Effects of smoking and smoking abstinence on cognition in adolescent tobacco smokers.

BACKGROUND: In adult animals and humans, nicotine can produce short-term cognitive enhancement and, in some cases, neuroprotection. Recent work in animals, however, suggests that exposure to nicotine during adolescence might be neurotoxic. We tested for evidence of acute and chronic effects of tobacco smoking on cognition in adolescents who smoked tobacco daily and were compared with adolescent nonsmokers. METHODS: Verbal working memory, verbal learning and memory, selective, divided, sustained attention, mood, symptoms of nicotine withdrawal, and tobacco craving were examined in 41 adolescent daily smokers and 32 nonsmokers who were similar in age, gender, and education. Analyses were controlled for general intelligence, reading achievement, parental educational attainment, baseline affective symptoms, and lifetime exposure to alcohol and cannabis. RESULTS: In adolescent smokers, cessation of tobacco use increased tobacco craving, symptoms of nicotine withdrawal, and depressed mood. Adolescent smokers were found to have impairments in accuracy of working memory performance irrespective of recency of smoking. Performance decrements were more severe with earlier age of onset of smoking. Adolescent smokers experienced further disruption of working memory and verbal memory during smoking cessation. As a group, male smokers initiated smoking at an earlier age than female smokers and were significantly more impaired during tests of selective and divided attention than female smokers and nonsmokers. CONCLUSIONS: Adolescent daily tobacco smokers experience acute impairments of verbal memory and working memory after smoking cessation, along with chronic decrements in cognitive performance that are consistent with preclinical evidence that neurotoxic effects of nicotine are more severe when exposure to nicotine occurs at earlier periods in development.     

Effect of {beta}-carotene and wheat bran fiber on colonic aberrant crypt and tumor formation in rats exposed to azoxymethane and high dietary fat

The typical high-fat, low-fiber American diet promotes coloncancer. An alternative to radical changes in dietary habitsis to reinforce the diet with cancer protectors. Experimentsto evaluate the effects of ß-carotene in the presenceof high fat and low and high dietary levels of wheat bran fiberwere designed using the Fischer-344 rat colon cancer model.Rats (20/group), were given either high fat (20% w/w), low wheatbran fiber (1% w/w) diets, or high fat (20% w/w) high wheatbran fiber (8% w/w) diets, with different levels of ß-carotene.After 2 weeks of adaptation, half were given two weekly s.c.injections of azoxymethane (AOM, 15 mg/kg body wt); and halftwo weekly s.c. injections of saline. Six weeks later, fiverats from each dietary group were killed to evaluate the comparativeeffect of different dietary regimens on the induction of colonaberrant crypt foci (ACF). The remaining rats were maintainedon their respective diets for an additional 20 weeks to examinethe effect on colon tumor incidence. The total number of ACE/ratin the low-fiber groups declined from 44.0 ± 4.18 to12.8 ± 1.95 in response to increasing amounts of ß-carotenefrom 1 to 20 mg/kg diet. A similar progressive reduction intotal ACF/rat was also seen in the high-fiber groups (20.8 ±2.92 to 9.2 ± 0.58). ACF did not develop in the saline-exposedgroups. Similarly colon tumor incidence declined from 73% to20% in high-fiber groups and from 27% to 13% in low-fiber groupsIn response to increasing amounts ß-carotene from1 to 20 mg/kg diet. The results showed that ß-caroteneand wheat bran, individually and when combined, protected thecolon in rats consuming high-fat, western-style diets from ACFand benign or malignant tumor formation.     

A brief review for orthopedic surgeons: Fatigue damage (microdamage) in bone (its determinants and clinical implications)

Bone modeling can slowly strengthen bones to keep their strains below bone's microdamage (MDx) threshold. When that condition is satisfied the slow basic multicellular unit (BMU)-based remodeling can usually repair the little MDx that occurs anyway, and some always does. While this arrangement minimizes fatigue fractures of whole bones or trabeculae, they can still happen if: (A) drugs, disease, or dead bone impair MDx repair; (B) if bone loads increase faster than the sluggish modeling can strengthen bone to meet the new loads, and/or faster than remodeling can repair the increased MDx; (C) if a cyst, tumor, or surgery removes enough bone to let strains in the remaining bone reach or exceed the MDx threshold; (D) if abnormal properties of bone as a material cause too much MDx to repair; (E) if altered modeling and remodeling thresholds cause an osteopenia that lets normal activities cause bone strains in or above the MDx threshold range; (F) or if strains in the bone supporting a load-bearing implant reach or exceed bone's MDx threshold. Received for publication on Dec. 15, 1997; accepted on April 7, 1998     

An Analysis of 37 Reversals on 504 Biliopancreatic Surgeries over 12 Years

Of 504 biliopancreatic diversions, 37 patients (7%) had to be reversed. There were many underlying causes for the nutritional compromise that preceded each reversal, but nearly two-thirds were due to either the nausea/hyperemesis syndrome or to protein malnutrition and anemia. Poor patient compliance with respect to supplements was a major contributory factor. The procedure can be reversed by either a proximal enteroenterostomy or restoration of anatomical continuity. The simpler enteroenterostomy, the method of choice, was done in 70% of the cases. There are specific indications for the more complex anatomical restoration. Reversals have proved to be successful in correcting the nutritional defects.