Objective assessment of movement competence in children using wearable sensors: An instrumented version of the TGMD-2 locomotor subtest.

Movement competence (MC) is defined as the development of sufficient skill to assure successful performance in different physical activities. Monitoring children MC during maturation is fundamental to detect early minor delays and define effective intervention. To this purpose, several MC assessment batteries are available. When evaluating movement strategies, with the aim of identifying specific skill components that may need improving, widespread MC assessment is limited by high time consumption for scoring and the need for trained operators to ensure reliability. This work aims to facilitate and support the assessment by designing, implementing and validating an instrumented version of the TGMD-2 locomotor subtest based on Inertial Measurement Units (IMUs) to quantify MC in children rapidly and objectively. 45 typically developing children, aged 6-10, performed the TGMD-2 locomotor subtest (six skills). During the tests, children wore five IMUs mounted on lower back, on ankles and on wrists. Sensor and video recordings of the tests were collected. Three expert evaluators performed the standard assessment of TGMD-2. Using theoretical and modelling approaches, algorithms were implemented to automatically score children tests based on IMUs' data. The automatic assessment, compared to the standard one, showed an agreement higher than 87% on average on the entire group for each skill and a reduction of time for scoring from 15 to 2min per participant. Results support the use of IMUs for MC assessment: this approach will allow improving the usability of MC assessment, supporting objectively evaluator decisions and reducing time requirement for the evaluation of large groups.

Laparoscopic cholecystectomy performed under regional anesthesia in patients with chronic obstructive pulmonary disease.

BACKGROUND: Laparoscopic cholecystectomy has been successfully performed using epidural anesthesia. We evaluated our experience with this surgical approach in high-risk patients. METHODS: We present the results of 29 patients with gallstones who, between 1998 and 1999, underwent laparoscopic cholecystectomy with epidural anesthesia. All but 1 patient had chronic obstructive pulmonary disease. RESULTS: All 29 surgeries were successfully completed via laparoscopy and with the patients under epidural anesthesia. No patient required endotracheal intubation during surgery or pain medication afterward. Postoperatively, 1 patient developed a wound infection and 3 patients developed urinary retention. At last follow-up (12 months postop), all patients were in good health. CONCLUSION: In this series, laparoscopic cholecystectomy was feasible under epidural anesthesia and it eliminated the need for postoperative analgesia. We believe that this approach should be considered for patients who require biliary surgery but who are not good candidates for general anesthesia due to cardiorespiratory problems.

Effects of metformin treatment on whole-body and splanchnic amino acid turnover in mild type 2 diabetes.

The effects of metformin therapy on whole body and splanchnic amino acid turnover are not known. Therefore, we have studied fasting and postprandial phenylalanine kinetics in type 2 diabetic subjects (non-insulin-dependent diabetes mellitus), previously treated with diet only, both before and after 4 weeks of either metformin (850 mg twice a day) (n = 11) or placebo administration (n = 6). Phenylalanine kinetic was evaluated by means of a multiple isotope technique: tritiated phenylalanine was infused i.v., whereas carbon-labeled phenylalanine was incorporated into a chemically-defined meal. Compared with placebo, metformin administration decreased both fasting (from 162 +/- 17 to 141 +/- 20 mg/dl) and postprandial (from 217 +/- 20 to 164 +/- 20 mg/dl) glucose concentrations (P < 0.05-P < 0.01). Fasting insulin concentrations were unaffected, but postmeal insulin tended to be lower (P < 0.06) after metformin. Compared with the pretreatment period, metformin administration did not change total phenylalanine rate of appearance (fasted state, 0.74 +/- 0.10 vs. 0.71 +/- 0.08 mumol/kg.min; fed state, 0.77 +/- 0.10 vs. 0.75 +/- 0.08 mumol/kg.min, respectively), dietary and endogenous phenylalanine rate of appearance, dietary phenylalanine oxidation, and splanchnic uptake, similar to what was observed in the placebo group. Our data indicate that, at least after a 4-week treatment, metformin does not affect fasting and postprandial protein turnover, as indicated by phenylalanine data, in subjects with mild non-insulin-dependent diabetes mellitus.

Fasting and postmeal phenylalanine metabolism in mild type 2 diabetes.

We have investigated postabsorptive and postprandial phenylalanine kinetics in non-obese type 2 diabetic patients [non-insulin-dependent diabetes mellitus (NIDDM)], using a double-isotope technique and the constant oral administration of a synthetic mixed meal. Fasting and postmeal glucose levels were increased (P < 0.01) in NIDDM (165 +/- 16 to 226 +/- 24 mg/dl), with respect to normal controls (85 +/- 3 to 102 +/- 6 mg/dl). Fasting insulin concentrations were comparable in NIDDM (13 +/- 2 microU/ml) and in normals (12 +/- 2 microU/ml), but after the meal it increased less (P < 0.07) in NIDDM vs. normals (to 36 +/- 5 vs. 56 +/- 12 microU/ml, respectively; P < 0.01 vs. basal for both). Postabsorptive phenylalanine rate of appearance (R(a)) in NIDDM (0.63 +/- 0.08 mumol.kg-1 x min-1) was comparable to that of controls (0.73 +/- 0.05 mumol.kg-1 x min-1, not significant). During the meal, total and endogenous phenylalanine R(a), splanchnic uptake, oxidation, and nonoxidative disposal of the ingested phenylalanine were also comparable in the two groups. These data indicate that fasting and postprandial kinetics of the essential amino acid phenylalanine are normal in NIDDM.

Suppressor cell activity in viral and non-viral chronic active hepatitis.

Suppressor cell function was studied in twenty-nine patients with chronic active hepatitis (CAH) in relation to possible aetiological causes and activity of liver disease. All fifteen patients with evidence of viral aetiology (ten HBsAg-positive CAH and five non-A, non-B CAH) showed normal suppressor cell function independently of severity of liver damage. In contrast, fourteen patients with HBsAg-negative CAH, including four cases with circulating antibodies to the hepatitis B virus, demonstrated a significant reduction in supprpessor cell activity compared to control subjects. No significant difference was found in this group between cases with and without circulating autoantibodies. In four out of five HBsAg-negative patients tested serially suppressor cell defect correlated with disease activity suggesting an abnormality in the regulation rather than a depletion of suppressor cells. These results suggest that different mechanisms are responsible for autoimmunity to the liver in virus and non-virus-related CAH.