A case of mesenteric cystic lymphangioma in an adult which caused duodenal stenosis after resection

INTRODUCTIONWe present a rare case of mesenteric lymphangioma in a middle-aged female.PRESENTATION OF CASEA 56-year-old female was admitted to the hospital with upper abdominal pain. Abdominal computed tomography revealed a multicystic mass surrounding the mesentery. We made the decision to resect the mass, suspecting that was a mesenteric lymphangioma based on additional imaging studies. The tumor adhered strongly to parts of the duodenum and the upper jejunum. In order to preserve the jejunum, we dissected its serosa away from the tumor. Approximately 1 week after surgery the patient experienced a constriction of the third portion of the duodenum. Her symptoms were improved with conservative therapy, and she was discharged from the hospital 62 days after surgery.DISCUSSIONLymphangioma originating from the mesentery may have cause adhesions due to exfoliated tumor cells; it is necessary to be concerned about postoperative obstruction.CONCLUSIONThe preoperative diagnosis of lymphangioma is based on various imaging modalities.     

Influence of oxygen inhibition on the surface free energy and enamel bond strength of self-etch adhesives

We compared the surface free energies and enamel bond strengths of single-step self-etch adhesives with and without an oxygen-inhibited layer. The adhesives were applied to the enamel surfaces of bovine incisors, light irradiated, and the oxygen-inhibited layer was either retained or removed with ethanol. The surface free energies and their components (γ(S)(LW), γ(S)(+), and γ(S)(-)) were determined by measuring the contact angles of three test liquids placed on the cured adhesives. The enamel bond strengths of specimens with and without the oxygen-inhibited layer were measured. For all surfaces, the value of the estimated surface tension component γ(S)(LW) was relatively constant. The value of the γ(S)(+) component increased slightly when the oxygen-inhibited layer was removed, whereas that of the γ(S)(-) component decreased significantly. The enamel bond strengths of the self-etch adhesives were significantly lower in the specimens without an oxygen-inhibited layer. The oxygen-inhibited layer therefore appeared to promote higher enamel bond strength.     

Renal p38 MAP kinase activity in experimental diabetes

Renal cell activity of p38 mitogen-activated protein kinase (p38) is increased in the diabetic milieu. p38 mediates signals relevant for the development of diabetic nephropathy (DN). However, renal p38 in Type 1 diabetes in vivo, particularly in conditions reflecting the differences in metabolic control, and its activity in advanced stages of DN, has received less attention. We examined the p38 pathway in renal cortex of rats with streptozotocin diabetes (4 weeks) with poor (DS), moderate (DM), and intensive (DII) metabolic control, achieved by varying doses of insulin therapy. Renal p38 was also studied in 12-month diabetic rats with established nephropathy (DM12) and compared with age-matched controls. p38 activity (in vitro kinase assay and expression of phosphorylated (active) p38 (P-p38)) was increased in DM and DS rats, as compared with non-diabetic controls, and attenuated by intensive insulin treatment. In all groups, P-p38 was predominantly localized in macula densa cells. Diabetic rats also demonstrated P-p38 immunoreactivity in the distal tubule and glomeruli. Enhanced p38 activity in DS and DM rats was not associated with increases in expression of active mitogen-activated protein kinase 3/6, an activator of p38, but paralleled with increased expression of scaffolding protein transforming growth factor-beta-activated protein kinase 1-binding protein 1. Expression of mitogen-activated protein phosphatase-1 (MKP-1), one of the phosphatases involved in inactivation of mitogen-activated protein kinase signaling, was increased in all diabetic groups, irrespective of metabolic control. Renal p38 activation was also detectable in D12 rats with established albuminuria and glomerulosclerosis. In summary, renal cortical p38 activity was increased in diabetic rats at early and advanced stages of nephropathy, as compared with non-diabetic animals, and attenuated by improved metabolic control. p38 activation in diabetes is likely to occur via multiple pathways and cannot be explained by downregulation of MKP-1.     

Transsphenoidal cyst cisternostomy with a keyhole dural opening for sellar arachnoid cysts: technical note

A less invasive transsphenoidal approach with a keyhole dural opening for intrasellar arachnoid cysts is described. This approach was used to address seven sellar cystic lesions with suprasellar extension; they were six intrasellar arachnoid cysts (IACs) and one Rathke’s cleft cyst (RCC). In all cases, preoperative MRI revealed cerebrospinal fluid (CSF) intensity on both T1- and T2-weighted images. On preoperative contrast-enhanced MRI, five of the six IACs manifested posterior displacement of the flattened pituitary gland toward the dorsum sellae; one of the six IACs and the RCC exhibited a flattened pituitary gland on the anterior surface of the cyst. Wide cyst cisternostomy through a keyhole dural opening was carried out safely using a microscope with the support of a thin angled endoscope (30° and/or 70°, diameter 2.7 mm). As we aimed to avoid iatrogenic injury of the pituitary function, we found it difficult to obtain a sufficiently wide and precise opening of the cyst wall when the pituitary gland was located on the anterior surface of the cyst wall. Our approach facilitates safe cyst cisternostomy as wide as that obtainable by transcranial manipulation. In addition, CSF leakage is prevented by dural plasty using the fascia lata and stitching with 6-0 monofilament sutures. This technique can be adapted to address various sellar cystic lesions. However, as the posterior or anterior displacement of the normal pituitary gland in the presence of IACs or RCCs, respectively, affects the width of the cyst opening, our technique is more suitable for IACs than RCCs.     

Spontaneously regressed granulomatosis with polyangiitis: A case report

A 71-year-old woman presented with chest pain, cough, and back pain. A chest roentgenogram showed multiple nodular shadows in both lungs. She was diagnosed with granulomatosis with polyangiitis (GPA). The multiple nodular shadows in both lungs regressed spontaneously in a few months. There are few reports of spontaneous regression of GPA, and the underlying mechanism is unclear. Neutrophil extracellular traps (NETs) have been recently shown to be involved in GPA. NETs may also be related to the natural regression of GPA.     

Endoscopic imaging modalities for diagnosing the invasion depth of superficial esophageal squamous cell carcinoma: a systematic review

Esophagus - Endoscopic diagnosis of the invasion depth of superficial esophageal squamous cell carcinoma (ESCC) is an important determinant of the treatment strategy. The three endoscopic imaging...     

Detection of glutamate release from neurons by genetically encoded surface-displayed FRET nanosensors

Glutamate is the predominant excitatory neurotransmitter in the mammalian brain. Once released, its rapid removal from the synaptic cleft is critical for preventing excitotoxicity and spillover to neighboring synapses. Despite consensus on the role of glutamate in normal and disease physiology, technical issues limit our understanding of its metabolism in intact cells. To monitor glutamate levels inside and at the surface of living cells, genetically encoded nanosensors were developed. The fluorescent indicator protein for glutamate (FLIPE) consists of the glutamate/aspartate binding protein ybeJ from Escherichia coli fused to two variants of the green fluorescent protein. Three sensors with lower affinities for glutamate were created by mutation of residues peristeric to the ybeJ binding pocket. In the presence of ligands, FLIPEs show a concentration-dependent decrease in FRET efficiency. When expressed on the surface of rat hippocampal neurons or PC12 cells, the sensors respond to extracellular glutamate with a reversible concentration-dependent decrease in FRET efficiency. Depolarization of neurons leads to a reduction in FRET efficiency corresponding to 300 nM glutamate at the cell surface. No change in FRET was observed when cells expressing sensors in the cytosol were superfused with up to 20 mM glutamate, consistent with a minimal contribution of glutamate uptake to cytosolic glutamate levels. The results demonstrate that FLIPE sensors can be used for real-time monitoring of glutamate metabolism in living cells, in tissues, or in intact organisms, providing tools for studying metabolism or for drug discovery.