact muscle fibers. However, the rate of net Cl efflux from muscle fibers which were Cl-loaded by overnight storage at 6 degrees C could be slowed by SITS treatment. Two classes of anions were defined based upon their effects on Cl efflux. Methanesulfonate and nitrate inhibited Cl efflux either when they replaced external chloride or when they were added to a constant external chloride concentration. The other group of anions (propionate, formate) stimulated both Cl efflux and influx and such stimulation could be blocked by SITS. Propionate influx was not nearly as large as the stimulated Cl efflux and was unaffected by SITS. Neither the effects of SITS nor those of the anion substitutes could be simply accounted for by changes in the membrane resting potential or conductance. These results suggest a mediated transport system for chloride across the barnacle sarcolemma.
The squid giant axon was internally dialyzed while the unidirectional fluxes of either Cl or Na were measured. The effects of varying the internal or external concentration of either Na or Cl were studied. Chloride influx was directly proportional to the external Na concentration whereas Cl efflux was unaffected by changes of the external Na concentration between 0 and 425 mM. Neither Cl influx nor efflux were affected by changes of internal Na concentration over the range of 8-158 mM. After ouabain and TTX treatment a portion of the remaining Na influx was directly dependent on the extracellular Cl concentration. Furthermore, when the internal Cl concentration was increased from 0 to 150 mM, the influxes of Cl and Na were decreased by 14 and 11 pmol/cm2.s, respectively. The influx of both ions could be substantially reduced when the axon was depleted of ATP. The influxes of both ions were inhibited by furosemide but unaffected by ouabain. It is concluded that the squid axolemma has an ATP-dependent coupled Na-Cl co-transport uptake mechanism.
Among 481 children with myelomeningocele seen at the North Carolina Baptist Hospital since 1949, 46 have undergone a urinary diversion procedure, as follows: ileal loop in 43; sigmoid loop in two; and transverse colon conduit in one. The indications for diversion were incontinence in 28, urinary infection or pyelonephritis in 27, and hydronephrosis, pyelocaliectasis, and reflux in 12 patients. No deaths resulted from the diversionary procedures. One patient required early surgical revision and seven patients required late surgical revision. Two patients have since died, 44 have been followed for an average of 7.9 years, 15 for more than 10 years. Overall, of 26 patients with normal prediversionary intravenous pyelograms (IVP's), 88% now have normal or nearly normal IVP's; of 14 patients with abnormal prediversionary IVP's, 79% now have normal, improved, or unaltered IVP's. Renal function has remained normal in all 44 patients, and renal calculi have developed in 10 patients. Ileal loop diversion appears to convert a high-pressure system into a low-pressure system, thereby helping to prevent further renal damage. This procedure tends to stabilize, rather than improve, urinary-tract function. For these children already so incapacitated by their basic disease, this goal is acceptable, particularly since it also provides continence and independence from parental nursing.
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The papillae are involved in renal disease and, hence, are an inextricable consideration in intrarenal surgical procedures. Guide lines for their management are newly emergent and, consequently, tentative. If divided along intra-arterial planes they appear to heal with little functional impairment. Resections of papillae, which are limited to the intracaliceal portions, involve no medullary structures and heal without apparent dysfunction.
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The level of intracellular free chloride in Aplysia giant neurons can be made to decline by pretreatment with 50 mM NH4+ solution followed by washing with 10 mM HCO3-/0.4% CO2-containing fluids. This effect can be completely blocked by the anion flux inhibitor, 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid (SITS). The net change of free chloride in the cell cannot be explained by changes in the electrochemical gradient of chloride. These results support the hypothesis that at least one mechanism for intracellular pH regulation involves a Cl-/HCO-3 exchange process.
The use and placement of ureteric stents either endoscopically or as part of an open procedure are outlined. The ureteric stent can replace the pyelostomy or nephrostomy tube and significantly reduce the postoperative morbidity.
Two methods were used to study effects of the antibiotics, nystatin, on giant neurons of Aplysia. In the first method the effects of various concentrations of nystatin on the current-voltage relationship were evaluated at a fixed time after exposure to the antibiotic using a two-microelectrode voltage clamp. Nystatin increased membrane conductance in a dose-dependent manner. The dose-response relation was very steep, with little or no effect below 15 mg/liter and an effect too large to measure at concentrations greater than 30 mg/liter. Upon return to antibiotic-free solution, membrane conductance returned to pre-treatment levels within 30 minutes. The second type of experiment involved use of ion-specific microelectrodes to measure changes of intracellular univalent ion activities which attended the nystatin-induced permeability. Nystatin-induced permeability changes mainly involved univalent cations, but Cl permeability was also increased. Nystatin may therefore be used to selectively rearrange the internal ionic milieu to study the effect of such a change on membrane transport or electrical properties.
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Measurements were made of 36C1 influx into squid giant axons whose internal solutes were controlled by means of internal dialysis. When the intracellular chloride concentration was 50mM and the internal concentration of adenosine 5'-triphosphate (ATP) was 4mM, the average chloride influx was 11.6 pmoles/cm2 x sec. When the axons were dialyzed with an ATP-free solution, the average influx fell to 5.1 pmoles/cm2 x sec. The effect was fully reversible upon the return of ATP to the dialysis fluid. Chloride-36 influx in the presence and absence of ATP was found to be inversely related to the internal chloride concentration.
Calcium-45 fluxes have been examined in isolated giant barnacle muscle fibers subjected to internal solute control by means of "internal dialysis". The 45Ca efflux was dependent upon the concentrations of both total and ionized internal Ca (Ca2+ buffered with EGTA). With a total Ca concentration of 2.0 mM and a 1:2 Ca/EGTA ratio (nominal [Ca2+]i =0.13 muM), the Ca efflux averaged 1.2 pmoles/cm2 sec. Under identical conditions, the mean Ca influx was only 0.36 pmoles/cm2 sec. The Ca efflux may not be attributed to leak of the CaEGTA complex, since a 2.5-fold increase in the EGTA concentration (nominal [Ca2+]i=0.032 muM) reduced the 45Ca efflux by one-third. Furthermore, when EDTA was used to buffer the internal Ca concentration (in the absence of internal Mg), the steady efflux of 14C-EDTA was only about 10% of the 45Ca efflux (in parallel experiments). The timecourse of the 45Ca fluxes also appeared anomalous in the 45Ca influx reached a steady level much more rapidly than 45Ca efflux in fibers of comparable diameters. If the muscle fibers are treated as right circular cylinders, these data imply that the apparent diffusion coefficient for inwardly-moving Ca is much larger than for outwardly-moving Ca. In contrast to Ca efflux, the outward diffusion of 22Na, 14C-EDTA and 3H2O appears to be limited primarily by the permeability of the dialysis tube wall. Some, but not all, of the anomalous behavior of the Ca fluxes can be reconciled if the deep, branched infoldings of the barnacle muscle surface membrane are taken into account.
The influx and efflux of calcium (as 45Ca) and influx of sodium (as 24Na) were studied in internally dialyzed squid giant axons. The axons were poisoned with cyanide and ATP was omitted from the dialysis fluid. The internal ionized Ca2+ concentration ([Ca2+]i) was controlled with Ca-EGTA buffers. With [Ca2+]i greater than 0.5 muM, 45Ca efflux was largely dependent upon external Na and Ca. The Nao-dependent Ca efflux into Ca-free media appeared to saturate as [Ca2+]i was increased to 160 muM; the half-saturation concentration was about 8 muM Ca2+. In two experiments 24Na influx was measured; when [Ca2+]i was decreased from 160 muM to less than 0.5 muM, Na influx declined by about 5 pmoles/cm2 sec. The Nao-dependent Ca efflux averaged 1.6 pmoles/cm2 sec in axons with a [Ca2+]i of 160 muM, and was negligible in axons with a [Ca2+]i of less than 0.5 muM. Taken together, the Na influx and Ca efflux data may indicate that the fluxes are coupled with a stoichiometry of about 3 Na+-to-1 Ca2+. Ca efflux into Na-free media required the presence of both Ca and an alkali metal ion (but not Cs) in the external medium. Ca influx from Li-containing media was greatly reduced when [Ca2+]i was decreased from 160 to 0.23 muM, or when external Li was replaced by choline. These data provide evidence for a Ca-Ca exchange mechanism which is activated by certain alkali metal ions. The observations are consistent with a mobile carrier mechanism which can exchange Ca2+ ions from the axoplasm for either 3 Na+ ions, or one Ca2+ and an alkali metal ion (but not Cs) from the external medium. This mechanism may utilize energy from the Na electrochemical gradient to help extrude Ca against an electrochemical gradient.
In a giant neuron of Aplysia californica, permeabilities and conductances obtained by measuring net fluxes of Na+, K+ and Cl-minus with ion-specific microelectrodes were compared with those obtained by measuring transmembrane current and potential changes when the three ions were varied in the external solution. Net fluxes were measured with ion-specific microelectrodes, after blocking metabolic processes, thus allowing movement of ions down their electrochemical gradients. Premeabilities and conductances obtained from the "chemical" measurements (i.e., ion-specific electrodes) were generally comparable to the values obtained from "electrical" measurements (i.e., ion-specific electrodes) were generally comparable to the values obtained from "electrical" measurements. Where discrepancies occurred, they could be explained by showing that some of the assumptions necessary to use the "electrical" method were not quantitatively true in this system. The absolute magnitudes of the permeabilities are significantly less than those found in many axonal preparations. There is also a relatively high PNa/PK ratio. The selectivity of the membrane against ions such as Tris" and MeSO3-minus is not good, Tris+ being nearly as permeable as Na+ and MeSO3-minus about one-half as permeables as Cl-minus. These properties may be characteristic of somal membranes.