An artificial neural network for nasogastric tube position decision support

Purpose: To develop and validate a deep learning model for detection of nasogastric tube (NGT) malposition on chest radiographs and assess model impact as a clinical decision support tool for junior physicians to help determine whether feeding can be safely performed in patients (feed/do not feed). Materials and Methods: A neural network ensemble was pretrained on 1 132 142 retrospectively collected (June 2007–August 2019) frontal chest radiographs and further fine-tuned on 7081 chest radiographs labeled by three radiologists. Clinical relevance was assessed on an independent set of 335 images. Five junior emergency medicine physicians assessed chest radiographs and made feed/do not feed decisions without and with artificial intelligence (AI)-generated NGT malposition probabilities placed above chest radiographs. Decisions from the radiologists served as ground truths. Model performance was evaluated using receiver operating characteristic analysis. Agreement between junior physician and radiologist decision was determined using the Cohen κ coefficient. Results: In the testing set, the ensemble achieved area under the receiver operating characteristic curve values of 0.82 (95% CI: 0.78, 0.86), 0.77 (95% CI: 0.71, 0.83), and 0.98 (95% CI: 0.96, 1.00) for satisfactory, malpositioned, and bronchial positions, respectively. In the clinical evaluation set, mean interreader agreement for feed/do not feed decisions among junior physicians was 0.65 ± 0.03 (SD) and 0.77 ± 0.13 without and with AI support, respectively. Mean agreement between junior physicians and radiologists was 0.53 ± 0.05 (unaided) and 0.65 ± 0.09 (AI-aided). Conclusion: A simple classifier for NGT malposition may help junior physicians determine the safety of feeding in patients with NGTs

State-Dependent and -Independent Effects of Dialyzing Excitatory Neuromodulator Receptor Antagonists into the Ventral Respiratory Column

Unilateral dialysis of the broad-spectrum muscarinic receptor antagonist atropine (50 mM) into the ventral respiratory column [(VRC) including the pre-Bötzinger complex region] of awake goats increased pulmonary ventilation (V̇i) and breathing frequency (f), conceivably due to local compensatory increases in serotonin (5-HT) and substance P (SP) measured in effluent mock cerebral spinal fluid (mCSF). In contrast, unilateral dialysis of a triple cocktail of antagonists to muscarinic (atropine; 5 mM), neurokinin-1, and 5-HT receptors does not alter V̇i or f, but increases local SP. Herein, we tested hypotheses that 1) local compensatory 5-HT and SP responses to 50 mM atropine dialyzed into the VRC of goats will not differ between anesthetized and awake states; and 2) bilateral dialysis of the triple cocktail of antagonists into the VRC of awake goats will not alter V̇i or f, but will increase local excitatory neuromodulators. Through microtubules implanted into the VRC of goats, probes were inserted to dialyze mCSF alone (time control), 50 mM atropine, or the triple cocktail of antagonists. We found 1) equivalent increases in local 5-HT and SP with 50 mM atropine dialysis during wakefulness compared with isoflurane anesthesia, but V̇i and f only increased while awake; and 2) dialyses of the triple cocktail of antagonists increased V̇i, f, 5-HT, and SP

Wireless networks of injectable microelectronic stimulators based on rectification of volume conducted high frequency currents

Objective. To develop and in vivo demonstrate threadlike wireless implantable neuromuscular microstimulators that are digitally addressable. Approach. These devices perform, through its two electrodes, electronic rectification of innocuous high frequency current bursts delivered by volume conduction via epidermal textile electrodes. By avoiding the need of large components to obtain electrical energy, this approach allows the development of thin devices that can be intramuscularly implanted by minimally invasive procedures such as injection. For compliance with electrical safety standards, this approach requires a minimum distance, in the order of millimeters or a very few centimeters, between the implant electrodes. Additionally, the devices must cause minimal mechanical damage to tissues, avoid dislocation and be adequate for long-term implantation. Considering these requirements, the implants were conceived as tubular and flexible devices with two electrodes at opposite ends and, at the middle section, a hermetic metallic capsule housing the electronics. Main results. The developed implants have a submillimetric diameter (0.97 mm diameter, 35 mm length) and consist of a microcircuit, which contains a single custom-developed integrated circuit, housed within a titanium capsule (0.7 mm diameter, 6.5 mm length), and two platinum–iridium coils that form two electrodes (3 mm length) located at opposite ends of a silicone body. These neuromuscular stimulators are addressable, allowing to establish a network of microstimulators that can be controlled independently. Their operation was demonstrated in an acute study by injecting a few of them in the hind limb of anesthetized rabbits and inducing controlled and independent contractions. Significance. These results show the feasibility of manufacturing threadlike wireless addressable neuromuscular stimulators by using fabrication techniques and materials well established for chronic electronic implants. Although long-term operation still must be demonstrated, the obtained results pave the way to the clinical development of advanced motor neuroprostheses formed by dense networks of such wireless devices.European Research Council (ERC) 724244ICREA under the ICREA Academia programm

Hypothalamic Deep Brain Stimulation Reduces Weight Gain in an Obesity-Animal Model

Prior studies of appetite regulatory networks, primarily in rodents, have established that targeted electrical stimulation of ventromedial hypothalamus (VMH) can alter food intake patterns and metabolic homeostasis. Consideration of this method for weight modulation in humans with severe overeating disorders and morbid obesity can be further advanced by modeling procedures and assessing endpoints that can provide preclinical data on efficacy and safety. In this study we adapted human deep brain stimulation (DBS) stereotactic methods and instrumentation to demonstrate in a large animal model the modulation of weight gain with VMH-DBS. Female Göttingen minipigs were used because of their dietary habits, physiologic characteristics, and brain structures that resemble those of primates. Further, these animals become obese on extra-feeding regimens. DBS electrodes were first bilaterally implanted into the VMH of the animals (n = 8) which were then maintained on a restricted food regimen for 1 mo following the surgery. The daily amount of food was then doubled for the next 2 mo in all animals to produce obesity associated with extra calorie intake, with half of the animals (n = 4) concurrently receiving continuous low frequency (50 Hz) VMH-DBS. Adverse motoric or behavioral effects were not observed subsequent to the surgical procedure or during the DBS period. Throughout this 2 mo DBS period, all animals consumed the doubled amount of daily food. However, the animals that had received VMH-DBS showed a cumulative weight gain (6.1±0.4 kg; mean ± SEM) that was lower than the nonstimulated VMH-DBS animals (9.4±1.3 kg; p<0.05), suggestive of a DBS-associated increase in metabolic rate. These results in a porcine obesity model demonstrate the efficacy and behavioral safety of a low frequency VMH-DBS application as a potential clinical strategy for modulation of body weight

A study of the effects of the neurokinin peptides on respiratory function in sheep

The respiratory responses, including changes in pulmonary resistance (RL) and dynamic compliance (Cdyn), to the neurokinin peptides substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) were assessed in anaesthetised normal Suffolk-cross and conscious Texel-cross asthmatic sheepIn normal sheep (n=l 1) intravenous SP was a more potent bronchoconstrictor than NKA (n=9) and this was similar to findings in sheep with a naturally acquired airway allergy to Ascaris suum antigen (asthmatic) (n=5) where peptides were administered by inhalation. NKB (n=4) was assessed only in normal sheep and caused insignificant changes in bronchomotor tone. Intravenous SP and NKA, in normal anaesthetised sheep, caused a dose-dependent reduction in respiratory rate and this was similar for both peptides.The bronchomotor response to SP in normal sheep demonstrated age-related changes. In sheep under 6 months of age there was a pronounced bronchoconstriction, with a subsequent reduction in the response as animals approach maturity. In old sheep, aged approximately four years, there was minimal bronchomotor response, however, there was dose-dependent apnoea.The bronchomotor response to SP in anaesthetised normal sheep was significantly antagonised after pre-treatment with atropine (lmg/kg; n=6), hexamethonium (20mg/Kg; n=3) and the NK-1 antagonist CP 96,345 (0.1 and 0.5mg/Kg; n=5), but not by the HI receptor antagonist chlorpheniramine (2mg/Kg; n=5) or the neurokinin antagonist spantide (lOug/kg/min; n=3). The anti-asthma drug nedocromil sodium (0.1 and l.Omg/kg; n=4) had a variable effect on the response. In the isolated sheep trachealis muscle preparation the contractile effect of SP was inhibited by atropine (n=4) and the Ml receptor antagonist pirenzepine (n=8), with IC₅₀ values of 5.6xl0⁻⁸ and 5xl0⁻¹⁰ M respectively, while spantide (n=7) and the NK-2 receptor antagonist L-659,874 (n=6) were ineffective.In several normal sheep (n=10) intravenous SP consistently caused augmented breaths. Bilateral vagotomy (n=7) abolished, and cooling of the right cervical vagus (n=7), after section of the left vagus, to temperatures below 7° C significantly attenuated the bronchomotor response to SP in normal sheep.The conclusion of this study is that the order of potency for the bronchomotor effects of the neurokinins is similar to rabbits and pigs but different from that reported for most other species, including man. The mechanism of action of SP is largely indirect, involving activation of vagal reflex mechanisms and/or modulation of ganglionic neurotransmission and acetylcholine release from cholinergic nerve endings

Lateral habenula regulation of emotional hyperthermia: mediation via the medullary raphé

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.The lateral habenula (LHb) has an important role in the behavioural response to salient, usually aversive, events. We previously demonstrated that activation of neurons in the LHb increases brown adipose tissue (BAT) thermogenesis and constricts the cutaneous vascular bed, indicating that the LHb contributes to the central control of sympathetic outflow to thermoregulatory effector organs. We have now investigated whether the LHb mediates BAT thermogenesis elicited by emotional stress, and whether the LHb modulates thermoregulatory sympathetic outflow via the rostral medullary raphé, a key integrative lower brainstem sympathetic control centre. In conscious animals, lesioning the LHb attenuated emotional BAT thermogenesis, suggesting that the LHb is part of the central circuitry mediating emotional hyperthermia. In anesthetized animals, inhibition of neurons in the rostral medullary raphé reversed BAT thermogenesis and cutaneous vasoconstriction elicited by activation of neurons in the LHb, indicating that the LHb-induced autonomic responses are mediated through activation of the rostral medullary raphé neurons. The latency to activate BAT sympathetic discharge from electrical stimulation of the LHb was substantially greater than the corresponding latency after stimulation of the medullary raphé, suggesting that the neuronal pathway connecting those two nuclei is quite indirect