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Leptin is a recently identified hormone produced by the adipocyte ob gene which acts as a negative feedback signal critical to the normal control of food intake and body weight. A number of proinflammatory cytokines, such as interleukin 6, tumor necrosis factor alpha, and interferon gamma, have been proposed as mediators of cancer cachexia; these data suggest that abnormalities in leptin production/release or in its feedback mechanism play a role in cancer patients. We therefore studied the relationship between serum leptin and serum cytokines interleukin 6 and tumor necrosis factor alpha levels in advanced-stage cancer patients. Twenty-nine advanced stage cancer patients (all but one stage IV) with tumors at various sites were included in the study. A direct correlation between body mass index and serum leptin levels was found both in cancer patients and in healthy individuals. The serum levels of interleukin 6 were significantly higher in cancer patients than in healthy individuals. In cancer patients an inverse correlation was found between serum levels of leptin and proinflammatory cytokines. There was an inverse correlation between the Eastern Cooperative Oncology Group performance status scale and serum levels of leptin. Regarding survival, patients with very high serum levels of proinflammatory cytokines and very low levels of leptin had very short survival. Although obtained in a cancer patient population not overtly cachectic, our results provide further evidence that a simple dysregulation of leptin production and/or release cannot be involved in cancer-associated pathophysiological changes leading to cachexia.

Changes in brain serotonin levels are correlated with the latency of an early component of auditory evoked potentials (EAEP) in rats. In fact 5-hidroxytryptophan provokes an increase both in serotonin brain synthesis and in the latency of EAEP. On the other hand, PCPA provokes an opposite effect.

Cyclic passive movements of the right arm at 1Hz induce an increase in pulmonary ventilation in man. This results from an increase in frequency of the respiratory cycles, mainly due to a shortening of the expiratory phase, and from an increase of the instantaneous flow. The delay between the beginning of the arm movements and the onset of the increase in flow is about 450msec.

Increments in pulmonary ventilation were shown to occur in anaesthetized cats during long-lasting stimulation of a peripherally cut extensor muscle nerve at maximal intensity for group I afferent fibers. However, these increments tended to gradually adapt to a lower value when stimuli were delivered at high frequency and constant rate whereas a tendency to potentiation, up to a steady state, occurred when stimulation was intermittent. End-tidal PCO2 initially decreased with a tendency to adaptation in the case of continuous stimulation, and decreased progressively in the case of intermittent stimulation. It is concluded that the nervous mechanisms producing hyperpnoea exhibit fatigue during their constant excitation while their effects sum up during intermittent stimulation.

An increase in the instantaneous pulmonary flow and a decrease in the respiratory frequency has been found in man as a consequence of isometric contraction of either flexor or extensor muscles of the elbow. The delay of 200 to 900msec between the onset of the muscle contraction and the beginning of the flow increment suggests that the respiratory system increases its activity due to the proprioreceptor activation. As there is no significant difference in the results obtained during flexor or extensor contraction, the contribution of the two different receptor groups appears to be the same.

Passive leg movements induced in man at a frequency of 1 Hz by an electric cycle increase pulmonary ventilation after a delay of 200-400 msec. No chemical stimuli can account for this effect since a longer delay of 1 to 5 respiratory acts (7) is required for them to drive the respiratory system. Consequently the hypothesis is made that a neural mechanism, put into action by the moving legs, provides the adequate stimuli.

Brief contraction of arm muscles affects respiratory ventilation either by increasing respiratory frequency or by increasing the instantaneous flow. Both these changes occur at a time subsequent to muscle contraction and can be attributed to a reflex mechanism originating from the muscles.

We have studied the latency behaviour of an early component of the cortical acoustic evoked potentials (EAEP) in albino rats after administration of p-chlorophenylalanine (PCPA), a rather selective tryptophan-hydroxylase inhibitor, at a dose of 100 mg/kg daily for 3 days. The rats were implanted with 3 chronic electrodes: one in the bregma, one in the nasion and 3rd inserted in the periauricular skin. Series of clicks originating from a square pulse of 0.12 msec duration were administrated. Brain responses were amplified by an EEG and averaged by a computer with different post-stimuli analysis times. A first group of 4 rats was tested with clicks of 100 dB (HTL) intensity and brain responses were analysed at 5,10,25,50,100 msec post-stimuli times. Results demonstrate that after PCPA administration there is a latency reduction of EAEP components that have a latency higher than 20 msec. In a second group of 4 rats we have analysed those EAEP components with an intensity of clicks ranging from 60 to 110 dB and results demonstrate that, when PCPA was administered, Latencies of those components were significatively lower than the controls at each stimuli intensity tested. We concluded that 5-HT may influence the acoustic pathways activity and this is according to remarks of other A.A. that found a correlation between acoustic stress and brain 5-HT levels.