Denosumab salvage therapy in an 11-year-old boy with locally recurrent unresectable giant cell tumor of the lumbar spine after surgery.

Giant cell tumors (GCTs) of the bone are locally aggressive primary bone tumors with a benign character. Spinal involvement is rare which accounts for approximately 5% of all primary bone tumors and it is quite rare in the lumbar spine. An 11-year-old boy patient presented with pain of low back and bilateral low extremities. Lumbar CT and MRI revealed a lytic lesion of the L4 vertebra corpus. The patient earned remarkable and timely recovery with 2 surgical interventions and the use of denosumab. Surgical resection for GCTs is still preferable as the initial treatment, denosumab should be utilized after tumor resection whether based on the purpose of prevention or treatment of tumor recurrence.

Hyperglycemia and Hypokalemia in a 16-Year-Old Overweight Female Patient Misdiagnosed with Cushing Syndrome at First and Ultimately Diagnosed with Carney Complex Proven by PRKAR1A Gene Test: a Case Report and Literature Review.

BACKGROUND: Here we report on a 16-year-old female patient with typical Cushingoid features who was admitted because of purple striae, menostasis, and microsomia for 1 year, and laboratory tests showed hyperglycemia and hypokalemia. METHODS: For diagnosis, we employed a hormone test, abdominal and pituitary computed tomography scan, ultrasonography to detect endocrine and cardiocutaneous lesions. DNA sequencing to detect PRKAR1A gene mutation to make differential diagnosis for Cushing Syndrome. RESULTS: Hormone test revealed hypercortisolism, images demonstrated right adrenal nodular hyperplasia and hyperparathyroid hyperplasia. DNA sequencing analysis revealed a heterozygous C.680 G>A substitution in PRKAR1A. CONCLUSIONS: We describe here an atypical Carney Complex (CNC) patient magnified Cushing Syndrome with a nonsense mutation in the PRKAR1A gene, which cannot sustain the diagnosis except for the RKAR1A gene sequencing for analysis.

Biofilm Formation Plays a Role in the Formation of Multidrug-Resistant Escherichia coli Toward Nutrients in Microcosm Experiments.

In this study, microcosms were established to determine the effect of nitrogen (N) and phosphorus (P) on the multidrug resistance and biofilm-forming abilities of Escherichia coli. The expression of biofilm-formation-related genes was detected to establish correlations between genotype and phenotype. Different concentrations of N and P were added to make one control group and four treatment groups. The glass tube method was used to determine biofilm-forming capabilities. Real-time PCR was used to detect the mRNA abundance of six biofilm-formation-related genes in E. coli. No resistant strains were isolated from the control group; meanwhile, multidrug resistance rates were high in the treatment groups. Expression of the biofilm-associated genes luxS, flhD, fliA, motA, and fimH was detected in all treatment groups; however, there was no expression of mqsR. The expression of luxS, flhD, fliA, motA, and fimH significantly correlated with the concentration of N and P, as well as with the appearance and duration of multidrug resistance in different groups. Overall, the results of this study suggest that biofilm-forming ability plays a key role in the formation of multidrug resistance in E. coli after the addition of N and P to a microcosm.

Analogous on-axis interference topographic phase microscopy (AOITPM).

The refractive index (RI) of a sample as an endogenous contrast agent plays an important role in transparent live cell imaging. In tomographic phase microscopy (TPM), 3D quantitative RI maps can be reconstructed based on the measured projections of the RI in multiple directions. The resolution of the RI maps not only depends on the numerical aperture of the employed objective lens, but also is determined by the accuracy of the quantitative phase of the sample measured at multiple scanning illumination angles. This paper reports an analogous on-axis interference TPM, where the interference angle between the sample and reference beams is kept constant for projections in multiple directions to improve the accuracy of the phase maps and the resolution of RI tomograms. The system has been validated with both silica beads and red blood cells. Compared with conventional TPM, the proposed system acquires quantitative RI maps with higher resolution (420 nm @λ = 633 nm) and signal-to-noise ratio that can be beneficial for live cell imaging in biomedical applications.

Clozapine directly increases insulin and glucagon secretion from islets: implications for impairment of glucose tolerance.

Second generation antipsychotics cause derangements in glucose metabolism that are often interpreted as insulin resistance. In previous studies we have shown that this is not classical insulin resistance but the drugs were actually inducing a hyperglycaemic state associated with elevated hepatic glucose output (HGO) and increased levels of glucagon and insulin. However, it remains unclear whether these effects are directly elicited by drug actions in the liver and pancreas, or whether they are indirectly mediated. Here we investigated if clozapine is capable of inducing insulin resistance in the liver or enhancing insulin and glucagon secretion from the pancreas. It was observed that insulin signalling was elevated in livers from animals treated with clozapine indicating there was no insulin resistance in the early steps of insulin signalling. To explore whether the defects arise at later stages of insulin action we used an isolated perfused liver system. In this model, clozapine had no direct effect on insulin's counter regulatory effect on epinephrine-induced HGO. In isolated mouse islets clozapine significantly increased glucose-stimulated insulin secretion while simultaneously blocking glucose-induced reductions in glucagon secretion. We also show that the non-peptidic glucagon receptor like peptide-1 (GLP-1) receptor agonist Boc5 was able to overcome the inhibitory effects of clozapine on glucose metabolism. Taken together these results suggest that clozapine does not have any direct effect on glucose metabolism in the liver but it simultaneously stimulates insulin and glucagon secretion, a situation that would allow for the concurrent presence of high glucose and high insulin levels in treated animals.