Qualitative research in family therapy: a substantive and methodological review.

Over the last decade, marriage and family therapy (MFT) researchers have developed a growing interest in qualitative research. In this article, we review substantive and methodological trends in the published qualitative studies within the MFT field. The research is compared and contrasted in the following areas: General topic, epistemological theory, methodological theory, sampling and sample, data collection, data analysis procedure, and approach to reliability and validity. We also provide recommendations for future research.

Client experience of gender in therapeutic relationships: an interpretive ethnography.

The purpose of this study was to explore clients' experiences of gender in therapeutic relationships in order to inform therapists of critical issues from clients' perspectives. To capture clients' views, the researchers chose an interpretive ethnographic design that used unstructured, collaborative interviews with clients who had worked with both female and male therapists. The interviews were analyzed using procedures developed by Kvale (1996), who emphasizes the importance of including the client's voice in data gathering, analysis, and final presentation. The results were reviewed with the clients to insure accurate presentation of their views. The final results were organized into six themes: client-therapist connection, male therapists, female therapists, topics discussed, effectiveness, and confounding factors. Researchers discuss the implications of gender-stereotyped behavior in therapy, the relationship between therapist gender and therapeutic alliance, and recommendations for practicing gender-sensitive therapy.

Changes in hormone and metabolite concentrations in plasma of steers during a prolonged fast.

Two Brown Swiss and two Holstein steers, average weight of 226 kg, were fasted 8 d. Two days before the fast, jugular vein catheters were installed. Blood samples were collected every 15 min from 0800 to 1400 h on d 0, 2, 5 and 8 of fasting. Plasma from each sample was analyzed for concentrations of growth hormone, and from selected samples for insulin, glucagon, glucose, beta-hydroxybutyrate, free fatty acids, urea N and glycerol. Both growth hormone and insulin concentrations decreased by d 2 of the fast and remained at that concentration. Glucagon, however, remained constant. From d 0 to 2, concentrations of beta-hydroxybutyrate, free fatty acids and glycerol increased but then changed little for d 5 and 8. From d 0 to 2, glucose decreased and urea N increased. In contrast to the other metabolites, glucose and urea N concentrations stabilized between 3 and 5 d of fasting. The ratio of growth hormone to insulin decreased threefold and the ratio of glucagon to insulin decreased fivefold from d 0 to 2; both ratios remained constant during the rest of the fast. The data indicate that fasting cattle adapt by decreasing concentrations in plasma of growth hormone and insulin but not glucagon. These endocrine changes, therefore, seem responsible for greater rates of free fatty acid mobilization and glucose sparing during an energy deficit.

Glucose kinetics, plasma metabolites, and endocrine responses during experimental ketosis in steers.

Phlorizin and 1,3-butanediol were used to determine effects of glucosuria and ketonemia on concentrations of metabolites in blood plasma and on kinetics of glucose metabolism. Four steers received four treatments (control; control plus dietary 1,3-butanediol; control plus phlorizin injections; and control plus phlorizin and 1,3-butanediol) in a Latin square design. Treatments lasted 14 days. All steers received a 30% grain, 70% forage ration in equal meals every 2 h. Metabolite concentrations in blood plasma and urine and glucose kinetics were measured on each of the last 3 days of each treatment period. Phlorizin caused glucosuria; decreased plasma glucose, glucose total entry rate, and glucose recycling; and increased plasma free fatty acids and glucose irreversible loss. Glucose pool size was increased by 1,3-butanediol. Phlorizin plus 1,3-butanediol caused glucosuria and ketonuria; decreased plasma glucose; and increased blood ketone bodies, plasma free fatty acids, glucose irreversible loss, and glucose pool size. Growth hormone, insulin, and glucagon were not affected by treatment. Physiological perturbations in these steers were characteristic of some of those in ketotic cows.

Plasma and liver metabolites and glucose kinetics as affected by prolonged ketonemia-glucosuria and fasting in steers.

For 28 days, four steers received 1,3-butanediol, which causes ketonemia, and phlorizin, which causes glucosuria. Steers also were fasted for 9 days. Effects of treatments on concentrations of metabolites in blood and liver and on kinetics of glucose metabolism were determined. Treatments were: control, control with dietary butanediol plus injected phlorizin, and fasting. Fasting caused hypoinsulinemia and decreased liver glycogen by 60%. Butanediol plus phlorizin and fasting caused 18 and 19% decreases of plasma glucose and 2.5- and 6-fold increases of free fatty acid concentrations in blood plasma. Glucose irreversible loss averaged 371, 541, and 182 g/day during control, butanediol plus phlorizin treatment, and fasting. Butanediol plus phlorizin increased liver ketone body concentrations, caused glucosuria, ketonuria, and ketonemia, but did not affect insulin, glucagon, or growth hormone concentrations in plasma or triglyceride and glycogen contents in liver. Steers given butanediol plus phlorizin did not show all the usual signs of lactation ketosis, but the treatment still offers promise for studying causes and effects of ketosis.

In vitro hepatic gluconeogenesis during experimental ketosis produced in steers by 1,3-butanediol and phlorizin.

Adaptations of in vitro incorporation of gluconeogenic substrates into glucose and adaptations of metabolite concentrations of liver to subcutaneous phlorizin and dietary 1,3-butanediol were examined for liver samples from dairy steers. Later, the same adaptations were examined after 6 days of feed restriction. Feeding 1,3-butanediol significantly decreased conversion of carbon-14 of lactate and propionate to glucose and to carbon dioxide. There were no changes of concentrations of hepatic glycogen or triglyceride, and increases were only minor for beta-hydroxybutyrate concentration. Both phlorizin, with or without 1,3-butanediol, and feed restriction significantly increased rates of carbon incorporation into glucose from aspartate, lactate, and propionate but did not change rates of oxidation to carbon dioxide. Phlorizin had no effect on hepatic glycogen or triglyceride concentrations, but feed restriction decreased liver glycogen and increased triglyceride concentrations. Changes associated with either phlorizin treatment or feed restriction are consistent with a decreased ratio of insulin to glucagon of blood plasma. When combined, phlorizin and 1,3-butanediol seem to have some utility for developing a ketosis model.

In vitro hepatic gluconeogenesis and ketogenesis as affected by prolonged ketonemia-glucosuria and fasting in steers.

Both 1,3-butanediol, which causes ketonemia, and phlorizin, which causes glucosuria, were given to four steers for 28 days to determine effects of prolonged ketonemia and glucosuria on in vitro hepatic gluconeogenesis and ketogenesis. Treatments were: control ration; control with butanediol plus phlorizin; and fasting for 9 days. Liver slices, obtained by biopsy, were incubated with carbon-14 substrates. Substrate converted to glucose [mumol/(h X g liver)] during control, butanediol plus phlorizin, and fasting averaged 2.34, 7.21, and 12.00 for propionate; .99, 3.80, and 12.26 for lactate; .30, .76, and 2.20 for alanine; and 2.06, 5.37, and 5.78 for glycerol. Omission of calcium++ eliminated increases of gluconeogenesis caused by butanediol plus phlorizin and by fasting. Ketone bodies, octanoate, and bovine serum albumin did not affect glucose production markedly. Stearate inhibited gluconeogenesis during all periods except fasting. Production of beta-hydroxybutyrate [mumol/(h X g liver)] during control, butanediol plus phlorizin, and fasting averaged 2.07, 4.27, and 3.25 from butyrate and .06, .27, and .02 from palmitate. Results demonstrate that the gluconeogenic capacity of bovine liver is responsive to physiological and nutritional status.