Thermoregulatory Model

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Mitsuaki Yamamoto - One of the best experts on this subject based on the ideXlab platform.

  • a Model based interpretation of the biphasic daily pattern of sleepiness
    Biological Cybernetics, 1999
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Hikaru Nishiyama, Mitsuaki Yamamoto
    Abstract:

    We developed a Thermoregulatory Model of sleep control based on the hypothesis that non-rapid eye-movement sleep participates in homeostatic thermoregulation. This Model successfully reproduced several qualitative features of human sleep/wake cycles during entrained as well as the internally desynchronized states. Among the reproduced features, generation mechanisms of the biphasic sleepiness distribution are studied here in the light of the Model structure. Harmonic analysis is employed for this purpose. Through linearizations and confining the harmonics of the masking process to the fundamental component, a simplified representation of sleepiness is obtained. The simplified sleepiness is constructed with the fundamental circadian, the second harmonic components, and the constant (DC). The bimodality of the sleepiness is shown to be made by the second harmonic which is added to the fundamental component. The behavior of their amplitudes and phase positions are investigated under the varied sleep/wake durations and phase differences between the oscillators. Since the sleepiness generated by our Model is roughly mimicked by the simplified representation under diverse conditions, this simplification can be regarded as adequate. From the behavior of the constituents of respective harmonic components, the fundamental component is shown to originate from the sleep/wake masking process and the circadian oscillators; the second harmonic from the multiplicative interactions between the circadian oscillators and the sleep/wake masking process. These results indicate that the rhythmic processes are principal constituents of the sleepiness, at least in the steady state.

  • Thermoregulatory Model of sleep control: losing the heat memory.
    Journal of Biological Rhythms, 1999
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    Thermoregulatory mechanisms were hypothesized to provide primary control of non-rapid-eye-movement sleep (NREM). On the basis of this hypothesis, we incorporated the Thermoregulatory feedback loops...

  • Thermoregulatory Model of sleep control: losing the heat memory.
    Journal of biological rhythms, 1999
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    Thermoregulatory mechanisms were hypothesized to provide primary control of non-rapid-eye-movement sleep (NREM). On the basis of this hypothesis, we incorporated the Thermoregulatory feedback loops mediated by the "heat memory," heat load, and loss processes associated with sleep-wake cycles, which were modulated by two circadian oscillators. In addition, hypnogenic warm-sensitive neurons (HWSNs) were assumed to integrate thermoregulation and NREM control. The heat memory described above could be mediated by some sleep-promoting substances. In this paper, considering the possible carrier of the heat memory, its losing process is newly included in the Model. The newly developed Model can generate the appropriate features of human sleep-wake patterns. One of the special features of the Model is to generate the bimodal distribution of the sleepiness. This bimodality becomes distinct, as the losing rate of the heat memory decreases or the amplitude of the Y oscillator increases. The theoretical analysis shows the losing rate of the heat memory control's rapidity of Model response to a thermal perturbation, which is confirmed by simulating the responses with various losing rates to transient heat loads ("heat load pulse"). The sleepiness exhibits large responses to the heat load pulses applied in the early and late phases of wake period, while the response is significantly reduced to the pulse applied in the supposed wake-maintenance zone. This bimodality of the response appears to reflect the sensitivity of the HWSNs. In addition, the early pulse raises the immediate sleepiness rather than the nocturnal sleepiness, while the heat load pulse applied in the later phase of waking period significantly raises the sleepiness during a nocturnal sleep. In simulations of sleep deprivation, the discontinuous relationship between recovery sleep length and deprivation time is reproduced, where the critical sleep deprivation time at which the recovery sleep length jumps is extended as the losing rate increases. This is possibly due to the dissipation of the heat memory accumulated by the sleep deprivation. The simulation results here qualitatively reproduce the experimental observations or predict the intriguing phenomena of human circadian rhythms. Therefore, our Model could provide a novel framework for investigating the relationship between thermoregulation and sleep control processes.

  • A Thermoregulatory Model of Sleep Control
    The Japanese journal of physiology, 1995
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    We hypothesize that non-rapid-eye-movement sleep (NREM) is controlled by Thermoregulatory mechanisms of the preoptic/anterior hypothalamus. Circadian and homeostatic Thermoregulatory processes may be integrated in this brain area. To investigate this hypothesis, we have developed a mathematical Model of qualitative features of human sleep-waking behavior based on a Thermoregulatory feedback control mechanism, with modulation by two circadian oscillators, one a temperature rhythm, the other modulating sleepiness. Homeostatic features of the sleep rhythm are generated by integration of a heat load associated with waking. Simulations under entrained conditions show that the Model closely mimics typical features of human sleep rhythms, including a biphasic daily pattern of sleepiness and sleep-onsets and awakenings fixed in a descending phase and an ascending phase of the temperature rhythm, respectively. Sleep duration is strongly controlled by the phase difference between the two oscillators with the same period; these could represent two phase-differentiated expressions of a single oscillator. In addition, the simulation of sleep deprivation provides a natural interpretation of the experimentally observed phenomena, which shows that the homeostatic and the oscillatory aspects of the human circadian system is successfully integrated in our Model. The promising results obtained suggest that the control of sleep-wake rhythm could be understood within the framework of the thermoregulation.

  • Dynamical Features of Thermoregulatory Model of Sleep Control
    The Japanese journal of physiology, 1995
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    We have developed a quantitative Model of human sleep-wake rhythms based on a Thermoregulatory feedback control mechanism modulated by two circadian oscillators. Homeostatic features of sleep regulation are realized through the heat memory which represents the history of the masking process associated with sleep-wake cycles: heat load during wake and heat loss during sleep. Simulations under entrained conditions showed that the Model closely mimics well-known features of human sleep-wake rhythm, and that the homeostatic and the oscillatory aspects of the human circadian system are successfully integrated in our Model. In this paper, parameter dependency of the Model behavior is studied by simulations. Because of its physiology-based structure, the parameter dependency could show the possible underlying mechanism for the typical features of human sleep-wake rhythm. In addition, the Model stability is analyzed by the linear system theory and the simulations, which establishes the stability condition and suggests that the presented simulation results are basically stable. These results are informative to apply our Model to actual data of sleep-wake rhythms, and to interpret them from the physiological point of view.

Arcangelo Merla - One of the best experts on this subject based on the ideXlab platform.

  • Functional-Thermoregulatory Model for the differential diagnosis of psoriatic arthritis
    Biomedical engineering online, 2014
    Co-Authors: Enas Ismail, Paolo Amerio, Alessandra Capo, Arcangelo Merla
    Abstract:

    Introduction Psoriasis arthritis (PsA) is a chronic inflammatory arthritis of joints of uncertain pathogenesis. PsA may lead to severe disabilities even in the absence of any clinical symptom. Therefore, PsA diagnosis in its early stages is critical.

  • Functional-Thermoregulatory Model for the differential diagnosis of psoriatic arthritis
    BioMedical Engineering OnLine, 2014
    Co-Authors: Enas Ismail, Paolo Amerio, Alessandra Capo, Arcangelo Merla
    Abstract:

    Introduction Psoriasis arthritis (PsA) is a chronic inflammatory arthritis of joints of uncertain pathogenesis. PsA may lead to severe disabilities even in the absence of any clinical symptom. Therefore, PsA diagnosis in its early stages is critical. Material and methods This study uses Control System theory to Model finger skin Thermoregulatory processes overlying the hand joint in response to an isometric exercise. The proposed Model is based on a homeostatic negative feedback loop characterized by four distinct parameters that describe how the control mechanisms are activated and maintained. Thermal infrared imaging was used to record a total of 280 temperature curves of 14 finger joints for each of 11 PsA patients and 9 healthy controls. Result and conclusion PsA patients presented delayed and prolonged re-warming processes characterized by the undershoot onset after the end of the isometric exercise followed by a faster temperature increase. Region classification on the basis of the Model parameters demonstrated that the interphalageal joint region of thumb better discriminates between patients and controls, providing 100% true-positive discrimination for PsA affected regions and 88.89% of correct classification of healthy regions. Even proved over a limited number of subjects, the proposed method may provide useful hints for early differential diagnosis in the IR assessment of PsA disease.

  • Scrotal Thermoregulatory Model and Assessment of the Impairment of Scrotal Temperature Control in Varicocele
    Annals of Biomedical Engineering, 2011
    Co-Authors: Alessandro Mariotti, Giuseppe Orlando, Gian Luca Romani, Luigi Carlo, Maria Letizia Corradini, Luigi Donato, Paolo Pompa, Roberto Iezzi, Antonio Raffaele Cotroneo, Arcangelo Merla
    Abstract:

    Varicocele is defined as the pathological dilatation of the pampiniform plexus and scrotal veins with venous blood reflux. Varicocele may impair scrotal thermoregulation and spermatogenesis, even when present in asymptomatic forms. In this study, we use the control system theory to Model scrotal thermoregulation in response to a standardized cold challenge in order to study the functional thermal impairment secondary to varicocele. The proposed Model is based on a homeostatic negative feedback loop, characterized by four distinct parameters, which describe how the control mechanisms are activated and maintained. Thermal infrared images series from 49 young patients suffering from left varicocele and 17 healthy controls were processed. With respect to healthy controls, left varicocele patients presented higher basal scrotal temperature and faster recovery of the left hemiscrotum. The Model indicated that varicocele alters local heat exchange processes among cutaneous layers and inner structures. The estimated Model parameters help in the assessment of the scrotal Thermoregulatory impairment secondary to the disease.

  • Finger Thermoregulatory Model Assessing Functional Impairment in Raynaud’s Phenomenon
    Annals of Biomedical Engineering, 2009
    Co-Authors: Alessandro Mariotti, Giuliana Grossi, Paolo Amerio, Giuseppe Orlando, Peter A. Mattei, Antonio Tulli, Gian Luca Romani, Arcangelo Merla
    Abstract:

    Raynaud’s Phenomenon (RP) is a paroxysmal vasospastic disorder of small arteries, pre-capillary arteries, and cutaneous arteriovenous shunts of the extremities, typically induced by cold exposure and emotional stress. RP is either primary (PRP) or secondary to systemic sclerosis. In this study we use Control System Theory to Model finger Thermoregulatory processes in response to a standardized cold challenge (a diagnostic test routinely performed for differential diagnosis of RP). The proposed Model is based on a homeostatic negative feedback loop, characterized by five distinct parameters which describe how the control mechanisms are activated and maintained. Thermal infrared imaging data from 14 systemic sclerosis subjects (SSc), 14 PRP, and 16 healthy control subjects (HCS) were processed. HCS presented the fastest active recovery, with the highest gain. PRP presented the slowest and weakest recovery, mostly due to passive heat exchange with the environment. SSc presented an intermediate behavior, with the longest delay of response onset. The estimated Model parameters elucidated the level of functional impairment expressed in the various forms of this disease.

  • finger Thermoregulatory Model assessing functional impairment in raynaud s phenomenon
    Annals of Biomedical Engineering, 2009
    Co-Authors: Alessandro Mariotti, Giuliana Grossi, Paolo Amerio, Giuseppe Orlando, Peter A. Mattei, Antonio Tulli, Gian Luca Romani, Arcangelo Merla
    Abstract:

    Raynaud’s Phenomenon (RP) is a paroxysmal vasospastic disorder of small arteries, pre-capillary arteries, and cutaneous arteriovenous shunts of the extremities, typically induced by cold exposure and emotional stress. RP is either primary (PRP) or secondary to systemic sclerosis. In this study we use Control System Theory to Model finger Thermoregulatory processes in response to a standardized cold challenge (a diagnostic test routinely performed for differential diagnosis of RP). The proposed Model is based on a homeostatic negative feedback loop, characterized by five distinct parameters which describe how the control mechanisms are activated and maintained. Thermal infrared imaging data from 14 systemic sclerosis subjects (SSc), 14 PRP, and 16 healthy control subjects (HCS) were processed. HCS presented the fastest active recovery, with the highest gain. PRP presented the slowest and weakest recovery, mostly due to passive heat exchange with the environment. SSc presented an intermediate behavior, with the longest delay of response onset. The estimated Model parameters elucidated the level of functional impairment expressed in the various forms of this disease.

Mitsuyuki Nakao - One of the best experts on this subject based on the ideXlab platform.

  • Integrated Model incorporating circadian phase dynamics and the Thermoregulatory mechanism of sleep
    Sleep and Biological Rhythms, 2007
    Co-Authors: Daiki Ishiura, Akihiro Karashima, Norihiro Katayama, Mitsuyuki Nakao
    Abstract:

    Recently, physiological findings have suggested the existence of an integrated regulatory mechanism for sleep-wake rhythms, as follows. Homeostatic regulation of the sleep-wake pattern and body temperature involves circadian oscillators and the history of activity patterns. In addition, the rest-activity pattern can modulate the dynamics of circadian oscillators via feedback mechanisms. We have developed Models of sleep-wake rhythms based on the Thermoregulatory function of sleep and the multi-oscillator mechanism with feedback. The former Model is tentatively called the “Thermoregulatory Model” and the latter the “multi-oscillator Model”. The application of the Thermoregulatory Model is confined to internally or externally entrained situations in which steady circadian oscillation and fixed-phase relationships between the oscillators can be expected to be retained. On the other hand, prediction by the multi-oscillator Model is confined to the dynamics of oscillator phase, since the Model consists of phase oscillators without amplitude. Making use of the mutual complementarity of these two Models, an integrated Model of the regulatory mechanism of sleep-wake rhythms was obtained by combining them. Although the integrated Model could be valid under conditions of concurrency in which the sleep-wake/rest-activity patterns of the two Models can be considered rhythmic and synchronized, the results of a simulation show that the Model can be applied to predict the behavior of sleepiness as well as circadian oscillators in a wide variety of situations, such as internally or externally entrained steady states, trans-meridian flight and rotating shift work. The integrated Model could provide a general framework for exploring possible physiological and dynamical regulatory mechanisms of sleep-wake rhythms as well as appropriate design of work schedules.

  • a Model based interpretation of the biphasic daily pattern of sleepiness
    Biological Cybernetics, 1999
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Hikaru Nishiyama, Mitsuaki Yamamoto
    Abstract:

    We developed a Thermoregulatory Model of sleep control based on the hypothesis that non-rapid eye-movement sleep participates in homeostatic thermoregulation. This Model successfully reproduced several qualitative features of human sleep/wake cycles during entrained as well as the internally desynchronized states. Among the reproduced features, generation mechanisms of the biphasic sleepiness distribution are studied here in the light of the Model structure. Harmonic analysis is employed for this purpose. Through linearizations and confining the harmonics of the masking process to the fundamental component, a simplified representation of sleepiness is obtained. The simplified sleepiness is constructed with the fundamental circadian, the second harmonic components, and the constant (DC). The bimodality of the sleepiness is shown to be made by the second harmonic which is added to the fundamental component. The behavior of their amplitudes and phase positions are investigated under the varied sleep/wake durations and phase differences between the oscillators. Since the sleepiness generated by our Model is roughly mimicked by the simplified representation under diverse conditions, this simplification can be regarded as adequate. From the behavior of the constituents of respective harmonic components, the fundamental component is shown to originate from the sleep/wake masking process and the circadian oscillators; the second harmonic from the multiplicative interactions between the circadian oscillators and the sleep/wake masking process. These results indicate that the rhythmic processes are principal constituents of the sleepiness, at least in the steady state.

  • Thermoregulatory Model of sleep control: losing the heat memory.
    Journal of Biological Rhythms, 1999
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    Thermoregulatory mechanisms were hypothesized to provide primary control of non-rapid-eye-movement sleep (NREM). On the basis of this hypothesis, we incorporated the Thermoregulatory feedback loops...

  • Thermoregulatory Model of sleep control: losing the heat memory.
    Journal of biological rhythms, 1999
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    Thermoregulatory mechanisms were hypothesized to provide primary control of non-rapid-eye-movement sleep (NREM). On the basis of this hypothesis, we incorporated the Thermoregulatory feedback loops mediated by the "heat memory," heat load, and loss processes associated with sleep-wake cycles, which were modulated by two circadian oscillators. In addition, hypnogenic warm-sensitive neurons (HWSNs) were assumed to integrate thermoregulation and NREM control. The heat memory described above could be mediated by some sleep-promoting substances. In this paper, considering the possible carrier of the heat memory, its losing process is newly included in the Model. The newly developed Model can generate the appropriate features of human sleep-wake patterns. One of the special features of the Model is to generate the bimodal distribution of the sleepiness. This bimodality becomes distinct, as the losing rate of the heat memory decreases or the amplitude of the Y oscillator increases. The theoretical analysis shows the losing rate of the heat memory control's rapidity of Model response to a thermal perturbation, which is confirmed by simulating the responses with various losing rates to transient heat loads ("heat load pulse"). The sleepiness exhibits large responses to the heat load pulses applied in the early and late phases of wake period, while the response is significantly reduced to the pulse applied in the supposed wake-maintenance zone. This bimodality of the response appears to reflect the sensitivity of the HWSNs. In addition, the early pulse raises the immediate sleepiness rather than the nocturnal sleepiness, while the heat load pulse applied in the later phase of waking period significantly raises the sleepiness during a nocturnal sleep. In simulations of sleep deprivation, the discontinuous relationship between recovery sleep length and deprivation time is reproduced, where the critical sleep deprivation time at which the recovery sleep length jumps is extended as the losing rate increases. This is possibly due to the dissipation of the heat memory accumulated by the sleep deprivation. The simulation results here qualitatively reproduce the experimental observations or predict the intriguing phenomena of human circadian rhythms. Therefore, our Model could provide a novel framework for investigating the relationship between thermoregulation and sleep control processes.

  • A Thermoregulatory Model of Sleep Control
    The Japanese journal of physiology, 1995
    Co-Authors: Mitsuyuki Nakao, D. Mcginty, Ronald Szymusiak, Mitsuaki Yamamoto
    Abstract:

    We hypothesize that non-rapid-eye-movement sleep (NREM) is controlled by Thermoregulatory mechanisms of the preoptic/anterior hypothalamus. Circadian and homeostatic Thermoregulatory processes may be integrated in this brain area. To investigate this hypothesis, we have developed a mathematical Model of qualitative features of human sleep-waking behavior based on a Thermoregulatory feedback control mechanism, with modulation by two circadian oscillators, one a temperature rhythm, the other modulating sleepiness. Homeostatic features of the sleep rhythm are generated by integration of a heat load associated with waking. Simulations under entrained conditions show that the Model closely mimics typical features of human sleep rhythms, including a biphasic daily pattern of sleepiness and sleep-onsets and awakenings fixed in a descending phase and an ascending phase of the temperature rhythm, respectively. Sleep duration is strongly controlled by the phase difference between the two oscillators with the same period; these could represent two phase-differentiated expressions of a single oscillator. In addition, the simulation of sleep deprivation provides a natural interpretation of the experimentally observed phenomena, which shows that the homeostatic and the oscillatory aspects of the human circadian system is successfully integrated in our Model. The promising results obtained suggest that the control of sleep-wake rhythm could be understood within the framework of the thermoregulation.

Karen A Matthews - One of the best experts on this subject based on the ideXlab platform.

  • gains in body fat and vasomotor symptom reporting over the menopausal transition the study of women s health across the nation
    American Journal of Epidemiology, 2009
    Co-Authors: Rebecca C Thurston, Maryfran Sowers, Barbara Sternfeld, Ellen B Gold, Joyce T Bromberger, Yuefang Chang, Hadine Joffe, Carolyn J Crandall, Elaine L Waetjen, Karen A Matthews
    Abstract:

    Most women living in the United States report vasomotor symptoms (hot flashes and/or night sweats) during the menopausal transition (1). Vasomotor symptoms are sensations of intense heat accompanied by sweating and flushing. Usually experienced as bothersome (2), vasomotor symptoms are associated with poorer quality of life (3), mood (4), memory performance (5), and sleep quality (6). Because hormone therapy, the most effective treatment for vasomotor symptoms, has been linked to health risk among certain women (7), the etiology, risk factors, and nonhormonal approaches to managing vasomotor symptoms are the subject of increased scientific interest (8). Obesity and its relation to vasomotor symptoms have been of particular interest. Early work hypothesized that body fat protected against vasomotor symptoms because of the aromatization of androgens to estrogens in fat tissue (9, 10). However, evidence indicates that higher body mass index (1, 11), and body fat in particular (12, 13), is associated with greater vasomotor symptom reporting, primarily hot flashes. These findings are consistent with a Thermoregulatory Model of vasomotor symptoms in which body fat acts as an insulator, rendering vasomotor symptoms, a putative heat dissipation event, more likely (14). The existing research linking body fat to vasomotor symptoms is cross-sectional, and the directionality or longitudinal nature of these associations is unclear. Of particular importance is whether fat gains are related to greater vasomotor symptom reporting over time. Women typically show progressive gains in body fat over midlife (15, 16), but the influence of these gains on vasomotor symptoms is unknown. Longitudinal research links higher body mass index to more reported vasomotor symptoms (1) and increases in reported weight across 2 time points (17) to higher vasomotor symptom reporting. However, body mass index, a ratio of weight to the square of height, is a rough proxy for body fat; reported weight is typically underestimated among women (18); and neither measure distinguishes between lean and fat mass. Given the importance of body fat to vasomotor symptoms, research with more precise estimates of body fat is important. No investigations have evaluated whether fat gains are related to vasomotor symptom reporting over time. We hypothesized that gains in body fat would be associated with an increased annual prevalence of reported hot flashes and night sweats. We also examined the role of reproductive hormones in these associations, particularly estradiol; follicle-stimulating hormone, a gonadotropin associated with both gains in body fat and vasomotor symptoms (15, 19); and the free estradiol index, an estimate of the portion of estradiol circulating unbound to sex hormone-binding globulin (SHBG) and thereby biologically available. Given the variations in body composition and vasomotor symptom reporting by race/ethnicity and menopausal stage (1, 15), interactions by race/ethnicity and menopausal stage were examined.

  • adiposity and reporting of vasomotor symptoms among midlife women the study of women s health across the nation
    American Journal of Epidemiology, 2007
    Co-Authors: Rebecca C Thurston, Maryfran Sowers, Barbara Sternfeld, Ellen B Gold, Yuefang Chang, Janet M. Johnston, Karen A Matthews
    Abstract:

    It has long been hypothesized that increased adiposity would be associated with decreased vasomotor symptoms during menopause because of conversion of androgens to estrogens in body fat. However, recent Thermoregulatory Models have postulated that increased adipose tissue would be associated with a greater likelihood of vasomotor symptoms. The authors evaluated these hypotheses in the Study of Women's Health Across the Nation, a multiethnic, community-based observational study of US women transitioning through menopause. The sample included 1,776 women aged 47-59 years with an intact uterus and at least one ovary who completed bioelectrical impedance analysis for assessment of body composition at the sixth annual study visit (2002-2004). Assessments also included reported vasomotor symptoms (hot flashes, night sweats) and serum levels of follicle-stimulating hormone, estradiol, and sex hormone-binding globulin-adjusted estradiol (free estradiol index). Results indicated that a higher percentage of body fat was associated with increased odds of reporting vasomotor symptoms (per standard deviation increase in percent body fat, odds ratio = 1.27, 95% confidence interval: 1.14, 1.42) in age- and site-adjusted Models. Associations persisted in fully adjusted Models and were not reduced when Models included reproductive hormones. These findings support a Thermoregulatory Model of vasomotor symptoms.

Alessandro Mariotti - One of the best experts on this subject based on the ideXlab platform.

  • Scrotal Thermoregulatory Model and Assessment of the Impairment of Scrotal Temperature Control in Varicocele
    Annals of Biomedical Engineering, 2011
    Co-Authors: Alessandro Mariotti, Giuseppe Orlando, Gian Luca Romani, Luigi Carlo, Maria Letizia Corradini, Luigi Donato, Paolo Pompa, Roberto Iezzi, Antonio Raffaele Cotroneo, Arcangelo Merla
    Abstract:

    Varicocele is defined as the pathological dilatation of the pampiniform plexus and scrotal veins with venous blood reflux. Varicocele may impair scrotal thermoregulation and spermatogenesis, even when present in asymptomatic forms. In this study, we use the control system theory to Model scrotal thermoregulation in response to a standardized cold challenge in order to study the functional thermal impairment secondary to varicocele. The proposed Model is based on a homeostatic negative feedback loop, characterized by four distinct parameters, which describe how the control mechanisms are activated and maintained. Thermal infrared images series from 49 young patients suffering from left varicocele and 17 healthy controls were processed. With respect to healthy controls, left varicocele patients presented higher basal scrotal temperature and faster recovery of the left hemiscrotum. The Model indicated that varicocele alters local heat exchange processes among cutaneous layers and inner structures. The estimated Model parameters help in the assessment of the scrotal Thermoregulatory impairment secondary to the disease.

  • Finger Thermoregulatory Model Assessing Functional Impairment in Raynaud’s Phenomenon
    Annals of Biomedical Engineering, 2009
    Co-Authors: Alessandro Mariotti, Giuliana Grossi, Paolo Amerio, Giuseppe Orlando, Peter A. Mattei, Antonio Tulli, Gian Luca Romani, Arcangelo Merla
    Abstract:

    Raynaud’s Phenomenon (RP) is a paroxysmal vasospastic disorder of small arteries, pre-capillary arteries, and cutaneous arteriovenous shunts of the extremities, typically induced by cold exposure and emotional stress. RP is either primary (PRP) or secondary to systemic sclerosis. In this study we use Control System Theory to Model finger Thermoregulatory processes in response to a standardized cold challenge (a diagnostic test routinely performed for differential diagnosis of RP). The proposed Model is based on a homeostatic negative feedback loop, characterized by five distinct parameters which describe how the control mechanisms are activated and maintained. Thermal infrared imaging data from 14 systemic sclerosis subjects (SSc), 14 PRP, and 16 healthy control subjects (HCS) were processed. HCS presented the fastest active recovery, with the highest gain. PRP presented the slowest and weakest recovery, mostly due to passive heat exchange with the environment. SSc presented an intermediate behavior, with the longest delay of response onset. The estimated Model parameters elucidated the level of functional impairment expressed in the various forms of this disease.

  • finger Thermoregulatory Model assessing functional impairment in raynaud s phenomenon
    Annals of Biomedical Engineering, 2009
    Co-Authors: Alessandro Mariotti, Giuliana Grossi, Paolo Amerio, Giuseppe Orlando, Peter A. Mattei, Antonio Tulli, Gian Luca Romani, Arcangelo Merla
    Abstract:

    Raynaud’s Phenomenon (RP) is a paroxysmal vasospastic disorder of small arteries, pre-capillary arteries, and cutaneous arteriovenous shunts of the extremities, typically induced by cold exposure and emotional stress. RP is either primary (PRP) or secondary to systemic sclerosis. In this study we use Control System Theory to Model finger Thermoregulatory processes in response to a standardized cold challenge (a diagnostic test routinely performed for differential diagnosis of RP). The proposed Model is based on a homeostatic negative feedback loop, characterized by five distinct parameters which describe how the control mechanisms are activated and maintained. Thermal infrared imaging data from 14 systemic sclerosis subjects (SSc), 14 PRP, and 16 healthy control subjects (HCS) were processed. HCS presented the fastest active recovery, with the highest gain. PRP presented the slowest and weakest recovery, mostly due to passive heat exchange with the environment. SSc presented an intermediate behavior, with the longest delay of response onset. The estimated Model parameters elucidated the level of functional impairment expressed in the various forms of this disease.