Calculations of temperature rise produced in body tissue by a spherical electrode

Two estimates of temperature rise produced in body tissue when a spherical electrode passes current have been calculated. The estimates bracket the expected temperature rise. Time-transient and steady-state results have been obtained. The effects of heat transfer through the highly conductive metal electrode and irreversible. Faradaic reactions have been considered. The calculations indicate that electrodes smaller than about 2 μm in radius produce a peak temperature rise of about 1°C when driven by typical square current pulses of 25 μA intensity and 200 μs duration. The results are presented in a graphic form allowing for quick estimation of the expected peak temperature rise around electrodes of a specific radius, which are driven with a pulse of known current density and duration.     

Learned anticipatory rise in body temperature due to handling

Hyperthermia produced by handling becomes evident at the initial daily measurement if temperature is measured at a consistent time. This hyperthermia may be a learned effect occurring in anticipation of handling. In Experiment One male Wistar rats were either unhandled or had their temperatures measured daily in the dark or the light part of the day. All animals had their temperatures measured on Day 29, in the dark. Rats usually tested in the dark were hyperthermic, 38.8 degrees C, relative to rats previously handled only in the light, 38.1 degrees C, and to naive rats, 37.9 degrees C. In Experiment Two rats were handled three times daily in either the light or the dark. On Day 9 each group was divided in two, and temperatures were measured at either the usual time or at the other time. Rats tested at their usual time were hyperthermic, relative to rats normally handled in the other part of the cycle. This suggests a conditioned hyperthermia occurs in response to stimuli predictive of handling.     

Transient stress lymphocytosis: an immunophenotypic characterization of the most common cause of newly identified adult lymphocytosis in a tertiary hospital

We prospectively evaluated 52 consecutive cases of newly identified absolute lymphocytosis to determine the hematologic and immunophenotypic features of transient stress lymphocytosis (TSL). The lymphocytosis in all cases was associated with an acute stressful event and ranged from 4,000 to 10,400/microL (4.0-10.4 x 10(9)/L). Compared with healthy individuals, patients with TSL showed an increase in the total WBC, absolute lymphocyte (ALC), absolute neutrophil (ANC), and platelet counts with no difference in hemoglobin levels. Immunophenotypic analyses of 38 cases revealed increases in absolute numbers of T B, and natural killer cells. Both CD4+ and CD8+ T cells were increased, predominantly accountedfor by an increase in memory cell subsets, with no change in gamma/delta T cells. Follow-up studies showed a significant reduction in the ALC with a concurrent increase in the ANC and reduction in hemoglobin values. The reduction in lymphocytes at resolution was accompanied by reduction in all broad Iymphocyte subsets. However, naive and memory subsets showed different patterns of alteration within the CD4+ and CD8+ populations, suggesting that acute stress differentially affects the in vivo distribution of these subsets.     

Periodontitis: a newly identified comorbidity in psoriasis and psoriatic arthritis

ABSTRACT

Introduction: Psoriasis is a chronic autoimmune skin disease with strong genetic background and environmental triggers. Patients with psoriasis and psoriatic arthritis are at greater risk of developing other chronic and potentially severe comorbidities, such as psoriatic arthritis, hyperlipidemia, type 2 diabetes mellitus, obesity, metabolic syndrome, cardiovascular diseases or depression. Recently, accumulating epidemiologic, genetic and pathogenetic evidence indicates that psoriasis is also associated with periodontitis, a chronic progressive inflammatory disease, which may result in tooth loss without early and adequate therapy.

Areas covered: In this review article we summarize and discuss in detail the available epidemiologic, genetic, microbiological and immunological links between psoriasis and periodontitis.

Expert opinion: Periodontitis, via the immunomodulatory effect of the oral microbiota, may play both a direct and indirect role in the development or exacerbation of psoriasis, and may influence the efficacy of antipsoriatic therapy. These new findings indicate a need for increased awareness, early recognition and focus on prevention of periodontitis for patients with psoriasis.     

TRH decreases food intake and increases water intake and body temperature in rats

Thyrotropin-releasing hormone (TRH) is a key regulator of the hypothalamus-pituitary-thyroid axis, which plays an important role in energy homeostasis and is involved in the regulation of feeding behavior. In the present study, we investigated the effects of acute and chronic TRH treatment on water intake, body temperature and feeding behavior in rats. TRH (0, 4, 16 and 64 mg/kg) was injected subcutaneously twice a day (06:00 and 18:00 h) in rats fed ad libitum. TRH decreased food and water intake in the first few hours (P < .05). There was a small reduction in food intake over the 24-h period, but body weight was not affected (P < .05). When TRH was injected at a dose of 32 mg/kg twice a day (06:00 and 18:00 h) for 5 days, T(3) and T(4) concentrations were increased (P < .05). TRH increased body temperature for 2 h after injection. Water intake was markedly increased (P < .05), but there was no effect on food intake or body weight. These results show that whereas a single injection of TRH decreases short-term food and water intake in rats, repeated daily treatments stimulate water intake but not food intake, and, thus, the increase in water consumption is mediated independently of food intake under these conditions.     

ADAM33: a newly identified gene in the pathogenesis of asthma

There is much to find out about this fascinating and complex molecule in relation to the development and progression of asthma. Added to it are three further new asthma/allergy genes identified by positional cloning: PDH Finger Protein II (PHF11) on chromosome 13q14, which encodes NY-REN-34 a protein first described in patients with renal cell carcinoma [67]; Dipeptidyl diptidase 10 (DDP10) on chromosome 2q14 [68]; and G protein-coupled receptor for asthma susceptibility (GPRA) on chromosome 7p [69]. For each of these genes, as is the case for ADAM33, determining their normal function(s) and how these become disordered in asthma is the future challenge.     

Cunninghamella: a newly recognized cause of rhinocerebral mucormycosis

Cunninghamella, a zygomycete in the order Mucorales, is an extremely rare cause of human infection. Of the five reported cases of human disease caused by this fungus, none involved rhinocerebral infection. Here, the authors document what appears to be the first case of rhinocerebral mucormycosis caused by Cunninghamella bertholletiae in an elderly man who had diabetes with sideroblastic anemia and hemochromatosis. The disease was rapidly fatal. The mycology and classification of this organism are presented, and the previous case reports in the literature are reviewed.     

DNA repair deficiency in a newly identified neurological disease

Mutations in PNKP cause microcephaly, seizures and defects in DNA repair Shen et al. (2010) Nature Genetics 42(3): 245–249     

Food intake and body temperature responses of rats to recombinant human interleukin-1 beta and a tripeptide interleukin-1 beta antagonist.

Food intake and body temperature are two of many factors affected by IL-1 beta, a cytokine which is produced in response to tissue injury and inflammatory processes. In the present experiment, a tripeptide IL-1 beta antagonist which blocked IL-1 beta-induced hyperalgesia was tested for the ability to block IL-1 beta-induced effects on food intake and body temperature. Food intake was decreased 4-22 h after intraperitoneal (IP) administration of 1.25, 1.88, or 2.50 micrograms IL-1 beta/rat, and 0-22 h food intake was decreased by 1.88 and 2.50 micrograms IL-1 beta/rat. The effect of 1.25 micrograms IL-1 beta/rat on food intake measured 4 and 22 h after (IP) injection was blocked by coadministration of 5 mg tripeptide IL-1 beta antagonist. However, 25 mg tripeptide IL-1 beta antagonist/rat plus 1.25 micrograms IL-1 beta/rat decreased 0-22 h food intake more than IL-1 beta alone. Administration (IP) of 1.25 micrograms IL-1 beta/rat increased body temperature 1 degrees C 4 h later, and 5 and 25 mg tripeptide IL-1 beta antagonist/rat blocked this increase. Although food intake remained decreased after IL-1 beta administration alone or with 25 mg tripeptide IL-1 beta antagonist/rat for 22 h, body temperature returned to normal under these conditions. Thus, a tripeptide IL-1 beta antagonist shown to block IL-1 beta-induced hyperalgesia also blocked food intake and body temperature responses to IL-1 beta, although the effective doses of IL-1 beta and the tripeptide IL-1 beta antagonist differ by 4,000-fold when both are administered peripherally.     

The effect of a rise in body temperature on the central-chemoreflex ventilatory response to carbon dioxide

We assessed the central-chemoreflex ventilatory responses to carbon dioxide in six male volunteers using a hyperoxic rebreathing technique. Hyperventilation prior to rebreathing allowed both the threshold and the sensitivity of the response to be measured. We used immersion in water to control the body temperature (tympanic). The water temperature was adjusted to be either thermo-neutral or hot so that body temperature either remained normal [+ 0.2 (0.04)°C, mean (SEM)] or was elevated by 1.5 (0.08)°C. The sensitivities of the central-chemoreflex ventilatory responses to carbon dioxide were increased at elevated body temperatures, changing from a mean of 1.8 (0.2) 1·min^–1. Torr^–1 to 2.7 (0.1) 1·min^–1·Torr^–1. However, the thresholds did not change with temperature, and the mean threshold was 48(1) Torr at both normal and elevated temperatures. For all of the volunteers, ventilation was increased at elevated body temperatures for all levels of carbon dioxide, mainly by changes in respiratory frequency due to reductions in expiratory times. At subthreshold levels of carbon dioxide, mean ventilation changed significantly from 6.3 (1.1) 1·min^–1 at normal temperatures to 10.8 (1.9) 1 · min^–1 at elevated temperatures. Heart rates also increased significantly with temperature, changing from a mean of 66 (4) beats·min^–1 to 102 (3) beats·min^–1 at threshold levels of carbon dioxide. The mean rates of rise of carbon dioxide partial pressure during rebreathing were significantly increased with temperature as well, changing from 0.075 (0.008) Torr·min^–1 to 0.089 (0.004) Torr·min^–1. We concluded that elevating the body temperatures of our subjects not only increased their ventilation, heart rates and metabolic rates at all levels of carbon dioxide, but it also increased the sensitivity of their central chemoreflex ventilatory responses to carbon dioxide. Despite these increases, the thresholds of the central-chemoreflex ventilatory responses to carbon dioxide remained unchanged.     

Stress-induced rise of body temperature in rats is the same in warm and cool environments

Several forms of psychological stress result in a rise in body temperature in rats. In this study, we report that rats housed at a low ambient temperature (11.1 degrees C) develop stress-induced rises in body temperature that do not differ from the responses seen when the animals are kept at a temperature within their thermoneutral zone (24.7 degrees C). These data support the hypothesis that stress-induced "hyperthermia" is a regulated rise in temperature (i.e., a rise in thermoregulatory "set-point," or fever), and is not simply the result of metabolic changes associated with the stress response itself.     

Food intake of rats administered with glycerol

The effect of glycerol on rats food intake was determined when it was administered either via bolus gastric intubation, or by a continuous 24 hr infusion into the aorta. Both of these treatments resulted in a suppression of the 24 hr food consumption to an extent which was greater than that accounted for by the caloric value of the administered metabolite. Gastric loading with urea solutions equiosmotic to glycerol or with glucose solutions equicaloric to glycerol were less effective than glycerol in reducing the 24 hr food intake. The time course effect on food intake varied between gastric loading with glycerol and with equicaloric glucose solutions, with the former usually exerting a more delayed and longer lasting effect. Continuous intraaortal infusions of glycerol were more effective than glucose solutions in suppressing 24 hr food intake even though the latter had twice the caloric value of the former. Our data suggest that the action of glycerol on food intake is not mediated through its conversion to glucose. The possibility that glycerol may participate in a lipostatic control mechanism of food intake is discussed.     

Hereditary angioedema: A decade of management with stanozolol

Thirty-seven patients with hereditary angioedema, who, without therapy, had attacks of cutaneous angioedema, gastrointestinal colic, and/or upper respiratory symptoms at a frequency and severity sufficient to prompt treatment with an attenuated androgen, have been evaluated for the incidence of side effects and biochemical toxicity during various schedules leading to the minimal effective dose. Stanozolol was administered in a 2 mg daily dose, initially, and after the symptoms and signs were adequately controlled for 2 months at this dose or at 1 mg per day, the drug was administered every other day at 4 mg. Patients who responded adequately to this schedule were administered 2 or 1 mg every other day, and then the interval between doses was gradually increased to 1 week, after which the agent was stopped. Eighteen patients experienced adverse reactions to stanozolol while the minimal effective dose was attained. In each instance the side effect subsided with a reduction in dosage. The most common adverse reactions were biochemical evidence of hepatic dysfunction and, to a lesser extent, hirsutism and menstrual irregularities. Although 21 of 27 patients in an initial study of the minimal effective dose were maintained with daily therapy in 1980, by 1986 this group and 10 additional patients were distributed so that three patients were receiving daily maintenance, 18 were receiving alternate-day maintenance, and 16 patients were receiving no maintenance therapy [corrected]. Thus, stanozolol appears to be a safe and effective agent for management of hereditary angioedema when patients are continually monitored to define the minimal effective dose or the feasibility of stopping the drug.