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Sleep is an essential function of human life, underlying both biological and cultural processes. Dramatic changes in sleep occur during infancy, in terms of night awakenings, which tend to diminish over time, and day/night sleep duration, with newborns sleeping up to 16-17 hours per day and gradually decreasing to 9-13 hours between 6-11 months of age. Remarkably, research indicates that changes in infant sleep are in interaction with important acquisitions in other domains of child development. In the present study, we aimed at investigating concurrent and longitudinal relations between sleep and cognitive maturation during infancy, by collecting data on 156 infants at 4 months of age and on a subsample of 103 infants at 8 months of age. Infants’ sleep was assessed through the Brief Infant Sleep Questionnaire (BISQ; Sadeh, 2004), whereas cognitive maturation was evaluated using the Developmental ProfileTM 3 (Alpern 2007). We also examined infants’ language understanding through the Italian version of the MacArthur–Bates Communicative Development Inventory (MCDI): Words and Gestures (Caselli & Casadio, 1995; Fenson et al., 1994). Finally, information about infants’ temperament and maternal practices potentially relevant for sleep quality, such as the use of a pacifier at nighttime, co-sleeping and exclusive breastfeeding, was detected. Results showed that night and day sleep were differently related to infants’ development at 4 and 8 months of age, but there were no robust longitudinal relationships.

To investigate whether colour Doppler US can demonstrate haemodynamic differences in patients with renal colic after pharmacological treatment with indomethacin and ketorolac.We studied 180 consecutive patients with unilateral acute renal colic with colour Doppler US; 90 were treated with indomethacin, 90 with ketorolac. Furthermore, 37 consecutive patients without obstruction (17 treated with indomethacin and 20 with ketorolac) were also examined and considered normal controls.In the patients with renal colic the average resistive index (RI) was significantly greater on the side of the colic after administration of either indomethacin or ketorolac (p0.001). The average RI in the obstructed kidneys was significantly higher in the patients treated with ketorolac than with indomethacin (p0.005). No statistically significant differences were shown between the average RIs of the non obstructed kidneys of the patients with renal colic and between the kidneys of the control patients treated with either indomethacin or ketorolac.Doppler evaluation of patients with renal colic requires careful interpretation after the administration of nonsteroidal anti-inflammatory drugs (NSAIDs), since values of renal RI depend on the drug that has been used to relieve symptoms.

There is increasing evidence that NF-kappaB is a major, if not the major transcription factor regulating inflammation and immunity. While this implies that blocking NF-kappaB might be therapeutically beneficial, it raises clear questions regarding the balance between efficacy and safety. In this brief review we discuss the effects of NF-kappaB blockade in rheumatoid arthritis, inflammation and immunity, and consider possible therapeutic targets within the NF-kappaB family.

Nutlin-3, a small molecule inhibitor of the MDM2/p53 interaction, has been recently taken into consideration as a promising therapeutic tool for tumor treatment based on its ability to stabilize and activate the p53 transcription factor pathway. Since Nutlin-3 displays non cell-autonomous tumor-suppressor activities, we wanted to investigate its effect on dendritic cell functions, given the central role of these cells in the modulation of the immune response. We found that Nutlin-3 alone slightly affected the levels of major histocompatibility complex and costimulatory molecules and significantly promoted the ability of dendritic cells to stimulate T cells in the mixed lymphocyte reaction. Taken together, our findings suggest that the ability of Nutlin-3 to modulate dendritic cell functions and therefore lymphocyte proliferation might represent an additional important mechanism by which Nutlin-3 exerts its non cell-autonomous tumor-suppression function.

Objectives Vascularization of the female urethra is an important factor contributing to the sealing effect responsible for the normal urethral closing system. The aim of this study was to assess whether contrast enhanced ultrasonography can be used to evaluate changes in urethral vascularization between pre- and postmenopausal women. Methods We studied the vascularization of female urethra in 11 healthy premenopausal females during the midfollicular phase of the menstrual cycle and 10 healthy postmenopausal volunteers using ultrasound contrast agents with a 2–5MHz curved-array transducer by a translabial approach. Reperfusion curves were analyzed by a blinded investigator. Ultrasound contrast agents were measured with specifically designed software, and results were evaluated using the Mann-Whitney U- test. Results The data suggest that the enhancement characteristics of the urethra were different in pre- and postmenopausal women and that the percent of blood volume and blood flow decreased with age. No changes were observed between pre- and postmenopausal women regarding the velocity of blood flow. Conclusions The study of female urethra vascularization by ultrasound contrast agents is safe, feasible, and noninvasive.

We previously showed that a metalloprotease and a serine protease mediate shedding of the TNF-R75 (75-kDa tumor necrosis factor receptor) in neutrophils. Here we show that elastase is the TNF-R75 solubilizing serine protease. Release of the TNF-R75 by resting cells was almost totally inhibited by the serine protease inhibitor diisopropylfluorophosphate (DFP), by two synthetic, chemically unrelated, elastase-specific inhibitors and by α1-protease inhibitor. Release after TNF or FMLP (N-formyl- L -methionyl- L -leucyl- L -phenylalanine) stimulation was blocked by DFP and a metalloprotease inhibitor used in combination. Supernatants from resting neutrophils contained a 28-kDa fragment of the receptor, compatible with that generated by elastase, whose appearance was inhibited by DFP. Upon FMLP stimulation, the release of 28-kDa and 40-kDa fragments was observed, which was inhibited by DFP and a metalloprotease inhibitor, respectively. We conclude that elastase is the TNF-R75 sheddase of resting neutrophils and that it contributes to shedding of this receptor in stimulated cells.