The effect of dietary fiber supplementation in man. I. Modification of eating habits

Six subjects were studied for an 8-week period that consisted of a 3-week control period, followed by a 3-week period during which their daily diets were supplemented with 3 oz of a high fiber breakfast food, All-bran, and a final 2 weeks on their regular diet. Daily diet records of food intake were recorded and analyzed for seven dietary constituents; carbohydrates, proteins, fats, cholesterol, fiber, alcohol, and total calories. The most significant change in eating behavior due to the fiber food supplementation was a decrease in eating eggs, butter, and breakfast meats. These foods were most often replaced because all six subjects chose to eat the major portion of All-bran during breakfast. An increase in milk and fruit also occurred during the supplemented feeding. These particular foods were added to make All-bran more palatable and served to increase carbohydrate and protein intake. Five subjects added the supplement to the between meal-time intake and thus caused an increase in total daily caloric intake. At lunch and dinner few foods were altered with no particular pattern of substitution. Notwithstanding the knowledge that increased fiber content may have beneficial effects, none of the subjects modified his eating behavior to include even 1 oz of a high fiber food daily after the experimental period was concluded. Thus behavior modification by forced diet intake of a high fiber breakfast food resulted in definite diet pattern changes that did not persist following the experimental period.     

Treatment of idiopathic membranous nephropathy

In a retrospective study of the effect of treatment in biopsy-proved idiopathic membranous nephropathy, 91 adults and 12 children were followed for periods up to 29 years after clinical onset (mean, 6.5 years). Forty-four were treated with corticosteroids, 15 with corticosteroids and immunosuppressants; 44 had no treatment and served as a control group. Clinical cure and improvement were significantly greater in the treated than in the nontreated group (P less than 0.01). The recurrence rate, occurrence of renal failure and probability of death were significantly greater in the nontreated group, although some of these patients eventually showed improvement. Prognosis was better in patients who responded to therapy. These data strongly suggest that steroid therapy is beneficial in patients with membranous nephropathy.     

Favorable effects of oral maintenance digoxin therapy on left ventricular performance in normal subjects: echocardiographic study

Left ventricular performance was assessed with echocardiography in 10 normal subjects before and during maintenance therapy with digoxin (0.5 mg/day orally) in the basal state and after acute pressure loading with intravenously administered phenylephrine. During digoxin therapy, despite a decrease in mean heart rate of 5 beats/min in the basal state, mean left ventricular ejection fraction increased from 74 +/- 2 to 79 +/- 1 percent (standard error, P less than 0.03); percent shortening of a left ventricular minor dimension increased from 37 +/- 2 to 41 +/- 1 percent (P less than 0.04) and the mean rate of left ventricular dimension shortening increased from 5.66 +/- 0.22 to 6.31 +/- 0.23 cm/sec (P = 0.05). During acute pressure loading with phenylephrine there was no change in mean heart rate after digoxin and mean ejection fraction increased from 69 +/- 3 to 75 +/- 2 percent; mean percent shortening increased from 33 +/- 2 to 38 +/- 2 percent; mean rate of shortening increased from 5.46 +/- 0.32 to 6.48 +/- 0.33 cm/sec and mean normalized rate of shortening increased from 1.11 +/- 0.06 to 1.29 +/- 0.05 sec-1 (all P less than 0.01). In a few subjects the response to digoxin did not coincide with the mean data for the whole group. This variability was largely due to difficulties in exactly matching heart rate between the control and digoxin studies. These data (1) support the concept that long-term oral digoxin therapy exerts a positive inotropic effect on the normal left ventricle, and (2) demonstrate the usefulness of echocardiography in nonivasive assessment of the effects of drugs on left ventricular performance.     

Hepatitis C--associated glomerular disease in liver transplant recipients

Hepatitis C virus (HCV) infection may be associated with extrahepatic illness including renal disease. We investigated the clinical and virological characteristics of three patients who developed a mesangial proliferative and sclerosing glomerulopathy alone or in association with membranoproliferative glomerulonephritis after liver transplantation for end-stage liver disease secondary to HCV infection. Using polymerase chain reaction technology and the IgM RIBA assay, viral load, genotype and IgM antibody response to HCV in the setting of glomerulonephritis was evaluated. Within 1 year of transplantation, the patients showed decreased renal function, proteinuria and recurrent hepatitis C liver disease. Likewise, HCV viral load increased following transplantation, whereas the viral genotypes remained unchanged. Although the first patient presented with classic type II cryoglobulinemia in association with glomerulonephritis, the second patient developed an IgM directed specifically against the hepatitis C core antigen. The third patient developed a low-titered IgM directed against the hepatitis C core antigen with rheumatoid factor activity but without cryoglobulinemia. All of the patients show IgM in glomerular capillary walls by biopsy. One patient has shown a clinical response to interferon (IFN) alfa-2b therapy without evidence of hepatic allograft rejection. The second and third patients have not responded to IFN or developed hepatic rejection. This study suggests that HCV-associated glomerulonephritis may complicate liver transplantation in conjunction with the production of increased amounts of IgM of variable specificity. The posttransplant setting may provide a unique situation in which to investigate the specific requirements for the onset of renal disease.     

Ventral pallidal GABA-A receptors regulate prepulse inhibition of acoustic startle

Prepulse inhibition (PPI) of the acoustic startle reflex occurs when a weak auditory stimulus is presented 30-500 ms before the startling stimulus. Previous studies have shown that PPI is modulated by GABAergic projections from the ventral striatum to the ventral pallidum (VP). To evaluate the anatomical and pharmacological substrates of pallidal modulation of PPI, we measured PPI after intrapallidal infusion of GABA-B and GABA-A antagonists. Intrapallidal infusion of the GABA-B antagonist, 2-OH-saclofen (0.025-0.10 microgram), did not significantly alter PPI, startle amplitude or peak startle latency. Infusion of the GABA-A antagonist, picrotoxin (0.02-0.08 microgram), into the medial or central VP significantly reduced PPI; this effect appeared somewhat weaker after picrotoxin infusion into the lateral VP and was absent after infusion into the adjacent fundus striatum (FS). There was no significant effect of picrotoxin infusion into any of the VP sites or FS on startle amplitude or peak startle latency. Thus, ventral striato-pallidal GABAergic modulation of PPI appears to be mediated solely by GABA-A receptors and this modulatory substrate is predominantly distributed across the medial and central portions of the VP.     

Regulation of nuclear factor-kappa B and its inhibitor I kappa B-alpha/MAD-3 in monocytes by Mycobacterium tuberculosis and during human tuberculosis

Blood monocytes from patients with active tuberculosis are activated in vivo, as evidenced by an increase in the stimulated release of proinflammatory cytokines, such as TNF-alpha, and the spontaneous expression of IL-2R. Further, monocytes from patients demonstrate an augmented susceptibility to a productive infection with HIV-1 in vitro. Mycobacterium tuberculosis and its components are strong signals to activate monocytes to production of cytokines. In this study we examined the basis of activation of monocytes during active tuberculosis and by M. tuberculosis. We found a constitutive degradation of I kappa B-alpha, the major cytoplasmic inhibitor of nuclear factor kappa B (NF-kappa B), in freshly isolated PBMC and monocytes from patients with tuberculosis. In contrast, I kappa B-alpha levels in PBMC and monocytes from healthy subjects or from patients with nontuberculous pulmonary conditions were intact. Further, by electrophoretic mobility shift assay, NF-kappa B was activated in monocytes from tuberculous patients. The expression of I kappa B-alpha gene, which is responsive to activation by NF-kappa B, was up-regulated in PBMC and monocytes from patients, but not in mononuclear cells from healthy subjects or those with nontuberculous lung diseases. By contrast, the expression of other adherence-associated early genes, such as IL-8 and IL-1 beta, was not up-regulated in PBMC of tuberculous patients. Further, M. tuberculosis and its tuberculin, purified protein derivative, induced the degradation of I kappa B-alpha and the expression of I kappa B-alpha mRNA, and purified protein derivative induced the activation of NF-kappa B in monocytes.     

Research in long-term care: what do we know, what can we use?

Urinary incontinence is a significant problem for nurses in long-term care. However, there is sufficient research to show that it is a treatable condition, Risk and associated factors have been identified. Impairments in mobility and cognition play a role in the development of incontinence and must be addressed in any strategy used to prevent incontinence from occurring in dry residents. Nurses must become comfortable in reading research reports and applying the findings to their facility. Using assessment techniques, including a voiding record and determining whether an individual is appropriate for one of the several behavioral techniques, are critical nursing actions. Administrative support including the delegation of authority and provision of resources is necessary as nurses change practice from traditional methods to evidence-based practice.