Changes in the smoking behavior of elderly Mexican Americans in the Southwest from 1982-1984 to 1993-1994

OBJECTIVES: The aim of this work was to examine changes in the smoking behavior of elderly Mexican Americans in the southwestern United States from the early 1980s to the early 1990s. METHODS: Data from the 1993-1994 Hispanic EPESE study (n = 2,809) on persons ages 65 to 74 and 75 to 84 residing in the five southwestern states were compared with data from the 1982-1984 Hispanic HANES study (n = 753, persons ages 55 to 74), which included a Mexican American sample from the same five southwestern states. RESULTS: Rates of current smoking in 1993-1994 for persons ages 65 to 74 were approximately half the rates for persons of the same age a decade earlier. Smoking rates for persons ages 75 to 84 in 1993-1994 were significantly lower than rates for persons ages 65 to 74 a decade earlier. Finally, rates for persons ages 65 to 74 in 1993-1994 were significantly lower than those for persons ages 55 to 64 in 1982-1984. CONCLUSIONS: Although some of the declines in smoking in recent years represent aging effects (including declines due to greater mortality among smokers), the much lower rates for same-age people (65 to 74) over the 10-year period are more significant in that they represent cohort differences. It appears that the broader public health message that is causing the general population to quit smoking is reaching the elderly Mexican American population of the Southwest.     

Nutritional status of pavement dweller children of Calcutta City

Pavement dwelling is likely to aggravate malnutrition among its residents due to extreme poverty, lack of dwelling and access to food and their exposure to polluted environment. Paucity of information about nutritional status of street children compared to that among urban slum dwellers, squatters or rural/tribal population is quite evident. The present study revealed the magnitude of Protein Energy Malnutrition (PEM) and few associated factors among a sample of 435 underfives belonging to pavement dweller families and selected randomly from clusters of such families, from each of the five geographical sectors of Calcutta city. Overall prevalence of PEM was found almost similar (about 70%) to that among other 'urban poor' children viz. slum dwellers etc., but about 16% of them were found severely undernourished (Grade III & V of IAP classification of PEM). About 35% and 70% of street dweller children had wasting and stunting respectively. Severe PEM (Grade III & IV) was more prevalent among 12-23 months old, girl child, those belonged to illiterate parents and housewife mothers rather than wage earners. It also did increase with increase of birth rate of decrease of birth interval.     

Second-trimester serum chorionic gonadotropin concentrations and complications and outcome of pregnancy

BACKGROUND: Maternal serum chorionic gonadotropin is measured to screen for fetal chromosomal abnormalities. Whether the results can also be used to predict the risk of complications or an adverse outcome of pregnancy is not known. METHODS: We reviewed the medical records of 28,743 girls and women in whom chorionic gonadotropin was measured during the second trimester of pregnancy (between July 1, 1995, and January 31, 1997), seeking information about the complications and outcome of their pregnancies. We excluded girls and women who had preexisting risk factors for complications or an adverse outcome of pregnancy. RESULTS: Higher serum chorionic gonadotropin concentrations were associated with higher rates of stillbirth (odds ratio for every increase in chorionic gonadotropin of 1 multiple of the median, 1.4; 95 percent confidence interval, 1.1 to 1.9). There was no relation between higher serum chorionic gonadotropin concentrations and the risk of gestational diabetes, premature rupture of membranes or intrauterine growth retardation or small size for gestational age (odds ratio, 1.1; 95 percent confidence interval, 0.9 to 1.2). Higher serum chorionic gonadotropin concentrations were associated with a risk of placental abnormalities (odds ratio, 1.5; 95 percent confidence interval, 1.3 to 1.7), pregnancy-induced hypertension (odds ratio, 1.4; 95 percent confidence interval, 1.3 to 1.5), and preterm delivery without pregnancy-induced hypertension (odds ratio, 1.1; 95 percent confidence interval, 1.0 to 1.2). Inclusion in certain racial or ethnic categories (black, Filipino or Pacific Islander, unknown race or ethnic group, and "other," which included those of Middle Eastern descent and Native Americans) was a better predictor of the risk of an adverse outcome than serum chorionic gonadotropin values. CONCLUSIONS: Measurements of serum chorionic gonadotropin are of little clinical value for predicting the risk of complications and the outcome of pregnancy.     

Serum thyroxine binding capacity-dependent bias in an automated free thyroxine assay

The magnitude of serum thyroxine (T4) binding capacity (sBC) dependent bias in the AXSYM free thyroxine (FT4) assay was assessed using two recently described tests. One of the tests uses a direct equilibrium dialysis (ED) FT4 assay as the reference method. The results obtained with the AXSYM method were compared with those obtained by the ED FT4 method in patient sera having a wide range of sBC. The other test involves comparison of the FT4 results obtained following dilution of sera by an inert buffer, to theoretically derived FT4 results. As serum dilution causes a predictable decrease in sBC, the demonstration of a negative bias whose magnitude increases in parallel to the dilution, is indicative of an sBC-dependent bias. The AXSYM FT4 assay exhibited a significant sBC-dependent bias. This sBC-dependent bias is likely to have been caused by the presence of significant amounts of T4 binding proteins in the assay reagents.     

Physiology of perception: cortical stimulation and recording in humans

OBJECTIVES: 1) To determine the effect of stimulus train duration (TD) on sensory perception using direct stimulation of somatosensory and visual cortices. 2) To investigate the occurrence of evoked potentials in response to stimulation that is subthreshold for perception. BACKGROUND: Studies of the mechanisms of conscious perception using direct cortical stimulation and recording techniques are rare. The clinical necessity to implant subdural electrode grids in epilepsy patients undergoing evaluation for surgery offers an opportunity to examine the role of stimulus parameters and evoked potentials in conscious perception. METHODS: Subjects included epilepsy patients with grids over somatosensory or occipital cortex. Single pulses (100 microseconds) and stimulus trains were applied to electrodes, and thresholds for perception were found. Evoked potentials were recorded in response to peripheral stimulation at intensities at, above, and below sensory threshold. RESULTS: During cortical stimulation, sensory threshold changed little for stimulus trains of 250 milliseconds and longer, but increased sharply as TD decreased below this level. Primary evoked activity was recorded in response to peripheral stimulations that were subthreshold for conscious perception. CONCLUSIONS: The results confirm a previous report of the effects of stimulus TD on sensory threshold. However, no motor responses occurred following somatosensory stimulation with short trains, as previously reported. The TD threshold pattern was similar in visual cortex. In agreement with the previous report, early components of the primary evoked response were not correlated with conscious sensory awareness.     

The effects of (+)-UH232 and (−)-DS121 on local cerebral glucose utilization in rats

Summary. Although (+)-UH232 (cis-(+)-5-methoxy-1-methyl-2-(n-dipropylamino)tetralin) and (−)-DS121 (S(−)-3-(3-(cyanophenyl)-N-n-propylpiperidine) are both preferential dopamine autoreceptor antagonists, (−)-DS121 is a more effective behavioral stimulant and dopamine releasing agent. To further compare these two agents, Sokoloff's 2-deoxyglucose autoradiography method was used to study the effects of (+)-UH232 and (−)-DS121 on regional brain energy metabolism. (+)-UH232, 30 mg/kg i.p., depressed metabolism in 37 of 65 brain regions and antagonized the stimulant effects of amphetamine. (−)-DS121, 30 mg/kg i.p., exhibited a strong, non-significant trend towards an increase in regional brain energy metabolism by itself and enhanced the stimulant effects of amphetamine. The data demonstrate dramatic differences in the effects of two autoreceptor antagonists on regional brain energy metabolism. It is concluded that, compared to (+)-UH232, (−)-DS121 is a more effective stimulant of brain energy metabolism and autoreceptor antagonist owing to its greater ability to increase DA release. Received March 5, 1998; accepted June 29, 1998     

Epidemiology of device-associated infections related to a long-term implantable vascular access device.

OBJECTIVE: To examine risk factors for, and determine the incidence of, device-associated infections among patients with an implantable vascular access device. SETTING: Grady Health System, including a 1,000-bed, inner-city, public, teaching hospital and human immunodeficiency virus (HIV), oncology, and sickle cell clinics in Atlanta, Georgia. PATIENTS: 123 consecutive patients who received a PAS-Port implantable venous access device between January 1 and June 30, 1995. DESIGN: Retrospective cohort study with follow-up > or = 1 year following device implantation. RESULTS: Underlying illnesses included HIV infection in 66 patients (median CD4 count, 24.4 cells/mm3), malignancy in 51, and sickle cell disease in 6. Mean age of patients was 43.7 years, 50% were male, and 74% were black. Thirty-one (25%) of 123 patients developed a primary or device-associated bloodstream infection (BSI), and 3 of the 31 patients experienced two separate episodes of infection. The overall rate of infection was 1.23 primary BSIs per 1,000 device days. Patients with cancer had a lower rate of infection than those with HIV infection, but the difference was not statistically significant (0.96 vs 1.50 BSIs/1,000 device days; relative risk, 0.58; 95% confidence interval, 0.27-1.26). Subgroup analysis of patients with different malignancies indicated that infection rates differed according to type of cancer, and there was a trend for heterogeneity across the different cancer strata (P=.06). Gram-positive pathogens accounted for 60% of the pathogens recovered. Six (19%) of 31 patients who developed an infection did so within the first 14 days after implantation. In 11 (32%) of the 34 BSIs, the port required removal; two patient deaths were attributed to device-associated bacteremias (0.072 deaths/1,000 device days). CONCLUSIONS: Approximately one fourth of patients who had a vascular access device implanted developed a primary BSI, but the overall infection rate (per 1,000 device days) was relatively low, even among those with HIV infection. Primary BSI rates in patients with vascular access devices appeared to differ according to the specific underlying illness.     

Acetaminophen-induced cytotoxicity in cultured mouse hepatocytes: effects of Ca(2+)-endonuclease, DNA repair, and glutathione depletion inhibitors on DNA fragmentation and cell death.

Hepatotoxic alkylation of mouse liver cells by acetaminophen is characterized by an early loss of ion regulation, accumulation of Ca2+ in the nucleus, and fragmentation of DNA in vitro and in vivo. Acetaminophen-induced DNA cleavage is accompanied by the formation of a "ladder" of DNA fragments characteristic of Ca(2+)-mediated endonuclease activation. These events unfold well in advance of cytotoxicity and the development of necrosis. The present study utilized cultured mouse hepatocytes and mechanistic probes to test whether DNA fragmentation and cell death might be related in a "cause-and-effect" manner. Cells were isolated by collagenase perfusion, cultured in Williams' E medium for 22-26 hr, and exposed to acetaminophen. Aurintricarboxylic acid, a general Ca(2+)-endonuclease inhibitor, and EGTA, a chelator of Ca2+ required for endonuclease activation, significantly decreased DNA fragmentation at 6 and 12 hr and virtually abolished cytotoxicity. N-Acetylcysteine also eliminated DNA fragmentation and cytotoxicity. 3-Aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase-stimulated DNA repair, failed to alter the amount of DNA fragmentation at 6 hr but substantially increased acetaminophen cytotoxicity in hepatocytes at 12 hr. With the exception of when DNA repair was inhibited by 3-aminobenzamide, Ca2+ accumulation in the nucleus, DNA fragmentation, and hepatocyte death varied consistently and predictably with one another. Collectively, these findings suggest that unrepaired damage to DNA contributes to acetaminophen-induced cell death in vivo and may play a role in necrosis in vivo.