Specific Hemagglutinin and a Modulator of Complement in Cockroach Hemolymph

Natural hemagglutinin activity against vertebrate erythrocytes is present in the hemolymph of the cockroach Blabarus craniifer. The hemagglutinin titer against rabbit erythrocytes is high, whereas sheep and horse red cells agglutinate weakly. Hemagglutinin activity was depressed by the complement inhibitor, cobra venom factor. Cockroach hemagglutinin is heat-labile; all activity is destroyed by heating at 56 C for 1 hr. A humoral factor similar to the complement component 3 proactivator is also present in cockroach hemolymph. The formation of the cobra venom factor-hemolymph "complex" is dependent on the presence of divalent cations and will not proceed at 56 C. The hemolytic intermediate formed after treatment of cockroach hemolymph with cobra venom factor was active in the presence of serum treated with ethylenediaminetetraacetic acid to inactivate the early complement components.     

Interstitial deletions 4q21.1q25 and 4q25q27: Phenotypic variability and relation to Rieger anomaly

We describe clinical and chromosomal findings in two patients with del(4q). Patient 1, with interstitial deletion (4)(q21.1q25), had craniofacial and skeletal anomalies and died at 8 months of hydrocephalus. Patient 2, with interstitial deletion (4)(q25q27), had craniofacial and skeletal anomalies with congenital hypotonia and developmental delay. These patients shared certain manifestations with other del(4q) patients but did not have Rieger anomaly. Clinical variability among patients with interstitial deletions of 4q may be related to variable expression, variable deletion, or imprinting of genes within the 4q region. © 1995 Wiley-Liss, Inc.     

Women with asthma: a review of potential variables and preferred medical management.

OBJECTIVES: To summarize the potential variables that contribute to the increased risk of asthma in women, outline therapeutic strategies that address these variables, and review current treatment recommendations for both pregnant and nonpregnant women with asthma. DATA SOURCES: Literature searches (MEDLINE and cross-references) were performed using the keywords asthma and women in combination with the terms compliance, depression, emergency department, hormones, menstruation, mortality, National Asthma Education and Prevention Program, osteoporosis, pregnancy, prevalence, smoking, and treatment. Searches were limited to human studies with data published before 2005. STUDY SELECTION: The author selected relevant articles for inclusion in this review. RESULTS: Fluctuations in sex hormones, menstruation, pregnancy, obesity, depression, medication nonadherence, and smoking may contribute to increased asthma symptoms or severity in women. Asthma control may be improved if physicians address conditions and behaviors associated with asthma variability and severity in women. Notably, asthma must be managed aggressively in pregnant women, because uncontrolled asthma can lead to perinatal complications. Asthma treatment in women is optimized through patient and physician adherence to national guideline recommendations, including provision of patient education and asthma action plans. CONCLUSIONS: Multiple variables throughout the female life cycle may influence asthma control. Successful asthma management requires an ongoing partnership between the patient and her physician to address physiologic (eg, sex hormones, pregnancy, obesity, depression) and nonphysiologic (eg, smoking, medication nonadherence) factors that may contribute to decreased asthma control.     

Genome-wide linkage analysis of families with obsessive-compulsive disorder ascertained through pediatric probands

The goal of this study was to identify chromosomal regions likely to contain susceptibility alleles for early-onset obsessive-compulsive disorder (OCD). A genome scan was done in 56 individuals from seven families ascertained through pediatric OCD probands; 27 of the 56 subjects had a lifetime diagnosis of definite OCD. Denser mapping of regions on chromosomes 2, 9, and 16 was subsequently done with those subjects and ten additional subjects from the largest family in the study. Direct interviews were completed with 65 of the 66 genotyped individuals. Relatives were interviewed blind to proband status. Of the 65 interviewed individuals, 32 had a lifetime diagnosis of definite OCD. Three of the seven probands had a history of Tourette disorder. Two of the 25 relatives with OCD had a tic history, whereas none of the 33 relatives without OCD had tics. The genome scan consisted of 349 microsatellite markers with an average between-marker distance of 11.3 centiMorgan (cM). Fine mapping was done with 24 additional markers at an average spacing of 1.6 cM. Parametric and nonparametric linkage analyses were conducted using GENEHUNTER(+). The maximum multipoint LOD score with a dominant model was 2.25 on 9p. However, with fine mapping and additional subjects, that LOD score decreased to 1.97. The maximum multipoint nonparametric LOD* score was 1.73 on 19q. The maximum multipoint LOD score with a recessive model was 1.40 on 6p. The results provide suggestive evidence for linkage on 9p and identify regions requiring further study with much larger samples.     

The vascularization of the hypothalamic-hypophyseal region of the eastern brook trout,Salvelinus fontinalis

The hypophysis of the brook trout is irrigated by blood vessels which originate from the internal carotid arteries. These are: (1) branches of the ventral hypothalamic arteries that give rise to an extensive capillary plexus in the neurohypophysis from which vessels extend into all regions of the adenohypophysis; (2) branches of the caudal hypothalamic artery that irrigate the saccus vasculosus and continue anteriorly to supply the ventral areas of the meta-adenohypophysis; (3) a caudal hypophyseal artery which vascularizes a portion of the meta-adenohypophysis however, this vessel is not always present; (4) a pair of small arteries which supply the peripheral regions of the gland directly from the carotids. Most of the neurosecretory fibers of the preoptic-hypophyseal tract terminate close to capillaries in the neurohypophysis. A few axons extend into meso-adenohypophyseal tissue. It is suggested that the secretory activities of the pro-, meso- and metaadenohypophyses are governed by hypothalamic factors that are chiefly transmitted to the gland cells via the vascular system (indirect control). However, the activity of the meso-adenohypophysis may also be regulated by factors which are transmitted directly to the cells from the endings of neurosecretory fibers which have traversed the neurohypophysis (direct control). The distribution and abundance of neurosecretion in the ventral hypophysis suggest the possibility of storage of hypothalamic products within this region.     

T cell developmental defects in 'viable motheaten' mice deficient in SHP-1 protein-tyrosine phosphatase. Developmental defects are corrected in vitro in the presence of normal hematopoietic-origin stromal cells and in vivo by exogenous IL-7

Defects in the gene that encodes SHP-1 protein tyrosine phosphatase result in multiple hematopoietic abnormalities and generalized autoimmunity in viable motheaten (me(v)) mice. These mice also exhibit early thymic involution and abnormalities in T cell development. Here, we describe the use of fetal thymic organ culture (FTOC) and bone marrow adoptive transfer to study the effects of SHP-1 deficiency on thymocyte development. Chimeric FTOC established with normal bone marrow placed onto deoxyguanosine-treated fetal thymic lobes or onto scid fetal thymic lobes generated T cells. Bone marrow from SHP-1-deficient me(v)/ me(v) mice generated decreased numbers of T cells in chimeric FTOC established using deoxyguanosine-treated thymi but generated normal numbers in chimeric FTOC established using scid thymi. However, scid fetal thymi seeded with me(v)/ me(v) bone marrow also exhibited morphological abnormalities and contained elevated numbers of macrophages. Addition of IL-7 to me(v)/ me(v) bone marrow-seeded scid FTOC led to increased cell numbers, particularly of macrophages. Intrathymic injection of IL-7 partially restored the ability of progenitor cells in me(v)/ me(v) bone marrow to populate the thymus of adoptive recipients. We conclude that abnormal T cell development in me(v)/ me(v) mice may in part be due to defects in the ability of bone marrow-derived accessory cells to provide bioavailable IL-7 to developing thymocytes.     

Comparison of Ashdown's medium, Burkholderia cepacia medium, and Burkholderia pseudomallei selective agar for clinical isolation of Burkholderia pseudomallei

Ashdown's medium, Burkholderia pseudomallei selective agar (BPSA), and a commercial Burkholderia cepacia medium were compared for their abilities to grow B. pseudomallei from 155 clinical specimens that proved positive for this organism. The sensitivity of each was equivalent; the selectivity of BPSA was lower than that of Ashdown's or B. cepacia medium.     

Bipedal distribution of human vestibular-evoked postural responses during asymmetrical standing

Galvanic vestibular stimulation (GVS) evokes responses in muscles of both legs when bilateral stimuli are applied during normal stance. We have used this technique to assess whether asymmetrical standing alters the distribution of responses in the two legs. Subjects stood either asymmetrically with 75 % of their body weight on one leg or symmetrically with each leg taking 50 % of their body weight. The net response in each leg was taken from changes in ground reaction force measured from separate force plates under each foot. The net force profile consisted of a small initial force change that peaked at ∼200 ms followed by an oppositely directed larger component that peaked at ∼450 ms. We analysed the second force component since it was responsible for the kinematic response of lateral body sway and tilt towards the anode. In the horizontal plane, both legs produced lateral force responses that were in the same direction but larger in the leg ipsilateral to the cathodal ear. There were also vertical force responses that were of equal size in both legs but acted in opposite directions. When subjects stood asymmetrically the directions of the force responses remained the same but their magnitudes changed. The lateral force response became 2-3 times larger for the more loaded leg and the vertical forces increased 1.5 times on average for both legs. Control experiments showed that these changes could not be explained by either the consistent (< 5 deg) head tilt towards the side of the loaded leg or the changes in background muscle activity associated with the asymmetrical posture. We conclude that the redistribution of force responses in the two legs arises from a load-sensing mechanism. We suggest there is a central interaction between load-related afferent input from the periphery and descending motor signals from balance centres.     

Malaria transmission and naturally acquired immunity to PfEMP-1

Why there are so few gametocytes (the transmission stage of malaria) in the blood of humans infected with Plasmodium spp. is intriguing. This may be due either to reproductive restraint by the parasite or to unidentified gametocyte-specific immune-mediated clearance mechanisms. We propose another mechanism, a cross-stage immunity to Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP-1). This molecule is expressed on the surface of the erythrocyte infected with either trophozoite or early gametocyte parasites. Immunoglobulin G antibodies to PfEMP-1, expressed on both life cycle stages, were measured in residents from an area where malaria is endemic, Papua New Guinea. Anti-PfEMP-1 prevalence increased with age, mirroring the decline in both the prevalence and the density of asexual and transmission stages in erythrocytes. These data led us to propose that immunity to PfEMP-1 may influence malaria transmission by regulation of the production of gametocytes. This regulation may be achieved in two ways: (i) by controlling asexual proliferation and density and (ii) by affecting gametocyte maturation.     

Nonmyeloablative bone marrow transplantation: Infectious complications in 65 recipients of HLA-identical and mismatched transplants.

Infections are a common complication of allogeneic bone marrow transplantation and the leading cause of transplantation-related mortality. It had been hypothesized that transplantation following nonmyeloablative preparative regimens would result in fewer infections by causing less mucosal injury, less graft-versus-host disease, and allowing earlier immune reconstitution. We have retrospectively reviewed the infectious complications of 65 consecutive patients with advanced hematologic malignancies who underwent bone marrow transplantation using a novel preparative regimen consisting of cyclophosphamide, thymic irradiation, and in vivo T-cell depletion. Cytomegalovirus (CMV) infection occurred in 52% of cases in which the donor or recipient had evidence of prior CMV exposure. Using a strategy of preemptive therapy and secondary prophylaxis with ganciclovir, no CMV disease occurred. Infections with gram-positive bacteria predominated over the first 100 days after bone marrow transplantation. Thereafter, the relative proportion of gram-negative infections increased without a significant increase in episodes of neutropenia. The rate of bacterial infections was not influenced by relapse of the underlying malignancy. Seven patients developed infections with Aspergillus species, which was the most common infectious cause of death in these patients. Infections with viruses other than CMV (n=10) and with protozoan organisms (n=2) also occurred. The use of HLA-mismatched donors, the occurrence of grade II-IV acute graft-versus-host disease, and treatment with corticosteroids did not influence the risk of CMV or bacterial or fungal infections in patients who underwent transplantation following this preparative regimen. Overall, the incidence and spectrum of infections in this series was similar to the reported incidence of infections following conventional myeloablative allogeneic stem cell transplantation. We conclude that a quantitative T-cell deficiency in these extensively T-cell depleted patients may be a risk factor for infection, even in the absence of graft-versus-host disease.