Also, the charge of the outer membrane affects the distribution a

Also, the charge of the outer membrane affects the distribution and stability of the liposome. Negatively charged selleck catalog liposomes were believed to be more rapidly removed from circulation than neutral or positively charged liposomes; later studies have indicated that the type of negatively charged lipid affects the rate of liposome uptake by the reticule-endothelial system. For example, liposomes containing negatively charged lipids that are not sterically shielded (phosphatidylserine, phosphatidic acid, and phosphatidylglycerol)

are cleared more rapidly than neutral liposomes of similar composition. However, liposomes containing sterically shielded lipids (ganglioside-GM1 and phosphatidylinositol) are cleared Inhibitors,research,lifescience,medical even more slowly than neutral liposomes [35]. Consequently, scientists have attempted to modify the liposomal structure in order to improve liposomal penetration across biological membranes and into their target Inhibitors,research,lifescience,medical organs. Targeted liposome-based system was suggested after conventional stealth liposomes failed to evade uptake of active molecules by

sensitive normal cells or nonspecific targets [39]. In addition, a targeted ligand can further increase the rate of liposomal drug accumulation in the ideal Inhibitors,research,lifescience,medical tissue or cells via overexpressed receptors, antigen and unregulated selectin [40, 41]. Peptides, proteins, and antibodies have been mostly studied as a ligand for directing drug-loaded liposomes into sites of action, due to their molecular Inhibitors,research,lifescience,medical structures, which are essentially composed by known amino acid sequences (Figure 1). The main advantage of these sellckchem structures is the relatively large quantities of drug that can be incorporated into one compartment. However, liposome structures present various problems Inhibitors,research,lifescience,medical related to the administration pathway. Orally administration is difficult because the low pH of the stomach

and the presence of bile salts tend to destabilize the liposome complex. Liposomes are very sensitive to pH, light, magnetism, temperature, and ultrasonic waves besides, liposomes are highly susceptible to destruction via uptake by the reticule-endothelial system of the macrophages. A way of protecting liposomes was studied and patented and consisted in increasing stable bilayers and regulating the release profile of the liposome [36, 40]. Although liposomes contain Dacomitinib an outer lipophilic membrane that increases their permeability across membranes, some biological barriers such as the BBB remain impenetrable. The development of a suitable liposomal carrier to encapsulate active compounds is very promising. These liposomes, also named targeted liposomes, are stable enough to be carried out to the brain across the BBB, with the appropriate surface characteristics for an effective targeting and for an active membrane transport.

Table III Trade-off between strictness of mild cognitive impairm

Table III. Trade-off between strictness of mild cognitive impairment (MCI) criterion (based on New York University [NYU] delayed paragraph recall) and decliners missed. GDS, Global Deterioration Score. Recalculated from data in Kluger et al.48 Pathological basis of MCI Most MCI patients identified in research clinics who decline to dementia can be retrospectively diagnosed with probable early stage Inhibitors,research,lifescience,medical AD. Such patients may therefore already harbor neuritic plaques and neurofibrillary tangles (NFTs), the classically recognized histolopathological hallmarks of

AD. In a large study of 109 community-dwelling older adults without dementia,63 33% were found at autopsy to have selleck bio neocortical neuritic plaques and NFTs suggesting a pathological diagnosis of AD. Methodological considerations preclude knowing how many of these cases actually had MCI, but the findings prompt speculation that gradations of AD-related pathology could explain the milder degrees of intellectual dysfunction prevalent in nondemented Inhibitors,research,lifescience,medical populations. The nature Inhibitors,research,lifescience,medical of the brain changes that distinguish pathological from normal aging and constitute the basis for MCI are

now becoming less obscure. On the basis of a large autopsy series of 2661 cases, Braak and Braak64 identified six age-associated stages of neurofibrillary change where early NFT formation is restricted to the entorhinal and transentorhinal regions of the medial temporal lobe and occurs in the absence of amyloid plaques. In autopsy studies of normal subjects without any cognitive impairment (CDR=0), investigators have found NFTs to be ubiquitous, but generally confined to the entorhinal cortex Inhibitors,research,lifescience,medical and hippocampus65 with densities, particularly for the CA1 region, that increase exponentially with advancing age.66 While most of these cognitively normal cases had either no amyloid deposition or only diffuse nonfibrillar plaques, between 18% and 45% may also exhibit neuritic plaques that are predominately concentrated in the limbic regions of the medial temporal lobe.65-67 It is therefore

apparent that some cognitively normal subjects harbor Inhibitors,research,lifescience,medical “preclinical” brain changes consistent with a pathological diagnosis of early AD; presumably, such individuals will nearly eventually develop MCI and dementia upon longitudinal observation. Virtually all CDR=0.5 (MCI) subjects studied by Price and Morris were found to have neuritic plaques AV-951 distributed more diffusely, involving neocortical as well as limbic regions.21,66 These data indicate that MCI, defined as CDR=0.5, may represent early AD more often than previously believed. Such observations, however, must be reconciled with the widely disparate rates of longitudinal decline exhibited by MCI subjects. As discussed previously, the etiological heterogeneity of MCI is most likely influenced by clinical diagnostic criteria as well as the characteristics of the population sampled.

Discussion It has been shown that HO-1 is an inducible enzyme, wh

Discussion It has been shown that HO-1 is an inducible enzyme, whose expression is often increased by those oxidative stresses, which produce reactive oxygen

species.3,14 In spite of the cytoprotective affects of HO-1 on healthy tissues following their exposure to harmful stimuli, it can also protect tumor cells. Such a protection can result in the progression Inhibitors,research,lifescience,medical of the disease. Different studies have shown that higher levels of HO-1 expression are associated with faster growth of tumors, as indicated by bigger volumes of nodules or by more numerous cancer cells.11,15 Although some studies have reported a selective decrease in the expression of HO-1 in a few malignant cells such as adenocarcinoma or tongue squamous carcinoma, most studies have shown that the expression of HO-1 is strongly up-regulated in various tumors. Therefore, it seems that HO-1 represent a molecular target in some cancers. The current Inhibitors,research,lifescience,medical study was designed to determine the expression pattern of HO-1 gene in five cancer cell lines that are highly prevalent in . Until now, only limited data are available on the expression of HO-1 in the cell lines investigated here. Among Inhibitors,research,lifescience,medical the cell line studied, HEPG2 cell line showed the highest expression of HO-1 based on the level of mRNA measured. The increased

expression of HO-1 mRNA in HEPG2 cell line in the present study is in agreement with the high levels of expression of HO-1 in tissues of hepatocellular carcinoma described by Doi and colleagues.16 Thus, based on these results, we suggest HEPG2 cell line is the best model for future analysis Inhibitors,research,lifescience,medical of biology and regulation of HO-1 in hepatocellular carcinoma cell lines. The gene of HO-1 was found by RT-PCR to be expressed in MCF7 cell line as well as in A549 cell line. Human lung adenocarcinoma A549 cells constitutively express HO-1, which help them to resist against toxic compounds Inhibitors,research,lifescience,medical and antitumor drugs.17 Concerning MCF7, our results are in line with the results obtained by Hill et al. who reported overexpression

of HO-1 protein in MCF-7 cells.18 A moderate level of HO-1 expression could be observed in myeloid leukemia-derived cell line K562. Given the up-regulation of HO-1 expression in myeloid leukemia cell line and based on the function of HO-1 as a survival factor in chronic myeloid leukemia,19 it can be suggested that there is an authentic Dacomitinib pattern of HO-1 expression related to chronic myeloid leukemia. Based on our results the LS174T cell line was the only one amongst the investigated cancer cell lines to reveal no HO-1 expression. In contrast to our results, Fang and co-workers indicated that up-regulation of HO-1 expression in colon cancer was a main factor for resistance against anticancer therapy, since the HO-1 inhibitors or targeted knocking down of the HO-1 expression made the cultured tumor cell lines much more sensitive to anticancer therapy.20 This discrepancy could be due to difference in the colon cell lines.

Although there were no ill effects noted in either case, perhaps

Although there were no ill effects noted in either case, perhaps due to the brief exposure of both dexamethasone and imatinib, a more prolonged exposure of the two medications may benefit from possible monitoring of plasma imatinib levels especially in the setting of metastatic GIST (case one). always find useful information Modifications to the treatment could include increasing the dosage of imatinib, decreasing the dosage of dexamethasone, or administering another anti-emetic in lieu of dexamethasone. Conclusion There have Inhibitors,research,lifescience,medical been very few incidences of synchronous colorectal cancer and GISTs reported in literature. Most

of the cases described were found due to other malignancies or discovered incidentally during surgery (3),(5),(15). The two Inhibitors,research,lifescience,medical cases

presented above underline the importance of being aware of this particular coexistence as well as the unlikely metastatic spread of GIST to lymph nodes, development of other primary tumours during treatment of metastatic GIST, and the importance of a multidisciplinary approach to cancer treatment. Footnotes No potential conflict of interest.
Due to the variety of therapeutic options that are currently available for patients diagnosed with Barrett’s-related high-grade dysplasia (BE-HGD), the choice of optimal management continues to be a topic of discussion among gastroenterologists, surgeons, oncologists, Inhibitors,research,lifescience,medical pathologists, and patients. Per the current American College of Gastroenterology guidelines, HGD is considered a threshold for therapeutic intervention (1). The choice of management ranges from the most conservative approach – continued endoscopic surveillance (2),(3) to the most aggressive option – esophagectomy, with Inhibitors,research,lifescience,medical endoscopic therapies such as endoscopic mucosal resection (4) and ablation therapy somewhere in the middle

(5). The potential to completely eradicate the diseased segment Inhibitors,research,lifescience,medical as well as the fact that 12.7%-75% (mean-39.3%) of patients with a pre-operative diagnosis of HGD will harbor adenocarcinoma on esophageal resection (6) are the most compelling reasons in favor Entinostat of esophagectomy. Esophagectomy, however, is associated with significant mortality and morbidity, with estimates of mortality ranging from 0%-2% at high-volume centers to 8%-10% at low volume centers (7). On the contrary, with significant advances in endoscopic techniques, the role of selleck Lenalidomide Esophagectomy is becoming restricted to patients diagnosed with multifocal dysplasia who have failed endoscopic therapy and patients in whom pre-operative imaging modalities such as endoscopic ultrasound staging (EUS) suggest the presence of at least submucosal disease. Compared to that which had been found in earlier studies, where up to 40% of patients with a pre-operative diagnosis of HGD demonstrated adenocarcinoma on resection, Konda et al in a meta-analysis of 23 studies found that only 12.

2002) These findings demonstrate that plaque components (lipid c

2002). These findings demonstrate that plaque components (lipid core and fibrous cap rupture) may be visualized on HRMRI

in ICAD. However, correlation between the HRMRI features and pathological specimens in ICAD has not yet been demonstrated. In addition, studies to determine the reliability of HRMRI for detecting high-risk plaque features and the prevalence of these features in ICAD are needed before their prognostic value can be determined. Figure 2 HRMRI of basilar atherosclerosis at level of the stenosis. Top row (A) T1 pre- and selleck catalog postcontrast, T2, and Inhibitors,research,lifescience,medical FLAIR images. Bottom row (B) shows same images with white dashed circle outlining artery and thin white circle outlining lumen. Lipid (white +) is … Conclusion HRMRI with 3D image acquisition can visualize basilar artery plaque in multiple planes, allowing identification of plaque features that may contribute to the clinical presentation. The addition of FLAIR sequences helps localize arterial wall pathology by suppressing the surrounding CSF signal. Inhibitors,research,lifescience,medical Conflict of Interest None declared.
Functional Inhibitors,research,lifescience,medical near-infrared spectroscopy (fNIRS) has become an increasingly promising imaging technique for mapping cortical activation related to cognitive tasks. This technique allows the measurement of hemodynamic responses associated with

neuronal activity by projecting near-infrared light at two different wavelengths (between the 650- and 900-nm spectrum), then recording intensity modulations of the reflected light from each Inhibitors,research,lifescience,medical wavelength that are absorbed by oxygenated (HbO) and deoxygenated (HbR) hemoglobin (Villringer and Chance 1997; Gratton et al. 2000). It has been used in various research domains with pediatric and adult populations without any neurological disorders (Watson et al. 2004; Gallagher et al. 2007; Kovelman et al. 2008) as well as with epileptic participants (Watanabe et al. 1998; Gallagher et al. 2007, 2008; Ota et al. 2011; see Dieler et al. 2012 for a review). The fNIRS Inhibitors,research,lifescience,medical studies conducted with healthy

adults have mainly focused on the hemodynamic changes associated with language-related processes. Hull et al. (2009) examined cortical activity in bilateral temporal regions during an overt picture-naming task in 10 English-speaking healthy adults. fNIRS recordings were not affected by verbalization Batimastat artifacts and the results revealed robust activation in the left temporal region with no significant changes in the analogous right-hemisphere region. Ehlis et al. (2007) used a verbal fluency task (letter and category) to investigate changes in the concentrations of HbO and HbR in the left hemisphere (including prefrontal, temporal, and central regions) in a group of 12 healthy participants. The participants exhibited strong increases of [HbO] in large areas of the left frontal cortex while performing the overt verbal fluency task during three 30-sec periods. Gallagher et al.

25 The resulting amino acid change in the PER2 protein affects it

25 The resulting amino acid change in the PER2 protein affects its phosphorylation by CKIδ/ε, and its stability and intracellular localization, hence the short period and advanced sleep phase of the patients.26,27 Interestingly, in another FASPD family, a mutation was found in the gene encoding CKIδ.28 A number of studies have focused on a polymorphism In the human PER3 gene. In one study, this polymorphism was found to be associated with delayed sleep phase dis? order (DSPD).29,30 PER3 variants

have also been associated with morning-evening preference, in this study, possibly through an effect on sleep structure, but not circadian timing. Viola and colleagues31 Inhibitors,research,lifescience,medical found that individuals homozygous for the PER35 allele showed marked differences in sleep compared with those homozygous for PER3,4 including greater sleep propensity, increased slow-wave sleep (SWS) and greater susceptibility Inhibitors,research,lifescience,medical to the effects of sleep deprivation. However, the circadian rhythms of melatonin, Cortisol, and activity were similar in both groups.31 This suggests that different clock genes may affect chronotype, selleck kinase inhibitor either via direct effects on the clock, or

through other mechanisms such as sleep homeostasis. Polymorphism of the human Inhibitors,research,lifescience,medical CLOCK gene has also been associated with evening preference and delayed timing of the sleep-wake cycle32,33 (but there are also conflicting results34). Subjects carrying one or two copies of the CLOCK 31 11C allele showed increased eveningness and reduced mornlngness, Inhibitors,research,lifescience,medical while 3111T/T subjects showed higher morningness scores.32,33 Although

the 3111C/C genotype is also associated with delayed sleep timing and greater daytime sleepiness in a Japanese population,33 thus far there is insufficient evidence to draw the same conclusions in Caucasians.32 There is currently no evidence Inhibitors,research,lifescience,medical to support an association between the 3111C/C genotype and DSPD.34,35 There is evidence to suggest that evening chronotype could increase the risk of psychiatric disorders.36 Both bipolar disorder (BPD) and schlzophrenla/schizoaffective patients show greater eveningness selleck products scores than controls. In BPD this observation appears Brefeldin_A to be correlated with age (ie, younger BPD patients were more extreme “evening types”), while schizophrenla/schizoaffectlve subjects tended to show greater eveningness at all ages. Being classified as an “evening type” could account for some of the sleep disturbances reported by BPD patients36 and could increase the severity of BPD as evidenced by an earlier age at onset of treatment, greater likelihood of self-reported rapid mood swings, and rapidcycling mood changes.36 Some work suggests there may be a relationship between DSPD and personality disorder.37 In one study, 16% of institutionalized mentally 111 adolescents were also diagnosed with DSPS,38 as compared with 7.3% of adolescents in Western countries.

4) In the remaining cases of suicide, a spectrum of toxic agents

4). In the remaining cases of suicide, a spectrum of toxic agents was used. Ethanol was the second most common main toxic agent in accidental deaths (11%). Table 4 Evaluated intention and main toxic agents in fatal poisonings in Oslo during one year. Anti-depressants (SSRIs, TCAs, or others) were found as the main or additional toxic agent in 28 (27%) of the deaths: 15 (22%) of men, and 13 (38%) of women. Thirty-one per cent of those who committed suicide had taken anti-depressants (n = 10), as had 25% of those with accidental death (n = 18). Among those Inhibitors,research,lifescience,medical who were alcohol dependent, 42% (n = 5) had taken anti-depressants.

Seventeen per cent of illegal drug abusers had used anti-depressants (n = 9), whereas 50% Inhibitors,research,lifescience,medical of those abusing prescription drugs had used such agents (n = 3). Toxic agents in fatal vs. non-fatal acute poisonings During the study period, 2998 acute selleck inhibitor poisoning episodes were registered in Oslo. Of these, 103 were fatal, of whom one episode were recognized as result of fatal poisoning only at the autopsy, and therefore not included in studies presented earlier [4,12]. The percentage of deaths per acute poisoning episode

was 3% in total (95% C.I., 0.03-0.04). Opiates or opioids were the main Inhibitors,research,lifescience,medical toxic agent in the majority of the fatal poisonings, whereas ethanol, opiates or opioids, and benzodiazepines dominated among those who survived the acute poisoning episode (Table ​(Table5).5). The case fatality rate was 0.07 or 7% for opiates or opioids Inhibitors,research,lifescience,medical (95% C.I., 0.06-0.09) and 0.9% for ethanol (95% C.I., 0.004-0.02). Acute poisonings caused by methanol, TCAs, and antihistamines resulted most often in fatal poisonings when the total number of such poisonings was taken into account. Methanol poisoning was fatal in 33% Inhibitors,research,lifescience,medical of the cases (95% C.I., 0.008-0.91), TCAs in 14% (95% C.I., 0.04-0.33), and antihistamines in 10% (95% C.I., 0.02-0.27)

of all registered poisoning episodes by these substances, respectively. Table 5 Comparison of main toxic agents between fatal and non-fatal acute poisonings during one year in Oslo. Discussion Three per cent of all acute poisonings were fatal. Previous studies of acute poisonings have focused Entinostat on in-hospital mortality [15,16], although a register-based study for the whole of Norway found that 80% of deaths occurred outside hospital [11]. In the present study from Oslo, the mortality rate was 24 per 100 000 inhabitants, whereas the register-based study including all of Norway found a lower mortality rate (10.8 per 100 000) [11]. This may indicate a higher mortality rate in Oslo, an urban setting, which usually has a larger population of drug addicts compared with the average of the whole country, including rural areas. However, it may also indicate that retrospective register-based studies tend to underestimate mortality.

The first step should be to attempt reduction or cessation of hyp

The first step should be to attempt reduction or cessation of hypotensive medication. 2 Following this, if unsatisfactory, fludrocortisone and midodrine are the drugs supplier INK 128 typically considered, but both are contraindicated in hypertensive patients. Little trial evidence is available to guide the physician. One trial, a RCT, included some vasodepressor CSS patients with a measure of success, but the trial was very small in size and without prolonged follow-up. 42 Recent discussions of the aggressiveness of blood pressure

control are relevant to these patients 43 and it is reasonable to allow higher than recommended levels of blood pressure to gain benefit at times of hypotension. A newly-available drug, droxidopa, may have some value in these patients but no evidence is yet available in CSS management. The most frequently considered drug is midodrine but one of its common side effects in males is urinary retention, making it untenable in many

who might benefit. Conclusions Carotid sinus syndrome is a relatively common cause of syncope in patients >40 years old but it is, even today, too infrequently sought as a possible cause. It occurs dominantly in males of advanced age and is diagnosed by CSM with reproduction of spontaneous symptoms. Carotid sinus hypersensitivity is a positive result of massage in the absence of clinical symptoms. Thus, these two conditions must be held as distinct entities. CSS is present in 8.8% of patients with syncope unexplained after initial evaluation, cardiac syncope is present in 10% of all patients presenting syncope and in 5% of those unexplained after initial evaluation, thus CSS is more frequent than all types of cardiac syncope combined. Cardioinhibitory

CSS is treated with acceptable success by pacing dual chamber in all those showing sinus rhythm. Greatest success may be expected in those patients who are tilt-test negative. Treatment of vasodepressor CSS is difficult and often unsatisfactory. Reduction of hypotensive medication and fluid intake increase should be the first step in management if the patient has been taking anti-hypertensive therapy. If recurrent syncope cannot be controlled, careful use of midodrine together with acceptance Anacetrapib of higher than usually accepted blood pressure levels is recommended. Tilt-test positive patients may have recurrence of syncope despite adequate pacing. They may benefit from measures to control the vasodepressor component of the reflex.
Base metal dental alloys are often used as alternatives to precious alloys due their cost considerations, mechanical properties, and low density.1,2 Currently, there is growing concern about nickel (Ni) being an allergen and beryllium (Be) being a toxic element.

5-5 Hz, causes LTD 21 In addition, direct activation of NMDARs or

5-5 Hz, causes LTD.21 In addition, direct activation of NMDARs or Group I metabotropic glutamate (mGlu) receptors can cause LTD.22,23 AMPA receptors nilotinib mechanism of action AMPARs mediate the overwhelming majority of fast excitatory neurotransmission in the central nervous system (CNS) and are critically important for nearly all aspects of brain function, including learning, memory, and cognition. They are ligand-gated ion channels composed of combinations of four separate subunits (GluA1-4). AMPARs are highly mobile proteins that undergo constitutive and activity-dependent translocation to; recycling at, and removal from, synapses.24,25

All subunits share a common membrane topology with Inhibitors,research,lifescience,medical each other, and with NMDAR and kainate receptor subunits (Figure Inhibitors,research,lifescience,medical 1). Complex combinations of signaling pathways regulated by global network activity and by the history of activity at the synapse control the number,

synaptic localization, and subunit composition of synaptic AMPARs. Increases in the number as well as changes in the composition and/or properties of synaptic AMPARs mediate LTP and LTD, Inhibitors,research,lifescience,medical which occur at synapses throughout the CNS26 (Figure 2). Furthermore, as discussed below, aberrant AMPAR trafficking is implicated in neurodegenerative diseases. Figure 1. AMPAR subunit topology, interacting partners and diverse intracellular c-termini. A) The membrane topology of an AMPA receptor subunit (AMPAR). AMPAR subunits have large extracellular N-termini, three full transmembrane domains, and a cytoplasmic re-entrant … Figure 2. Basic principles of AMPAR trafficking and synaptic plasticity. Long-term changes in synaptic function can be induced by activation of postsynaptic N-methyl-D-aspartate (NMDA) receptors, which alter synaptic strength through regulating the number Inhibitors,research,lifescience,medical of postsynaptic … AMPAR subunit composition, assembly, and ER exit AMPARs

assemble in the endoplasmic Inhibitors,research,lifescience,medical reticulum (ER) first as dimers, which then come together to form dimers of dimers to make a tetramer.27,28 In adult rat hippocampal neurons AMPARs mainly comprise combinations of GluA1/2 or GluA2/3 subunits,29 and synaptic AMPARs are predominantly GSK-3 combinations of GluA1 and GluA2.30 The GluA2 subunit contains an RNA editing site that replaces the glutamine residue Q607 coded for in the genomic DNA to an arginine residue (Q/R editing) and almost all GluA2 is edited in adult neurons.31 This residue forms part of the channel lining, and the switch to arginine functions both to act as an ER retention motif and to render GluA2-containing AMPARs impermeable to calcium.32-34 GluA1, which lacks this motif, is both calcium permeable and rapidly exported from the ER and trafficked to the plasma membrane.35 Transmembrane AMPAR regulatory proteins (TARPs) which, as discussed below, facilitate correct AMPAR folding and modify channel properties, also participate in export of AMPARs from the ER.

The Gaussian beam focusing was employed as the main method of cha

The Gaussian beam focusing was employed as the main method of characterizati
From the time of its inception, Nutlin-3a IC50 Synthetic Aperture Radar (SAR) imaging systems have provided a remote sensing resource complementary to optical and thermal-infrared sensors. SAR Imagery has been applied in a gamut of areas including ecological observation, surface monitoring, target detection, and mapping. Primary among the advantages of SAR imaging are day-night and all-weather operation, wide area coverage and sensor height-independent image resolution. These functionalities have also led to an escalating interest in the last decade towards the usage of SAR imagery for ocean environment monitoring.Nevertheless, the multiplicative speckle noise caused by microwave illumination degrades the quality of the SAR imagery. Speckle impedes visual interpretation of SAR images and may lead to interclass confusion. This is particularly so in the quick detection of oil slicks on the sea surface. The low backscatter cross section of the surface of oil spillages causes Bragg wave dampening effects on the sea. As a result of this an oil spill comes out on the image as a dark slick or dark spot, whereas the surrounding water appears bright. Consequently, oil slicks in SAR images are characterized by a high noise and low contrast, disturbing their extraction and analysis.A variety of methods have been developed to reduce speckles. For example, geometric filters such as those of Frost [1] and Lee [2] have been designed. However, convolving the image with filters could reduce the segmentation accuracy by blurring the feature boundaries due to high noise [3]. Traditional edge segmentation methods, such as border tracing, have drawbacks as well. In these methods, use of a small convolution window to preserve image resolution generates an edge map with incomplete feature boundaries and spurious edge points, due to high noise. In recent years, several novel methods have been attempted for reducing speckles while preserving edges such as Markov Random Fields [4][5] and wavelet methods [6]. Unlike these methods, level set provides a new option that is able to remove high noise and simultaneously delineate a smooth and stable boundary [7].Level set was proposed by Osher and Sethian [8] as an interface propagation technique for various applications including image segmentation. In this method, a curve is embedded as a zero level set of a higher dimensional surface. Following that, the entire surface is evolved to minimize a metric defined by the curvature and image gradient, i.e. the speed terms of the level set will reduce to zero when reaching the object boundary. The level set interface can propagate with topological changes, significant protrusion and narrow regions.In the traditional level set technique, instead of tracking the points on the interface itself, the interface is embedded as the zero level set propagates by iterations.