Codistribution of a sensory gating deficit and schizophrenia in multi-affected families.

Because the clinical diagnosis of schizophrenia has not generally been an adequate phenotypic marker to detect the genes that convey risk for schizophrenia, efforts have been directed toward the identification of more elementary neuronal dysfunctions in schizophrenic patients and their families. Psychophysiological studies of sensory gating and selective attention suggest that defects in these brain functions are present in schizophrenic patients and some of their relatives. This study examines one of these defects in sensory gating, failure to suppress the P50 evoked response to repeated auditory stimuli. Six pedigrees, chosen because of the presence of large sibships containing several cases of schizophrenia, were studied. A mathematical model was developed to assess the familial association of the P50 defect with schizophrenia. The model preserves the quantitative nature of the data and is suitable for use in a sample with small numbers of pedigrees comprising many individuals. It is thus suitable for the evaluation of putative phenotypes in families to be studied by linkage analysis with polymorphic genetic markers. The results suggest that the P50 defect is familially associated with schizophrenia.     

Aggressive therapy of infants with renal failure

Nine infants, who presented with renal failure within the first 3 months of life, were treated with continuous ambulatory peritoneal dialysis (CAPD). Seven infants survived to an age of 12–15 months, when they received transplants. Two patients died while on CAPD. Six infants are alive with a functioning renal allograft, at an average age of 35.5 months and an average of 22 months post-transplant. Neurological development is normal in four of the six infants tested. The mean current height of the six transplant recipients is just below 2 SD from the mean.     

Gating of the Auditory Evoked Potential in Children and Adults

Auditory evoked potentials were recorded from 163 subjects, aged IS months to 55 years. A conditioning-testing paradigm was used to assess sensory gating. In this paradigm, click stimuli are presented in pairs to the subjects with a 0.5-second intrapair interval. In normal adults, the first stimulus activates or “conditions” sensory gating mechanisms. The strength of these mechanisms is “tested” by the second stimulus, which produces a response whose amplitude is significantly suppressed. This aspect of sensory gating was not reliably observed in our subjects until age 18 years. Younger subjects varied widely in their ability to demonstrate sensory gating. Mean levels of suppression increased during late childhood and adolescence, with no relationship to other changes in evoked potential amplitude and latency. Sensory gating would appear to be a late developing aspect of human sensory physiology.     

Decreased infectivity despite unaltered C3 binding by a DeltahbhA mutant of Mycobacterium tuberculosis

HbhA of Mycobacterium tuberculosis is a multifunctional binding protein, binding to both sulfated sugars such as heparin and to human complement component C3. HbhA may therefore interact with host molecules and/or host cells during M. tuberculosis infection and play a role in the pathogenesis of this bacterium. The purpose of this study was to use allelic exchange to create an M. tuberculosis strain deficient in expression of HbhA to determine whether this protein's C3-binding activity plays a role in the pathogenesis of M. tuberculosis. An in-frame, 576-bp unmarked deletion in the hbhA gene was created using sacB as a counterselectable marker. Southern blotting and PCR analyses confirmed deletion of hbhA in the DeltahbhA mutant. The DeltahbhA mutant strain grew at a rate similar to that of the parent in broth culture and in J774.A1 murine macrophage-like cells but was deficient in growth compared to the parent strain in the lungs, liver, and spleen of infected mice. In addition, the DeltahbhA mutation did not reduce binding of M. tuberculosis to human C3 or to J774.A1 cells in the presence or absence of serum, suggesting that in the absence of HbhA, other molecules serve as C3-binding molecules on the M. tuberculosis surface. Taken together, these data indicate that HbhA is important in the infectivity of M. tuberculosis, but its ability to bind C3 is not required for mycobacterial adherence to macrophage-like cells. Using the DeltahbhA mutant strain, a second M. tuberculosis C3-binding protein similar in size to HbhA was identified as HupB, but the role of HupB as a C3-binding protein in intact organisms remains to be determined.     

Psychiatric symptoms, type A behavior, and arrhythmias following coronary bypass

One hundred four patients undergoing coronary bypass surgery were evaluated for psychiatric symptoms and their association with postoperative arrhythmias occurring within 48 hours after surgery. Patients high in type A behavior had increased risk of ventricular arrhythmias, while those scoring relatively high in depression and anxiety had fewer atrial arrhythmias than patients low in these measures. No significant association was found between postoperative arrhythmias and obesity, heavy tobacco use, or number of bypasses. A history of arrhythmias correlated significantly with postoperative arrhythmias. Anxious or depressed patients who deny their symptoms may be at increased risk for postoperative atrial arrhythmias.     

Oncocytic change in mucoepidermoid carcinoma of the parotid gland.

Among the morphological features of an oncocytic mucoepidermoid carcinoma of the parotid salivary gland in a 78-year-old man, the oncocytes had granular eosinophilic cytoplasm that was characterized ultrastructurally by large numbers of mitochondria that displayed minimal abnormalities. Complex cell-to-cell relationship, well-developed junctival complexes, and microvillous-like surface projections suggestive of ductal differentiation were present; epidermoid features in the form of dense focal aggregates of cytoplasmic fibrils were also seen.