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Objective: Unusual clinical course. Background: Rapidly involuting congenital hemangioma (RICH) of the fetal skull is an extremely rare vascular disease which undergoes proliferation only in utero and progresses with maximal size at birth. RICH can be detected by prenatal imaging but is easily misdiagnose. Case Report: A 28-year-old nulliparous woman was referred at 38 weeks of gestation for routine screening with obstetric ultrasonography. The ultrasonography revealed a female fetus with a previously undetected head tumor (32×22 mm). Certain unusual sonographic features were observed: the lesion was fusiform, with a wide base adjacent to the frontal bone. Tumor growth appeared to be toward the brain parenchyma rather than outwards (ie, toward the skull), which suggested that the mass may have been derived from the skull. The mass may have remained undiagnosed due to its small size or due to the superimposition of the skull in poor quality ultrasound images. On the basis of ultrasound findings, the lesion was diagnosed as an intracranial tumor, but fetal MRI findings led to the suspicion of RICH of the fetal skull. Finally, the patient was followed up until 1 year after birth, by which time the lesion had completely disappeared. Conclusions: Careful evaluation of prenatal ultrasound is necessary to ensure detection of any mass adjacent to the skull, and the ultrasonography technician should carefully examine the features of any suspected mass to diagnose it correctly to avoid affecting the treatment strategy. [ABSTRACT FROM AUTHOR]

Aconitum species are commonly used in traditional Chinese medicine, and they have a narrow therapy window due to the possibility of aconitine poisoning. Aconitine poisoning deaths appear infrequently in forensic practice. It is important to collect valuable body samples in time due to the rapid absorption and excretion of aconitine. However, it is unknown whether postmortem samples have value for toxicological analysis if the deceased has experienced long-term treatment before death. Herein, we present a case of a woman who died after 12 days of failed active treatment for aconitine poisoning. Aconitine was detected in the liver tissue. To our knowledge, this is the first case report describing the detection of aconitine in a decedent after long-term active treatment. The findings indicated that the aconitine concentration in liver tissue can be maintained after long-term treatment; this information may therefore serve as a reference in forensic practice. [ABSTRACT FROM AUTHOR]

Traumatic axonal injury (TAI) accounts for a large proportion of the mortality of traumatic brain injury (TBI). The diagnosis of TAI is currently of limited use for medicolegal purposes. It is known that axons in TAI are diffusely damaged by secondary processes other than direct head injury. However, the physiopathological mechanism of TAI is still elusive. The present study used RGD peptide, an antagonist of the mechanotransduction protein integrin, to explore the role of integrin-transmitted mechanical signalling in the pathogenesis of rat TAI. The rats were subjected to a linearly accelerating load, and changes in beta-amyloid precursor protein (β-APP) expression, skeleton ultrastructure, skeleton protein neurofilament light (NF-L), and α-tubulin in the brainstem were observed, indicating that RGD could relieve the severity of axonal injury in TAI rats. In addition, the expression of β-integrin was stronger and centralized in the brainstem of the deceased died from TAI compared to other nonviolent causes. This study examined the pathophysiology and biomechanics of TAI and assessed the role of integrin in the injury of microtubules and neurofilaments in TAI. Thus, we propose that integrin-mediated cytoskeletal injury plays an important role in TAI and that integrin has the potential as a biomarker for TAI. [ABSTRACT FROM AUTHOR]

• We report an extremely rare case of sudden death due to acute necrotizing encephalopathy(ANE) caused by influena A infection. • The expression of influenza A virus antigen in the brain by immuno-histochemistry is helpful for diagnosis of ANE due to influenza virus A virus. • The present case emphasizes the neuropathological features of ANE. Influenza occasionally causes central nervous system disorders. Acute necrotizing encephalopathy (ANE) is one of the most severe influenza-associated complications, predominantly affecting infants and young children under 5 years of age. We present this case as it involves a very rare complication of influenza infection that is known to have a high rate of mortality. A 5-year-old girl presented with a high fever and convulsions. Her condition deteriorated rapidly, and she died within 24 h. Autopsy revealed extensive brain edema, multifocal perivascular hemorrhage, and necrosis of neurons without inflammatory cell infiltration in the pons and bilateral thalamus. Tests for influenza virus A and antibodies to it were positive. The girl's death was attributed to ANE associated with influenza A infection based on the clinical presentation, the postmortem neuropathology, and identification of the virus. The goal of this report is to draw attention to the potentially serious complications of influenza A infection. We hope that the lethal outcome of this disease will be fully recognized by medical personnel. [ABSTRACT FROM AUTHOR]