Unsupervised graph learning techniques have garnered increasing interest among researchers. These methods employ the technique of maximizing mutual information to generate representations of nodes and graphs. We show that these methods are susceptible to backdoor attacks, wherein the adversary can poison a small portion of unlabeled graph data (e.g., node features and graph structure) by introducing triggers into the graph. This tampering disrupts the representations and increases the risk to various downstream applications. Previous backdoor attacks in supervised learning primarily operate directly on the label space and may not be suitable for unlabeled graph data. To tackle this challenge, we introduce GRBA,1 a gradient-based first-order backdoor attack method. To the best of our knowledge, this constitutes a pioneering endeavor in investigating backdoor attacks within the domain of unsupervised graph learning. The initiation of this method does not necessitate prior knowledge of downstream tasks, as it directly focuses on representations. Furthermore, it is versatile and can be applied to various downstream tasks, including node classification, node clustering and graph classification. We evaluate GRBA on state-of-the-art unsupervised learning models, and the experimental results substantiate the effectiveness and evasiveness of GRBA in both node-level and graph-level tasks.

Paroxysmal movement disorders include two groups of intermittent neurologic disorders: paroxysmal dyskinesia, in which episodes of involuntary hyperkinetic movements (mainly chorea and/or dystonia) occur with preserved consciousness, and episodic ataxias, which are characterized by discrete attacks of cerebellar dysfunction, sometimes associated with progressive ataxia. Since episodic ataxias are individually discussed in Chapter 8 of this volume, we herein provide a deep overview of phenotypic, genetic, pathophysiologic, diagnostic, and treatment aspects of paroxysmal dyskinesia, following the trigger-based nomenclature which distinguishes paroxysmal kinesigenic dyskinesia, paroxysmal nonkinesigenic dyskinesia, and paroxysmal exercise-induced dyskinesia. Emerging paroxysmal dyskinesia not fulfilling the criteria for the above-mentioned subtypes will also be discussed. Phenotypic and genotypic overlap among paroxysmal movement disorders, epilepsy, and migraine have progressively emerged, thus shedding light on a shared pathophysiologic framework. Advances in our understanding of the pathomechanisms underlying paroxysmal movement disorders, which involve dysfunctions of ion channels, proteins associated with the vesical synaptic cycle machinery, and proteins involved in neuronal energy metabolism, point toward a discrete number of converging pathophysiologic pathways and may lay foundations for developing target-specific therapies.

Zoonotic infections can result in life-threatening complications that can manifest with hemophagocytic lymphohistiocytosis (HLH)/cytokine storm syndrome (CSS). Bacteria constitute the largest group of zoonotic infection-related HLH cases. The growing list of zoonotic bacterial infections associated with HLH/CSS include Brucella spp., Rickettsia spp., Ehrlichia, Coxiella burnetii, Mycobacterium spp., and Bartonella spp. Patients most commonly present with fever, cytopenias, hepatosplenomegaly, myalgias, and less frequently with rash, jaundice, and lymphadenopathy.

OBJECTIVE: Peripherally induced movement disorders (PIMD) are hyperkinetic movement disorders that can occur after injury to a part of the body. This study aimed to identify PIMD in the stomatognathic system following dental or oral surgical procedures.
METHODS: A total of 229 patients with PIMD (144 women and 85 men; mean age: 53.4 years) triggered by oral surgical or dental interventions were evaluated retrospectively.
RESULTS: The average latency between the procedures and onset of PIMD was 14.3 days. Oral surgery (40.2%), including tooth extraction, trauma treatment, and other surgical procedures, was the most frequent trigger of PIMD. This was followed by general dental treatment, including periodontal, endodontic, and restorative procedures (36.7%), prosthetic treatment (19.7%), and orthodontic treatment (3.5%). PIMD consisted of oromandibular dystonia (73.8%), functional (psychogenic) movement disorders (11.4%), orolingual dyskinesia (7.9%), and hemimasticatory spasms (5.7%).
CONCLUSIONS: These results suggest that even minor alterations in normal anatomy or physiology after dental procedures may result in PIMD in predisposing patients.
CONCLUSIONS: Dental professionals should be aware that although infrequently, PIMD can develop after various dental treatments. If such symptoms precipitate, the attending physician should properly explain them to the patient and provide appropriate treatment or consultation with a movement disorder specialist.

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Two studies were conducted to explore the influence of bystander features of displaced aggression in provocative situations among male juvenile delinquents. Study 1 examined the differences in displaced aggression between provoked male juvenile delinquents in the presence or absence of bystanders. The results revealed that provoked male juvenile delinquents exhibited significantly higher levels of displaced aggression when bystanders were present compared to when they were not. Study 2 further manipulated the bystanders\' trigger level and investigated the differences in displaced aggression exhibited by provoked male juvenile delinquents towards highly versus lowly triggered bystanders. The results indicated that after low provocation, male juvenile delinquents exhibited significantly higher levels of displaced aggression towards highly triggered bystanders compared to lowly triggered bystanders. These findings demonstrated that male juvenile delinquents exhibited a high level of displaced aggression towards bystanders in provocative situations, particularly with highly triggered bystanders. This study supported the personality and social model of displaced aggression, emphasizing that bystanders, especially those with high triggers, were more likely to become targets of displaced aggression. The current study provides references for subsequent criminal rehabilitation and crime prevention.

BACKGROUND: Transcranial magnetic stimulation (TMS), when applied over the primary motor cortex, elicits a motor-evoked potential (MEP) in electromyograms measured from peripheral muscles. MEP amplitude has often been observed to fluctuate trial to trial, even with a constant stimulus. Many factors cause MEP fluctuations in TMS. One of the primary factors is the weak stationarity and instability of cortical activity in the brain, from which we assumed MEP fluctuations originate. We hypothesized that MEP fluctuations are suppressed when TMS is delivered to the primary motor cortex at a time when several electroencephalogram (EEG) channels measured on the scalp are highly similar in the frequency domain.
OBJECTIVE: We developed a TMS triggering system to suppress MEP fluctuations using EEG coherence analysis, which was performed to detect the EEG signal similarity between the 2 channels in the frequency domain.
METHODS: Seven healthy adults participated in the experiment to confirm whether the TMS trigger system works adequately, and the mean amplitude and coefficient of the MEP variation were recorded and compared with the values obtained during the control task. We also determined the experimental time under each condition and verified whether it was within the predicted time.
RESULTS: The coefficient of variation of MEP amplitude decreased in 5 of the 7 participants, and significant differences (P=.02) were confirmed in 2 of the participants according to an F test. The coefficient of variation of the experimental time required for each stimulus after threshold modification was less than that without threshold modification, and a significant difference (P<.001) was confirmed by performing an F test.
CONCLUSIONS: We found that MEP could be suppressed using the system developed in this study and that the TMS trigger system could also stabilize the experimental time by changing the triggering threshold automatically.

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It has not been fully elucidated which patients with persistent atrial fibrillation (PerAF) should undergo substrate ablation plus pulmonary vein isolation (PVI). This study aimed to identify PerAF patients who required substrate ablation using intraprocedural assessment of the baseline rhythm and the origin of atrial fibrillation (AF) triggers.
This was a post hoc subanalysis using extended data of the EARNEST-PVI trial, a prospective multicenter randomized trial comparing PVI-alone and PVI-plus (i.e., PVI with added catheter ablation) arms. We divided 492 patients into 4 groups according to baseline rhythm and the location of AF triggers before PVI: Group A (n=22), sinus rhythm with pulmonary vein (PV)-specific AF triggers (defined as reproducible AF initiation from PVs only); Group B (n=211), AF with PV-specific AF triggers; Group C (n=94), sinus rhythm with no PV-specific AF trigger; Group D (n=165), AF with no PV-specific AF trigger. Among the 4 groups, only in Group D (AF at baseline and no PV-specific AF triggers) was arrhythmia-free survival significantly lower in the PVI-alone than PVI-plus arm (P=0.032; hazard ratio 1.68; 95% confidence interval 1.04-2.70).
Patients with sinus rhythm or PV-specific AF triggers did not receive any benefit from substrate ablation, whereas patients with AF and no PV-specific AF trigger benefited from substrate ablation.

Graves\' disease (GD) is the most common cause of hyperthyroidism while Hashimoto or autoimmune thyroiditis is the most common cause of hypothyroidism. Spontaneous hypothyroidism may develop after successful medical treatment of GD in up to 20% of cases. This report presents a gentleman who is a known smoker and was diagnosed with GD at the age of 64 years. He was counseled about smoking cessation and started with medical treatment using carbimazole (CBZ). He was adequately controlled using medical treatment, yet he continued to smoke. After 2 years of medical treatment, CBZ was stopped due to developing hypothyroidism on the minimum dose of treatment. Celebrating the discontinuation of treatment, the patient decided to quit smoking. One month later, he was euthyroid; however, 4 months later, he developed overt hypothyroidism. He received levothyroxine replacement therapy and titrated to achieve euthyroidism and remained on levothyroxine for more than 5 years. The possibility that quitting smoking may have triggered the development of hypothyroidism was raised due to the coincidence of developing hypothyroidism only 4 months after quitting smoking. Current smoking is associated with a higher risk of developing both GD and Graves\' orbitopathy. Quitting smoking is associated with a higher risk of developing new-onset thyroid autoimmunity. Quitting smoking is also associated with a sevenfold higher risk of autoimmune hypothyroidism especially in the first year of smoking cessation. Involved mechanisms may include a sudden increase in oxidative stress, a sudden increase in iodide delivery to thyroid follicles, or promoting T-helper 1-mediated autoimmune thyroiditis after quitting smoking. The present case suggests that quitting smoking may be a triggering factor for the development of hypothyroidism following successful medical treatment of GD, a phenomenon that may affect one-fifth of GD patients without previously reported triggers.
Quitting smoking may trigger hypothyroidism in previously treated Graves’ disease patients Graves’ disease is the commonest cause of hyperthyroidism. Medical treatment is the mainstay treatment, and about 5-20% of patients may develop hypothyroidism after successful medical treatment. The triggers to this conversion are not known. The present case, a 64 years old gentleman who is a smoker, after being diagnosed with graves’ disease, receives medical treatment for 2 years. On the occasion of stopping medical treatment for graves’ disease, he decides to quit smoking. One month later he is euthyroid off medications, but 4 months later, he develops severe hypothyroidism, for which he receives replacement therapy for the following five years. The possibility that quitting smoking may have triggered this conversion was raised. Smoking is associated with a 2-folds higher risk of having graves’ disease. Quitting smoking on the other hand increases the risk of acquiring thyroid autoantibodies, and new onset autoimmune hypothyroidism. Quitting smoking is also associated with symptoms of weight gain, constipation, and depression, all of which may also occur in hypothyroidism. That is why, ordering thyroid function tests is recommended in recent quitters if they develop such symptoms. Thus, quitting smoking in the present case may have triggered this severe hypothyroidism. Underlying mechanisms may involve increased oxidative stress or autoimmune reactions favoring the occurrence of autoimmune thyroiditis.