Langerhans cell histiocytosis misdiagnosed as cow protein allergy: a case report.

BACKGROUND: Langerhans cell histiocytosis (LCH) is a heterogeneous disease with diverse clinical manifestations. Abdominal organ involvement is rare. Early diagnosis and active treatment are needed. The purpose of this article is to enable readers to have a better knowledge of LCH and prevent misdiagnosis. CASE PRESENTATION: A 2-month-old boy had diarrhea, hematochezia, and a rash, and was diagnosed as having a cow milk protein allergy (CMPA). He was given an amino acid-based formula, but there was no sign of improvement in his condition. The patient then had a skin biopsy and was diagnosed as having multisystem Langerhans cell histiocytosis (MS-LCH). The general condition of the child deteriorated after the first two doses of chemotherapy, and the child died. CONCLUSIONS: MS-LCH is a protracted and progressive condition with poor prognosis. Early diagnosis and treatment are essential for survival. If a child has chronic diarrhea and hematochezia in the presence of a characteristic rash, the pediatrician should consider the possibility of this disease to avoid misdiagnosis.

Circadian clock disruption attenuated growth hormone(GH)-mediated signalling.

The circadian molecular clock is an internal time-keeping system, which regulates various physiological processes through the generation of approximately 24-hour circadian rhythms. BMAL1 (brain and muscle arnt-like 1) is a core component of the circadian clock. Previous studies have shown that the circadian clock correlates with rhythmic secretion of endocrine hormone (such as growth hormone, GH). Currently, the effect of circadian clock on the GH-mediated biological activities is not fully understood. In this work, we used BMAL1 gene knockout mice (BMAL-/- mice) model to explore the effect of circadian clock dysfunction on GH's activities, and the results from in vivo and in vitro experiments showed that GH-induced signaling is down-regulated. In vivo, GH/GHR-mediated tyrosine phosphorylation of signaling molecules (such as the Janus kinase-signal transducer and activator of transcription, JAK-STAT) in BMAL-/- mice was significantly lower compared to control mice. In vitro, GH/GHR-mediated signaling in the hepatocytes from BMAL-/- mice is decreased compared to hepatocytes from control mice. Furthermore, we explore the mechanism by which GH/GHR-mediated signalling is down-regulated in BMAL-/- mice, and results indicated that the expression levels of negative regulators of cytokine signaling (such as the suppressor of cytokine signaling (SOCS) and protein phosphatase) were increased, which may be one of the factors that cause the GH signaling downregulation. In summary, our results show that the circadian clock affects the biological activities of GH. This finding lays the foundation for future investigations into the relationship between the circadian clock and biological activities of GH.

Oxycodone protects cardiomyocytes from ischemia-reperfusion-induced apoptosis via PI3K/Akt pathway.

Ischemia/reperfusion (I/R) cause secondary myocardial damage following a blood reflow after myocardial infarction. This study aimed to explore oxycodone as a myocardial protector after an I/R injury in rats. Oxycodone reduced myocardial infarction volume, an I/R-induced apoptosis of the cardiomyocytes, the serum levels of CK-MB and LDH. The ejection fraction and fraction shortening in the I/R rats also increased. From the molecular mechanism, it was evident that oxycodone not only decreased the expression levels of Bax, active-caspase 3 protein but also increased the expression levels of Bcl2, p-PI3K, and p-Akt protein in heart tissue of the I/R rats. In vitro, oxycodone induced anti-H9c2 cell apoptosis after hypoxia/reoxygenation (H/R). However, its ability to act as a myocardial protector deteriorated in the presence of a PI3K/Akt pathway inhibitor.

Acute sleep deprivation leads to growth hormone (GH) resistance in rats.

Sleep is an essential physiological process that is required by all higher animals. Sleep has many important physiological functions. Previous studies have focused on the relationship between sleep and growth hormone secretion patterns. However, to date, whether sleep affects the biological activities of GH remains unclear. Here, we investigated this issue by evaluating the growth hormone receptor (GHR)-mediated intracellular signalling pathway in a sleep-deprived rat model. The results showed that GH's signalling ability is decreased in an acute sleep deprivation rat model. JAK2-STAT signalling was decreased significantly compared to that in control rats. We further analysed the possible molecular mechanism of GH signal inhibition in sleep-deprived rats. The results showed that the protein expression levels of SOCS3 (suppressors of cytokine signalling 3, which functions as the negative regulatory molecule of GH's signalling) increased; however, other negative regulatory proteins, such as protein phosphatase (PTP1B), did not change. In addition, acute sleep deprivation results in a significant increase in serum FFA (free fatty acid) level, which is also one of the factors contributing to GH inhibition. These findings suggest that GH signal resistance may be caused by a combination of factors. This study could serve as an important reference for related studies on the effect of sleep deprivation on endocrine systems.

Successful removal of multiple magnetic foreign bodies in the digestive tract of children by gastroscopy: Two case reports.

RATIONALE: Gastrointestinal foreign body (FB) is an emergency commonly encountered by the pediatric gastroenterology department. Management of their extraction requires knowledge and careful consideration of removal techniques. PATIENT CONCERNS: Two little girls swallowed multiple magnets that stuck together for >3 days, which was an indication for surgery. DIAGNOSIS: X-ray revealed dense shadows in the left abdomen. However, the abdominal examination revealed a soft abdomen without tenderness, rebound tenderness, or muscle rigidity. INTERVENTION: The multiple magnets were removed by endoscopy instead of surgery. OUTCOME: We conducted sufficient preoperative assessment and preparation. Eventually, we successfully removed the multiple magnets by endoscopy, and no perforation or fistula formation was observed. Surgery was avoided. LESSONS: Swallowing multiple magnets isn't a rare emergency in children. Physicians must be aware that surgery is not the only option even if multiple magnets are swallowed for >12 hours. Endoscopic removal can be considered if there is no obstruction, perforation, or fistula formation upon careful patient assessment. If endoscopic removal fails, surgical treatment should be performed as soon as possible to avoid serious complications.

catena-Poly[[tri-aqua-copper(II)]-µ-5-carb-oxy-benzene-1,3-di-carboxyl-ato-κ(2) O (1):O (3)].

In the title complex, [Cu(C9H4O6)(H2O)3] n , the Cu(II) cation exhibits a distorted square-pyramidal coordination geometry involving five O atoms from two monodentate 5-carb-oxy-benzene-1,3-di-carboxyl-ate anions and three water mol-ecules. The 5-carb-oxy-benzene-1,3-di-carboxyl-ate anions bridge Cu(II) cations into zigzag polymeric chains running along the b-axis direction. These chains are further linked by O-H⋯O hydrogen bonds between coordinating water mol-ecules or carboxyl groups and carboxylate groups into a three-dimensional supra-molecular architecture. In the crystal, π-π stacking is observed between parallel benzene rings of adjacent chains, the centroid-centroid distances being 3.584 (3) and 3.684 (3) Å.

Poly[di-µ9-citrato-tetra-sodiumzinc].

In the title compound, [Na4Zn(C6H5O7)2] n , the Zn(II) ion lies on an inversion center and is coordinated by six O atoms from two citrate ligands, forming a distorted octa-hedral geometry. There are two crystallographically independent Na(+) cations in the asymmetric unit. One Na(+) cation exhibits a distorted square-pyramidal geometry defined by five O atoms from four citrate ligands. The other Na(+) cation is surrounded by six O atoms from five citrate ligands in a distorted octa-hedral geometry. The Na(+) cations are bridged by citrate carboxyl-ate groups, forming a layer parallel to (100). The layers are further assembled into a three-dimensional network with the [Zn(citrate)2](4-) building units as 'pillars'; O-H⋯O hydrogen bonds also stabilize the structure.