Posterior insular stroke causing selective loss of contralateral nonpainful thermal sensation.
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Differential Threshold↗
Biomedical subjects
L Cattaneo
Publications and source records attributed to L Cattaneo.
The localization of facial motor impairment in sporadic Möbius syndrome.
OBJECTIVE: To investigate the neurophysiologic aspects of facial motor control in patients with sporadic Möbius syndrome defined as nonprogressive congenital facial and abducens palsy. METHODS: The authors assessed 24 patients with sporadic Möbius syndrome by performing a complete clinical examination and neurophysiologic tests including facial nerve conduction studies, needle electromyography examination of facial muscles, and recording of the blink reflex and of the trigeminofacial inhibitory reflex. RESULTS: Two distinct groups of patients were identified according to neurophysiologic testing. The first group was characterized by increased facial distal motor latencies (DMLs) and poor recruitment of small and polyphasic motor unit action potentials (MUAPs). The second group was characterized by normal facial DMLs and neuropathic MUAPs. It is hypothesized that in the first group, the disorder is due to a rhombencephalic maldevelopment with selective sparing of small-size MUs, and in the second group, the disorder is related to an acquired nervous injury during intrauterine life, with subsequent neurogenic remodeling of MUs. The trigeminofacial reflexes showed that in most subjects of both groups, the functional impairment of facial movements was caused by a nuclear or peripheral site of lesion, with little evidence of brainstem interneuronal involvement. CONCLUSION: Two different neurophysiologically defined phenotypes can be distinguished in sporadic Möbius syndrome, with different pathogenetic implications.
Adolescent↗
Capillary blood viscosity in microcirculation.
As known, at the arteriolar level there is the highest resistance to the flow due to the section and to the velocity with an average pressure fall of 50 mmHg (from 85 to 35 mmHg). This resistance is expressed in sec(-1) by the ratio W/2r. This ratio is very high with an average value of 332 sec(-1) and viscosity at this high shear-rate is negligible. At the capillary level the pressure fall is 11.5 mmHg but the vascular resistance W/2r is much lower, on average 32 sec(-1). We can say that if a resistance of 333 sec(-1) corresponds with a pressure fall of 50 mmHg, then a resistance of 32 sec(-1) should correspond with a pressure fall of 4.8 mmHg. The highest pressure fall is due to another kind of resistance which we can define as "Capillary Blood Viscosity" because it depends on the rheological and structural characteristics of the blood. Our instrument reproduces the structure of the capillary district in an experimental model and measures the General Blood Viscosity (GBV) and the Capillary Blood Viscosity (CBV) at the same shear-rate and in particular at the low shear-rate when in non-Newtonian fluids the highest increase in viscosity appears. Consequently, at the capillary, viscosity is dominant with respect to the other geometric and physical resistances. Moreover, the percentage ratio between the GBV and the CBV gives a physical measure of erythrocyte deformability. Knowing viscosity at shear-rate present in the circulatory system, we can obtain the size of RBCs aggregates in the different circulatory districts and their characteristics expressed like "aggregation bond". Changes in CBV are the only possibility in clinical practice to improve the circulatory flow in the capillary district because it is not sure that changes in the arteriolar section can improve the capillary flow or rather open arterio-venous anastomosis. Moreover, in the systemic circulation the aggregate size allows us to point out the phenomenon of cell adhesion because the presence of several receptors involves also the other blood cells. Finally the size and the stability of the RBCs aggregates can modify the endothelial thrombo-resistance.
Arthritis, Rheumatoid↗
Pathological yawning as a presenting symptom of brain stem ischaemia in two patients.
Two cases of brain stem stroke involving the upper pons and the ponto-mesencephalic junction presented with transient excessive pathological yawning, associated with gait ataxia and in one subject with upper limb and facial hemiparesis. A causal relation is hypothesised between the brain stem lesion and pathological yawning, possibly related to denervation hypersensitivity of a putative brain stem yawn centre. Excessive yawning may herald brain stem ischaemia.
Aged↗
A cortico-cortical mechanism mediating object-driven grasp in humans.
Humans and other primates demonstrate an exquisite ability to precisely shape their hand when reaching out to grasp an object. Here we used a recently developed transcranial magnetic stimulation paradigm to examine how information about an object's geometric properties is transformed into specific motor programs. Pairs of transcranial magnetic stimulation pulses were delivered at precise intervals to detect changes in the excitability of cortico-cortical inputs to motor cortex when subjects prepared to grasp different objects. We show that at least 600 ms before movement, there is an enhancement in the excitability of these inputs to the corticospinal neurons projecting from motor cortex to the specific muscles that will be used for the grasp. These changes were object- and muscle-specific, and the degree of modulation in the inputs was correlated with the pattern of muscular activity used later by individual subjects to grasp the objects. In a number of control experiments, we demonstrated that no change in excitability was observed during object presentation alone, under conditions in which subjects imagined grasping the object, or before movements involving the same muscles but without an object. This finding demonstrates a cortico-cortical mechanism subserving the transformation from the geometrical properties of an object to the outputs from motor cortex before grasp that is specific for object-driven movements.
Adult↗
Small fibers peroneal mononeuropathy in a patient with Sjögren's syndrome.
Sjögren's syndrome (SS) is an autoimmune epithelitis characterized by lymphocytic infiltration of exocrine glands and epithelia in multiple sites. One third of the patients present with peripheral nervous system involvement. We describe the case of a woman aged 62 affected by a peroneal nerve mononeuropathy with painful disturbances secondary to a prevalent involvement of small fibers as demonstrated by electrophysiological investigations and skin biopsy. Asymmetric peripheral nerve involvement is not uncommon in SS, though, to our knowledge, it has never been reported of a mononeuropathy involving primarily small fibers.
Ankle↗
Combined antiestrogen, antiangiogenic and anti-invasion therapy inhibits primary and metastatic tumor growth in the MMTVneu model of breast cancer.
Treatments available to women with locally advanced breast cancer are unsatisfactory, since most patients succumb to metastatic spread. Therefore, there is a need to devise novel therapeutic combinations that effectively inhibit metastatization and to test them in animal models of breast cancer showing strong similarities with their human counterpart, including the ability to give rise to metastases. With these considerations in mind, tamoxifen (TAM), 4-hydrotamoxifen (4-HT) or liposome-complexed DNA constructs coding for antiangiogenic/anti-invasion proteins (angiostatin, TIMP-2, IFN-alpha(1), sFLT-1) were individually administered to MMTVneu transgenic mice. Significant inhibition of primary tumor growth was obtained with TAM (40% inhibition, P=0.049), angiostatin (85% inhibition, P=0.001) and TIMP-2 (60% inhibition, P=0.015). No lung metastasis was observed in any of these treated mice at 5 months, compared with a rate of 70% in control groups. These observations were the basis for designing a combined treatment with all these compounds. The association of angiostatin, TIMP-2 and TAM was greatly effective at the primary tumor level (90% inhibition, P=0.01). Moreover, all the mice treated with this association were metastasis free at a time point (6 months) in which seven out of nine control mice were either dead from disseminated cancer or showed lung metastasis. This combined therapy could become an important component of anticancer therapy in humans.
Angiogenesis Inhibitors↗
Combined effects on tumor growth and metastasis by anti-estrogenic and antiangiogenic therapies in MMTV-neu mice.
Breast tumor growth and metastasization are both hormone-sensitive and angiogenesis-dependent. Recent work carried out in our laboratory on a transgenic model of breast cancer displaying many similarities to its human counterpart, has shown that liposome-mediated angiostatin cDNA delivery partially inhibits both local and metastatic growth. However, it is now recognized that anti-angiogenesis strategy alone cannot completely arrest tumor growth and spread, and this led to the suggestion that approaches based on different molecular mechanisms could usefully be combined. In the present work, we investigated whether tamoxifen, a classical antiestrogen agent widely used in human therapy, could improve the results obtained with angiostatin alone. Further reduction of local growth was achieved with the combined regimen with respect to angiostatin or tamoxifen alone, while, as expected, no metastatic growth was detected in either group. We therefore conclude that a combination of angiogenesis inhibitors with antiestrogen drugs might be useful in humans and that other associations between conventional and gene transfer-mediated therapy are worth investigating and will soon become important components of anticancer therapy.
Angiogenesis Inhibitors↗
Sural nerve abnormalities in sacral perineural (Tarlov) cysts.
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Adult↗
Masseteric repetitive nerve stimulation in the diagnosis of myasthenia gravis.
OBJECTIVE: (1) to develop a method for masseteric repetitive nerve stimulation (RNS) and to obtain normative data for amplitude and area decrement of the muscle (M) response. (2) To investigate myasthenia gravis (MG) patients with masseteric RNS. Masticatory muscles are frequently affected in MG, but no RNS test is available to investigate this district. METHODS: Fifteen healthy subjects and 17 MG patients were examined. The masseteric nerve was stimulated by a monopolar needle (cathode), inserted between the mandibular incisure and the zygomatic arch, and a surface electrode (anode), on the contralateral cheek. Masseteric M response was recorded using surface electrodes on the muscle belly and below the mandibular angle. Stimuli were delivered at 3 Hz in trains of 9, at rest and after isometric effort. RESULTS: Normal subjects: mean amplitude decrement was 0.3+/-1.2% at rest, and 1.9+/-1.3% after isometric effort. PATIENTS: 15 patients (88%) were positive on masseteric RNS; in 3 of these it was the only positive RNS test. The extent of decrement observed in masseter muscle was significantly greater than in trapezius muscle. CONCLUSIONS: Masseteric RNS is a simple and well-tolerated procedure; it offers a new possibility in testing the cranial muscles in disorders of neuromuscular transmission.
Accessory Nerve↗
Trigemino-facial reflex inhibitory responses in some lower facial muscles.
The effects of electrical trigeminal stimulation on activated facial muscles were studied in 20 normal subjects in order to evaluate whether excitatory or inhibitory responses are present and to investigate whether the reflex organization is similar in all the facial muscles. No inhibition was observed in frontalis, orbicularis oculi, orbicularis oris, and mentalis muscles. By contrast, a clear suppression of electromyographic (EMG) activity (late silent period or SP2) was present in the levator labii superioris, depressor anguli oris, and depressor labii inferioris muscles, with a mean latency ranging from 41.8 to 50.2 ms, and a mean duration ranging from 27.5 to 40.9 ms. An early suppression of EMG activity (early silent period or SP1) was observed, with a latency of 16 to 20 ms and a duration of 10 ms, mainly in inferior perioral muscles. Our findings show a selective trigeminal inhibitory influence upon some specific lower facial muscles.
Adult↗
Hypothalamic neuropeptide Y and galanin in overweight rats fed a cafeteria diet.
We evaluated neuropeptide Y (NPY) and galanin (GAL) immunoreactivity (IR) and mRNA in the paraventricular and arcuate nucleus, respectively, in rats that became overweight (Ov) or not (NOv) when fed a cafeteria diet. After 2 months of diet, NOv rats showed a significant increase in NPY IR, whereas Ov rats showed a significant increase in GAL mRNA levels. None of these changes was present in rats overfed for 6.5 months. These differential changes in hypothalamic GAL and NPY transmissions may contribute to the different susceptibility of the two rat subpopulations to the weight-promoting effects of the hypercaloric diet.
Animals↗
Muscle reinnervation following neonatal nerve crush. Interactive effects of glycosaminoglycans and insulin-like growth factor-I.
This study shows that glycosaminoglycans promote muscle reinnervation following neonatal sciatic nerve injury. Such an effect appears to be mediated by insulin-like growth factor-1. The glycosaminoglycan moiety of proteoglycans is a constituent of the basal lamina active on nerve regeneration by means of the interaction with laminin and with several growth factors. We have previously shown that supplementation of glycosaminoglycans affects neuronal degeneration and regeneration. In this study we report that following neonatal lesion of the rat sciatic nerve glycosaminoglycan treatment promoted extensor digitorum longus muscle reinnervation with consequent improvement of muscle morphology. In saline-treated rats, reinnervation was only partial and there was a marked muscle fibre atrophy. In addition glycosaminoglycan treatment of lesioned rats increased insulin-like growth factor-I messenger RNA and protein in the reinnervated muscle, and insulin-like growth factor-I and insulin-like growth factor binding protein-3 plasma levels. Similarly, treatment of nerve lesioned rats with insulin-like growth factor-I promoted muscle reinnervation and prevention of muscle fibre atrophy, higher levels of insulin-like growth factor-I in the reinnervated muscle and of insulin-like growth factor-I and insulin-like growth factor binding proteins in plasma. These data suggest that glycosaminoglycans are potent stimulants of muscle reinnervation and that their effects may be mediated by increased levels of insulin-like growth factor-I.
Acetylcholinesterase↗
Different phototransduction kinetics of phytochrome A and phytochrome B in Arabidopsis thaliana.
The kinetics of phototransduction of phytochrome A (phyA) and phytochrome B (phyB) were compared in etiolated Arabidopsis thaliana seedlings. The responses of hypocotyl growth, cotyledon unfolding, and expression of a light-harvesting chlorophyll a/b-binding protein of the photosystem II gene promoter fused to the coding region of beta-glucuronidase (used as a reporter enzyme) were mediated by phyA under continuous far-red light (FR) and by phyB under continuous red light (R). The seedlings were exposed hourly either to n min of FR followed by 60 minus n min in darkness or to n min of R, 3 min of FR (to back-convert phyB to its inactive form), and 57 minus n min of darkness. For the three processes investigated here, the kinetics of phototransduction of phyB were faster than that of phyA. For instance, 15 min R h-1 (terminated with a FR pulse) were almost as effective as continuous R, whereas 15 min of FR h-1 caused less than 30% of the effect of continuous FR. This difference is interpreted in terms of divergence of signal transduction pathways downstream from phyA and phyB.
Arabidopsis↗
Growth hormone responses to growth hormone-releasing hormone and hexarelin in fed and fasted dogs: effect of somatostatin infusion or pretreatment with pirenzepine.
Using unanesthetized young male and female beagle dogs, before and after a 2-day fast, we studied the effect of an i.v. infusion of 0.9% saline (5 ml/h), somatostatin (SS, 4 or 8 micrograms/kg/h), or pretreatment with pirenzepine (PZ, 0.6 mg/kg i.v.), a muscarinic cholinergic antagonist which allegedly releases SS, on the GH release evoked by acute administration of GHRH (2 micrograms/kg i.v.), hexarelin (HEXA), a member of the GH-releasing peptide family (250 micrograms/kg i.v.) or GHRH plus HEXA. In fasted dogs, GHRH delivered during saline infusion induced a clear-cut rise in plasma GH levels, significantly higher than that which it induced in fed dogs. In contrast, HEXA, although very effective in causing the release of GH, only slightly increased GH secretion in fasted dogs over that which it induced in fed dogs. Co-administration of GHRH plus HEXA into fed dogs induced a synergic GH response that further increased with fasting. The action of GHRH in fed dogs was abolished by the lower dose of SS, whereas SS at either dose was ineffective in suppressing the GH-releasing effect during fasting. Infusion of the lower dose of SS failed to counter the action of HEXA, either before or during fasting, whilst the higher SS dose partially reduced it in both conditions. In contrast to SS, PZ reduced the GH-releasing effect of GHRH and HEXA, both in the fed state and, though to a lesser extent, during fasting. Pirenzepine only slightly reduced the robust GH rise elicited by GHRH plus HEXA in fed dogs. The suppressive effect of PZ on the GH response to combined administration of the peptides was lowest in fasted dogs. These data show that: (1) fasting augmented the GH response to GHRH and (to a lesser degree) to HEXA; (2) SS inhibited the GH response to GHRH in the fed state, but not in the fasted state; (3) only the higher dose of SS partially reduced the GH stimulation by HEXA in either the fed or the fasted state; (4) PZ lowered the GH response to GHRH and to HEXA in both the fed and (to a lesser degree) the fasted state; (5) PZ did not modify the GH release due to the combined administration of GHRH and HEXA. It is suggested that: (1) during fasting the greatly enhanced GH response to GHRH alone or GHRH plus HEXA probably reflects an augmented GHRH secretion; (2) somatotrope refractoriness to SS may contribute to the enhanced GH secretion in states of calorie deprivation; (3) in contrast to a general belief, muscarinic cholinergic antagonists, e.g. PZ, do not act exclusively via release of SS, but probably also through inhibition of GHRH function.
Analysis of Variance↗
Effect of long-term administration of Hexarelin on the somatotrophic axis in aged rats.
The growth hormone-releasing peptide Hexarelin (Hexa; 80 micrograms/kg-1, s.c.) was administered for 30 and 60 days to old rats. The GH-releasing effect of Hexa was maintained during chronic treatment. At the end of the treatment, old rats were administered once with Hexa which elicited a greater GH response in rats chronically treated with the peptide than in those receiving a placebo. Pituitary GHmRNA concentrations were significantly lower in the older rats than in the younger animals, irrespective of Hexa treatment, while the GH protein content was similar in all the groups studied. The same was true for hypothalamic GHRH, whose synthesis was reduced in all the older animals but not in the young, in the presence of maintained concentrations of the peptide. Somatostatin mRNA concentrations were significantly higher in the hypothalami of older rats and administration of Hexa for 30 or 60 days brought the concentrations of somatostatin mRNA of aged rats to 'young' levels. Treatments with Hexa failed to alter the circulating levels of IGF-1. The data reported in this article indicate that long-term treatment with Hexa normalized some biological indices of somatotrophic function in aged rats.
Aging↗
Hypothalamo-pituitary-IGF-1 axis in female rats made obese by overfeeding.
A gender-related impairment of the somatotrophic axis is present in obese Zucker rats, female rats being better preserved than males. We showed that another animal model of obesity, i.e., male rats made obese by feeding a hypercaloric diet had a reduced function of somatotrophic axis which was likely related to impairment of gonadal function. Aim of this work was that of studying the function of somatotrophic axis in female overfed rats and comparing it to that of male rats of the previous study. Sprague-Dawley female rats were fed an energy-rich palatable diet for seven months. At the end of overfeeding, according to the degree of overweight, rats were divided into overtly obese (Obese), overweight (Overweight) and Non-Obese, i.e. rats whose weights were similar to those of controls. Rats fed ad libitum with the standard pellet chow served as controls (Controls). Acute administration of a supramaximal dose of GHRH (2 microg/rat, iv) elicited a plasma GH rise similar to that of Controls in all the groups, except in Obese which had a lower GH response. Growth hormone responses after GHRH administration were inversely related to plasma levels of free fatty acids (FFA). Pituitary GH content and gene expression as well as hypothalamic GHRH and SS mRNA content, were similar in all experimental groups and in Controls and the same was true for plasma concentrations of free IGF-I. These results indicate that, similarly to obese female Zucker rats, also overfed female rats had a better preservation of the somatotrophic axis than their male counterparts. In diet-induced obese rats, also the etiology of the impairment of somatotrophic axis seems to be gender-related i.e. due to a reduction of gonadal function in males and to an elevation of FFA in females.
Animals↗
Worsening of ischemic damage in hearts from rats with selective growth hormone deficiency.
The effects of growth hormone (GH) deficiency on cardiac function were studied in young male rats administered an anti-GH-releasing hormone (GHRH) serum from postnatal day 20 to 40. Dependence of heart abnormalities on GH deficiency was ascertained by giving a group of anti-GHRH serum-treated rats GH replacement therapy. Heart preparations from anti-GHRH serum-treated rats, undergoing low-flow ischemia, showed a progressive increase in left ventricular end-diastolic pressure with poor recovery of mechanical activity and increased coronary perfusion pressure upon reperfusion. Hearts from anti-GHRH serum + GH-treated rats, undergoing global reduction to the flow, showed only a minimal increase of left ventricular end-diastolic pressure and, upon reperfusion, cardiac mechanical activity recovered almost completely. Similar findings were also observed in heart preparations from control (normal rabbit serum-treated) rats. Infusion of acetylcholine (10(-6) M) into heart preparations in the preischemic period increased coronary perfusion pressure values more markedly in hearts from normal rabbit serum- and anti-GHRH serum + GH-treated rats than in those from anti-GHRH serum-treated rats. These results indicate that selective GH deficiency in young male rats renders the heart more sensitive to ischemic damage and leads to an impairment of cardiac muscarinic receptor function.
Acetylcholine↗