Biomedical subjects

D L Kaminski

Publications and source records attributed to D L Kaminski.

At least 19 recordsLinked to original sources

PubMed1995

Comparative evaluation of educational methods in surgical resident education.

OBJECTIVE: To determine the influence of study methods on American Board of Surgery (ABS) examination performance. DESIGN: Performance on ABS examinations by and faculty evaluations of 54 categorical surgical residents from 1976 to 1992 were correlated with the residents' use of commonly available educational methods (textbooks, Selected Readings in General Surgery, grand rounds, preceptor guidance, clinical surgery review courses, surgical science review courses, Surgical Education and Self-Assessment Program [SESAP], and continuing medical education lectures) in early, late, and after residency. SETTING: An average-sized midwestern US university surgical residency. RESULTS: Residents who consistently scored above the 33rd percentile on ABS examinations had used texts early, Selected Readings later, and SESAP after residency more frequently than those with ABS In-Training Examination scores in the lower one third. Selected Readings and clinical review courses were associated with significant increases in ABS percentile scores when used in late or after residency and, along with SESAP, were used when residents improved their low ABS In-Training Examination scores. CONCLUSIONS: Independent study methods are the most effective pathway to successful ABS examination performance. Formal surgical review courses may help improve the ABS examination scores of residents at a higher risk of failure.

Clinical Competence↗

PubMed1995

Evidence for a colonic PAF receptor.

We sought to determine the effect of exogenously administered platelet-activating factor (PAF) on eicosanoid release from the left colon of the rabbit. Using an isolated buffer-perfused rabbit left colon preparation, 1.0- or 5.0-micrograms doses of PAF were infused into the inferior mesenteric artery. Effluents from the inferior mesenteric vein and colonic lumen were collected and the concentrations of the eicosanoids, prostaglandin E, 6-ketoprostaglandin F1 alpha, thromboxane B2, and leukotriene B4 (LTB4), were measured by ELISA. During PAF infusion there was a significant increase of all prostanoids, but not LTB4 into the venous effluent and colonic luminal perfusate when compared to control experiments. Additional studies were performed by pretreating the colons with the PAF antagonists WEB-2170 or alprazolam prior to PAF infusion. Both venous and luminal effluent prostanoid release was effectively blocked by WEB-2170, but not by alprazolam. Colons pretreated with WEB-2170 prior to PAF had markedly diminished tissue injury when compared to colons treated with PAF alone. Inhibition of PAF-stimulated prostanoid release by WEB-2170 suggests that a PAF-sensitive receptor is present in rabbit colonic tissue which may induce eicosanoid-mediated tissue injury.

Animals↗

PubMed1995

Gallbladder mucosal protein secretion during development of experimental cholecystitis.

The development of experimental cholecystitis produced by lysophosphatidylcholine is associated with reversal of the normal absorptive characteristics of gallbladder mucosa, resulting in the intraluminal accumulation of water, glycoprotein, and protein. The purpose of the present study was to attempt to ascertain if the protein leaks into the lumen because of the cytolytic properties of lysophosphatidylcholine or if it is due to an active secretory process and to characterize the protein produced. Experiments were performed on anesthetized cats undergoing gallbladder perfusion with and without lysophosphatidylcholine. The amount of protein in the perfusate was measured and albumin clearance from blood to gallbladder lumen was calculated with and without the administration of vesicular transport inhibitors. In separate experiments, control and lysophosphatidylcholine (LPC) produced gallbladder perfusates were collected and the protein subjected to SDS-PAGE to ascertain the nature of the protein secreted. Inhibitors of both microtubular and microfilament activity decreased the protein accumulation and clearance produced by lysophosphatidylcholine. Gallbladder white blood cell accumulation and inflammation as evaluated by beta-glucuronidase and prostaglandin E levels were not significantly altered by cytochalasin or colchicine administration. Lysophosphatidylcholine also produced significant increases in perfusate LDH levels. The protein produced was primarily a 66-kDa protein. Transfer of the protein to a nitrocellulose membrane and immunoblotting with anti-albumin antibody demonstrated that the protein was albumin. The results suggest that during the development of cholecystitis, lysophosphatidylcholine produces albumin accumulation in the gallbladder primarily by inducing an active secretory process resulting in gallbladder distension.

Albumins↗

PubMed1995

Lysophosphatidylcholine-stimulated protein and glycoprotein production by human gallbladder mucosal cells.

It has been demonstrated in experimental cholecystitis in cats produced by lysophosphatidylcholine that the development of inflammation is associated with the exsorption of a large amount of protein into the gallbladder lumen. It was subsequently demonstrated that in feline experimental cholecystitis the protein produced was albumin and that its production was decreased by vesicular transport inhibitors, suggesting an active secretory process. In the present study, the effect of lysophosphatidylcholine on protein production by fresh, isolated human gallbladder mucosal cells was evaluated. Isolated gallbladder mucosal cells were incubated with [14C]leucine for 24 hr in tissue culture medium. The cells readily incorporated the radioactive label into cellular protein, a process inhibited by cycloheximide. Exposure of the cells to lysophosphatidylcholine for 1 hr in buffer solution resulted in loss of intracellular protein into the buffer solution. Exposure of the cells for 1 hr prior to lysophosphatidylcholine administration to vesicular transport inhibitors, colchicine, and cytochalasin B and to 4 degrees C culture conditions failed to alter the lysophosphatidylcholine-produced passage of the 14C label extracellularly. SDS-PAGE evaluation of the protein produced demonstrated that human gallbladder mucosal cells continuously produced a 66-kDa protein that was not increased by increasing concentration of lysophosphatidylcholine and a 14-kDa protein that increased with increasing concentrations of lysophosphatidylcholine. Employing Western blotting with specific antibodies, the 66-kDa protein was demonstrated to not be albumin but a 66-kDa glycoprotein, and the 14-kDa protein was demonstrated to contain phospholipase A2. Human gallbladder mucosal cells produced a protein and glycoprotein in response to lysophosphatidylcholine by a mechanism not related to vesicular transport.

Carbon Radioisotopes↗

PubMed1995

Improved outcome by identification of high-risk nonocclusive mesenteric ischemia, aggressive reexploration, and delayed anastomosis.

BACKGROUND: The factors associated with outcome of patients with nonocclusive mesenteric ischemia are poorly defined. METHODS: Over a 7-year period, 34 consecutive patients with nonocclusive mesenteric ischemia were identified. RESULTS: The mean age of the study patients was 63 years (range 31 to 94); 21 of 34 (62%) were men. The mean delay in diagnosis was 31 hours (range 7 hours to 6 days). Seven of 34 (21%) underwent preoperative visceral arteriography. Two of these 7 required surgery, and both died as a result of intestinal infarction. The remaining 27 had the diagnosis made at celiotomy. Among the 29 who were explored, 16 of 29 (55%) had intestinal infarction. Twenty-one of 29 (72%) had segmental bowel injury whereas 8 of 29 (28%) had massive injury. Among those with segmental infarction, primary anastomosis was performed in 12 of 21 patients (57%); 5 of the 12 (42%) died. Nine of 21 patients (43%) underwent delayed anastomosis; 2 of the 9 (22%) died. No patient with massive injury underwent primary anastomosis. Second-look laparotomy was performed on 22 of 29 (76%). Eleven of those 22 (50%) had a further bowel resection. Overall, 16 of 29 (55%) who underwent surgery for nonocclusive mesenteric ischemia are alive. CONCLUSIONS: Improved survival from nonocclusive mesenteric ischemia is dependent upon the identification of high-risk groups, aggressive reexploration, and delayed intestinal anastomosis.

Acute Disease↗

PubMed1995

Rifampicin induction of lidocaine metabolism in cultured human hepatocytes.

In our laboratory, cultured human hepatocytes are being evaluated as an experimental system to study drug interactions. We report the effect of a known cytochrome P450 (CYP) inducer, rifampicin, on the metabolism of lidocaine by primary human hepatocytes. Rifampicin has been shown to induce CYP3A4, a major human hepatic CYP isozyme that is known to metabolize lidocaine to its primary metabolite, monoethylglycinexylidide. Human hepatocytes were cultured on collagen-coated plates in serum-free, hormone-supplemented Waymouth medium for a 3-day period before they were treated with rifampicin at 50 microM for 1 to 3 days. Hepatocytes isolated from five individuals were studied, and, in all cases, lidocaine metabolism was found to be induced by rifampicin, as demonstrated by a higher rate of monoethylglycinexylidide formation than concurrent controls. For three of the hepatocyte cultures, lidocaine metabolism was evaluated at various times after treatment. Induction was observed at 1 day after treatment, and reached higher levels at day 2 or 3. The level of induction was found to be approximately 100% for two hepatocyte isolations and approximately 600% for one isolation. In a separate experiment, hepatocytes were treated with rifampicin for a 2-day period. Rate of lidocaine metabolism at multiple substrate concentrations (10-120 microM) were then studied. Rifampicin induction of lidocaine metabolism (approximately 100%) was observed at all the lidocaine concentrations studied. Lineweaver-Burk plot of the data showed an increase in Vmax and a less significant change in Km. Induction of lidocaine metabolism by rifampicin (concentrations of 0.1-50 microM) was found to be dose-dependent, with significant induction observed at 1 microM and higher concentrations. (ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

Glutamine transport in isolated human hepatocytes and transformed liver cells.

The transport of L-glutamine was examined in isolated adult and fetal human hepatocytes as well as in the human hepatoma cell lines HepG2 and SK-Hep. In all cells studied, glutamine uptake was at least 85% Na(+)-dependent. Kinetic analysis of the Na(+)-dependent component indicated mediation by a single transporter in three human hepatocyte preparations and in SK-Hep cells, whereas two transporters appeared to be responsible for glutamine uptake in HepG2 cells and in hepatocytes from the liver of one male patient. Amino acid inhibition analysis showed primary mediation by System N in fetal and adult hepatocytes, whereas System ASC was principally responsible for glutamine uptake in transformed cells. Similar to the rat transporter, human System N was pH-sensitive, stereospecific, and responsive to treatment with steroid hormones. Although the human carrier was less tolerant of Li(+)- for Na+ substitution, glutamine transport in primary human hepatocytes was stimulated by treatment with hypotonic buffer (cell swelling), as reported in rat parenchymal cells. In contrast, glutamine transport in hepatoma cells was relatively insensitive to changes in extracellular pH and failed to show enhanced activity in response to hypoosmotic challenge. Collectively, the data suggest that markedly distinct plasma membrane transporters mediate the concentrative uptake of glutamine in normal and transformed human hepatocytes, and that the salient properties of System N have been largely conserved from rat to man.

Adult↗

PubMed1994

Effect of platelet-activating factor and its antagonists on colonic dysmotility and tissue levels of colonic neuropeptides.

We investigated whether platelet-activating factor (PAF) alters colonic tissue levels of substance P and vasoactive intestinal peptide (VIP), two neuropeptides that regulate colonic motility. Left colons were harvested from NZ White Rabbits and underwent vascular perfusion via the inferior mesenteric artery. Strain gauge transducers were sewn onto the serosal surface of the colon to evaluate colonic motility. Colons were perfused with either buffered saline alone or with 5.0 x 10(-5) M PAF. PAF administration increased tissue VIP and substance P levels and decreased the force of colonic contractions. Pretreatment with WEB-2170 or alprazolam decreased concentrations of both tissue neuropeptides, and decreased the force of colonic contractions and minute motility index. These results suggest that both VIP and substance P are stimulated by PAF and may participate in colonic dysmotility during inflammatory states.

Alprazolam↗

PubMed1994

Hyperbilirubinemia without common bile duct abnormalities and hyperamylasemia without pancreatitis in patients with gallbladder disease.

OBJECTIVE: To determine the incidence of jaundice and hyperamylasemia in the absence of common bile duct abnormalities or clinical pancreatitis in patients undergoing cholecystectomy. DESIGN: A continuous, prospective analysis of a consecutive case series was performed on all patients undergoing cholecystectomy. SETTING: An urban, tertiary care university hospital. PATIENTS: Adult patients with gallbladder disease. INTERVENTION: All patients underwent cholecystectomy. MAIN OUTCOME MEASURES: The presence or absence of common bile duct abnormalities was evaluated by cholangiography, and pancreatitis was identified by clinical signs, imaging studies, and direct visual inspection during cholecystectomy. RESULTS: All patients (N = 1746) undergoing cholecystectomy were prospectively categorized as having chronic calculous (n = 1410), acute calculous (n = 217), chronic acalculous (n = 70), or acute acalculous (n = 49) gallbladder disease. It was uncommon for patients with chronic calculous cholecystitis to have an elevated bilirubin level with no choledocholithiasis and a normal common bile duct or to have hyperamylasemia without pancreatitis. Twenty-five percent of the patients with acute calculous cholecystitis had a serum bilirubin level between 34 and 86 mumol/L (2.0 and 5.0 mg/dL) with no common bile duct abnormality and 4% had hyperamylasemia without pancreatitis. Over one third of the patients with acute acalculous cholecystitis had an elevated bilirubin level with a normal common bile duct or an elevated amylase level without pancreatitis. CONCLUSION: Jaundice and hyperamylasemia can be produced by gallbladder disease alone.

Acute Disease↗

PubMed1994

Laparoscopic cancer surgery. Lessons from gallbladder cancer.

Laparoscopic cholecystectomy (LC) may inhibit the discovery of unsuspected gallbladder cancer, and the effect of LC on the prognosis of gallbladder cancer is unknown. We present two cases of unsuspected gallbladder cancer removed laparoscopically and report the discovery of peritoneal tumor implantation at the umbilical port site 21 days after LC. Although gallbladder carcinoma flow cytometry has been reported to be of prognostic value by Japanese investigators, this technique did not distinguish herein between an invasive adenocarcinoma and carcinoma in situ. A cellular doubling time of 56 h was calculated from one tumor. When unsuspected invasive gallbladder cancer is found after LC, laparoscopic port sites should be inspected at reoperation and, at a minimum, the port site through which the gallbladder was removed should be widely excised. This demonstration of cancer recurrence in laparoscopic port sites may limit the application of laparoscopy to elective cancer resection.

Adenocarcinoma↗

PubMed1994

The effect of Clostridium difficile toxin on colonocyte prostanoid activity.

Antibiotic-associated colitis is caused by Clostridium difficile toxin. However, the pathophysiology of this entity is poorly understood. The aim of this study was to determine the effects of C. difficile toxin on colonocyte cyclooxygenase and phospholipase A2 (PLA2) activity. A transformed colonocyte cell line (Caco-2) was grown to confluency on 6 well plates. The cells were stimulated with graded concentrations of C. difficile toxin. In separate experiments, the cells were pretreated for one hour prior to stimulation with the cyclooxygenase inhibitor, indomethacin, or the glucocorticoid, dexamethasone. The culture media was collected one hour following C. difficile stimulation. Prostaglandin E2 (PGE2), 6-keto prostaglandin F1 alpha (6KPGF), thromboxane B2 (TxB2) and leukotriene B4 (LTB4) levels were determined in the media by an ELISA. Platelet activating factor (PAF) concentration was determined by a RIA. C. difficile toxin stimulated PGE2 and 6KPGF levels in a dose dependent fashion but failed to stimulate TxB2, LTB4 or PAF. Prostanoid production was inhibited by indomethacin dose dependently but was not inhibited by dexamethasone. The presence of indomethacin resulted in production of PAF. Our results show that the effects of C. difficile toxin on colonocytes are mediated by cyclooxygenase activity. The increase in PAF formation associated with indomethacin administration suggests that the prostanoids modulate PLA2 activity and inhibit PAF formation.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Studies on the etiology of acute acalculous cholecystitis: the effect of lipopolysaccharide on human gallbladder mucosal cells.

Previous studies in animals have shown that lipopolysaccharide produces experimental cholecystitis possibly through a platelet-activating factor-prostanoid mediated process. In this study it was intended to evaluate the effect of LPS on primary cultures of human gallbladder mucosal cells. Gallbladder mucosal cells were isolated from gallbladders removed during routine cholecystectomies or other operations. The cells were cultured for 24 h before treatment. Unstimulated cells produced low levels of prostanoids and significant basal levels of PAF. LPS produced stimulation of eicosanoid and PAF secretion. The increased prostanoid formation was not enhanced when LPS and PAF were administered together. Prostanoid synthesis was inhibited by the administration of a cyclooxygenase inhibitor while administration of a PAF receptor antagonist significantly increased prostanoid formation, suggesting that increased PAF levels function as a negative control mechanism to decrease prostanoid synthesis. The results suggest that endotoxemia may produce a cascade of inflammatory processes in human gallbladder mucosal cells resulting in the development of acute acalculous cholecystitis.

Acute Disease↗

PubMed1994

The production of experimental cholecystitis by endotoxin.

Acute acalculous cholecystitis (AAC) is a severe inflammatory disorder of the gallbladder. It occurs primarily in patients acutely ill from other disorders and is related to sepsis and shock. We previously found that platelet-activating factor (PAF), a phospholipid autacoid purported to be a mediator of the shock response, produced AAC. This study was performed to determine the effect of intravenous lipopolysaccharide (LPS) on feline gallbladders. Anesthetized cats underwent LPS administration with and without administration of a cyclooxygenase inhibitor and PAF antagonist. Gallbladder inflammation was evaluated by quantitation of luminal water transport and tissue myeloperoxidase levels. In an attempt to understand the mechanisms of the response, gallbladder perfusate and tissue prostanoid and PAF levels were quantitated as were serum PAF levels. LPS administration resulted in alteration of the normal absorptive pattern of the gallbladder mucosa to exsorption of fluid into the gallbladder lumen, increased tissue myeloperoxidase levels and increased serum PAF levels. This was associated with increased gallbladder tissue and perfusate prostanoid levels and increased perfusate PAF levels. Indomethacin prevented the pro-inflammatory changes in the gallbladder produced by LPS. The PAF antagonist, alprazolam, increased gallbladder prostanoid production when administered alone and with LPS. The administration of LPS resulted in the production of acute changes in the gallbladder consistent with cholecystitis. These changes being prevented by a cyclooxygenase inhibitor suggests that development of AAC may be related to the release of systemic and local pro-inflammatory substances.

Alprazolam↗

PubMed1994

Platelet-activating factor mediates trinitrobenzene induced colitis.

Platelet-activating factor (PAF) is an endogenous phospholipid which may be an important mediator of shock and inflammation. Recent evidence suggests that PAF plays a role in the development of ischemic colitis and inflammatory bowel disease. Its effects are mediated by second messengers, including the arachidonic acid metabolites. Using an ex vivo isolated left colon rabbit perfusion model, our aims were to determine whether exogenously administered trinitrobenzene sulfonic acid (TNB), which produces experimental colitis, stimulates both PAF and eicosanoid release in the colon, and if so, whether this effect can be blocked by a PAF antagonist. Colonic inflammation was induced by the intracolonic administration of 0.25 ml of 50% ethanol containing 30 mg of TNB. Tissue and perfusate concentrations of the eicosanoids, [prostaglandin E (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2), leukotriene B4 (LTB4)] and the autocoid PAF were measured by ELISA. During TNB infusion there was a significant increase in tissue levels of PAF compared to control colons. Additional studies performed pretreating the colons with the PAF receptor antagonist WEB-2170 prior to TNB infusion blocked PAF release. TNB stimulated release of luminal eicosanoids except LTB4 and suppressed release of tissue prostanoids. Pretreatment with WEB-2170 prior to TNB inhibited luminal eicosanoids, and inhibited PGE2 and prostacyclin, but not TX tissue suppression. Inhibition of TNB-stimulated PAF release by WEB-2170 suggests that PAF may play a role in TNB-induced colitis and this phenomenon may mediate tissue injury.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Noncardiac operations in patients supported with mechanical circulatory support devices.

BACKGROUND: Recent advances in technology as well as refinements of patient selection criteria have improved results of ventricular assistance in patients with end-stage heart disease. With a "normal" cardiac output and the resultant improvement in end-organ perfusion, some patients revert to normal or near normal physiology. Seven patients supported with cardiac assist devices who have undergone general surgical, nonassist device related procedures with the assist device in place are presented. STUDY DESIGN: This is a historical review of seven cases. RESULTS: The surgical procedures included three cholecystectomies, one dialysis catheter placement, and one thoracoscopy. Six patients had Thoratec ventricular assist devices (Thoratec Laboratories Corp., Berkeley, CA) and one was supported with a Jarvik (Symbion, Inc., Tempe, AZ) total artificial heart. In one patient, postcholecystectomy bleeding was the only complication that may have been directly attributable to having an assist device in place. Four patients underwent successful transplantation and three patients died, two during support and one after transplantation. CONCLUSIONS: As heart transplant waiting lists become longer and when permanent ventricular assist devices become available, an increasing number of patients on ventricular assistance will have noncardiac related pathology requiring operative intervention. In our experience, patients supported on mechanical assist devices tolerated these procedures well.

Adult↗

PubMed1994

Acute acalculous cholecystitis in the critically ill.

Acute acalculous cholecystitis, inflammation of the gall-bladder without evidence of calculi, accounts for 2 to 15% of all cases of acute cholecystitis. The incidence of acute acalculous cholecystitis in adults undergoing cholecystectomy may be as high as 15 per cent and up to 32 per cent in the pediatric population. During the past 10 years, 22 patients who were being treated in the intensive care unit for other reasons underwent cholecystectomy for acute acalculous cholecystitis. Eighteen (82%) of the patients were male, the average age was 61 years, and patients spent an average of 19 days in the intensive care unit prior to cholecystectomy. The most common clinical findings were right upper quadrant tenderness and pain. Fifteen (68%) of the patients had a previous operative procedure. HIDA scans were positive in all 12 patients in which they were performed. Ultrasounds were positive in 13 of 17 (76%) patients, and CT scans 7 of 9 (78%). Nine (41%) patients died. Early diagnosis with rapid intervention is crucial in managing this disease if outcome is to be improved. Gangrene and/or necrosis of the gallbladder was present in 13 (59%) of patients, suggesting that cholecystectomy may be the best approach to management.

Abdominal Pain↗

PubMed1993

Preoperative pulmonary function evaluation for laparoscopic cholecystectomy.

OBJECTIVE: Hypercarbia with respiratory acidosis is a recognized complication of laparoscopic cholecystectomy. This study was performed to identify preoperatively those patients who may develop hypercarbia and acidosis during the procedure. DESIGN: Retrospective analysis of preoperative variables. PATIENTS: Thirty-one consecutive patients underwent laparoscopic cholecystectomy at one institution who were receiving both preoperative pulmonary function tests and arterial blood gas analysis. RESULTS: More than 80 demographic, laboratory, and perioperative variables were entered into a univariate analysis to identify predictors of intraoperative acidosis (pH, < 7.35). Patient age, duration of the procedure, and preoperative blood gas values were not predictors of intraoperative acidosis. Several univariant predictors for patients experiencing carbon dioxide pneumoperitoneum-induced hypercarbia were identified; these included an elevated American Society of Anesthesiologists classification and significant decreases in forced expiratory flow at 25% of maximum, maximal forced expiratory flow, maximal voluntary ventilation, vital capacity, inspiratory capacity, and diffusing capacity of the lung for carbon monoxide. CONCLUSIONS: This study suggests that neither age nor preoperative arterial blood gas values are predictive of intraoperative hypercarbia and acidosis during periods of carbon dioxide pneumoperitoneum. However, preoperative pulmonary function measures of decreased flow, limited capacity, and compromised diffusion do correspond to the development of intraoperative acidosis. Preoperative evaluation with pulmonary function tests demonstrating forced expiratory volumes less than 70% of predicted values and diffusion defects less than 80% of predicted values can identify those patients who are at risk of developing hypercarbia and acidosis.

Acidosis, Respiratory↗

PubMed1993

Clinical skills acquired during third-year surgical clerkships.

An instrument was developed to survey third-year medical students about their experience with 18 clinical skills that are generally recognized as required learning for the third-year surgical clerkship. The same instrument was adapted to ascertain which surgical skills 25 fourth-year medical students, 25 surgical residents, and 25 practicing surgeons thought should be acquired during the third-year surgical clerkship. None of these evaluators had completed medical school or residency at our institution. A remarkable degree of conformity was found in the rankings of the 18 clinical skills by senior students, surgical residents, and practicing surgeons; fourth-year students rated only central venous line placement and simple operative procedures as significantly more important than did more senior evaluators. The third-year medical students' actual surgical clerkship experience with 10 out of the 18 skills was significantly below the overall competency levels desired by the graduate groups. Our survey demonstrates that both students and graduates attach similar importance to the acquisition of clinical skills in the third-year surgical curriculum. The instrument utilized in this study to measure students' experience and satisfaction with this phase of their education was reliable, the measurements were consistent, and this information was useful in the evaluation and modification of the curriculum.

Catheterization, Central Venous↗