Bridging gaps between mind, body, & spirit. Healing the whole person.

Fifty percent of visits of primary care providers are for psychiatric problems making it desirable to screen for mental, addictive, or behavioral disorders at the level of primary care. Psychiatric/mental health nurses prepared at the master's level to practice in the blended clinical specialist/nurse practitioner role are well placed to treat or collaborate in the treatment of people who present with symptoms of physical or psychological problems. The role of the clinical specialist/nurse practitioner is evolving in response to changes in health demographics, epidemiology, scientific and technological advances, and changes in managed care. Advanced practice nursing education must continue to anticipate and meet on-going changes and challenges.

Antisocial personality disorder: diagnostic, ethical and treatment issues.

Antisocial personality disorder (ASPD) is a complex disorder that creates a diagnostic, ethical, and treatment dilemma for mental health professionals. Psychosocial, biological, and cultural influences play a role in the development of ASPD. People with ASPD often had harsh early childhoods that impaired their ability to trust in adulthood. Research supports intriguing biological links, but it remains unclear if biological differences are the cause or the effect of ASPD. Individualism, patriarchy, and widespread media violence create the cultural context for the development of ASPD. ASPD is difficult to clinically diagnose and treat, and there is controversy concerning whether ASPD is a psychiatric or a legal-ethical problem. However, the management of ASPD often falls to mental health services. This article addresses treatment and primary prevention of ASPD in a way that is relevant to mental health practice.

Evaluation of APHA and AOAC II methods for phosphatase in butter and differentiation of milk and microbial phosphatases by agarose-gel electrophoresis.

Salted and unsalted butters with 3 levels of phosphatase were prepared with both raw and pasteurized cream containing 36% fat. Test samples were analyzed for phosphatase by the modified method of the American Public Health Association (APHA) and the official AOAC method, 16.256 (1984, 14th Ed., 1990 15th Ed., 946.02). In the APHA method, weighing of solid frozen butter for testing yielded repeatable results. Addition of 0.0-1.0 mg magnesium to the butter had little effect on phosphatase activity in the APHA modified rapid colorimetric method (MRCM), but caused the phosphatase activity to decrease in the AOAC method. Phosphatase in salted and unsalted butters was quite stable at -17 +/- 1 degrees C and at 3.0 +/- 0.5 degrees C; however, within 2 to 4 days, freshly prepared butters stored at 22 +/- 1 degrees C developed reactivated and/or microbial phosphatases that were both heat-labile and heat-stable. At 22 +/- 1 degrees C, frozen butters showed decreased milk phosphatase activity before producing microbial phosphatase. Heat-labile phosphatases in salted and unsalted butters were inactivated at 62.8 degrees C for 10 min, and the phosphatase lability was partially due to the heat-denaturing effect of NaCl in salted butter. Some heat-stable phosphatases in unsalted butter survived at 66 degrees C for 30 min. Differentiation of milk phosphatase from microbial phosphatases was difficult by both methods; however, they were successfully differentiated by the agarose-gel electrophoretic technique.

Melanogenesis in murine B16 cells exposed to Aeromonas hydrophila cytotoxic enterotoxin.

Specific markers (growth, melanogenesis) of B16 murine melanoma cells in culture were used as indicators of toxin production by Aeromonas hydrophila. Cytotonic enterotoxinlike activity (inhibited growth, raised tyrosinase activity, and melanin accumulation) occurred at cytotoxic end points of purified beta-hemolysin and several culture filtrates. Antihemolysin rabbit serum inhibited this activity. A hemolysin-neutralized culture filtrate concentrate (10X) failed to elevate tyrosinase relative to untreated and cholera toxin treated controls. Similar dilution profiles using Chinese hamster ovary cells showed limited cell extension only at cytotoxic end points with antihemolysin inhibiting this activity. Cytotoxicity of Chinese hamster ovary cells and B16 cells was proportional to hemolytic activity, with B16 cells showing about 100-fold greater sensitivity on a per cell basis. Cell culture cytotoxicity attributed to beta-hemolysin correlated with reactivity in rabbit ileal loop assays. The ADP-ribosyl transferase activity of concentrated (10X) A. hydrophila culture filtrates and fractions thereof was negative. Apparently sublethal doses of A. hydrophila beta-hemolysin can nonspecifically stimulate cyclic adenosine monophosphate mediated events in melanoma and Chinese hamster ovary cell assays, producing lower activities than cholera toxin with shorter lag times.

Reactivation of alkaline phosphatase in ultra high-temperature, short-time processed liquid milk products.

Alkaline phosphatase (enzyme) reactivation was studied in liquid milk products heated to 87.8 to 121.1 C for less than 1 s in a continuous, two-phase, slug-flow heat exchanger. The effects of magnesium concentration, pH, incubation temperature, homogenization pressure, processing temperature, fat content, and initial enzyme concentration were investigated. Jersey milk from one farm showed seasonal variations in enzyme concentration and its reactivation behavior. Increased reactivation in products with high fat content was due to high initial enzyme concentration in the product. Homogenization of products before heating decreased reactivation. Maximum reactivation occurred in products heated to 104.4 C, incubated at 34 C, and adjusted to pH 6.5. Maximum velocity of reactivation and reactivation constant varied with milk samples. Activation energy for the control and samples with magnesium was 22.646 +/- .118 and 24.100 +/- .210 kJ mole-1, respectively. The enzyme from raw and reactivated cream contained two major isozymes, and the reactivated isozyme differed from the control. The official method for differentiating residual and reactivated enzymes was modified in terms of magnesium concentration and extent of reactivation of the enzyme in the reactivated product.