, 1996, Namkoong, 2002, McKinnel, 2002, Bariteau, 2003 and Aravan

, 1996, Namkoong, 2002, McKinnel, 2002, Bariteau, 2003 and Aravanopoulos, 2011) and much scientific attention has been paid to evolutionary and adaptive processes (e.g. Eriksson et al., 1993; Namkoong et al., 2002; Le Corre and Kremer, 2003 and Le Corre and Kremer, 2012) as a basis. However, a general application and scaling-up of the verifiers

proposed by Namkoong Venetoclax solubility dmso et al. (2002) have not yet been feasible due to the difficulties summarized above. Any relevant set of indicators for trends in genetic diversity must include components at different scales (local/landscape/national/regional/global), involving the amount of diversity and how it is distributed in space. There is a need to identify genetically appropriate indicators and, at the same time, not to inflate the already large number of indicators that exist at global and regional scales. The State–Pressure–Benefit–Response (S–P–B–R) loop developed by UNEP/CBD/AHTEG, 2011a and UNEP/CBD/AHTEG,

2011b and Sparks et al. (2011) provides a well-considered and appropriate framework to ensure that the suggested set of indicators meet the requirements of being scientifically sound, LDN-193189 mouse realistic, and policy relevant; and the framework has been adopted for implementation by BIP, 2013. The identification of indicators of tree genetic diversity should therefore preferably take place within such a framework and result in a set of S–P–B–R indicators. In Table 5 we list what we consider to be relevant operational indicators

and their type (state, pressure, benefit, response) at different geographic levels (global, regional/national and local) under the headline indicator trends in genetic diversity of tree species. Our table is not necessarily exhaustive, but proposes a fairly complete set of indicators Thalidomide and has been made in congruence with Table 2. However, no separate pressure indicators are identified. Pressure indicators of genetic diversity are intrinsically linked with state indicators and the identification of the impact of any kind of pressure will have to rely on the knowledge of the state. Response indicators are referred to as response–benefit, because the rationale for a response is typically based on benefit. In Table 5 we subdivide the headline indicator trends in genetic diversity of tree species into seven operational indicators. These are appraised based on 21 verifiable indicators using a total of 34 verifiers. Genetic diversity indicators that are proposed in order to assess the adaptive potential of forest tree species from the global to the local level present different characteristics, such as indicator classification (state, pressure, benefit, response), reference level (global, regional, national, local), type of work needed (field, lab, web-based search, etc.), feasibility and type of expertise (direct measurement, or based on experimental analysis), level of informativeness, and cost.

This system

integrates routine laboratory steps by perfor

This system

integrates routine laboratory steps by performing cell lysis, DNA isolation, STR amplification, electrophoretic separation, fluorescent detection, and data analysis to generate DNA profiles in under two hours. Previously, PowerPlex® 16 HS chemistry (Promega Corp., Madison, WI), a find more 16 marker assay, was validated on the RapidHIT System [3] and [4]. However, the Federal Bureau of Investigation (FBI), European Network of Forensic Science Institute (ENFSI) and European DNA Profiling Group (EDNAP) have all agreed to the addition of STR loci to the European Standard Set (ESS) and to the core CODIS loci to increase cross-border data sharing, increase discrimination power, and reduce adventitious matches [5], [6], [7] and [8]. Furthermore, the Prüm treaty [9] and [10] was enacted into European 3-Methyladenine in vivo Union legislation which requires member states to submit the five additional loci that are part of the new expanded 12 ESS [11]. This led manufacturers to develop and commercialize products that include all the required and/or recommended loci as requested by ENFSI, EDNAP and the core CODIS Loci Working group [12] and [13]. The GlobalFiler Express PCR Amplification Kit from ThermoFisher Scientific (Waltham, MA),

an NDIS approved chemistry, contains all the required and recommended loci [6] and [8]. The kit contains 21 autosomal STR loci (D3S1358, vWA, D16S539, CSF1PO, TPOX,

D8S1179, D21S11, D18S51, D2S441, D19S433, TH01, FGA, D22S1045, D5S818, D13S317, D7S820, SE33, D10S1248, D1S1656, D12S391, D2S1338) and 3 sex determining markers (Amelogenin, DYS391, Y-indel). Use of fluorescent six-dye technology enables the amplicon sizes to be less than 400 bp (except SE33, 442 bp). To support the community worldwide, increase level of discrimination, facilitate international DNA profile comparison, and reduce risk of adventitious matches, the GlobalFiler Express assay was integrated and validated on the RapidHIT System. The developmental validation experiments presented here were performed according to the quality assurance standards issued by ioxilan the Director of the FBI [14] and the revised guidelines published by the Scientific Working Group on DNA Analysis (SWGDAM) [15]. The results confirm the reliability of the NDIS-approved GlobalFiler® Express assay on the RapidHIT System for generating DNA profiles from reference samples. The profiles can be uploaded after forensic expert review to national and international databases once laboratories have completed their internal validation. Buccal swab samples were collected from consenting donors using 3 inch cotton-tipped swabs from Puritan Medical Products Company (Guilford, ME). Each donor was instructed to swipe the inside of the cheek ten times and contribute swabs daily to generate aged swabs for stability studies.

Using stepwise analysis only SNiP was retained as an independent

Using stepwise analysis only SNiP was retained as an independent correlate (r2 0.72, p = 0.0009) ( Table 3 and Fig. 2). The acute effect of NIV was studied in six patients who were already established users of nocturnal home NIV. One subject declined to have further stimulations

after the end of the period on ventilation so post-NIV data was only available in 5 subjects. NIV significantly reduced the work of breathing with a decrease in diaphragm pressure time product from 269 ± 45 cm H2O s−1 min−1 to 34 ± 13 cm H2O s−1 min−1 (p = 0.003). End expiratory pressures at which stimulations were delivered did not differ significantly in the three periods ( Table 4). NIV was associated with a significant decrease in normalized selleck amplitude of the diaphragm MEPTS (p = 0.02), but it did not alter motor threshold or MEP latency ( Table 5). NIV did not alter the excitability of intracortical inhibitory or facilitatory pathways assessed using paired stimulation. NIV was also not associated with significant changes in the amplitude of rectus abdominis MEPTS. The main findings of this study were firstly that the

excitability of corticospinal pathways to the respiratory muscles of patients with COPD who have been established on home NIV did not differ from those who do not require NIV. Secondly, the excitability of intracortical facilitatory and inhibitory circuits assessed using paired stimulation LBH589 molecular weight was strongly correlated with indices of disease severity, namely inspiratory muscle

strength and hypercapnia respectively. Finally, although the acute use of NIV in chronic users did reduce the excitability of the corticospinal pathway to the diaphragm it did not, in contrast to our findings in healthy subjects (Sharshar et al., 2004b), alter the excitability of intracortical inhibitory or facilitatory circuits. By studying an expanded cohort of patients we have been able to establish more clearly the relationship between cortical responses and pathophysiological parameters in patients with COPD. Specifically, next decreased intracortical facilitation was most closely related to reduced inspiratory muscle strength while greater intracortical inhibition was associated with higher levels of PaCO2. This suggests that excitatory circuits are influenced predominantly by neuromechanical feedback and inhibitory ones by chemical inputs. It is interesting in this context to note that isocapnic non-invasive ventilation in healthy subjects had a greater effect on intracortical facilitation than on inhibition supporting a role for neuromechanical feedback as the principle driver for this adaptation (Sharshar et al., 2004b).

Using temperature changes measured at the optical sensor site, it

Using temperature changes measured at the optical sensor site, it had been demonstrated previously that the switch-over of the two blood streams occurred within 50 ms at the sensor surface ( Chen

et al., 2012b), which is certainly fast enough to indicate that the mechanical switch-over of the two blood streams did not affect our results in any way. Any diminution in recorded ΔPO2 with increasing Akt inhibitor simulated RR would therefore be due to sensor performance, rather than test rig limitation. Studies investigating cyclical atelectasis in the Acute Respiratory Distress Syndrome (ARDS), where PO2PO2 varies widely within breaths, require very fast response intravascular oxygen sensors, which motivated the present study. PO2PO2 and SaO2 oscillations in arterial blood have been studied for several decades; an overview of the most important findings in this field is presented and discussed in the following paragraph. Cyclic variations in blood oxygenation within the respiratory cycle were reported in 1961 in

an open chest experimental animal model (Bergman, 1961a and Bergman, 1961b). In this model, femoral arterial blood was withdrawn from a small catheter through a fast response external oximetry cuvette at a constant rate by a motor-driven syringe, and variations in oxyhaemoglobin saturation (SaO2) were recorded in real time. SaO2 was used as a surrogate for arterial oxygen tension (PO2)(PO2), and rapid cyclic variations of up to 20% in SaO2 (ΔSaO2) were recorded. Using these saturation figures and a standard dissociation curve,

Etoposide cell line these values translate to a PO2PO2 oscillation amplitude of 15 mmHg at a mean PO2PO2 of 36 mmHg (Whiteley et al., 2003). Despite the evidence suggesting that the cause of the observed fluctuations in arterial saturation might be due to variations in pulmonary shunt, it was concluded that these large variations in PaO2/SaO2PaO2/SaO2 might be due to cyclical changes in Linifanib (ABT-869) alveolar oxygen tension. Much later on, in a computer model, it was shown that large changes in PaO2PaO2 could only be generated by large intra-breath changes in pulmonary shunt caused, most likely, by cyclical atelectasis (Whiteley et al., 2003). Oscillations in carotid artery PO2PO2, which had the same period as respiration, were demonstrated in the cat, and in the newborn lamb in the first hours after birth (Purves, 1965 and Purves, 1966). Although recognising that changes in venous admixture occur during the respiratory cycle and that there was a significant degree of venous admixture during the experiments, the conclusion was drawn that the cyclical oscillations in carotid PO2 (ΔPaO2) in these animal studies were due to changes in alveolar PO2PO2. Thirteen years later, in an experimental cat model, it was shown that the amplitude of ΔPaO2 increased with increasing tidal volume, with increasing mean PaO2PaO2, and decreasing ventilator frequency (Folgering et al., 1978). Some of these studies were conducted at a mean PaO2PaO2 of 150 mmHg, i.e.

One such model suggests that channel size

One such model suggests that channel size Selleck CH5424802 and incision depth influence post-incision processes, with controls on widening from accumulation of material at the base of eroding banks acting as a limit on lateral channel migration (Beechie et al., 2008). In Robinson Creek, the incision and bank erosion occurring is consistent

with the initial deepening stages of the cycle in relatively narrow portions and subsequent stages in the relatively wider portions of the channel, where erosion control measures have not been implemented. However, if incision continues, currently wider areas with bars and potential for vegetation establishment may destabilize as the incision–erosion cycle continues. Evidence for this scenario is evident from Robinson Creek field surveys that show upstream incision even in Ku-0059436 relatively wide zones over a three year period. In such an actively incising channel,

dynamic changes and complex responses may create spatial variability in geomorphic responses and complexity in channel recovery as multiple knickzones migrate upstream into reaches where cycles of local incision and aggradation have already occurred. Erosion control measures that limit widening may alter future channel adjustments. Both positive and negative feedback loops operate in coupled human–landscapes (Chin et al., 2013) such as incised alluvial systems. A positive feedback is an initial change to the system that causes more change in the same direction. In contrast, a negative feedback is a modification that limits the initial change. With respect to channel incision processes, positive feedback may occur because as a channel incises, high magnitude flood flows become confined (instead of spreading onto former floodplains) causing flow depth, transport capacity,

and shear stress to increase and further erode the bed of the channel. Negative feedback may occur when bank height increases L-NAME HCl beyond a critical threshold, causing bank erosion and channel widening to occur, and limit flow depth and shear stress such that aggradation occurs. Considering coupled human–landscape feedbacks is critical in understanding how human activities contribute to positive feedback that may exacerbate incision versus negative feedback that may minimize incision and promote resilience over various time scales. For example, human responses such as constructing bank erosion control structures that address a symptom of incision—namely bank erosion—but not the cause (Spink et al., 2008), may intensify incision that can undercut the structure itself, and thus are not likely to be effective over the long term. Similar conclusions have been noted in other dynamic rivers (Miller and Kochel, 2010). Another problem is lack of attention, as structures intended to limit erosion are rarely monitored (Shields, 2009).

g , Oosterberg and Bogdan, 2000) In the Mississippi delta, nutri

g., Oosterberg and Bogdan, 2000). In the Mississippi delta, nutrient excess delivered via diversions to freshwater marshes have been blamed for their apparent

vulnerability to hurricanes (e.g., Kearney BIBF 1120 et al., 2011). For successful schemes of channelization, a comprehensive adaptive management plan for water, sediment and nutrients would be needed to protect the ecological characteristics in addition of maintaining the physical appearance of the delta plain. If increases in the sediment trapped on the fluvial delta plain may aid to balance the effects of sea level rise, a similar approach for the external, marine delta plain would completely change the landscape of that region. Composed of fossilized sandy beach and barrier ridges that receive little new sand once encased on the delta plain, the marine delta would be transformed by channelization into an environment akin to the fluvial delta with lakes and marshes. In the absence of other solutions, such as hard protection dikes and short of abandonment, channelization could potentially raise the ground locally on these strandplains and barrier plains. Instead, with no new sediment input, the marine delta would

in time result in its partial drowning; sand ridge sets of higher relief will transform into barrier systems and thus, with water on both sides, become dynamic again rather than being fossilized on the delta plain. This will provide in turn some protection to the remaining Crizotinib cell line mainland delta coast because Idoxuridine dynamic barrier systems with sand sources nearby (i.e., the delta lobes themselves) are

free to adjust to dynamic sea level and wave conditions by overwash, foredune construction, and roll over. However, it is clear that the most vulnerable part of the Danube delta is the deltaic coastal fringe where most of sediment deficit is felt. In order to tackle erosion along the delta coast, a series of large scale diversion solutions have been proposed since the early 20th century (see e.g., compilation by Petrescu, 1957). However, the entire Danube currently debouches only about half the amount of sediment that Chilia distributary used to deliver annually to construct its lobe in pre-damming era! Our study suggests instead that small but dense diversions similar to the natural Chilia secondary channels, thus another type of channelization mimicking natural processes, may minimize erosion in the nearshore. Hard structures such as breakwaters and groins that curtail offshore and alongshore sediment loss may also provide some temporary, if imperfect, relief. However, waves along the coast of Danube delta are a very efficient and relentless sediment redistribution machine, and in the long run erosion will remain a problem. Erosion of moribund lobes, such as it appears to be the case with the current St. George lobe, can provide enough sand if it is abandoned. Reworking of the St.

The authors declare no conflicts of interest The authors would l

The authors declare no conflicts of interest. The authors would like to thank all Brazilian pediatric intensivists that have been strenuously devoted to the study and care of critically-ill children, especially those affected by acute respiratory failure. “
“Acute viral bronchiolitis (AVB) caused by respiratory syncytial virus (RSV) is the primary infection of the lower airways

in children under 2 years of age worldwide, and it is the main cause of hospitalization in this age group in developed countries.1 Although all children are infected with RSV by the age of three, most infections are mild and have no sequelae. The mechanisms involved with the severity of AVB caused by RSV are not yet fully understood. Why does RSV infection present Ipatasertib cost such variable evolution in different patients? Why does one child with RSV remain asymptomatic and another child dies? When assessing the severity of AVB caused by RSV, which factors are more often associated: genetic and/or epidemiological/environmental factors? These questions have intrigued researchers and remain without definitive answers. There are 3,000 to 4,000 deaths annually

in the United States due to AVB caused by RSV.2 The prevalence of hospitalization due to RSV in the United States is 48.9 per 1,000 in children younger than 3 months, 26 per 1,000 in those younger than 1 year, Epigenetics Compound Library and 1.8 per 1,000 in children aged 1 to 5 years, with 132,000 to 172,000 hospitalizations/year due to

RSV in children under 5 years.3 In the United States, there are, on average, 22.8 visits to the emergency room caused by RSV per 1,000 infants; 29% of whom are Oxymatrine hospitalized. That represents an annual spending of 50.5 million dollars on emergency room visits and 650 million dollars on hospitalizations.4 In other regions, the rate of hospitalization per 1,000 infants with RSV varies from 8.7 in Australia5 to 60 in Japan.6 In Australia, the incidence of RSV is from 110.0 to 226.5 per 1,000 infants, and the annual cost is estimated at $ 50 million dollars, which is more significant than the costs of Influenza and Rotavirus infections. 5 In Europe, RSV is responsible for 45% of hospitalizations for lower respiratory infection in children younger than 2 years. 6 In Brazil, a study of 5,304 children younger than 1 year showed that 113 (2.1%) were hospitalized due to AVB.7 Among the children hospitalized for RSV, 2.7% were admitted to the intensive care unit (ICU), 1.5% required assisted ventilation, and 0.2% died.8 Infection by RSV has variable severity with clinical manifestations from mild symptoms in the upper respiratory tract to bronchiolitis and pneumonia, and may develop into the severe form, requiring ICU admission and mechanical ventilation, and at times leading to death. To date, the treatment of AVB by RSV is supportive. It has been demonstrated that, in the United States, of 1.

Indeed, there was no marked exacerbation of cough or sputum in al

Indeed, there was no marked exacerbation of cough or sputum in all four cases. In addition, sequential PFT (available in cases 1 and 4), and HRCT (available in cases 1, 3 and 4), and chest X-ray of the four cases did not show any see more marked worsening, thus suggesting

that parenchymal lung disease was not the primary cause of the advancing symptoms/signs. Third, respiratory infection was not indicated by symptoms/signs, blood tests or imaging studies in the four cases. We thus used PAH-specific vasodilators and had favorable outcomes in patient symptoms/signs and pulmonary hemodynamics. The degree of hemodynamic improvement was marked in the four cases. Indeed, MPAP and PVR reduced by 19 ± 15% and 45 ± 8%, respectively. In addition, CI and CMR-derived RVEF improved by 28 ± 9% and 51 ± 10%, respectively. These clinical courses suggested that PAH-specific vasodilators improved pulmonary hemodynamics along with right heart function, which subsequently appeared to improve patient symptoms such as exertional dyspnea and peripheral edema. The underlying pathophysiology of the vascular response to PAH-specific treatment was not elucidated in this observational study. However, it is of clinical interest how the vasodilators could have improved pulmonary hemodynamics. First, it can be speculated that vascular lesions appeared to have more or less reversible components. Indeed,

PAH-specific vasodilators would have been less efficacious if vessel loss or ablation Everolimus in the damaged lung parenchyma was the primary mechanism of increased PVR. Second, it can also be assumed that PAH-specific treatment was efficacious because the vasculopathy was in its early phase. In fact, pulmonary vasculopathy why would respond poorly to any vasodilator if the vascular lesion is progressed to heavily fibrotic or hyalinized phase.12 Finally, the target proteins

of vasodilators, particularly of sildenafil, might have been expressed in the diseased vessels.13 Deterioration of hypoxia is the major concern when using vasodilators in hypoxic PH patients with lung disease. Theoretically, vasodilators can dilate vessels in the poorly ventilated lung fields, leading to further deterioration of ventilation/perfusion mismatch and hypoxia.3 In this regard, PDE-5 inhibitors enhance the nitric oxide pathway in the well-ventilated lung areas,14 minimizing the worsening of perfusion/ventilation mismatch when compared with other PAH-specific agents. In addition, sildenafil is reported to better improve arterial oxygenation as compared with other PDE-5 inhibitors.15 We therefore used sildenafil as the first line agent in all four cases, whereas beraprost (case 1) and bosentan (case 3) were added for the purpose of further decreases in MPAP. Importantly, the change in pulmonary oxygenation varied among the cases. In fact, pulmonary oxygenation improved in case 2, deteriorated in case 1, and did not change markedly in cases 3 and 4.

However, all eligible children with CKD from the Nephrology Pedia

However, all eligible children with CKD from the Nephrology Pediatric Center of IMIP were selleckchem included. It is noteworthy, however, that this study is the in Brazil to evaluate QoL through PedsQLTM in children and adolescents with CKD. Finally, it is concluded

that the study sample showed a significant reduction in QoL, functional capacity, and physical activity in children and adolescents with CKD. Positive associations were also found between functional capacity, pulmonary function, and QoL. However, no correlation was found between respiratory muscle strength and functional capacity, suggesting the need for new studies to better elucidate this finding. The authors declare no conflicts of interest. “
“Neoplasms have become important in the epidemiological scenario, as they represent one of the leading causes of death of in the 1 to 19 years age group in Brazil, second only to external causes, in 2010, despite the rarity of

childhood cancer when compared to adults.1 In children, tumors are usually categorized into 12 specialty groups, according to the Third Edition of the International Classification of Childhood Cancer (ICCC). Leukemias constitute Group I, which comprises the subgroups: acute lymphocytic leukemia; acute myeloid leukemia; and chronic myeloproliferative disorders, including chronic myeloid leukemia and unspecific or combined types. Chronic lymphocytic leukemia is extremely rare in children and was therefore included in the subgroup selleck kinase inhibitor of acute lymphocytic leukemia, the predominant type of leukemia in children, without affecting the incidence rates in this subgroup.2 Acute lymphoblastic leukemia represents the majority of cases among the diagnostic groups of lymphocytic leukemias (99%), so that the diagnosis

group of ICCC becomes synonymous with acute lymphocytic leukemia. Likewise, acute nonlymphocytic leukemias are referred to as acute myeloid leukemia (representing 69%) and chronic myeloid leukemia, with 6-7% representation in its group.3 Leukemias have the highest incidence rates among childhood tumors in Brazil and worldwide. In a study conducted Methane monooxygenase in the United States, of all neoplasms, leukemias showed a frequency of 26.3%. In Brazil, they were also the most prevalent in 20 population-based cancer registries, with a median percentage of 29%, with the highest incidence occurring in the age group 1-4 years, with a median percentage of 31.6%. Leukemia was the leading cause of death among cancers in children and adolescents (1-18 years) from 2001 to 2005 in Brazil, with 1,897 deaths in females and 2,539 deaths in males.4 The present study aimed to assess the trend of mortality from childhood leukemia in Brazil from 1980 to 2010. This is an ecological, retrospective, time-series study based on secondary data.

3D) was greater than samples with equimolar RGES ( Fig 3E) The

3D) was greater than samples with equimolar RGES ( Fig. 3E). The decline in aggregation frequency and concomitantly more uniform distribution of the hemocytes treated with RGDS (5 mM; Fig. 3D) compared to the

samples with RGES (5 mM; Fig. 3E) and the buffer control (CTX only; Fig. 3C) likely represents inhibition of integrin-mediated in vitro microaggregate formation. The number of circulating hemocytes may vary, counts declining or increasing (a form of hemocyte mobilization) as the hemocytes adhere to or lose affinity for surrounding tissues [77] and [32]. Unlike the in vitro results ( Fig. 1), incubation duration for acute CTX (0, 6, 60 nM) effects on circulating hemocytes in vivo was greatest at 20 min ( Fig. 4). This discrepancy with the in vitro results ( Fig. 1) was expected since reaction times are shorter in vivo than in vitro due to possible differences caused by plasma factors and their concentrations Cilengitide [28]; 20 min was chosen for subsequent in vivo experiments. The influence of CTX and its moieties on circulating hemocytes in vivo was determined with increasing concentrations CTX and CTA (ranging from 1.2 to 120 nM), and CTB (ranging from 0 to 600 nM). Levels of circulating hemocytes peaked at 6 nM

CTX, followed by a drop at 12 nM and rose to a plateau level by 60 nM, the latter hemocyte levels being similar to those at 6 nM CTX ( Fig. 5A). CTB caused an initial decrease in circulating hemocytes plateauing Selleckchem FRAX597 from 6 nM to 150 nM, followed thereafter to a maximum increase that plateaued starting at 300 nM, the latter two effects being similar to the corresponding concentrations of CTX ( Fig. 5A). Molar equivalents of CTA had no statistically significant effect (p>0.05) on circulating hemocyte counts ( Fig. 5A). The effect of CTX in vivo on circulating hemocytes was mirror image the pattern seen in vitro ( Fig. 2A), albeit the reaction taking place

at higher levels of CTX in vivo suggesting a tissue dilution effect in vivo in which other tissues might interact with CTX lowering the amount of holotoxin available for reaction with the hemocytes. To determine if CTX or its moieties affected the adhesiveness of the hemocytes remaining in circulation larvae were injected with these molecules and the hemocyte counts determined. Concentrations of 0, 6, second 12, and 60 nM CTX (corresponding to 0, 30, 60, and 300 nM CTB) were chosen since 6 and 60 nM represent the most pronounced effects of CTX in vivo and 12 nM CTX represents a lower intermediate effect ( Fig. 5A). The total number of adhering hemocytes decreased in 6 nM CTX-injected insects compared with PBS-injected insects, whereas adhesion levels increased from insects injected with 12 and 60 nM CTX ( Fig. 5B). Levels of attached granular cells and plasmatocytes followed the same pattern in insects injected with 0, 6, and 12 nM CTX, levels of adhering granular cells between 6 and 60 nM CTX increased faster than plasmatocytes ( Fig. 5B).