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According to information-processing models of alcohol use, alcohol expectancies constitute representations in long-term memorythat may be activated in the presence of drinking-related cues, thereby influencing alcohol consumption. A fundamental implication of this approach is that primed expectancies should affect drinking only for those individuals who possess the specific expectancies primed. To test this notion, in the present study, participants were initially assessed on three distinct domains of positive alcohol expectancies. Approximately one week later, they completed an ad libitum drinking study during which only a single expectancy domain (sociability) was primed in the experimental condition. Consistent with predictions, following exposure to sociability primes, but not control primes, individuals with stronger expectancies that alcohol would enhance sociability uniquely showed increased placebo consumption of nonalcoholic beer. These results, which demonstrate the moderating role of compatibility between the specific content of primes and that of underlying expectancies, offer new, direct support for memory network-based models of drinking behavior.

Previous research has shown that primes associated with alcohol influence behavior consistent with specific alcohol expectancies. The present study examined whether exposure to marijuana-related primes and marijuana expectancies interact to produce similar effects. Specifically, the present study examined whether marijuana primes and marijuana expectancies regarding cognitive and behavioral impairment interact to influence performance on an arithmetic task.Two independent samples (N = 260) of undergraduate students (both marijuana users and nonusers) first completed measures of marijuana-outcome expectancies associated with cognitive and behavioral impairment and with general negative effects (Sample 2). Later in the semester, participants were exposed to marijuana-related (or neutral) primes and then completed an arithmetic task.Results from Sample 1 indicated that participants who were exposed to marijuana-themed magazine covers performed more poorly on the arithmetic task if they expected that marijuana would lead to cognitive and behavioral impairment. Results from Sample 2 indicated that, for marijuana users, cognitive and behavioral impairment expectancies, but not expectancies regarding general negative effects, similarly moderated arithmetic performance for participants exposed to marijuana-related words.Results support the hypothesis that the implicit activation of specific marijuana-outcome expectancies can influence cognitive processes. Implications for research on marijuana are discussed.

Twin and adoption Studies have convincingly established that a substantial proportion of variance in the risk for alcohol use and dependence is attributable to additive genetic influences (for reviews see Heath, 1995; McGue, 1999). However, the identification of genes explaining unique variance in alcohol-related behavior has proven difficult, largely because alcohol use and dependence reflect complex, multigenic behaviors that are heterogeneous across individuals and subject to environmental as well as genetic influence (Dick and Foroud, 2003; Li, 2000; Schuckit, 2000). Instances in which individual genes predict significant variability in the risk for alcohol dependence can provide unique opportunities to evaluate how specific genetic factors act additively or interactively with other genetic or environmental factors to influence alcohol-related behavior (Heath et al., 2001; Li et al., 2001). The 2 genes with the strongest associations with alcohol use and dependence are ALDH2 (12q24) and ADH1B (4q22). These genes encode the major enzymes involved in alcohol metabolism and have functional variations that are protective against alcohol dependence (Edenberg, 2007; Wall, 2005). The major pathway of alcohol elimination involves conversion of ethanol to acetaldehyde by alcohol dehydrogenase (ADH) enzymes, followed by oxidation of acetaldehyde to acetate via mitochondrial aldehyde dehydrogenase (ALDH) (Edenberg, 2007; Thomasson and Li, 1993). The ADH1B*2 allele encodes an ADH enzyme subunit whose catalytic properties lead to more rapid conversion of ethanol to acetaldehyde, whereas the ALDH2*2 allele encodes an ALDH enzyme subunit that is functionally inactive, impairing the conversion of acetaldehyde to acetate (for reviews see Li, 2000; Thomasson and Li, 1993; Wall, 2005). Theoretically, these variants protect against the risk for alcohol dependence by promoting increased transient acetaldehyde during alcohol metabolism and, in turn, decreased consumption (Edenberg, 2007; Wall, 2005). The ALDH2*2 allele, found exclusively among individuals of northeast Asian heritage (Chinese, Koreans, and Japanese; Goedde et al., 1992), shows the strongest association with drinking behavior. Individuals with ALDH2*2 show significantly lower rates of alcohol use, heavy drinking and alcohol dependence compared to those without this variant (Chen et al., 1996; Higuchi et al., 1996; Luczak et al., 2001, 2004; Takeshita and Morimoto, 1999; Thomasson and Li, 1993; Thomasson et al., 1991; Wall et al., 2001). A meta-analysis comprising 15 case–control studies and over 4,500 participants showed that ALDH2*2 heterozygotes have approximately one-fourth the risk for alcohol dependence compared to ALDH2*1 homozygotes (Luczak et al., 2006), and case–control and population studies have found only 3 individuals homozygous for ALDH2*2 who were classified as alcohol-dependent (Chen et al., 1999; Luczak et al., 2004). ALDH2*2 is associated with heightened blood acetaldehyde and cardiovascular responses following alcohol ingestion (Peng et al., 1999, 2007; Wall et al., 1997), as well as greater self-reported sensitivity to alcohol (Duranceaux et al., 2008), lending support for a protective mechanism involving increased acetaldehyde levels and alcohol sensitivity among those with ALDH2*2. The ADH1B*2 allele is highly prevalent among northeast Asians and moderately prevalent in Caucasians, in particular those of Jewish and Russian ancestry (Goedde et al., 1992; Hasin et al., 2002). ADH1B*2 is associated with a decreased risk of alcohol dependence in both Asian and Caucasian populations (e.g., Chen et al., 1999; Higuchi, 1994; Luczak et al., 2006; Thomasson et al., 1991; Whitfield et al., 1998). In Asian samples, significant protective effects of ADH1B*2 have been observed after controlling for ALDH2 status in some (Chen et al., 1999; Thomasson et al., 1991) but not all studies (e.g., Luczak et al., 2004, 2006; Peng et al., 2002). The aforementioned meta-analysis showed that the protective effects of ADH1B*2 were somewhat greater for individuals who also had the ALDH2*2 allele (Luczak et al., 2006), suggesting possible interactive effects between these genes. ADH1B*2 has not been associated with measured acetaldehyde levels in vivo (e.g., Peng et al., 2007), but is associated with increased sensitivity to alcohol as measured by skin flushing, self-reported physiologic symptoms and post-intoxication body sway (Chen et al., 1998; Cook et al., 2005; Duranceaux et al., 2006; Takeshita et al., 1996; Wall et al., 2005). In some research, effects of ADH1B*2 on alcohol sensitivity are limited to individuals with ALDH2*2 (Cook et al., 2005; Takeshita et al., 2001), again suggesting the possibility of interactive effects. Much of the research on ALDH2 and ADH1B has utilized case–control studies that rely predominantly on adult, male participants and focus on dichotomous diagnostic outcomes. Research with younger populations may be important given evidence of possible age differences in the effects of ALDH2 and ADH1B on drinking behavior (Carr et al., 2002; Doran et al., 2007; Hendershot et al., 2005), consistent with increasing genetic influences on alcohol use during the transition from adolescence to adulthood (e.g., Koopmans and Boomsma, 1996; Pagan et al., 2006). It has also been suggested that the examination of multiple, continuous phenotypes is preferable to a focus on dichotomous diagnostic variables (e.g., Dick et al., 2008; Hutchison et al., 2004). For example, in samples with relatively lower rates of alcohol dependence, restricted variability in diagnostic outcomes may obscure genetic effects, whereas examination of subclinical phenotypes may reveal these effects (e.g., Irons et al., 2007). This study evaluated additive and interactive effects of ALDH2 and ADH1B genotypes on alcohol-related outcomes in a mixed-gender sample of Chinese and Korean young adults. Whereas most studies of Asian-American young adults have included participants at or above legal drinking age, this study included participants 18 years and older, most of whom were under age 21. This study also emphasized evaluation of continuous phenotypes, including heavy episodic drinking, alcohol sensitivity, hazardous drinking, and alcohol-related consequences. Genetic effects were estimated using generalized linear models while controlling for ethnicity, thus allowing estimation of unique contributions of cultural and genetic influences on drinking behavior.

Alarge body of research has shown that an individual's response to alcohol serves as a marker of risk for alcohol-use disorders and alcohol-related consequences. Individual differences in response to alcohol have been shown to influence risk for alcohol dependence (Schuckit and Smith, 2001) and to relate to increased heavy alcohol use (Conrod et al., 2001). Alcohol response has also been found to be heritable (Heath and Martin, 1991; Heath et al., 1999; Viken et al., 2003) and to differentiate between children of alcoholics and controls (Schuckit, 1985; Schuckit and Gold, 1988). These findings lend support to the construct of alcohol response as an endophenotype for alcohol-use disorders (Schuckit et al., 2007). The present study examined subjective response to alcohol as a marker of alcoholism risk in African Americans. Considerable research evidence shows that the alcoholism risk process differs for African Americans and whites. Results from the National Comorbidity Survey Replication data found that the lifetime prevalence of alcohol-use disorders was lower for African Americans (9.5%) compared with whites (13.4%) and that African Americans have a lower lifetime risk of developing a substance-use disorder (Breslau et al., 2006). Additionally, in college populations, African Americans report lower rates of heavy drinking compared with whites (O'Malley and Johnston, 2002). However, despite lower rates of alcohol-use disorders, there is some evidence for increased persistence of alcohol dependence and more frequent engagement in heavy drinking occasions in African Americans in mid-adulthood (Dawson, 1998). Because of the ethnic differences in polymorphisms of the alcohol metabolizing enzymes (alcohol dehydrogenase [ADH] and aldehyde dehydrogenase [ALDH]), response to alcohol has been studied across a variety of racial groups (e.g., Asian: Luczak et al., 2002; Native American: Garcia-Andrade et al., 1997; Latino: Schuckit et al., 2004). However, despite recent findings showing that ADH polymorphisms (e.g., ADH1B*3) may be linked to decreased risk for alcoholism in African Americans (Ehlers et al., 2001, 2003), studies have not examined how response to alcohol relates to drinking behavior in this group. Individual differences in acute response to alcohol are frequently assessed through alcohol-challenge studies, where participants report on their subjective feelings of intoxication and/or physiological measures of response are obtained (e.g., heart rate) following a specified dose of alcohol. Such studies provide a fairly direct assessment of response and also allow for the examination of alcohol response on both the ascending and descending limbs of the blood alcohol curve. In their review and synthesis of the literature, Newlin and Thompson (1990) argued for the importance of examining response separately for the ascending and descending limbs of the blood alcohol curve. Alcoholism risk would be associated with dampened response to the sedating effects of alcohol (King et al., 2002; Schuckit, 1980, 1984; Schuckit and Smith, 2001) on the descending limb and with increased response to the stimulating effects (Conrod et al., 1995, 2001; Erblich and Earleywine, 2003; Finn et al., 1990; King et al., 2002) on the ascending limb. Despite the advantages of the alcohol-challenge paradigm, such studies are time consuming, expensive, and—in the United States—restricted to individuals age 21 or older. Schuckit and colleagues (1997a) developed a self-report measure designed to assess response to alcohol (Self-Rating of the Effects of Alcohol scale [SRE]) that can be used when alcohol-challenge studies are not feasible. Recently, Schuckit and colleagues (2007) showed that the SRE prospectively predicts alcohol-related problems and heavy use. One goal of the present study is to test the convergent validity of the SRE in an African-American sample, demonstrating that it is associated with acute response to alcohol in an alcohol challenge, as well as self-reported drinking behavior and a family history of alcoholism. The present study had two primary aims. Our first aim was to test the association between acute subjective response to alcohol and drinking behavior in African Americans. We hypothesized that increased stimulation from alcohol on the ascending limb and diminished sedation on the descending limb would be related to having higher levels of drinking, experiencing alcohol-related problems, meeting lifetime criteria for an alcohol-use disorder, and having a family history of alcoholism. Our second aim was to examine the convergent validity of the SRE in an African-American sample. We hypothesized that higher scores on the SRE (i.e., reporting drinking more drinks to experience the effect) would be associated with having increased drinking behavior, experiencing decreased acute sedation on the descending limb of the breath alcohol curve, experiencing alcohol-related problems, having an increased likelihood of an alcohol-use disorder, and having a family history of alcoholism. Based on the content of the SRE items (e.g., passing out, slurring speech), we hypothesized that the SRE would not be related to acute stimulation on the ascending limb of the breath alcohol curve.

This article examines recently noted major epidemiologic trends in peptic ulcer disease and their implications for the elderly. Aspects of the natural history, diagnosis, management, and outcome of peptic ulcer and its complications that are peculiar to the elderly, together with the effects of aging on responses to the commonly used drugs, are reviewed. Diagnostic vigilance by physicians for atypical presentations of serious disease is seen as the factor most likely to reduce morbidity and mortality.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause acute diffuse injury to the gastroduodenal mucosa, and also cause chronic focal ulcers that may bleed or perforate without warning symptoms. Acute and chronic lesions are distinct, are pathogenetically different, respond differently to drugs, and require different management strategies. The principal rationale for antiulcer therapy in NSAID users is to prevent or reduce potentially fatal outcomes; to date no evaluated drug meets this criterion for efficacy. Antacids and H2-receptor antagonists, based on open uncontrolled studies, appear to heal both gastric and duodenal ulcers, and maintain them healed during continued NSAID use; larger gastric ulcers show delayed healing with conventional doses of H2-receptor antagonists during NSAID therapy. No such delay occurs with omeprazole therapy. The suggests that if NSAID-associated gastric ulcers are treated with H2-receptor antagonists, larger doses should be given for longer periods. In patients with no pre-existing ulcer disease, H2-receptor antagonists given prophylactically prevent duodenal but not gastric ulcers; sucralfate does the same. In individuals without peptic ulcer disease taking NSAIDs, misoprostol, given as prophylaxis, reduces the development of gastric ulcers; its beneficial effects on ulcer healing or symptoms during continued NSAID therapy, or its ability to prevent duodenal ulcers or ulcer complications, are not established. Because of diarrhea, the 400 micrograms/day dosage is recommended, especially in the elderly.

Στόχοι: Οι μεταβλητές της κοινωνικοοικονομικής κατάστασης (SES) για το εκπαιδευτικό επίπεδο και τη λειτουργικότητα στην εργασία βρέθηκε ότι εμφανίζουν αρνητική συσχέτιση με τη χρήση αλκοόλ. Η παρούσα μελέτη εξέτασε προοπτικά τη σχεση ανάμεσα στις μετρήσεις λειτουργικότητας, τις προσδοκίες από το αλκοόλ και την εμπλοκή με το αλκοόλ. Υποστηρίχθηκε ότι οι προσδοκίες λειτουργούν ως διαμεσολαβητής για τη σχέση ανάμεσα στις εκπαιδευτικές / επαγγελματικές επιδόσεις και τη συμπεριφορά κατανάλωσης αλκοόλ. Υποθέσαμε ότι οι αλλαγές στη λειτουργικότητα του νεαρού ενηλίκου σχετίζονται με αλλαγές σε κοινωνικό περιβάλλον και/ή τη διαθεσιμότητα παραγόντων ενίσχυσης που δεν σχετίζονται με το αλκοόλ, οι οποίοι με τη σειρά τους επηρεάζουν την αναμενόμενη ενίσχυση από το αλκοόλ. Συμμετέχοντες και σχεδιασμός: Οι συμμετέχοντες ήταν 172 νεαροί ενήλικες από μια εν εξελίξει διαχρονική μελέτη για τη μακροπρόθεσμη πορεία της θεραπείας των εφήβων από την τοξικοεξάρτηση. Για αυτές τις αναλύσεις χρησιμοποιήθηκαν τα στοιχεία από το follow up που πραγματοποιήθηκε στο έκτο και όγδοο έτος. Το δείγμα που είχε λάβει θεραπεία (n=100) εντοπίστηκε από θεραπευτικά προγράμματα διαμονής για εφήβους. Ένα δείγμα από την κοινότητα (n=72) εντοπίστηκε με ίδια χαρακτηριστικά κατά την εισαγωγή, όσον αφορά το οικογενειακό ιστορικό χρήσης ουσιών και την κοινωνικο-οικονομική κατάσταση. Ευρήματα: H ανάλυση πολλαπλής συσχέτισης έδειξε ότι η εκπαίδευση είχε μια μοναδική διαχρονική σχέση με την προσδοκία από τη χρήση αλκοόλ τόσο για το δείγμα που είχε λάβει θεραπεία όσο και εκείνο από την κοινότητα, περισσότερο από οποιαδήποτε προηγούμενη χρήση και προσδοκία από τη χρήση αλκοόλ. Οι μεταβλητές για την απασχόληση δεν εμφάνισαν διαχρονική σχέση με τη χρήση ή με την προσδοκία από το αλκοόλ για καμία ομάδα δείγματος. Οι προσδοκίες επηρέασαν τη σχέση εκπαίδευσης / κατανάλωσης αλκοόλ για το δείγμα που είχε λάβει θεραπεία μόνο. Συμπεράσματα: Αυτά τα αποτελέσματα παρουσιάζουν έναν από τους τρόπους με τους οποίους οι αλλαγές στη λειτουργικότητα μπορεί να διαφοροποιούν την εμπλοκή με το αλκοόλ μέσα στο χρόνο: μεταβάλλεται η προσδόκιμη ενίσχυση από το αλκοόλ. Λέξεις κλειδιά: αλκοόλ, προσδοκία από τη χρήση αλκοόλ, εκπαίδευση, απασχόληση.

The present study tested convergent, discriminant, and incremental validity of implicit and explicit measures of alcohol and smoking cognitions. College-aged participants (n = 264) completed questionnaire measures of alcohol and smoking expectancies and behavior. Participants also completed the Implicit Association Test (IAT; Greenwald, McGhee, & Schwartz, 1998) for alcohol and smoking on two occasions, approximately 1 month apart. Psychometric qualities of these IATs were evaluated. Modest associations were found between implicit and explicit measures for the same substance. Both implicit and explicit measures had unique associations with use. Discriminant validity was stronger for alcohol measures than for smoking measures. These results support the utility of the IAT as a technique for assessing implicit associations about alcohol and smoking. They also provide some evidence that smoking motivations may make unique contributions to alcohol use.

The present study constructs and provides initial validation for a measure of positive expectancies for drinking and driving for use with adolescents and young adults (PEDD-Y). In Study 1, items were generated through open-ended responses from high school- and college-age youth. Data collected from a 2nd sample of college students (n = 404) identified a 29 item, 4 factor questionnaire. Two of the PEDD-Y factors (Convenience, Avoiding Consequences) explained additional variance in drinking and driving behavior above and beyond other cognitions about drinking and driving. Study 2 extended these results to a high school sample (n = 185). Study 3 demonstrated test-retest reliability of the PEDD-Y in college-age youth (n = 165). These results provide initial evidence for the utility of the PEDD-Y in assessing drinking and driving risk in adolescents and college students.

Renal solitary fibrous tumors (SFTs) have been reported infrequently. We report a 76-year-old man with a left renal mass that had previously been shown radiographically to be stable, but was now growing. Grossly, the mass measured 12 cm, was poorly circumscribed, and invaded beyond the renal capsule. Approximately 10% of the neoplasm consisted of haphazardly arranged spindle cells admixed with dense collagenous bands, which is typical of benign SFT. However, the remainder of the mass was composed of pleomorphic, spindled sarcoma cells with frequent mitoses and foci of necrosis. Immunohistochemically, we observed CD34 labeling in the benign SFT component with loss of expression in the sarcomatous component, focal labeling for Bcl-2 protein in both areas, and absence of labeling for cytokeratin, renal cell carcinoma marker, S100 protein, CD117, and muscle markers in both areas. To our knowledge, this is the first reported case of malignant renal SFT, likely representing transformation from a histologically documented benign SFT component.

The term "gastropathy", and discussion surrounding the adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) on the gastrointestinal (GI) tract, suggests that most of the complications arise from injury to the gastric mucosa, resulting in gastric ulcers that develop complications. The commonest GI complication is bleeding, which results principally from thrombocytopathy or impaired platelet function in the presence of various underlying GI conditions, including but not confined to antecedent peptic ulcer disease, and in some cases ulcers caused by NSAIDs. In unselected cases, bleeding as a result of aspirin or NSAID may occur early in the course of treatment, much of it predictable from a careful history, taken to identify well-defined risk factors, including previous peptic ulcer disease, GI bleeding, or concomitant treatment with steroids, anticoagulants, or anti-platelet drugs. Only in the presence of such risk factors is NSAID use likely to be associated with a serious GI complication. Although GI complications are common in such cases, attributability of the event solely to NSAIDs is low. Attributability of the complication to the drug is highest when NSAID use is the sole risk factor: the estimated incidence of complications in this setting is only about 10% of all NSAID-associated GI complications. In estimating the likely outcome of therapy, the risk factors identifiable from the history in each case before treatment are more important than the choice of NSAID. Independently analysed, the VIGOR and CLASS trials showed that use of rofecoxib or celecoxib caused fewer clinical ulcers and bleeding, but much of the bleeding observed did not arise from ulcers or from sites proximal to the ligament of Treitz. This suggests that the main value of these drugs is the absence of thrombocytopathy: their safety is substantially reduced by concomitant treatment with low doses of aspirin. This paper analyses the separate roles of COX 2-selective agents, H. pylori eradication, and concomitant aspirin prophylaxis or treatment with acid-suppressant drugs.

Drinking in elementary school, despite its low base rate, has been shown to predict alcohol use in middle school (Wilson, Battistich, Syme, & Boyce, 2002), which in turn predicts alcohol abuse or dependence in young adults (Guo, Collins, Hill, & Hawkins, 2000). The authors report 1 of the 1st examinations of the relationship between personality and psychosocial learning risk factors and drinking behavior among elementary school students. Fifth-grade students completed measures of disinhibition, positive and negative alcohol expectancies, and drinking. MIMIC modeling, tests of mediation, and tests of moderation were completed to test these relations. It was found that disinhibition and positive alcohol expectancies were each related to drinking in 5th graders. Disinhibition moderated the relation between positive alcohol expectancies and drinking in some cases. Mediation was not supported.

This study examined sample bias related to parental consent procedures in school-based survey research on alcohol-related behavior. Alcohol prevalence and severity of use estimates from a high school student survey using traditional-active parental consent (N = 1,429) were compared with estimates from 2 student surveys using alternative parental consent procedures (passive consent; N = 2,210 and N = 3,231). Traditional-active parental consent procedures resulted in underrepresentation of lifetime drinkers. Furthermore, traditional-active parental consent procedures resulted in lower levels of high-risk drinking, and this bias was most evident for Caucasians and both boys and girls. Findings accentuate the need for administrators, policymakers, and researchers to consider the impact consent procedure related bias may have on results and interpretation of findings from school-based substance use research.

This study tested whether obtaining a driver's license was associated with increases in alcohol and other drug involvement and changes in alcohol-related cognitions for youth, and whether drinking and driving behavior increased with driving experience.Confidential, anonymous surveys were conducted at two time points (fall, spring) with students at four high schools in San Diego county (N = 2,865, 51% female). Data were collected on alcohol, cigarette and marijuana use, license status, alcohol use by peers, attitudes towards drinking and driving and drinking and driving behaviors.Nondrivers (60%), new drivers (obtained a license between Time 1 and Time 2) and experienced drivers (26%) were compared on study variables at both time points and over time. Initially obtaining a driver's license was associated with increased frequency of substance use. Results were not significant for quantity of alcohol use, frequency of heavy drinking or perceived alcohol use norms. Attitudes towards drinking and driving reflected an increase in the perceived dangerousness of this behavior for new drivers. Drinking and driving behavior during the last 30 days increased with increased driving experience.The results indicate a number of changes in substance involvement after obtaining a driver's license. However, initially this transition may also indicate a period of protection against drinking and driving. These results may have implications for the target and content of drinking and driving interventions.

Although many youths reduce or stop drinking without formal treatment, little is known of cognitive mechanisms influencing such alcohol change efforts during adolescence. The present research examines alcohol cessation expectancies of adolescents in the context of a cognitive-behavioral de-escalation model of alcohol use. Grounded in Developmental Social Information Processing theory (Coie and Dodge, 1998) and empirical findings on adolescent self-change process, alcohol cessation expectancies are defined as anticipated consequences of ceasing or decreasing drinking. The present study is the first to develop a measure of adolescent alcohol cessation expectancies.A 23-item measure was administered to 5,446 high school students (51% female) as part of a survey on alcohol and drug use.Using data for adolescents who reported any history of alcohol use (N = 3,098), exploratory and confirmatory factor analyses identified expectations of global changes and social effects. Expectancy factor structure was examined within drinking groups (light, moderate, heavy drinkers) and as a function of age and change goal (reduction and cessation). Predictive validity of the expectancy measure was examined for youth who reported efforts to decrease or stop drinking during the prior year. Our results suggest greater differentiation in cessation expectancies with increased alcohol experience. The findings also provide evidence that youth cessation expectancies uniquely predict alcohol change efforts over and above alcohol use and problems.Youths maintain several types of alcohol reduction/cessation expectancies predictive of behavioral change efforts. Articulation of this construct for youth contributes to an understanding of mechanisms involved in adolescent efforts to reduce or stop drinking.

Heartburn is a common, often disabling condition. Twenty percent of adults exhibit symptoms at least once weekly. Few obtain complete satisfactory relief of their symptoms without the simultaneous implementation of significant lifestyle modifications and appropriate pharmacologic intervention. Poor sleep and chronic symptoms impair the QoL in 25% to 30% of such cases. Nocturnal symptoms are more troublesome, more difficult to treat, and are often manifested by extraesophageal symptoms. Several patients, however, unknown to their physicians continue to experience heartburn, despite lifestyle changes and taking prescription drugs. Adequate acid suppression is currently essential to effective management of the condition.

A bovine collagen matrix is sometimes used as a delivery medium during direct intratumoral injection of a chemotherapeutic agent. The bovine collagen enhances the dose and duration of local drug delivery and limits systemic toxicity. Although this strategy is advocated as a means of easy and effective delivery of chemotherapeutic drugs, the associated risks are not well defined. We report the case of a 71-year-old man with hepatocellular carcinoma who underwent weekly intratumoral injections of cisplatin in a bovine collagen matrix. During the third injection, he suddenly and unexpectedly underwent cardiac arrest and died. An autopsy disclosed diffuse occlusion of the pulmonary microcirculation by bovine collagen. The collagen emboli were associated with an inflammatory infiltrate typical of bovine collagen–induced hypersensitivity. This case identifies a fatal complication of intratumoral chemotherapy injections using a bovine collagen matrix, which does not appear to have been previously reported. This case underscores the valuable role of the traditional autopsy examination as a means of identifying possible complications of novel oncologic strategies, which are being rapidly developed and implemented.

Although the majority of youth and adults resolve alcohol problems without formal treatment, we know little about the strategies used by youth in their efforts to decrease alcohol use. Recent studies have begun to address change efforts that adolescents report being helpful in cutting down or stopping alcohol use. The current study seeks to improve our understanding of adolescent change processes in alcohol use by examining the perceptions of high school students.As part of a secondary alcohol intervention study of high school students (ages 12-18; 51% male), 1069 participants completed an anonymous supplemental questionnaire on change strategies for cutting down and stopping alcohol use. Based on content analysis of youth-generated responses, a classification system consisting of nine broad categories was developed (e.g., informal-interpersonal supports, formal aids, alternative activities). Participant responses were independently coded by two raters trained to criterion. Cases with full agreement (n = 934; 96%) were used for data analyses of methods for cutting down drinking, stopping drinking, and strategies recommended for a friend.The five most frequently youth-generated change strategies to alter drinking were environmental exposure management (e.g., avoid drinking situations, 19%); informal interpersonal supports (e.g., talk to a friend, 18%); formal aids (e.g., peer support group, counselor, 17%); behavioral self-management (e.g., limit consumption, 14%); and alternative activities (e.g., recreation, sports, 10%). Whereas informal interpersonal supports were consistently endorsed for all change situations, behavioral self-management strategies were viewed as more useful for reduction of drinking and formal aids more critical for cessation efforts. Some differences were observed in youth-generated strategies for changing their own drinking compared with efforts to help friends, with environmental changes (e.g., reducing exposure to risk situations and people, formal aids) more often considered when changing youth's own behavior, and strategies reflecting a need for personal change (e.g., education) recommended to others.Our findings support theoretical conceptualizations of alcohol and drug problem resolution that accommodates multiple pathways to recovery. The normative information about specific change strategies generated by youth may further aid in the design of interventions more acceptable for adolescents.

Objective To clarify race differences in eating disorder risk factors and symptoms, by comparing Caucasian and African American samples on the factor structures, intercorrelations, and mean levels of endorsement on a set of risk and symptom measures. Method A sample of 300 Caucasian and 200 African American undergraduates completed measures of eating and thinness/dieting expectancies, the Three-Factor Eating Questionnaire (TFEQ), and the BULIT. Results The factor structures of each measure were invariant across race. Intercorrelations among the measures generally did not differ across race. On the three expectancy measures predictive of symptomatology, two of three scales of the TFEQ, and the BULIT, African American women had lower mean scores than Caucasian women. Socioeconomic status did not account for the results: in this sample, it was unrelated to race and correlated with only 1 of 20 measures. Discussion The factor-based meaning of these measures appears to be consistent across race. The measures correlate similarly across race, suggesting that the risk process may be similar for both races, but African American women endorsed significantly fewer risk factors and fewer symptoms. © 2002 by Wiley Periodicals, Inc. Int J Eat Disord 32: 326–334, 2002.

Between January 1997 and February 2000, 101 fine-needle pancreatic aspirates were obtained. After a cytologic diagnosis was made, possible molecular alterations were determined on the 94 aspirates with adequate tissue using a molecular panel (K-ras, p53, and DPC4 [MAD4] genes). The 94 aspirates were categorized as follows: diagnostic of adenocarcinoma, 48 (51%); atypical (suggestive of, but not diagnostic of, adenocarcinoma), 19 (20%); negative for adenocarcinoma, 25 (27%); diagnostic of a neoplasm other than adenocarcinoma, 2 (2%). Clinical follow-up revealed that 3 patients (12%) with negative cytologic diagnoses and 12 patients (63%) with atypical cytologic diagnoses had adenocarcinoma. Of 63 with a final diagnosis of adenocarcinoma, 42 (67%) had an alteration in at least 1 of the genes analyzed. In contrast, only 2 (6%) of 31 patients without adenocarcinoma had an alteration in 1 gene on the panel. Overall, the molecular analyses supported the diagnosis of adenocarcinoma in 6 (32%) of 19 aspirates originally diagnosed as atypical by cytology alone. A molecular panel that includes the Kras, p53, and DPC4 (MAD4) genes correlates with and can supplement traditional cytologic diagnosis of pancreatic fine-needle aspirates.

The socio-economic status (SES) variables of education level and occupational functioning have been found to be correlated negatively with alcohol use. The present study examined prospectively the relationship between these functioning measures, alcohol expectancies and alcohol involvement. We propose that expectancies function as a mediator of the relationship between educational/occupational attainment and drinking behavior. We hypothesized that changes in young adult functioning are linked to changes in social context and/or the availability of non-alcohol reinforcers, which in turn affect the reinforcement expected from alcohol.Participants were 172 young adults from an ongoing longitudinal study of long-term clinical course of adolescent substance use treatment. Data from 6- and 8-year follow-ups were used in the present analyses. The treated sample (n=100) was recruited from in-patient substance abuse treatment programs for adolescents. A community sample (n=72) was matched on family history of substance abuse and SES at intake.A cross-lag panel analysis indicated that education had a unique longitudinal relationship with expectancy for both the treated and community sample, over and above previous alcohol use and expectancy. Occupational variables did not have a longitudinal relationship with alcohol use and expectancy for either sample. Expectancies mediated the education/drinking relationship for the treated sample only.These results suggest one means through which changes in functioning may alter alcohol involvement over time: alteration of the reinforcement expected from alcohol.

Much controversy surrounds the interaction of Helicobacter pylori infection and the use of Aspirin (ASA) or non-aspirin nonsteroidal anti-inflammatory drugs (NANSAIDs). The issue is comprised of many components, best dealt with singly. In summary, the severity of drug-associated gastritis, but not its incidence or prevalence, is influenced by infection prior to ASA or NANSAID therapy. Furthermore, the severity of dyspeptic symptoms appears worse in infected drug users. Both Chemical and Helicobacter gastritis, by increasing neutrophils in the tissue, lead to ulcers, although the induction of prostaglandin synthesis by inflammation in some circumstances may also be mildly protective. More ulcers are found in Hp+ve than Hp-ve users of NSAIDS, but ulcers in the stomach may heal more easily with acid suppressive therapy in infected patients. Eradication of infection is beneficial in aspirin users and in those beginning NANSAID therapy. Adaptation to aspirin is confined to Hp-ve cases. However, in long-term users of NANSAIDs, H. pylori eradication does not appear to speed ulcer healing, reduce recurrence, or prevent complications. These are best achieved by long-term maintenance therapy with a proton-pump inhibitor drug.

The mechanisms by which aspirin(ASA) and non-steroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal symptoms are poorly understood. They probably arise from several causes, including direct and indirect mucosal injury, exacerbation of underlying peptic ulcer disease or non-ulcer dyspepsia, exacerbation of Helicobacter pylori gastritis, and possibly motility disorders. No single form of therapy has been generally successful. Because, in most cases, symptoms abate fairly rapidly with continued treatment, there is little evidence that benefit associated with any symptom-directed drug therapy is superior to placebo beyond 4 weeks. Exceptions may be the subsets of patients with pre-existing ulcer disease or heartburn, exacerbated by the NSAID therapy, who usually benefit from acid-suppressive drug treatment. Different NSAIDs vary in the frequency with which their use leads to gastrointestinal(GI) complications such as haemorrhage, perforation, obstruction, or the symptomatic ulcers from which about 40% of the complications arise. Most gastroduodenal ulcers heal over time, albeit more slowly, with conventional doses of any of the available anti-ulcer drugs. Maintenance therapy may be needed in many patients who continue NSAID therapy. Anti-ulcer drugs have not, thus far, been shown to be more effective than placebo in preventing ulcer complications or their recurrence. The use of COX-2-selective inhibitors appears, in outcome studies, to reduce gastrointestinal bleeding, including bleeding from ulcers, but it is not established that the ulcers protected were caused by NSAIDs, as distinct from ulcers exacerbating or recurring from antecedent peptic ulcer disease. To-date, perforation or obstruction have not been shown to be affected by selective COX-2 inhibitor drugs. If the major problem giving rise to severe NSAID complications is pre-existing peptic ulcer disease, it may yet emerge that the most effective approach will be the use of proton pump inhibitor drugs, for the duration of NSAID therapy, in a small subset of high-risk patients. Most other low-risk patients may not need any special care. Co-morbid conditions have a major impact on outcome of NSAID therapy. Morbidity or even death attributable solely to NSAIDs is probably small in normal patients, and requires little in the way of prophylaxis.

Knowledge of treatment response for alcohol and drug problems among adults is mounting; less is known about long-term outcome for adolescents who receive treatment for alcohol and drug problems. The current study examined youth substance involvement over 4 years (using five waves of data collection) following treatment for alcohol and drug abuse.A cohort of youth (N = 162, 60% male) treated during adolescence (mean age = 16 years) was followed into young adulthood, a period associated with stabilization of alcohol use patterns and elevated risk for life problems secondary to both alcohol and drug use. Participants (14-18 years old) were consecutive admissions to inpatient adolescent alcohol and drug treatment centers in San Diego that were abstinence focused and based on the 12-step approach.Alcohol and other drug use were reduced during the 4 years posttreatment, with the exception of nicotine. The greatest prevalence reduction occurred for stimulants; modest changes were evident in alcohol and marijuana use. Nicotine was the most commonly used substance throughout the 4 years after treatment. Several distinct substance involvement trajectories were evident during the 4 years following treatment.Alcohol and drug use patterns during the 4 years following treatment highlight both changes and diversity in substance involvement as youth make the transitions from middle to late adolescence and into young adulthood. Findings demonstrate the importance of identifying transitional periods and the need for alternative intervention strategies that may help the progression of this population into young adulthood.

This study tested several predictions of the "acquired preparedness" model in both black and white samples of college students. The acquired preparedness model holds that trait disinhibition affects alcohol-related learning and, ultimately, alcohol use. This model maintains that the reward focus typical of disinhibited individuals increases the likelihood of forming overly positive expectancies about the effects of alcohol. Alcohol expectancy, then, acts as a mediator of the relationship of disinhibition and drinking behavior.Participants (N = 479, 341 women) were 279 white and 200 black college students. Self-reported alcohol expectancy, disinhibition and drinking behavior were assessed. Covariance structure analysis was used to test hypotheses separately for each sample, controlling for socioeconomic status.Black participants scored significantly lower on disinhibition, expectancy and drinking. However, invariance testing indicated that the relationships between these variables were not different across groups. Results were consistent with the stated hypotheses in both samples--alcohol expectancy functioned as a mediator of the disinhibition-drinking relationship. Results did not differ across expectancy content.These results provide support for the validity of the acquired preparedness model. Despite mean differences in risk and drinking levels between black and white samples, psychosocial learning appears to mediate the influence of disinhibition on drinking for both groups.

To compare the gastrointestinal (GI) toxicities of various nonsteroidal anti-inflammatory drugs (NSAIDs), it is first necessary to dismantle the imprecise entity "NSAID gastropathy" into its component conditions, and understand their pathogenesis. In this article, toxicities are reviewed only in so far as they affect the upper GI tract, the site of approximately 80% of GI injuries caused by NSAIDs. The phenomena discussed are platelet dysfunction, causing hemorrhage from various lesions, including but not confined to ulcers; various mucosal injuries, ranging from small erosions to large ulcers; and "complications," such as bleeding or perforations, causing admission to hospital, that may arise from ulcers but may also arise from other lesions. Ulcers, when complicated, may either be those caused by an NSAID or "peptic" ulcers that preceded NSAID therapy (having a high prevalence in the population) and gave rise to complications resulting from NSAID effects on platelets, tissues, or biologic processes, for example, healing, necrosis/apoptosis, leukocyte adherence, vasoconstriction, or generation of free radicals. NSAIDs have been compared in various ways, including fecal blood loss, endoscopic lesion development, prospective preclinical cohort studies measuring perforations, ulcers, and bleeds, post-marketing surveillance studies, and studies of the incidence of serious adverse events in populations followed in large databases linked to each individual patient record with regard to drug consumption and outcome. All methods show considerable differences between NSAIDs. Modern studies on the relative toxicities of NSAIDs are summarized and reviewed, and a number of marketed and emerging drugs that appear less toxic than classic NSAIDs are identified.

Nonsteroidal anti-inflammatory drug (NSAID)-associated gastrointestinal (GI) toxicity is a broad topic encompassing symptoms as well as severe GI complications. GI bleeding and perforation are the 2 overlapping components that account for the majority of deaths and disability associated with these drugs. Abnormal gastric endoscopic profiles as well as symptoms such as heartburn, pain, and dyspepsia are common in NSAID users, but no correlation has been found between these factors and the occurrence of the more severe complications; therefore, neither symptoms nor endoscopic observations can necessarily be considered reliable predictors of future outcomes. Confounding factors can increase the risk of complications, and specific NSAIDs vary in the magnitude and type of risk attending their use. Recent studies have focused on the contribution of nonprescription NSAIDs to total complications, and combined with evidence suggesting that the risk is greatest during the first month of NSAID use, it is apparent that NSAID toxicity is an acute as well as a chronic problem.

Vitamin B12 deficiency can result in neurological, psychiatric, and hematological symptoms. The neurological symptoms, which may vary from person to person, depend on the degree and duration of the...

Researchers rely on adolescents' self-reports of alcohol consumption and alcohol-related problems, despite little evidence concerning their validity. We assessed the reliability and validity of adolescents' self-reports, employing collateral validation and focusing on the understudied transitional years of early adolescence.Subjects were 214 boys and 247 girls who participated in school-wide surveys that assessed drinking, drunkenness and alcohol-related problems each year for 3 years. These measures were validated by collateral (peer) reports and by separate, 7-day drinking calenders. Internal consistency and test-retest reliability were also assessed.Results replicated findings with older adolescents that drinking/drunkenness and alcohol-related problems fall on two partially overlapping dimensions. Scales assessing each dimension had moderate to high internal consistency and high test-retest stability. Correlations with collateral reports were relatively strong for the drinking/drunkenness scale, moderate for a dichotomous variable reflecting the presence or absence of alcohol-related problems, and more modest for the alcohol-related problems scale. Correlations with diary reports of drinking behavior were strong for drinking/drunkenness. Results generally replicated across gender and over time.Researchers can have some confidence in the reliability and validity of early adolescents' survey self-reports, particularly of alcohol consumption (alcohol-related problems occurred with low base rates, perhaps limiting validity coefficients). Because drinking/drunkenness and alcohol-related problems shared 30% of their variance, factors other than consumption (e.g., personality factors) apparently influenced the experience of alcohol-related problems.

Until recently, peptic ulcer disease implied lifelong susceptibility to symptomatic, asymptomatic or complicated ulcer recurrences. Only about 50% of the ulcers seen endoscopically ever become symptomatic. Asymptomatic ulcers appear ciinically unimportant, except in the setting of aspirin (ASA) or NSAID use, where they may lead without warning to fatal complications. Until recently, ulcer disease could not be cured medically: no drug has been shown to prevent ulcer complications occurring in patients taking ASA/ NSAIDs. Low-dose maintenance therapy with H2-antagonists reduces recurrences and complications, but is expensive and requires indefinite use. Other anti-ulcer drugs have not been studied enough to conclude with confidence that they are similarly effective. Over 80% of recurrences are infrequent and can be treated when they occur.n 20% of ulcer patients have 3 recurrences/yr, ulcer complications, or such poor health that recurrence might prove fatal. Ulcers recurring during maintenance therapy rarely complicate and heal with increasing and maintaining dosage. Eradication of H. Pylori (HP) infection, while difficult, abolishes most recurrences without maintenance therapy. Maintenace therapy is therefore indicated principally when HP can not be eradicated. Surgery is rarely required for uncomplicated idsease.

Evidence has accumulated that nonsteroidal anti-inflammatory drugs (NSAIDs) cause clinically important gastroduodenal ulcers. The pathogenesis, which involves the impairment of mucosal resistance to injury in an acid-peptic environment, is multifactorial and controversial. Ulcers caused by NSAIDs can occur either in mucosa inflamed because of infection with Helicobacter pylori or in histologically normal mucosa. The use of these drugs has been linked to an unexpectedly high incidence of ulcer complications, and a history of peptic ulcer disease is common in such cases. Nonsteroidal anti-inflammatory drugs thus appear both to exacerbate an underlying peptic diathesis and to cause de novo ulcers. The association between the use of these drugs and ulcer complications is supported by ulcer prevalence data from cross-sectional studies, and by data from case-controlled and cohort studies, and from randomized, experimental trials. Drug-induced gastric ulcers have been prevented by misoprostol, but not by H2 blocker therapy. Several therapies have been reported to promote ulcer healing despite continued use of NSAIDs, but adequate controlled trials have not been done. Small gastric and duodenal ulcers readily heal, whereas larger gastric ulcers require vigorous and prolonged therapy. The relative efficacies of various therapies in preventing ulcers, healing ulcers, or preventing complications remain to be established.

Merkel cell (neuroendocrine) carcinoma is a small round blue cell malignant neoplasm that primarily presents in the skin. The diagnosis of Merkel cell carcinoma in a pleural fluid is challenging because of the morphological similarity to many other malignant neoplasms. Immunohistochemical stains can be essential to establish the diagnosis of Merkel cell carcinoma.

Dr. Fang: The patient, a 33-yr-old white fewas admitted to George Washington University Hospital on January 3, 1978, with a 10 mo history of diarrhea and a 20 lb weight loss. In March, 1977, she noted a change from her normal pattern of one stool daily to passage of 1-2 brownish semiformed stools/day. The frequency of the stools increased to five-six times a day in September, 1977. She did not use drugs or drink alcohol. By October, 1977, she had developed epigastric cramps with intermittent nausea. Occasional vomiting began in November, 1977, and at one time, she vomited coffee ground material. She drank bottled water shipped from Arkansas. Her private physician obtained a barium enema and an oral cholecystogram in October, both of which were normal. An upper gastrointestinal series revealed an enlarged duodenal bulb and a dilated jejunum with thickened jejunal folds. No ulcers were seen. She was hospitalized on November 23, 1977, for a work-up of the diarrhea. Physical examination revealed occasional high-pitched bowel sounds and mild diffuse abdominal tenderness. The stool was hemoccult negative and negative for fat by Sudan stain. The hematocrit was 45; white blood count was 7,700; transaminases were normal; serum albumin was 4.2 g/dl; serum cholesterol was 194 mg/dl. A small bowel biopsy specimen obtained at the duode

A 15-year-old girl with hereditary spherocytosis was admitted for evaluation of recurrent pleural effusions containing amylase in high concentration and was found to have biliary obstruction, pancreatitis, and a congenital duplication of the duodenum attached to an accessory lobe of the pancreas via the duct of Santorini, a unique entity. Successful surgical management of these disorders included common duct clearance and anastomosis of the duplication to the adjacent duodenum.

Endoscopic distinction between ulcers and erosions is difficult. Consequently, existing literature, which must be taken at face value, may be misleading. Nevertheless, from published studies most gastric and duodenal ulcers associated with nonsteroidal antiinflammatory drugs appear to heal on antacids or H2-antagonists. Sucralfate appears useful for duodenal but not gastric ulcers. Continuing nonsteroidal antiinflammatory drugs does not prevent or delay healing of duodenal or small gastric ulcers; their effects on large gastric ulcers remain uncertain. Thus far, only full doses of H2-antagonists, or their combinations with antacids, have been shown to heal ulcers and prevent recurrences. Ulcer recurrences and complications have occurred in small numbers of patients on maintenance doses of H2-antagonists. Available antiulcer drugs (antacids, H2-antagonists, sucralfate) reduce severe acute injury when taken before or with nonsteroidal antiinflammatory drugs. They also reduce ulcerlike symptoms due to nonsteroidal antiinflammatory drugs. Inexplicably, chronic prophylaxis with H2-antagonists for 4 wk or more appears ineffective in preventing gastric ulcers, although duodenal injury is reduced. As the efficacy of available prophylactic therapy (H2-antagonists, sucralfate, and antacids) has not been established, routine use in all cases seems unjustified at present.

In the present study we explored whether the presence or absence of symptoms could provide a reliable way of assessing the adequacy of control of gastric secretion in patients with Zollinger-Ellison syndrome who were treated medically. Over a 5-yr period, 26 Zollinger-Ellison syndrome patients were entered into a prospective study which examined the presence or absence of symptoms that are associated with gastric hypersecretion, the presence or absence of upper gastrointestinal pathology, and the degree of control of gastric acid secretion. During their last admission, 15 of the 26 patients (58%) were symptomatic, but post-drug gastric acid secretion for the 2 h before the next dose of medication was not significantly different from that in asymptomatic patients. This lack of correlation between the presence or absence of symptoms and post-drug gastric acid secretion was evident for the group as a whole, as well as for 8 of 12 patients who underwent multiple admissions. Of 23 patients who underwent upper gastrointestinal endoscopy or x-rays, or both, on their last admission, 12 had pathology. Post-drug gastric acid secretion was less in patients without pathology than in those with pathology. Furthermore, in patients in whom post-drug gastric acid secretion was ≤ 10 mEq/h, the criterion of acceptable control used in this study, pathology did not occur. These findings demonstrate that the presence or absence of symptoms cannot be used to assess the adequacy of medical control of gastric acid secretion in patients with Zollinger-Ellison syndrome. In our opinion, maintenance of post-drug gastric acid secretion ≤ 10 mEq/h for the 2 h before the next dose of medication is an acceptable criterion for long-term control of gastric secretion in patients with Zollinger-Ellison syndrome.

Sixty-one cases of the Zollinger-Ellison syndrome, encountered over a 2-year period, have been treated with cimetidine, half of them for over 1 year. Two-thirds of the patients responded to 300 mg of the drug every 6 hr by mouth. Others required up to 600 mg every 6 hr. In adequate doses the drug was highly effective: it controlled pain and dyspepsia, restored weight, abolished diarrhea, and allowed healing of ulcers and other inflammatory conditions. Missed or reduced doses led to rapid return of symptoms. Progression of the basic neoplastic process, with associated secretory drive, was unimpeded. Patient acceptance of the drug was 100%, and apart from minor transient abnormalities, gynecomastia (5 cases) and liver dysfunction (3 cases), which resolved while treatment continued, no serious adverse effects were seen. Of 61 patients 48 are still on the drug, 3 who were well controlled were treated surgically, 5 died for reasons unrelated to therapy, and 5 had significant problems. The drug provides an alternative to total gastrectomy and can be recommended with confidence for the suitably selected patient. The drug was also beneficial in some cases of the short bowel syndrome, systemic mastocytosis, and endogenous hyperhistaminemia due to leukemia.

In a study of changes in digestive enzymes after massive intestinal resection and the mechanisms by which such changes occur, rats were sacrified 4 wk after removal of the proximal two-thirds of the small intestine. Alterations in the mucosal levels of sucrase, enterokinase, and dipeptide hydrolase (L-leucyl-L-alanine substrate) were examined in the light of associated changes in protein. DNA and wet mucosal weight, measured in standardized gut segments from various regions of intestine. Metabolic studies showed that normal growth patterns were reestablished after the operation but significant elevations in stool weight and fecal nitrogen occurred in the second postoperative week, falling towards normal by the 4th wk. In standard gut segments wet weight of mucosa, protein, and DNA rose, especially in distal segments, DNA increasing disproportionately. Mucosal levels of the proximally distributed and membrane-bound enzymes, sucrase and enterokinase, showed similar patterns of change: when enzyme activity was expressed in terms of the total per segment, proximally there were considerable increases in both enzymes, but, expressed in terms of specific activity, that of sucrase fell and that of enterokinase was unaltered. By contrast, the largely soluble and more distally distributed dipeptide hydrolase increased more in distal segments and the increases in total activity were accompanied by lesser increases in specific activity. However, in spite of increases in total activity, enzyme activity per milligram DNA fell by over 50% in postanastomotic segments. Subcellular distribution studies showed no change in the percentage of the total activity which was membrane-bound and zymograms confirmed that no new dipeptide hydrolase had appeared after resection. It is concluded that increases in the segmental totals of various enzymes seen after resection are achieved by disproportinate increases in the number of mucosal cells per segment and that the greatest change in a particular enzyme occurs in the region where the enzyme is normally found in highest concentration.