Vaccination of Lewis rats with temperature-sensitive mutants of Mycoplasma pulmonis: adoptive transfer of immunity by spleen cells but not by sera.

Temperature-sensitive mutant vaccines protect rats against Mycoplasma pulmonis infection. The role of the humoral or cellular immune response in resistance to mycoplasma infection was investigated by adoptive-transfer experiments. Spleen cells from Lewis rats vaccinated but not challenged with wild-type organisms (vaccinated) and spleen cells from rats vaccinated (or not) and challenged were effective in preventing syngeneic recipients from developing respiratory disease. There was also a significant reduction in the incidence and number of challenging organisms in the respiratory system. In contrast, sera from the same donors had no detectable effect on the number of mycoplasmas recovered or on lesion development in the respiratory tract. We conclude that cellular immunity rather than humoral immunity generated in vaccinated rats confers protection against subsequent infection.     

Sequential occurrence of IgA nephropathy and Henoch-Schönlein purpura: support for common pathogenesis

We report a patient who developed Henoch-Schönlein purpura (HSP) 13 years after he presented with IgA nephropathy (IgAN). In both HSP and IgAN renal biopsy most commonly reveals focal proliferative glomerulonephritis on light microscopy and immunofluorescence displays mesangial IgA deposits. In addition, patients with HSP or IgAN have elevated serum IgA levels, circulating IgA immune complexes, IgA-bearing lymphocytes, immunoglobulin-producing cells, and binding of IgG to glomerular components of similar molecular weight. The occurrence of both diseases in the same patient or the same families and the presence of immune abnormalities compatible with HSP or IgAN in relatives of patients with these diseases suggest a common pathogenesis.     

Difficult or Impossible Ventilation after Sufentanil-induced Anesthesia Is Caused Primarily by Vocal Cord Closure

Introduction: Opioid-induced rigidity often makes bag-mask ventilation difficult or impossible during induction of anesthesia. Difficult ventilation may result from chest wall rigidity, upper airway closure, or both. This study further defines the contribution of vocal cord closure to this phenomenon.

Methods: With institutional review board approval, 30 patients undergoing elective cardiac surgery participated in the study. Morphine (0.1 mg/kg) and scopolamine (6 micro gram/kg) given intramuscularly provided sedation along with intravenous midazolam as needed. Lidocaine 10% spray provided topical anesthesia of the oropharynx. A fiberoptic bronchoscope positioned in the airway photographed the glottis before induction of anesthesia. A second photograph was obtained after induction with 3 micro gram/kg sufentanil administered during a period of 2 min. A mechanical ventilator provided 10 ml/kg breaths at 10/min via mask and oral airway with jaw thrust. A side-stream spirometer captured objective pulmonary compliance data. Subjective airway compliance was scored. Pancuronium (0.1 mg/kg) provided muscle relaxation. One minute after the muscle relaxant was given, a third photograph was taken and compliance measurements and scores were repeated. Photographs were scored in a random, blinded manner by one investigator. Wilcoxon signed rank tests compared groups, with Bonferroni correction. Differences were considered significant at P <0.05.

Results: Twenty-eight of 30 patients exhibited decreased pulmonary compliance and closed vocal cords after opioid induction. Two patients with neither objective nor subjective changes in pulmonary compliance had open vocal cords after opioid administration. Both subjective and objective compliances increased from severely compromised values after narcotic-induced anesthesia to normal values (P = 0.000002) after patients received a relaxant. Photo scores document open cords before induction, progressing to closed cords after the opioid (P = 0.00002), and opening again after a relaxant was administered (P = 0.00005).     

Altered corticomotor representation in patients with Parkinson's disease.

In 6 patients with Parkinson's disease (PD) and 6 age-matched controls, transcranial magnetic stimulation was applied at 56 regions over the motor cortex and premotor cortex of each hemisphere, with the first dorsal interosseous (FDI) muscle of both hands activated at 15% maximum voluntary contraction during stimulation. For each site, motor evoked potential (MEP) landmarks were recovered, including MEP amplitude, MEP onset latency, and silent period duration. Scaled MEP amplitudes were used to construct individual cortical maps of the FDI muscles. The maps revealed an anterior displacement of the muscle representation in PD patients. This anterior shift over motor cortical areas may reflect increased contributions of corticocortical connections between motor cortex and premotor cortical areas, possibly enhanced by the visual feedback aspect of the task. These alterations may reflect adaptations to the impairments in striatocortical circuits in PD.     

IDENTIFICATION OF NEURODEVELOPMENTAL ABNORMALITY AT FOUR AND EIGHT MONTHS BY THE MOVEMENT ASSESSMENT OF INFANTS

The predictive validity of infant neuromotor evaluation by the Movement Assessment of Infants (MAI) was investigated in low-birthweight infants. Motor performance at four and eight months was examined in relation to neurodevelopmental outcome at 18 months of age. Correlations were equally strong between total MAI risk scores at four and eight months and performance on the Bayley Scales. Muscle tone observations were more discriminating at four months, and automatic reactions and volitional movement were most predictive at eight months. The MAI was highly sensitive to neurodevelopmental abnormality at four and eight months and more sensitive than the Bayley Motor Scale; both assessment tools had lower specificity at eight months. The high false-positive rate is attributed to transient neuromotor abnormalities and immaturity of motor function in low-birthweight infants with normal outcome.     

Recombinant human nerve growth factor is biologically active and labels novel high-affinity binding sites in rat brain.

Iodinated recombinant human nerve growth factor (125I-rhNGF) stimulated neurite formation in PC12 cell cultures with a half-maximal potency of 35-49 pg/ml, compared with 39-52 pg/ml for rhNGF. In quantitative ligand autoradiography, the in vitro equilibrium binding of 125I-rhNGF to brain sections showed a 10-fold regional variation in density and was saturable, reversible, and specifically displaced by up to 74% with rhNGF or murine NGF (muNGF). At equilibrium, 125I-rhNGF bound to these sites with high affinity (Kd 52-85 pM) and low capacity (Bmax less than or equal to 13.2 fmol/mg of protein). Calculation of 125I-rhNGF binding affinity by kinetic methods gave average Kd values of 24 and 31 pM. Computer-generated maps revealed binding in brain regions not identified previously with 125I-muNGF, including hippocampus; dentate gyrus; amygdala; paraventricular thalamus; frontal, parietal, occipital, and cingulate cortices; nucleus accumbens; olfactory tubercle; subiculum; pineal gland; and medial geniculate nucleus. NGF binding sites were distributed in a 2-fold increasing medial-lateral gradient in the caudate-putamen and a 2-fold lateral-medial gradient in the nucleus accumbens. 125I-rhNGF binding sites were also found in most areas labeled by 125I-muNGF, including the interpedunucular nucleus, cerebellum, forebrain cholinergic nuclei, caudoventral caudate-putamen, and trigeminal nerve nucleus. 125I-rhNGF binding sites were absent from areas replete with low-affinity NGF binding sites, including circumventricular organs, myelinated fiber bundles, and choroid plexus. The present analysis provides an anatomical differentiation of high-affinity 125I-rhNGF binding sites and greatly expands the number of brain structures that may respond to endogenous NGF or exogenously administered rhNGF.     

Industrial back belts and low back pain: Mechanisms and outcomes

The recent increased utilization of industrial back belts as personal protective equipment in the workplace has generated considerable controversy among occupational health and safety professionals in the United States. The purpose of this article is to review the literature regarding proposed mechanisms of action of these devices and studies related to outcome of belt utilization in the prevention of low back pain and disability in the workplace. At the present time, neither the suspected mechanisms of action nor the efficacy of these devices in the primary, secondary, and tertiary prevention of work-related low back pain has been adequately demonstrated in clinical trials. As a result, generally accepted guidelines regarding the safe use of belts in the occupational setting have not been established. Based on this review it is recommended that further well-controlled, prospective, randomized clinical trials are necessary to evaluate the effectiveness of these devices as personal protective equipment. During the interim, the decision to prescribe belts to employees in the workplace should be at the discretion of an adequately trained occupational health care provider. These devices should not be provided as an alternative to appropriate administrative and/or engineering controls.