Psychosocial and environmental correlates of violence perpetration among African-American urban youth.

PURPOSE: To ascertain the proportion of youths involved in acts of violence; to examine individual, social, and environmental factors associated with perpetration; and to determine the relationship among victimization, witnessing, and perpetration of violence. METHODS: A cross-sectional survey was completed by 349 volunteer males and females, aged 9-15 years, 96% of whom were African-American. The youths were recruited from recreation centers associated with 10 public-housing communities in an eastern city. Survey instruments included the Child Health and Illness Profile, Survey of Children's Exposure to Community Violence, and other standardized questionnaires. Statistical analyses included Chi-square, correlation, regression, and test for linear trends. RESULTS: Half of the youths self-reported at least one act of violence perpetration, with similar distributions among males and females. One-third of the youths reported both personal victimization and the witnessing of violent events. Victim and witness status were moderately correlated. Individual risk behaviors and victimization made significant contributions to perpetration status. Further analysis demonstrated a linear relationship between acts of perpetration and number of victimization events. CONCLUSIONS: Participation in problem behaviors may place youths in circumstances in which they may be victim, witness, or aggressor. The chronic and high levels of community violence to which many youths are exposed are likely to contribute to an individual's participation in acts of violence.

Parent-youth concordance regarding violence exposure: relationship to youth psychosocial functioning.

PURPOSE: To examine the relationship between parent-youth concordance with regard to youth exposures to violence and youth psychosocial functioning, including perpetration of violence, distress symptomatology, and social skillfulness. METHODS: A battery of self-report questionnaires were completed by 333 parent-youth dyads residing in urban public housing developments. Concordance status (<50%, 50-80%, and >80%) was based on dyad agreement regarding youth's violence exposures. The relationship between concordance and psychosocial factors was assessed by a series of analyses of covariance tests. RESULTS: Parents underestimated the extent to which their children were victims of or witnesses to violence and suffered from distress symptoms. Low concordance status was associated with youth perpetration of violence and distress symptomatology, as well as lower self-esteem and problem-solving skillfulness. Youth in the low concordance group characterized their families as exhibiting less involvement, open communication, and parental monitoring. CONCLUSIONS: Concordance between parents and youth is associated with youth psychosocial competence and strong family functioning. Findings underscore the need to incorporate a parent component in primary and secondary violence-prevention programs. Further examination of the processes which contribute to concordance may enhance our ability to prevent youth engagement in violence and its untoward psychosocial sequelae.

Nonsurgical management of gallstone disease.

Cholelithiasis is a common disease in the United States associated with significant morbidity. Surgical treatment with cholecystectomy has been increasing with a significant cost to the health care system. Surgical management is not without risk. Cholecystectomy has also been associated with a significant morbidity and mortality in elderly patients. Cholecystectomies are often performed unnecessarily in gallstone patients for nonspecific symptoms. Many patients with nonspecific pain, which may have a psychogenic component, continue to experience similar pain after cholecystectomy. There are problems in determining the symptom status of patients. Patients who believe surgery will relieve symptoms may maximize their symptoms, whereas patients who are reluctant to undergo surgery may minimize their symptoms. Although cholecystectomy is the mainstay of gallstone treatment, bile acid therapy and, if available, ESWL and topical dissolution are nonsurgical treatment alternatives in selected patients. In selected cases, in particular in the elderly and in other patients at increased risk from surgery, nonsurgical management offers lower morbidity and mortality than does operative treatment. The decision for surgical versus nonsurgical management should be based on both objective selection criteria and patient choice.

Dopamine D2-receptor isoforms expressed in AtT20 cells inhibit Q-type high-voltage-activated Ca2+ channels via a membrane-delimited pathway.

Dopamine D2 receptors both acutely and chronically inhibit high-voltage-activated Ca2+ channels (HVA-CCs). Two alternatively spliced isoforms, D2L (long) and D2S (short), are expressed at high levels in rat pituitary intermediate lobe melanotropes but are lacking in anterior lobe corticotropes. We stably transfected D2L and D2S into corticotrope-derived AtT20 cells. Both isoforms coupled to inhibition of Q-type calcium channels through pertussis toxin-sensitive G proteins. Thus, we have created a model system in which to study the kinetics of D2-receptor regulation of Ca2+ channels. Rapid inhibition of HVA-CCs was characterized using a novel fluorescence video imaging technique for the measurement of millisecond kinetic events. We measured the time elapsed (lag time) between the arrival of depolarizing isotonic 66 mM K+, sensed by fluorescence from included carboxy-X-rhodamine (CXR), and the beginning of increased intracellular Ca2+ levels (sensed by changes in indo 1 fluorescence ratio). The lag time averaged 350-550 ms, with no significant differences among cell types. Addition of the D2-agonist quinpirole (250 microM) to the K+/CXR solution significantly increased the lag times for D2-expressing cells but did not alter the lag time for AtT20 controls. The increased lag times for D2L- and D2S-transfected cells suggest that at least a fraction of the Ca2+ channels was inhibited within the initial 350-550 ms. As this inhibition time is too fast for a multistep second messenger pathway, we conclude that inhibition occurs via a membrane-delimited diffusion mechanism.

Hereditary angioedema. Complex symptoms can make diagnosis difficult.

Although rare, hereditary angioedema is a potentially life-threatening disorder that can be difficult to diagnose. It is characterized by a deficiency in C1 esterase inhibitor (C1 INH). Manifestations include gastrointestinal, subcutaneous, and respiratory edema. Factors that trigger episodes vary. Symptoms typically last 48 to 72 hours, but they can last 4 hours to 1 week. Treatment includes prophylactic therapy with attenuated androgens or antifibrinolytic agents. Acute episodes can be medical emergencies, and airway management is a major concern. The treatment of choice in an acute episode is administration of plasma concentrate of C1 INH.

Dilation of the influenza hemagglutinin fusion pore revealed by the kinetics of individual cell-cell fusion events.

We have monitored kinetics of fusion between cell pairs consisting of a single influenza hemaglutinin (HA)-expressing cell and a single erythrocyte (RBC) that had been labeled with both a fluorescent lipid (Dil) in the membrane and a fluorescent solute (calcein) in the aqueous space. Initial fusion pore opening between the RBC and HA-expressing cell produced a change in RBC membrane potential (delta psi) that was monitored by a decrease in Dil fluorescence. This event was followed by two distinct stages of fusion pore dilation: the flux of fluorescent lipid (phi L) and the flux of a large aqueous fluorescent dye (phi s). We have analyzed the kinetics of events that occur as a result of transitions between a fusion pore (FP) and a solute permissive fusion pore (FPs). Our data are consistent with a fusion pore comprising six HA trimers.

Searching for resilience among African-American youth exposed to community violence: theoretical issues.

PURPOSE: The exploration of resilience factors which may moderate the impact of violence exposure on African-American youth living in high-crime neighborhoods has received scant research attention. Yet, how these adolescents appraise and cope with exposures to violent events has implications for social adaptation and resilience. This article attempts to organize diverse literatures and cross-disciplinary perspectives into an integrative framework for the study of resilience among African-American youth exposed to violence. METHODS: The search for protective factors requires critical examination of both the ethnocentric bias in traditional developmental frameworks and the decontextualization of sociocultural and environmental influences on adaptation. A paradigmatic refocusing is necessary, one which highlights the capacities for coping and adaptation resulting from the engagement of personal resources, family strengths, and community support systems. RESULTS: To facilitate this research, an appraisal and coping model of violence is presented. This model emphasizes the need to identify and assess the appraisal processes and coping strategies initiated by African-American families as they attempt to thrive amidst community violence. CONCLUSIONS: Protective factors, operative at different junctures and within different ecologies, may reduce the likelihood of maladaptation or promote social competence in African-American youth exposed to violence. This search for resilience must address the meaning of competence and mechanisms of familial and external support that are salient within the African-American community.

Simultaneous imaging of intracellular [Ca2+] and pH in single MDCK and glomerular epithelial cells.

The interrelationships between changes in intracellular calcium concentration ([Ca2+]i) and intracellular pH in Madin-Darby canine kidney cells and kidney glomerular epithelial cells exposed to various stimuli were analyzed simultaneously using a new design of a fluorescence video microscope. Cells were double labeled with indo 1 and SNARF 1 dyes and were excited simultaneously at 350 and 540 nm. Images at four emission wavelengths were captured simultaneously at 405, 475, 575, and 640 nm at 30 frames/s for the two ratio dyes. SNARF sensitivity to pH between 6.5 and 8.0 was unchanged by [Ca2+]i. The SNARF ratio maps were used to correct the pH-dependent changes in the calculation of local cell calcium. NH4Cl loading produced the expected alkalinization and a concurrent rise in [Ca2+]i. When the NH4Cl was removed and the cells became acidic, a second rise in [Ca2+]i was recorded. Both changes in [Ca2+]i were from intracellular stores since they persisted in the absence of extracellular calcium. The findings demonstrate the need for pH correction of indo 1 recordings.

Calcium regulation of intracellular pH in pituitary intermediate lobe melanotropes.

The regulatory activities of both intracellular calcium ([Ca2+]i) and intracellular pH (pHi) have greatly increased interest in the study of their interdependence. We have designed an epifluorescence video microscope that will image the fluorescence from two ratio dyes, indo-1 (for [Ca2+]i) and SNARF-1 (for pHi) at video rates. We examined primary cultures of pituitary intermediate lobe melanotropes loaded with both dyes. After experimentation, cells were positively identified by fluorescence immunohistochemistry. K(+)-induced depolarization of melanotropes produced increases in [Ca2+]i due to activation of L-type Ca channels. A secondary Ca2+ peak or oscillations were often seen. After treatment with carbonyl cyanide m-chlorophenylhydrozone, depolarization produced a rise in intracellular [Ca2+]i as well as oscillations. After thapsigargin or cyclopiazonic acid treatment, depolarization produced a primary Ca2+ elevation, but the secondary Ca2+ changes disappeared. This suggests that the oscillations were due to Ca2+ release from an endoplasmic reticulum type of intracellular store. All of these increases in [Ca2+]i were also directly coupled to a rise in intracellular H+. The close association between intracellular Ca2+ and H+ suggests that the observed pHi changes were due to the release of H+ upon binding of Ca2+ to intracellular buffers. This direct obligate coupling of intracellular Ca2+ and H+ suggests the possibility that pH-dependent cellular processes are directly activated by sudden increases in intracellular Ca2+ levels. This second messenger type of signaling system would be activated whether the Ca2+ was released from intracellular stores or entered the cell via plasma membrane Ca2+ channels.

Calcium influx mediated by the Escherichia coli heat-stable enterotoxin B (STB).

The heat-stable enterotoxin B (STB) of Escherichia coli is a 48-amino acid extracellular peptide that induces rapid fluid accumulation in animal intestinal models. Unlike other E. coli enterotoxins that elicit cAMP or cGMP responses in the gut [heat-labile toxin (LT) and heat-stable toxin A (STA), respectively], STB induces fluid loss by an undefined mechanism that is independent of cyclic nucleotide elevation. Here we studied the effects of STB on intracellular calcium concentration ([Ca2+]i), another known mediator of intestinal ion and fluid movement. Ca2+ and pH measurements were performed on different cell types including Madin-Darby canine kidney (MDCK), HT-29/C1 intestinal epithelial cells, and primary rat pituitary cells. Ca2+ and pH determinations were performed by simultaneous real-time fluorescence imaging at four emission wavelengths. This allowed dual imaging of the Ca(2+)- and pH-specific ratio dyes (indo-1 and SNARF-1, respectively). STB treatment induced a dose-dependent increase in [Ca2+]i with virtually no effect on internal pH in all of the cell types tested. STB-mediated [Ca2+]i elevation was not inhibited by drugs that block voltage-gated Ca2+ channels including nitrendipine, verapamil (L-type), omega-conotoxin (N-type), and Ni2+ (T-type). The increase in [Ca2+]i was dependent on a source of extracellular Ca2+ and was not affected by prior treatment of MDCK cells with thapsigargin or cyclopiazonic acid, agents that deplete and block internal Ca2+ stores. In contrast to these results, somatostatin and pertussis toxin pretreatment of MDCK cells completely blocked the STB-induced increase in [Ca2+]i. Taken together, these data suggest that STB opens a GTP-binding regulatory protein-linked receptor-operated Ca2+ channel in the plasma membrane. The nature of the STB-sensitive Ca2+ channel is presently under investigation.