A record-high EQE of 7.65%@3300 cd m-2 achieved in non-doped near-ultraviolet OLEDs based on novel D'-D-A type bipolar fluorophores upon molecular configuration engineering.

Developing a high-performance near-ultraviolet (NUV) material and its simple non-doped device with a small efficiency roll-off and good color purity is a promising but challenging task. Here, we proposed a novel donor'-donor-acceptor (D'-D-A) type molecular strategy to largely solve the intrinsic contradictions among wide-bandgap NUV emission, fluorescence efficiency, carrier injection and transport. An efficient NUV fluorophore, 3,6-mPPICNC3, exhibiting a hybridized local and charge-transfer state, is achieved through precise molecular configuration engineering, realizing similar hole and electron mobilities at both low and high electric fields. Moreover, the planarized intramolecular charge transfer excited state and steric hindrance effect endow 3,6-mPPICNC3 with a considerable luminous efficiency and good color purity in the aggregation state. Consequently, the non-doped device emitting stable NUV light with Commission Internationale de l'Eclairage (CIE) coordinates of (0.160, 0.032) and a narrow full width at half maximum of 44 nm exhibits a state-of-the-art external quantum efficiency (EQE) of 7.67% and negligible efficiency roll-off over a luminance range from 0 to 3300 cd m-2. This is a record-high efficiency among all the reported non-doped NUV devices. Amazingly, an EQE of 7.85% and CIE coordinates of (0.161, 0.025) are achieved in the doped device. This demonstrates that the D'-D-A-type molecular structure has great potential for developing high-performance organic light-emitting materials and their optoelectronic applications.

Case Report: Lower Limb Muscle Weakness in a Child With Kawasaki Disease.

Kawasaki disease (KD) is a systemic vasculitis that may impact multiple organ systems in children. Myositis is an unusual presentation of KD that presents with muscle weakness. To date, a few pediatric patients with KD and myositis have been reported. Diffuse muscle weakness involving the 4 limbs was the most common presentation in these children. However, isolated lower limb involvement was rarely reported before. Here, we report lower limb muscle weakness in an 18-month-old child with KD. He presented with fever, rash, conjunctival injection, peeling over fingers and toes, and progressive muscle weakness of the lower limbs. Muscle enzymes were normal, but electromyography indicated myositis. The symptom of fever was relieved quickly by intravenous immunoglobulin and aspirin, which were ineffective for myositis. However, lower limb muscle weakness fully recovered 5 days after prednisolone treatment. This rare case might add value to the growing literature exploring the association of KD with myositis.

Case Report: Fatal Neurotoxicity Following Resmethrin Poisoning in a Child.

Resmethrin, a type I pyrethroid insecticide, can activate sodium channels, causing neurotoxicity in both mammals and insects. Possible routes of poisoning include inhalation, dermal contact and ingestion. There are no specific symptoms for resmethrin poisoning. Until now, no antidote has been available for resmethrin. Resmethrin poisoning is rarely reported in children. Here, we report a fatal case of resmethrin poisoning that might have been caused by accidental ingestion by a 26-month-old child. He presented with neurotoxic symptoms that included vomiting, recurrent seizures, and coma. The cranial CT showed extensive lesions of low intensity in the bilateral white matter, thalamus, brainstem, and cerebellum. Lumbar punctures showed increased intracranial pressure (ICP > 25 mmHg). Cerebrospinal fluid (CSF) tests revealed that protein was elevated to 289.2 mg/dL without pleocytosis. Resmethrin was detected in his blood by liquid chromatography-mass spectrometry, which confirmed the diagnosis of resmethrin poisoning. The child developed brain stem herniation and then was declared brain dead at the 77th h after admission. Resmethrin poisoning can be fatal, and it requires immediate diagnosis and treatment. Previous studies reported that cranial CT and CSF analyses were all normal in patients with pyrethroid poisoning. This case might extend the knowledge of neuroimaging and CSF analysis in children with resmethrin poisoning.

Fulminant encephalopathy in a child with hyperferritinemic sepsis: a case report.

BACKGROUND: Sepsis-associated encephalopathy (SAE) is epidemic in intensive care units and recognized as a fatal complication of sepsis. SAE is characterized by diffuse brain dysfunction and the correct diagnosis of SAE requires ruling out direct central nervous system (CNS) infection or other types of encephalopathy, such as hepatic encephalopathy, pulmonary encephalopathy, and other encephalopathy. CASE PRESENTATION: We reported a rare case of a 5-year-old girl who presented with abdominal pain, vomiting, recurrent seizures, and coma. Brain magnetic resonance imaging (MRI) showed diffuse white matter abnormalities in the brain on day 1. Cerebrospinal fluid (CSF) tests revealed that protein levels and glucose levels were normal without pleocytosis. CSF PCRs for pathogens were all negative. The electroencephalography examination demonstrated diffuse, generalized and slow background activity. The patient showed the symptom of hyperferritinemic sepsis with multiple organ dysfunction syndrome (MODS). SAE was also diagnosed by ruling out other encephalitis or encephalopathy. The patient made marked improvements of clinical symptoms and the lesions on brain imaging disappeared completely within two months after appropriate treatment including antibiotic treatments, methylprednisolone, intravenous immunoglobulin, membrane-based therapeutic plasma exchange (TPE), and continuous renal replacement therapy (CRRT). CONCLUSIONS: SAE can be a fatal complication of sepsis which asks for immediate diagnosis and treatment. Few reports have focus on MRI imaging findings on the early onset of hyperferritinemic sepsis with MODS since these children were too ill to undergo an MRI scan. However, SAE might appear before other systemic features of sepsis are obvious, and MRI could show abnormal lesion in the brain during the early course. Therefore, MRI should be performed early to diagnose this fatal complication which would play important roles in improving the clinical outcomes by early initiation with appropriate treatments.