The progress in the relationship between trace elements and acute lymphoblastic leukemia.

Trace elements are very important substances with low content in the human body. If the content of some trace elements changes, they are also related to diseases. Acute lymphoblastic leukemia (ALL) is a malignant blood tumor, and its relationship with trace elements has also been a concern by scholars. Not only have the trace element levels in ALL patients changed, but the efficacy of different treatment methods has also been linked to the corresponding trace element changes. The characteristics of ALL may be related to the dysregulation of differentiation and proliferation of lymphoid precursor cells. Cell proliferation and differentiation are often affected by changes in DNA levels. However, trace elements are involved in DNA damage and repair mechanisms. In recent years, as an increasing number of studies believe that ALL is related to the abnormal metabolism of trace elements in the body, this paper intends to discuss the research progress on the relationship between trace elements and ALL to provide more information on trace elements for the diagnosis, treatment, and prevention of ALL.

[Fever for 2 months and disturbance of consciousness for 1 week in a preschool-aged girl].

Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation syndrome (ROHHADS) is a rare multi-system disease, and delayed diagnosis and treatment may lead to catastrophic cardiopulmonary complications. As far as we know, no patient with ROHHADS has been reported in China, and this article reports a child with ROHHADS to improve the awareness of this disease among clinicians. A girl, aged 3 years, had the clinical manifestations of rapid weight gain, fever, disturbance of consciousness, and convulsion. The physical examination showed a body weight of 20 kg, somnolence, irregular breathing, and stiff neck. She had increased blood levels of prolactin and follicle-stimulating hormone and hyponatremia. The lumbar puncture showed an increased intracranial pressure. The brain MRI and magnetic resonance venography showed symmetrical lesions in the periventricular region and venous thrombosis in the right transverse sinus and the superior sagittal sinus. The sleep monitoring showed hypopnea. The girl was finally diagnosed with ROHHADS and intracranial venous thrombosis. She recovered after symptomatic treatment including decreasing intracranial pressure, anticoagulation, and respiratory support. The possibility of ROHHADS should be considered for patients with unexplained obesity, fever, and hypoventilation, with or without central nervous system symptoms. Early diagnosis and standardized follow-up can improve the prognosis of children with ROHHADS.

The ERK signaling pathway is involved in cardiotrophin-1-induced neural differentiation of human umbilical cord blood mesenchymal stem cells in vitro.

Central nervous system diseases remain the most challenging pathologies, with limited or even no therapeutic possibilities and a poor prognosis. This study aimed to investigate the differentiation properties of human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) transfected with recombinant adenovirus expressing enhanced green fluorescence protein cardiotrophin-1 (Adv-EGFP-CT-1) and the possible mechanisms involved. Cells were isolated, and MSC immunophenotypes were confirmed. The resulting differentiated cells treated with Adv-EGFP-CT-1 and cultured in neural induction medium (NIM) expressed higher levels of Nestin, neuronal nuclei (NeuN) and glial fibrillary acidic protein (GFAP) markers than cells in other treatments. Expression of glycoprotein 130/leukemia inhibitory factor receptor ß (gp130/LiFRß), Raf-1, phosphorylated Raf-1 (p-Raf-1), extracellular signal-regulated kinase 1/2 (ERK1/2) and phospho-ERK1/2 (p-ERK1/2) increased gradually within 72 h after transfection with Adv-EGFP-CT-1 and NIM culture. Additionally, inhibition of extracellular signal-regulated kinase kinase (MEK) abrogated expression of p-ERK1/2, Nestin, GFAP and NeuN. Thus, the ERK1/2 pathway may contribute to CT1-stimulated neural differentiation of hUCB-MSCs.