Effects of ethmoidal nerve stimulation on respiration-related neurones in the dorsal medulla of the cat

Stimulation of the nasal mucosa produces a number of respiratory reflexes the afferent limb of which is provided by the ethmoidal nerve, a branch of the trigeminal nerve. In the cat this nerve terminates within the trigeminal nucleus. It has no direct projection to brainstem respiratory centres. This study examines the response of respiratory-related neurones in the nucleus of the solitary tract (NTS) to ethmoidal stimulation. It demonstrates that these neurones show both excitatory and inhibitory responses to ethmoidal stimulation. Thus, the NTS appears to be involved in respiratory reflexes initiated by stimulation of the nasal mucosa.     

Collaborative Practice Through Nursing Case Management

A 528-bed community teaching hospital redesigned its patient care delivery system, implementing a collaborative practice model on the 30-bed inpatient rehabilitation unit in April 1990. This model is a patient-centered delivery model that encourages the healthcare team to facilitate the achievement of patient outcomes within effective time frames and with an appropriate use of resources. The collaborative practice model includes a nurse case manager's role for the staff nurse, which had as its framework the concept of nursing case management. Tested project management techniques were used to ensure a successful implementation process. Various strategies, such as using project teams and providing educational programs, were used to respond to the issues of role conflict and overlap, especially between social workers and nurse case managers. The implementation of this model provided a number of benefits, including improved interdisciplinary relationships and decreased length of stay.     

CD40 ligand-independent B cell activation revealed by CD40 ligand-deficient T cell clones: evidence for distinct activation requirements for antibody formation and B cell proliferation

We report the capacity of CD40 ligand (CD40L)-negative T cell clones to activate human B cells. CD40L-negative T cells induce a level of B cell proliferation 10–20% of that seen with normal T cells. The signal provided by the negative clones is synergistic with that derived from a CD40L transfectant, and restores B cell proliferation to normal levels, showing that CD40L-negative T cell clones are not inherently inhibitory for B cells. Although their capacity to induce proliferation was much reduced, CD40L-negative T cell clones were still strong inducers of B cell differentiation to plasma cells. This differentiation to plasma cells was inhibited by a CD40L transfectant. The data are discussed with regard to the normal in vivo mechanism for maintaining B cell memory and memory antibody responses to T-dependent antigens.     

Impaired Microvascular Function in Normal Children: Effects of Adiposity and Poor Glucose Handling

Clustering of cardiovascular risk factors is thought to occur early in life. The endothelium is an important regulator of microvascular function. We investigated the relationship between microvascular function and cardiovascular risk factors in 145 normal, healthy children aged 11-14 years. Skin microvascular responses, measured using laser Doppler imaging, to iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), were negatively correlated with percentage body fat ( r =−0.20, P < 0.05 and r =−0.18, P < 0.05, respectively). Subjects were stratified into quintiles based on 2-h, post-feeding glucose levels. Subjects in the upper glucose quintile (range 7.4-11.4 mmol l⁻¹) showed significantly lower vasodilatation to both ACh (   P < 0.005  ) and SNP (   P < 0.02  ) than those in the lower quintile (range 3.9-4.9 mmol l⁻¹). Waist-to-hip ratio and the fasting insulin resistance index were significantly greater in subjects in the upper quintile than those in the lower quintile ( P < 0.001 and P < 0.05, respectively). Additionally, in subjects in the upper glucose quintile, fasting triglyceride correlated with fasting insulin ( r = 0.59, P < 0.001) and with the fasting insulin resistance index ( r = 0.49, P < 0.009), and plasma levels of cholesterol and 2-h glucose were also correlated ( r = 0.40, P < 0.05). In a cross-section of normal children, microvascular function was negatively associated with adiposity. Additionally, in a subgroup of subjects, there was a clustering of high post-feeding glucose, impaired microvascular function, increased insulin resistance and higher central fat distribution. These findings suggest that risk factors for adult cardiovascular disease begin to cluster in normal children, which might have important consequences for development of atherosclerosis later in life.     

Formation of rabbit reaginic antibodies to protein and hapten—protein conjugates

The capacities of BSA and DNP—protein conjugates to evoke reagin formation in rabbits were compared. Reagins to DNP generally appeared earlier and disappeared more rapidly from the circulation than did anti-BSA reagins. Initial formation of reagins proceeded with a logarithmic phase indicating a doubling time of 7–8 hours. Booster antigen injections resulted in some cases in a reagin response after a shorter latent phase than that observed after primary immunization. A secondary reagin response was more readily evoked in rabbits with low titres of agglutinating antibodies than in those with high titres. Anti-DNP reagins were demonstrable in a higher percentage of the injected rabbits than were anti-BSA reagins. The two types of reagins were equally sensitive to heat and 2-mercaptoethanol. A positive correlation between serum levels of anti-DNP but not anti-BSA reagins and agglutinating antibodies was demonstrated. Some evidence that a low antigen dose was more efficient than a high dose in evoking reagin formation was obtained. Treatment of rabbits with 6-mercaptopurine during the 1st week following antigen injection resulted in an increased latent phase and an enhancement of the production of anti-BSA reagins and some suppression of the formation of anti-DNP reagins.     

Kinesiophobia and symptomatology in chronic fatigue syndrome: A psychometric study of two questionnaires

Objectives. The aims of the study were to examine the reliability of the Dutch and French versions of the Tampa scale kinesiophobia (TSK) version chronic fatigue syndrome (CFS), and to examine the reliability and validity of the Dutch and French versions of the CFS symptom list. Design. Repeated‐measures design. Methods. Native Dutch speakers (N=100) and native French (N=48) speakers fulfilling the diagnostic criteria for CFS were asked to list the five most important symptoms and to complete the TSK–CFS, the CFS symptom list, and the Short Form 36 Health Status Survey or SF‐36. A modified version of the TSK–CFS and the CFS symptom list was filled in within 24 hours of the first assessment. Results. The French and Dutch version of the TSK–CFS and CFS symptom lists displayed good reliability (ICC≥.83). The CFS symptom list was internally consistent (Cronbach's α≥.93) and concurrently valid with the SF‐36. For the native Dutch and French speakers, respectively, 82 and 78% of the self‐reported symptoms matched the content of CFS symptom list. Conclusions. The results are in support of the psychometric properties of the French and Dutch versions of both the TSK–CFS and the CFS symptom list for assessing kinesiophobia and symptom severity, respectively.     

Intratracheal administration of liposomal clodronate accelerates alveolar macrophage reconstitution following fetal liver transplantation

To facilitate study of alveolar macrophages in vivo, we developed a method to rapidly and efficiently replace resident alveolar macrophages with macrophages of a different (donor) genotype. Chimeric mice were generated by lethal irradiation followed by fetal liver transplantation (FLT) using green fluorescent protein (GFP) transgenic reporter mice as donors. Kinetics of peripheral blood monocyte (PBM) and alveolar macrophage reconstitution was determined 4 and 10 weeks post-FLT by quantifying the percentage of GFP+ cells. To enhance the recruitment of donor monocytes into the lung after FLT, mice were treated with intratracheal administration of liposomal clodronate to deplete host alveolar macrophages at 6 weeks post-FLT. PBM reconstitution occurred by 4 weeks after FLT (85.7+/-1.6% of CD11b+/Gr-1+ monocytes were GFP+), and minimal alveolar macrophage repopulation was observed (9.5% GFP+). By 10 weeks following FLT, 48% of alveolar macrophages were GFP+ by immunostaining of macrophages on lung tissue sections, and 55.1 +/- 1.6% of lung lavage macrophages were GFP+ by fluorescein-activated cell sorter analysis. Clodronate treatment resulted in a significant increase in GFP+ alveolar macrophages 10 weeks after FLT. By immunostaining, 90% of macrophages were GFP+ on lung tissue sections and 87.5 +/- 1.1% GFP+ in lung lavage (compared with GFP-transgenic controls). The ability of newly recruited alveolar macrophages to clear Pseudomonas aeruginosa and activate nuclear factor-kappaB in response to Eschericia coli lipopolysaccharide demonstrated normal macrophage function. Optimizing this methodology provides an important tool for the study of specific genes and their contribution to alveolar macrophage function in vivo.     

Upregulation of TGF-beta, FOXP3, and CD4+CD25+ regulatory T cells correlates with more rapid parasite growth in human malaria infection

Understanding the regulation of immune responses is central for control of autoimmune and infectious disease. In murine models of autoimmunity and chronic inflammatory disease, potent regulatory T lymphocytes have recently been characterized. Despite an explosion of interest in these cells, their relevance to human disease has been uncertain. In a longitudinal study of malaria sporozoite infection via the natural route, we provide evidence that regulatory T cells have modifying effects on blood-stage infection in vivo in humans. Cells with the characteristics of regulatory T cells are rapidly induced following blood-stage infection and are associated with a burst of TGF-beta production, decreased proinflammatory cytokine production, and decreased antigen-specific immune responses. Both the production of TGF-beta and the presence of CD4+CD25+FOXP3+ regulatory T cells are associated with higher rates of parasite growth in vivo. P. falciparum-mediated induction of regulatory T cells may represent a parasite-specific virulence factor.