Goal attainment scaling in post-acute outpatient brain injury rehabilitation.

Therapists continuously strive for efficiency in clinical practice. Goal Attainment Scaling (GAS) is a tool that can provide both a structure for objective documentation of patient progress and a means of program evaluation. This article describes the application of GAS in a comprehensive outpatient brain injury rehabilitation program. The benefits of GAS include: (1) objective data in monitoring participants' progress, (2) a structure for team confer-. ences, (3) facilitation of on oing rehabilitation planning and decision- making, (4) concise relevant information to funding sources, referral sources, and family members, and (5) a mechanism for program evaluation. For the brain injured person, GAS serves as a focus for an arra of multiple, often abstract rogram goals. GAS can also increase the participant's awareness of deficits being addressed in the program and of progress towards resolving these problems.

Long-term preservation of segmental pancreas autografts.

Clinical pancreas transplantation is logistically difficult because of uncertainty concerning how long pancreas grafts can be preserved. We studied the viability of canine segmental (tail) pancreatic autografts transplanted after 24 to 72 hours of hypothermic preservation in either modified Collins' solution or modified silica gel filtered dog plasma (SGF). All grafts stored for 24 to 48 hours functioned immediately (plasma glucose less than 140 mg/dl in recipients). Grafts that failed did so between 2 and 7 days, and five dogs died with functioning grafts. The long-term functional success rate was 80% for fresh transplants; 67% and 40% for grafts stored in Collins' solution for 24 and 48 hours, respectively; and 75%, 75%, and 30% for grafts stored in SGF for 24, 48, and 72 hours, respectively. If technical failures are excluded. 50% of grafts stored in Collins' solution and 100% of grafts stored in SGF for 48 hours functioned long term. K values for the intravenous glucose tolerance test at 2 weeks in dogs with functioning grafts ranged from -1.44% to -1.78% and were similar in all groups. In conclusion, pancreatic grafts can be preserved for 48 hours by simple cold storage, but SGF is more reliable than Collins' solution (P = 0.015). Four human pancreas grafts were stored in SGF for 7 to 22 hours, one with and three without prior warm ischemia, and all three of the latter functioned after transplantation.

The effect of atropine and duct decompression on the evolution of Diazinon-induced acute canine pancreatitis.

Three groups of eight dogs each were studied to evaluate the early evolution of the hyperamylasemia, hyperlipasemia, and acinar cell pathology at the light and electron microscopic levels during acute Diazinon-induced pancreatitis. Two more groups of five dogs each were evaluated for the effects of cholinergic receptor blockade with atropine and ductal decompression on the evolution of serum enzyme changes and acinar cell pathology. Group I dogs received a secretin infusion of 2 units/kg/hr, and a Diazinon infusion of 75 mg/kg, and demonstrated significant increases in serum amylase and lipase at one, two and three hours. Light microscopy revealed acinar cell vacuolization and progressive interstitial edema. Electron microscopy revealed the formation of large intracytoplasmic vacuoles filled with flocculent material, the fusion of these vacuoles with basolateral membrane, and the formation of interstitial edema. In both group II dogs (that received secretin alone) and Group III dogs (that received atropine, 200 micrograms/kg IV prior to secretin and Diazinon), the serum enzyme levels and histologic results were normal. In group IV dogs, pancreatic duct cannulation to prevent hypertension prevented the hyperamylasemia and hyperlipasemia, but not the acinar cell vacuolization and interstitial edema. This model for acute interstitial pancreatitis is apparently cholinergic-receptor mediated, the serum enzyme elevations are due primarily to ductal hypertension, and the acinar cell pathology is primarily due to cholinergic stimulation and occurs independent of ductal hypertension.

Remote tumor effects on lactic dehydrogenase of mouse muscle fibers with different glycolytic--oxidative metabolic potentials.

The total lactic dehydrogenase (LD) activity and the isoenzyme pattern were studied in muscles of mice during the progressive growth of a distally transplanted methylcholanthrene-induced tumor. The thigh muscles as a group (a mixture of fibers with different oxidative-glycolytic metabolic potentials), the gastrocnemius muscle (primarily glycolytic), the soleus muscle (predominantly oxidative), the heart (purely oxidative), and the diaphragm (primarily oxidative) were evaluated. The total LD activity increased in muscles with a high glycolytic metabolic potential. In such muscles a significant increase of the muscle type and a significant decrease of the heart type of LD were observed. After 3 weeks of tumor growth the tumor was resected, and the LD activity and isoenzyme distribution returned toward normal values 2 weeks later.

Muscle and serum enzymes and isoenzymes in muscular dystrophies.

Total activity of creatine kinase (CK), lactate dehydrogenase (LD), aldolase (Ald), glutamico-oxaloacetic transaminase (GOT), and LD-isoenzyme distribution was studied in serum and muscle biopsies from normal persons and 117 patients with different types of muscular dystrophy: 82 Duchenne type (DMD), 12 BEcker type, 7 facioscapulohumeral (FSHMD), and 16 limb girdle (LGMD). Total enzyme activity in sera and muscle homogenates was determined by spectrophotometric assays. LD isoenzymes were separated by electrophoresis on agarose gel plates in barbital buffer (pH 8.6), scanned and quantitated. The amounts of the 2 types (M and H) of LD isoenzymes were calculated and the ratio of M/H in serum and muscle was used as an index to differentiate among the types of muscular dystrophy. Serum enzyme activity was elevated to variable degrees reflecting a corresponding decrease in muscle enzymes in the different muscular dystrophies. Patterns of LD isoenzymes in serum and muscle were specific to each type of muscle disease. Increase in serum LD5 (the muscle LD fraction) was a common feature in muscle damage. Changes in the amounts of M and H types in the subunits of LD correlated to the existence and severity of muscle damage. The mean muscle M/H ratio was 6.4 in controls, 1.8 in early DMD, 0.1 in late DMD, 3.0 in Becker type, 3.8 in FSHMD and 3.9 in LGMD. The muscle LD isoenzyme distribution in DMD showed a shift toward a more aerobic fetal muscle pattern. This is a result of the gradual disappearance of the mature anaerobic LD-type (M) and the increase in synthesis of the aerobic fetal LD-type (H) during the progression of the disease. This report provides a comparative study of the LD isoenzyme patterns in muscular dystrophies which may help in differential diagnosis.