A 50-year-old woman underwent endoscopic placement of a biliary self-expandable metallic stent (SEMS) and a 22 × 90 mm WallFlex™ duodenal stent (Boston Scientific, Natick, Massachusetts, USA) across an inoperable periampullary adenocarcinoma. Eighteen months later, the patient presented with nonbilious vomiting. A clinical diagnosis of gastric outlet obstruction due to disease progression was made. Endoscopy revealed a normal esophagus, dilated stomach, and narrowing between the first and second parts of the duodenum, but the stent was not clearly visualized. One week later, the patient underwent a water-soluble contrast study for assessment of the gastric outlet obstruction. Preliminary fluoroscopy revealed a radiopaque foreign body in the cervical esophagus, which was presumed to be the displaced fragment of the stent ([ Fig. 1 a ]). Fig. 1 a Preliminary fluoroscopy revealed a fractured stent fragment with partially disrupted mesh in the cervical esophagus (arrow). b Contrast was entrapped in the interstices of the mesh in the empty phase (arrow). There was no mediastinal leak. There was free flow of contrast across the fragment ([ Fig. 1 b ]). Luminal obstruction was apparent at the proximal end of the fractured stent in the second part of the duodenum with abrupt cutoff and prestenotic dilatation of the proximal duodenum and stomach ([ Fig. 2 ]). Fig. 2 The fractured enteral stent (arrows) with duodenal obstruction and prestenotic dilatation. At endoscopy, the stent fragment, with a partially disrupted mesh, was seen just below the cricopharynx ([ Fig. 3 a ]). Fig. 3 a On endoscopy, the fractured fragment was visualized just below the cricopharynx. There was no evidence of deep esophageal injury. b Post-retrieval specimen. It was retrieved by grasping it by its sides with two forceps, using a double-channel endoscope (Fujinon, Tokyo, Japan) ([ Fig. 3 b ]). Migration is a known complication of enteral SEMS with reported rates of up to 5 % [ 1 ]. Distal migration is the norm and proximal migration is an exceptional event. The incidence of SEMS fracture and the exact reasons for this complication are elusive. Acid corrosion, thermal overstrain induced by laser application, and defective material at the time of deployment are some of the proposed explanations [ 2 ] [ 3 ]. However, there was no obvious reason for the cervical esophageal migration of the fractured segment in our patient, and we hypothesize that the reverse peristalsis accompanying the frequent episodes of vomiting was responsible for this unusual presentation. Endoscopic removal of stents that have migrated into the esophagus should be considered after ruling out potential complications with a water-soluble contrast study. Endoscopy_UCTN_Code_CPL_1AH_2AD

Sleep is important for cognitive and physical performance. Sleep deprivation not only affects neural functions but also results in muscular fatigue. A good night’s sleep reverses these functional derangements caused by sleep deprivation. The role of sleep in brain function has been extensively studied. However, its role in neuromuscular junction (NMJ) or skeletal muscle morphology is sparsely addressed although skeletal muscle atonia and suspended thermoregulation during rapid eye movement sleep possibly provide a conducive environment for the muscle to rest and repair; somewhat similar to slow-wave sleep for synaptic downscaling. In the present study, we have investigated the effect of 24 h sleep deprivation on the NMJ morphology and neurochemistry using electron microscopy and immunohistochemistry in the rat soleus muscle. Acute sleep deprivation altered synaptic ultra-structure viz. mitochondria, synaptic vesicle, synaptic proteins, basal lamina, and junctional folds needed for neuromuscular transmission. Further acute sleep deprivation showed the depletion of the neurotransmitter acetylcholine and the overactivity of its degrading enzyme acetylcholine esterase at the NMJ. The impact of sleep deprivation on synaptic homeostasis in the brain has been extensively reported recently. The present evidence from our studies shows new information on the role of sleep on the NMJ homeostasis and its functioning.

Background: Gliosis and dendritic loss is reported to be secondary to the amyloid beta (Aß) and hyperphosphorylated tau (hp‐tau) production in Alzheimer’s disease(AD) brain. STZ administration is reported to induce sporadic AD. Previous clinical or preclinical studies on effect of rTMS treatment in AD patients or APP23 mice showed cognitive improvement alone or as adjuvant therapy along‐with amelioration of the glial aggravation in the hippocampus. However, studies on the effect of magnetic field stimulation on the gliosis related dendritic trimming in animal models of sporadic AD is elusive. Therefore, in the present study we have looked in to the effect of extremely low frequency magnetic field stimulation (ELF‐MF; 17.96µT, 50Hz, 2hr/day) for one month post‐injection of STZ (bilateral, 3mg/kg).Method: Total 45 animals were (ethical no. 937/IAEC/2016) randomly divided into five groups: Control, Sham, AD, Sham+MF and AD+MF. After assessing retention of spatial and avoidance memory using Morris water maze and passive avoidance step down test on 30th day, animals were sacrificed and tissues processed for oxidative stress and immunofluorescence, Golgi‐Cox staining.Result: Behavioural analysis revealed spatial memory improvement with no effect on the avoidance memory loss in AD+MF group as compared to AD group. We also found significant decrease in superoxide dismutase, catalase, GSH and increase in malon‐di‐aldehyde (MDA) in AD group. ELF‐MF treatment only reduced MDA level in hippocampus and frontal cortex. GFAP, IBA‐1 and hp‐tau (ser356) positive cells were found to be reduced in AD+MF group, as compared to all groups except Control. Sholl analysis revealed partial improvement of reduction in the number of intersection, bifurcation and length in basal and apical dendrite in the AD group after ELF‐MF treatment in CA3 layer. Convex hull analysis revealed a contradictory result showing reduction in apical (p = 0.018) and increase in basal dendrite (p = 0.038) of AD group as compared to control.Conclusion: These findings suggests dual role of ELF‐MF exposure on STZ model of AD showing improvement of spatial memory by reducing the gliosis induced dendritic loss but loss in avoidance memory.