Safety and feasibility of revisional bariatric surgery following Laparoscopic Adjustable Gastric Band - Outcomes from a large UK private practice.

Background: Revisional bariatric surgery is unavoidable in a proportion of patients. Despite its need, the development of this speciality has been hampered by its complexity and preferred delivery in institutional set ups. Although primary bariatric surgery can be delivered in the private sector; safety and feasibility of revisional bariatric surgery remains unexplored in this setting.

Physiologic levels of resistin induce a shift from proliferation to apoptosis in macrophage and VSMC co-culture.

Background: Resistin, an adipokine with inflammatory properties, has been associated with plaque vulnerability. Vascular smooth muscle cells and macrophages are the major cellular components in advanced atherosclerotic plaques and interdependently affect plaque stability. The purpose of this study was to examine the effects of resistin on the interactions of vascular smooth muscle cells and macrophages using co-culture systems.

Volumetric Analysis of Extent of Resection, Survival, and Surgical Outcomes for Insular Gliomas.

Background: Insular gliomas are challenging tumors to surgically resect owing to the anatomy surrounding them. This study evaluates the role of extent of resection (EOR) and molecular markers in surgical outcome and survival for insular gliomas.

Methods: Seventy-four patients who had undergone initial resection for insular glioma by the same surgeon between 2006 and 2016 were analyzed.

PKC-epsilon and TLR4 synergistically regulate resistin-mediated inflammation in human macrophages.

Background And Aims: Resistin has been associated with atherosclerotic inflammation and cardiovascular complications. We and others have previously shown that PKC-epsilon (PKCε) is involved in resistin-induced smooth muscle cell (VSMC) dysfunction at a high pathological concentration. This study aimed to evaluate the role and potential pathways of resistin at a physiological concentration, in atherosclerosis-related inflammation.

Eotaxin Augments Calcification in Vascular Smooth Muscle Cells.

Calcification of atherosclerotic plaques in elderly patients represents a potent risk marker of cardiovascular events. Plasma analyses of patients with or without calcified plaques reveal significant differences in chemokines, particularly eotaxin, which escalates with increased calcification. We therefore, hypothesize that eotaxin in circulation augments calcification of vascular smooth muscle cells (VSMCs) possibly via oxidative stress in the vasculature.

PKCε mediates resistin-induced NADPH oxidase activation and inflammation leading to smooth muscle cell dysfunction and intimal hyperplasia.

Background And Aims: Resistin has been implicated in cardiovascular disease and poor interventional cardiovascular outcomes. Previous studies by our group demonstrated resistin promoted vascular smooth muscle cell (VSMC) migration through protein kinase C epsilon (PKCε) pathways, while few others showed that resistin induced reactive oxygen species (ROS) generation in various cell types. In this study, we aim to systemically examine the functional role of resistin at the cellular and tissue levels as well as the potential mechanistic relationship between resistin-induced PKCε activation and ROS production.

A Prospective Evaluation of Systemic Biomarkers and Cognitive Function Associated with Carotid Revascularization.

Objective: To determine factors affecting cognition and identify predictors of long-term cognitive impairment following carotid revascularization procedures.

Background: Cognitive impairment is common in older patients with carotid occlusive diseases.

Methods: Patients undergoing carotid intervention for severe occlusive diseases were prospectively recruited.

Protein kinase G-regulated production of H2S governs oxygen sensing.

Reflexes initiated by the carotid body, the principal O2-sensing organ, are critical for maintaining cardiorespiratory homeostasis during hypoxia. O2 sensing by the carotid body requires carbon monoxide (CO) generation by heme oxygenase-2 (HO-2) and hydrogen sulfide (H2S) synthesis by cystathionine-γ-lyase (CSE). We report that O2 stimulated the generation of CO, but not that of H2S, and required two cysteine residues in the heme regulatory motif (Cys(265) and Cys(282)) of HO-2.

Inherent variations in CO-H2S-mediated carotid body O2 sensing mediate hypertension and pulmonary edema.

Oxygen (O2) sensing by the carotid body and its chemosensory reflex is critical for homeostatic regulation of breathing and blood pressure. Humans and animals exhibit substantial interindividual variation in this chemosensory reflex response, with profound effects on cardiorespiratory functions. However, the underlying mechanisms are not known.

Role of oxidative stress-induced endothelin-converting enzyme activity in the alteration of carotid body function by chronic intermittent hypoxia.

Chronic intermittent hypoxia (CIH) leads to remodelling of the carotid body function, manifested by an augmented sensory response to hypoxia and induction of sensory long-term facilitation (LTF). It was proposed that endothelin-1 (ET-1) contributes to CIH-induced hypoxic hypersensitivity of the carotid body. The objectives of the present study were as follows: (i) to delineate the mechanisms by which CIH upregulates ET-1 expression in the carotid body; and (ii) to assess whether ET-1 also contributes to sensory LTF.

Volkman's Contracture, Persistent Limb Ischaemia, and Amputation: A Complication of Brachial Artery Catheterisation for Haemodynamic Monitoring Using PiCCO.

We report a case of a 64-year-old woman who was admitted to intensive care unit with multiorgan failure secondary to Plasmodium falciparum malaria. Haemodynamic monitoring using the transpulmonary thermodilution with pulse contour analysis system (PiCCO) was achieved via the left brachial artery. Two days later, a flexion deformity of the left hand was noted, and examination revealed left lower arm ischaemia.

Differential regulation of tyrosine hydroxylase by continuous and intermittent hypoxia.

Although continuous hypoxia (CH) and intermittent hypoxia (IH) cause reduction in oxygen availability, organisms adapt to the effects of chronic CH whereas IH adversely impacts autonomic functions. Catecholamines are expressed both in the central and peripheral nervous systems and they play important roles in the regulation of cardio-respiratory functions during hypoxia. Tyrosine hydroxylase (TH) is the rate-limiting enzyme for catecholamine synthesis.

Endogenous H2S is required for hypoxic sensing by carotid body glomus cells.

H(2)S generated by the enzyme cystathionine-γ-lyase (CSE) has been implicated in O(2) sensing by the carotid body. The objectives of the present study were to determine whether glomus cells, the primary site of hypoxic sensing in the carotid body, generate H(2)S in an O(2)-sensitive manner and whether endogenous H(2)S is required for O(2) sensing by glomus cells. Experiments were performed on glomus cells harvested from anesthetized adult rats as well as age and sex-matched CSE(+/+) and CSE(-/-) mice.

NADPH oxidase-derived H(2)O(2) contributes to angiotensin II-induced aldosterone synthesis in human and rat adrenal cortical cells.

Background: The Renin-Angiotensin-Aldosterone-System plays a pivotal role in hypertension. Angiotensin II (Ang II) is a major regulator of aldosterone synthesis and secretion, and it is known to facilitate reactive oxygen species (ROS) generation in many cell types.

Aims: Here, we assessed the role of ROS signaling in Ang II-induced aldosterone synthesis by focusing on the regulation of aldosterone synthase (CYP11B2), a cytochrome P450 oxidase that catalyzes the final step in aldosterone biosynthetic pathway.

Endothelin-1 mediates attenuated carotid baroreceptor activity by intermittent hypoxia.

The objectives of the present study were to examine the effects of intermittent hypoxia (IH) on arterial baroreflex function and assess the underlying mechanism(s). Experiments were performed on adult male rats treated with 14 days of IH (15 s of hypoxia, 5 min of normoxia; 8 h/day) or normoxia (control). Arterial blood pressures were elevated in IH-treated rats, and this effect was associated with attenuated heart rate and splanchnic sympathetic nerve responses to arterial baroreflex activation.

Angiotensin II evokes sensory long-term facilitation of the carotid body via NADPH oxidase.

We previously reported that reactive oxygen species generated by NADPH oxidase 2 (Nox2) induces sensory plasticity of the carotid body, manifested as a progressive increase in baseline sensory activity or sensory long-term facilitation (sLTF). ANG II, a peptide generated within the carotid body, is a potent activator of Nox2. In the present study, we tested the hypothesis that ANG II evokes sLTF of the carotid body via Nox2 activation.

Post-translational modification of glutamic acid decarboxylase 67 by intermittent hypoxia: evidence for the involvement of dopamine D1 receptor signaling.

Intermittent hypoxia (IH) associated with sleep apnea leads to cardio-respiratory morbidities. Previous studies have shown that IH alters the synthesis of neurotransmitters including catecholamines and neuropeptides in brainstem regions associated with regulation of cardio-respiratory functions. GABA, a major inhibitory neurotransmitter in the CNS, has been implicated in cardio-respiratory control.

Enhanced neuropeptide Y synthesis during intermittent hypoxia in the rat adrenal medulla: role of reactive oxygen species-dependent alterations in precursor peptide processing.

Intermittent hypoxia (IH) associated with recurrent apneas often leads to cardiovascular abnormalities. Previously, we showed that IH treatment elevates blood pressure and increases plasma catecholamines (CAs) in rats via reactive oxygen species (ROS)-dependent enhanced synthesis and secretion from the adrenal medulla (AM). Neuropeptide Y (NPY), a sympathetic neurotransmitter that colocalizes with CA in the AM, has been implicated in blood pressure regulation during persistent stress.

H2S mediates O2 sensing in the carotid body.

Gaseousmessengers, nitric oxide and carbon monoxide, have been implicated in O2 sensing by the carotid body, a sensory organ that monitors arterial blood O2 levels and stimulates breathing in response to hypoxia. We now show that hydrogen sulfide (H2S) is a physiologic gasotransmitter of the carotid body, enhancing its sensory response to hypoxia. Glomus cells, the site of O2 sensing in the carotid body, express cystathionine gamma-lyase (CSE), an H2S-generating enzyme, with hypoxia increasing H2S generation in a stimulus-dependent manner.

Attachment of polymer films to solid surfaces via thermal activation of self-assembled monolayers containing sulphonyl azide group.

We report on a simple and effective way to attach thin polymer films to solid surfaces. The system is based on a thermosensitive sulphonyl azide derivative that is immobilized to SiO(2) surfaces via chlorosilane anchoring group and subsequently covered with a polymer film. Upon heating the sulfonyl azide decomposes, leading to a C-H insertion reaction from the adjacent polymer chain resulting in a covalent attachment of the polymer to the surface.

A randomised controlled trial comparing Mediwrap heat retention and forced air warming for maintaining normothermia in thoracic surgery.

Hypothermia is one of the common complications in the perioperative period. Currently, normothermia is maintained with forced air warming (FAW) or passive heat retention methods. We compared the efficacy of the Mediwrap blanket with FAW in maintaining normothermia during intra-operative period in thoracic surgery in a prospective randomised controlled trial on 30 patients.

Pattern-specific sustained activation of tyrosine hydroxylase by intermittent hypoxia: role of reactive oxygen species-dependent downregulation of protein phosphatase 2A and upregulation of protein kinases.

We investigated the role of protein phosphatases (PP) and protein kinases in tyrosine hydroxylase (TH) activation by two patterns of intermittent hypoxia (IH) in rat brainstem. Rats exposed to either IH(15s) (15 s, 5% O(2); 5 min, 21%O(2)) or IH(90s) (90 s each of 10% O(2) & 21%O(2)) for 10 days were used. IH(15s) but not IH(90s) caused a robust increase in TH activity, dopamine (DA) level, and TH phosphorylation at Ser-31 and Ser-40 in the medulla but not in the pons.

Intermittent hypoxia activates peptidylglycine alpha-amidating monooxygenase in rat brain stem via reactive oxygen species-mediated proteolytic processing.

Intermittent hypoxia (IH) associated with sleep apneas leads to cardiorespiratory abnormalities that may involve altered neuropeptide signaling. The effects of IH on neuropeptide synthesis have not been investigated. Peptidylglycine alpha-amidating monooxygenase (PAM; EC 1.