The association between osteoporotic hip fractures and actinic lesions as a biomarker for cumulative sun exposure in older people-a retrospective case-control study in Argentina.

The aim of this study was to analyze the association between the presence of actinic lesions (solar keratosis and non-melanoma skin cancer) and osteoporotic hip fractures in older patients. Both pathologies are common conditions in this age group. Since cumulative sun exposure is difficult to quantify, the presence of actinic lesions can be used to indirectly analyze the association between ultraviolet radiation and osteoporotic hip fractures. This was an observational case-control study. We reviewed the centralized medical records of patients with hip fracture (cases, n = 51) and patients with other diseases hospitalized in the same institution and period (controls, n = 59). The mean age of the patients was 80 ± 8.3 years (range 50-103 years). Differences in maternal hip fracture history were found between cases and controls (14.8 and 8 %, respectively; p = 0.047). Falls history in the past year was higher in cases than in controls (p < 0.0001). Actinic lesions were observed in 32.7 % of patients (prevalence rate 23.5 % in cases, 40.7 % in controls; p = 0.04). When considering patients with actinic lesions, controls have a higher FRAX score compared with cases. Although sun exposure is recommended for bone health, it represents a risk factor for actinic lesions. The presence of actinic lesions may indicate a lower osteoporotic hip fracture risk. A balance between adequate lifetime sun exposure and protection against its adverse effects is required for each patient, in the context of geographic location.

A simple anthropometric tool for the assessment of pre-sarcopenia in postmenopausal women.

OBJECTIVES: The purpose of this research was to explore the performance of anthropometric tools in the assessment of low muscle mass in a group of postmenopausal women. METHOD: Fifty consecutive ambulatory postmenopausal women were studied. A complete clinical examination and an anthropometric evaluation following a standardized procedure were performed. Three indicators were devised: upper limb adjusted perimeter (ULAP), lower limb adjusted perimeter (LLAP), and appendicular adjusted perimeter (AAP). RESULTS: Sixteen sarcopenic patients (32%) were identified using the DXA appendicular lean mass/h2 threshold. ULAP and AAP correctly classified 82% of the patients, while LLAP showed a lower performance (72%). The sensitivity and specificity values of ULAP and AAP were higher than those obtained using LLAP; their positive and negative predictive values were 65.2%, 96.3% and 68.4%, 90.3%, respectively. A highly significant concordance was observed for the three anthropometric indicators. CONCLUSION: The availability of reliable and simple clinical instruments to identify low muscle mass is of great relevance. Anthropometric methods reported in this paper could represent an innovative resource for muscle mass assessment in daily practice. The contribution of these approaches in the detection and management of sarcopenia should allow the physician to make early interventions and thus prevent or modify its relevant health consequences.

Ants modulate stridulatory signals depending on the behavioural context.

Insect societies require an effective communication system to coordinate members' activities. Although eusocial species primarily use chemical communication to convey information to conspecifics, there is increasing evidence suggesting that vibroacoustic communication plays a significant role in the behavioural contexts of colony life. In this study, we sought to determine whether stridulation can convey information in ant societies. We tested three main hypotheses using the Mediterranean ant Crematogaster scutellaris: (i) stridulation informs about the emitter'caste; (ii) workers can modulate stridulation based on specific needs, such as communicating the profitability of a food resource, or (iii) behavioural contexts. We recorded the stridulations of individuals from the three castes, restrained on a substrate, and the signals emitted by foragers workers feeding on honey drops of various sizes. Signals emitted by workers and sexuates were quantitatively and qualitatively distinct as was stridulation emitted by workers on different honey drops. Comparing across the experimental setups, we demonstrated that signals emitted in different contexts (restraining vs feeding) differed in emission patterns as well as certain parameters (dominant frequency, amplitude, duration of chirp). Our findings suggest that vibrational signaling represents a flexible communication channel paralleling the well-known chemical communication system.

Effect of insulin on systemic and renal handling of albumin in nondiabetic and NIDDM subjects.

Insulin resistance and hyperinsulinemia cluster with microalbuminuria in both diabetic and nondiabetic subjects, but the mechanism underlying this association is unknown. To test the hypothesis that insulin influences protein permeability, we measured the albumin transcapillary escape rate (TER) by the (131)I-labeled albumin technique in 12 healthy volunteers and 12 normoalbuminuric NIDDM patients (fasting plasma glucose, 10.9 +/- 1.3 mmol/l) during 4 h of isoglycemia with high (1.1 mU x min(-1) x kg(-1)) or, on a different day, low (0.1 mU x min(-1) x kg(-1)) insulin infusion. In both patients and control subjects, high insulin was associated with a 7% decrease in blood volume (P = 0.006) and a 6% decrease in diastolic blood pressure (P < 0.02), these two changes being related to one another (r = 0.56, P < 0.01). Basal albumin TER was similar in patients (8.4 +/- 0.5% x h(-1)) and control subjects (7.7 +/- 0.7% x h(-1)) and was not significantly changed by high insulin in either group (patients vs. control subjects, 7.3 +/- 0.9 vs. 6.2 +/- 0.4% x h(-1); NS vs. low insulin). In contrast, high insulin increased renal albumin excretion (from 3.6 +/- 0.8 to 5.4 +/- 1.1 microg/min, P < 0.01) and clearance rate (0.09 +/- 0.02 to 0.13 +/- 0.03 microl/min, P < 0.001) in patients but not in control subjects. To localize the effect of insulin along the nephron, we measured the urinary excretion of N-acetyl-beta-D-glucosaminidase (beta-NAG), released by the proximal tubule; retinol-binding protein (RBP), reabsorbed by the proximal tubule; and Tamm-Horsfall protein (THP) and epidermal growth factor (EGF), both secreted by the distal tubule. For both beta-NAG and RBP, but not EGF or THP, insulin enhanced urinary excretion (diabetics vs. controls: beta-NAG, 0.48 vs. -0.15 microU/min [P = 0.03]; RBP, 78 vs. -32 ng/min [P = 0.05]). In conclusion, physiological hyperinsulinemia does not affect systemic albumin permeability in healthy subjects or normoalbuminuric NIDDM patients. In contrast, in NIDDM patients, but not in healthy subjects, insulin increases the urinary excretion of albumin and protein markers of proximal tubular function. The significance of this finding for the pathogenesis of diabetic nephropathy remains to be established.

The natural history of kyphosis in postmenopausal women.

A cross-sectional study of vertebral morphometry in 449 unscreened postmenopausal women, from the ages of 40 to 80, is reported. The wedge angles of thoracic vertebrae T4-12 were found to increase exponentially as a function of age, up to 70 years. In addition to age, the wedging phenomenon was found to be accentuated by increased bone turnover due to low calcium intake, reduced physical activity, each successive delivery, and breast feeding. Most of these variables were not correlated with isolated vertebral wedge angles, but rather with the sum of them (Sigma, sigma), assumed to assess the impact of those variables on thoracic kyphosis. In a subset of women, sigma was found to be inversely correlated with low spinal mineral density at L2-4. T-11 and T-12 were the vertebrae most frequently deformed (wedge angle exceeding mean +/- 3 SD in a group of 50 young healthy women, 25-45 years old). The distribution of deformed vertebrae was found to be significantly different from those qualified as "fractured" according to Kleerekoper et al.'s (1984) and Melton et al.'s (1989) criteria. The overall information afforded by past and present data indicates that in postmenopausal women, vertebral deformation may occur with the help of mechanical solicitations plus high bone remodeling rates, as well as by structural collapse (fracture). The information obtained does not allow one to quantify the relative contribution of each set of factors to the wedging phenomenon.

Effects of amiodarone on supraventricular tachycardia involving bypass tracts.

This study evaluates whether the electrophysiologic effects of i.v. amiodarone in patients with reentrant supraventricular tachycardia (SVT) can predict the efficacy of long-term oral therapy with this drug. The effects of oral and i.v. amiodarone were studied in 27 patients with SVT. In 14 the SVT circuit involved a concealed atrioventricular bypass for retrograde conduction (Group I), and in 13 a concealed atrio-His bypass (Group II). Intravenous amiodarone induced significant prolongation of the AH interval, the refractory periods of the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium. The ventriculoatrial interval was slightly prolonged in Group I patients and did not change in Group II patients after i.v. administration of the drug. In both groups, the effective refractory period (ERP) of the concealed bypass was prolonged by i.v. amiodarone. During control state, SVT could be induced in all patients; after i.v. administration of the drug, SVT was presented in 6 patients in Group I and in 8 patients in Group II. In all cases, in which i.v. amiodarone prolonged the ERP of the concealed bypass to more than 350 ms, the drug always prevented SVT even when given orally. All but 2 patients--1 from Group I and 1 from Group II--remained asymptomatic after oral amiodarone. In the patient from Group I, SVT had been prevented by i.v. amiodarone, whereas in the patient from Group II SVT could not be induced by ventricular stimulation during the control state, but appeared after i.v. administration of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Inappropriate growth hormone response to luteinizing hormone-releasing hormone in diabetes mellitus.

We randomly administered luteinizing hormone-releasing hormone (LHRH) or thyrotropin releasing hormone (TRH) (25 micrograms and 200 micrograms, respectively, as a bolus), to 16 diabetic male subjects (9 type I, 7 type II) and to 9 healthy male controls in two different mornings. While GH in the basal state was similar in type I, type II, and normal subjects, LHRH administration surprisingly evoked a significant GH release in 7 (5 type 1, 2 type II) diabetic patients. GH-responders had higher glycated hemoglobin than non-responders (11 +/- 1 nu 8.3 +/- 0.5%) but superimposable fasting and intratest average glucose levels. Only one patient among the GH-responders to LHRH showed a GH release also after TRH. These data support the hypothesis that GH secretion in diabetes, especially when poorly controlled, is abnormal.

Insulin sensitivity in familial hypercholesterolemia.

Insulin resistance is found in association with obesity, non-insulin-dependent diabetes mellitus, and essential hypertension, which are all risk factors for atherosclerotic cardiovascular disease. Furthermore, hyperinsulinemia has been reported in familial combined hyperlipoproteinemia and endogenous hypertriglyceridemia. Finally, relatively high serum triglyceride and low high-density lipoprotein (HDL) cholesterol concentrations invariably accompany hyperinsulinemia. Whether insulin sensitivity is affected by the isolated presence of high levels of serum low-density lipoprotein (LDL) cholesterol has not been clearly established. We studied 13 subjects with heterozygous familial hypercholesterolemia (FHC) and 15 normocholesterolemic subjects selected to be free of any other known cause of insulin resistance. Thus FHC patients and controls had normal body weight and fat distribution, glucose tolerance, blood pressure, and serum triglyceride and HDL cholesterol concentrations, but were completely separated on plasma LDL cholesterol concentrations (6.05 +/- 0.38 v 3.27 +/- 0.15 mmol/L, P < .0001). Fasting plasma levels of glucose, insulin, free fatty acids (FFA), and potassium and fasting rates of net carbohydrate and lipid oxidation were superimposable in the two study groups. During a 2-hour euglycemic (approximately 5 mmol/L) hyperinsulinemic (approximately 340 pmol/L) clamp, whole-body glucose disposal rates averaged 30.4 +/- 2.3 and 31.1 +/- 3.0 mumol.kg-1 x min-1 in FHC and control subjects, respectively (P = 0.88). The ability of exogenous hyperinsulinemia to stimulate carbohydrate oxidation and energy expenditure and suppress lipid oxidation and plasma FFA and potassium levels was equivalent in FHC and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin decreases circulating vitamin E levels in humans.

Both hyperinsulinemia and free oxygen radicals have been implicated in the pathogenesis of atherosclerosis, but the relationship between insulin levels or insulin action and the oxidant/antioxidant balance has not been explored. We measured the effect of physiologic hyperinsulinemia on plasma concentrations of vitamin E, a major free radical scavenger molecule. Isoglycemic clamps (at an insulin infusion rate of 6 pmol . min-1 . kg-1) were performed in four groups of subjects: (1) 12 non-insulin-dependent diabetic (NIDDM) patients, (2) eight patients with essential hypertension, (3) 11 nondiabetic obese individuals, and (4) 12 healthy subjects. In 10 healthy volunteers, a time-control experiment was performed by replacing the insulin infusion with normal saline. Vitamin E and plasma lipid levels were determined at baseline and after 2 hours of insulin/saline infusion. Insulin sensitivity was reduced in diabetic, obese, and hypertensive groups in comparison to healthy controls, but fasting plasma vitamin E concentrations were similar in all groups. A consistent decrement in plasma vitamin E concentrations (averaging 12% of baseline, P < .0001) was observed in all subjects receiving insulin regardless of the level of insulin sensitivity, whereas no significant changes in plasma vitamin E were seen in subjects receiving saline infusion (P < .001 v insulin infusion groups). The insulin-induced decrement persisted in all study groups when plasma vitamin E concentrations were corrected for total serum cholesterol levels (-8.9% +/- 1.2% v -0.4 +/- 2.3% of saline controls, P = .0004) or serum low-density lipoprotein (LDL(-10.0% +/- 1.2% v -0.4% +/- 2.2%, P = .0002). We conclude that insulin infusion acutely depletes vitamin E in circulating lipids regardless of insulin resistance. This effect may represent a physiologic means of transferring vitamin E into cell membranes; alternatively, it might reflect a pro-oxidant action of insulin in vivo.

Reproducibility of electrophysiological parameters of sinus node following autonomic blockade.

We investigated the reproducibility of sinus node cycle length (SCL), corrected sinus node recovery time (CSRT) and sino-atrial conduction time (SACT) during the control state and following autonomic blockade in 25 patients (mean age: 56.9 +/- 13.8 years). Autonomic blockade was induced by i.v. administration of propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). The electrophysiological study was repeated after 24 hr and the results were compared. The patients were divided into two groups: Group 1 (15) with normal and Group 2 (10) with abnormal intrinsic sinus node function. Following autonomic blockade in Group 1 the daily variations in SCL, CSRT and SACT were very slight whereas in Group 2 there was far greater variability in these parameters. However, in the latter group there were no patients who changed their status from prolonged to normal intrinsic CSRT on the second study, whereas SACT changed its status in 2 patients. In Group 1 the daily variations in sinus node parameters were much slighter following autonomic blockade than during the control state. In Group 2 the variations were very similar during control and following autonomic blockade. These data suggest that: (1) following autonomic blockade the reproducibility of sinus node parameters is very good in Group 1, whereas in Group 2 several patients show marked daily variations in sinus node parameters; (2) following autonomic blockade the sinus node electrophysiological parameters are meaningful in diagnosing an involvement of intrinsic sinus node function; and (3) in patients with abnormal sinus node parameters during control state, but with normal intrinsic sinus node function, the daily variations are mainly due to change in autonomic tone, whereas when the intrinsic sinus node function is abnormal, the day to day variations during control state appear due predominantly to intrinsic sinus node abnormalities.

A method for evaluating different modes of action of an antiarrhythmic drug in man. The effects of propafenone on sinus nodal functions.

In vitro experiments have shown that the antiarrhythmic effects of propafenone are due to a direct depressant action and to a beta-blocking activity. In this study a method was used to evaluate the direct effect and the autonomically mediated actions of an antiarrhythmic agent in a clinical setting. An electrophysiological study was performed twice, at an interval of 24 hr, in 17 patients (age: 52 +/- 17 years) with normal resting and intrinsic heart rate. In the first study the overall effect of intravenous propafenone (1.5-2 mg/kg) was evaluated by comparing the sinus node parameters obtained during the basal state and after drug administration. In the second study the direct depressant effect of the drug was evaluated by comparing the electrophysiological variables obtained following autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg) and after propafenone. In the first study there was no significant change in the sinus cycle length and corrected sinus node recovery time and only a small (9.1%) increase in sinuatrial conduction time, whereas in the second study these variables increased significantly. The degree of increase in sinus cycle length and corrected sinus node recovery time was significantly higher in the second study than in the first one. These data suggest that: (1) propafenone has direct depressant effect on sinus automaticity but this effect is counteracted by autonomically mediated actions (most likely of vagolytic type); (2) the beta-blocking effect of the drug demonstrated in isolated atria is not seen in a clinical setting.

[Effects of low-dose oral contraceptives on sugar metabolism]. / Effetti dei contraccettivi orali a basse dosi sul metabolismo glucidico.

The effects on carbohydrate metabolism by four low-dose oral contraceptives were evaluated in four low-dose oral contraceptives were evaluated-66 young women randomly divided in four groups. In the various preparations there were a different dosage of estrogen (ethinylestradiol) together different doses and types of progestogen (desogestrel, gestodene, cyproterone acetate). After six months of treatment, in all groups a slight increase of glycemic and insulinemic responses during OGTT was observed; the significance was achieved with the preparation containing cyproterone acetate alone. Glycated hemoglobin did not change. Our results suggest that these new low-dose oral contraceptives induced negligible metabolic side effects.

In postmenopausal osteoporosis the bone increasing effect of monofluorophosphate is not dependent on serum fluoride.

According to previous pharmacokinetic studies the bioavailability of fluorine (F) from sodium monofluorophosphate (MFP) doubles that of sodium fluoride (NaF). This paper reports a study designed to verify whether the vertebral bone mass increasing effect of NaF (30 mg F/day) was comparable to that of MFP (15 mg F/day), given for 18 months to osteoporotic postmenopausal women. The BMD of lumbar vertebrae of both groups showed significant increases (MFP: 60 +/- 15 mg/cm2, NaF: and 71 +/- 12 mg/cm2) over basal levels (P < 0.001). The difference between treatments was not significant (P = 0.532). The serum levels of ionic F (the mitogenic species on osteoblasts) were not related to the above mentioned effects. In NaF-treated patients, the fasting levels of total serum F increased significantly (6.7 +/- 0.9 microM vs. Basal: 2.0 +/- 0.8 microM; P < 0.001). This phenomenon was accounted for by ionic fluoride that increased over 20-fold (6.5 +/- 1.9 microM vs. Basal: 0.3 +/- 0.04 microM). In MFP-treated patients the fasting serum levels of total (7.0 +/- 0.7 microM vs. Basal: 2.2 +/- 0.9 M) and diffusible F (0.5 +/- 0.02 microM vs. Basal 0.2 +/- 0.02 microM) increased significantly (P < 0.001). The increase in the non diffusible F fraction is accounted for by protein-bound F, probably by the complexes formed between MFP and alpha 2-macroglobulin and C3. Serum diffusible F was formed by two fractions: ionic F and F bound to low molecular weight macromolecule/s (2,200 +/- 600 Da), in approximately equal amounts. The general information afforded by the present observations support the hypothesis that ionic F is released progressively during the metabolism of MFP bound to alpha 2-macroglobulin and C3. These phenomena explain why comparable effects to those obtained with 30 mg F/d of NaF could by obtained with one half the dose of MFP.