Sinoaortic denervation does not increase cardiovascular/endocrine responses to stress.

Sinoaortic baroreceptor denervation is reported to produce exaggerated centrally derived cardiovascular and endocrine responses. We examined the effect of sinoaortic denervation (SAD) on the cardiovascular and endocrine responses to two acute stressors, footshock and immobilization, in male Sprague-Dawley rats. Parameters measured were mean arterial pressure (MAP), heart rate (HR) and plasma levels of oxytocin (OT) and vasopressin (VP). Baseline MAP was elevated in the SAD group (approximately 25 mm Hg) and footshock stress increased arterial pressure equivalently in both groups. This stress caused tachycardia and increased plasma OT, with a tendency for the SAD group to show blunted responses. Immobilization increased HR but caused no change in MAP and no significant difference between the groups. This form of stress also increased plasma OT, and again the SAD group showed a diminished response. Plasma VP was not significantly altered by either stressor. The results of these studies indicate that SAD does not uniformly increase the cardiovascular and endocrine responses to all stressors or centrally derived stimuli. These results also suggest that the lack of an increase in plasma VP is not related to baroreceptor-mediated inhibition of secretion under stressful conditions.     

Helicobacter pylori Infection in Infants and Toddlers in South America: Concordance between [13C]Urea Breath Test and Monoclonal H. pylori Stool Antigen Test

Accurate noninvasive tests for diagnosing Helicobacter pylori infection in very young children are strongly required. We investigated the agreement between the [¹³C]urea breath test ([¹³C]UBT) and a monoclonal ELISA (HpSA) for detection of H. pylori antigen in stool. From October 2007 to July 2011, we enrolled 414 infants (123 from Brazil and 291 from Peru) of ages 6 to 30 months. Breath and stool samples were obtained at intervals of at least 3 months from Brazilian (n = 415) and Peruvian (n = 908) infants. [¹³C]UBT and stool test results concurred with each other in 1,255 (94.86%) cases (kappa coefficient = 0.90; 95% confidence interval [CI] = 0.87 to 0.92). In the H. pylori-positive group, delta-over-baseline (DOB) and optical density (OD) values were positively correlated (r = 0.62; P < 0.001). The positivity of the tests was higher (P < 0.001; odds ratio [OR] = 6.01; 95% CI = 4.50 to 8.04) in Peru (546/878; 62.2%) than in Brazil (81/377; 21.5%) and increased with increasing age in Brazil (P = 0.02), whereas in Peru it decreased with increasing age (P < 0.001). The disagreement between the test results was associated with birth in Brazil and female gender but not with age and diarrhea. Our results suggest that both [¹³C]UBT and the stool monoclonal test are reliable for diagnosing H. pylori infection in very young children, which will facilitate robust epidemiological studies in infants and toddlers.     

A phylogenetic analysis using multidirectional chromosome painting of three species (Uroderma magnirostrum, U. bilobatum and Artibeus obscurus) of subfamily Stenodermatinae (Chiroptera-Phyllostomidae)

The species of genera Uroderma and Artibeus are medium-sized bats belonging to the family Phyllostomidae and subfamily Stenodermatinae (Mammalia, Chiroptera) from South America. They have a wide distribution in the Neotropical region, with two currently recognized species in Uroderma and approximately 20 species in Artibeus. These two genera have different rates of chromosome evolution, with Artibeus probably having retained the ancestral karyotype for the subfamily. We used whole chromosome paint probe sets from Carollia brevicauda and Phyllostomus hastatus on Uroderma magnirostrum, Uroderma bilobatum, and Artibeus obscurus. With the aim of testing the previous phylogenies of these bats using cytogenetics, we compared these results with published painting maps on Phyllostomidae. The genome-wide comparative maps based on chromosome painting and chromosome banding reveal the chromosome forms that characterize each taxonomic level within the Phyllostomidae and show the chromosome evolution of this family. Based on this, we are able to suggest an ancestral karyotype for Phyllostomidae. Our cladistic analysis is an independent confirmation using multidirectional chromosome painting of the previous Phyllostomidae phylogenies.     

Facile Synthesis of Well‐Defined Telechelic Alkyne‐Terminated Polystyrene in Polar Media Using ATRP With Mixed Fe/Cu Transition Metal Catalyst

The synthesis of polystyrene (PS) by atom transfer radical polymerization using the Fe(0)/CuBr₂ catalytic system in dimethylformamide is reported. The effects of temperature, ligand, initiator structure, and monomer to solvent ratio on the polymerization kinetics are evaluated. PS with high molecular weight, low polydispersity, and telechelic structure are achieved and successfully used for further reinitiation or the copper(I)‐catalyzed Huisgen 1,3‐dipolar cycloaddition click reaction between alkyne‐ and azide‐terminated PS. For the first time, suitable styrene polymerization rates are achieved using this cost‐effective and environmentally attractive catalytic system. This method can be very useful in macromolecular engineering to afford PS‐based materials with well‐controlled structure.     

Renal involvement in patients with hepatosplenic Schistosomiasis mansoni.

In a prospective study of renal involvement in 100 consecutively hospitalized patients with hepatosplenic schistosomiasis mansoni, 15 exhibited persistent proteinuria of varying degree, which in 6 instances was accompanied by hypertension. Nine patients had the nephrotic syndrome. The most common glomerular lesion in this group was membrano-proliferative glomerulonephritis. Surgical biospy obtained during splenectomy in 15 patients without clinical evidence of renal involvement showed glomerular lesions in 6 instances. Focal proliferative glomerulonephritis was the most common lesion in this group. The detection of silent glomerular lesions in patients with Schistosoma mansoni infection suggests that the glomerular alterations may precede clinical manifestations of renal disease.     

Delayed-type Necrosis after Soft-tissue Augmentation with Hyaluronic Acid

The growing use of dermal fillers, specifically the use of hyaluronic acid, can be explained by their effectiveness and versatility as well as their favorable safety profiles. Nevertheless, early and late complications with varying levels of severity may occur. The incidence of complications is low and the majority of adverse events are mild (edema, erythema, and local ecchymosis) and of limited duration. However, more severe events, such as ischemia and necrosis, may occur. The symptoms of ischemia can occur immediately after the injection or several hours after the procedure. Here, the authors report three cases of necrosis after hyaluronic acid injection with the first symptoms presenting only several hours after the procedure. The patients were treated immediately after the diagnosis. The aim of this review is to communicate the possibility of the delayed-type presentation of necrosis, present the signs and symptoms that lead to early diagnosis, and review the treatment possibilities of this severe complication.Dermal fillers have been injected with increasing frequency over the past three decades for soft-tissue augmentation by volume expansion in the management of the aging face. In 2012, there were about two million procedures using dermal fillers, according to the American Society of Plastic Surgeons, five percent more than in 2011 and 205 percent more than in 2000, second only to botulinum toxin type A. These minimally invasive and nonsurgical cosmetic procedures were the two most commonly performed in this range of time studied.1,2The growing use of dermal fillers, specifically the use of hyaluronic acid (HA), can be explained by their effectiveness and versatility as well as their favorable safety profiles. Nevertheless, early and late complications with varying levels of severity may occur. The incidence of complications is low and the majority of adverse events are mild (edema, erythema, and local ecchymosis) and of limited duration. However, more severe events, such as ischemia and necrosis, may occur.Injection necrosis is a rare, but important, complication associated with dermal fillers. Necrosis can be attributed to one of two factors—an interruption of vascular supply due to compression or frank obstruction of vessels by direct injection of the material into a vessel itself. The glabella is the injection site commonly believed to be at greater risk for necrosis, but it can also occur at the nasolabial fold.3 Risk factors for intravascular injection include site of application (deep injection of filler products at or near the site of named vessels), volume applied (larger amounts of product can cause a proportionally greater degree of arterial obstruction), and previous scarring (deep tissue scars may stabilize and fix arteries in place, making them easier to penetrate with small sharp needles).4The initial presentation of vascular events may include pain and discomfort disproportionate to what is typically experienced following filler treatments and clinical findings, including blanching, livedo pattern, or violaceous discoloration.4 Although many cases report this immediate post-injection presentation as the typical background seen in a necrosis event, there are few reports with the first symptom presenting only hours after augmentation. See Figures 1 through ​through3,3, where the authors present three cases of vascular compromise after soft-tissue augmentation with delayed-type presentation. Open in a separate windowOpen in a separate windowFigures 2Aand 2B.Case 2: Necrosis and secondary infection 48 hours after the HA injection (a). Discrete scars in the affected area after treatment (b). Open in a separate windowOpen in a separate windowFigures 1Aand 1B.Case 1: Edema, erythema, and progressive violaceous reticulated patch, livedoid area were observed on the left cheek 36 hours after the injection (a). Complete healing five days after hyaluronidase application and nine days after the HA injection (b). Open in a separate windowOpen in a separate windowFigures 3Aand 3B.Case 3: Necrosis and secondary infection 48 hours after the HA injection (a). Erythema, hipercromia, and discreet scars in the affected area after treatment (b).