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DockerChannel is a software suite for investigating possible information leakages of Docker containers. Its main scope is to support developers to fully assess the impact of the “loose” isolation of statistics provided by the container engine. It can also help researchers to investigate new attacks leveraging the orchestration of malicious containers. DockerChannel is built around an extensible Python class abstracting the creation of the covert communication mechanism and it can be used both in a general-purpose manner or “bundled” within pre-existing containers, e.g., to check leakages in real cloud-native deployments.

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Currently, there are no clear guidelines for the implementation of rehabilitative exercise training (RET) in burned individuals. Therefore, we quantified the training logs for exercise intensity, frequency, and duration of 6 weeks of this program to develop a basic framework for outpatient RET in patients recovering from severe burns. Thirty-three children (11 female, [mean ± SD] 12 ± 3 years, 145 ± 18 cm, 40 ± 11 kg, 49 ± 31 BMI percentile) with severe burns (49 ± 15% total body surface area burned, with 35 ± 22% third-degree burns) completed our 6-week resistance and aerobic exercise training program. Cardiorespiratory fitness (peak VO2), strength, power, and lean body mass (LBM) were measured before and after RET. Outcome measures were analyzed as a relative percentage of values in age- and sex-matched nonburned children (11 female, 12 ± 3 years, 154 ± 20 cm, 49 ± 22 kg, 56 ± 25 BMI percentile). At discharge, burned children had lower LBM (77% of age-sex–matched nonburn values), peak torque (53%), power (62%), and cardiorespiratory fitness (56%). After 6 weeks of training, LBM increased by 5% (82% of nonburn values), peak torque by 18% (71%), power by 20% (81%), and cardiorespiratory fitness by 18% (74%; P< .0001 for all). Quantification of data in exercise training logs suggested that physical capacity can be improved by aerobic exercise training performed at five metabolic equivalents (>70% of peak VO2) at least 3 days/week and 150 minutes/week and by resistance training performed at volume loads (reps × sets × weight) of 131 kg for the upper body and 275 kg for the lower body for 2 days/week. We present for the first time the quantification of our RET and provide clear exercise prescription guidelines specific to children with severe burn injury.

Minimizing the deconditioning of burn injury through early rehabilitation programs (RP) in the intensive care unit (ICU) is of importance for improving the recovery time. The aim of this study was to assess current standard of care (SOC) for early ICU exercise programs in major burn centers. We designed a survey investigating exercise RP on the ICU for burn patients with >30% total burned surface area. The survey was composed of 23 questions and submitted electronically via SurveyMonkey®to six major (pediatric and adult) burn centers in Texas and California. All centers responded and reported exercise as part of their RP on the ICU. The characteristics of exercises implemented were not uniform. All centers reported to perform resistive and aerobic exercises but only 83% reported isotonic and isometric exercises. Determination of intensity of exercise varied with 50% of centers using patient tolerance and 17% using vital signs. Frequency of isotonic, isometric, aerobic, and resistive exercise was reported as daily by 80%, 80%, 83%, and 50% of centers, respectively. Duration for all types of exercises was extremely variable. Mobilization was used as a form of exercise by 100% of burn centers. Our results demonstrate that although early RP seem to be integral during burn survivor’s ICU stay, no SOC exists. Moreover, early RP are inconsistently administered and large variations exist in frequency, intensity, duration, and type of exercise. Thus, future prospective studies investigating the various components of exercise interventions are needed to establish a SOC and determine how and if early exercise benefits the burn survivor.

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Modern treatment of partial-thickness burns follows the paradigm of less frequent dressing changes to allow for undisturbed reepithelialization of the burn wound. We compared Mepilex Ag (M), a silver-impregnated foam dressing, and Suprathel (S), a DL-lactid acid polymer, in the outpatient treatment of partial-thickness burns in pediatric and adult patients. Patients were enrolled in a randomized, controlled, prospective clinical trial. We monitored time to reepithelialization, wound pain, discomfort during dressing changes, and treatment cost. Objective scar characteristics (elasticity, transepidermal water loss, hydration, and pigmentation) and subjective assessments (Patient and Observer Scar Assessment Scale) were measured at 1 month post burn. Data are presented as mean ± SEM, and significance was accepted at P< 0.05. Sixty-two patients (S n = 32; M n = 30) were enrolled; age, sex, and burn size were comparable between the groups. Time to reepithelialization was not different between the groups (12 days; P= 0.75). Pain ratings were significantly reduced during the first 5 days after burn in the Suprathel group in all patients (P= 0.03) and a pediatric subgroup (P< 0.001). Viscolelasticity of burned skin was elevated compared with unburned skin in the Mepilex Ag group at 1 month post burn. Patients treated with Suprathel reported better overall scar quality (S: 2; M: 4.5; P< 0.001). The cost of treatment per square centimeter for Mepilex Ag was considerably lower than that of Suprathel. Both dressings are feasible and efficacious for the outpatient treatment of minor and selected moderate partial-thickness burns. Reduced pain, especially in a pediatric patient population, may be advantageous, despite increased treatment cost.

Since the inception of the P50 Research Center in Injury and Peri-operative Sciences (RCIPS) funding mechanism, the National Institute of General Medical Sciences has supported a team approach to science. Many advances in critical care, particularly burns, have been driven by RCIPS teams. In fact, burns that were fatal in the early 1970s, prior to the inception of the P50 RCIPS program, are now routinely survived as a result of the P50-funded research. The advances in clinical care that led to the reduction in postburn death were made by optimizing resuscitation, incorporating early excision and grafting, bolstering acute care including support for inhalation injury, modulating the hypermetabolic response, augmenting the immune response, incorporating aerobic exercise, and developing antiscarring strategies. The work of the Burn RCIPS programs advanced our understanding of the pathophysiologic response to burn injury. As a result, the effects of a large burn on all organ systems have been studied, leading to the discovery of persistent dysfunction, elucidation of the underlying molecular mechanisms, and identification of potential therapeutic targets. Survival and subsequent patient satisfaction with quality of life have increased. In this review article, we describe the contributions of the Galveston P50 RCIPS that have changed postburn care and have considerably reduced postburn mortality.

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Chromosome conformation capture methods have identified subchromosomal structures of higher-order chromatin interactions called topologically associated domains (TADs) that are separated from each other by boundary regions. By subdividing the genome into discrete regulatory units, TADs restrict the contacts that enhancers establish with their target genes. However, the mechanisms that underlie partitioning of the genome into TADs remain poorly understood. Here we show by chromosome conformation capture (capture Hi-C and 4C-seq methods) that genomic duplications in patient cells and genetically modified mice can result in the formation of new chromatin domains (neo-TADs) and that this process determines their molecular pathology. Duplications of non-coding DNA within the mouse Sox9 TAD (intra-TAD) that cause female to male sex reversal in humans, showed increased contact of the duplicated regions within the TAD, but no change in the overall TAD structure. In contrast, overlapping duplications that extended over the next boundary into the neighbouring TAD (inter-TAD), resulted in the formation of a new chromatin domain (neo-TAD) that was isolated from the rest of the genome. As a consequence of this insulation, inter-TAD duplications had no phenotypic effect. However, incorporation of the next flanking gene, Kcnj2, in the neo-TAD resulted in ectopic contacts of Kcnj2 with the duplicated part of the Sox9 regulatory region, consecutive misexpression of Kcnj2, and a limb malformation phenotype. Our findings provide evidence that TADs are genomic regulatory units with a high degree of internal stability that can be sculptured by structural genomic variations. This process is important for the interpretation of copy number variations, as these variations are routinely detected in diagnostic tests for genetic disease and cancer. This finding also has relevance in an evolutionary setting because copy-number differences are thought to have a crucial role in the evolution of genome complexity.

Growth hormone (GH) secreting adenoma represents a therapeutic challenge in childhood. Because of its rarity no treatment guidelines are available and pediatric management often results from recommendations issued for adults. We report a case of a 4-year-old girl with somatotropinoma successfully treated with only medical treatment. She presented with tall stature and history of growth acceleration. Imaging and laboratory confirmed the diagnosis of GH secreting macroadenoma. She started medical treatment with a somatostatin analogue and a dopamine agonist. During an 8-year follow-up period, a good clinical control of the disease and a shrinkage of the adenoma have been demonstrated. At the last observation she achieved normal near-adult height and pubertal development. According to our experience and limited literature evidences, first line treatment with somatostatin analogues can be attempted in patients with somatotropinoma. This approach seems to be able to control the clinical course of the disease, allowing to postpone transphenoidal surgery to adult age or to avoid it.

Background:No data are available about the risk of thyroid disturbance after exposure to low-dose radiation due to the use of cardiac catheterization in the first years of life. Aim:To determine the risk of functional and morphological thyroid abnormalities in a homogeneous cohort of patients who underwent diagnostic low-dose radiation for heart catheterization during the first 18 months of life. Subjects and methods:Fifty-five patients, submitted to cardiac catheterization during the first 18 months of life, underwent evaluation of the thyroid function and structure after a median period of 13 yr since the first radiation exposure. Sixty-eight unexposed controls matched for age and sex, underwent the same protocol. Twenty-two patients were then re-evaluated after a median period of 22 yr. Results:Thyroid function resulted normal in both patients and controls. The prevalence of small thyroid nodules and inhomogeneous structures in ultrasound study was not augmented in irradiated patients compared to controls. No thyroid tumors or reduced thyroid volume were observed. Conclusions:Neither functional nor morphological disorders of the thyroid gland were demonstrated after a period up to 24 yr in patients exposed to diagnostic ionizing radiation for cardiac catheterization during the first 18 months of life.

Denial of service (DoS) attacks evolved and consolidated as severe security threats to network servers, not only for internet service providers but also for governments. Earlier DoS attacks involved high-bandwidth flood -based approaches exploiting vulnerabilities of networking and transport protocol layers. Subsequently, distributed DoS attacks have been introduced amplifying not only the overall attack bandwidth but also the attack source, thus eluding simple counter measures based on source filtering. Current low bit-rate approaches, instead, exploit vulnerabilities of application layer protocols to accomplish DoS or DDoS attacks. Slow DoS attacks like, e.g., slowloris are particularly dangerous because they can bring down a well equipped server using small attacker’s bandwidth, hence they can effectively run on low performance hosts, such as routers, game consoles, or mobile phones. In this paper, we study slow DoS attacks, analysing in detail the current threats and presenting a proper definition and categorisation for such attacks. Hopefully, our work will provide a useful framework for the study of this field, for the analysis of network vulnerabilities, and for the proposal of innovative intrusion detection methodologies.

Background/objective: Although pharmacological GH stimulation tests are still considered the gold standard for GH deficiency (GHD) diagnosis, they are burdened by poor specificity. The majority of children diagnosed as having GHD show normal GH responses when re-tested at the end of growth, thus questioning the initial diagnosis. We evaluated the concordance between IGF-I levels and GH responses to provocative tests. Methods: We analyzed 105 GHRH plus arginine tests, 79 arginine tests, and 124 clonidine tests performed in 192 short children. IGF-I levels ≤2SD score (SDS) were considered suggestive for high likelihood of GHD. The percentage of positive and negative results for each test was determined and compared with IGF-I levels, clinical follow-up and response to therapy. Results: In children with IGF-I>-2SDS the arginine test showed a concordance rate of 6.9%, the clonidine test of 28.6%, and GHRH plus arginine test of 70%. In children with IGF-I≤2SDS the concordance was 96.1%, 85.7%, and 46.4%, respectively. The overall concordance was 66.7% for GHRH plus arginine, 42.7% for clonidine, and 27.8% for arginine tests. Conclusion: Our results suggest that GHRH plus arginine test provides the best concordance with the assessment of IGF-I levels thus suggesting that the combination of the two procedures may significantly reduce the need of a second provocative test.

To date, 43 patients have been described with mutations in or involving the CDKL5gene. The typical phenotype includes early‐onset, often intractable epileptic seizures and severe mental retardation with very limited progress in psychomotor development. Most patients also show impaired social interaction with avoidance of eye‐to‐eye contact, and some clinical features reminiscent of Rett syndrome (RTT), including stereotypic hand movements, lack of purposeful hand use, acquired microcephaly, and generalized hypotonia. We report on the case of a 5‐year‐old girl with a de novo CDKL5gene mutation who developed early puberty, which has not been described before. © 2009 Wiley‐Liss, Inc.

AbstractBackground: Autosomal-dominant isolated GH deficiency (IGHD) is a rare disorder that is commonly believed to be due to heterozygous mutations in the GH-1 gene (GH-1). These mutations cause the production of a protein that affects the release of the product of the normal allele. Rarely, heterozygous mutations in the gene encoding for HESX-1 gene (HESX-1) may cause autosomal-dominant IGHD, with penetrance that has been shown to be variable in both humans and mice. Subjects and Methods: We have sequenced the whole GH-1 in the index cases of 30 families with autosomal-dominant IGHD. In all the families other possible causes of GH deficiency and other pituitary hormones deficits were excluded. We here describe the clinical, biochemical and radiological picture of the families without GH-1 mutations. In these families, we also sequenced the HESX-1. Results: The index cases of the five families with autosomal-dominant IGHD had normal GH-1, including the intronic sequences. They had no HESX-1 mutations. Conclusion: This study shows that GH-1 mutations are absent in 5/30 (16.6%) of the families with autosomal-dominant IGHD and raises the possibility that mutations in other gene(s) may be involved in IGHD with this mode of transmission.Copyright © 2006 S. Karger AG, Basel

Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplatelet-mediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab′)2fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for γ-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through γ-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents. (Blood. 2004;104:2102-2106)

Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplatelet-mediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab′)2 fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for γ-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through γ-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents. (Blood. 2004;104:2102-2106)

Antigens encoded by MAGE genes and recognized by T cells are of interest for cancer immunotherapy because of their strict tumoral specificity and because they are shared by many tumors. Several MAGE-1 peptide that are recognized by CD8⁺ cytolytic T lymphocytes have been used in therapeutic vaccination trials. To obtain anti-tumor immune response, vaccines combining peptides recognized by CD8⁺ and peptides recognized by CD4⁺ T cells might be optimal. We focused therefore on the identification of MAGE peptides recognized by CD4⁺ T cells. We report here the identification of MAGE-1 epitope EYVIKVSARVRF, which is presented to CD4⁺ T lymphocytes by HLA-DR15. This HLA allele is present in 29 % of Asians and 17 % of Caucasians.

Patients with microdeletion of chromosome 22q11.2 (del22q11) were studied, in order to evaluate auxological parameters and to correlate growth patterns with the presence of main clinical characteristics of the syndrome.

Purpose: Patients with microdeletion of chromosome 22q11.2 (del22q11) were studied, in order to evaluate auxological parameters and to correlate growth patterns with the presence of main clinical characteristics of the syndrome.Methods: Between January 1995 and March 2000, auxological parameters (weight, height, head circumference, and bone age) of 73 patients with del22q11 were collected. Five subgroups of patients were distinguished: Group I (37 patients) included patients aged between 0.3 and 4 years, Group II (20 patients) included patients aged between 5 and 10 years, Group III (16 patients) included patients aged between 11 and 16.3 years. The presence or absence of some clinical features was correlated to growth patterns.Results: Weight: in Group I, 5 of 37 (13.5%) patients were below the 3rd percentile, 29 of 37 (78.3%) were below the mean percentile, none was overweight; in Group II, 13 of 20 (65%) patients were between the 10th and the 50th percentiles; in Group III, weight corresponded to the 97th percentile in 5 of 16 (31.2%) patients, and in 2/16 (12.5%) adolescents, the weight measurements were even above the 97th percentile. Height: short stature was detected in 7 of 73 (9.6%) of the total patients; the patients with short stature were all < 10 years old; the height was within the normal age in all adolescent patients. Head circumference: it was below the 3rd percentile in 7 of 73 (9.6%), between the 3rd and the 25th percentiles in 36 of 73 (49.3%) patients, between the 25th and the 75th percentiles in 20 of 73 (27.3%) patients, and between the 75th and the 97th percentiles in 10 of 73 (13.7%) patients. Bone age: mean ± sd bone age was -0.25 ± 0.78 years. Comparisons: the only statistically significant correlation was that between the presence of feeding difficulties and underweight.Conclusion: Auxological parameters of children with del22q11 are characterized by: (1) weight deficiency in the first years of age, (2) weight normalization in the following years, (3) development of obesity in adolescence, (4) short stature in 10% of the patients, (5) normal height in adolescents, (6) slight delay in bone age in infancy, (7) microcephaly in 10% of the patients.

AbstractUrinary cotinine was measured according to its inhibitory activity on the agglutination of cotinine-coated latex particles by anti-cotinine antibodies, the agglutination being measured by optical counting of the remaining non-agglutinated particles (particle counting, PaC). The detection limit was 0.03 μg/ml and the practical range extended from 0.03 to 3.9 μg/ml. The correlation results of 320 urine samples with those of high pressure liquid chromatography, enzyme-linked (Coti-Tracq EIA, Serex Inc., Maywood, NJ, USA), and fluorescence polarization immunoassay (TDX instrument, Abbott, Abbott Park, IL, USA) were r = 0.90, r = 0.69, r = 0.87, respectively, whereas the correlation coefficients between the assays other than particle counting ranged from 0.62 to 0.88. PaC does not require any separation step and can thus be easily automated.

The helical muscle fibers of Enchytraeus minutus (Annelida, Enchytraeidae) have been investigated with respect to their development. We have shown that longitudinal fibers, in the cocoon, begin to develop as platymyarian fibers, then develop into shallow coelomyarian ones and finally, just before hatching, reach a flat circomyarian stage. After hatching, the fibers grow only in size due to an increase in contractile material in the helical sarcomere system. Indications are given as to the ways this process can take place.

We report the effect of growth hormone (GH) treatment for 4 to 10 years in 15 prepubertal non-GH-deficient short children (10 boys, 5 girls, aged 7.4 to 13.2 years). In 7 patients, GH was administered at a dosage of 0.5 U/kg per week (group 1: 4 boys, 3 girls) and in 8 patients (group 2: 6 boys, 2 girls) at a dosage of 1.0 U/kg per week. After the first year, mean linear growth velocity had significantly increased in both groups. The increase in growth velocity was sustained during the first 4 years and then declined to pretreatment values in the majority of subjects. Treatment with GH did not induce an earlier onset of puberty, but there was a tendency toward faster skeletal maturation. The mean final height standard deviation score (SDS) was similar in the two groups and was significantly higher than the height SDS for chronologic age before treatment, but it did not differ from mean pretreatment predicted adult height SDS nor from mean target height SDS in both groups. Final height was significantly correlated with target height in both groups. These preliminary observations indicate that GH treatment does not generally increase final height over target height in short non-GH-deficient children. (J PEDIATR1994;125:196-200)

We evaluated the effect of six-month treatment with growth hormone (GH) or low-dose oxandrolone in a group of boys with constitutional growth delay (CGD). Sixteen boys were randomly assigned to two treatment groups. Group 1 received GH (0.6 U/kg/week sc 5–6 times/week) and Group 2 received oxandrolone (0.07 mg/kg po). The boys of the two groups were closely matched for age (13.7 ± 0.5 and 12.8 ± 0.4 years) (mean ± SE), chronologic age/bone age ratio (1.15 ± 0.04 and 1.16 ± 0.02), height standard deviation score (SDS; −2.7 ± 0.4 and −2.5 ± 0.3) and pretreatment height velocity (HV) (3.7 ± 0.8 and 4.0 ± 0.4 cm/year). Other known causes of short stature were excluded in all subjects, and none had taken long-term medication prior to the study. After 6 months of treatment HV increased to 7.5 ± 0.4 and to 8.1 ± 0.5 cm/year in group 1 and 2, respectively. Plasma IGF-I concentrations rose significantly after treatment in both groups. Predicted adult height was not significantly affected by either GH or oxandrolone treatment. We conclude that a short-term course of low-dose oxandrolone is as effective as GH to accelerate growth in boys with CGD. Low-dose oxandrolone represents an effective, cheap, and convenient therapeutic approach in boys with CGD.

A mouse monoclonal anti-idiotypic (anti-id) immunoglobulin M (IgM) antibody, called MAb2, was raised against a mouse monoclonal anti-cholera toxin (anti-CT) antibody (MAb1). The MAb2 was shown, by competition with CT for MAb1, to bear the internal image of an epitope of CT. MAb2 immunization of rats was performed via the intraperitoneal, intragastric, and intrajejunal routes and compared with immunization of rats with either a control, isotype- and allotype-matched MAb or with CT via the same routes. Both serum IgG and bile IgA anti-CT Ab3's were detected by enzyme-linked immunosorbent assay in anti-id MAb2-immunized rats, although their titers were lower than those in CT-immunized rats. No anti-CT antibodies were detected in sera and bile of rats immunized with the control MAb. When tested for degree of gut protection against a CT challenge, rats immunized with MAb2 by the intrajejunal route showed a rather high degree of protection, which was only slightly lower than that of rats immunized with CT via the same route; all rats but one immunized with the control MAb were unprotected. There was, however, no correlation between serum or bile anti-CT titers and degree of gut protection in MAb2-immunized rats. Their serum anti-CT Ab3's were purified by adsorption and elution from a CT immunosorbent and resembled anti-CT MAb1 in their unique reactivity with MAb2. This constitutes to our knowledge the second report of protection against a pathogen by anti-id immunization via the enteric route.

The boundary conditions at a solid–solid interface are analyzed in the transition from a solid–solid interface to a liquid–solid interface. This transition is mathematically performed by means of a limit process, that is, by letting the Lame´ shear coefficient of one medium tend to zero. The behavior of the reflection coefficient for transverse waves in the transition can be derived from the boundary conditions. In particular, a linear shear‐velocity dependence of its magnitude has been found. As a consequence, the magnitudes of the other reflection and transmission coefficients are also linear. Numerical calculations of the coefficients have been performed. The results confirm the theoretical analysis and point out some critical angles where the linear trend does not occur.

We have previously reported on the induction, in mice, of a systemic (splenic) immune response with IgA as the dominant antibody, as a result of a short (4 day) intragastric immunization course with foreign erythrocytes. This response was followed by a prolonged period of hyporesponsiveness to similarly administered antigen. Here it is shown that this hyporesponsiveness is also manifested towards antigen given intraperitoneally, and that one is therefore dealing with tolerance, not with failure to absorb antigen from the gut. In contrast, mice primed parenterally and then challenged intragastrically behaved as if never having any previous contact with the antigen, i.e., with a primary-type splenic response of predominant IgA character. This agrees with our former conclusion that splenic responses to enterically absorbed antigen reflect colonization of the spleen by cells sensitized locally in the gut wall, a site not readily primed by the parenteral route. Serum from intragastrically immunized mice contained a very active tolerogen. In vivo, it was capable of conferring tolerance to nonimmune recipient mice. In vitro, it paralyzed the activity of antibody-producing cells. Inhibitory sera has weak antibody activity, restricted to the IgA class, and contained immune complexes reacting with rheumatoid factor but not with C1q. Elimination of these complexes by means by insolubilized rheumatoid factor abolished the tolerogenic effect. In conclusion, the enterically induced tolerogen seems to consist of immune complexes with IgA as the antibody.

An assay of immunoglobulin M (IgM) antitoxoplasma antibodies which is rapid (less than 30 min), homogeneous, and reliable (interassay coefficient of variation, less than 11%) is proposed. Its principle is based on the observation that a suspension of latex particles coated with toxoplasma antigens, after treatment with proteinase K, becomes less agglutinable by IgG antibodies but more agglutinable by IgM antibodies. The difference between the activities of the two classes of antibodies is increased by the addition of a monoclonal antibody directed against the Fc region of IgM. Agglutination is measured with a special instrument which optically counts the particles that remain free after the reaction. Turbidimetric reading, although less sensitive, is also suitable. No significant interferences either by IgG antitoxoplasma antibodies or by rheumatoid factor or antinuclear antibodies were observed. The sensitivity was similar to that of the immunosorbent agglutination assay.

CIRCULATING antigen–antibody (AgAb) complexes are important pathogenic factors in various diseases. In addition to their inflammatory effect, immune complexes can interfere with cellular immunity. For instance, in cancer, the so-called blocking factors are apparently circulating AgAb complexes1,2. Factors interfering with cellular immunity specifically directed against placental and foetal antigens have also been described in pregnancy serum3–5, and some data suggest a role of immune complexes as blocking factors in pregnancy6. We report here that circulating AgAb complexes are a constant feature of every normal pregnancy. This, of course, raises interesting questions as to the possible involvement of such complexes in the tolerance of the foetus by the mother.