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Wildfires strongly alter hydrological processes and surface and groundwater quality in forested environments. The paired-watershed method, consisting of comparing a burnt (altered) watershed with an unburnt (control) watershed, is commonly adopted in studies addressing the hydrological effects of wildfires. This approach requires a calibration period to assess the pre-perturbation differences and relationships between the control and the altered watershed. Unfortunately, in many studies, the calibration phase is lacking due to the unpredictability of wildfires and the large number of processes that should be investigated. So far, no information is available on the possible bias induced by the lack of the calibration period in the paired-watershed method when assessing the hydrological impacts of wildfires. Through a literature review, the consequences of the lack of calibration on the assessment of wildfire hydrological changes were evaluated, along with the most used watershed pairing strategies. The literature analysis showed that if calibration is lacking, misestimation of wildfire impacts is likely, particularly when addressing low-severity or long-term wildfire effects. The Euclidean distance based on physical descriptors (geology, morphology, vegetation) was proposed as a metric of watersheds similarity and tested in mountain watersheds in Central Italy. The Euclidean distance proved to be an effective metric for selecting the most similar watershed pairs. This work raises awareness of biases exerted by lacking calibration in paired-watershed studies and proposes a rigorous and objective methodology for future studies on the hydrological effects of wildfires.

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The authors describe the case of a 3-year-old girl with acute lymphoblastic leukemia which was diagnosed several months after the appearance of the first symptoms. The delay can be attributed to the vague symptoms at onset in the form of a single laterocervical adenopathy which responded to antibiotic and antiphlogistic therapy, the total absence of any indicative hematological symptoms and the patient s persistent excellent general conditions. In the light of this unusual case, the authors stress the need to carry out invasive diagnostic tests on lymph node lesions that are often defined as aspecific given that they may occasionally disguise more severe lymphoproliferative diseases.

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Our previous studies indicate the Sertoli cell as a target for thyroid hormone action at testis level. In the present study we evaluated the effect of thyroid hormone on Sertoli cell oxidative capacity measured by specific cytochrome oxidase (COX) activity and intracellular adenosine triphosphate (ATP) content. Sertoli cells were isolated from 21-day-old rats. Hypothyroidism, induced from the day of birth by administration of 0.025% methimazole, was characterized by a severe delay of body and testis growth and resulted in a lower COX activity (-40%, p < or = 0.01) and a lower ATP content (-35%, p < or = 0.01) by isolated Sertoli cells. Administration of triiodothyronine (10 micrograms/100 g body wt on alternate days) to hypothyroid rats improved body and testis growth and restored both COX activity and ATP content. The presence of high-affinity, low-capacity binding sites for triiodothyronine in Sertoli cell mitochondria also was demonstrated. This study, unlike that carried out on the whole testis from adult rats, demonstrates that thyroid hormone affects the energy metabolism of Sertoli cells from midpubertal rat testes.

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Previous work has demonstrated that thyroid hormones influence testis development. Specific receptors for tri-iodothyronine (T3) have been demonstrated in Sertoli cells. The aim of the present study was to examine the possible effect of thyroid hormone on its own receptor during pubertal development by evaluating the influence of thyroid status on T3-binding capacity, -binding affinity and receptor occupancy in nuclei isolated from immature rat testes. The binding capacity for T3 of nuclei from rat testis significantly decreased during pubertal development, being 375 +/- 32, 117 +/- 15 and 44 +/- 7 fmol/mg DNA in 7-, 21- and 35-day-old rats respectively, whereas the affinity of binding, as evaluated by the dissociation constant (Kd), did not change. Early induced hypothyroidism significantly affected the time-course of the postnatal decline of nuclear T3 receptors in the testis. At 21 days of age, the binding capacity for T3 in the testis of methimazole-treated rats was significantly higher with respect to euthyroid controls, being 173 +/- 21 and 117 +/- 15 mol/mg DNA respectively, while the Kd was unaffected. T3 replacement therapy completely prevented changes in T3 receptor number induced by hypothyroidism without modifying the Kd. Our results indicate that nuclear T3 receptors in the developing rat testis are modulated by thyroid hormone.

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The existence of nuclear tri-iodothyronine (T3) receptors in both Sertoli and Leydig cells isolated from immature piglet testes was investigated. The results demonstrated the presence of high-affinity (Kd = 1.09 +/- 0.25 nM), low-capacity (185 +/- 24 pg T3/mg DNA) binding sites for T3 in nuclei from freshly isolated Sertoli cells. No specific binding for T3 was observed in nuclei isolated from Leydig cells. The localization of specific T3 receptors, which might mediate the onset of thyroid hormone action, at Sertoli cell level confirms that these cells are a target for thyroid hormone and strongly sustain the role of the thyroid in the regulation of testicular functions during postnatal development.

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The influence of Insulin-like Growth Factor I (IGF-I) on some metabolic functions of Sertoli cells from peripubertal rats was investigated. Sertoli cells were isolated from the testes of 24-day-old animals and cultured at 32 degrees C in Eagle's MEM with or without 1 nM IGF-I. Sertoli cells cultured in the presence of IGF-I showed increased nuclear RNA polymerase activity (+80%) and augmented protein synthesis (+50%).

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The effects of thyroid status on the binding capacity, association constant (Ka) and receptor occupancy during postnatal rat testis development were evaluated. Hypothyroidism (induced by oral administration of 0.05% methimazole from the day of birth) increased the total T3 binding capacity in the testis, retarding the normal developmental decrease in T3 receptor number (mean maximal binding capacities estimated by Scatchard analysis for 21-day-old eu- and hypothyroid rats were 117 and 173 fmol/mg DNA, respectively). The rat thyroid status also affected the percentage of T3 receptor occupancy but not the affinity of binding (as measured by Ka). The postnatal developmental changes in T3 binding capacity induced by hypothyroidism were completely reversed by T3 replacement. These results suggest that T3 nuclear receptors in the developing rat testis are modulated by thyroid hormones.

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