Fear and the startle reflex: Blink modulation and autonomic response patterns in animal and mutilation fearful subjects

The present study was designed to examine the pattern of startle reflex modulation and autonomic responses for individuals high in animal or blood-injury fear when viewing pictures of their feared objects. Sixteen individuals in each fear group and 16 low-fear control individuals viewed 32 color slides depicting fear-relevant, unpleasant but fear-unrelated, neutral, and pleasant scenes. Free viewing times were assessed in a second phase of the procedure as an index of avoidance behavior. Exposure to pictures of feared objects resulted in a consistent startle reflex potentiation and behavioral avoidance in both fear groups. This activation of the basic aversive system was independent of the autonomic pattern of the fear responses, which differed for the high-fear groups. These results suggest that the probe startle response indexes the organism's basic motivational disposition and add new information to the assessment of fear.     

Apolipoprotein E genotype and cerebral palsy

Aim Apolipoprotein E (APOE, protein; [ApoE, gene]) is a lipid transport protein abundantly present in brain cells. We investigated whether the APOE genotype is associated with cerebral palsy (CP) and whether patients with CP with comorbid conditions and more severe neurological deficits are likely to have a particular genotype. Method In a cross‐sectional study, 243 individuals with spastic CP (135 males, 108 females; mean age at data collection 11 year ([SD 6y 7mo], 34% with hemiplegia, 37% with diplegia, 29% with triplegia/tetraplegia; 44% with mild motor involvement), 31% with moderate motor involvement, 25% with severe motor involvement, were compared with healthy individuals matched by age, race, and sex to analyse the association between APOE genotype and the incidence of CP. Associations between the APOE genotype and the incidence of comorbidities and neurological deficits were studied in the group with CP. Results The APOE ε2ε3 genotype was significantly more prevalent in the group with CP (11%) than the comparison group (5%) (odds ratio [OR] 2.8; 95% confidence interval [CI] 1.01–7.66). The presence of the ε2 allele raised the probability of having CP (OR 3.2; 95% CI 1.27–8.27). The presence of ApoE ε4 was not significantly different among groups. No relation was found between APOE genotype and severity of neurological deficit or distribution of motor involvement. Four patients with CP presented the ε4ε4 genotype, and all exhibited epilepsy and microcephaly. Eleven of 12 individuals with CP and macrocephaly carried the ε3ε3 genotype. Interpretation A higher prevalence of the APOE ε2 genotype was found among those with CP. The association of microcephaly and epilepsy with the ε4ε4 genotype and the association of macrocephaly with ε3 demand further investigation.     

Local Repolarization Abnormalities Induced by Transcatheter Radiofrequency Ablation in Pigs

Radiofrequency (RF) ablation alters action potential repolarization of myocardial cells and, theoretically, tbis should induce ST-T segment changes in the ECG. Since these ECG abnormalities have been rarely reported in patients submitted to RF ablation we assess the ability of the procedure to caase ST-T segment changes in local electrograms. Epicardial ECG mapping was performed in 17 anesthetized open chest pigs submitted to endocardial (n = 9) or to epicardial (n = 8) unipolar radiofrequency ablation (500 kHz, 20 W for 5-10 s). To characterize the cellular electrophysiological alterations induced by RE ablation transmembrane action potentials were recorded at various distances from the ablation lesion; these were compared with seven control pigs. Endocardial RE ablation induced a transient (< 5 min) change of 6.1 ± 2.4 m V in T wave amplitude (baseline: 12.8 ± 5.6 mV, P < O.OOl) in 141 out of 269 epicardial electrodes. T wave changes were associated with shortening in local activation time (20.1 ± 2.3 ms at baseline vs 18.5 ± 2.5 ms at 60 s after ablation, P = 0.03). RE current caused persistent ST segment elevation at the center of the ablation lesion with no transmural expansion. Intracellular potentials along a 2-6-mm wide myocardial band bordering the RE lesion showed lower amplitude (101 ± 7.0 mV vs 71 ± 23 mV, P < 0.01) and shorter duration (254 ± 44 ms vs 156 ± 29 ms, P < 0.01) than control hearts. The center of the ablation lesion was electrically anexcitable. We concluded that RF ablation alters cellular electrophysiology in small areas surrounding the ablation lesion and this causes short-lasting transmural changes in T wave amplitude and nontransmural ST segment elevation.     

Voltage Dip in Pacemaker Battery Supply: A New Cause of Pacemaker Mediated Tachycardia

A new cause of pacemaker medialed tachycardia was observed in a patient equipped with a Vitatron® Quintech 931 DDD pacemaker. In this type of pacemaker the microprocessor is switched off during the atrial refractory period. Beyond the recommended replacemenl lime, the internal resistance of the battery may increase to such an extent that switching on and off the microprocessor may cause voltage dips. Those voltage dips are erroneously interpreted as P waves hy the atrial sensing amplifier, which may cause self-triggering of the pacemaker and initiate a pacemaker mediated tachycardia.     

Modulation of T-cell responsiveness during Trypanosoma cruzi infection: analysis in different lymphoid compartments

Spleen and lymph node cells of Trypanosoma cruzi-infected mice were studied for mitogen-induced responsiveness in terms of proliferation and lymphokine production (IL-2, IFN-gamma). Splenocyte (SP) as well as lymph node cell (LN) proliferation and IL-2 production were depressed during the acute phase of the infection. Proliferative capacity of LN cells recovered completely and that of SP partially during the chronic phase. In contrast to these suppressive effects, the mitogen-induced IFN-gamma response was enhanced. In vitro co-incubation of normal SP or LN cells with trypomastigotes resulted in a reduced mitogen-induced cell proliferation and IL-2 secretion, similar to those seen with cells taken from infected mice. In contrast, trypomastigotes exerted a stimulatory activity on the mitogen-induced IFN-gamma response of both SP and LN cells. Addition of lymph node cells from T. cruzi-infected mice (LN-I) to lymph node cells of control mice (LN-C) suppressed strongly the mitogen-induced responsiveness of such cocultures. A marginal level of suppression was recorded in cocultures of spleen cells from infected mice (SP-I) and control spleen cells (SP-C). The potent suppressive cells within LN-I populations were identified as macrophage-like and such cells were absent in SP-C and peritoneal exudate cells from T. cruzi infected animals.     

Renal Tubular Excretion of the N4-Acetyl Metabolites of Sulphasomidine and Sulphadimethoxine in the Dog

Abstract— To investigate whether dogs are able to excrete acetylated drugs by active transport, the plasma kinetics and renal excretion of the N₄-acetyl metabolites of sulphasomidine and sulphadimethoxine were studied in the beagle dog after a rapid intravenous bolus injection. Two doses of N₄-acetylsulphasomidine (1050 and 105 mg) and one dose of N₄-acetylsulphadimethoxine (472 mg) were administered on separate occasions. The renal clearance (CL_R) was as follows: N₄-acetylsulphasomidine (1050 mg) 34 mL min^?1; N₄-acetylsulphasomidine (105 mg) 28 mL min^?1; and N₄-acetylsulphadimethoxine (472 mg) 24 mL min^?1. CL_R was higher than expected on the basis of the measured glomerular filtration rate, indicating that the N₄-acetyl metabolites may be excreted by the renal tubules by active tubular transport. Saturation of the excretion process of N₄-acetylsulphasomidine occurred with a transport maximum of 930 ± 190 μg min^?1 and a Michaelis-Menten constant of 37 ± 10 μg mL^?1. It may be concluded that the dog renal organic anion transport system is able to secrete acetylated sulphonamides.     

Long-term results of vocal rehabilitation after total laryngectomy with the low-resistance,indwelling ProvoxTM Voice prosthesis system

A low-resistance indwelling prosthesis for vocal rehabilitation after total laryngectomy, Provox^TM was developed in the Netherlands Cancer Institute 5 years ago. The long-term results in 132 patients using this prosthesis are now reported. The mean and median device life of the prosthesis in the 75 patients in long-term follow-up are 235 and 141 days respectively. Good to fair vocal rehabilitation was achieved in 92% of the patients. Statistical analysis revealed a significant relationship of the device life with the original tumour site (P=0.0078). Radiotherapy had a borderline (P=0.0652) negative influence on the device life but not on prosthesis-related complications. Increasing follow-up time has a positive influence on the device life of the prosthesis (P < 0.0001).     

Ploidy status and the response of T1 glottic carcinoma to radiotherapy

Flow cytometric DNA ploidy measurements were performed on formalin fixed paraffin embedded tumour specimens from patients with a T₁ glottic laryngeal carcinoma in order to evaluate the role of DNA content in relation to local control. From 1980 to 1987, a consecutive series of 90 patients with a T₁ glottic laryngeal carcinoma were treated by radiotherapy with curative intent. Biopsies from 44 of these patients were readily available for DNA flow cytometry. In this group aneuploidy was associated with a significantly higher risk (P= 0.018) of local recurrence within 2 years after completion of radiotherapy (38% vs. 9% in the diploid group).