Cat scratch disease with generalized bone lesions in an immunocompetent child.

A 9-year-old immunocompetent girl with prolonged fever for 1 month was suspected of having a malignancy because of generalized bone abnormalities identified by MRI. Histopathology of liver tissues indicated the diagnosis of cat-scratch disease (CSD). Results of NGS, immunofluorescence and immunochemical assay confirmed the causative agent was Bartonella henselae. Paediatricians should increase their awareness of CSD as a cause for bone lesions, except for malignancy.

Evaluation of efficacy and safety of propofol in the treatment of procedural sedation/anesthesia in neonates: A protocol for systematic review and meta-analysis.

BACKGROUND: In newborns, propofol anesthesia is commonly utilized. Propofol is increasingly being shown to be effective and safe in treating procedural sedation and anesthesia in neonates. This research aims to evaluate the efficacy and safety of propofol in neonates using systematic review and meta-analysis methodologies. METHODS: A thorough review and meta-analysis of studies on propofol anesthesia in neonates will be conducted. Conduct comprehensive searches in Web of Science, PubMed, Cochrane Library, EMBASE database, WanFang database, and Chinese biomedical literature database before May 25, 2021, to obtain published and qualified research. Two reviewers will assess the quality of the included papers and extract the data independently. Then, for meta-analysis, we will utilize RevMan 5.3 software. RESULTS: This study will pool the data of separate trials to analyze the efficacy and safety of propofol in the treatment of procedural sedation/anesthesia in neonates. CONCLUSION: Our findings will give strong data for determining whether propofol is an effective treatment for procedural anesthesia in neonates.

Anesthetic management of a patient with an unusual broken tracheostomy tube: a case report.

OBJECTIVE: This study was performed to investigate the management of general anesthesia in an unusual case involving a patient with a broken tracheostomy tube presenting as an airway foreign body. METHODS: We herein describe the anesthetic management of a patient with a broken tracheostomy tube. A 77-year-old Chinese man who had been involved in a car accident underwent a tracheostomy. One year later, he presented with cough and bleeding at the tracheostomy site. Preoperative evaluation revealed that the metal tracheostomy tube was lodged in his left main bronchus. General anesthesia was induced to maintain spontaneous breathing, and adequate topical anesthesia of the airway was administered. RESULTS: The metal tracheostomy tube was successful removed, and a new tracheal tube was put in place. CONCLUSIONS: General anesthesia to maintain spontaneous breathing and adequate topical anesthesia of the airway can be safely used when removing broken tracheostomy tubes.

Ketamine destabilizes growth of dendritic spines in developing hippocampal neurons in vitro via a Rho­dependent mechanism.

The safety of anesthetics on the developing brain has caused concern. Ketamine, an N­methyl­D­aspartate receptor antagonist, is widely used as a general pediatric anesthetic. Recent studies suggested that ketamine alters the plasticity of dendritic spines in the developing brain and may be an important contributing factor to learning and cognitive impairment. However, the underlying molecular mechanism remains poorly understood. Therefore, the aim of the present study was to investigate the effect of ketamine on the plasticity of dendritic spines in cultured hippocampal neurons and the potential underlying mechanisms. After 5 days in vitro, rat hippocampal neurons were exposed to different concentrations (100, 300 and 500 µM) of ketamine for 6 h. Ketamine decreased the number and length of dendritic spines in a dose­dependent manner. Ketamine at a concentration of 300 µM caused an upregulation of transforming protein RhoA (RhoA) and Rho­associated kinase (ROCK) protein. These effects were inhibited by the ROCK inhibitor Y27632. These results suggested that ketamine induces loss and shortening of dendritic spines in hippocampal neurons via activation of the RhoA/ROCK signaling pathway.

Dexmedetomidine mitigates sevoflurane-induced cell cycle arrest in hippocampus.

BACKGROUND: Epidemiologic studies suggest the possibility of a modestly elevated risk of adverse neurodevelopmental outcomes in children exposed to anesthesia during early childhood. Sevoflurane is widely used in pediatric anesthetic practice because of its rapid induction and lower pungency. However, it is reported that sevoflurane leads to the long-term cognitive impairment. Some evidence revealed that the selective α2-adrenoreceptor agonist dexmedetomidine (DEX) exerts neuroprotective effects in various brain injury models of animals. But the role of DEX on sevoflurane-induced neuro-damage remains elusive. MATERIALS AND METHODS: In our study, we isolated the hippocampal neuron cells from newborn neonatal rats and verified the purity of neurons by immunocytochemistry. We employed the flow cytometry and western blot to examine the effect of sevoflurane, DEX and α2-adrenergic receptor antagonist yohimbine on cell cycle distribution. RESULTS: Immunocytochemistry results showed the purity of neurons > 94%, which provided a good model for neural pharmacology experiments. The exposure of sevoflurane-induced cell cycle arrest at S phase and suppressed the expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB). The addition of DEX suppressed sevoflurane-induced cell cycle arrest and the inhibitory of BDNF and TrkB expression. But the function of DEX was partly blocked by a α2 adrenergic receptor blocker yohimbine. CONCLUSION: Sevoflurane suppressed neuron cell proliferation via inhibiting the expression of BDNF and TrkB, and DEX relieved the neurotoxicity induced by sevoflurane via α2 adrenergic receptor. These findings provided new evidence that DEX exerted as a neuroprotective strategy in sevoflurane-induced neuro-damage, and provided new basis for the clinical application of DEX.

Ketamine-induced neurotoxicity blocked by N-Methyl-d-aspartate is mediated through activation of PKC/ERK pathway in developing hippocampal neurons.

Ketamine, a non-competitive N-methyl d-aspartate (NMDA) receptor antagonist, is widely used in pediatric clinical practice. However, prolonged exposure to ketamine results in widespread anesthetic neurotoxicity and long-term neurocognitive deficits. The molecular mechanisms that underlie this important event are poorly understood. We investigated effects of anesthetic ketamine on neuroapoptosis and further explored role of NMDA receptors in ketamine-induced neurotoxicity. Here we demonstrate that ketamine induces activation of cell cycle entry, resulting in cycle-related neuronal apoptosis. On the other hand, ketamine administration alters early and late apoptosis of cultured hippocampus neurons by inhibiting PKC/ERK pathway, whereas excitatory NMDA receptor activation reverses these effects. Ketamine-induced neurotoxicity blocked by NMDA is mediated through activation of PKC/ERK pathway in developing hippocampal neurons.

The protective effect of the Rho-kinase inhibitor hydroxyfasudil on propofol-induced hippocampal neuron apoptosis in neonatal rats.

Propofol is widely applied for anesthesia induction in pediatric patients. However, accumulating evidence has proved that propofol is neurotoxic to the immature or developing brain. In the present study, we found that hydroxyfasudil, a specific inhibitor of Rho kinase, alleviated the apoptotic neurodegeneration induced by propofol in the developing rat brain. A spatial probe test and Morris water maze test revealed that hydroxyfasudil showed a potential improvement of the tendency towards cognitive impairments induced by propofol. Mechanistically, hydroxyfasudil markedly ameliorated the activation of RhoA and the expression of Rock1, Rock2, Bak, Bax, and Bad induced by propofol and rescued the expression of Bcl2 suppressed by propofol. Our findings suggest that hydroxyfasudil may serve as an effective agent to reduce the propofol-induced neurotoxic effects in pediatric medical procedures.

In vitro dose-dependent inhibition of the intracellular spontaneous calcium oscillations in developing hippocampal neurons by ketamine.

Spatial and temporal abnormalities in the frequency and amplitude of the cytosolic calcium oscillations can impact the normal physiological functions of neuronal cells. Recent studies have shown that ketamine can affect the growth and development and even induce the apoptotic death of neurons. This study used isolated developing hippocampal neurons as its study subjects to observe the effect of ketamine on the intracellular calcium oscillations in developing hippocampal neurons and to further explore its underlying mechanism using Fluo-4-loaded laser scanning confocal microscopy. Using a semi-quantitative method to analyze the spontaneous calcium oscillatory activities, a typical type of calcium oscillation was observed in developing hippocampal neurons. In addition, the administration of NMDA (N-Methyl-D-aspartate) at a concentration of 100 µM increased the calcium oscillation amplitude. The administration of MK801 at a concentration of 40 µM inhibited the amplitude and frequency of the calcium oscillations. Our results demonstrated that an increase in the ketamine concentration, starting from 30 µM, gradually decreased the neuronal calcium oscillation amplitude. The inhibition of the calcium oscillation frequency by 300 µM ketamine was statistically significant, and the neuronal calcium oscillations were completely eliminated with the administration of 3,000 µM Ketamine. The administration of 100, 300, and 1,000 µM NMDA to the 1 mM ketamine-pretreated hippocampal neurons restored the frequency and amplitude of the calcium oscillations in a dose-dependent manner. In fact, a concentration of 1,000 µM NMDA completely reversed the decrease in the calcium oscillation frequency and amplitude that was induced by 1 mM ketamine. This study revealed that ketamine can inhibit the frequency and amplitude of the calcium oscillations in developing hippocampal neurons though the NMDAR (NMDA receptor) in a dose-dependent manner, which might highlight a possible underlying mechanism of ketamine toxicity on the rat hippocampal neurons during development.