Fístula arteriovenosa pulmonar tratada mediante lobectomía por VATS uniportal / Pulmonary Arteriovenous Fistula Treated by Uniportal VATS Lobectomy

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[Translated article] Pulmonary Arteriovenous Fistula Treated by Uniportal Vats Lobectomy / Fístula arteriovenosa pulmonar tratada mediante lobectomía por VATS uniportal

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Standardized surgical technique for uniportal video-assisted thoracoscopic lobectomy.

SUMMARY: Uniportal video-assisted thoracoscopic surgery may be the approach for any thoracic procedure, from minor resections to complex reconstructive surgery. However, anatomical lobectomy represents its most common and clinically proven usage. A wide variety of information about uniportal video-assisted thoracoscopic lobectomies can be found in the literature and multimedia sources. This article focuses on updating the surgical technique and includes important aspects such as the geometric approach, anaesthesia considerations, operating room set-up, tips about the incision, instrumentation management and the operative technique to perform the 5 lobectomies. The following issues are explained for each lobectomy: anatomical considerations, surgical steps and technical advice. Medical illustrations and videos are included to clarify the text with the goal of describing a standard surgical practice.

Current role of uniportal video-assisted thoracic surgery for lung cancer treatment.

The use of video-assisted thoracic surgery (VATS) as an approach for early-stage lung cancer treatment has revealed benefits compared to open surgery by minimizing trauma to the patients. This trend has brought the evolution of VATS to less and less invasive methods, eventually leading to the development of Uniportal VATS (UniVATS) technique. This new approach has shown to be resourceful, proving its feasibility even for complex oncological procedures. Furthermore, data is starting to express some benefits over multiport VATS, thus spurring on its development towards newer and more complex procedures. It is also been adopted by the surgical community achieving fast evolution and worldwide diffusion. Here, we review the evolution of UniVATS, its current state of evidence, some basic technical aspects, the present role it has in lung cancer treatment and the ongoing development of the technique. RELEVANCE FOR PATIENTS: This article could help patients to understand how the UniVATS technique developed as part of the evolution of VATS, sharing its benefits and indications. Furthermore, patients would be able to understand technical aspects and the current applications of UniVATS for lung cancer treatment.

Uniportal VATS for non-small cell lung cancer.

The video-assisted thoracic surgery (VATS) technique has evolved from its multiport origins to even less invasive approaches grounded in its proven benefits over open surgery for the treatment of early stage lung cancer. In this evolution process, the Uniportal VATS (UniVATS) strategy emerged. This technique is giving some evidence of benefits when compared to the multiport VATS and has been embraced by the surgical community spreading its geographical and surgical boundaries. Moreover, UniVATS has proven its feasibility for numerous and more complex procedures for lung cancer diagnosis and treatment, which are reviewed in this document as well as its current and future development.

Resolution of acenocoumarol-associated calciphylaxis with drug withdrawal.

Calciphylaxis is a syndrome of cutaneous ischaemic necrosis and ulceration due to arteriolar calcification with subsequent thrombosis, which rarely presents in patients without terminal kidney disease. Recently, several reports of coumarins-associated calciphylaxis have stressed the relevance of anticoagulant therapy as an important risk factor for the development of this condition. We report five cases of acenocoumarol-associated, biopsy-proven calciphylaxis in women aged between 64 and 92 years. The drug had been prescribed for atrial fibrillation and was taken without interruption from 14 to 224 months. Lesions were present for months in all cases and were resistant to multiple therapeutic options, but they resolved only with simple wound care measures 6-14 months after changing the anticoagulant therapy.

Altered Fetal Head Growth in Preeclampsia: A Retrospective Cohort Proof-Of-Concept Study.

BACKGROUND: Preeclampsia is associated with fetal growth restriction and low birth weights. Neurotrophins, which mediate neuronal growth and development, are also increased in the placenta and cord blood in preeclampsia. Hence, the aim of this study was to determine whether fetal head growth is altered in preeclampsia, adjusting for growth restriction and other confounding variables. METHODS: This research included a retrospective cohort study, looking at fetal head circumference at birth, plus a case-control study examining fetal head circumference at mid-gestation. The head circumference at birth analysis consisted of 14,607 pregnancies (preeclampsia = 382, control = 14,225), delivered between July 2006 and June 2012 at Nepean Hospital, Australia. Head circumference at birth, in addition to other maternal and fetal variables, was sourced from the Nepean Obstetric Database. The head circumference at mid-gestation study consisted of 756 pregnancies (preeclampsia = 248, control = 508), delivered within the same data collection period at Nepean Hospital. Head circumference at mid-gestation was retrieved from an earlier ultrasound scan. Exclusion criteria included >1 fetus, illegal drug use, alcohol consumption, and chronic or gestational hypertension. Generalized linear models were used to analyze fetal head circumference in preeclampsia versus controls, adjusting for confounding variables. RESULTS: Head circumference increased at a greater rate in preeclampsia versus controls, adjusted for gestation, fetal gender, birth weight and length, smoking, maternal BMI, and growth restriction. At mid-gestation, there was no difference in head circumference between preeclampsia and controls. CONCLUSION: For the first time, this research has suggested increased fetal head growth in preeclampsia, adjusted for confounders. This finding may be explained by altered fetal exposure to neurotrophins in preeclampsia. The long-term neurodevelopmental consequences of preeclampsia remain unclear.

In utero Head Circumference is Associated with Childhood Allergy.

BACKGROUND: Altered fetal growth is known to be associated with allergic disease. Specifically, increased head circumference at birth has been linked to asthma and elevated IgE. However, few studies have examined a link between early fetal anthropometry and allergic disease. The aim of this study was to examine head circumference at mid-gestation in children diagnosed with allergy. METHODS: This was a retrospective cohort study, comprising pregnancies delivered between 10/2006 and 9/2010 at Nepean Hospital, Australia. Exclusion criteria were illegal drug use, alcohol consumption, gestation <35 weeks, and gestational hypertension. Pregnancy data were sourced from the Nepean Obstetric Database. Atopic diseases (asthma, atopic dermatitis, and IgE-mediated food allergy) were assessed by questionnaire at age 1-5 years. Infants from pregnancies with completed questionnaires, who also had a mid-gestation ultrasound scan, were included (N = 121). Multiple logistic regression techniques were used to model head circumference against the development of allergies. RESULTS: Smaller head circumference at mid-gestation was associated with increased odds of allergic disease in children aged 1-5 years. A 1 mm smaller head circumference was associated with a 7% increased chance of allergies being later diagnosed, adjusted for gestation (95% CI: 1-14%, p = 0.036). Head circumference at mid-gestation was also inversely correlated with the presence of multiple atopic disease. CONCLUSION: Smaller mid-gestational head circumference is associated with early childhood allergic disease, which suggests that fetal programing of allergic disease occurs before mid-gestation. This suggests that mediators such as brain-derived neurotrophic factor may be dysregulated early in utero in a milieu, which also predisposes to atopic disease.

Validation of a Comprehensive Early Childhood Allergy Questionnaire.

BACKGROUND: Parental questionnaires to assess incidence of pediatric allergic disease have been validated for use in school-aged children. Currently, there is no validated questionnaire-based assessment of food allergy, atopic dermatitis (AD), and asthma for infants and young children. METHODS: The Comprehensive Early Childhood Allergy Questionnaire was designed for detecting AD, asthma, and IgE-mediated food allergies in children aged 1-5 years. A nested case-control design was applied. Parents of 150 children attending pediatric outpatient clinics completed the questionnaire before being clinically assessed by a pediatrician for allergies. Sensitivity, specificity, and reproducibility of the questionnaire were assessed. RESULTS: Seventy-seven children were diagnosed with one or more current allergic diseases. The questionnaire demonstrated high overall sensitivity of 0.93 (95% CI 0.86-0.98) with a specificity of 0.79 (95% CI 0.68-0.88). Questionnaire reproducibility was good with a kappa agreement rate for symptom-related questions of 0.45-0.90. CONCLUSIONS: Comprehensive Early Childhood Allergy Questionnaire accurately and reliably reflects the presence of allergies in children aged 1-5 years. Its use is warranted as a tool for determining prevalence of allergies in this pediatric age group.

Neurosteroid vitamin D system as a nontraditional drug target in neuropsychopharmacology.

Vitamin D is becoming increasingly recognized as a nontraditional drug target for different brain pathologies. Although widely known for their role in calcium metabolism, vitamin D and its receptor have been linked to several brain disorders, including cognitive decline, epilepsy, affective disorders, and schizophrenia. Here we discuss mounting evidence, and parallel recent clinical and animal behavioral, genetic and pharmacological data to emphasize the emerging role of the neurosteroid vitamin D system in brain function.

Premature aging in vitamin D receptor mutant mice.

Hypervitaminosis vitamin D(3) has been recently implicated in premature aging through the regulation of 1alpha hydroxylase expression by klotho and fibroblast growth factor-23 (Fgf-23). Here we examined whether the lack of hormonal function of vitamin D(3) in mice is linked to aging phenomena. For this, we used vitamin D(3) receptor (VDR) "Tokyo" knockout (KO) mice (fed with a special rescue diet) and analyzed their growth, skin and cerebellar morphology, as well as overall motor performance. We also studied the expression of aging-related genes, such as Fgf-23, nuclear factor kappaB (NF-kappaB), p53, insulin like growth factor 1 (IGF1) and IGF1 receptor (IGF1R), in liver, as well as klotho in liver, kidney and prostate tissues. Overall, VDR KO mice showed several aging related phenotypes, including poorer survival, early alopecia, thickened skin, enlarged sebaceous glands and development of epidermal cysts. There was no difference either in the structure of cerebellum or in the number of Purkinje cells. Unlike the wildtype controls, VDR KO mice lose their ability to swim after 6 months of age. Expression of all the genes was lower in old VDR KO mice, but only NF-kappaB, Fgf-23, p53 and IGF1R were significantly lower. Since the phenotype of aged VDR knockout mice is similar to mouse models with hypervitaminosis D(3), our study suggests that VDR genetic ablation promotes premature aging in mice, and that vitamin D(3) homeostasis regulates physiological aging.

Serum cholesterol and expression of ApoAI, LXRbeta and SREBP2 in vitamin D receptor knock-out mice.

Vitamin D insufficiency has been reported to be associated with increased blood cholesterol concentrations. Here we used two strains of VDR knock-out (VDR-KO) mice to study whether a lack of vitamin D action has any effect on cholesterol metabolism. In 129S1 mice, both in male and female VDR-KO mice serum total cholesterol levels were significantly higher than those in wild type (WT) mice (20.7% (P=0.05) and 22.2% (P=0.03), respectively). In addition, the serum high-density lipoprotein-bound cholesterol (HDL-C) level was 22% (P=0.03), respectively higher in male VDR-KO mice than in WT mice. The mRNA expression levels of five cholesterol metabolism related genes in livers of 129S1 mice were studied using quantitative real-time PCR (QRT-PCR): ATP-binding cassette transporter A1 (ABCA1), regulatory element binding protein (SREBP2), apolipoprotein A-I (ApoAI), low-density lipoprotein receptor (LDLR) and liver X receptor beta (LXRbeta). In the mutant male mice, the mRNA level of ApoAI and LXRbeta were 49.2% (P=0.005) and 38.8% (P=0.034) higher than in the WT mice. These changes were not observed in mutant female mice, but the female mutant mice showed 52.5% (P=0.006) decrease of SREBP2 mRNA expression compared to WT mice. Because the mutant mice were fed with a special rescue diet, we wanted to test whether the increased cholesterol levels in mutant mice were due to the diet. Both the WT and mutant NMRI mice were given the same diet for 3 weeks before the blood sampling. No difference in cholesterol or in HDL-C between WT and mutant mice was found. The results suggest that the food, gender and genetic background have an effect on the cholesterol metabolism. Although VDR seems to regulate some of the genes involved in cholesterol metabolism, its role in the regulation of serum cholesterol seems to be minimal.

Vestibular dysfunction in vitamin D receptor mutant mice.

The vitamin D endocrine system is essential for calcium and bone homeostasis. Vitamin D deficits are associated with muscle weakness and osteoporosis, whereas vitamin D supplementation may improve muscle function, body sway and frequency of falls, growth and mineral homeostasis of bones. The loss of muscle strength and mass, as well as deficits in bone formation, lead to poor balance. Poor balance is one of the main causes of falls, and may lead to dangerous injuries. Here we examine balance functions in vitamin D receptor deficient (VDR-/-) mice, an animal model of vitamin D-dependent rickets type II, and in 1alpha-hydroxylase deficient (1alpha-OHase-/-) mice, an animal model of pseudovitamin D-deficiency rickets. Recently developed methods (tilting box, rotating tube test), swim test, and modified accelerating rotarod protocol were used to examine whether the absence of functional VDR, or the lack of a key vitamin D-activating enzyme, could lead to mouse vestibular dysfunctions. Overall, VDR-/- mice, but not 1alpha-OHase-/- mice, showed shorter latency to fall from the rotarod, smaller fall angle in the tilting box test, and aberrant poor swimming. These data suggest that VDR deficiency in mice is associated with decreased balance function, and may be relevant to poorer balance/posture control in humans with low levels of vitamin D.

Progressive hearing loss in mice with a mutated vitamin D receptor gene.

BACKGROUND: Both hypo- and hypervitaminosis D can cause sensorineural hearing loss, and aural symptoms due to vitamin D insufficiency are especially common during gravidity. Hormonal forms of vitamin D regulate transcription by binding with the high-affinity vitamin D receptor (VDR). OBJECTIVE: To assess the effects of impaired vitamin D action in VDR knockout (KO) mice on hearing, cochlear morphology, and cochlear gene expression. MATERIALS AND METHODS: Eighteen young male and female mice (10 VDR KO and 8 wild type, WT, < or =6 months old), 33 adult male and female mice (16 VDR KO and 17 WT, between 7 and 14 months old), and 11 aged male and female mice (5 VDR KO and 6 WT, > or =15 months old) on 129S1 genetic background were studied. Auditory thresholds were evaluated by auditory brain stem response. Morphological changes were analyzed using plastic embedding and light microscopy. The expression of key genes (known to play a role in the regulation of cochlear function), and caspase 3 activity, were assessed using immunofluorescent confocal microscopy. RESULTS: There was a statistically significant difference between the young and the adult groups, and between the adult and aged groups of WT mice. There was also a statistically significant difference between the adult and aged groups in VDR KO mice, and between the young WT group and the young VDR KO group. Spiral ganglion cell loss was observed in the basal turn of adult VDR KO mice, a phenomenon infrequently found in WT mice. Expression of connexin 26, KCNJ10, and transient receptor potential channel vanilloid subfamily 4/6 was not affected by VDR KO-mediated hearing loss. Caspase 3 activation was detected in the spiral ganglion cell and its satellite cells, stria vascularis, spiral ligament fibrocytes, and the organ of Corti in both genotypes. However, the percentage of positive cells and the staining intensity were lower in the VDR KO (compared to the WT) mice. CONCLUSION: These data suggest that sensorineural hearing loss progressively developed at an earlier age in VDR KO mice. While the fundamental gene expressions in the cochlea were not influenced by VDR mutation, it resulted in decrease of caspase 3 activation, which may be one of the factors underlying accelerating age-related hearing loss observed in VDR KO mice.

The regular and light-dark Suok tests of anxiety and sensorimotor integration: utility for behavioral characterization in laboratory rodents.

Animal behavioral models are crucial for neurobiological research, allowing for the thorough investigation of brain pathogenesis to be performed. In both animals and humans, anxiety has long been linked to vestibular disorders. However, although there are many tests of anxiety and vestibular deficits, there are few protocols that address the interplay between these two domains. The Suok test and its light-dark modification presented here appear to be suitable for testing this pathogenetic link in laboratory rodents. This protocol adds a new dimension to previously used tests by assessing animal anxiety and balancing simultaneously, resulting in efficient, high-throughput screens for testing psychotropic drugs, phenotyping genetically modified animals, and modeling clusters of human disorders related to stress/anxiety and balancing.

Neophobia, sensory and cognitive functions, and hedonic responses in vitamin D receptor mutant mice.

Vitamin D is a seco-steroid hormone with multiple actions in the brain, mediated through the nuclear vitamin D receptor (VDR). We have recently shown that mutant mice lacking functional VDR demonstrate altered emotional behavior and specific motor deficits. Here we further examine phenotype of these mice, testing their novelty responses, as well as cognitive and sensory (olfactory and gustatory) functions in the novel food, two-trial Y-maze and tastant consumption tests. In addition, we study depression-like behavior in these mice, using anhedonia-based sucrose preference test. Overall, VDR mutant mice showed neophobic response in several different tests, but displayed unimpaired olfactory and gustatory functions, spatial memory and baseline hedonic responses. Collectively, these data confirm that mutation of VDR in mice leads to altering emotional/anxiety states, but does not play a major role in depression, as well as in the regulation of some sensory and cognitive processes. These results support the role of the vitamin D/VDR neuroendocrine system in the regulation of behavior, and may have clinical relevance, enabling a better focus on psychiatric and behavioral disorders associated with dysfunctions in this neuroendocrine system.

Aberrant nest building and prolactin secretion in vitamin D receptor mutant mice.

1Alpha,25(OH)2D3, the hormonal form of vitamin D, is a neuroactive seco-steroid hormone with multiple functions in the brain. Most of these effects are mediated through the nuclear vitamin D receptor (VDR), widely distributed in the central nervous system. Our earlier studies showed that mutant mice lacking functional VDR have specific behavioural abnormalities, including anxiety and aberrant maternal behaviour, which may be hormonally regulated. Here we describe impaired nest building behaviour in VDR mutant mice. Since prolactin plays a key role in the regulation of nest building in both sexes, we also examine whether VDR mutant mice have altered prolactin levels. Overall, serum prolactin levels were increased in VDR mutant mice, accompanied by marked impairments in their nest building activity. In contrast, there were no differences in prolactin mRNA expression levels between wildtype control mice and VDR mutant mice. Collectively, these data suggest that partial genetic ablation of VDR affects prolactin system in mice, and that altered serum prolactin levels in VDR mutants may underlie some of their behavioural abnormalities, such as impaired nest building.

Influence of paternal genotypes on F1 behaviors: lessons from several mouse strains.

F1 and F2 mouse hybrids derived from different parental strains are becoming a useful tool in behavioral research, underlining the importance of their in-depth behavioral phenotyping. 129S1/SvImJ (S1), C57BL/6 (B6), NMRI (N) and BALB/c (BC) mice are commonly used in behavioral neuroscience, demonstrating marked behavioral differences. Here, we assess behavioral phenotypes of male mice of S1 and several hybrid strains (S1B6, S1N, S1BC) in a battery of behavioral tests, including the open field, novel odor exposure, novelty-induced grooming, horizontal rod (Suok) and the elevated plus maze tests. In addition, we assessed aggression and social barbering in these strains. Overall, the substantial differences observed here between these strains allow us to determine the influence of different genetic backgrounds on mouse behaviors, and more fully understand how different strain-specific behaviors overlap in the F1 progeny. Our results imply complex interplay between parental genotypes in anxiety, activity, grooming, aggression and barbering of their F1 progeny, further confirming the utility of F1 hybrids in behavioral neurogenetics.

Thalamic calcification in vitamin D receptor knockout mice.

Vitamin D is a steroid hormone with many important functions in the brain, mediated through the nuclear vitamin D receptor. Here, we report that aging nuclear vitamin D receptor knockout mice demonstrate a symmetric thalamic calcification with numerous Ca/P-containing laminated bodies. These results are consistent with clinical findings showing brain calcification in patients with vitamin D deficiency. Our results suggest that nuclear vitamin D receptor deficiency leads to brain mineralization in vitamin D receptor knockout mice, which may represent an experimental model of intracranial calcification.