Association of Autofluorescence-Based Detection of the Parathyroid Glands During Total Thyroidectomy With Postoperative Hypocalcemia Risk: Results of the PARAFLUO Multicenter Randomized Clinical Trial.

Importance: Because inadvertent damage of parathyroid glands can lead to postoperative hypocalcemia, their identification and preservation, which can be challenging, are pivotal during total thyroidectomy.

Objective: To determine if intraoperative imaging systems using near-infrared autofluorescence (NIRAF) light to identify parathyroid glands could improve parathyroid preservation and reduce postoperative hypocalcemia.

Design, Setting, And Participants: This randomized clinical trial was conducted from September 2016 to October 2018, with a 6-month follow-up at 3 referral hospitals in France.

Systematic Endoscopy 5 Years After Sleeve Gastrectomy Results in a High Rate of Barrett's Esophagus: Results of a Multicenter Study.

Background: Recent evidence has indicated an increased risk of Barrett's esophagus (BE) in the long term after sleeve gastrectomy (SG).

Aim: The aim of the study is to investigate the spectrum of gastroesophageal reflux disease (GERD) symptoms as well as the prevalence of BE, at minimum 5 years after SG in patients who underwent SG in different bariatric centers of two countries: France and Italy.

Patients And Methods: Five high volume outpatient centers dedicated to bariatric surgery that routinely perform upper GI endoscopy before any bariatric procedures were invited to participate in the study.

Reduction of Venous Thromboembolism in Surgical Patients Using a Mandatory Risk-Scoring System: 5-Year Follow-Up of an American College of Surgeons National Surgical Quality Improvement Program.

Background: Sheikh Khalifa Medical City's (SKMC) surgery institute was identified as a high outlier in the incidence of venous thromboembolism (VTE; deep vein thrombosis [DVT] and pulmonary embolism [PE]) based on the semiannual report of the American College of Surgeon's National Surgical Quality Improvement Program (ACS NSQIP) in June 2010.

Aim: To report our rates of VTE at SKMC, the results, and 5-year follow-up after an ACS NSQIP quality improvement program.

Methods: A multidisciplinary VTE task force was established in June 2010.

Screening colonoscopy in the initial workup of bariatric surgery patients: guidelines are needed.

Background: Cancer is one of the most common causes of death among morbidly obese individuals. Obese individuals have a well-documented increased risk of colon cancer. No guidelines are available for the workup of bariatric surgery patients in relation to colon cancer.

Are results of bariatric surgery different in the Middle East? Early experience of an international bariatric surgery program and an ACS NSQIP outcomes comparison.

Background: Bariatric operations performed at the Bariatric and Metabolic Institute Abu Dhabi are submitted randomly from the entire surgery volume at Sheikh Khalifa Medical City to the American College of Surgeons (ACS) NSQIP. Our aim is to report our early experience and compare our bariatric surgery outcomes with ACS NSQIP hospitals of similar size.

Study Design: We queried the ACS NSQIP database for bariatric surgery codes between August 2009 and August 2012 for hospitals with >500 beds.

Tenecteplase in prosthetic mitral valve thrombosis.

In the few reported cases of prosthetic mitral valve thrombosis, where surgical intervention was considered as high risk, fibrinolytic therapy had proved life saving. The authors present clinical, laboratory, and imaging data from such a patient, with prosthetic mitral valve thrombosis and its successful management with tenecteplase. The use of tenecteplase as a viable fibrinolytic agent for the first time was justified, due to the lack of immunogenicity concerns compared to streptokinase.

Central nervous system Toll-like receptor expression in response to Theiler's murine encephalomyelitis virus-induced demyelination disease in resistant and susceptible mouse strains.

Background: In immunopathological diseases, such as multiple sclerosis (MS), genetic and environmental factors that contribute to the initiation and progression of the disease are often discussed. The Theiler murine encephalomyelitis virus-induced demyelination disease (TMEV-IDD) model used to study MS reflects this: genetically susceptible mice infected intra-cerebrally with TMEV develop a chronic demyelination disease. TMEV-IDD can be induced in resistant mouse strains by inducing innate immunity with lipopolysaccharide (LPS).

Irradiation does not compromise or exacerbate the innate immune response in the brains of mice that were transplanted with bone marrow stem cells.

Microglia and invading macrophages play key roles in the brain immune response. The contributions of these two populations of cells in health and diseases have yet to be clearly established. The use of chimeric mice receiving bone marrow-derived stem cell grafts from green fluorescent protein (GFP)-expressing mice has provided an invaluable tool to distinguish between local and blood-derived monocytic populations.

Molecular and cellular immune mediators of neuroprotection.

Our view of the immune privileged status of the brain has dramatically changed during the past two decades. Even though systemic immune stimuli have the ability to activate different populations of neurons, cells of monocytic lineage also have access to the neuronal tissue and populate it as microglia. Although such a phenomenon is limited in intact brains, it is greatly increased during neurodegenerative processes associated with innate immunity and the release of pro-inflammatory molecules by either resident microglia or those derived from the bone marrow stem cells.

Tumor necrosis factor alpha but not interleukin 1 beta mediates neuroprotection in response to acute nitric oxide excitotoxicity.

Neurodegenerative processes in the brain are accompanied by activation of innate immunity, which involves the release of proinflammatory cytokines by microglia and infiltrating macrophages. The beneficial or detrimental roles of these cytokines, including interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha), remain to be clarified. These cytokines have numerous overlapping activities that make it difficult to interpret data generated by mice that have a mutation in the gene encoding either TNF-alpha or IL-1beta.

Cyclooxygenase 2 (COX-2) inhibition increases the inflammatory response in the brain during systemic immune stimuli.

Non-steroidal anti-inflammatory drugs (NSAIDs) and inhibitors of the cyclooxygenase (COX) pathways are currently recommended for the prevention and treatment of several inflammatory diseases, including neurodegenerative disorders. However non-selective blockade of COX was found to have pro-inflammatory properties, because they have the ability to alter the plasma glucocorticoid levels that play a critical role in the control of the innate immune response. The present study investigated the role of non-selective (ketorolac or indomethacin) or specific inhibitors of COX-1 (SC-560) and COX-2 (NS-398) in these effects.

Unraveling the molecular details involved in the intimate link between the immune and neuroendocrine systems.

During systemic infections, the immune system can signal the brain and act on different neuronal circuits via soluble molecules, such as proinflammatory cytokines, that act on the cells forming the blood-brain barrier and the circumventricular organs. These activated cells release prostaglandin of the E(2) type (PGE(2)), which is the endogenous ligand that triggers the pathways involved in the control of autonomic functions necessary to restore homeostasis and provide inhibitory feedback to innate immunity. Among these neurophysiological functions, activation of the circuits that control the plasma release of glucocorticoids is probably the most critical to the survival of the host in the presence of pathogens.

Closure of small bowel stomas on postoperative day 10.

Objective: To find out if early closure of a defunctioning small bowel stoma (day 10) was feasible and safe.

Design: Prospective non-randomised study.

Setting: University hospital, France.

Influence of chronic interleukin-2 infusion and stressors on sickness behaviors and neurochemical change in mice.

Objectives: Major depression is associated with increased circulating interleukin-2 (IL-2) levels, and IL-2 immunotherapy may provoke depressive symptoms, leading to the suggestion that this cytokine may contribute to the evolution of affective disorders. Although depression is a relatively chronic condition, and immunotherapy involves repeated cytokine administration, animal studies have typically assessed the consequences of acute cytokine treatment. The present investigation assessed several behavioral and neurochemical effects of chronic IL-2 infusion.

Innate immune reaction in response to seizures: implications for the neuropathology associated with epilepsy.

In the present study, the expression of pro-inflammatory transcripts was assessed across the brain of mice having undertaken pilocarpine-induced seizures. Pilocarpine-induced marked neurodegeneration and demyelination in multiple regions of the forebrain. The pattern of genes encoding toll-like receptor type 2 (TLR2) and I kappa B alpha (index of NF-kappa B activation) was associated with the neurodegenerating areas, but this was not the case for the mRNA encoding other inflammatory proteins.

Interleukin-1beta system in anorectic catabolic tumor-bearing rats.

Purpose Of Review: The onset of cancer anorexia and the accompanying neurological symptoms and signs involve the general influence of cytokines on the brain. Using methylcholanthrene to induce tumors in Fischer 344 rats, we measured various specific components of the cytokine-induced anorectic reaction, including: (1) IL-1beta system components (ligand, signaling receptor, receptor accessory proteins, and receptor antagonist); (2) TNF-alpha; (3) TGF-beta1; and (4) IFN-gamma in the tumor tissue, the liver and the brain.

Recent Findings: The data show that IL-1beta, TNF-alpha and IFN-gamma messenger RNA were detected in the tumor tissue of anorectic tumor-bearing rats.

Neurochemical sensitization associated with systemic administration of tumor necrosis factor-alpha: adjuvant action in combination with bovine serum albumin.

Tumor necrosis factor-alpha (TNF-alpha) provokes a time-dependent sensitization of brain monoamine activity, plasma corticosterone activity and sickness behavior, the latter being reminiscent of septic or anaphylactic shock. In this investigation, bovine serum albumin (BSA) elicited similar corticosterone and sickness profiles, whereas the monoamine changes were not observed. The sensitization elicited by mTNF-alpha plus BSA was markedly greater than that elicited by BSA alone.

[Early closure of temporary stoma of the small bowel].

Aim: Transient small bowel stoma is usually closed 9-12 weeks after initial operation (late closure). Since these stoma have a poor physiological and psychological impact with frequent social consequences, we wanted to estimate feasibility and results of early closure of small bowel stoma.

Patients And Method: From January 1998 to December 2001, 39 patients (21 women and 18 men, mean age: 64 years) with a transient small bowel stoma were elected for early closure.

Cytokines as a stressor: implications for depressive illness.

Stressful events have been implicated in the provocation of depressive illness. Inasmuch as immunological challenge, and particularly cytokine administration, engender neuroendocrine and central neurochemical changes reminiscent of those provoked by psychogenic stressors, it was suggested that immune activation may also contribute to affective illness. The present report provides a brief overview of the neurochemical sequelae of acute and repeated interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and IL-2 treatment, describes some of the synergisms associated with these treatments, as well as their potential interactions with psychogenic stressors.

Pro-inflammatory and anti-inflammatory cytokine mRNA induction in the periphery and brain following intraperitoneal administration of bacterial lipopolysaccharide.

Gram-negative bacteria-derived lipopolysaccharide (LPS or endotoxin) is known to play an important role in immune and neurological manifestations during bacterial infections. LPS exerts its effects through cytokines, and peripheral or brain administration of LPS activates cytokine production in the brain. In this study, we investigated cytokine and neuropeptide mRNA profiles in specific brain regions and peripheral organs, as well as serum tumor necrosis factor (TNF)-alpha protein levels, in response to the intraperitoneal administration of LPS.

Neither acute nor chronic exposure to a naturalistic (predator) stressor influences the interleukin-1beta system, tumor necrosis factor-alpha, transforming growth factor-beta1, and neuropeptide mRNAs in specific brain regions.

Physical (neurogenic) stressors may influence immune functioning and interleukin-1beta (IL-1beta) mRNA levels within several brain regions. The present study assessed the effects of an acute or repeated naturalistic, psychogenic stressor (predator exposure) on brain cytokine and neuropeptide mRNAs. Acute predator (ferret) exposure induced stress-like behavioral effects, including elicitation of a startle response and reduced exploratory behaviors; these responses diminished after 30 sessions.

Kindling modulates the IL-1beta system, TNF-alpha, TGF-beta1, and neuropeptide mRNAs in specific brain regions.

Cytokines and neuropeptides may be involved in seizure-associated processes. Following amygdala kindling in rats, we determined alterations of IL-1beta, IL-1 receptor antagonist (IL-1Ra), IL-1 receptor type I (IL-1RI), IL-1 receptor accessory proteins (IL-1R AcPs) I and II, TNF-alpha, TGF-beta1, neuropeptide Y (NPY), glycoprotein 130 (gp 130) and pro-opiomelanocortin (POMC) mRNA levels in the parietal, prefrontal and piriform cortices, amygdala, hippocampus and hypothalamus. Messenger RNAs expression in all brain regions was determined 2 h or 3 weeks following the last generalized convulsive seizure triggered from the ipsilateral kindled amygdala.

Cytokine-cytokine interactions and the brain.

Cytokine-cytokine interactions play a role in health and are crucial during immunological and inflammatory responses in disease. Cytokine interactions can result in additive, antagonist, or synergistic activities in maintaining physiological functions such as feeding, body temperature, and sleep, as well as in anorectic, pyrogenic, and somnogenic neurological manifestations of acute and chronic disease. These interactions involve signaling homology, convergence of signaling pathways, and/or positive or negative feedbacks within and among cytokine systems.

Cytokine interactions and cytokine balance in the brain: relevance to neurology and psychiatry.

Cytokine-cytokine and cytokine-neurotransmitter-neuropeptide interactions are pivotal for the magnitude of neurological and psychiatric manifestations, neuroimmunological and neuroinflammatory responses, and neurological complications of disorders associated with increased cytokine production.