Artificial urinary sphincters: plain radiography of malfunction and complications

Inflatable artificial urinary sphincters provide excellent voluntary continence. Eighty-four consecutive patients underwent implantation of artificial urinary sphincters for intractable urinary incontinence; 33 patients had 58 episodes of sphincter malfunction, and eight patients had eight complications involving a functional prosthetic sphincter. Retrospective analysis was performed to determine the value of plain radiography of the pelvis in patients with sphincter malfunction or complication. The cause of malfunction in the majority of patients was a system leak and subsequent loss of hydraulic fluid (31 occurrences; 53%). Plain radiography permitted correct identification of all instances of fluid leakage in patients with opacified prostheses. Plain radiographs were of no value in examining patients with nonopacified prostheses or the complications of cuff erosion or wound infection. Due to the low cost and noninvasive nature of plain radiography of the pelvis, we conclude that it should be used as the initial diagnostic modality in patients with previously opacified but currently dysfunctional artificial urinary sphincters.     

p18INK4C基因敲除加重顺铂诱导的小鼠急性肾损伤

目的 探讨周期素依赖性激酶抑制基因p18INK4C敲除对顺铂诱导的小鼠急性肾损伤(AKI)的影响,并分析其可能机制.方法 利用已引种的杂合p18INK4C基因敲除小鼠p18INK4C+/-繁育p18INK4C基因敲除小鼠P18INK4C-/-(KO组),以同窝野生型小鼠p18INK4C+/+作为对照(WT组).腹腔注射顺铂制备AKI模型,观察两组小鼠的存活情况,并检测给药后第2、3、5天血肌酐、尿素氮的变化及肾组织的病理变化.结果 WT组小鼠在第3天出现死亡,第7天存活率为46.7%(14/30).KO组小鼠自第2天出现死亡,至第7天全部死亡(100.0%,30/30).KO组的死亡率显著高于WT组(P<0.05).自给药后第2天起,KO组小鼠的肾功能恶化明显,此后继续加重.给药后第2、3、5天,KO组的尿素氮、肌酐均显著高于WT组(P值均<0.05).WT和KO组小鼠均以给药后第3天肾脏病变最为严重.结论 p18INK4C基因敲除加速了顺铂诱导的小鼠AKl的进展,可能与其增加小管上皮损伤及加剧炎性反应有关.     

Identification of primary lysosomes in human megakaryocytes and platelets

The presence of lysosomal enzymes in human platelets is well documented; the identity of the "lysosome," however, has been the subject of some disagreement. In order to determine the time of appearance and subcellular localization of two lysosomal enzymes in megakaryocytes (MK) and platelets, we examined normal human bone marrow and blood by electron microscopy and cytochemistry. Acid phosphatase (AcPase) was present in the Golgi region in the youngest recognizable MK, as well as in those with a considerable degree of cytoplasmic maturation. Heavy reaction product was usually confined to one or two Golgi-associated cisternae and coated vesicles; other Golgi cisternae were sometimes lightly reactive. In mature MK, reaction product was limited to vesicles of variable size, but smaller than alpha-granules. Another lysosomal enzyme, arylsulfatase (AS), was localized in similar small vesicles in MK of all stages; it could not be demonstrated in the Golgi complex. Vesicles containing AS were also found in about 25% of platelet profiles, whereas vesicles containing AcPase were found in only about 15% of platelet profiles. The alpha-granules of all MK and platelets examined were negative for both enzymes. We conclude that the enzyme-containing vesicles in these cells constitute the lysosomes and that they are distinct from other platelet organelles. Since there was no evidence that they had participated in any digestive event, we believe that they are primary lysosomes, whose contents are secreted during platelet aggregation and the release reaction.     

Specificity Improvement for Network Distributed Physiologic Alarms Based on a Simple Deterministic Reactive Intelligent Agent in the Critical Care Environment

Automated physiologic alarms are available in most commercial physiologic monitors. However, due to the variability of data coming from the physiologic sensors describing the state of patients, false positive alarms frequently occur. Each alarm requires review and documentation, which consumes clinicians’ time, may reduce patient safety through ‹alert fatigue’ and makes automated physician paging infeasible. To address these issues a computerized architecture based on simple reactive intelligent agent technology has been developed and implemented in a live critical care unit to facilitate the investigation of deterministic algorithms for the improvement of the sensitivity and specificity of physiologic alarms. The initial proposed algorithm uses a combination of median filters and production rules to make decisions about what alarms to generate. The alarms are used to classify the state of patients and alerts can be easily viewed and distributed using standard network, SQL database and Internet technologies. To evaluate the proposed algorithm, a 28 day study was conducted in the University of Michigan Medical Center’s 14 bed Cardiothoracic Intensive Care Unit. Alarms generated by patient monitors, the intelligent agent and alerts documented on patient flow sheets were compared. Significant improvements in the specificity of the physiologic alarms based on systolic and mean blood pressure was found on average to be 99% and 88% respectively. Even through significant improvements were noted based on this algorithm much work still needs to be done to ensure the sensitivity of alarms and methods to handle spurious sensor data due to patient or sensor movement and other influences. Blum JM, Kruger GH, Sanders KL, Gutierrez J, Rosenberg AL. Specificity improvement for network distributed physiologic alarms based on a simple deterministic reactive intelligent agent in the critical care environment.     

Deoxygenation inhibits the volume-stimulated, Cl(-)-dependent K+ efflux in SS and young AA cells: a cytosolic Mg2+ modulation

We recently reported that the Cl(-)-dependent K+ (K:Cl) efflux, which can be stimulated by cell swelling in the presence of inhibitors of the Na+ pump (ouabain) and of the Na-K-Cl cotransport (bumetanide), is highly active in young AA and SS RBCs. We report here that deoxygenation inhibits volume-stimulated K:Cl efflux in SS and reticulocyte-enriched density-separated SS and AA RBCs. In SS whole blood, the K:Cl efflux stimulated by hypotonic (220 mOsm) swelling was reduced from 9.2 +/- 2 (mean +/- SE) in oxygen to 2.7 +/- 1.9 (mmol/L cell/h = flux units = FU) (n = 4) under deoxygenated conditions (P less than .005). Deoxygenation also decreased the acid pH-stimulated K:Cl efflux from 5.9 +/- 1.5 to 3.7 +/- 1.1 FU (n = 3) (P less than .025) but did not inhibit NEM-stimulated K:Cl transport. The effect of deoxygenation on density-separated SS cells is similar: When fraction SS2 (reversible discocytes) is deoxygenated under hypotonic conditions, the K:Cl efflux is reduced by 50%. In reticulocyte-enriched AA cells obtained from anemic patients, deoxygenation under hypotonic conditions also reduces K+ efflux by 50%. In SS cells only, deoxygenation under isotonic conditions results in an increased Cl(-)-independent K+ efflux. Because ionized Mg2+ in the cytosol increases during deoxygenation, we investigated the effect of external and internal Mg2+ on the volume-stimulated K:Cl efflux. Removal of external Mg2+ did not influence the rate of transport in oxygenated cells. When internal Mg2+ was clamped at 0.15 mmol/L with A23187 and EDTA at ionized cytosolic Ca2+ = O, however, the inhibitory effect of deoxygenation on the K:Cl efflux was eliminated. We conclude that deoxygenation inhibits the volume-stimulated, Cl(-)-dependent K+ efflux in AA and SS young red cells by concomitantly increasing ionized cytosolic Mg2+.