Our study examined the cross-presentation of NP396, NP205, GP33, and GP276 using primary and pAPC cell lines (Fig. 2B). All pAPC showed comparable capacities to cross-present the LCMV antigens. Clearly, the NP396 epitope was the most efficient epitope to be cross-presented especially 24 h p.i. (Fig. 2B). The other three epitopes were cross-presented with less efficiency, with GP33 being the least efficient (Fig. 2B). Overall, these results confirmed that cross-presentation of cell-associated LCMV proteins did occur with different efficiencies. The CTL lines

used in this study were tested for their ability to produce IFN-γ in response to various concentrations of click here LCMV peptides (10−7–10−12 M) SB203580 ic50 (Fig. 2C) when incubated with peptide-labeled APC. The data indicate that the relative quality of different epitope-specific CTL were comparable. Therefore, the differences in the data recorded with cross-presentation were not due to different qualities or sensitivities of the epitope-specific CTL. Thus far, we found that NP396 and GP276 (located in different proteins) were the most efficient epitopes to be cross-presented. By further studying their kinetics of cross-presentation, we could detect significant cross-presentation for both epitopes as early as 3 h postincubation (Fig. 2D), but the peak of cross-presentation varied. GP276 peaked around 12 h, and NP396 was best detected at 18 h (Fig.

2D), where both epitopes were cross-presented similarly by DC and Mø. We next addressed the question if the viral RNA, which would normally complex with LCMV-NP during virus assembly, is contributing to the efficiency of this cross-presentation. We approached this aim by treating LCMV-infected cells with the endonuclease RNase A to degrade the RNA in the ADC after infection and confirmed RNA degradation by inspecting 28S and 18S rRNA. In Fig. 3A, these two bands are clearly visible in the intact RNA control samples (L1 and L2), whereas in the treated sample (Fig. 3A, L3) only a lower molecular weight smear

was obtained indicating RNA degradation. We also confirmed that the RNase treatment did result in the loss of LCMV proteins from the ADC (Fig. 3B). As shown in Fig. 3C, we tested several conditions and examined the Phosphatidylinositol diacylglycerol-lyase cross-presentation of NP396 and GP276 and included the standard LyUV-treated cells (Fig. 3C, i). In order to use the RNAase, pellet from lysed infected cells were incubated at room temperature (RT) for 20 min and then UV treated. The appropriate controls for this treatment are shown in Fig. 3C (ii and iii). Treatment of ADC with RNase degraded the RNA (Fig. 3A, L3), and caused a small but significant reduction in the cross-presentation of NP396 but not GP276 (Fig. 3C, iv). Thus, degrading the ADC’s RNA did not abolish cross-presentation and rules out a possible role for de novo protein translation in APC.

PPAR-γ also plays a critical role in natural regulatory T cell (Treg) suppressive function and in the differentiation and stability of inducible Tregs [8-10]. In fact, PPAR-γ was shown recently to have a direct effect on visceral adipose tissue Treg accumulation, phenotype and function [11]. Consistent with the immunoregulatory effects of PPAR-γ, a number of PPAR-γ agonists have been used to treat effectively murine experimental autoimmune encephalomyelitis (EAE), colitis, asthma and allergic disease [12-19]. In humans, PPAR-γ agonists have demonstrated clinical efficacy in treating Crohn’s disease,

psoriasis and multiple sclerosis, reflecting a beneficial effect in cell-mediated autoimmune diseases [20-23]. During recent years, the relationship between inflammation, cytokine production, insulin resistance and subsequent Y-27632 molecular weight development

of type 2 diabetes mellitus (T2DM) has become apparent. Inflammation in CP-690550 research buy the pancreatic islets of T2DM patients includes inflammatory cytokines [24, 25] and proinflammatory immune cells [25, 26]. The chronic systemic inflammation associated with T2DM patients has been hypothesized to contribute to the development of T cell islet-specific autoimmunity in some phenotypic T2DM patients [27-31]. Activation of islet-specific T cells (T+) in phenotypic T2DM patients has been found to be more common than appreciated previously [31], and correlated positively with a more severe β cell lesion [31, 32]. Treatment of T2D patients with PPAR-γ agonists, such as rosiglitazone or pioglitazone, have been shown previously to have beneficial effects on glycaemic control, insulin sensitivity, insulin secretion and plasma adipokine levels [33]. Recently, the cumulative incidence of monotherapy failure at 5 years was shown to be significantly lower in phenotypic T2DM patients treated with the PPAR-γ agonist, rosiglitazone,

compared to T2DM patients treated with metformin or glyburide. The 4-Aminobutyrate aminotransferase clinical efficacy of rosiglitazone was believed to be due, in part, to a slower decline in beta cell function in rosiglitazone-treated patients [34]. We hypothesized that the beneficial effects of PPAR-γ agonists in T2DM patients might be due, in part, to the immunosuppressive properties on T cell islet autoimmunity and inflammatory cytokine production. In this study we compared the islet-specific T cell responses (T+), IL-12 production, IFN-γ production and glucagon-stimulated beta cell function in autoimmune phenotypic T2DM patients treated with the PPAR-γ agonist, rosiglitazone, to autoimmune T2DM patients treated with glyburide.

9a,b) in a STIM1-dependent manner and by CD28-dependent store-independent activation of Ca2+ entry, potentially in a STIM2/ORAI1 or ORAI3-dependent manner. The CD28-dependent Ca2+ entry can occur in the context of the IS formation. If only CD28 is expressed, we would therefore not expect differences in

Ca2+ signals between CD80 or CD86 costimulation because CD28 is recruited to the IS independent of the type of costimulation (Fig. 9a). This is the case in Jurkat E6-1 and naïve primary T cells. However, if both CD28 and CTLA-4 are present at high concentrations, as in the case of effector T cells, it is expected that CD80 should preferentially bind to CTLA-4 and not so much to CD28, with the opposite being true for CD86.37 Therefore, CD86 should enhance CD28 recruitment to the IS and CD80 should inhibit CD28 recruitment by recruiting CTLA-4 instead. Through an unknown mechanism Selleckchem H 89 CD86, but not CD80, somehow enhances the store-independent activation of the CRAC channel,21,53 most likely in a STIM2/ORAI1 and/or ORAI3-dependent manner (Fig. 9b). In this model, the negative effect of CTLA-4 on T-cell activation is caused by the inhibition of CD28 recruitment to the IS. The knowledge of the fine-tuned difference in T-cell activation mediated by costimulatory molecules is of utmost importance not only to understand the underlying biology, but may also lead to novel therapeutic strategies that aim to activate the immune system against infectious

and malignant diseases. Super-agonistic antibodies targeting costimulatory molecules and activating T cells

by bypassing selleck the first signal have been developed in recent years.58 These super-agonistic antibodies bind to receptor domains that are not physiologically recognized by naturally occurring ligands, CYTH4 circumvent the need for TCR specificity and, most importantly, are no longer regulated by the human immune system. This last issue has recently gained significant attention because a clinical trial using a CD28 super-agonistic antibody (TGN1412) confirmed in a dramatic manner that no model systems exists today that can predict immune mechanisms induced by super-agonistic molecules.58 In an early clinical trial performed in healthy volunteers, it was expected that activation of regulatory T cells by TGN1412 would further suppress the immune system and that the antibody would, eventually, be developed to treat patients with autoimmune diseases. As the CD28 antigen is expressed on the vast majority of T cells and not only on the small proportion of regulatory T cells, a broad T-cell activation pattern was observed resulting in a life-threatening cytokine release syndrome requiring treatement in the intensive-care unit. This clinical experience has demonstrated that the nature of super-agonistic, non-physiological ligands is unpredictable when tested in vivo. Along that line, a CTLA4–immunoglobulin has been developed for blockage of the CD28-CD80/CD86 pathway.

Electrophysiological and algesimetry tests were performed serially along 4 months follow-up, and histomorphometric analysis was performed at the end of the study. Both groups with chitosan tubes showed similar degree of functional recovery, and similar number of BMN 673 research buy myelinated nerve fibers at mid tube after 4 months of implantation. The results with chitosan tubes were significantly better compared to SIL tubes (P < 0.01), but lower than with

AG (P < 0.01). In contrast to AG, in which all the rats had effective regeneration and target reinnervation, chitosan tubes from DAI and DAII achieved 43 and 57% success, respectively, whereas regeneration failed in all the animals repaired with SIL tubes. This study suggests that chitosan guides are promising conduits to construct artificial nerve grafts. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. "
“The treatment of wound complications and deep infection after hemipelvectomy is challenging.

We describe a 17-year-old woman with Ewing sarcoma in the pelvis who underwent hemipelvectomy and reconstruction with an artificial hip joint and bone cement. Selleckchem Erismodegib After the operation, skin necrosis and deep infection with methicillin-resistant Staphylococcus aureus (MRSA) were observed. Debridement resulted in exposure of the artificial joint and bone cement. Topical negative pressure (TNP) and irrigation successfully Monoiodotyrosine eradicated the infection. The skin and soft-tissue defect was subsequently reconstructed using a combination of free latissimus dorsi myocutaneous flap and serratus anterior muscle flap. To our knowledge, this is the first described case of combined TNP and irrigation with myocutaneous flap for the treatment of pelvic infection and skin and soft-tissue defect with endoprosthesis exposure. © 2011 Wiley Periodicals, Inc. Microsurgery, 2011. “
“Surgeons believe that in high ulnar nerve lesion distal interphalangeal joint (DIP) flexion of the ring and little finger is abolished. In this article, we present the results of a study on innervation of the flexor

digitorum profundus of the ring and little fingers in five patients with high ulnar nerve injury and in 19 patients with a brachial plexus, posterior cord, or radial nerve injury. Patients with ulnar nerve lesion were assessed clinically and during surgery for ulnar nerve repair we confirmed complete lesion of the ulnar nerve in all cases. In the remaining 19 patients, during surgery, either the median nerve (MN) or the anterior interosseous nerve (AIN) was stimulated electrically and DIP flexion of the ring and little fingers evaluated. All patients with high ulnar nerve lesions had active DIP flexion of the ring and little fingers. Strength scored M4 in the ring and M3-M4 in the little finger. Electrical stimulation of either the MN or AIN produced DIP flexion of the ring and little fingers.

However, significantly higher levels of T cells were detected

in NSG mice that were implanted in the renal subcapsular space of the kidneys compared to the subcutaneous site (Fig. 4b). No structural differences were observed between thymus tissues recovered from either site (Fig. 4d–k), although the size of the tissue recovered from the subcutaneous site was consistently smaller. Moreover, well-formed Hassall’s corpuscles, a structure characteristic of human thymus, were detected readily within the thymic medulla of tissues recovered from either renal subcapsular or subcutaneous sites (Fig. 4e,i,g,k) [61]. Significantly higher levels of B cells were detected in NSG mice implanted in the subcutaneous site (Fig. 4c), although no significant differences were detected in human IgM and IgG in the plasma of mice from either group (Fig. 4l,m). Doxorubicin chemical structure These findings indicate that subcutaneous implantation of human fetal thymic tissues is less efficient than subrenal implantation for generation of human T cells in the BLT model.

To evaluate the long-term maintenance of human cell chimerism Pirfenidone mw in BLT mice, NSG mice were irradiated (200 cGy), implanted with human thymic and liver tissues and injected with human HSC as described in Materials and methods. Between 26 and 28 weeks post-implant, NSG–BLT mice were screened for total human cell chimerism (CD45+ cells) for human T cell (CD3+ cells) and B cell (CD20+ cells) development in the blood and spleen (Fig. 5a–c). Human leucocyte levels were very high in mice new that had been engrafted for greater than 25 weeks. However, both T and B cells were transitioning to an activated phenotype at these later time-points. For example, there was a significant decrease in the percentage of CD45RA+ CD4 and CD8 T cells in the blood at 26 weeks compared

to 12 weeks (Fig. 5d). CD45RA is not expressed exclusively by naive T cells, but still provides a reliable estimation of the activation status [62]. In the spleen of BLT mice, the average percentage of CD45RA+ CD4 and CD8 T cells was less than 60% between 26 and 28 weeks after implant (Fig. 5e). Moreover, there was a significant increase in human IgM and IgG levels in plasma of BLT mice at 26 to 28 weeks after implant compared to 12 and 19 weeks (Fig. 5f,g). The activation of the human immune system also correlated with a decrease in platelet (PLT), red blood cell (RBC) and haemoglobin (HGB) values (Fig. 5h–j, respectively). Together these data suggest that human cell chimerism is maintained long term in BLT mice, but the human immune system becomes activated spontaneously. NSG–BLT mice support the human immune system engraftment for an extended time-frame; however, these animals have been reported to develop a xeno-GVHD late after implant [54]. At approximately week 20 post-implant, NSG–BLT mice generated in our laboratory displayed a significantly increased rate of mortality compared to NSG mice that were only irradiated (P = 0·026, Fig.

Because our findings so far suggested direct crosstalk between TNFα and Fas signaling, we performed a detailed analysis of the components of the two signaling pathways. We recently reported that FasL-induced apoptosis of collagen-cultured primary mouse hepatocytes occurred independently of Bid. This was in contrast to apoptosis induced by TNFα/ActD, which still required Bid (type II signaling).12 We therefore tested whether this was also the case for the sensitization effect of TNFα

on FasL-induced apoptosis. Indeed, although Bid−/− hepatocytes showed the same caspase-3/caspase-7 activation in response to FasL that WT cells showed, the increased caspase-3/caspase-7 activation due to treatment with TNFα and FasL was entirely abolished (Fig. 4A). Both cell Pexidartinib price death (based on the MTT assay; Supporting Fig. 5A) and apoptosis-associated DNA fragmentation (Supporting Fig. 5B) were reduced in Bid−/− hepatocytes versus WT cells when they were treated with TNFα and FasL, and this supported the caspase data. Additionally, Bid was processed into its active selleck inhibitor form (tBid) in cells treated with TNFα and FasL, whereas TNFα alone did not lead to any tBid formation (Fig. 4B). However, TNFα

induced increased expression of the Bid protein (Fig. 4B) and mRNA (Fig. 4C) and further strengthened a crucial role of this protein in the sensitizing mechanism. Bid processing

was also observed with FasL alone, but this did not contribute to apoptosis induction (Fig. 4A). Thus, our results show that although Bid is not required for FasL-induced apoptosis on collagen-cultured hepatocytes, it is absolutely crucial for the TNFα sensitization of this process. XIAP is an endogenous inhibitor of caspase-9 and effector caspase-3/caspase-7 and restrains apoptosis along the type I pathway unless it is neutralized by apoptogenic factors emanating from mitochondria. Accordingly, as we previously showed, XIAP−/− hepatocytes exhibited 10-fold higher caspase-3/caspase-7 activity in response to FasL than WT cells (Supporting Fig. 6). This activity was not further increased by TNFα preincubation. However, a slight selleck compound sensitization was seen at low FasL doses (10-20 ng/mL). This indicates that deletion of XIAP does not abrogate the TNFα sensitization to FasL-induced apoptosis. Importantly, XIAP protein (Supporting Fig. 7) and mRNA (Supporting Fig. 16C) remained nearly unchanged during TNFα preincubation. Thus, XIAP turned out to be dispensable for the sensitizing effect of TNFα. Activation of JNK has been implicated in TNFα-induced apoptosis in several cell types, including hepatocytes.19, 20 We therefore monitored the active phosphorylated form of JNK by anti–phospho-JNK western blot analysis in primary mouse hepatocytes treated with TNFα.

5-HT7 receptor expression was determined by Real Time PCR. Routine histopathology and immunhistochemical staining for TNF-a were also performed in liver sections. Potential role of 5-HT7 receptors were investigated by administration of LP44 (5-HT7 receptor agonist) and SB269970 (5-HT7 receptor antagonist) at two different doses. Results: At 4th, 8th and 12th hours after PARA administration, AST and

ALT were significantly increased and GSH was significantly decreased when compared to control. Agonist administration to PARA click here given rats significantly improved liver conditions in terms of AST, ALT, GSH and TNF-α. However antagonist administration worsened liver functions, those results were also supported histopathological and immunohistochemical analyses. Real Time PCR results showed that liver 5-HT7 receptor expression decreased in a time dependent manner after PARA administration. Agonist administration increased 5-HT7 receptor expression back in all time points while antagonist had no effect. Conclusions: In conclusion, this study demonstrated for the first time that 5-HT7 receptor expression

in liver tissue is decreased during PARA induced hepatotoxicity. Agonist administration can be a new therapeutic approach for PARA induced liver damage. Also 5-HT7 receptors may be a promising new therapeutic target selleck kinase inhibitor for prevention of drug and other chemicals induced hepatotoxicity. This study may N-acetylglucosamine-1-phosphate transferase also provide a new glimpse into drug induced hepatic damage’s pathophysiology. Disclosures: Beyzagul Polat – Grant/Research Support: TUBITAK Emre Karakus – Grant/Research Support: TUBITAK The following people have nothing to disclose: Zekai Halici, Elif Cadirci, Yasin Bayir, Abdulmecit Albayrak, Deniz Unal Although the progression of alcoholic liver disease is well-described, the mechanisms leading to alcohol-induced liver

damage remain elusive. Previously, we determined that microtubules are hyperacetylated and more stable in ethanol-treated WIF-B cells, liver slices and in livers from ethanol-fed rats. Our focus is to determine whether tubulin hyperacetylation can explain alcohol-induced defects in microtubule-dependent protein trafficking. Previously, we determined that transport of newly synthesized proteins from the Golgi to the basolateral surface and STAT5B nuclear translocation are impaired by alcohol metabolism. Recently, we confirmed that delivery of apical proteins from the basolateral-to-apical membrane via transcytosis is also impaired in ethanol-treated WIF-B cells. Similar to STAT5B nuclear translocation, transcytosis is mediated by dynein (a minus-end directed motor) and dynactin (a dynein activating complex). Unlike control cells, transcytosing proteins accumulated sub-apically and aligned along acetylated microtubules in ethanol-treated cells indicating that impairment was due to vesicle translocation, not basolateral internalization.

1 mL. To ensure the stability of the protein, the package insert for onabotulinumtoxinA (BOTOX®) recommends reconstitution with preservative-free normal saline (0.9% Sodium Chloride, USP).50 Once a 100 U vial

of onabotulinumtoxinA has been reconstituted, it must be injected or immediately stored in a refrigerator at 2-8°C in the original vial (not in a syringe) and used within 24 hours50 or as indicated in the local package insert. In the development of a treatment paradigm for onabotulinumtoxinA injections, perhaps the greatest evolution has been in the selection of sites for the injections. As mentioned above, 2 approaches have been widely used: fixed-site/fixed-dose and follow-the-pain. It was previously believed that the type of approach depended on the type of headache, but whether one approach should be preferred over the other has not previously been firmly MK-1775 clinical trial established. Early headache studies

generally used a fixed-site approach, identifying sites in the forehead and glabellar region while generally avoiding the occipital and neck regions.10,51 The fixed-site approach distributes onabotulinumtoxinA to muscles that align with the peripheral nerve distribution of the cervical and trigeminal sensory system, which is believed to be the target-end organ for onabotulinumtoxinA in treating CM. These sites remain unchanged regardless of where the patient’s pain is located. The PREEMPT injection BAY 57-1293 concentration paradigm, which uses a combination of fixed and FTP injection sites, provides optimal distribution of onabotulinumtoxinA based on individual patient symptoms.8,24 The muscle groups chosen in PREEMPT were based on in-depth analysis of the interaction effects of muscle group dose on efficacy variables in patients who were not using prophylactic headache medication during baseline, and in-depth analyses of the safety and tolerability of the dose and dosage paradigm used in the 2 Allergan-sponsored phase 2 studies of patients with CDH.8,24 The findings from these analyses,

which are discussed further below, serve as the foundation for the choice of muscles, dose, and dilution used in the PREEMPT studies. Frontalis, Corrugator, and Procerus (Frontal/Glabellar Region).— enough In the phase 2 trials,8,24 patients reported that the frontal/glabellar region was the most frequent location where their head pain started and ended. In the first trial, doses for the frontal/glabellar region were not specified; only a total dose was specified for the overall region, which was administered across the frontalis, corrugator, and procerus muscles. In the second trial, the frontalis and corrugator muscles of the forehead were injected, but not the procerus muscle. Overall, the first trial had better signals for efficacy than the second trial.

Here, we hypothesized that PBGs are populated by mature and undifferentiated cells capable of proliferation in pathological states. To address this hypothesis, we developed a novel whole-mount immunostaining assay that preserves the anatomical integrity of EHBDs coupled with confocal microscopy and found that PBGs populate the entire length of the extrahepatic biliary tract, except the gallbladder. Notably, in addition to the typical position of PBGs adjacent to the duct mucosa, PBGs elongate and form intricate intramural epithelial networks that communicate between different

segments of the bile duct mucosa. Network formation begins where the cystic duct combines with hepatic ducts to form the common bile duct (CBD) and continues along the CBD. Pexidartinib nmr Cells of PBGs and the peribiliary network stain positively for α-tubulin, mucins, and chromogranin A, as well as for endoderm transcription factors SRY (sex determining region Y)-box 17 and pancreatic and duodenal homeobox 1, and proliferate robustly subsequent to duct injury induced GSK1120212 solubility dmso by virus infection and bile duct ligation. Conclusion: PBGs form elaborate epithelial networks within the walls of EHBDs, contain cells of mature and immature phenotypes, and proliferate in response to bile duct injury. The anatomical organization of the epithelial network in tubules and the link with PBGs support an expanded cellular reservoir with the potential to restore

the integrity and function of the bile duct mucosa in diseased states. (Hepatology 2013;58:1486–1496) Anatomical and molecular relationships among hepatic and biliary cells are critical to normal development and to the regenerative response after an injury. In the liver, molecular circuits targeting hepatocytes, cholangiocytes, and nonparenchymal cells work coordinately Vildagliptin to control embryogenesis and restore lobular organization and functional integrity after an insult.[1, 2] Although these principles may apply to the development and repair of the intrahepatic and extrahepatic biliary tract, the functional

relationships among individual cell types and molecular pathways in bile ducts are less well defined.[3] Recent advances suggest that the embryogenesis of individual segments of the extrahepatic biliary tract (gallbladder, cystic duct, hepatic ducts, and the common bile duct [CBD]) is regulated, at least in part, by separate genes, as supported by the isolated defects in mice with mutations in Inversin, Foxf1, Hes1, or Lgr4.[4-7] Interestingly, a molecular signature of embryonic endoderm has also been reported in cells of peribiliary glands (PBGs), which appear to have phenotypic plasticity typical of cells with progenitor properties.[8] PBGs are clusters of epithelial cells adjacent to the mucosal lining of intrahepatic and extrahepatic bile ducts, described in several animal species including mice and humans.

Chronic myelogenous leukemia

(CML) is a clonal bone marrow stem cell disorder with proliferation of granulocytes and their precursors. It is associated with the characteristic chromosomal translocation, the Philadelphia chromosome. Patients Ivacaftor datasheet are often asymptomatic, presenting with an elevated white blood cell count. Others may have malaise, easy bruising, enlarged spleen, increased susceptibility to infection, and anemia. The reported autopsy incidence of gross gastrointestinal (GI) involvement in leukemia ranges from 14.8 to 25%,1,2 more common in acute than chronic leukemia and situated mainly in the mucosa and submucosa.1 Except for an occasional report,3 GI involvement occurs when the leukemia is in relapse. Its presence varies according to the type of leukemia4 and has been decreasing over time due to improved chemotherapy. Gross leukemic lesions are most common in the stomach, ileum, and proximal colon1,5 and include nodules, plaques, diffuse infiltrates, polyps, and a convoluted brain-like appearance of the mucosal folds.1 Leukemia can affect different and multiple anatomical sites of the GI tract.6 In almost 3% of cases, extensive segments of the GI tract are involved.1 Because leukemic plaques involve the submucosa or muscle

coats, they RO4929097 molecular weight may be associated with ulcerations and intestinal perforation. Nodular lesions, in contrast, tend to affect the mucosa and submucosa and are associated with intussusception and intestinal obstruction. Patients with leukemic infiltrates are usually asymptomatic or have vague, non-specific complaints. They may present with abdominal pain, diarrhea,7 or GI bleeding.2 Four types of esophageal lesions are found.2 Hemorrhagic lesions range from petechiae and ecchymoses to erosions and ulcers. Leukemic infiltrates range from microscopic lesions to gross nodular infiltrates that tend to undergo necrosis with secondary infection Obatoclax Mesylate (GX15-070) and hemorrhage. There is agranulocytic and pseudomembranous esophagitis with an eroded mucosa

covered by an adherent membrane of necrotic debris, fibrin, and bacterial colonies, usually with little associated inflammation. Finally, a fungal esophagitis, most commonly candida, occurs with diffuse mycelial growth and necrosis with little or no inflammatory reaction. It is more common in acute than chronic leukemias.8 Fungal lesions can be found throughout the GI tract and are promoted by the use of antibiotics, cytotoxic agents, corticosteroids, and the leukemic process itself. While Aspergillus most commonly affects the lung, it can occasionally cause esophagitis, as can other invasive fungal organisms such as Mucor, Histoplasma, and Cryptococcus species.9 These organisms are diagnosed by endoscopic biopsy and brushings.