The new FCSEMS is short but has a wide flare to prevent migration. This appears to be effective, because we observed asymptomatic migration in only 1 case. In this case, the stent migrated outward. We assumed that the stent migrated out because of shrinkage of the cyst. Recently, an FCSEMS with a novel shape and delivery system specially designed for enterocystostomy was described.11 and 12 The authors reported that enterocystostomy using this lumen-apposing stent was accomplished with high technical and clinical success in this pilot observational study. Compared with a lumen-apposing stent, the new FCSEMS has some marked advantages,

the main ones being its wide lumen diameter and the thin and simple delivery system. The diameter of this stent is 16 mm, and the delivery system is 10F. In all cases, the stent was inserted without changing to an endoscope with a larger channel Compound Library diameter. When DEN was performed, the diameter of the stent was large enough to insert a normal or a therapeutic endoscope. The new FCSEMS was inserted and expanded successfully in all cases. Stent replacement was not necessary

in any patient. Although the stent was large in diameter, minimal pre-dilation of the tract was needed, which appeared to reduce the risk of leakage. In the pancreatic pseudocyst cases, stent insertion was effective for drainage. In BIBW2992 price the WOPN cases, DEN was performed successfully through the endoscope. Because DEN cannot be performed through a plastic stent, the FCSEMS is superior in this regard. Multiple sessions of DEN were required to achieve complete Ergoloid removal of necrosis, but the initial stent placement avoided the need for tract dilation before each endoscopic procedure. The FCSEMS appears to be useful for both drainage and DEN. However, in the WOPN cases without appropriate debridement, the result was unfavorable. The clinical success rate indicates that, even when a large-diameter tract was maintained, solid necrosis could not be completely drained spontaneously. There was one serious complication where

bleeding occurred. Angiography revealed that the point of bleeding was distinct from the stent, and we believe that the vessel damage was not related to the stent but was the result of inflammation or necrosectomy. Because this was a pilot study, the complication rate was not fully analyzed and needs to be evaluated more thoroughly in a larger study. One limitation of this study is that it was a retrospective evaluation of a small number of cases. Second, the FCSEMS was inserted via the transgastric route in every case. Stent insertion via the transduodenal route could be associated with different complications, such as migration or leakage. Third, the follow-up duration was short, so recurrence and other complications might have been underestimated. Further studies are needed to evaluate these aspects.

Without research on those factors, the source of variation cannot be controlled, and the inherent variability might be so high that the biomarker is invalidated as part of a field monitoring program. Minimizing the effects of confounding factors can reduce systematic sampling error. For example the data set used in the present exercise included only non reproductively-active Ku-0059436 cost adult fish to reduce the high variability of EROD activity

among female fish at the onset of spawning. Estrogen is known to down-regulate the cyp1a gene, so that assays of EROD activity in sexually maturing female fish approaching spawning will inflate the variance of EROD activities of a mixed sample of male and female fish ( Forlin and Haux, 1990). If the biomarker selected is influenced by the gender of the fish, the data provided in Table 3 represents the number of fish per sex to selleck chemical be collected at each site, assuming that the variance is equal between sexes. It is worthwhile to note that in field studies, seasonality in biomarkers of fish health often introduces variability that is higher than inter-site variability ( Hanson et al., 2010), making it increasingly difficult to relate cause and effects. A rigorous

sampling program with an adequate number of fish sampled will offer a reasonable potential to offset high seasonal variability. While the influence of confounding factors might be minimized, the analytical variability can still be surprisingly high. In an inter-laboratory round-robin, Munkittrick et al. (1993) found that EROD activities measured in sub-samples of fish livers varied considerably. For seven laboratories reporting EROD activities measured with 9000g supernatants (S-9 fractions), the coefficients of variation of arithmetic mean EROD activities of six fish per site sampled from reference and pulp

mill sites ranged from 46–80% (calculated from Table 2, Munkittrick et al., 1993). However, the variation in induction (i.e. the proportional increase in activity between reference and exposed sites) was much less, with a cv of only 30% among the seven independent labs. This indicates that the variance among labs was likely related Dynein to differences in methods that affected induced and uninduced fish equally. Standardization and improvement of analytical protocols can reduce analytical variability (van den Heuvel et al., 1995), thereby increasing the probability of detecting an inter-site difference. Because this variability is entirely within the control of the monitoring agency, it can be beneficial to develop Quality Assurance/Quality Control (QA/QC) protocols for each biomarker. For example, in addition to variations among fish of EROD activity, variation in EROD assays can be generated from each step of the assay, including preparation of S-9 fractions, the biochemical assay, and the analysis of data.

Furthermore, in exploratory analyses of the BATTLE study, in which patients with pretreated NSCLC selleck products were randomized to four separate phase II targeted therapies including erlotinib monotherapy, clinical outcomes of patients aged >65 years were comparable with those of younger patients [12]. POLARSTAR (POst-Launch All-patient-Registration Surveillance in TARceva®-treated NSCLC patients) was a large-scale surveillance program, including all Japanese patients with NSCLC treated with erlotinib [13]. The study was undertaken

as a post-approval commitment to monitor the efficacy and safety of erlotinib in Japanese patients, and more than 10,000 patients were registered. The primary endpoints were patterns of occurrence of interstitial lung disease (ILD) and risk factors for onset of ILD, given the small but important risk in Japanese patients [8], [9] and [10]. Interim safety and efficacy data supported the clinical benefits of erlotinib in Japanese NSCLC patients, with no new safety signals observed [13]. I-BET-762 ic50 ILD (all grades) was confirmed in 4.5% of the interim analysis population with a mortality rate of 1.6%. Significant ILD risk factors included concomitant or previous ILD, smoking history, concomitant or previous lung infection, and Eastern Cooperative Oncology

Group (ECOG) performance status (PS) 2–4. The median progression-free survival (PFS) and OS were 64 and 260 days, respectively.

The present analysis of the POLARSTAR surveillance study compared the efficacy and safety of erlotinib treatment for elderly (stratified as ≥75 years or 75–84 years or ≥85 years) versus non-elderly (<75 years) Japanese patients with Alectinib NSCLC. All patients with unresectable, recurrent and/or advanced NSCLC who were treated with erlotinib in Japan between December 2007 and October 2009 were enrolled. Eligible patients received oral erlotinib (150 mg once daily) from 1027 institutions that could prescribe erlotinib (up to 12 October 2009) and were monitored until erlotinib therapy termination or completion of 12 months of treatment. The study was conducted in accordance with relevant national and local guidelines, and with ethics committee approval. Demographic and baseline data were collected for each patient, including age, gender, body mass index, tumor histology, ECOG PS, smoking history, and medical history (including hepatic dysfunction, renal dysfunction, cardiovascular disease, and lung disorders). Safety data were collected at 1, 6, and 12 months after the start of erlotinib therapy. All AE reports were collected and graded using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 3.0 and coded using the Medical Dictionary for Regulatory Activities (MedDRA) version 14.1 thesaurus terms.

The amplification reaction contained the template oligonucleotides in a 0.1 μM concentration, the amplification primers in a 1 μM concentration, 250 μM of each deoxynucleotide triphosphate and 2 U of the thermostable recombinant Taq polymerase. The

reactions were subjected to initial denaturation of 4 min at 95 °C and subsequent 40 cycles that consisted of denaturing the DNA at 95 °C for 1 min, annealing at 55 °C for 1 min and elongation at 72 °C for 1 min. The PCR product was purified using the QIAquick TM Gel Extraction kit (Qiagen, USA), digested with Bsa I and Xba I and cloned into pE-SUMO LIC Vector. The plasmid obtained (6xHis-SUMO-PnTx3-4) encodes a fusion protein composed of an 18.0 kDa Yeast SUMO protein (Smt3) fused at the N-terminal with a 6xHis tag and at the C-terminal with the PnTx3-4 toxin (8.0 kDa). The sequence of the recombinant plasmid was confirmed by automatic sequencing Ku0059436 using the dideoxynucleotide chain-termination reaction ( Sanger et al., 1977). E. coli ORIGAMI (DE3) cells containing pGro7 chaperone plasmid were transformed with 6xHis-SUMO-PnTx3-4. An isolated colony was inoculated Osimertinib in vitro in 10 mL of LB medium supplemented with Ampicillin (100 μg mL−1) and Chloramphenicol (20 μg mL−1) for cultivation at 30 °C overnight. The culture was then

diluted 100-fold in 1 L of LB medium (with antibiotics) containing 0.5 mg mL−1 of l-arabinose (for chaperones expression) and cultured to an OD600 of 0.5–0.8. The expression of the recombinant fusion protein was induced with 0.6 mM Isopropyl β-d-1-thiogalactopyranoside (IPTG), overnight, at 18 °C with shaking. Cells were harvested by centrifugation at 5000 g for 15 min, suspended in 30 mL of Resuspension buffer (20 mM Tris–HCl, 150 mM NaCl, pH 7.5) containing protease inhibitor cocktail (CALBIOCHEM), lysed by passing twice through a French Press (16,000–18,000 psi) dipyridamole and cell debris were removed by centrifugation. The recombinant toxin expressed in the supernatant was purified by affinity chromatography

using a Ni-NTA agarose resin (Qiagen). After purification, elutions were pooled and dialyzed against 20 mM Tris–HCl, 150 mM NaCl, pH 7.5 for 24 h to remove imidazole. To purify the recombinant toxin present in inclusion bodies, the pellet obtained after cell lysis was solubilised in a denaturing buffer (6 M Guanidine-HCl, 100 mM NaH2PO4, 10 mM Tris, 20 mM Imidazole pH 8.0) and incubated for 1 h at RT. The sample was then centrifuged at 32,000 g for 30 min and the supernatant was purified by affinity chromatography using a Ni-NTA agarose resin. The elutions were dialyzed first against 1 M Guanidine-HCl, 0.05 M Tris, 0.15 M NaCl, pH 8.0 and later against 0.1 M Gnd-HCl, 0.05 M Tris, 0.15 M NaCl, 1 mM DTT, pH 8.0.

We have previously designed and synthesized several series of bifunctional alkylating agents that were found to have potent activity against a variety of cancer xenograft

models [28], [29] and [30]. Among these agents, the compound BO-1012 (Figure W1A), which is a bis(methylcarbamate) derivative of 3a-aza-cyclopenta[α]indene, was shown to have potent therapeutic efficacy against inherited resistance H460 cells and bladder cancer cells with acquired cisplatin resistance (NTUB1/P) in nude mice when used in combination with arsenic trioxide [31]. Another derivative, BO-1090, was found to be effective PARP inhibitor against a variety of oral cancer cells both in vitro and in vivo [30]. Compound BO-1012 displays potent therapeutic efficacy and was selected as a lead compound for further development as an antitumor agent. However, this agent was not suitable for large-scale preparation because of the explosive and severely hazardous properties of methyl isocyanate, which was used to introduce the bis(methylcarbamate) functional group into the final product. For lead optimization, we synthesized compound 3-(4-methoxyphenyl)-9H-pyrrolo[1,2-a]indole-1,2-diyl)bis(methylene)

bis(ethylcarbamate) (BO-1509) ( Figure W1), which bears a bis(ethylcarbamate) group and can be prepared in large amounts. Notably, we found that BO-1509 possessed the ability to kill various cancer cell lines. ICLs formed by bifunctional alkylating agents are usually repaired by a complex pathway [32]. The combination of a PI3K inhibitor MEK inhibitor with an anticancer agent is therefore believed to increase the efficacy of the drug or to decrease drug resistance [33] and [34]. In this study, we investigated the anticancer activity of BO-1509 in combination with LY294002 against non–small cell lung cancer (NSCLC), which accounts for approximately 80% of lung cancer cases [35]. Protirelin More than half of patients with NSCLC have epidermal growth factor receptor (EGFR) mutations and are promisingly treated with tyrosine kinase inhibitors (TKIs), such as erlotinib or gefitinib [36], [37], [38] and [39]. Unfortunately, the emergence of resistance to targeted therapeutics

occurs nearly in all patients in a short period [40]. Therefore, in this study, we demonstrated that the combination of BO-1509 with LY294002 significantly suppressed the growth of several lung cancer cell lines, including EGFR-mutant NSCLC lines, PC9 and PC9/gef B4 cells, both in vitro and in vivo. H460 and A549 cells were obtained from the American Type Culture Collection (Manassas, VA). Gefitinib-sensitive (PC9) and gefitinib-resistant (PC9/gef B4) cells were kindly provided by Dr Chih-Hsin Yang (Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan) [41]. CL1-5, CL83, and CL25 cells were provided by Dr Pan-Chyr Yang (Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan) [42]. A549 cells were maintained in Dulbecco’s modified Eagle’s medium.

WRKY gene family expansion may arise from whole-genome duplication events, rather than from genome size, given that Selleckchem Caspase inhibitor the grapevine genome has not undergone recent genome duplication [48]. The Populus genome has undergone salicoid duplication (p event) [47] and [49], duplication events (β, α) have occurred in Arabidopsis and Gossypium, and Gossypium has undergone one more duplication event than Arabidopsis [49], [50] and [51]. The WRKY family, one of the most important transcription

factor families, regulates plant responses to various physiological processes, especially biotic and abiotic stresses [45] and [52]. Under salt stress, 26 WRKY genes were induced in Arabidopsis, based on comprehensive microarray analysis of the root transcriptome [53]. Of the 64 GmWRKY genes in soybean (Glycine max Merr.), 25 WRKY genes show differential expression in response to at least one abiotic treatment [15]. In rice, at least 54 WRKY genes respond to http://www.selleckchem.com/products/17-AAG(Geldanamycin).html abiotic stress [54]. In addition, the transcripts of 49 WRKY genes in Arabidopsis are expressed in response to bacterial infection and salicylic acid (SA) treatment [55]. In cotton, eight WRKY genes from different cotton species have previously been reported. GaWRKY1 participates

in the regulation of sesquiterpene biosynthesis in cotton, and GhWRKY3 may function in plant defense responses [19] and [56]. In the present study, we further identified 12 WRKY genes induced by salt stress, 16 induced by drought stress, and 14 induced in response to V. dahliae VD8 infection. As shown in Table 2, 11 WRKY genes were simultaneously induced by both drought and salt treatment, and six WRKY genes were simultaneously induced by drought, salt, and pathogen treatments. These results indicate that WRKY genes are important regulators in cotton stress responses. Notably, GhWRKY59 and GhWRKY80 exhibited sustained responses to V. dahliae inoculation from 48 h to 144 h. They are two of the six WRKY genes simultaneously induced by the three stressors (drought, salt, and V. dahliae inoculation). This finding indicates that GhWRKY59 and GhWRKY80 have multi-functional roles in stress

tolerance, and may potentially be applied in breeding for new cotton cultivars with increased stress resistance. Homologous Rebamipide genes from different plant species may play diverse roles. In Arabidopsis, WRKY genes (AtWRKY2, AtWRKY17, and AtWRKY33) are induced under NaCl treatment [53], [57] and [58], whereas AtWRKY63 may function in drought tolerance [59] and AtWRKY4 and AtWRKY60 function in plant responses to pathogens [7] and [60]. Genes homologous to all of these Arabidopsis WRKY genes except AtWRKY63 were identified in cotton. According to qRT-PCR analysis, WRKY22 and WRKY41, which are homologous to AtWRKY33 and AtWRKY17, respectively, were downregulated in response to NaCl treatment but significantly upregulated under drought treatment and post-inoculation.

4G). Whereas no effect on the phagocytosis of E. coli was observed with the Aβ(1-x) isoforms, the phagocytosis of E. coli was strongly and exclusively enhanced by N-terminally GDC-0980 cell line truncated Aβ(2–42). A tendency to induce phagocytosis was also observed for Aβ(3p–42). This

finding confirms that N-terminally truncated Aβ(x–42) also induces phagocytosis when bound to E. coli. As previously observed during the phagocytosis of PSPs, the opsonizing effect of Aβ(3p–42) was less pronounced in THP-macrophages than in primary human phagocytes. As differentiation and polarization have a great impact on the phagocytic activity of macrophages, primary human monocyte-derived GM-CSF- and M-CSF-elicited macrophages were compared. The differentiation and polarization of monocytes by GM-CSF and

M-CSF were confirmed by phase contrast microscopy, iNOS immunofluorescence, flow cytometry MK-2206 molecular weight and ELISA (Fig. 4A). GM-CSF-derived macrophages displayed higher expression of iNOS and CD206. The expression of MSRI, HLA-DR and CD14 was higher in M-CSF-elicited macrophages (Fig. 4B). Furthermore, the secretion of TNFα tended to be higher in GM-CSF-derived macrophages, whereas that of IL-10 was higher in M-CSF-derived macrophages (Fig. 4C). Therefore, GM-CSF-elicited macrophages shared several, but not all, of the features of M1 macrophages, whereas M-CSF-derived macrophages rather resembled M2 macrophages. Again, Aβ-peptides terminating at amino acid position 40 did not increase the uptake of AF488-labeled ADAM7 E. coli. Pre-incubation with n-truncated Aβ(x–42) increased the uptake of E. coli most effectively, independent of macrophage polarization. In GM-CSF-derived macrophages, coating with Aβ(1–42), Aβ(2–42) and Aβ(3p–42) resulted in 55–70% increases in the uptake of E. coli (p < 0.01). Most interestingly, Aβx–42 induced phagocytosis even more effectively than a commercial opsonizing (OpsR) reagent intended to facilitate the phagocytosis of E. coli ( Fig. 4D). Aβ5–42 also induced

the phagocytosis of pHrhodo Green-labeled E. coli. However, this effect was weaker than that with Aβ1–42 ( Fig. 4F). Although a coating concentration of 1 mg/mL was chosen for the comparison of the Aβ peptide variants, a dose response analysis with Aβ1–42 revealed 500 μg/mL to be the least effective coating concentration when applied in our paradigm ( Supplementary Fig. 1). In the M-CSF-derived macrophages, similar effects were obvious (Fig. 4E). N-terminally truncated Aβ(3p–42) stimulated the uptake of E. coli most efficiently. The MFI values increased by 67% (p < 0.0001). This effect was only slightly stronger after coating the E. coli with the opsonizing reagent (OpsR). Aβ(1–42) was again more effective than Aβ(1–40), which did not influence phagocytic activity (p < 0.0001). The good correlation of fluorescent signal intensities between cultures with and without cytochalasin D (r = 0.78 for GM-CSF- and r = 0.74 for M-CSF-elicited macrophages, both p < 0.

Increasingly government departments funding these institutions tend to focus on the number of people coming through the doors to see exhibitions, often so called “blockbuster shows”, rather than the critical research being undertaken behind the scenes documenting biodiversity and how this is being affected by climate change as well as the increasing urbanisation and coastal development in Australia. Governments fail to recognise that much of this research only occurs in museums and without it we cannot answer questions; such as how distribution patterns are changing associated with

climate change and loss of habitats, critical in the development and management of marine parks, for example. Loss of this taxonomic expertise will lead to a loss of students as they can see 5-FU concentration no future in the discipline, and hence the loss of the next generation of taxonomists. People do not become taxonomists overnight, and it is critical that students are mentored by today’s practising taxonomists. As already mentioned, there is an amazing proliferation of coastal and offshore development, often associated with selleck the mining industry, here in Australia. For example along the Queensland coast there are proposals for eight port developments, in some cases new ports,

in others expansion of existing ports, to allow the export of minerals, primarily coal. All these developments include dredging and disposal of dredge Forskolin order spoils off shore and within the Great Barrier Reef World Heritage Area (Grech et al., 2013). Similar developments are occurring along the northwest Australian coast. Yet the composition of the benthic communities is poorly known in both these areas and increasingly it is difficult

to find the experts able to identify the fauna or obtain funds to support these experts. This often this leads to studies where the fauna is just identified to major groups which means that only limited information can be extracted from the data and which certainly cannot be compared with other areas or allow time series analyses. In some cases the material is deposited in the relevant state museum but, increasingly, they are limited in their ability to incorporate this material into collections and make it available for research. Australian institutions continue to fund expensive offshore sampling programmes but fail to allocate funds to actually identify the material collected (Kenchington and Hutchings, 2012, and references therein) and with it support the remaining taxonomists. Often these taxonomists, who have spent a lifetime studying their groups, can provide useful information on the ecology and habitat requirements of the fauna which can add value to the data being analysed. Increasingly they are using molecular data to complement the morphological data, which may reveal cryptic species as well as contributing to phylogenetic studies.

Importantly, the likely benefits of even limited visual restoration to a blind individual are often under appreciated by sighted individuals (Lane et al., 2012). Even rudimentary prosthetic vision in the setting of profound blindness may have significant positive psychological and functional ramifications for a blind individual, contributing to reduced feelings of isolation and depression (Dagnelie, 2008). Only a

few reproducible phosphenes may be ERK inhibitor clinical trial required to improve an individual׳s quality of life. For example, a recipient of the Dobelle implant was able to navigate independently and read letters on a Snellen chart with only 21 phosphenes at his disposal (Dobelle, 2000). In the most simple

of demonstrations, the reported elation felt by blind volunteers stimulated with only 4 occipital electrodes, in addition to their ability to independently locate a light source (Button and Putnam, 1962), suggests that questions of what constitutes “acceptable” performance by both recipients and treating physicians alike, needs to be carefully balanced. Progression to functional testing of a cortical implant is predicated on an uneventful implantation procedure and postoperative recovery. As discussed in Section 6.1.3, optimal surgical outcomes will depend partly on careful selection of implant recipients, for whom good general health will likely be a pre-requisite. Beyond this, there is a paucity of data on which to base firm statements about the risk of postoperative complications find more in current-generation cortical visual prosthesis recipients per se, however inferences can be made by drawing from older studies, the general (-)-p-Bromotetramisole Oxalate neurosurgical literature and recent reports on neuroprostheses implanted for other CNS disorders. The works of Brindley and Dobelle provide historical insights into the risks of cortical implant surgery,

although miniaturization of implant hardware, and improvements in operative technique and infection prophylaxis probably render these of little contemporary relevance. Nonetheless, recipients of implants from both groups reportedly suffered implant-related infections (Naumann, 2012 and Rushton et al., 1989). More recent large-series reports describe infection rates of 3.1% following the implantation of deep brain stimulators (DBS) (Fenoy and Simpson, 2014), 3.5% for hydrocephalus shunts (Parker et al., 2014) and 2.3% for subdural recording electrodes (Arya et al., 2013). While these figures are more informative, several factors suggest that these studies may overestimate the likely risk for future visual cortex implant recipients. Firstly, shunt candidates often present with comorbidities that increase their infection risk, while subdural recording electrodes incorporate externalized wires that provide a pathway for the intracranial migration of bacteria.

1% of total samples tested), of which there were 41 discrepant κ FLC results and 20 discrepant λ FLC results. Further investigations on these discrepant samples revealed that elevated levels of FLC, or an Natural Product Library elevated FLC ratio, on the Freelite™ assay was not supported by the mAb assay or serum IFE, and may have reflected cross-reactivity on the Freelite™ assay with whole immunoglobulin paraprotein or hindrance from the Freelite ‘gaps’ (see Fig. 6); for detailed assessment, see supplementary results. Results from the mAb assay were supported by serum IFE, as well as investigations on matched urine and analysis of patient history, where available. In summary, results indicated that all serum samples with abnormal FLC levels, or an abnormal

κ:λ ratio, were detected by the mAb assay from 1000 consecutive serum samples. Further investigations

revealed that both anti-κ FLC mAbs (BUCIS 01 and BUCIS 04) were diagnostically similar, and either could be used to indicate a sample containing an abnormal κ FLC level. Similarly, both anti-λ FLC mAbs (BUCIS 03 and BUCIS 09) were diagnostically similar, and either could be used to indicate a sample containing an abnormal λ FLC level. Results from 13,090 urine samples analysed routinely by the CIS on the mAb assay and on urine IFE were compared to assess the specificity and sensitivity of the mAbs at detecting FLC in urine. Urine IFE was conducted using ABT-263 cell line antisera against κ and λ LCs that did not distinguish between free and bound LC. Flucloronide Of the 13,090 urines, 12,242 samples were from patients who had a known serum paraprotein, 641 samples had no paraprotein present, and 207 had an unknown admission diagnosis. After initial comparisons between the mAb assay and IFE, 199 discrepancies were identified (1.52% of all samples tested). 143 of these samples had polyclonal LC by IFE but < 10 mg/L of the relevant FLC on the mAb assay. The other 56 samples had monoclonal LC present in the urine, but

< 10 mg/L of the relevant FLC on the mAb assay. These samples were re-tested on the mAb assay to exclude the possibility of user error, and all samples were re-analysed by full IFE analysis to distinguish between FLC and LC bound to whole immunoglobulin. Results from this process revealed that all samples with FLC detected by IFE were also detected by the mAb assay. Complementary analyses of matched serums and patient history also supported these findings. In summary, the mAbs detected FLC in all 2995 urine samples containing monoclonal κ FLC and all 1180 urine samples containing monoclonal λ FLC, as detected by IFE specific for FLC. Assay imprecision, or CV%, was measured in pools of serum samples with low, medium and high κ or λ FLC levels. For κ FLC, at 8.00 mg/L, 16.85 mg/L, and 238.94 mg/L, the intra-assay CV% was 4.46%, 4.69%, and 4.85%, respectively; and the inter-assay CV% was 6.45%, 6.50%, and 5.31%, respectively. For λ FLC, at 7.27 mg/L, 10.38 mg/L, and 91.13 mg/L, the intra-assay CV% was 5.69%, 4.86%, and 2.