Congenital retroparietal fibrolipoma and osteochondroma in a calf.
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Biomedical subjects
Publications and source records attributed to A Salvaggio.
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Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.
BACKGROUND: The aims of this study were to compare compliance to treatment with fixed CPAP and with autoCPAP, subjective preference for type of CPAP treatment, and factors associated to preference for autoCPAP in patients with OSAS. PATIENTS AND METHODS: Twenty-two subjects were studied in a randomized, single blind cross-over fashion. They were treated for one month by fixed CPAP (Elite Sullivan V, ResMed, Sydney, Australia) and one month by autoCPAP (Autoset T, ResMed, Sydney, Australia). RESULTS: Four subjects who stated a preference for fixed CPAP and four who expressed no preference were pooled together; fourteen preferred autoCPAP. Compliance to treatment using the two machines did not differ in the first group (3.8 (1.9) vs. 3.8 (1.5)h/day, fixed vs autoCPAP), but was higher with autoCPAP in the second group (4.8 (1.8) vs 5.5 (1.5)h/day, P<0.05). Baseline apnea/hypopnea index (AHI) was high in both groups, but was higher in the second group P<0.02. First treatment was always fixed CPAP in patients who preferred fixed CPAP, while it was either in the other subjects. CONCLUSIONS: Compliance to autoCPAP differs among OSAS patients. As long as factors predicting higher compliance to autoCPAP are not found, a trial with autoCPAP in patients poorly compliant to fixed CPAP may be warranted.
The aim of this study was to investigate whether chronic continuous positive airway pressure (CPAP) affects blood pressure (BP) responsiveness to obstructive events occurring on the first night of CPAP withdrawal in obstructive sleep apnoea (OSA) after chronic treatment. Thirteen male subjects with severe OSA underwent nocturnal polysomnography with beat-by-beat BP monitoring before treatment and after 4.9 +/- 3.4 months of home CPAP (mean daily use 5.1 +/- 1.7 h). Variations in oxyhaemoglobin saturation (deltaSa,O2), systolic (deltaPs), and diastolic (deltaPd) BP within nonrapid eye movement apnoeas and hypopnoeas were measured on a sample of pre- and post-treatment events. In addition, a pretreatment sample was selected for deltaSa,O2 to match post-treatment events. The higher the mean deltaSa,O2 was in the full pretreatment sample, the more deltaSa,O2, deltaPs and deltaPd were attenuated after treatment. Mean deltaPs decreased from 47.3 +/- 8.5 in the full pretreatment sample to 42.2 +/- 6.9 in the selected pretreatment sample, to 31.5 +/- 5.9 mmHg in the post-treatment sample. The post-treatment value differed significantly from both the pretreatment values. The corresponding values for mean deltaPd were 27.0 +/- 3.5, 24.0 +/- 3.1 and 19.6 +/- 3.7 mmHg, with all values differing significantly from each other. Chronic continuous positive airway pressure is followed by a decrease in apnoea/ hypopnoea-related blood pressure swings, possibly secondary to both reduced severity of event-related hypoxaemia and decreased responsiveness to obstructive events secondary to chronic prevention of nocturnal intermittent hypoxaemia.
Hepatic biliary cystadenoma is a well-delineated neoplasm in some domestic animals, especially in cats, but it has not been reported in equines. We report on a case of hepatic biliary tumor, incidentally found in a 10-year-old horse, with gross and microscopic features similar to those observed in biliary adenofibroma of humans. The tumor presented as a solid mass measuring 16 cm in diameter and histologically was composed of complex tubulocystic biliary components embedded in an abundant fibrotic stroma. We regarded this tumor as a morphological variant of biliary cystadenoma of domestic animals. Differential diagnoses from other hepatic biliary tumor-like and tumor lesions are provided.
We have studied the effects of treatment with recombinant human (rh)IL-6 on clinical, histological and immunological parameters of protracted relapsing (PR) experimental allergic encephalomyelitis (EAE) in DA rats. rhIL-6 (50 microg/rat subcutaneously/day) was given under three different regimens, as early prophylaxis, from 1 day prior to 14 days after immunization, in late prophylaxis, from day +7 until day 21 post-immunization (p.i.) and therapeutically to rats with clinical signs of EAE from day 14 to day 28 p.i. Although rhIL-6 failed to modulate the course of PR-EAE when administered as the early prophylactic regimen, it exerted clear-cut favourable effects on the course of the disease if was administered either as later prophylactic or as therapeutic treatment. Under these conditions, rhIL-6 accelerated recovery from EAE attacks and reduced/milded subsequent EAE episodes as compared to either PBS- or heat-inactivated rhIL-6-treated control rats. In agreement with this clinical effect, relative to PBS-treated rats, the animals injected with rhIL-6 exhibited lower numbers of MHC class II(+) and CD4(+) cells in their spinal cords. rhIL-6-treatment also profoundly modulated the endogenous cytokine network, the treated rats displaying increased numbers of spleen cells expressing mRNA transcripts of the anti-inflammatory cytokines IL-10 and TGF-beta along with simultaneously reduced numbers of mRNAs for TNF-alpha. In addition, upon ex vivo exposure to either myelin basic protein peptide 63-88 (MBP63-88) or to phytoaemagglutinin A, the numbers of IFN-gamma secreting splenocytes was also significantly reduced (ELISPOT analysis) in rhIL-6-treated rats as compared to PBS-treated controls.
Electrical stimulation of the spinal cord at C7D1 evoked triphasic descending spinal cord evoked potentials (DSCEP) from an oesophago-vertebral recording at D8D8 or D1OD1O. Ascending SCEPs (ASCEP) larger and similar in shape were also observed when the orientation of the stimulating and recording dipoles was reversed. Both SCEPs are in part generated by descending and ascending synchronous excitation of neuronal volume-conducted spinal cord dipoles.
The reliability of a POLYMESAM (PM) instrument in the detection of ventilatory disorders and in the diagnosis of obstructive sleep apnea syndrome (OSAS) was evaluated in 50 subjects suspected for OSAS, simultaneously studied by polysomnography (PSG) in a sleep laboratory. Recordings were analysed by separate scorers, blinded to the results of the paired recording. The number of central (Ac), obstructive (Ao) or mixed apneas (Am), of hypopneas (H), and the total number of ventilatory disorders (AH) per hour of time in bed (TIB) calculated on the two recordings were significantly correlated. Bland and Altman analysis showed a good agreement between AH/TIB, Ac/TIB, Am/TIB and mean AH duration; a lower Ao/TIB at PM was mirrored by a higher H/TIB. Forty-two subjects had OSAS according to an apnea/hypopnea index (AHI) > or = 10 at PSG. Due to low sleep efficiency, AH/TIB was substantially lower than AHI. However an AH/TIB > or = 5 at PM showed a sensitivity of 100% and a specificity of 71.4%, while an AH/TIB > or = 10 showed a sensitivity of 95.2% and a specificity of 100%. In conclusion, PM proved reliable for recognition of the characteristics of ventilatory disorders and for diagnosis of OSAS.
Blood pressure (BP) variability during sleep is high in obstructive sleep apnoea syndrome (OSAS). How BP sampling interval affects the estimate of mean nocturnal BP in OSAS and control subjects was investigated. Nine subjects with apnoea/hypopnoea index (AHI) <5 and 18 OSAS patients with AHI >30 underwent nocturnal polysomnography with beat-by-beat BP monitoring. Mean nocturnal BP was evaluated averaging: a) all systolic (Ps) and diastolic (Pd) BP values; b) Ps and Pd sampled every 5, 10, 15, 20, and 30 min. The sampling starting point was repeatedly shifted, and several mean BP estimates for each sampling interval were obtained. Differences (deltaPs and deltaPd) between means obtained by sampling BP and by averaging all BP values were calculated. In both groups deltaPs and deltaPd scatter increased as sampling interval increased; their variance was always higher in OSAS subjects (p<0.001). Over 95% of deltaPs and deltaPd were <5% of the beat-by-beat mean values at all sampling intervals in controls, but this occurred only at sampling intervals < or =10 min in OSAS subjects. To conclude, for each blood pressure sampling time, a larger number of inaccurate nocturnal mean blood pressure estimates are obtained in obstructive sleep apnoea syndrome than in control subjects. Obstructive sleep apnoea syndrome subjects require more frequent blood pressure measurements to obtain a similar accuracy in nocturnal blood pressure evaluation.
Concanavalin A (ConA)-induced hepatitis is a cell-mediated immunoinflammatory condition similar to human autoimmune hepatitis. We investigated the role of interleukin 12 (IL-12) in hepatitis induced in NMRI and C57/BL6 mice by a single injection of ConA. Recombinant murine IL-12 administered 24 hours and 1 hour prior to ConA exacerbated both transaminase activities in plasma and histologic signs of hepatitis. These markers of liver injury were significantly reduced by prophylactic, but not therapeutic treatment with anti-IL-12 monoclonal antibody (mAb). The disease-modulatory effects of IL-12 and anti-IL-12 mAb were associated with profound and reverse modifications of a ConA-induced increase in the circulating levels of IL-4, IL-6, interferon gamma (IFN-gamma) and tumor necrosis factor (TNF). Relative to control animals receiving ConA alone, the plasma levels of these cytokines were all augmented in IL-12/ConA-treated mice and diminished in anti-IL-12 mAb/ConA-treated mice. Anti-IFN-gamma mAb also impeded the appearance of IL-12/ConA-induced hepatitis. Thus, IL-12-induced production of IFN-gamma might play a role in mediating the hepatitis-inducing effect of ConA. However, IL-12p40-deficient C57/BL6 mice were as susceptible as wild-type controls to the hepatitis-inducing effect of ConA.
OBJECTIVE: To evaluate the effects of a diet therapy in patients with rheumatoid arthritis (RA). METHODS: Fifty RA patients entered a 24-week double-blind, randomised, controlled-study of two different dietary regimens (an experimental diet high in unsaturated fats, low in saturated fats with hypoallergenic foods vs. a control well-balanced diet). The primary end points of the study were 20% and 50% improvement in disease activity according to composite symptoms (Paulus index) of arthritis. Other end points were the other measures of disease activity at 12 and 24 weeks of diet treatment. RESULTS: The 2 groups were comparable at inclusion. Diet treatment was well tolerated and the rate of drop-outs was low. Percentage of patients with global 20 or 50% response didn't differ between experimental and control group after the 24-week of diet treatment. The experimental diet group did better for all the variables considered but only four variables (Ritchie's index, tender and swollen joints, and ESR) reached a statistical difference by multivariate analysis. Adjusting these data for weight variations, the number of tender joints (p=0.014) and ESR (p=0.025) were still statistically significant. CONCLUSIONS: Dietary manipulation, either by modifying food supplements or by reducing weight, may give some clinical benefit although no significant improvement can be observed assessing the results with a composite index.
The ventilatory and arterial blood pressure (ABP) responses to isocapnic hypoxia during wakefulness progressively increased in normal subjects staying 4 wk at 5,050 m (Insalaco G, Romano S, Salvaggio A, Braghiroli A, Lanfranchi P, Patruno V, Donner CF, and Bonsignore G; J Appl Physiol 80: 1724-1730, 1996). In the same subjects (n = 5, age 28-34 yr) and expedition, nocturnal polysomnography with ABP and heart rate (HR) recordings were obtained during the 1st and 4th week to study the cardiovascular effects of phasic (i.e., periodic breathing-dependent) vs. tonic (i. e., acclimatization-dependent) hypoxia during sleep. Both ABP and HR fluctuated during non-rapid eye movement sleep periodic breathing. None of the subjects exhibited an ABP increase during the ventilatory phases that correlated with the lowest arterial oxygen saturation of the preceding pauses. Despite attenuation of hypoxemia, ABP and HR behaviors during sleep in the 4th wk were similar to those in the 1st wk. Because ABP during periodic breathing in the ventilatory phase increased similarly to the ABP response to progressive hypoxia during wakefulness, ABP variations during ventilatory phases may reflect ABP responsiveness to peripheral chemoreflex sensitivity rather than the absolute value of hypoxemia, suggesting a major tonic effect of hypoxia on cardiorespiratory control at high altitude.
A possible role for human endogenous retroviruses (HERV) in the pathogenesis of MS was investigated by analyzing HERV peptides-stimulated proliferation and cytokine production in MS patients with acute (AMS) or stable (SMS) disease. HERV peptides specific-proliferation and type 1 cytokine production by peripheral blood mononuclear cells was observed in AMS but not in SMS individuals, in whom a type 2 cytokine profile dominates. HERV peptides-stimulated immune responses were modified by changes in disease expression; mediated by CD4+ T lymphocytes; and not related to HLA class II molecules. These data suggest the possibility of a pathogenic role for HERV and HERV-specific immune responses in MS.
BACKGROUND: The thymus is the organ responsible for the maturation and selection of T lymphocytes and is thus pivotal in allowing the development of a functional immune system. Because in HIV infection cell-mediated immune responses are severely impaired, we studied the role of thymus in the control of the progression of HIV infection to AIDS. METHODS: Thymic volume was analysed by magnetic resonance imaging in 31 vertically HIV-infected children. Plasma HIV viral load and phenotypic and functional cellular immunity-defining parameters were examined in the same patients. RESULTS: Thymic volume was not correlated with age or nutritional status; thymic volume was nevertheless correlated with CD4 T-lymphocyte counts and with the percentage and absolute number of CD45RA+CD62L+ (naive) T lymphocytes. In addition, the ability of peripheral blood mononuclear cells to proliferate upon tetanus stimulation was directly proportional to thymic volume. Finally, a negative correlation was detected between thymic volume and HIV viral load. CONCLUSION: Because low HIV plasma viraemia and preserved immune function are favourable prognostic indices in HIV disease, these data indicate that an immunological, thymic-dependent control of the progression of HIV infection might be possible, at least in vertically transmitted HIV infection.
PURPOSE: Hemorrhoids and rectal diseases are very frequent in HIV-positive patients, especially in those with homosexual habits. This study was designed to compare posthemorrhoidectomy healing time in such patients, and evaluate the role of various factors related to their HIV-positive status. METHODS: The study involved a prospective series of 48 male patients (32 HIV-seropositive and 16 with acquired immunodeficiency syndrome) who underwent hemorrhoidectomy between 1992 and 1996; 20 age-matched and gender-matched seronegative patients were retrospectively identified as controls. Healing times, postoperative complications, and wound infections were recorded, and the delaying effect of CD4+, Karnofsky Index scores, and HIV-ribonucleic acid were evaluated. Between-group differences were analyzed using Cox's model, Student's t-test, chi-squared test, and Fisher's exact probability test. P values of <0.05 were considered statistically significant. RESULTS: Cox's model revealed that HIV positivity and the presence of acquired immunodeficiency syndrome significantly delayed wound healing, which also correlated with the presence of infection. The healing rate in HIV-positive patients was 66 percent after 14 weeks and 100 percent after 32 weeks; the corresponding figures for patients with acquired immunodeficiency syndrome were 0 and 50 percent. All of the controls were healed after 14 weeks (P < 0.01 vs. both the patients with acquired immunodeficiency syndrome and HIV+ patients). Centers for Disease Control and Prevention HIV-positive status (including CD4+ counts) and the performance status proved to be of prognostic value. CONCLUSIONS: Our data suggest that the indications for hemorrhoidectomy in patients with acquired immunodeficiency syndrome need to be considered extremely carefully because of the high incidence of delayed wound healing.
The role of sleep in the pathogenesis of coronary ischaemic events such as myocardial infarction, transient myocardial ischaemia, or cardiac sudden death, is unclear. This review will analyse the available data on the subject according to: (i) the autonomic and cardiovascular changes during sleep that may potentially favour myocardial ischaemia; (ii) the evidence of a circadian distribution of coronary events; and (iii) the factors possibly involved in the pathogenesis of nocturnal angina. Available data suggest that myocardial ischaemia may occur by different mechanisms in non-rapid eye movement (NREM) (decreased coronary perfusion pressure) and rapid eye movement (REM) sleep (increased myocardial oxygen demand). Coronary events show a major peak of occurrence between 6.00 a.m. and noon; however, the myocardial ischaemic threshold, defined as the heart rate value at which myocardial ischaemia develops, may be lower at night than during the daytime, suggesting an unexpectedly higher susceptibility to myocardial ischaemia during sleep than during wakefulness. These data warrant further study on the pathophysiology of coronary circulation during sleep. Finally, some evidence is available that sleep disordered breathing may precipitate nocturnal angina especially in REM sleep, through decreased arterial oxygen content secondary to hypoventilation or true apnoeas. More data are needed to better understand the effects of sleep on the coronary circulation, and to improve the therapeutic approach of nocturnal angina.
Vaccination of HIV-infected individuals increases HIV viral load, reduces CD4 cell counts, and might influence disease progression. Because these deleterious effects are postulated to be secondary to a direct activation of T lymphocytes induced by the immunogen, we compared immunologic and virologic effects of a T cell-dependent and a T cell-independent vaccine. Seventeen HIV-infected children were immunized with influenza (FLU) (T cell-dependent) or pneumococcal (PNEUMO) (T cell-independent) vaccines. HIV viral load and type 1 (IL-2 and IFN-gamma) and type 2 (IL-4 and IL-10) cytokine production were evaluated before and 7, 14, and 28 days after vaccination. Slopes of CD4 cell counts analyzed 6 months before and 6 months after vaccination were not significantly different. HIV viral load increased in both groups of children despite the fact that type 1 cytokine production and the type 1-to-type 2 ratio increased in FLU-vaccinated but not in PNEUMO-vaccinated patients. Thus, an increase in HIV viral load in the absence of T cell activation (as measured by cytokine production) was observed in PNEUMO-vaccinated children. Because polysaccharides of the bacterial cell wall stimulate TNF-alpha production by monocyte-macrophages and TNF-alpha was shown to stimulate HIV replication directly on activation of NF-kappa b after binding the long terminal repeat (LTR) sequences of HIV, we measured TNF-alpha production and observed a significant increase in both groups of vaccines. These data suggest that an increase in HIV viral load can be observed in vaccinated HIV-infected children even independent of direct antigen-induced activation of T lymphocytes, and that augmented production of TNF-alpha might play a role in this phenomenon.