These areas were rebiopsied 1 and 3 years after the initial biopsy, without significant change in the pathologic findings. Four years after initial presentation, the patient was again taken to the operating room for cystoscopy and biopsy. On this examination, multiple papillary tumors were noted and biopsied. The largest was approximately 5 cm in diameter with several satellite Dabrafenib lesions. Representative biopsy revealed squamous papillomas. After counseling the patient regarding these findings, we recommended continuing follow-up with cystoscopy and periodic rebiopsy. A review of the urologic literature reveals

only 12 reported cases of squamous papilloma. Current literature suggests that although the appearance and presentation may mimic urothelial carcinoma, squamous papilloma is benign and not thought to be a risk factor for Modulators bladder cancer.2 Extensive keratinization of the bladder has been associated with bladder contracture and risk

of development of metachronous bladder cancer.4 For this reason, we suggest that it is prudent to continue surveillance with periodic rebiopsy in patients with keratinizing squamous metaplasia that does not resolve with conservative therapy. To our knowledge, this is the first published case of keratinizing squamous metaplasia with melanotic deposits of an unknown material with synchronous development of squamous papilloma. “
“Primary signet ring cell adenocarcinoma of the urinary bladder, also called linitis plastica urinary bladder, is rare, accounting for only 0.24% of all VE-821 malignant tumors of the urinary bladder.1 A 72-year-old patient consulted for intermittent painless total gross hematuria, urgency, and pollakiuria. The medical and familial histories were unremarkable. Physical examination was normal. The abdominal and pelvic ultrasound showed a bilateral hydroureteronephrosis with thickening of the urinary bladder wall. Cystoscopy visualized a solid mass in the left-side wall of the urinary bladder. Histologic examination of cystoscopic biopsy showed a proliferation Oxymatrine of

round-cell aspect of signet ring. An immunohistochemical study demonstrated positivity for cytokeratin 7 and negativity for cytokeratin 20. The diagnosis of signet ring cell adenocarcinoma of the bladder was established. Abdominal computed tomography (CT) showed no locoregional lymph nodes, metastases, or a primary tumor in other abdominal or pelvic organs. We performed a complete gastrointestinal endoscopic evaluation to exclude an extravesical primary tumor site, but no other primary site was found. The tumor was therefore treated as a primary signet ring cell carcinoma (SRCC) of the urinary bladder. The patient underwent a radical cystoprostatectomy. The intraoperative examination found a budding tumor inserted to the left-side wall. Histologic examination concluded to a signet ring cell adenocarcinoma with a colloid component estimated about 40%.

2010), and other insoluble factors on the plasma membrane (Sudo et al. 1998). Microglia activated by signals from damaged neurons may produce harmful factors that further contribute to neurodegeneration, or by phagocytizing the dying neurons. However, when the neuronal damage is not severe enough to induce neuronal death, microglia may become neuroprotective Inhibitors,research,lifescience,medical and promote neuronal survival by releasing various neuroprotective factors. This duality of function by microglia has long been proposed (Kreutzberg 1996; Streit et al. 1999; Cullheim and Thams 2007), and agents

that change the microglial phenotype from destructive to protective have been sought for a long time as treatments for neurological disorders. This Trametinib cell line cytokine mixture may have this microglial phenotype-changing

activity. The beneficial effect of this cytokine mixture may also be related to its ability to increase the expression of Bcl-xL Inhibitors,research,lifescience,medical in neurons. This effect may promote the survival of damaged neurons, activate the neuroprotective actions of surrounding microglia, and further bolster neuronal survival. Expression of NG2 by microglia may be another hallmark of their activation (Yokoyama et al. 2006; Kitamura et al. 2010; Zhu et al. 2010). Although NG2+ microglia have been reported to express a neuroprotective factor, GDNF (Kitamura et al. 2010), it appears that in the present scenario this neuroprotective factor did not contribute Inhibitors,research,lifescience,medical to neuronal survival in the 6-OHDA-induced Parkinsonism model. This is because NG2+ microglia were present following 6-OHDA treatment without

and with cytokine treatment. 6-OHDA-induced neurotoxicity has been attributed to oxidative stress (Glinka et al. 1997). Inhibitors,research,lifescience,medical Astrocytes have strong antioxidant properties (Tanaka et al. 1999; Inhibitors,research,lifescience,medical Miyazaki et al. 2011), and activated astrocytes are known to prevent DArgic neurodegeneration (Asanuma et al. 2010; Choudhury et al. 2011). Activated astrocytes were also evident in this study and the expression of mRNAs encoding Cu/Zn SOD and metallothionein 2, both of which play critical roles in suppressing oxidative stress, were upregulated in parallel with increased GFAP expression in the SNpc of the saline group. However, the activation of astrocytes and the upregulation of antioxidant factors did not lead to improved survival of neurons. Furthermore, when neurodegeneration was suppressed the with the cytokine mixture, both astrocytic activation and the expression of antioxidative factors were also suppressed, suggesting that astrocytes and the antioxidative factors do not contribute to DArgic neuronal survival in the presence of the cytokines. On the other hand, NG2 glia may contribute to the survival of DArgic neurons. NG2 glia are abundantly distributed throughout the brain and the spinal cord, representing 5–15% of nonneuronal cells (Staugaitis and Trapp 2009; Trotter et al. 2010). Some of these cells are also oligodendrocyte progenitor cells.

There has been considerable argument on whether a “true” sham or masked TMS exists. The one-wing, twowing, 45-degrec, and 90-dcgrcc positions have been explored and have nevertheless been found to induce a modest, amount of magnetic field in the cortex.21 The use of sham coils seems to be the preferred method (Neotonus, Marietta, Ga, USA), though there have been no published research using this coil. Side effects associated with TMS

and rTMS Inhibitors,research,lifescience,medical Overall, TMS and rTMS have so far been remarkably safe. Initial concerns about, the possibility of the induction of seizures have been allayed since the introduction of the guidelines for the safe administration of TMS. Additional concerns like headaches, cognitive effects, effects of irradiation, and local facial or scalp pain during the administration of TMS are rare.7 TMS studies in depression Following the observations

that TMS could provoke transient mood elevations or acute crying in normal volunteers,22,23 several researchers described the antidepressant effects of single-pulse Inhibitors,research,lifescience,medical TMS in small sample of patients with major depression.24-28 Hoflich and collaborators from Germany published the first report on the antidepressant effects of TMS.27 Inhibitors,research,lifescience,medical These authors treated two patients with delusional major GDC 0449 depressive disorder (MOD) with 10 sessions of TMS (14-mm round coil, 250 stimulations at 0.3 Hz per day, at the vertex, and at 5% to 30% above MT) and followed these treatments with 10 sessions of electroconvulsive therapy Inhibitors,research,lifescience,medical (ECT). ECT was superior to TMS in both patients; however, a mild antidepressant effect, of TMS was observed in one of the patients. Additional sTMS studies are those of Kolbinger et al,28 Grisaru et al,24 Conca et al,25; and Geller et al.25 These studies

were all performed with round coils, at relatively low frequencies, and with coil locations at, either the vertex or the LDLPFC. The antidepressant effects of TMS in these studies were very modest. Conca et al24 compared the Inhibitors,research,lifescience,medical effects of TMS as an add-on Adenosine treatment to ongoing antidepressant medication in patients with MDD without delusions. The authors randomly assigned patients to one of two groups, one treated with sTMS and medication, and the other with medication alone. TMS was administered over several cortical regions with a round coil. The authors found a greater remission of depressive symptoms in the sTMS group after just, three sTMS sessions; this difference was even more significant by the end of the 10th and final sTMS session. Conca et al repeated this design in a follow-up study of 12 MDD patients without, delusions.29 These authors administered 500 pulses a day for up to 10 days at maximal machine output, and over several cortical regions. They reported a significant, response rate for sTMS-treated patients.

Our results also provide relevant prognostic information for the DPAM subtype for the purpose of staging and prioritizing urgency of surgery, as even in patients with apparently indolent disease, survival outcomes vary widely. In addition, elevated CA 19-9 may be useful in identifying patients who would potentially benefit from adjuvant therapy and/or closer post-operative surveillance. Acknowledgements Disclosure: The authors declare no conflict of interest.
The KRAS and BRAF gene amplification was conducted by Primus 96 Advanced PCR-instrument (PeqLab). Primers and fragment

details are described in Table 1. For all 50 samples, (25 samples before and 25 samples Inhibitors,research,lifescience,medical after neoadjuvant Inhibitors,research,lifescience,medical radiochemotherapy), the existence of amplified KRAS and BRAF fragment was revealed by 2% agarose gel electrophoresis prior to SNaPshot- and sequence analysis. Table 1 Applied primers for KRAS- and BRAF-PCR analysis Sequencing and SNaPshot Sequencing analysis was based on Sanger method and the SNaPshot analysis on single base extension (Table 2. Applied primers) carried Inhibitors,research,lifescience,medical out according to the recommendation of Applied Biosystems, Germany. Different sets of primers were used to amplify KRAS and BRAF genes, (Table 2). The GeneMapper®

software v4.0 and the Sequencing Analysis Software v5.2 was applied to size and genotype the data. Inhibitors,research,lifescience,medical The GeneScan™-120 LIZ® size standard was used to indicate the size of labeled fragments. The SNaPshot reaction was purified by 1 µL SAP (1 U/mL) and the sequence-product by the application of the Dye Ex Kit 2.0 (QIAGEN, Germany). Table 2 Applied primers

for KRAS- and BRAF- sequencing and SNaPshot analysis Microsatellite instability analysis The microsatellite analysis was conducted using a fluorescent multiplex PCR-based method. Typical allelic profiles of microsatellite markers (as listed in Table 3), generated by amplification Inhibitors,research,lifescience,medical of matching tumor and normal tissue, were compared. Panel 1 and panel 2 (Table 3) include two distinct analyses of five microsatellite systems, respectively. Therefore in total 10 microsatellite markers were used for MSI testing. Table 3 Microsatellite marker used in the present study. BAT25, BAT26 and BAT40 are mononucleotide repeats. D5S346, D1S123, D17S250, D10S197 and D18S69 are dinucleotide of repeats and MYCL1 presents a tetranucleotide repeat If more than 30% of a tumor’s markers are unstable, it is scored as MSI-H. The tumor is designated as MSI-L if at least one, but fewer than 30% of markers are unstable (Table 3). Statistics and mathematics The JMP statistical software version 6.0 (JMP, Germany) and SPSS 17.0 (IBM, Germany) were used for all statistical analyses. A selleck chemical P-value of 0.05 or less was usually regarded as relevant.

2 sec. Subjects were instructed to name each picture as fast and accurately as possible and to attend to the distractor word as it may but need not RG-7204 assist word finding. RT analysis and interrater reliability After fMRI sessions, responses were consulted for scoring of each participant’s correctness of naming responses and for the analysis of RTs including visual inspection

of the waveform (see Rastle and Davis 2002). Contrary to automated analyses, the manual extraction of RTs from the sound files with high signal-to-noise ratio does not depend on such variables as initial phoneme, individual participant Inhibitors,research,lifescience,medical characteristics, or breathing into the microphone (see also Discussion section). Initial onsets were adequately Inhibitors,research,lifescience,medical balanced across our conditions. In order to control for subjective variability of manual RT extraction, we examined the interrater reliability for four randomly selected subjects assessed by two speech pathologists. Interrater reliability over all conditions was high (r = 0.997, P < 0.001) with a mean difference

of 11.8 msec (SE = 1.1 msec). Image acquisition, processing, Inhibitors,research,lifescience,medical and analysis Anatomical (MPRAGE: data matrix, 256 × 256; TR, 2.2 sec; TE, 2.6 msec; pixel size, 1 mm3) and functional images (EPI sequence: data matrix, 64 × 64; FOV, 19.2 cm; TE, 30 msec; TR, 2.19 sec) were recorded on a 3T Siemens TIM-Trio with an 8-element head coil in a circularly polarized mode. Using continuous acquisition, functional data were acquired from 36 interleaved slices with 3 mm thickness. Images were analyzed with SPM 5 (http://www.fil.ion.ucl.ac.uk/spm). Preprocessing included slice timing, coregistration and segmentation of the anatomical Inhibitors,research,lifescience,medical image, normalization

using the parameters estimated during segmentation, and smoothing with a 12-mm full-width half-maximum (FWHM). Realignment parameters were only estimated because motion and distortion correction had been Inhibitors,research,lifescience,medical performed beforehand by a scanner software (see Zaitsev et al. 2004). Trials that elicited acceptable naming responses (e.g., the distractor/picture pair Kugel/bowl and Kuchen/cake) were reclassified Isotretinoin accordingly (e.g., naming response Torte/tart, reclassified from phonological to unrelated condition; 0.9% of all trials). A total of 4.4% of all trials were discarded because of naming errors. Picture onsets were modeled as the critical event using the canonical hemodynamic response function (HRF), and estimated realignment parameters were applied as multiple regressors in SPM 5. Statistical analyses comprised a calculation of main effects on the first and standard repeated measures ANOVAs on the second level (subtraction and conjunction analyses [conjunction null]). We intended to compare the unrelated distractor condition (UNREL) to the related linguistic distractor conditions (REL).

Evidence suggests cross-talk between IGF-1R and EGFR, which might be crucial for the mitogenic and transforming activity of EGFR. More specifically, the IGF-1 downstream signaling cascade is thought to induce EGFR independent PIK3CA and AKT activity, which might be another explanation for the lack of efficacy of anti-EGFR monoclonal antibodies

Inhibitors,research,lifescience,medical in KRAS WT CRC (74). This is supported by Bohula et al. in their experiments which proved that IGF-1 and IGF-2 are ubiquitously produced protein hormones that interact with the IGF-1 receptor (IGF1R) to regulate growth, differentiation, and survival. The IGF1R activates both RAS/ERK- and PI3K/AKT-related signal transduction pathways, which act to promote proliferation and prevent apoptosis (75). A phase II study with the anti-IGF-1R monoclonal antibody

IMC-A12, either alone or in combination Inhibitors,research,lifescience,medical with CTX, was performed in patients with CTX or PAM-refractory mCRC. No antitumor activity was seen in the 23 patients treated with IMC-A12 monotherapy and of the 21 patients treated with the combination of IMC-A12 and Inhibitors,research,lifescience,medical CTX, 1 patient with KRAS WT achieved a partial response, with disease control lasting 6.5 months. No additional antitumor activity was observed in patients with the combination treatment (76). Concomitant blockade of IGF-1R and MEK has been shown to effectively prevent the occurrence of the EGFR-IGF1R cross-talk in BRAF mutated CRC preclinical models (77). Conclusions Despite the rapid advancement in EGFR targeted therapy, much remains to be studied to understand the mechanism of resistance in CRC. Clearly, KRAS codon 12 mutation is a leading cause of resistance to EGFR inhibitors. In the KRAS WT group several contributing factors appear to Inhibitors,research,lifescience,medical influence resistance and these include ligand expression, activation of the PI3K or IGFR-1 pathways. The role of RAS codon 13 mutations and BRAF mutations as a mechanism of resistance to EGFR inhibitors is an

area that requires further research. Identification of mechanism of resistance Inhibitors,research,lifescience,medical to EGFR inhibitors will improve our ability to select patients for personalized medicine approach as well as develop new combinations of therapies that can overcome resistance to current available treatments. Acknowledgements Disclosure: The authors declare no conflict those of interest.
Colorectal cancer remains one of the most common causes of cancer diagnoses and mortality in the United States. The treatment of Galunisertib cell line metastatic colorectal cancer has evolved significantly over the last decade with near-tripling of patient survival rate. A significant contribution to this outcome was the advent of novel targeted agents, such as the epidermal growth factor (EGFR) inhibitors. In an era of emphasis on refining therapy, the presence of KRAS mutation will predict for resistance and limit exposure to patients who are more likely to benefit. In contrast, the presence of BRAF mutations does not seem to have a predictive value.

The computerization of the study allowed the data to be presented to participants in a novel and more meaningful way. Data from rounds two and three were presented to participants as a color histogram (or heat map) where the depth of color indicated the frequency with which respondents in the previous round had chosen each rating. Figure 1 shows the frequency with which each of the five responses had been chosen in the previous round (dark being many, light being few). The grey circle shows the choice

that the current participant Inhibitors,research,lifescience,medical made on the previous round and the green circle shows the choice that they have made on the current round, (in round one each box was white as no previous selection had been made). In this way, participants could easily see how their responses compared to the consensus in the previous round and either confirm or update their response accordingly. Figure 1 An example from the website of a

color histogram of previous Inhibitors,research,lifescience,medical responses. Inhibitors,research,lifescience,medical The second question required a numeric answer. As the user sample size in each round exceeded 30 (and therefore the number of independent responses was sufficient to assume that the central limit theorem held with responses tending towards being PLX4032 in vivo normally distributed), we proceeded Inhibitors,research,lifescience,medical to adopt a parametric approach in the iterative feedback to users between rounds. Feedback to the user was given as a color again, but in this case, the depth of color indicated the number of standard deviations between the user’s response and the mean response (in other words, the z-score). As the scale for each answer was different, the normalized z-score

provided a consistent measure of agreement for each question. Z-scores were calculated as, z=x-μσ Where x was the value for which the z-score is to be calculated, μ was the mean of the values of the previous round and σ was the standard Inhibitors,research,lifescience,medical deviation of the values from the previous round. The z-score was translated into a color depth MycoClean Mycoplasma Removal Kit and shown around the input box for each item in the questionnaire. The mean value from the previous round, along with the participant’s own response from the previous round were also displayed on the questionnaire. An example of the quantity input box is given in Figure 2; the top box shows that the previous average quantity for this item was 73 and that this participant had said 53. The light color indicates the difference. The bottom box shows where the participant was in closer agreement in the last round. The numbers in the boxes show the participant’s updated response for this round. Figure 2 The quantity input box for two items as presented on the website.

Feeding and swallowing difficulties are quite common in infantile Pompe disease (12, 13). However, apart from few scattered single case reports (14, 15), poor attention has been generally paid to facial and bulbar symptoms in adult-onset Pompe disease and only recently few studies focused their attention on them (16-18). A vacuolar myopathy in genioglossus Inhibitors,research,lifescience,medical and proximal esophagus has also been described through autopsy study in Pompe disease (19) Furthermore, according to a nationwide prospective observational study in adults with Pompe disease in Netherlands, bulbar muscle weakness was detected in about one quarter

of patients and was significantly associated with scapular winging (20). We report on 3 family members with atypical lateonset Pompe disease, characterized by bulbar symptoms, in particular swallowing difficulty and tongue weakness, clinically relevant in all our patients and requiring assisted ventilation. In patient 1 and 3 bulbar symptoms were reported as first symptoms and Inhibitors,research,lifescience,medical in particular Inhibitors,research,lifescience,medical patient 1 was first investigated elsewhere for disease of central nervous system. Patient 2 – presenting increased CK values – was asymptomatic for many years and presented bulbar symptoms only 5 years after the onset of lower limb weakness, confirming the great phenotypic variability of the disease. Patient 1 complained also

difficulty in moving lips; facial muscle involvement was confirmed by neurological

examination and electromyography. Tongue involvement with macroglossia – traditionally described in infants Inhibitors,research,lifescience,medical with classic phenotype – was considered a rare finding in late-onset disease. However tongue weakness has been reported in 19 patients affected by late-onset Pompe disease (17), one third of them complaining for swallowing difficulties, such as impairment of oral bolus control, and not further investigated. In that Angiogenesis inhibitor series Inhibitors,research,lifescience,medical tongue weakness was mild and only detected on neurological examination, being usually underestimated by the patients. On the contrary in our patients tongue weakness was more marked according to criteria established by Dubrovski and colleagues and reported as first symptom by patient 1. Furthermore tongue weakness had a main role in swallowing difficulties as showed by videofluoroscopy swallowing examination performed in our patients. Differently from data reported by Dubrovski and Thymidine kinase colleagues, all our patients displayed also tongue hypotrophy. As a matter of fact tongue involvement detected in our patients was also supported by facial CT and MRI findings in patients 1 and 2, respectively, that showed fatty degeneration, according to previously reported studies (16, 17). Recently Hobson- Webb and colleagues reported that 3/12 patients affected by late-onset Pompe disease showed oropharyngeal dysphagia, although none of them as first symptom (18).

An example of a new indication for an old drug is that of inhaled corticosteroids in chronic obstructive pulmonary disease (COPD) and metformin, an anti-diabetic medication, which has been receiving much attention recently as a potential anti-cancer agent, primarily on the basis of several observational studies Inhibitors,research,lifescience,medical that reported impressive reductions in the incidence of and mortality from cancer. These observational

studies formed the impetus for the conduct of major large-scale randomized trials. In this paper, we show that the spectacular effects reported in many of the observational studies that have been conducted in this context are the result of time-related biases, particularly immortal time bias which tends to exaggerate the benefits observed with a drug. We also show how the studies could have avoided this bias, and the ones that did actually reported null effects. With this knowledge, it is unlikely Inhibitors,research,lifescience,medical that randomized trials would have been conducted. INHALED CORTICOSTEROIDS IN COPD Chronic obstructive pulmonary disease, a disease that encompasses emphysema, chronic obstructive bronchitis, and small airway obstruction, is characterized by largely irreversible airflow obstruction.10 It currently affects Inhibitors,research,lifescience,medical around 10% of the population over the age of 40 years

and has recently check details become the third leading cause of death in the US.11,12 The pharmacological treatment of COPD has generally consisted of bronchodilators. However, because of the presence of inflammation in COPD, inhaled corticosteroids, which had been shown to be highly effective for the treatment of asthma, were readily adopted in COPD in the 1980s despite the fact Inhibitors,research,lifescience,medical that no randomized controlled trials had yet evaluated their effectiveness in this indication. The earliest randomized controlled trials to evaluate inhaled

corticosteroids in the treatment of COPD were only published in the late 1990s. The first seven trials Inhibitors,research,lifescience,medical found no improvement in the decline of lung function over time and, except for the last two trials, found no reduction in exacerbation rates Montelukast Sodium with various inhaled corticosteroids (ICS) compared with placebo, over periods ranging from 6 months to 3 years.13–19 In the early 2000s, the next wave of randomized controlled trials all involved the evaluation of inhaled corticosteroids combined with a long-acting beta-agonist.20–25 Most of these trials reported significant effects on lung function and reductions in exacerbation rates with the combination therapy, while the effects of inhaled corticosteroids alone were equivocal. Thus, the totality of these trials can be concluded to imply that any effectiveness of these medications is driven primarily by the long-acting beta-agonist component.

However, pharmacokinetics of BPs require delivery method to escape bone and to target macrophages. Liposomes encapsulating CLO were successfully used to achieve temporary macrophage depletion in the spleen [21]. The authors

demonstrated that once phagocytosed, the liposomal membranes were disrupted by the phospholipases of the lysosomes, and the drug is released into the cell. Other studies Inhibitors,research,lifescience,medical confirmed macrophage elimination from the spleen, following intravenous (i.v.) injection of CLO entrapped into liposome by the absence of lysosomal acid phosphatase activity [21, 22] and surface markers of macrophages [23] as well as by the absence of cells with the MAPK inhibitor capacity to Inhibitors,research,lifescience,medical ingest and accumulate carbon particles from the circulation [22]. Ultrastructural studies also confirmed that macrophages not only lose some of their functional characteristics but are also physically removed from the circulation [26]. Growth inhibition of macrophages-like

cells by using liposomes encapsulating BP was also confirmed with other BPs, namely, PAM and ETI, on RAW 264 and CV1 cells [24]. In this study, free BPs were Inhibitors,research,lifescience,medical found to be even 1000 times less active, compared with the corresponding liposome-based formulations. Interestingly, the use of high calcium extracellular concentration resulted in a stronger macrophage depletion, suggesting the role of calcium to mediate BP cell uptake [24, 27]. The liposome Inhibitors,research,lifescience,medical type affected macrophage depletion, which was higher when using negatively charged unilamellar

liposomes [27]; however, this effect was found only in the case of CLO and ETI but not in the case of PAM. Finally, the use of calcium/bisphosphonate complex was found to lead to an enhanced uptake into cells but not to an inhibitory effect on the cytokine production by macrophages [27]. BP-encapsulating liposomes, when intravenously administered, led to elimination of macrophages from spleen and liver [25] but not those in other organs [23], reflecting the pharmacokinetics of the carrier. Accordingly, subcutaneous Inhibitors,research,lifescience,medical footpad administration of the BP-encapsulating liposomes resulted in macrophage elimination in draining lymph nodes [28] while intratracheal administration exclusively eliminates macrophages from lung tissues [29]. Liposome encapsulating BPs were used to enhance tumor growth in an experimental model of liver metastasis [30]. Rat inoculation with colon carcinoma unless cells resulted in a strong enhanced tumor growth in the liver only when the animals were pretreated with an i.v. injection of CLO-encapsulating liposomes. This effect was attributed to the effective elimination of all Kupffer cells that are preferential accumulation site for colloidal carriers. Accordingly, in the same experiment, nonphagocytic cells into the liver were not affected [30]. In contrast, liposome encapsulating CLO have been successfully used to inhibit the tumor growth.