27,28,31,32 The cationic nature of SLPI may also allow it to directly destabilize viral envelop. The mechanism for Elafin inhibition of HIV-1 is unknown, but may be similar to SLPI given their homology (approximately 40%).29,30 Lysozyme, another component of FRT secretions, derives its antibacterial activity from the ability to cleave peptidoglycan present on bacterial cell walls.13 Like

other antimicrobials, it can directly interact with cell membranes via its positively charged amino acids.13,33 It inhibits HIV-1 infection of target cells, most likely via its HL9 and HL18 peptide regions, by blocking viral entry and replication.8,34,35 Lactoferrin, EGFR inhibitor a homolog of the iron-carrier Metformin purchase protein transferrin, inhibits bacterial growth by sequestering

iron under acidic conditions similar to those in the lower FRT.13 It blocks HIV-1 infection of target cells by interfering with viral fusion and entry through interactions with the V3 loop of HIV-1 gp120.8,36 Furthermore, it inhibits HIV-1 adsorption to target cells. MIP3α/CCL20 is a neutrophil chemoattractant, and similar to other chemokines and cytokines, also functions as an antimicrobial agent.37 Recently, it was shown to inhibit HIV-1 infection of target cells through an unknown mechanism.38 The pioneering studies of Schumacher in the 1960s and 1970s demonstrated that components of the reproductive tract milieu vary with specific stages of the menstrual cycle. For example, IgG and IgA in cervical mucus both decrease at ovulation but remain elevated during the proliferative and secretory phases of the cycle. Reflecting this initial work, other investigators have shown that, in addition to antibodies, specific cytokines, chemokines and antimicrobials also change with the menstrual Cyclooxygenase (COX) cycle. As seen in Table III, HNPs 1–3, HBD2, lactoferrin,

and SLPI in cervico-vaginal lavages (CVL) transiently and dramatically decrease at mid-cycle/ovulation, before increasing during the latter portion of the secretory phase.39,40 A similar trend for lysozyme has also been reported elsewhere.41 The greatest decreases were observed in HNPs 1–3 (80%) and HBD2 (70%).39 Multiple cytokines, which potentially have antimicrobial activity,37 also demonstrated this trend.39 Some of the highest concentrations of antimicrobials (HNPs 1–3, HBD2 and SLPI) were detected during the menstrual phase. However, this is likely due to blood contamination of CVL during endometrial breakdown and may not reflect endogenous FRT production. In contrast to CVL findings, studies using tampons for collection of vaginal fluid reported increased levels of HNPs 1–3, HBD2, and lysozyme while lactoferrin, HBD1, and SLPI decreased from proliferative to secretory stages of the menstrual cycle with no apparent mid-cycle drop.

Our current and previous results suggest that CD8+ T cells freshly purified from the BM of normal lymphoreplete mice transiently retain some traits of their in vivo activation in this organ, including higher intracellular phospho-signal transducer and activator of transcription (STAT)-5 and phospho-p38 mitogen-activated protein kinase (MAPK), lower membrane CD127 expression, and reduced proliferative response to IL-7 [[11, 17]]. Although some of these traits may resemble those of T cells undergoing rapid homeostatic

expansion in lymphopenic hosts, for example low CD127 expression [[37]], other features are different, for example high Bcl-2 expression [[11]]. How much self-antigens and/or cytokines contribute MG-132 datasheet to memory CD8+ T-cell activation in the BM and how long such BM-driven activated cells live are still unsolved RAD001 purchase questions. Nevertheless our studies suggest that a prominent role is played by IL-15, and that BM seeding by recirculating

antigen-specific memory CD8+ T cells is associated with long-term memory [[10, 11, 16, 17]]. Future studies will be necessary to define the rate of homing and egress of memory CD8+ T cells in and out of LNs, spleen, and BM, as well as to determine the kinetics of CD127 expression by recirculating memory CD8+ T cells. Cyclical expression of a membrane molecule by recirculating T cells due to microenvironment-driven modulation has been demonstrated in the case of CD62L [[38]]. Our CD127 mRNA expression results together with the CD127tg cell findings point to regulatory noncoding regions as important

targets of IL-15-dependent transcriptional and/or post-transcriptional regulation. This is consistent with both in vitro studies showing IL-15-induced CD127 transcriptional inhibition in LN T cells [[6]] and in vivo observations showing impaired membrane CD127 downmodulation selleck kinase inhibitor by antigen-responding CD8+ T cells in IL-15 KO mice [[39]]. Our further investigation on the CD127 transactivator Foxo1 [[32]] showed that Foxo1 protein was less abundant in BM CD44high CD8+ T cells than in corresponding cells from spleen and LNs of both WT and IL-15 KO mice. We cannot completely exclude that Foxo1 low amount in the BM contributes to the reduced CD127 transcription by an IL-15-independent mechanism. Nevertheless, the fact that Foxo1 is low and yet CD127 is not downmodulated in IL-15 KO BM suggests that the contribution of Foxo1 has minor relevance, if any. Further studies are required to define the molecular mechanisms differentially regulating CD127 expression in WT versus IL-15 KO mice. Our results have implications for human therapies targeting membrane CD127 expressed by T cells. Based on mouse studies, it has been proposed to use anti-CD127 Ab in humans to inhibit either donor T cells in graft versus host disease (GVHD) [[40]] or recipient T cells in transplant rejection [[41]].

Therefore, IL-10 has been shown to synergize with IL-21 to induce the secretion of IgA by CD40L-stimulated human B cells, whereas IL-4 diminished it [9]. The stimulatory signalling through the IL-21R/γc complex, rather than other

γc-containing cytokine receptors, such as those for IL-2 or IL-4 has previously been demonstrated to be very important to induce switching to IgG and IgA [23]. Although this recognized importance, in this study, there were no differences between the mRNA expression of this receptor between periodontitis and healthy individuals. However, although the expression of IL-21R and CD40L were similar between groups, the expression of IL-21 and levels of IL-10 was upregulated in chronic CB-839 nmr periodontitis tissues when compared to healthy ones. In addition, the levels of IL-4 were lower in periodontitis tissues than healthy biopsies. Concomitant with the increased expression of IL-21 and IL-10 and decreased in IL-4 levels in periodontitis tissues; the amounts of salivary IgA were significantly higher

in periodontitis subjects. Together, these data suggest that the abovementioned role of IL-21, IL-10, and IL-4 in Ig isotype switching might also take place in chronic periodontitis and indicate an immunomodulation of the oral mucosal tissues in subjects under periodontal pathogens challenge. The role of these cytokines has been already investigated in periodontitis; however, the majority of the studies have focused on the functions of cytokines on CP-690550 research buy the Th1/Th2 or Th17/Treg responses. In according to the present results, previous studies showed that IL-21 was highly expressed in gingival biopsies of chronic periodontitis [24] and the levels of IL-21 in gingival crevicular Methane monooxygenase fluid decreased after treatment of chronic periodontitis [19]. Furthermore, our findings confirm previous observations in which lower levels of IL-4 [25, 26] and higher levels of IL-10 [27, 28] were associated with periodontitis. In addition, in agreement with present study, the levels of IgA against different pathogens have been found to be higher in subjects with periodontal disease [3, 4,

6]. Therefore, salivary IgA, the most abundant immunoglobulin isotype in saliva seems to be potentially protective against periodontal pathogens and their virulence factors [6, 29]. Accordingly, the selective IgA primary immunodeficiency (IgAD) predisposes to oral mucosal infections, supporting the role of IgA in inhibiting mucosal colonization and invasion of pathogens [30], although the loss of IgA did not result in an increase in periodontitis levels in IgAD individuals [30, 31]. In this study, we suggested that the higher amount of the IgA found in the saliva of the chronic periodontitis subjects may have a direct relationship with the higher expression of IL-21 and IL-10 and lower expression of IL-4 in periodontitis tissues.

05) (Table 1). The mean pre-operative QOL was 4.3 ± 0.7, while it was 1.15 ± 0.8 at 3 months and 1.3 ± 0.6 at 12 months postoperatively, which was a statistically significant difference between pre- and postoperatively at both 3 months (P < 0.01) and 12 months (P < 0.01), but the difference between 3 and 12 months

postoperatively was not statistically significant (P < 0.05) (Table 1). The mean pre-operative RU was 85.6 ± 6.0 mL while it was 25.6 ± 8.5 mL at 3 months and 27.1 ± 8.5 mL at 12 months postoperatively. The difference between pre-operative RU and postoperative both at 3 months (P < 0.01) and 12 months (P < 0.01), but the difference LY2157299 research buy between 3 and 12 months postoperatively was not statistically significant (P < 0.05) LY2606368 concentration (Table 1). According to the result of statistical analysis, which was summarized in Table 1, the patients become asymptomatic. Maximum urinary flow rate rose up to its normal range, good quality of life ensued, and no significant post-voiding residual urine appeared. This result indicates that TV pedicle flap urethroplasty is a safe and successful

procedure for patients with anterior urethral stricture. There were few changes in clinical parameters between 3 and 12 months postoperatively, but the differences were not statistically significant. An early postoperative complication was one case of wound infection and subsequent wound dehiscence in tabularized technique and also one case of hematoma formation in ventral onlay technique. Wound infection was resolved by 2-weeks of antibiotic therapy and the hematoma was drained. In one patient on the tabularized technique, re-stricture developed, while in the onlay technique, one case of urethro-cutaneous occurred.

Both of them were considered failed cases. There was no other complication like penile curvature (chordee) in our series. The total success rate in our study was 86.6% (13/15). Chlormezanone There was no statistically significant difference between success rate of tabularized and ventral onlay technique. A great variety of tissues from the genital and extra genital area have been tried both experimentally and clinically for a flap or free graft. These include the fasciocutaneous component of the penis, bucal mucosa graft, vesicle mucosa, small intestinal sub-mucosa and peritoneum.[4] Besides that, several surgical techniques have been launched to find an ideal substitute for the urethra, but it seems that the ideal graft or flap has not been identified yet. Based upon many previous experimental studies, we clinically evaluated the feasibility and usefulness of tunica vaginalis pedicle flap for reconstruction of anterior urethral stricture in the form of ventral onlay and tabularized techniques. Our sample comprised 15 adult men with bulbo-penile acquired urethral stricture, of which nine underwent TV-ventral onlay and six underwent TV-tubularized urethroplasty.

g. pathogen infection, protein ligands, endotoxins, and so on) and the recruited leukocyte subtypes. Given

such heterogeneity, it is difficult to make conclusion about the involvement of transcellular vs. paracellular translocation. Further, the majority of in vivo reports of transcellular translocation have been shown using methods that are often unequivocal (e.g. scanning electron microscopy, transmission electron microscopy, or confocal fluorescence microscopy); however, it is important to note when discussing such reports that some have employed single-section transmission electron microscopy only, Metabolism inhibitor which cannot conclusively determine the route of translocation. It is noteworthy that some pathogens may choose the easiest way for BBB translocation. Pathogens and infected leukocytes may preferentially translocate using paracellular route during in vitro experiments owing to the fact that cell–cell junctions are not well formed and developed compared to their in vivo counterparts (Hoshi & Ushiki, 1999). Moreover,

in vivo experiments may also depend on the microenvironment of the brain and BMECs that seems to be responsible for the differentiation of the BBB phenotype and astrocytic end-feet cover (Kacem et al., 1998; Rubin & Staddon, 1999; Abbott, 2002), which may influence the route of pathogen translocation. Relatively small number of pathogens is responsible for bacterial meningitis. Group B streptococci (GBS), L. monocytogenes, and S. pneumoniae account for the most cases of neonatal and early childhood bacterial meningitis (Garges et al., 2006). Streptococcus pneumoniae, Saracatinib price N. meningitidis, and H. influenzae

type b remain the most common causes of meningitis (Hart & Thomson, 2006), while meningococcus and pneumococcus cause 95% of cases of acute bacterial meningitis in children. Sporadic cases related to E. coli, M. tuberculosis, B. burgdorferi, and T. pallidum continue to be important. Fungal meningitis caused by C. neoformans, C. albicans, and Histoplasma capsulatum; and parasitic cerebral infestations caused by Acanthamoeba, Plasmodium falciparum, Trypanosoma, and Toxoplasma gondii are sporadic types of meningitis, often Dipeptidyl peptidase observed in patients with immune deficiency. Some GBS molecules, like fibrinogen-binding protein A (Tenenbaum et al., 2005), PilA, PilB (Maisey et al., 2007), laminin-binding protein (Tenenbaum et al., 2007), beta-hemolysin/cytolysin (Doran et al., 2003), serine-rich repeat-1 (van Sorge et al., 2009), and lipoteichoic acid (LTA) (Doran et al., 2005), mediate interaction of the pathogen with BMECs and penetration of the BBB. Many of these GBS ligands are known to bind ECM molecules such as fibronectin, fibrinogen, and laminin, which successively bind host-cell-surface proteins such as integrins. GBS ligands and their receptors on BMECs described earlier are depicted in Table 1.

Only 12 strains of 66 corresponded to the ‘classical’ B+P+I+ type. The prevalent type was B−, P−, I+, and it included 24 CoNS of the 66 studied strains. Despite the presence of ica genes in several species, no PNAG was detected in vitro. The inactivation of the ica operon could be attributed to several factors such as the insertion of the IS256 element (Ziebuhr et al., 1999), the action of the IcaR repressor (Conlon et al., Ivacaftor 2002), and post-transcriptional regulation (Knobloch

et al., 2002). Factually, the maximum transcription of icaADBC can be obtained with a persistence of PNAG and a biofilm-negative phenotype (Dobinsky et al., 2003). The reason for the absence of biofilm production Idasanutlin order despite the presence on the entire ica operon remains

unclear. Similar results were obtained in the ica operon expression studies on 10 strains of S. epidermidis (seven biofilm-positive and three biofilm-negative strains) (Cafiso et al., 2004). Because the strains were isolated from patients with infected implanted devices, PNAG and biofilm may be formed in vivo, but not in vitro. The two types of strains B+, P−, I+ (eight of 66 CoNS strains) and B+, P−, I− (two Staphylococcus lugdunensis of 66 strains) are very interesting, because they imply a possibility that different CoNS species could form a biofilm in vitro not containing PNAG. Selected biofilm-positive strains of this collection were then used for a detailed chemical analysis of their EPS. Having established the reliable method of analysis of the extracellular matrix of a staphylococcal biofilm (Sadovskaya et al., 2005), our group investigated the chemical composition of carbohydrate-containing polymers of a number of biofilm-positive staphylococcal

strains associated with the infections of orthopaedic implants (Kogan et al., 2006; Sadovskaya et al., 2006). Of the 15 biofilm-producing clinical staphylococcal strains studied, three produced high amounts of PNAG in vitro. The production of PNAG by one of them, S. epidermidis 5 (CIP 109562), was higher than that of the model strain S. epidermidis Montelukast Sodium RP62A, and therefore, this strain may be considered as a PNAG overproducer (Fig. 2a and b). Three strains (two S. epidermidis and one S. lugdunensis) were found to produce a small, but detectable amount of PNAG (Fig. 2c). Nine other strains (six S. epidermidis and one of each S. aureus, Staphylococcus warneri, and S. lugdunensis) did not produce in vitro PNAG in an amount that could be detected using direct chemical methods (Fig. 2d). While the presence of trace amounts of PNAG cannot be excluded, we suggested that biofilms of these strains contain mainly TA and protein components, which could be easily isolated from their extracellular extracts.

Volume and pressures were recorded at various sensations up to maximal capacity (MCC). Maximal capacity was considered a volume with strong feeling of fullness in lower PS-341 cell line abdomen or filling pressure of 30 cmH2O, whichever was reached earlier. At the end of the filling phase, the patient was asked to void in the uroflowmeter. He was encouraged to void with pelvic-floor relaxation along with Crede’s maneuver/straining. The following definitions were used: (i) Pouch compliance = MCC/end.fill.Ppouch; (ii) MCC = voided volume + PVR. This definition was used rather

than “volume filled” to account for the urine production during the study; (iii) clinically significant incontinence = leakage of over a few drops of urine. Urethral pressure profilometry was performed after filling 100 mL infusate into the pouch. The catheter was pulled at a constant rate (2 mm/sec) using motor-driven automated catheter puller and urethral pressures were recorded. The above evaluation was conducted initially at least 6 weeks after surgery and later at least 3 months after the initial

evaluation. All patients were counseled and trained to void on schedule by sphincter relaxation along with Crede’s maneuver SCH772984 order if required. The pelvic floor strengthening exercises were started in the preoperative period and continued thereafter. Pelvic floor rehabilitation was initiated just before removal of catheter. Data were analyzed using statistical package for social science (SPSS, version 17, Chicago, IL, USA). Normality of data were checked using one sample Kolmogorov–Smirnov test. The before-and-after comparisons were made using paired t-test (parametric), Wilcoxon signed rank test (non-parametric) or McNemar test (dichotomous categorical).

Correlations between clinical/QOL and urodynamic parameters were made using Pearson’s correlation (parametric) or Spearman’s rank correlation (non-parametric). Factors predicting continence status were examined using Mann–Whitney U-test (non-parametric dataset). Binominal logistic regression and stepwise linear regression analyses were conducted as appropriate. Total 17 patients with mean age 52.7 ± 11.3 years and body mass index 22.7 ± 3.3 kg/m2 were evaluated. All patients underwent cystoprostatectomy (radical in 16 patients with 3-oxoacyl-(acyl-carrier-protein) reductase bladder cancer and simple in one patient with genitourinary tuberculosis) and construction of orthotopic neobladder (ONB) with ileum of mean length 48 ± 7 cm (range 40–60 cm). Three patients of bladder cancer developed recurrence; one in corpus cavernosus of penis, one in the pelvis and one in both. All were treated with systemic chemotherapy and the latter two with pelvic radiotherapy in addition. The former patient had a complete remission of disease; the latter two succumbed to progressive disease and hence were excluded.

Candida albicans isolate (CIMR #5), a virulent and well-characterized isolate [eight citations given in Clemons et al. (2006)], stored at −80 °C, was plated on blood agar plates

(BAP) and incubated for 20 h at 35 °C. After passage of C. albicans on BAP, yeast growth was harvested into saline, pelleted by centrifugation (400 g, 10 min), and counted in a hemacytometer. Candida albicans was suspended in CTCM to the required concentration for challenging monocytes, neutrophils, or macrophages. The cells remain almost completely as yeasts during the brief exposure periods. Monocytes or peritoneal macrophages in duplicate cultures were treated with increasing concentrations of 3M-003 or IFN-γ, https://www.selleckchem.com/products/pci-32765.html or CTCM vehicle, 0.2 mL per well. After incubation for 20 h at 37 °C in a 5% CO2 incubator, the supernatants were aspirated and monocytes or macrophages were challenged with C. albicans in 0.2 mL of CTCM or CTCM+10% fresh mouse serum. Effector to target ratios (E : T) 10 : 1, 50 : 1, and 100 : 1

were tested; 100 : 1 was generally optimal for plating under these conditions. Following a 2–4-h incubation period at 37 °C, each culture was harvested by aspiration into distilled water and culture wells were washed 10 times with distilled water. Microscopic examination of harvested culture wells confirmed that the well contents were removed. Harvested material from each culture was plated on BAP in duplicate. Inoculated BAP were incubated at 35 °C for 20 h, and CFU per culture were calculated. 0.1 mL per well of SCH772984 106 neutrophils mL−1 CTCM in duplicate cultures were treated with increasing FER concentrations of 3M-003 or IFN-γ for 20 h at 37 °C in a 5% CO2 incubator. Following the incubation period, neutrophils were challenged in situ with 0.1 mL of C. albicans in CTCM for 2 h at 37 °C. Cultures were harvested and harvested material was plated on BAP as described above for monocytes and macrophages. After incubation of plated material on BAP for 20 h at 35 °C, colony counts were performed and CFU per culture was calculated. Blood

from BALB/c mice was collected by cardiac puncture into EDTA-containing vacutainer tubes. Blood was pooled, diluted 1 : 1 in phosphate-buffered saline, 3 mL of the mixture was layered over 3 mL of Accu-Paque (Accurate Chemical and Scientific Corp., Westbury, NY), and centrifuged (400 g) for 30 min. PBMC at the interface were collected into Hanks’ balanced salt solution and cells were pelleted by centrifugation (200 g, 7 min). The viability of PBMC was determined by trypan blue exclusion and PBMC were counted in a hemacytometer. PBMC were suspended in CTCM. Dilutions of 3M-003 in CTCM (0.25 mL) were prepared in flat bottom 48-well tissue culture plates (Costar). Sets (eight wells per set) of 3M-003 dilutions were inoculated with PBMC (0.25 mL per well of 4 × 106 mL−1) and cultures were incubated for 24 h at 37 °C and 5% CO2.

13 Nocturia is multifactorial, with causes beyond the urinary tract itself.1,14 Metabolic syndrome (MetS) consists of a clustering of cardiovascular risk factors, such as obesity, high blood pressure, impaired glucose tolerance, and dyslipidemia. Kupelian et al. reported an association of individual urological

symptoms with MetS.15 Thus, we examined the association between components of MetS and nocturia. Tikkinen reported that obesity was associated with increased nocturia, more strongly among women than among men, in Finland.16 The factors underlying an association between find more nocturia and obesity are unclear. Lifestyle-related factors may also be more common among the obese. It is possible that nocturia in some obese persons is related to excessive nighttime eating or drinking, especially consumption of alcohol.16 Moreover, obesity is a multifactorial disease with adverse health consequences, such as cardiovascular disease, type 2 diabetes, hypertension (HT), sleep apnea, and possibly depression, which may result independently in nocturia.17 In previous studies in animals, an association between HT and the development of LUTS was demonstrated. Spontaneously hypertensive rats, which

develop autonomic hyperactivity at an early age, have been found to have pronounced Selleck AZD1208 bladder overactivity.18 These animals void at least three times more frequently than normotensive control rats, and have been shown to have increased noradrenergic bladder innervation.19 The relation between nocturia and HT is not clear. Some authors reported that HT was an independent risk factor for nocturia among patients in Japan (odds ratio [OR], 1.64; 95% confidence interval [95% CI], 1.45–1.87),20 as well as in the USA (Michigan and

Boston) (OR, 1.52; 95% CI, 1.52–1.94 and OR, 2.00; 95% CI 1.24–3.14, respectively).21,15 But other studies reported no association between HT and nocturia among Dutch or Swedish patients.22,23 Treatment of HT with diuretics and calcium channel blockers can increase urine output.24 It has been reported that the mean blood pressure is higher in men with nocturnal polyuria than in controls. McKeigue hypothesized that HT and nocturnal polyuria each reflect the resetting of the normal pressure–natriuresis relationship in the Liothyronine Sodium kidney, resulting in sodium retention and increased blood pressure.25 Diabetes is a common cause of nocturia. Uncontrolled diabetes leads to hyperglycemia and an osmotic diuresis, predisposing patients to nocturia.26 Diabetes also leads to decrease in functional bladder capacity due to large residual urine volume. Ueda studied bladder function in asymptomatic Japanese patients with diabetes using cystometry.27 This study found that patients have increased bladder capacity at first sensation to void and decreased detrusor contractility. Moreover, 25% of diabetic patients had detrusor hyper-reflexia. More than half had no irritable urinary symptoms.

08 (2.98-3.18)) and MSAc cerebella (expression BAY 80-6946 cost change: 2.44 (2.14-2.88)). In the latter there was CysC overexpression in Pukinje

cells, Bergmann glia and dentate nucleus neurons. No cathepsin increase was detected in MSA cerebella. High mRNA levels of CST3 and cathepsins B and L1 were observed in SCA3 and CI brains. CysC changes are differentially present in the parkinsonian and cerebellar forms of MSA and may play an important role in the pathogenesis of this neurodegenerative condition. “
“Medulloblastoma is the most common paediatric malignant brain tumour. To identify altered genetic events in a comprehensive manner, we recently performed exome sequencing of a series of medulloblastomas [1]. This study identified mutations in genes involved in chromatin modification in 20% of patients examined, including the myeloid/lymphoid or mixed lineage leukaemia (MLL) family genes MLL2 and MLL3, which were not previously known to be associated with medulloblastoma [1]. The majority of those alterations were nonsense or frameshift mutations, indicating that MLL2 and MLL3 are new medulloblastoma tumour suppressor genes [1]. Subsequent exome sequencing studies further validated MLL2 pathway mutations as medulloblastoma

driver events [2-4]. In this report, we present detailed histopathological characteristics of three cases with MLL2/3 gene mutations. The male patient discussed in case 1 initially presented as a 5-year-old with a profound frontal headache associated with nausea and vomiting, following receipt of an immunization booster. Five days later the headache Edoxaban returned, and he was noted to have a gait imbalance; a magnetic resonance Ibrutinib order imaging scan showed a fourth ventricular mass (Figure 1A). Histopathological analysis revealed a medulloblastoma. Therapy consisted of craniospinal irradiation with a posterior fossa boost and chemotherapy consisting of a bone marrow transplant protocol

of vincristine, amifostine, cisplatin and cyclophosphamide. He is now 5 years post therapy without evidence of disease. Case 2 is of a male patient who presented as an 11-year-old who began to experience decreased appetite and headaches that awoke him, associated with nausea and vomiting. A computed tomography scan showed marked hydrocephalus with a 4-cm mass in the posterior fossa. Histopathological analysis identified a medulloblastoma. Post-operatively, he underwent craniospinal radiation therapy and chemotherapy with vincristine, cisplatin and cyclophosphamide supplemented with hyperalimentation via gastric tube placement. Now at 6 years post diagnosis, he is doing well at recent follow-up. Case 3 is a female patient who presented as a 7-year-old with a 3-week history of headache associated with morning nausea and vomiting, dizziness and recent onset of double vision. Radiographic studies revealed an enhancing mass lesion in the fourth ventricle. Axial and sagittal gadolinium-enhanced images demonstrated diffuse leptomeningeal spread of disease.