Biomedical subjects

G L Su

Publications and source records attributed to G L Su.

At least 19 recordsLinked to original sources

PubMed2005

Investigation of valence orbitals of propene by electron momentum spectroscopy.

The binding energy spectra and momentum distributions of all valence orbitals of propene were studied by electron momentum spectroscopy (EMS) as well as Hartree-Fock and density functional theoretical calculations. The experiment was carried out at impact energies of 1200 eV and 600 eV on the state-of-the-art EMS spectrometer developed at Tsinghua University recently. The experimental momentum profiles of the valence orbitals were obtained and compared with the various theoretical calculations. Moreover, the experiment with a new analysis method presents a strong support for the correct ordering of the orbital 8a' and 1a'', i.e., 9a' < 8a' < 1a'' < 7a'.

Journal Article↗

PubMed2005

Direct observation of distorted wave effects in ethylene using the (e,2e) reaction.

We report here the direct measurements of electron momentum distributions for ethylene using the (e,2e) reaction at different impact energies from 400 to 2400 eV. The "turn up" effects in the (e,2e) cross sections of the 1b(3g) orbital compared with the plane-wave impulse approximation calculations were observed at low and high momentum regions, and such discrepancies become smaller with the increase of the impact electron energies. It is suggested that the observed discrepancies are due to the distorted-wave effects in molecules, while appropriate theoretical calculations using distorted waves in molecules could not be achieved until now.

Journal Article↗

PubMed2005

An investigation of valence shell orbital momentum profiles of difluoromethane by binary (e,2e) spectroscopy.

The electron binding energy spectra and momentum profiles of the valence orbitals of difluoromethane, also known as HFC32 (HFC-hydrofluorocarbon) (CH(2)F(2)), have been studied by using a high resolution (e,2e) electron momentum spectrometer, at an impact energy of 1200 eV plus the binding energy, and by using symmetric noncoplanar kinematics. The experimental momentum profiles of the outer valence orbitals and 4a(1) inner valence orbital are compared with the theoretical momentum distributions calculated using Hartree-Fock and density functional theory (DFT) methods with various basis sets. In general, the shapes of the experimental momentum distributions are well described by both the Hartree-Fock and DFT calculations when large and diffuse basis sets are used. However, the result also shows that it is hard to choose the different calculations for some orbitals, including the methods and the size of the basis sets employed. The pole strength of the ionization peak from the 4a(1) inner valence orbital is estimated.

Journal Article↗

PubMed2004

The outer valance orbital electron densities of cyclopentane by binary (e,2e) spectroscopy.

The binding energy spectra and electron distributions in momentum space of the valence orbitals of cyclopentane (C(5)H(10)) are studied by Electron Momentum Spectroscopy (EMS) in a noncoplanar symmetric geometry. The impact energy was 1200 eV plus binding energy and energy resolution of the EMS spectrometer was 1.2 eV. The experimental momentum profiles of the outer valence orbitals are compared with the theoretical momentum distributions calculated using Hartree-Fock and density functional theory (DFT) methods. The shapes of the experimental momentum distributions are generally quite well described by both the Hartree-Fock and DFT calculations when the large and diffuse basis sets are used.

Journal Article↗

PubMed2001

Outcome of liver transplantation for hepatitis B: report of a single center's experience.

Results of liver transplantation (LT) for hepatitis B have improved significantly with the use of hepatitis B immune globulin (HBIG) and/or lamivudine. The aim of this study is to review the long-term outcome of patients who underwent LT for hepatitis B. Records of 41 patients who underwent LT for hepatitis B and survived 3 months or longer post-LT were reviewed. Twenty patients were administered no immunoprophylaxis or short-term intramuscular HBIG, whereas 21 patients were administered high-dose intravenous (IV) HBIG. Median post-LT follow-up in these 2 groups was 76 months (range, 4 to 155 months) and 25 months (range, 4 to 68 months), respectively. Hepatitis B recurred in 15 (75%) and 4 patients (19%) who underwent LT in the pre-HBIG and post-HBIG eras, respectively. Cumulative rates of recurrent hepatitis B at 1 and 3 years post-LT in these 2 groups were 66% and 77% and 20% and 20%, respectively (P <.001). Recurrent hepatitis B in the post-HBIG era correlated with antibody to hepatitis B surface antigen titer less than 100 IU/L. Nine patients with recurrent hepatitis B were administered lamivudine for 13 to 49 months (median, 28 months); 6 patients continued to have stable or improved liver disease, whereas 3 patients developed virological breakthrough with slow deterioration of liver disease. Long-term IV HBIG is effective in preventing recurrent hepatitis B. The risk for recurrent hepatitis B is negligible after the first year post-LT. Among patients with no virological breakthrough, lamivudine can stabilize or improve liver disease for up to 4 years in patients with recurrent hepatitis B post-LT.

Adult↗

PubMed2001

Protegrin-1 enhances bacterial killing in thermally injured skin.

OBJECTIVE: Septic complications and the emergence of drug-resistant microbes represent serious risks to patients. Recently, naturally occurring peptides have been discovered that possess potent and broad-spectrum antimicrobial activity. Protegrin-1 is particularly attractive for clinical use in human wounds because, unlike defensins, protegrin-1 retains broad antimicrobial and antifungal activity at physiologic salt concentration and in the presence of serum. The objective of this study was to examine the efficacy of protegrin-1 in killing multiple drug-resistant microbes isolated from human burn patients. DESIGN: For thein vitroexperiment, bilayer radial diffusion was performed comparing standard antibiotics with protegrin-1 on multiple-drug-resistant microbial organisms isolated from infected burn wounds. In vivo, rats received a 20% total body surface area partial-thickness burn by immersion in 60 degrees C water for 20 secs followed by wound seeding with 106 colony forming units of Silvadene-resistant Pseudomonas aeruginosa. SETTING: University of Michigan research laboratory. SUBJECTS: Adult, male Sprague-Dawley rats. INTERVENTIONS: Rats were randomized into three groups: those receiving synthetic protegrin-1, acetic acid (carrier), or gentamicin (positive control). Protegrin-1 was administered by topical application or intradermal injection. Wound tissues were harvested aseptically at different time points for quantitative bacterial counts. MEASUREMENTS AND MAIN RESULTS: In vivo and in vitro experiments revealed rapid and significant decreases in bacterial counts for protegrin-1-treated groups compared with controls. CONCLUSIONS: This study shows that protegrin-1 potentially may be used as an alternative or adjunct therapy to standard agents used to treat wound infections.

Administration, Topical↗

PubMed2001

Feasibility of biolistic gene therapy in burns.

Skin is an especially attractive target for genetic manipulation because it is readily accessible and easily monitored for both the presence and the expression of inserted genes. This study was designed to assess the feasibility of particle mediated gene transfer to burned skin and to compare the transfection efficiency, anatomic distribution, and duration of transgene expression achievable in normal versus burned skin. Two days following scald injury of varying depths in 60 degrees C water (10 s: superficial partial; 20 s: deep partial; 40 s: full thickness) reporter gene (beta-galactosidase) constructs were delivered using a gene gun at various helium pressures (200-600 psi) to normal and burned skin. A time course study was performed to examine the kinetics of transgene expression. Animals received a superficial partial thickness burn and were sacrificed 12 h, 1, 3, 5, 7, 14, or 21 days after gene transfer. India Ink injection and immunohistochemistry were used to assess the depth of the scald injury. Transfection efficiency was measured in skin homogenates 24 h after gene transfer by morphometric and chemoluminescent assays. We found that the extent of tissue damage was directly related to the duration of heat source exposure. Reporter gene activity was significantly higher in superficial partial thickness burns compared to normal controls and gradually declined with increasing tissue injury. No activity was seen in the full thickness burn group. Beta-galactosidase activity reached a maximum level 12 h after gene transfer in both normal and superficial partial thickness burned skin with no levels seen after 5 days post-transfection. These findings indicate that particle-mediated gene transfer in thermally injured skin is feasible and may provide a means of introducing biologic agents into injured tissue capable of enhancing bacterial clearance and improving wound healing.

Animals↗

PubMed2001

Comorbid illness is an important determinant of health-related quality of life in patients with chronic hepatitis C.

OBJECTIVES: Chronic hepatitis C (CHC) patients selected for entry into treatment trials have been reported to have impaired health-related quality of life (HRQOL). However, these trials have an inherent selection bias, and HRQOL in CHC patients may have been underestimated because of the exclusion of patients with comorbid illness. The aim of this study was to assess HRQOL in an unselected group of CHC patients and to identify factors associated with impairment in HRQOL. METHODS: A total of 220 consecutive eligible CHC patients were enrolled from a hepatology clinic. HRQOL was assessed by the short form 36 (SF-36) and comorbid illnesses were assessed by an interview. RESULTS: CHC patients had significantly lower SF-36 scores in all subscales and in the summary scales when compared to those of the healthy general population in the United States (p < 0.001). Compared to CHC patients entering treatment trials, our patients had lower SF-36 scores on five subscales (p < 0.001). The presence of comorbid illness was the most important predictor of HRQOL in CHC patients. However, CHC alone resulted in significantly lower SF-36 scores in all subscales and summary scales (p < or = 0.003) compared to those of the healthy U.S. population. There was no correlation between SF-36 scores and history of i.v. drug use or dependence. alcohol dependence. and serum aminotransferase levels. CONCLUSIONS: We conclude that unselected CHC patients presenting for medical evaluation have a reduced HRQOL, which is lower than that reported for CHC patients entering treatment trials. CHC alone is associated with significant impairment in HRQOL, but the presence of comorbid illness leads to further diminution in HRQOL.

Adult↗

PubMed2001

Increased severity of alcoholic liver injury in female rats: role of oxidative stress, endotoxin, and chemokines.

Alcoholic liver injury is more severe and rapidly developing in women than men. To evaluate the reason(s) for these gender-related differences, we determined whether pathogenic mechanisms important in alcoholic liver injury in male rats were further upregulated in female rats. Male and age-matched female rats (7/group) were fed ethanol and a diet containing fish oil for 4 wk by intragastric infusion. Dextrose isocalorically replaced ethanol in control rats. We analyzed liver histopathology, lipid peroxidation, cytochrome P-450 (CYP)2E1 activity, nonheme iron, endotoxin, nuclear factor-kappa B (NF-kappa B) activation, and mRNA levels of cyclooxygenase-1 (COX-1) and COX-2, tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-2 (MIP-2). Alcohol-induced liver injury was more severe in female vs. male rats. Female rats had higher endotoxin, lipid peroxidation, and nonheme iron levels and increased NF-kappa B activation and upregulation of the chemokines MCP-1 and MIP-2. CYP2E1 activity and TNF-alpha and COX-2 levels were similar in male and female rats. Remarkably, female rats fed fish oil and dextrose also showed necrosis and inflammation. Our findings in ethanol-fed rats suggest that increased endotoxemia and lipid peroxidation in females stimulate NF-kappa B activation and chemokine production, enhancing liver injury. TNF-alpha and COX-2 upregulation are probably important in causing liver injury but do not explain gender-related differences.

Animals↗

PubMed2000

Lipopolysaccharide-binding protein accelerates and augments Escherichia coli phagocytosis by alveolar macrophages.

BACKGROUND: The first step in bacterial clearance by leukocytes is attachment and phagocytosis. Although lipopolysaccharide-binding protein (LBP) is best known for potentiating LPS-induced cytokine production through a CD14-dependent pathway, recent studies suggest that LBP plays a critical role in clearance of gram-negative bacteria and is essential for survival after bacterial challenge. We therefore sought to examine LBP's effect on Escherichia coli phagocytosis by alveolar macrophages (AMs) and to determine if this effect is mediated through CD14. MATERIALS AND METHODS: Phosphatidylinositol-specific phospholipase C (PIPLC)-treated and untreated rat AMs were incubated in the presence of increasing doses of recombinant LBP or negative control protein (choramphenicol acetyltransferase) prior to E. coli-FITC (Ec-F) BioParticle challenge. Phagocytosed bacteria were assayed by fluorescence measurement. A time course study was also performed. RESULTS: LBP potentiated phagocytosis of Ec-F BioParticles by AMs in a dose-dependent fashion. Kinetic studies showed that LBP augmented Ec-F phagocytosis by 76% at 30 min. Treatment of AMs with PIPLC to remove CD14 resulted in only a partial decrease in LBP-mediated enhancement of phagocytosis. CONCLUSION: These results clearly demonstrate that LBP plays an important role in enhancing Ec-F binding and phagocytosis in a time- and dose-dependent manner. This observed increase may not require the presence of CD14 as significant potentiation of phagocytosis still occurred after PIPLC treatment. We postulate that the LBP-mediated increase in Ec-F phagocytosis can occur in the absence of CD14 through the presence of another receptor.

Acute-Phase Proteins↗

PubMed2000

Kupffer cell activation by lipopolysaccharide in rats: role for lipopolysaccharide binding protein and toll-like receptor 4.

Lipopolysaccharide (LPS) binding protein (LBP) is a key serum factor that mediates LPS activation of mononuclear cells. In the presence of LBP, 1/1,000 the concentration of LPS is sufficient to activate peripheral blood monocytes. Previous studies with Kupffer cells have shown a variable effect of serum on LPS activation of these cells and led to the conclusion that, unlike extrahepatic mononuclear cells, Kupffer cells do not respond to LPS in an LBP-dependent fashion. Because there are multiple components in serum other than LBP that might affect LPS activation, these reports with serum are difficult to interpret. To investigate the specific role of LBP in LPS activation of Kupffer cells, we produced a functional recombinant rat LBP using a baculovirus expression system, which we used to selectively examine the role of LBP's on Kupffer-cell function. Isolated Kupffer cells exposed to increasing concentrations of LPS (0, 1, 10 ng/mL) showed a dose-dependent increase in TNF-alpha production, which was augmented and accelerated by the presence of LBP. The effects of LBP on Kupffer cell activation by LPS are dependent on a functional Toll-like receptor 4 (Tlr 4) because Kupffer cells from C3H/HeJ mice failed to respond to LPS in the presence of LBP. LBP plays an important role in mediating Kupffer cell activation by LPS, and these effects are dependent on the presence of functioning Tlr 4.

Acute-Phase Proteins↗

PubMed2000

Mechanism of the alcohol cyclic pattern: role of the hypothalamic-pituitary-thyroid axis.

The cause of the cycle of urinary alcohol levels (UALs) in rats fed ethanol continually at a fixed rate is unknown. Rats were fed ethanol intragastrically at a constant dose for 2 mo, and daily body temperatures and UALs were recorded. Body temperature cycled inversely to UAL, suggesting that the rate of metabolism could be mechanistically involved in the rate of ethanol elimination during the cycle. To document this, whole body O(2) consumption rate was monitored daily during the cycle. The rate of O(2) consumption correlated positively with the change in body temperature and negatively with the change in UAL. Since the metabolic rate responds to changes in body temperature, thyroid hormone levels were measured during the UAL cycle. T(4) levels correlated positively with the O(2) consumption rate and negatively with the UALs. In a second experiment using propylthiouracil treatment, UALs did not cycle and a fall in body temperature failed to stimulate an increase in the rate of ethanol elimination. Consequently, rats died of overdose. Likewise, in a third experiment using rats with severed pituitary stalks, UALs failed to cycle and rats died of overdose. From these observations it was concluded that the UAL cycle depends on an intact hypothalamic-pituitary-thyroid axis response to the ethanol-induced drop in body temperature by increasing the rate of ethanol elimination.

Alanine Transaminase↗

PubMed1999

Activation of nuclear factor kappa B and cytokine imbalance in experimental alcoholic liver disease in the rat.

Inflammatory stimuli and lipid peroxidation activate nuclear factor kappa B (NF-kappaB) and upregulate proinflammatory cytokines and chemokines. The present study evaluated the relationship between pathological liver injury, endotoxemia, lipid peroxidation, and NF-kappaB activation and imbalance between pro- and anti-inflammatory cytokines. Rats (5 per group) were fed ethanol and a diet containing saturated fat, palm oil, corn oil, or fish oil by intragastric infusion. Dextrose isocalorically replaced ethanol in control rats. Pathological analysis was performed and measurements of endotoxin were taken, lipid peroxidation, NF-kappaB, and messenger RNA (mRNA) levels of proinflammatory cytokines (tumor necrosis factor-alpha [TNFalpha], interleukin-1 beta [IL-1beta], interferon-gamma, [IFN-gamma], and IL-12), C-C chemokines (regulated upon activation, normal T cell expressed and secreted [RANTES], monocyte chemotactic protein [MCP]-1, macrophage inflammatory protein [MIP]-1alpha), C-X-C chemokines (cytokine induced neutrophil chemoattractant (CINC), MIP-2, IP-10, and epithelial neutrophil activating protein [ENA]-78), and anti-inflammatory cytokines (IL-10, IL-4, and IL-13). Activation of NF-kappaB and increased expression of proinflammatory cytokines C-C and C-X-C chemokines was seen in the rats exhibiting necroinflammatory injury (fish oil-ethanol [FE] and corn oil-ethanol[CE]). These groups also had the highest levels of endotoxin and lipid peroxidation. Levels of IL-10 and IL-4 mRNA were lower in the group exhibiting inflammatory liver injury. Thus, activation of NF-kappaB occurs in the presence of proinflammatory stimuli and results in increased expression of proinflammatory cytokines and chemokines. The Kupffer cell is probably the major cell type showing activation of NF-kappaB although the contribution of endothelial cells and hepatocytes cannot be excluded. Downregulation of anti-inflammatory cytokines may additionally exacerbate liver injury.

Alanine Transaminase↗

PubMed1999

CD14 expression and production by human hepatocytes.

BACKGROUND/AIMS: CD14 has been identified as a receptor for LPS and is present both in a membrane-bound and a soluble form. Membrane CD14 (mCD14) is predominantly expressed on monocytes, macrophages and granulocytes. The source of soluble CD14 (sCD14) is as yet unclear. Previous investigation using monocytes has shown that sCD14 can be derived either from the shedding of mCD14 or from direct secretion by monocytes. Whether the monocyte is the sole or even the major source of sCD14 is as yet uncertain. Clearance of LPS from the bloodstream is thought to be primarily mediated by the liver. Production of CD14 by hepatocytes would potentially provide a powerful mechanism by which the liver could clear LPS, and therefore we examined the ability of human hepatocytes to produce CD14. METHODS: Human hepatocytes were isolated using collagenase perfusion. RESULTS: Human hepatocytes were found to have CD14 mRNA by Northern blot analysis. Western blot analysis and immunohistochemical staining confirmed CD14 protein in primary hepatocyte cultures. Further studies showed that a liver epithelial-like cell line AKN-1 is capable of producing CD14. Comparisons of the size of hepatocyte-derived CD14 protein with the sCD14 protein from the human monocytic leukemia cell line HL60 suggested that a slightly larger form of CD14 is expressed by human liver cells. CONCLUSION: This is the first study to demonstrate production of CD14 by human hepatocytes.

Cell Line↗

PubMed1998

Pulmonary LPS-binding protein (LBP) upregulation following LPS-mediated injury.

BACKGROUND: The acute respiratory distress syndrome (ARDS) causes significant morbidity and mortality among trauma patients. Although multiple factors have been implicated, pulmonary injury in this population may be due to inflammatory mediators released in response to stimuli such as endotoxin (LPS). LBP plays an integral part in LPS-mediated release of inflammatory cytokines and increased local expression of LBP as the result of a primary injury may prime the lung to secondary LPS-mediated damage. MATERIALS AND METHODS: To determine the magnitude of pulmonary LBP upregulation following LPS injury we challenged rats with either intravenous (IV) or intratracheal (IT) LPS. Animals from each group were euthanized at 1, 2, 4, and 8 h postchallenge. Lung LBP and CD14 mRNA levels were assayed by Northern blot. Serum and bronchoalveolar lavage (BAL) fluid were assayed for inflammatory cytokines (TNF-alpha, MCP-1, IL-1beta, IL-6, and IL-10) by ELISA. RESULTS: LBP and CD14 mRNA levels were found to increase significantly in lung tissue after both IV and IT LPS with the IV LPS animals having a greater increase over 8 h. Serum TNF-alpha was significantly elevated in the IV LPS group whereas very low levels were detected in the BAL. Only BAL TNF-alpha was increased in the IT group at 8 h. CONCLUSION: Local pulmonary LBP and CD14 mRNA are both upregulated after either systemic or local LPS exposure. Such upregulation may render thelung more susceptible to local immune overactivation and injury during subsequent exposures to LPS.

Acute-Phase Proteins↗

PubMed1998

Tissue coexpression of LBP and CD14 mRNA in a mouse model of sepsis.

BACKGROUND: Lipopolysaccharide binding protein (LBP) markedly increases the sensitivity of immune cells to LPS and CD14 expression correlates with cellular responsiveness to LPS. LBP gene expression can be induced in multiple organs following injury and CD14 upregulation on monocytes correlates with the infection and mortality rates in severely injured patients. We sought to determine the time-course induction of LBP and CD14 gene expression following experimental peritonitis. MATERIAL AND METHODS: BALB/c mice were subjected to laparotomy alone or laparotomy with cecal ligation and puncture and treated with Imipenem. At serial time points, animals were sacrificed and tissues harvested for isolation of RNA and protein. LBP, CD14, and cytokine mRNAs were analyzed by Northern blot analysis and TaqMan fluorescent quantitative RT-PCR. RESULTS: LBP and CD14 mRNA levels were significantly increased in all three organs from CLP mice compared to sham-operated mice. IL-1 mRNA levels increased in all three organs following CLP with significantly higher levels found in the lungs compared to the kidney and liver. No significant differences were noted in local TNF mRNA levels. CONCLUSIONS: LBP, CD14, and IL-1 mRNA levels are induced concurrently in the lung, kidney, and liver after cecal ligation and puncture. Given the synergistic affect of LBP and CD14 in potentiating LPS-induced production of inflammatory cytokines and the hypothesized role of such cytokines in the etiology of MSOF following injury and sepsis, our findings suggest a mechanism by which these organs may be rendered more susceptible to a "second hit" from endotoxemia after initial injury.

Acute Disease↗

PubMed1998

CD14 and lipopolysaccharide binding protein expression in a rat model of alcoholic liver disease.

Lipopolysaccharide-binding protein (LBP) and CD14 play key intermediary roles in the activation of cells by endotoxin. As endotoxin has been postulated to participate in promoting pathological liver injury in alcoholic liver disease, we investigated the role of LBP and CD14 in alcoholic liver injury. Rats were fed intragastrically ethanol or dextrose and either medium-chain triglycerides, corn oil, or fish oil for 4 weeks. Kupffer cells, endothelial cells, and hepatocytes were isolated. LBP and CD14 mRNA levels were measured in liver and individual cell types. The highest levels of LBP and CD14 mRNA levels in the liver were found in the fish oil/ethanol group, which was also the group with the greatest degree of pathological injury and inflammation. CD14 mRNA levels were also significantly elevated in groups fed unsaturated fatty acids with dextrose. CD14 expression was localized to the Kupffer cells and LBP expression to the hepatocytes. Expression of CD14 mRNA was also found in nonmyeloid cells in the two experimental groups (fish oil/ethanol and corn oil/ethanol) that had liver necrosis and inflammation. Our results suggest that enhanced LBP and CD14 expression correlates with the presence of pathological liver injury in alcoholic liver injury. Furthermore, unsaturated fatty acids may prime cells to respond to endotoxin by enhancing CD14 expression.

Acute-Phase Proteins↗

PubMed1996

Increased expression of interferon-gamma in a rat model of chronic intestinal allograft rejection.

Chronic rejection remains a major cause of late graft dysfunction. Although much research has focused on acute rejection, little is known about the mechanisms of chronic rejection. Our group has recently reported evidence of significant intestinal smooth muscle hypertrophy and hyperplasia associated with abnormal contractile and electrical activities in a rat model of chronic intestinal rejection. The changes in the smooth muscle layer are associated with a significant inflammatory infiltrate. In order to further delineate the immune mechanisms of chronic rejection, we sought to clarify the nature of this infiltrate. Orthotopic small bowel transplantation was performed using an allogeneic (ACI-Lewis) rat combination. The rats only received immunosuppression for the first 28 days posttransplantation (cyclosporine 15 mg/kg daily from postoperative day 0 to 6 and every other day from postoperative day 7 to 28). This led to chronic rejection of the graft by day 90, at which time the rats were sacrificed. Analysis by immunohistochemistry revealed NK and CD5+ leukocytes infiltrating the muscular layer. Examination of cytokine production by radiolabeled polymerase chain reaction showed high levels of steady state interferon-gamma mRNA in full thickness intestinal segments and within the isolated muscularis of chronically rejecting intestinal allografts as compared to syngeneic and control grafts. Interferon-gamma mRNA was localized to both the muscularis and mucosa. Interestingly, positively hybridized cells within the muscularis tended to preferentially localize to the myenteric and submucosal plexuses suggesting potential role for this cytokine in chronic intestinal ejection.

Animals↗