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Biomedical subjects

F J Kim

Publications and source records attributed to F J Kim.

17 recordsLinked to original sources
PubMed2004

Hypotension and acute pulmonary insufficiency following transfusion of autologous red blood cells during surgery: a case report and review of the literature.

Transfusion of autologous blood is associated with fewer complications, although all untoward events of transfusion may not be negated with this strategy. We report a case of acute pulmonary insufficiency and hypotension following transfusion of autologous packed red blood cells (PRBCs) in a patient, who was undergoing major surgery. Anti-HLA class-I and class-II and anti-granulocyte antibodies were measured in the unit and in the recipient. Neutrophil (PMN)-priming activity was measured as the augmentation of the formyl-Met-Leu-Phe-activated respiratory burst. No immunoglobulins were identified; however, significant lipid-priming activity was present in the implicated, autologous PRBC unit that primed PMNs from both healthy people and the recipient. In addition, lipids, identical to those that accumulate during PRBC storage, caused significant hypotension when infused into rats at similar concentrations found in stored PRBCs. We conclude that the observed transfusion-related acute lung injury reaction with significant hypotension may be the result of two independent events: the first is related to inherent host factors, in this case major surgery, and the second is the infusion of lipids that accumulate during the routine storage of PRBCs.

Adenocarcinoma↗
PubMed2001

Image-guided therapy in urology.

Technological breakthroughs have advanced the fields of urology, radiology, and minimally invasive surgery. Today, the various imaging modalities are increasingly applied to guiding therapy. Among the procedures now in use or under development are percutaneous cyst drainage or sclerotherapy; tissue ablation with high-intensity focused ultrasound, cold, heat, or photon radiation; and conformal radiation and brachytherapy. As current limitations are overcome, image-guided therapy will expand.

Animals↗
PubMed2000

Definition of an amino-terminal domain of the human T-cell leukemia virus type 1 envelope surface unit that extends the fusogenic range of an ecotropic murine leukemia virus.

Murine leukemia viruses (MuLV) and human T-cell leukemia viruses (HTLV) are phylogenetically highly divergent retroviruses with distinct envelope fusion properties. The MuLV envelope glycoprotein surface unit (SU) comprises a receptor-binding domain followed by a proline-rich region which modulates envelope conformational changes and fusogenicity. In contrast, the receptor-binding domain and SU organization of HTLV are undefined. Here, we describe an HTLV/MuLV envelope chimera in which the receptor-binding domain and proline-rich region of the ecotropic MuLV were replaced with the potentially corresponding domains of the HTLV-1 SU. This chimeric HTLV/MuLV envelope was processed, specifically interfered with HTLV-1 envelope-mediated fusion, and similar to MuLV envelopes, required cleavage of its cytoplasmic tail to exert significant fusogenic properties. Furthermore, the HTLV domain defined here broadened ecotropic MuLV envelope-induced fusion to human and simian cell lines.

Amino Acid Sequence↗
PubMed2000

Renal transplantation: laparoscopic live donor nephrectomy.

Laparoscopic nephrectomy is now performed at many centers worldwide. This technique for organ harvesting offers less postoperative pain, quicker convalescence, and an optimal cosmetic result when compared with the traditional open approach. With experience, the laparoscopic technique is accomplished without compromise to donor safety or allograft function, and complications are comparable with the rates in open historic series. Longer operative times and the need for disposable equipment result in greater hospital costs; however, the quicker convalescence permits patients to resume activity sooner, allowing marked cost savings for patients and employers. The laparoscopic technique is associated with a steep learning curve. Launching a successful laparoscopic living donor program requires a dedicated coordinated effort involving physicians, nurses, and hospital administration. The ultimate impact of this technique on the willingness of individuals to donate has not yet been determined.

Humans↗
PubMed1998

Complications of acucise endopyelotomy.

Endoscopic management of ureteropelvic junction (UPJ) obstruction has a success rate of 80% to 86%. We have been performing a ureteral cutting balloon procedure under fluoroscopic control (Acucise endopyelotomy) for UPJ obstruction at Loyola University Medical Center since 1991. The overall success rate in 77 patients was 78%. All patients had a preoperative intravenous urogram or a retrograde pyelogram, but none had vascular imaging studies. Acucise endopyelotomy consisted of a posterolateral incision of the UPJ and placement of an endopyelotomy or double-J stent. Foley catheter placement at the end of the procedure demonstrated significant gross hematuria in three patients (4%). All three remained hemodynamically stable but with significant drops in postprocedure hemoglobin levels, which necessitated blood transfusion. Aggressive management included angiographic studies and embolization of lower-pole branching arteries in two patients (3%). One patient stopped bleeding after being given two units of blood. None of the patients required an open exploratory procedure. Although the risk of vascular injury is low with Acucise endopyelotomy, prolonged postoperative gross hematuria does mandate investigation and observation. Angiographic embolization appears to be the therapeutic modality of choice for patients with hemorrhagic complications after an Acucise endopyelotomy.

Adolescent↗
PubMed1996

Differential expression of superoxide dismutases containing Ni and Fe/Zn in Streptomyces coelicolor.

Streptomyces coelicolor contains two distinct superoxide dismutase (SOD) activities detected on native PAGE. The level of each changed differently depending on growth media and scarcely responded to paraquat, a superoxide-generating agent. The total SOD activity doubled in late exponential phase compared with that in mid-exponential phase and less than double upon treatment with plumbagin, another superoxide-generating agent. The two SODs from S. coelicolor ATCC 10147 (Müller) strain were purified to near homogeneity. SOD1, a tetramer of 13.4-kDa subunits, was found to be a novel type of SOD containing 0.74 mol nickel/mol subunit as determined by atomic absorption spectroscopy. SOD2, a tetramer of 22.2-kDa subunits, was found to contain 0.36 mol iron and 0.26 mol zinc/mol subunit. The N-terminal amino acid sequences of both SODs were determined. SOD2 is similar to manganese-containing superoxide dismutases (MnSODs) and iron-containing superoxide dismutases (FeSODs) from other organisms, whereas SOD1 is less similar to known SODs but still contains a few conserved amino acids. The effects of metals and chelating agents on the expression of these two SODs were examined. The presence of nickel at micromolar concentrations in growth media induced the expression of SOD1 (nickel-containing superoxide dismutase; NiSOD), whereas the expression of SOD2 (iron/zinc-containing superoxide dismutase; FeZnSOD) was repressed. The changes in SOD activities were positively correlated with the amount of each enzyme as determined by immunoblotting, suggesting that metals do not modulate the activity per se but the amount of each protein.

Amino Acid Sequence↗
PubMed1996

Characterization of the nuclear export signal of human T-cell lymphotropic virus type 1 Rex reveals that nuclear export is mediated by position-variable hydrophobic interactions.

We previously determined that amino acids 64 to 120 of human T-cell lymphotropic virus type 1 (HTLV-1) Rex can restore the function of an effector domain mutant of human immunodeficiency virus type 1 (HIV-1) Rev (T. J. Hope, B. L. Bond, D. McDonald, N. P. Klein, and T. G. Parslow, J. Virol. 65:6001-6007, 1991). In this report, we (i) identify and characterize a position-independent 17-amino-acid region of HTLV-1 Rex that fully complements HIV-1 Rev effector domain mutants and (ii) show that this 17-amino-acid region and specific hydrophobic substitutions can serve as nuclear export signals. Mutagenesis studies revealed that four leucines within the minimal region were essential for function. Alignment of the minimal Rex region with the HIV-1 Rev effector domain suggested that the position of some of the conserved leucines is flexible. We found two of the leucines could each occupy one of two positions within the context of the full-length HTLV-1 Rex protein and maintain function. The idea of flexibility within the Rex effector domain was confirmed and extended by identifying functional substitutions by screening a library of effector domain mutants in which the two regions of flexibility were randomized. Secondly, the functional roles of the minimal Rex effector domain and hydrophobic substitutions were independently confirmed by demonstrating that these effector domains could serve as nuclear export signals when conjugated with bovine serum albumin. Nuclear export of the wild-type Rex conjugates was temperature dependent and sensitive to wheat germ agglutinin and was blocked by a 20-fold excess of unlabeled conjugates. Together, these studies reveal that position-variable hydrophobic interactions within the HTLV-1 Rex effector domain mediate nuclear export function.

Amino Acid Sequence↗
PubMed1995

Reperfused gut elaborates PAF that chemoattracts and primes neutrophils.

Our in vivo model of mesenteric ischemia/reperfusion (I/R) has shown that the gut serves as a priming bed for neutrophils (PMN). Activation of phospholipase A2 (PLA2) during ischemia temporally precedes PMN sequestration in the gut and the appearance of primed PMN in the portal circulation. Therefore, we hypothesized that reperfused gut secretes platelet activating factor (PAF) via PLA2 activation that is responsible for increased PMN chemotaxis and priming for superoxide (O2-) generation. Sprague-Dawley rats underwent gut ischemia/reperfusion (45 min SMA occlusion/2 hr reperfusion) or sham laparotomy. Distal ileum was harvested, rinsed with bacteriostatic saline/neomycin, and incubated for 1 hr at 37 degrees C in RPMI 1640 and the cell-free supernatant was collected. Normal human PMNs, isolated by plasma-Percoll gradients, were pretreated with or without a PAF receptor antagonist (WEB 2170). Chemotaxis toward gut supernatant was then measured by the agarose method. Additionally, PMNs were preincubated with or without WEB 2170 and their O2- release in response to 1 microM FMLP was measured by the Vmax of SOD-inhibitable cytochrome c reduction. Reperfused gut produced a chemotactic index of 2.1 +/- 0.1 compared to 0.2 +/- 0.9 following sham laparotomy (P < 0.05); this was reduced to 0.4 +/- 0.9 with PAF receptor blockade. Similarly, gut I/R supernatant primed PMNs for O2- (P < 0.05) compared to laparotomy, and this effect was abrogated by a PAF antagonist. These data suggest that reperfused gut can elaborate PAF which chemoattracts and primes PMNs for O2- generation.

Animals↗
PubMed1995

Postinjury neutrophil priming and activation: an early vulnerable window.

BACKGROUND: Generation of extracellular, cytotoxic superoxide anion (O2-) by polymorphonuclear neutrophils (PMNs) contributes to an unbridled inflammatory response that can precipitate multiple organ failure (MOF). Release of O2- is markedly enhanced when activated PMNs have been previously "primed" by inflammatory mediators, such as those expressed after trauma. We therefore hypothesized that PMN priming occurs as an integral part of the early inflammatory response to trauma. METHODS: PMNs were obtained from 17 high-risk patients with torso trauma at 3, 6, 12, 24, 48, and 72 hours after injury, as well as from 10 healthy donors, and the in vitro release of O2- was quantitated with a kinetic, superoxide dismutase (SOD)-inhibitable cytochrome c reduction assay. PMN O2- release was measured in the presence and absence of 1 mumol/L N-formyl-methionyl-leucyl-phenylalanine (fMLP) and after priming and activation with 20 nmol/L platelet-activating factor (PAF) and 1 mumol/L fMLP, respectively. RESULTS: In vitro PMN O2- release was used to determine whether postinjury PMNs were (1) activated in vivo, (2) primed in vivo, or (3) primable in vitro. Unstimulated PMNs from trauma patients spontaneously expressed modest amounts of O2- in vitro from 6 to 48 hours after injury, suggesting endogenous activation. Also, fMLP-activated PMNs collected between 3 and 24 hours after injury expressed more O2- than controls (p < or = 0.02), indicating in vivo, trauma-related priming. Furthermore, postinjury PMNs were maximally primed in vivo (i.e., in vitro exposure to PAF before fMLP activation failed to significantly enhance O2- release) as compared to PMNs treated with fMLP. CONCLUSIONS: These data indicate that major torso trauma (first hit) primes and activates PMNs within 3 to 6 hours after injury. Consequently, we postulate that postinjury priming of PMNs may create an early vulnerable window during which a second hit (e.g., a secondary operation or delayed hemorrhage) activates exuberant PMN O2- release, rendering the injured patient at high risk for MOF.

Adolescent↗
PubMed1995

CD11b blockade prevents lung injury despite neutrophil priming after gut ischemia/reperfusion.

Gut ischemia/reperfusion (I/R) provokes lung injury via a mechanism that involves neutrophils [polymorphonuclear neutrophils (PMNs)]. CD11b/CD18 (alpha mB2) is the integrin receptor on PMNs critical for adhesion-dependent oxidative burst. The purpose of this study was to investigate the mechanistic role of CD11b in the process of gut I/R-induced lung injury. Sprague-Dawley rats underwent 45 minutes of superior mesenteric artery (SMA) occlusion with and without CD11b monoclonal antibody treatment (IB6) (1 mg/kg, i.v.), before SMA clamping. At 2-hour reperfusion, PMN presence in tissue was quantitated by myeloperoxidase activity and circulating PMN priming determined by the difference in superoxide production with and without N-formyl-methionyl-leucyl-phenylalanine, whereas lung leak was assessed by 125I-albumin lung/blood ratio. In sum, CD11b blockade prevented gut I/R-induced lung leak, but did not attenuate gut I/R-induced PMN priming or tissue PMN accumulation. In conclusion, gut I/R promotes PMN priming and PMN adhesion in both local and distant beds via receptors other than CD11b, but this B2 integrin receptor is critical for PMN-mediated endothelial injury.

Animals↗
PubMed1995

Gut phospholipase A2 mediates neutrophil priming and lung injury after mesenteric ischemia-reperfusion.

Intestinal ischemia-reperfusion (I/R) provokes polymorphonuclear neutrophil (PMN)-mediated lung injury via a process characterized by circulating PMN priming, pulmonary PMN sequestration, and increased microvascular leak in the lung. We found in rats subjected to intestinal I/R (ischemia 45 min and reperfusion 6 h) that 1) intestinal phospholipase A2 (PLA2) was activated during ischemia, 2) circulating PMN priming (assessed by superoxide production with N-formyl-Met-Leu-Phe) occurred after 1 h reperfusion, and 3) exaggerated 125I-labeled albumin lung leak occurred after 2 h reperfusion, compared with sham-treated animals (P < 0.05). Treatment with a PLA2 inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA2 activity and abrogated subsequent PMN priming and lung leak (P < 0.05). However, when quinacrine was administered after 2 h of reperfusion, circulating PMN priming and lung leak continued to evolve despite suppression of intestinal PLA2 activity. We conclude that intestinal PLA2 activation may be a prerequisite for the sequelae of circulating PMN priming and pulmonary microvascular leak observed after intestinal I/R.

Animals↗
PubMed1994

Interleukin-6 potentiates neutrophil priming with platelet-activating factor.

BACKGROUND: Polymorphonuclear neutrophil (PMN) priming appears to be an important event in the pathogenesis of hyperinflammatory states, resulting in adult respiratory distress syndrome or multiple organ failure. Interleukin-6 (IL-6) is an integral mediator of the acute stress response to injury and infection, but excessive and prolonged systemic levels have been associated with morbidity and mortality following trauma, burns, and elective surgery. We hypothesized that IL-6 primed PMNs for exaggerated cytotoxicity. However, we have been unable to directly prime PMNs for superoxide release with IL-6. OBJECTIVE: To determine whether IL-6 acted in concert with another inflammatory mediator (platelet-activating factor [PAF]) to prime PMNs. METHODS: Polymorphonuclear neutrophils isolated from healthy human donors were incubated for varying times with IL-6 (0.01 to 100 ng/mL), PAF (0.01 to 100 ng/mL), or a combination of IL-6 and PAF. Superoxide production was then measured with and without the addition of the PMN-activating formylpeptide formyl-methionyleucylphenylalanine. RESULTS: Over the range of times (5 to 90 minutes) and doses tested, IL-6 did not prime PMNs, while PAF primed PMNs in a dose- and time-dependent manner. Interleukin 6 (10 ng/mL) combined with a nonpriming concentration of PAF (0.1 ng/mL) primed PMNs for superoxide production over a range of incubation times. CONCLUSION: The inflammatory mediators IL-6 and PAF act synergistically to prime PMNs in vitro. This observation may begin to elucidate the mechanistic role of IL-6 in pathologic clinical states.

Analysis of Variance↗
PubMed1994

Trauma surgeons can render definitive surgical care for major thoracic injuries.

Restrictions on the operative domain of general surgeons threaten the viability of trauma surgery as a career choice. Our study hypothesis is that an experienced trauma surgeon can provide definitive care for life-threatening thoracic trauma. This analysis is based on clinical outcomes at an ACS-verified level I center in which there are more than 3000 trauma admissions managed annually under the direction of four academic trauma surgeons. We selected penetrating cardiac wounds and blunt tears of the thoracic aorta because these injuries are managed exclusively by the trauma service and the endpoints are distinct. During the past 4 years, 40 patients with cardiac wounds were delivered to the ED; 23 patients arrived dead. In the remaining 17, injury mechanisms were 15 stab wounds (SW), one gunshot wound (GSW), and one shotgun (SGW). Four of these patients required ED thoracotomy, and the remaining 13 underwent some form of prethoracotomy pericardial decompression. Survival rate without neurologic deficit was 94% (16 of 17). During this same period, 19 patients with a torn thoracic aorta from blunt injuries arrived with signs of life. In this group the injury mechanisms were automobile crash in 15, and the mean ISS was 39.7 +/- 2.3. One patient was transferred for total cardiopulmonary bypass; 17 of the remaining patients underwent aortic repair employing partial left heart bypass. Sixteen of our 18 patients lived and none developed paraplegia. In summary, excluding patients who arrived dead, survival for penetrating cardiac wounds was 94% and for blunt thoracic aortic tears 89%. In conclusion, these data support our contention that trauma surgeons can render definitive care for thoracic injuries with survival rates comparable to those reported by cardiothoracic surgeons.

Adolescent↗
PubMed1994

The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure.

Our trauma research center program entitled, "Trauma Primes Cells" is based on the fundamental hypothesis that prior exposure to multiple, sequential, sublethal cellular insults primes constructive or destructive pathways of cellular responses of subsequent injury. A major objective is to design therapy that will reduce the incidence of multiple organ failure. Although a number of inflammatory cascades have been incriminated in the pathogenesis of multiple organ failure (MOF), diffuse PMN-mediated tissue injury remains an attractive unifying concept. We have developed a sequential insult rodent model in which the priming event consisted of superior mesenteric arterial (SMA) clamping for 45 minutes followed by 6 hours of reperfusion. Following this priming event, activation was induced with a low dose of endotoxin (2.5 mg/kg). We believe that these studies support our hypothesis: mesenteric ischemic/reperfusion primes circulating PMNs. When these have been activated they can then be provoked by endotoxin to provoke distant organ injury. Primed PMNs are released from the postischemic mesenteric bed and enter the systemic circulation. They subsequently sequester in the pulmonary vascular bed where they are relatively harmless until they are activated by low dose endotoxin. These activated PMNs then migrate across the endothelium cell and release reactive oxygen metabolites.

Animals↗
PubMed1994

Disparate signal transduction in neutrophil CD18 adhesion receptor expression versus superoxide generation.

BACKGROUND: We have previously shown that platelet-activating factor (PAF) primes polymorphonuclear neutrophils (PMNs) for superoxide generation and, concurrently, increases CD11/CD18 receptor expression; both events appear central to the pathogenesis of postinjury multiple organ failure. Recently, the counterinflammatory role of the neuroendocrine response to trauma has been emphasized, and, specifically, beta-adrenergic stimulation has been found to inhibit PMN activation. METHODS: Normal human PMNs were primed with PAF (10(-9) mol/L for 5 minutes) or pretreated with beta-receptor stimulation (isoproterenol, 10(-7) mol/L) or adenylate cyclase (AC) activation (forskoklin, 10(-7) mol/L) for 5 minutes and then primed with PAF. Superoxide generation in response to N-formyl-methionyl-leucyl-phenylalanine (10(-6) mol/L) was measured by superoxide dismutase inhibitable reduction of cytochrome C and CD18 expression determined by flow cytometry. RESULTS: PAF primed PMNs for superoxide generation (229.5 +/- 42.3 nmol/10(6) cells/min versus 18.7 +/- 6.5), whereas pretreatment with beta-adrenoreceptor stimulation (112.9 +/- 20.6) or AC activation (115.3 +/- 12.6) dramatically attenuated this process (p < 0.0001). PAF also enhanced CD18 expression (6.1 +/- 1.1 mean fluorescence intensity versus 10.3 +/- 2.3), but beta-adrenoreceptor stimulation (10.1 +/- 2.1) and AC activation (9.7 +/- 1.9) had no discernible effect. CONCLUSIONS: PAF priming of PMNs for superoxide generation was inhibited by the beta-adrenergic signal transduction pathway, but CD18 expression was not regulated via this pathway.

Adult↗