Τρίτη 10 Νοεμβρίου 2020

Laparoscopic Gastric Bypass Reversal with Concomitant Sleeve Gastrectomy (SG) for Refractory Hypoglycemia: an Unusual Procedure

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Abstract

Introduction

Post-bariatric surgery hypoglycemia is usually seen in patients with a history of gastric bypass surgery [1], and few experience severe symptoms [2]. The pathophysiology of post-gastric bypass surgery hypoglycemia is not well understood, and many theories have been proposed: excessive GLP-1, nesidioblastosis, and increased glucose effectiveness [3]. Thus, the etiology of this condition is complex. Laparoscopic GBP reversal is a very unusual procedure and indications may include excessive weight loss, unexplained GI tract symptoms, and severe hypoglycemia. Hypoglycemia should be managed non-surgically at first, but in case of medical therapy failure, surgical options may be considered. Surgical options include gastrostomy tube placement, gastric bypass reversal [4], or gastric bypass reversal with concomitant sleeve gastrectomy [57]. A partial reversal was also mentioned in the lite rature [6]. Laparoscopic conversion to a sleeve gastrectomy for hypoglycemia is unusual and converting an open gastric bypass to a laparoscopic sleeve gastrectomy is exceptional, even never reported. In this video (run time 6 min and 48 s), we present our procedure, which was performed by adopting a new technique.

Patient and Methods

A 52-year-old lady was referred to us for hypoglycemia following an open gastric bypass revision that was done in 2012. Her past surgical history includes 2 laparoscopic gastric band surgeries with subsequent removal of the bands, open bypass surgery in 2007 and open bypass surgery revision in 2012. History goes back to 12 months ago when the patient started complaining of fatigue, lassitude, and symptoms consistent with Whipple's triad. OGTT (oral glucose tolerance test) showed low glucose levels at 2 h (2.7 mmol/l) and at 3 h (3.3 mmol/l). Serum insulin level and C-peptide were normal. The patient was diagnosed as having early dumping syndrome (reactive hypoglycemia). She was started on sitagliptin 1 tab once daily with dietary changes. Despite this management, she was hospitalized several times for worsening of her symptoms. When referred to our department, the patient asked about the possibility of a laparoscopic intervention, sin ce she has suffered a lot from her previous laparotomy incisions. The laparoscopic surgery intervention was discussed with the patient and it was a challenging option in this case. The patient was placed in the lithotomy position with the surgeon standing between the patient's legs. An 11-mm trocar was inserted above the umbilicus. Under vision, 4 other trocars were inserted: a 12-mm trocar in the right midclavicular line and three 5-mm trocars in the epigastrium, left anterior axillary line, and left midclavicular line, respectively. We started with adhesiolysis in order to identify the gastro-jejunostomy and to free the abdominal esophagus. A subtle hiatal hernia was also reduced. Then, the jejuno-jejunostomy was identified, and the alimentary limb was measured. The latter was 70 cm in length, and the decision was to resect it, keeping the jejuno-jejunal anastomosis in place. The gastric pouch was divided just above the gastro-jejunal anastomosis. The alimentary limb was th en exteriorized. Then, the gastric remnant was freed from its omental attachment. The gastric remnant and the gastric pouch were calibrated with a 40-Fr Faucher tube, and appropriate sequential firing was done using endo-GIA. A gastro-gastrostomy was fashioned by the end of the sleeve division to create the gastric tube.

Results

The operative time was 245 min, with minor blood loss (less than 250 cc). The perioperative course was uneventful, with no intra-operative or post-operative morbidity. An upper GI series was done on post-operative day 2 and showed no evidence of leak. It has been 11 months since the procedure and the patient has become normoglycemic. Her last FBS was 4.4 mmol and she is currently free of symptoms.

Discussion and Conclusion

Post-bariatric surgery hypoglycemia is a challenging condition, for both surgeons and endocrinologists. Our patient has suffered severe symptoms that were refractory to medical treatment and dietary modifications. Few papers have discussed LGBP conversion to a sleeve gastrectomy for hypoglycemia, but results from small series are showing promising results. Our case was challenging because of the patient's previous multiple open surgeries and the technique we have adopted is unique, since we have fashioned the sleeve by firing 2 separate gastric pouches (gastric pouch and gastric remnant) to create a gastric tube and by performing a gastro-gastrostomy with intra-corporeal sutures.

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Vaccines, Vol. 8, Pages 670: Intratumoral Combinatorial Administration of CD1c (BDCA-1)+ Myeloid Dendritic Cells Plus Ipilimumab and Avelumab in Combination with Intravenous Low-Dose Nivolumab in Patients with Advanced Solid Tumors: A Phase IB Clinical Trial

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Via Vaccines

Vaccines, Vol. 8, Pages 670: Intratumoral Combinatorial Administration of CD1c (BDCA-1)+ Myeloid Dendritic Cells Plus Ipilimumab and Avelumab in Combination with Intravenous Low-Dose Nivolumab in Patients with Advanced Solid Tumors: A Phase IB Clinical Trial

Vaccines doi: 10.3390/vaccines8040670

Authors: Julia Katharina Schwarze Gil Awada Louise Cras Jens Tijtgat Ramses Forsyth Inès Dufait Sandra Tuyaerts Ivan Van Riet Bart Neyns

Intratumoral (IT) myeloid dendritic cells (myDCs) play a pivotal role in re-licensing antitumor cytotoxic T lymphocytes. IT injection of the IgG1 monoclonal antibodies ipilimumab and avelumab may induce antibody-dependent cellular cytotoxicity, thereby enhancing the release of tumor antigens that can be captured and processed by CD1c (BDCA-1)+ myDCs. Patients with advanced solid tumors after standard care were eligible for IT injections of ≥1 lesion with ipilimumab (10 mg) and avelumab (40 mg) and intravenous (IV) nivolumab (10 mg) on day 1, followed by IT injection of autologous CD1c (BDCA-1)+ myDCs on day 2. IT/IV administration of ipilimumab, avelumab, and nivolumab was repeated bi-weekly. Primary objectives were safety and feasibility. Nine patients were treated with a median of 21 × 106 CD1c (BDCA-1)+ myDCs, and a median of 4 IT/IV administrations of ipilimumab, avelumab, and nivolumab. The treatment was safe with mainly injection-site reactions, but also im mune-related pneumonitis (n = 2), colitis (n = 1), and bullous pemphigoid (n = 1). The best response was a durable partial response in a patient with stage IV melanoma who previously progressed on checkpoint inhibitors. Our combinatorial therapeutic approach, including IT injection of CD1c (BDCA-1)+ myDCs, is feasible and safe, and it resulted in encouraging signs of antitumor activity in patients with advanced solid tumors.

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Tau accumulation in astrocytes of the dentate gyrus induces neuronal dysfunction and memory deficits in Alzheimer’s disease

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Nature Neuroscience, Published online: 09 November 2020; doi:10.1038/s41593-020-00728-x

Alzheimer's disease is often considered a disease of neurons. This study reveals that astrocytes are also impaired by the disease and that these cells contribute more to memory deterioration than previously thought.
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A cerebello-olivary signal for negative prediction error is sufficient to cause extinction of associative motor learning

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Nature Neuroscience, Published online: 09 November 2020; doi:10.1038/s41593-020-00732-1

Learning to suppress maladaptive behaviors is critical for good mental health. Kim et al. show that mice can be taught to suppress previously acquired motor responses by selective and properly timed stimulation of the cerebello-olivary pathway.
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Prefrontal–amygdala circuits in social decision-making

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Nature Neuroscience, Published online: 09 November 2020; doi:10.1038/s41593-020-00738-9

Gangopadhyay, Chawla et al. examine the neural bases of social decision-making at different processing stages and across humans, non-human primates and rodents. These examinations underscore the importance of the medial prefrontal–amygdala pathways.
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Analysis of the Human Plasma Proteome Using Multi‐Nanoparticle Protein Corona for Detection of Alzheimer's Disease

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Analysis of the Human Plasma Proteome Using Multi‐Nanoparticle Protein Corona for Detection of Alzheimer's Disease

Protein coronas are formed on six varying nanoparticles in plasma of 11 Alzheimer's disease (AD), 16 healthy but later AD‐diagnosed, and 13 healthy patients. Random forest model detects prevalent AD with 99.96% sensitivity and 93.7% specificity, and incident AD with 97.6% sensitivity and 95.5% specificity. AD "importance scores" are also generated for more than 400 proteins from the protein corona.


Abstract

As the population affected by Alzheimer's disease (AD) grows, so does the need for a noninvasive and accurate diagnostic tool. Current research reveals that AD pathogenesis begins as early as decades before clinical symptoms. The unique properties of nanoparticles (NPs) may be exploited to develop noninvasive diagnostics for early detection of AD. After exposure of NPs to biological fluids, the NP surface is altered by an unbiased but selective and reproducible adsorption of biomolecules commonly referred to as the biomolecular corona or protein corona (PC). The discovery that the plasma proteome may be differentially altered during health and disease leads to the concept of disease‐specific PCs. Herein, the disease‐specific PCs formed around NPs in a multi‐NPs platform are employed to successfully identify subtle changes in plasma protein patterns and detect AD (>92% specificity and ≈100% sensitivity). Similar discrimination power is achieved using banked plasma sample s from a cohort of patients several years prior to their diagnosis with AD. With the nanoplatform's analytic ability to analyze pathological proteomic changes into a disease‐specific identifier, this promising, noninvasive technology with implications for early detection and intervention could benefit not only patients with AD but other diseases as well.

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Engineering Silk Fibroin‐Based Nerve Conduit with Neurotrophic Factors for Proximal Protection after Peripheral Nerve Injury

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Engineering Silk Fibroin‐Based Nerve Conduit with Neurotrophic Factors for Proximal Protection after Peripheral Nerve Injury

The incorporation and delivery of neurotrophic factors that stimulate nerve repair in previously developed tunable enzymatically crosslinked silk fibroin‐based conduits are presented. Glial cell line‐derived neurotrophic factor (GDNF), acting upon motor and sensory neurons, also instigating angiogenesis, uses these conduits as a platform for its controlled delivery, enhancing motor and sensory regeneration both in vivo and in vitro.


Abstract

Artificial nerve conduits capable of adequately releasing neurotrophic factors are extensively studied to bridge nerve defects. However, the lack of neurotrophic factors in the proximal area and their visible effects in axonal retrograde transport following nerve injury is one of the factors causing an incomplete nerve regeneration. Herein, an advanced conduit made of silk fibroin is produced, which can incorporate growth factors and promote an effective regeneration after injury. For that, enzymatically crosslinked silk fibroin‐based conduits are developed to be used as a platform for the controlled delivery of neurotrophic factors. Nerve growth factor and glial‐cell line derived neurotrophic factor (GDNF) are incorporated using two different methodologies: i) crosslinking and ii) absorption method. The release profile is measured by ELISA technique. The bioactivity of the neurotrophic factors is evaluated in vitro by using primary dorsal root ganglia. When implanted in a 10& nbsp;mm sciatic nerve defect in rats, GDNF‐loaded silk fibroin conduits reveal retrograde neuroprotection as compared to autografts and plain silk fibroin conduit. Therefore, the novel design presents a substantial improvement of retrograde trafficking, neurons' protection, and motor nerve reinnervation.

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