Ultrasonographic placental localization with respect to fetal position in utero

Ultrasonographic localization of the placental site was performed serially throughout pregnancy in 56 primigravidas with anteriorly located placentas. The placenta was found to be located on the right side of the uterus significantly more frequently than at any other site on the anterior uterine wall. Placental position was found to be related to the position of the fetus in utero. The role of placental location in determining the high incidence of the left occiput position at delivery is discussed.     

Glutamate and gamma-aminobutyric acid content and release of synaptosomes from temporal lobe epilepsy patients

During surgical intervention in medically refractory temporal lobe epilepsy (TLE) patients, diagnosed with either mesial temporal lobe sclerosis (MTS)- or tumor (T)-associated TLE, biopsies were taken from the anterior temporal neocortex and the hippocampal region. Synaptosomes, isolated from these biopsies were used to study intrasynaptosomal Ca(2+) levels ([Ca(2+)](i)), and glutamate and gamma-aminobutyric acid (GABA) contents and release. All synaptosomal preparations demonstrated a basal [Ca(2+)](i) of about 200 nM, except neocortical synaptosomes from MTS-associated TLE patients (420 nM). K(+)-induced depolarization resulted in a robust increase of the basal [Ca(2+)](i) in all preparations. Neocortical synaptosomes from TLE patients contained 22.9 +/- 3.0 nmol glutamate and 4.6 +/- 0.5 nmol GABA per milligram synaptosomal protein, whereas rat cortical synaptosomes contained twice as much glutamate and four times as much GABA. Hippocampal synaptosomes from MTS-associated TLE patients, unlike those from T-associated TLE patients, contained about 70% less glutamate and 55% less GABA than neocortical synaptosomes. Expressed as percentage of total synaptosomal content, synaptosomes from MTS-associated TLE patients exhibited an increased basal and a reduced K(+)-induced glutamate and GABA release compared to rat cortical synaptosomes. In MTS-associated TLE patients, only GABA release from neocortical synaptosomes was partially Ca(2+)-dependent. Control experiments in rat synaptosomes demonstrated that at least part of the reduction in K(+)-induced release can be ascribed to resection-induced hypoxia in biopsies. Thus, synaptosomes from MTS-associated TLE patients exhibit a significant K(+)-induced increase in [Ca(2+)](i), but the consequent release of glutamate and GABA is severely impaired. Our data show that at least part of the differences in glutamate and GABA content and release between human biopsy material and fresh rat tissue is due to the resection time.     

Activity-dependent increases in local oxygen consumption correlate with postsynaptic currents in the mouse cerebellum in vivo

Evoked neural activity correlates strongly with rises in cerebral metabolic rate of oxygen (CMRO(2)) and cerebral blood flow (CBF). Activity-dependent rises in CMRO(2) fluctuate with ATP turnover due to ion pumping. In vitro studies suggest that increases in cytosolic Ca(2+) stimulate oxidative metabolism via mitochondrial signaling, but whether this also occurs in the intact brain is unknown. Here we applied a pharmacological approach to dissect the effects of ionic currents and cytosolic Ca(2+) rises of neuronal origin on activity-dependent rises in CMRO(2). We used two-photon microscopy and current source density analysis to study real-time Ca(2+) dynamics and transmembrane ionic currents in relation to CMRO(2) in the mouse cerebellar cortex in vivo. We report a direct correlation between CMRO(2) and summed (i.e., the sum of excitatory, negative currents during the whole stimulation period) field EPSCs (∑fEPSCs) in Purkinje cells (PCs) in response to stimulation of the climbing fiber (CF) pathway. Blocking stimulus-evoked rises in cytosolic Ca(2+) in PCs with the P/Q-type channel blocker ω-agatoxin-IVA (ω-AGA), or the GABA(A) receptor agonist muscimol, did not lead to a time-locked reduction in CMRO(2), and excitatory synaptic or action potential currents. During stimulation, neither ω-AGA or (μ-oxo)-bis-(trans-formatotetramine-ruthenium) (Ru360), a mitochondrial Ca(2+) uniporter inhibitor, affected the ratio of CMRO(2) to fEPSCs or evoked local field potentials. However, baseline CBF and CMRO(2) decreased gradually with Ru360. Our data suggest that in vivo activity-dependent rises in CMRO(2) are correlated with synaptic currents and postsynaptic spiking in PCs. Our study did not reveal a unique role of neuronal cytosolic Ca(2+) signals in controlling CMRO(2) increases during CF stimulation.     

Tumor necrosis factor-α levels correlate with postoperative pain severity in lumbar disc hernia patients: opposite clinical effects between tumor necrosis factor receptor 1 and 2

Lumbar disc hernia (LDH) is a leading cause of chronic pain in adults. The underlying pathology of chronic pain after discectomy remains unclear. Chronic local inflammation is considered to underlie painful symptomatology. In this context, we investigated tumor necrosis factor (TNF)-α, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2) expression at the time of surgery in LDH patients and correlated it with the severity of postoperative pain. We analyzed protein and mRNA levels from muscle, ligamentum flavum (LF), annulus fibrosus (AF), and nucleus pulposus (NP) in LDH patients and scoliosis patients (SP), who served as controls. Pain assessment with the visual analogue scale (VAS) was performed 1 day before surgery and 6 weeks and 12 months postoperatively. TNF-α protein levels were detected in AF, LF, and NP in all LDH patients, but not in SP. TNF-α mRNA was significantly greater in LDH patients than in SP; ie, 5-fold in AF, 3-fold in NP, and 2-fold in LF. For NP, TNF-α protein levels correlated with VAS scores (r = 0.54 at 6-week and r = 0.65 at 12-month follow-up). Also, TNFR1 protein levels in NP positively correlated with VAS scores (r = 0.75 at 6-week and r = 0.80 at 12-month follow-up). However, TNFR2 protein levels in AF negatively correlated with VAS scores (r = −0.60 at 6 weeks and r = −0.60 at 12 months follow-up). These data indicate that TNF-α levels could determine the clinical outcome in LDH patients after discectomy. Moreover, the opposite correlation of TNF receptors with pain sensation suggests that an unbalanced expression plays a role in the generation of pain.     

Screening of blood donors for idiopathic CD4+ T-lymphocytopenia

BACKGROUND: The recent recognition of idiopathic CD4+ T-lymphocytopenia (ICL) had led to concern that an unknown immunodeficiency virus may be transmissible by transfusion. STUDY DESIGN AND METHODS: To evaluate the prevalence and significance of low CD4+ values among blood donors, CD4+ data on 2030 blood donors who were negative for antibody to human immunodeficiency virus type 1 (HIV-1) were compiled. Those with CD4+ values below ICL cutoffs (< 300 CD4+ T cells/microL, or < 20% CD4+ T cells) were recalled for follow-up investigations. Serial CD4+ data on 55 homosexual men who seroconverted during prospective follow-up and data on 139 anti-HIV-1-positive blood donors initially evaluated in 1986 were reviewed as well. RESULTS: Five seronegative donors (0.25%) had absolute CD4+ counts < 300 cells per microL and/or < 20 percent. On follow-up, all five donors had immunologic findings within normal ranges, lacked HIV risk factors, and tested negative for HIV types 1 and 2 and human T-lymphotropic virus type I and II infections by antibody and polymerase chain reaction assays. Four of five donors reported transient illness shortly after their low CD4+ count donations. The median interval from HIV-1 seroconversion to an initial CD4+ value below ICL CD4+ cutoffs was 63 months for infected homosexual men. Of 139 HIV-1-infected blood donors studied 1 to 2 years after seropositive donations, 34 (24%) had CD4+ counts < 300 cells per microL and/or < 20 percent. CONCLUSION: Low CD4+ counts are rare among anti- HIV-1-negative volunteer blood donors and are generally associated with transient illnesses. If any unknown virus progresses similarly to HIV- 1, CD4+ count donor screening would be a poor surrogate for its detection.     

Significance of antibody to hepatitis B core antigen in blood donors as determined by their serologic response to hepatitis B vaccine

Because large numbers of volunteer blood donors may be disqualified for "false-positive" results on tests for antibody to hepatitis B core antigen (anti-HBc), a more specific definition of anti-HBc enzyme immunoassay (EIA)-reactive was evaluated, including only those donor samples that were "strongly" reactive (sample-to-cutoff absorbance ratio, < 0.45). Results using this definition and other anti-HBc test methods were compared to the serologic response (antibody to hepatitis B surface antigen [anti-HBsAg]) to hepatitis B vaccination. Fifty-eight volunteer blood donors who had previously been deferred as donors, because of reactive anti-HBc tests (all other blood screening tests were negative, including those for HBsAg and anti-HBsAg) on two occasions, were vaccinated for hepatitis B. It was assumed that an anamnestic response to vaccine indicated past infection with hepatitis B, while a primary response to vaccine indicated lack of past infection. One (2%) of 43 donors with a historically "weak" anti-HBc (reactive absorbance ratio, > or = 0.45) had an anamnestic response to vaccine, compared to 8 (53%) of 15 with historically "strong" anti-HBc (reactive absorbance ratio, < 0.45) (p < 0.005). Anti-HBc testing using the microparticle EIA method also correlated well with hepatitis B vaccination results. The use of a narrower definition of "reactive" for anti-HBc EIA testing yielded much more specific, but slightly less sensitive, results.