Efficacy and safety of ND:YAG 1064 nm lasers for photoepilation: a systematic review

Lasers in Medical Science - Using light sources in phototherapy has presented promising results regarding several types of facial and body skin affections for centuries. The neodymium-doped yttrium...     

Familial stenosis of the pulmonary artery branches with a JAG1 mutation.

Although most congenital heart defects are isolated abnormalities of embryonic development, with little genetic contribution, a small number are components of syndromes. In such cases, an accurate diagnosis has important implications for individual prognosis and familial genetic counseling. Alagille syndrome (AGS) is a dominantly inherited multisystem developmental disorder, which primarily affects the liver, heart, eyes, skeleton, and face. In recent years, the identification of the AGS gene has drawn attention to the existence of subclinical carriers, and broadened the spectrum of phenotypical variation associated with this syndrome. The authors present a case of mother and son with benign stenosis of the pulmonary artery branches. Subtle facial aspects suggested the diagnosis of AGS, which was confirmed by molecular analysis. Relevant clinical investigations and diagnostic implications are discussed.     

Acute resynchronization with inhaled iloprost in a pregnant woman with idiopathic pulmonary artery hypertension.

We describe the case of a pregnant woman with idiopathic pulmonary arterial hypertension, a responder in right heart catheterization, followed since the first trimester in outpatient consultations, admitted to hospital at 23 weeks gestation. She was treated with inhaled iloprost until delivery (at 34 weeks gestation) and continuous infusion of iloprost throughout the perioperative period and following days. This line of therapy has proved efficacious in previous cases. The authors present echocardiographic images that document acute changes in ventricular synchrony during inhalation of iloprost.     

Pulmonary embolism.

Pulmonary embolism (PE) is an important health problem and often a major clinical challenge, not only because of the low specificity of its clinical manifestations but also because of the increasing number of medical circumstances that are risk factors for this illness and the importance of early identification, since prompt and appropriate treatment can decrease mortality from this disease by about 25%. In recent years research on PE has been extensive, directed mainly at trying to determine and characterize its risk factors, establish new clinical probability algorithms, develop new diagnostic methods and put existing ones into perspective, seek new therapeutic approaches (pharmacological and non-pharmacological), and above all establish protocols that can guide the clinician from the stage of clinical suspicion to measures to prevent recurrence. It was the authors' aim to review the most significant literature on this subject, in order to produce a text that reflects the state of the art concerning PE and that can be used as a guide in the clinical approach to this pathology.     

Interference of antihistamines and anti-allergic drugs with antigen-induced paw edema in boosted and unboosted mice.

The protective effects of two antihistamines and two anti-allergic drugs against anaphylactic paw edema were studied in immunized animals that had or had not received a booster injection of antigen. The injection of 1 or 10 micrograms/paw ovalbumin induced acute paw edema of similar intensity in both groups. The antihistamine meclizine and the mixed anti histamine/anti-5-HT antagonist cyproheptadine reduced the anaphylactic reaction by 55 and 84% respectively, in non-boosted animals and were less effective against edema induced by 1 microgram antigen in boosted animals. The effectiveness of these drugs was also reduced when boosted mice were challenged with 10 micrograms antigen, where meclizine and cyproheptadine inhibited edema by 31 and 59%, respectively. The anti-allergic compounds ketotifen and azelastine, although effective against allergic inflammation in non-boosted mice, had a reduced or no effect in boosted mice. Our results suggest that allergic edema is less sensitive to antihistamine and anti-allergic drugs in boosted mice, which may be accounted for by an increased role of other mediators.     

Lung responsiveness to antigen in sensitised mice of different strains

A new model of the isolated perfused lung from different strains of mice was developed. Lungs from Swiss, Balb/C and CBA mice actively sensitised to ovalbumin were challenged intratracheally (i.t.) by antigen on day 14. In Swiss mice instillation of ovalbumin led to the release of leukotriene (LT) C₄ significantly above basal values. Conversely, lungs from Balb/C and CBA mice were unresponsive to ovalbumin in terms of production of LTC₄. All strains failed to release histamine when challenged with antigen. Intratracheal instillation of platelet-activating factor (PAF), to lungs from non-sensitised animals, induced the release of comparable amounts of LTC₄, irrespective of the strain. In contrast, i.t. administration of fMLP to lungs from Swiss mice elicited release of significantly higher amounts of LTC₄ as compared to Balb/C and CBA mice. In separate experiments, ovalbumin was injected into the paws and anaphylactic oedema was evaluated. Balb/C and CBA required 1 μg to show an oedema formation, whereas the dose of ovalbumin for Swiss mice to develop a similar response was at least 30-fold lower. In conclusion, antigen provocation induced release of LTC₄ from lungs from Swiss mice but not from Balb/C or CBA. This difference may be accounted for by strain-dependent factors, such as antibody production and requires further investigation.