Computed Tomography-Derived Three-Dimensional Printed Models versus Two-Dimensional Transesophageal Echocardiography for Left Atrial Appendage Occlusion Device Planning: A Systematic Review and Meta-Analysis.

Objective: This systematic review and meta-analysis compared computed tomography (CT)-derived three-dimensional (3D) modeling versus two-dimensional transesophageal echocardiography (TEE) for left atrial appendage occluder (LAAO) device planning.

Background: LAAO device planning is commonly performed with TEE. However, procedures often require multiple devices and deployments due to inaccurate sizing from TEE.

Relationship between compliance and pulmonary vascular resistance in pulmonary arterial hypertension.

Background: Pulmonary arterial compliance (PAC) was previously shown to be an important prognostic factor in pulmonary arterial hypertension (PAH), in addition to the conventional pulmonary vascular resistance (PVR). The product of PAC and PVR, the arterial time (RC) constant, expresses the logarithmic relationship between the hemodynamic parameters. The objective of the study was to test RC constant stability in PAH patients followed beyond 12 months after diagnosis, and to report possible RC variations in different etiologies.

Report: effects of Camellia sinensis L. (green tea) extract on the body and testicular weight changes in adult Wistar rate.

This research was aimed to study the effects of oral administration of Camellia sinensis L. on the testicular and body weights of adult Wistar rats for short and long time periods. The adult Wistar rats were divided into 3 groups (A, B and C).

Characteristics of a large cohort of patients with diabetes having at-risk feet and outcomes in patients with foot ulceration referred to a tertiary care diabetes unit.

To identify in a large population cohort the clinical and biochemical characteristics of patients with diabetes at risk of foot ulceration and outcomes in those with foot ulcers. All patients with diabetes attending Baqai Institute of Diabetology and Endocrinology from January 2004 to April 2012 included in the study. Clinical, biochemical and socio-demographic data were collected and patients were categorised into those at no risk of ulceration, at risk of ulceration and those with foot ulcer, according to the University of Texas classification.

Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem.

Perinatal inflammation is associated with respiratory morbidity. Immune modulation of brainstem respiratory control centers may provide a link for this pathobiology. We exposed 11-day old rats to intratracheal lipopolysaccharide (LPS, 0.

Use of locally made off-loading techniques for diabetic plantar foot ulcer in Karachi, Pakistan.

The aim of this study was to evaluate the effectiveness of applying locally made pressure off-loading techniques on plantar foot ulcer in individuals with diabetes. This prospective study of 70 diabetic patients was conducted at the foot clinic of Baqai Institute of Diabetology & Endocrinology. Plantar foot ulcer, stages 1A and 2A according to the University of Texas classification, was treated by using three off-loading techniques: modified foot wear (sandal), modified plaster of Paris cast with plywood platform and Scotchcast boot.

L-citrulline supplementation reverses the impaired airway relaxation in neonatal rats exposed to hyperoxia.

Background: Hyperoxia is shown to impair airway relaxation via limiting L-arginine bioavailability to nitric oxide synthase (NOS) and reducing NO production as a consequence. L-arginine can also be synthesized by L-citrulline recycling. The role of L-citrulline supplementation was investigated in the reversing of hyperoxia-induced impaired relaxation of rat tracheal smooth muscle (TSM).

Role of arginase in impairing relaxation of lung parenchyma of hyperoxia-exposed neonatal rats.

Background: Prolonged exposure of immature lungs to hyperoxia contributes to neonatal lung injury and airway hyperreactivity. We have previously demonstrated that neonatal exposure of rat pups to ≥95% O2 impairs airway relaxation due to disruption of nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling.

Objective: We now hypothesize that these impaired relaxation responses are secondary to hyperoxia-induced upregulation of arginase, which competes with NO synthase for L-arginine.

Neurokinin-neurotrophin interactions in airway smooth muscle.

Neurally derived tachykinins such as substance P (SP) play a key role in modulating airway contractility (especially with inflammation). Separately, the neurotrophin brain-derived neurotrophic factor (BDNF; potentially derived from nerves as well as airway smooth muscle; ASM) and its tropomyosin-related kinase receptor, TrkB, are involved in enhanced airway contractility. In this study, we hypothesized that neurokinins and neurotrophins are linked in enhancing intracellular Ca(2+) concentration ([Ca(2+)](i)) regulation in ASM.

H. pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria.

Background And Aim: Our previous study of Helicobacter pylori-induced apoptosis showed the involvement of Bcl-2 family proteins and cytochrome c release from mitochondria. Here, we examine the release of other factors from mitochondria, such as apoptosis-inducing factor (AIF), and upstream events involving caspase-8 and Bid.

Methods: Human gastric adenocarcinoma (AGS) cells were incubated with a cagA-positive H.

Role of brain-derived neurotrophic factor in hyperoxia-induced enhancement of contractility and impairment of relaxation in lung parenchyma.

Prolonged hyperoxic exposure contributes to neonatal lung injury, and airway hyperreactivity is characterized by enhanced contraction and impaired relaxation of airway smooth muscle. Our previous data demonstrate that hyperoxia in rat pups upregulates expression of brain-derived neurotrophic factor (BDNF) mRNA and protein, disrupts NO-cGMP signaling, and impairs cAMP production in airway smooth muscle. We hypothesized that BDNF-tyrosine kinase B (TrkB) signaling plays a functional role in airway hyperreactivity via upregulation of cholinergic mechanisms in hyperoxia-exposed lungs.

Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma.

Exposure of immature lungs to hyperoxia for prolonged periods contributes to neonatal lung injury and airway hyperreactivity. We studied the role of disrupted nitric oxide-guanosine 3',5'-cyclic monophosphate (NO-cGMP) signaling in impairing the relaxant responses of lung tissue from hyperoxia-exposed rat pups. Pups were exposed to >/=95% O(2) or room air for 7 days starting from days 1, 5, or 14.

Neonatal lung and airway injury: a role for neurotrophins.

Maintenance of patency in distal airways is essential for gas exchange in neonatal life, and its disruption may have long-lasting effects on respiratory function. However, neural mechanisms that regulate caliber of intrapulmonary airways during early postnatal life, and their disruption by hyperoxic exposure, have not been well characterized. We have previously shown that cholinergically mediated airway contractile responses in rat pups are upregulated after hyperoxic exposure, and that increased expression of neuropeptides, such as substance P, may be contributory.

Adenosine A2A receptors are expressed by GABAergic neurons of medulla oblongata in developing rat.

During early development, adenosine contributes to the occurrence of respiratory depression and recurrent apneas. Recent physiological studies indicate that GABAergic mechanisms may be involved in this inhibitory action of adenosine, via their A(2A) receptors. In the present study, in situ hybridization with ribonucleotide probes for A(2A) receptor (A(2A)R) mRNA was combined with the immunolabeling technique for parvalbumin and transneuronal retrograde tracing method using green fluorescent protein expressing pseudorabies virus (GFP-PRV) to (1) characterize age-dependent changes in the expression of adenosine A(2A)Rs mRNA in brain stem regions where GABAergic neurons are located; (2) determine whether GABA-containing neurons express A(2A)R mRNA traits, and (3) identify whether bulbospinal GABAergic neurons projecting to phrenic nuclei contain A(2A)R mRNA.

Brain stem excitatory and inhibitory signaling pathways regulating bronchoconstrictive responses.

This review summarizes recent work on two basic processes of central nervous system (CNS) control of cholinergic outflow to the airways: 1) transmission of bronchoconstrictive signals from the airways to the airway-related vagal preganglionic neurons (AVPNs) and 2) regulation of AVPN responses to excitatory inputs by central GABAergic inhibitory pathways. In addition, the autocrine-paracrine modulation of AVPNs is briefly discussed. CNS influences on the tracheobronchopulmonary system are transmitted via AVPNs, whose discharge depends on the balance between excitatory and inhibitory impulses that they receive.

Airway-related vagal preganglionic neurons express brain-derived neurotrophic factor and TrkB receptors: implications for neuronal plasticity.

Recent evidence indicates that brain-derived neurotrophic factor (BDNF) is present in neurons and may affect neurotransmitter release, cell excitability, and synaptic plasticity via activation of tyrosine kinase B (TrkB) receptors. However, whether airway-related vagal preganglionic neurons (AVPNs) produce BDNF and contain TrkB receptors is not known. Hence, in ferrets, we examined BDNF and TrkB receptor expression in identified AVPNs using in situ hybridization and immunohistochemistry.

Characterization of the F198S prion protein mutation: enhanced glycosylation and defective refolding.

Prion diseases are associated with the accumulation of a misfolded, protease resistant form of the prion protein, PrPres. In humans there are a variety of different prion related diseases that are sporadic, inherited, or acquired by infection. Gerstmann-Straussler-Sheinker syndrome (GSS) is an inherited prion disease in which PrPres accumulates as amorphous aggregates as well as in amyloid plaques.

An astrocyte toxin influences the pattern of breathing and the ventilatory response to hypercapnia in neonatal rats.

Recent in vitro data suggest that astrocytes may modulate respiration. To examine this question in vivo, we treated 5-day-old rat pups with methionine sulfoximine (MS), a compound that alters carbohydrate and glutamate metabolism in astrocytes, but not neurons. MS-treated pups displayed a reduced breathing frequency (f) in baseline conditions relative to saline-treated pups.

Hyperoxia enhances brain-derived neurotrophic factor and tyrosine kinase B receptor expression in peribronchial smooth muscle of neonatal rats.

Airway hyperreactivity is one of the hallmarks of hyperoxic lung injury in early life. As neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are potent mediators of neuronal plasticity, we hypothesized that neurotrophin levels in the pulmonary system may be disturbed by hyperoxic exposure. We therefore evaluated the effects of hyperoxia on the expression of BDNF, NGF, and their corresponding high-affinity receptors, TrkB and TrkA, respectively, in the lung of rat pups.

Expression of alpha-7 nAChRs on spinal cord-brainstem neurons controlling inspiratory drive to the diaphragm.

In the present study, we determined whether alpha-7 subunit containing nicotinic acetylcholine receptors (nAChRs) are expressed by neurons within the pre-Botzinger complex (pre-BotC), bulbospinal, and phrenic motor nuclei in the rat. alpha-7 Immunohistochemistry combined with cholera toxin B (CTB), a retrograde tracer was used to detect expression of alpha-7 nAChRs by phrenic motor and bulbospinal neurons. Neurokinin-1 receptor immunoreactivity was used as a marker for pre-BotC neurons.

The Thr183Ala Mutation, Not the Loss of the First Glycosylation Site, Alters the Physical Properties of the Prion Protein.

The abnormal form of the prion protein has increased resistance to protease digestion and is insoluble in non-ionic detergents. The normal prion protein is modified by the non-obligatory addition of two N-linked glycans. One pathogenic mutation, Thr to Ala at residue 183 of the human prion protein, blocks addition of the first glycan to the Asp residue 181.