Arthroscopic or open Bankart procedures: what are the costs?

The cost implications and resource utilization of arthroscopic and open Bankart procedures were evaluated to determine if differences exist between these procedures when performed in a community setting. Billing and hospital records of consecutive patients who underwent either open or arthroscopic Bankart procedures at the three facilities in our city during an 18-month period were analyzed. Procedure type (open or arthroscopic), location (hospital or surgicenter), operation time, operating room time, postanesthesia care unit time, step-down area time, charges for each of these, and anesthesiologist charges were analyzed for 11 open and 13 arthroscopic Bankart procedures. Open procedures took longer and required more operating room time than arthroscopic procedures regardless of location (P < .01). Open procedures required longer postanesthesia care unit time than arthroscopic procedures (P < .01). Facility made no difference. Anesthesia fees were less for arthroscopic ($882) than open Bankarts ($1,075) (P = .002). Total facility and anesthesia fees were less for arthroscopic ($4,747) than for open Bankarts ($6,062) (P = .05). The arthroscopic Bankart repair was performed more quickly than the open Bankart procedure, regardless of facility choice, and resulted in lower total charges. A surgicenter is less expensive whether these procedures are performed arthroscopically or open.

Cross training: indices of training stress and performance.

Twenty well-trained runners (VO2max 4.6+/-0.5 L x min[-1]) were age and ability matched and assigned to either a cross training (CT) or run only group (RT). All subjects maintained normal running distance and intensity for 6 wk and reported for three additional training sessions per week. These workouts were performed outdoors on a 400-m track or measured road course (RT) or on a bicycle ergometer (CT). The sessions were as follows: (work x rest(-1) ratio = 1): 5 x 5 min at >95% VO2max/peak (Monday), 50-60 min at 70% VO2max/peak (Wednesday), and 3 x 2.5 min at >105% VO2max/peak, plus 6 x 1.25 min at >115% VO2max/peak (Friday). Subjects were tested before (PRE), after 3 wk (MID), and after 6 wk (POST) of intensified training. Blood samples were obtained from RT, CT, and ten controls (CON) at each time point (0600 h). Runners also completed a 10-min submaximal run at the same absolute intensity (velocity to elicit 75% of initial V02max) during which heart rate, RPE, and VO2 were measured. Each runner then completed a simulated 5-km race (time trial) on a treadmill. Total testosterone (TT), free testosterone (FT), cortisol (C), and creatine kinase activity (CK) were determined. Running economy was similar between RT and CT; however, RPE decreased significantly at MID and POST compared with that at PRE (P < 0.05; time effect). There were no significant differences among groups for TT, FT, or CK, but C was significantly lower in CON than in RT and CT. Performance was significantly faster (P < 0.05; time effect) in the 5-km race at MID (1076.1+/-81.4 s) and POST (1068.6+/-83.9) compared with PRE (1096.6+/-79.5) but was not different between CT and RT. In conclusion, RT and CT responded similarly to 6 wk of increased training, and both groups improved 5-km performance to a similar extent.

Dynamic interplay of TFIIA, TBP and TATA DNA.

The TATA binding protein (TBP) binds to the -30 region of eukaryotic and archaea promoters, where it assembles a transcription complex. For those genes transcribed by RNA polymerase II, transcription factor TFIIA binds TBP and positively regulates its activity, including enhancing TBP/ TATA interactions. Since little is known about the dynamic interplay among TFIIA, TBP and DNA, we set out to examine the stability of these interactions. Using the nitrocellulose filter binding assay, the koff of recombinant human TBP from TATA and non-specific DNA was determined to be 5.5(+/-0.1) x 10(-5) s-1 (t1/2 = 210 minutes) and 5.8(+/-0.1) x 10(-4) s-1 (t1/2 = 20 minutes), respectively. TFIIA/TBP complexes, containing either HeLa-derived or recombinant human TFIIA, possessed a nearly tenfold lower koff when bound to TATA. Interactions of TFIIA with DNA upstream of the TATA box did not appear to play a major role in stabilizing TBP/TATA interactions. Instead, the upstream DNA contacts appeared to be important for stabilizing the association of TFIIA with the TBP/TATA complex as measured in electrophoretic mobility shift assays: koff of TFIIA decreased from 1.4(+/-0.1) x 10(-3) s-1 (t1/2 = eight minutes) to 2.4(+/-0.2) x 10(-4) s-1 (t1/2 = 49 minutes) when upstream DNA contacts were allowed. The stability of TFIIA/TBP interactions was measured using a rapid "pull-down" assay, which employed-nickel agarose and polyhistidine-tagged TFIIA. In the absence of DNA, TFIIA dissociated from TBP with a koff = 4.9(+/-0.6) x 10(-3) s-1 (t1/2 = 2.4 minutes), which varied with solution conditions.

Sex differences in growth hormone (GH) secretion by rats administered GH-releasing hexapeptide.

The purpose of this study was to compare GH secretion after the administration of GH-releasing hexapeptide (GHRP-6) in conscious male and female rats. Plasma GH was significantly elevated in female rats (six of six) compared to male rats (three of six) 15 min after administration of a single sc injection of GHRP-6 (0.5 mg/kg). In male rats, GHRP-6 administration was associated with suppression of episodic GH secretion and desensitization to a second injection administered 6 h later, whereas in female rats, GH secretion occurred after both GHRP-6 injections. After 14 consecutive days of administering GHRP-6 twice per day, mean plasma GH concentrations in males decreased from 110 +/- 91 to 2.8 +/- 0.6 ng/ml (P less than 0.05) and in females increased from 170 +/- 53 ng/ml to 361 +/- 81 ng/ml (P less than 0.05). Desensitization to GHRP-6 in conscious male rats was not observed in pentobarbital-anesthetized male rats, suggesting that GHRP-6 administration enhanced somatostatin release in the conscious state. After 14 consecutive days of GHRP-6 administration, the mean pituitary GH concentration in female rats was significantly lower than that in male rats (5.1 +/- 0.2 vs. 12.9 +/- 1.2 micrograms/mg, respectively). Lower pituitary GH concentrations in females correlated with higher GH secretion after GHRP-6 administration. Desensitization to GHRP-6 in male rats is attributed to neurohumoral factors producing their unusual pattern of episodic GH secretion, and the response is probably not typical of other species.

Relative cerebellar weight: a potential indicator of developmental neurotoxicity.

Overt malformations do not always accompany behavioral changes resulting from perinatal exposure to certain drugs. However, the central nervous system (CNS) is the anatomical substrate for behavior, and functional defects may be accompanied by more subtle, structural alterations of the brain. The purpose of this study was to determine if changes in the weights of certain brain regions occur in rats exposed prenatally and/or perinatally to propylthiouracil (PTU) which retards functional development of the brain. Pregnant rats were dosed with PTU during gestation and/or lactation, and on postnatal day 28, auditory startle responses were measured to determine if PTU altered functional development. The brains of all pups were then dissected into 10 separate regions, dried and individually weighed. Brain weights were expressed in absolute and relative (to total brain weight) terms. Pups that were exposed to PTU from days 10 to 21 of gestation grew normally, but their startle responses to auditory stimuli were significantly different (p less than 0.05) from controls. Thus, for the purpose of this experiment, PTU acted as a developmental neurotoxicant because it altered performance on a test of neuromuscular function without being overtly teratogenic. The weights of most brain regions in PTU-treated rats were statistically comparable to controls. However, relative cerebellar weight was significantly (p less than 0.05) different. Therefore, these data suggested that relative cerebellar weight might be used to predict functional defects that appear during development following prenatal or perinatal exposure to certain neurotoxicants. Although cerebellar weight and auditory startle responses were altered by PTU, this study does not establish a causal relationship between the anatomical and functional changes that occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced disease in aged rats treated chronically with ibopamine, a catecholaminergic drug.

As part of preclinical safety testing for carcinogenicity, postpubertal (50 days old) rats were dosed (0, 30, 90 or 180 mg/kg/day) with ibopamine (N-methyldopamine, 0,0'-diisobutyroyl ester.HCl; SK&F 100168) for 730 consecutive days. Neoplastic and nonneoplastic lesions were identified histologically in all rats that died during the period of dosing, as well as in those that were killed after it was completed. Six neoplastic lesions (adrenal cortical, mammary, and pituitary adenoma, skin papilloma, pheochromocytoma and mammary adenocarcinoma) and five nonneoplastic lesions (chronic glomerulonephropathy, renal pelvic mineralization, hepatocellular proliferative nodule, galactoceles and chronic cardiomyopathy) were significantly reduced in a dose-related fashion in at least one sex of ibopamine-treated rats. In addition, age-related alopecia and atrophy of the adrenal zona glomerulosa were retarded by ibopamine treatment. Squamous cell skin carcinoma was the only lesion that was significantly (p less than 0.05) increased in the treated groups. Mortality during the study was not significantly different in treated and control groups, indicating that the lower incidence of disease in ibopamine-treated rats was a drug effect and not an artifact of differential survival. Although life span was not measured, ibopamine-treated rats had significantly less malignant lesions than controls at the end of dosing, suggesting a potentially positive effect of treatment on population survival. As the result of these beneficial effects, ibopamine may be useful for future study of factors affecting the occurrence of disease during aging.