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This article synthesizes research on resilience theory and its implications for prevention interventions to increase resilience in high-risk children and adolescents. In addition, this response to both the articles by Drs. Greenberg and Dishion summarizes their key points. Their papers discuss the neuroscience substrate behind two major mediators of antisocial behaviors, namely lack of self-regulation and executive function problems. In addition, we present an overall Resilience Framework that will help the reader organize the aspects of resilience discussed by these two researchers into a transactional process model. This article extends prior researchers' suggestion that resilience is the product of the interaction of genetic, biological, and environmental precursors to a further consideration of higher-level cognitive precursors, such as purpose in life and existential meaning. The relevance of resilience to the prevention of negative outcomes in high-risk children of alcoholics (COAs) and substance abusers is covered. Within this third wave of resilience research on prevention interventions, we present data suggesting that family strengthening approaches have the greatest impact on increasing resilience.

The balance between optimal levels of emotional arousal and cognitive performance reflects the integration of several dopaminergically and adrenergically regulated neural systems. The amygdalar system is a key region for gating stimulation to cortical regions and the medial amygdala appears to play an especially key role in mediating the fear response. More generally, these arousal regulatory neural systems are key to frustration or stress impact prefrontal cortical function. Further, the threshold for when the level of stress is overwhelming and hence impairs cognitive function reflects minimally genetic and experiential influence. An important interface between Drs. Lewis and Davis's work is how early experience, especially through early parenting, may set the threshold of responsiveness for these arousal regulatory neural systems.

Friend leukemia virus (FLV) leukemogenesis was prevented by treatment of the virus with Concanavalin A (Con A). Mice infected with the lectin-treated virus, however, showed evidence of a dormant infection since infectious virus could be recovered for as long as 100 days. Humoral immune responses to sheep erythrocytes (SRBC), a thymus-dependent antigen, and to E. coli lipopolysaccharide (LPS), a thymus-independent antigen, were depressed (approximately 80-90%) in mice given the Con A-treated FLV. Cell transfer studies indicated that the impaired responsiveness to SRBC was related to a defect in B-lymphocyte function, similar to the impairment in mice infected with untreated FLV. The mitogenic response of splenocytes from Con A-FLV mice to E. coli LPS was also depressed as was the ability of Ig-bearing spleen cells to redistribute these immunoglobulin receptors into polar caps. The impaired immune responsiveness in the Con A-FLV infected mice appeared associated with the persistent virus infection and not to neoplastic transformation generally associated with leukemogenic process.

TA3-HA nonspecific tumors growing in ascites form shed their membrane components into the ascites fluid. This product can induce tumor growth enhancement if given together with or after i.p. tumor inoculation in relatively large quantities, but if given i.m. in small quantities, several days before tumor challenge, the mice show an elevated resistance to the tumor. The strictly strain-specific TA3-St line does not release such membrane components into the ascites fluid. It has also been found that the TA3-HA cells have a larger membrane fluidity than the TA3-St cells, as measured by membrane microviscosity, using the Shinitzki procedure. Isolation and gross chemical analysis of the TA3-Ha ascites fluid component was carried out. Results, so far, indicate that the active site of this product is probably carbohydrate in nature. The possible mode of action of such component in tumor growth enhancement is most probably by overwhelming and neutralizing immunocytes capable of recognition and eventually cytotoxic action.

Several investigators1–4 have shown that burned animals are quite susceptible to systemic invasion by Pseudomonas aeruginosa. We have produced fatal septicemia in mice by immersion of the scalded tail (immersed in water at 70°C for five sec) in cultures of Pseudomonas strain 180. For purposes of local therapy the tails have been enclosed in rubber tubing held in place by stapling to the loose skin at the base of the tail (figure 1). Therapy consisted of suspending the drugs in a vanishing cream base and injecting the suspension into the tubes, which were then sealed with a cork. Treatment was given six hr after challenge. Details of the techniques employed may be found in recent publications.5,6 In a comparative study of eleven chemotherapeutic agents, six were highly effective in preventing death. (See table 1). The mortality with 8.5% sulfamylon acetate was 8%; 0.25% chloramphenicol, 0.5% gentamycin, 0.4% neomycin, and 1% streptomycin all produced zero mortality; 0.5 sulfadiazine gave 10% mortality. Little effect on survival was observed from 0.2% polymyxin, 0.1% colimycin, 0.25% tetracycline, 0.25% penicillin G, or 0.5% silver nitrate. Ninetythree% of untreated animals died and 90% with the vanishing cream alone.5 A similar study was carried out on mice treated systemically, and without local therapy. Treatment was begun six hr after the challenge and repeated once daily for four additional days. It was found that sulfadiazine given orally in doses of 100 to 500 mg/kg brought about complete survival, and streptomycin administered subcutaneously in doses of 100 mg/kg produced 90% survival (table 2). The drugs currently in use, polymyxin, colimycin, and gentamycin had little effect in the usual therapeutic doses. A comparison of in vivo activity with in vitro sensitivity revealed that test tube activity is not a reliable index of therapeutic action (table 3). Gentamycin, polymyxin, and colimycin were bacteriostatic at 1 μg per ml. Only gentamycin exhibited local activity, and colimycin was without effect systemically. Chloramphenicol, sulfadiazine, and streptomycin were equally active in vitro (25 μg/ml). All were effective locally, but systemically, chloramphenicol was inactive while sulfadiazine and streptomycin were most effective.

2 family planning programs operating in New Orleans and Lincoln Parish Louisiana between 1965 and 1967 are reviewed to refute the concept that indigent women and those who have experienced out-of-wedlock pregnancies are uninterested in fertility control. Studies conducted prior to the inception of both programs determined a lack of reproductive and contraceptive knowledge among lower socioeconomic couples rather than a lack of motivation. The population of rural Lincoln Parish is 41.8% black and the median annual family income ranges between $2000 and $3000. 50% had delivered out-of-wedlock the median age was 23.6 years and the majority displayed low parity. In the New Orleans program annual family incomes were below $4500 and 95.7% of the patients were black (primarily because poor whites were unwilling to attend integrated clinics). Birth records from public and charity hospitals were used to identify patients and priority contact was given to current postpartum patients followed by high-risk mothers who had delivered in the past 2 years. Low-risk women were contacted last. Contact with postpartum mothers was made 1 or 2 days after birth by a program nurse and included an individual education session literature and the offer of an appointment 4 to 6 weeks later. High and low-risk women were contacted by family planning auxiliary workers selected from the indigent population and trained in reproductive physiology contraceptive techniques and program orientation. Auxiliary workers were responsible for the program follow-up system which increased the total number of first admissions by 22% in New Orleans. Patients received a call or letter after missing their first appointment and a home visit after a second cancellation. Data from the Lincoln Parish programs second year of operation showed a significant decrease (47%) among indigent illegitimate births and other pertinent indices. In New Orleans 96% of the first admissions accepted some form of birth control. Oral contraceptives were chosen by 62% of the women and the IUD was chosen by 20% compared to previous usage levels of 24% and .2% respectively. 88% of the first admissions remained with the program over an 18-month period. Both Louisiana programs demonstrate that successful acceptance of family planning by indigents depends upon the design and provision of adequate maternal health services which stress privacy freedom of choice and sustained personal contact.

Leucocyte migration inhibition detected in vitro by the capillary tube technique (LMCT) has proved a useful tool for detection of tumor-specific cell-mediated hypersensitivity (TCMH) in man. Investigations in pateints with renal tumors are reported. It is shown that TCMH is a feature of hypernephroma in man, that the antigenic specificity is found in autologous as well as allogeneic tumor tissue and in fetal kidney tissue. The pattern of reactivity compared to postoperative survival and occurrence of metastases and postoperative clinical course shows a clear association between TCMH and tumor elimination. The capacity of hypernephroma patients to develop a cell-mediated immune response is generally not reduced. In allogeneic combinations, small noninvading tumors usually have a high antigenicity, whereas tumors with early dispersion show a low antigenicity. The development of TCMH and associated tumor elimination therefore may be depending preferably on the antigenicity of the tumor, less on the immune capacity of the tumor host.

The kinetics of the antitumor cellular immune response of mice with progressively growing syngeneic tumors were determined in vivo using a quantitative radioisotopic footpad assay. A close correlation was found between the size of the tumor and the degree of the cellular immune response. An initial phase of cellular immune stimulation was followed by specific suppression and subsequent immunologic paralysis as the tumor grew larger. This immune paralysis was attributed to increased tumor load since a homogenate of an SV40 transformed fibrosarcoma injected intraperitoneally into tumor-immune mice specifically depressed their cellular immune response. The fraction of the tumor homogenate that brought about this depression was present in the high speed supernatant and pellet of a 3M KCl extract of the tumor. The specificity of the depression was determined in vivo by the radioisotopic footpad assay and in vitro by a 51Cr cytolysis assay. Unwashed spleen cells harvested from mice bearing large tumors were unreactive in a local adoptive footpad assay. However, reactivity could be restored by repeatedly washing the spleen cells.