A case of severe pneumoconiosis with synchronous triple lung cancer]

A 70-year-old man who had worked in a stonepit for about fifty years was admitted to our hospital for detailed examination of the signs of pneumoconiosis (3/3, q) and a nodular shadow in the right upper lung field. Under a clinical diagnosis of lung cancer complicated with pneumoconiosis, right upper lobectomy with a right S6 resection was performed. Pathological examination revealed moderately differentiated adenocarcinoma of the right S2, well-differentiated adenocarcinoma of the right S6, and a squamous cell carcinoma of the right S1 which was not detected by chest CT. In addition to the difficulty of diagnosing lung cancer in a patient with severe pneumoconiosis, treatment for lung cancer may be limited by the poor pulmonary function that results from pneumoconiosis. Although the labor administration's decision that lung cancer patients with concomitant pneumoconiosis deserve compensation can be evaluated as a good one, the study of the relationship between pneumoconiosis and lung cancer needs further study through follow-up examination of pneumoconiosis cases.     

Magnetic resonance imaging appropriate for construction of subject-specific head models for diffuse optical tomography

Subject-specific head models of which their geometry is based on structural magnetic resonance images are essential to accurately estimate the spatial sensitivity profiles for image reconstruction in diffuse optical tomography. T1-weighted magnetic resonance images, which are commonly used for structural imaging, are not sufficient for the threshold-based segmentation of the superficial tissues. Two types of pulse sequences, which provide a high contrast among the superficial tissues, are introduced to complement the segmentation to construct the subject-specific head models. The magnetic resonance images acquired by the proposed pulse sequences are robust to the threshold level and adequate for the threshold-based segmentation of the superficial tissues compared to the T1- and T2-weighted images. The total scan time of the proposed pulse sequences is less than one-fourth of that for the T2-weighted pulse sequence.OCIS codes: (170.2655) Functional monitoring and imaging, (170.3660) Light propagation in tissues     

Changes in energy metabolism after induction therapy in patients with severe or moderate ulcerative colitis

We investigated the changes in energy expenditure during induction therapy in patients with severe or moderate ulcerative colitis. Thirteen patients (10 men, 3 women; mean age, 36.5 years) with ulcerative colitis admitted to the Shiga University Hospital were enrolled in this study. We measured the resting energy expenditure and respiratory quotients of these patients before and after induction therapy with indirect calorimetry. We analyzed the changes of nutritional status and serum inflammatory cytokine levels and also evaluated the relationship between energy metabolism and disease activity by using the Seo index and Lichtiger index. The resting energy expenditure was 26.3 ± 3.8 kcal/kg/day in the active stage and significantly decreased to 23.5 ± 2.4 kcal/kg/day after induction therapy (p<0.01). The resting energy expenditure changed in parallel with the disease activity index and C-reactive protein and inflammatory cytokine levels. The respiratory quotient significantly increased after induction therapy. Thus, moderate to severe ulcerative colitis patients had a hyper-metabolic status, and the energy metabolism of these patients significantly changed after induction therapy. Therefore, we recommend that nutritional management with 30–34 kcal/kg/day (calculated as measured resting energy expenditure × activity factor, 1.3) may be optimal for hospitalized ulcerative colitis patients.     

Chugging in patients on veno-venous extracorporeal membrane oxygenation: An under-recognized driver of intravenous fluid administration in patients with acute respiratory distress syndrome?

Background

Veno-venous extracorporeal membrane oxygenation (VV-ECMO) is increasingly utilized in the management of severe acute respiratory distress syndrome (ARDS). Providers who care for patients on VV-ECMO should be familiar with common circuit complications.

The regulation of two distinct glucose transporter (GLUT1 and GLUT4) gene expressions in cultured rat thyroid cells by thyrotropin.

We investigated the glucose transporter mRNAs expressed in FRTL5, a rat thyroid cell line, and their regulation by TSH by means of the polymerase chain reaction. FRTL5 cells as well as rat thyroid tissue expressed three types of glucose transporter mRNAs: GLUT1 or erythrocyte/HepG2/brain isoform, GLUT2 or pancreatic beta-cell/liver isoform, and GLUT4 or muscle/fat isoform. GLUT1 mRNA predominated, GLUT4 mRNA was minor, and GLUT2 mRNA expression was faint. Incubation of FRTL5 cells with TSH induced a time- and concentration-dependent increase in GLUT1 mRNA levels, while GLUT4 mRNA levels were decreased. The response of GLUT1 mRNA to TSH was evident at 3 h, and the maximal response was achieved at 12 h. TSH at a dose of 1 mU/ml elicited an approximately 3-fold increase in GLUT1 mRNA levels. (Bu)2cAMP (1 mM), 8-bromo-cAMP (1 mM), and forskolin (50 microM) mimicked the effect of TSH on GLUT1 and GLUT4 mRNA levels. The increase in GLUT1 mRNA by TSH was correlated with the increase in GLUT1 protein and the increase in 2-deoxyglucose transport activity. These observations suggest that in thyroid cells, TSH stimulates glucose transport at least in part by enhancing GLUT1 gene expression, and that the effect of TSH on GLUT1 and GLUT4 mRNA levels is mediated by a cAMP-dependent pathway.     

Identification of simultaneous mutation of fibrinogen alpha chain and protein C genes in a Japanese kindred

Afibrinogenaemia usually induces a bleeding tendency during infancy, whereas protein C deficiency increases susceptibility to thrombosis in children or adolescence. Mutations of these genes have been, therefore, established as independent risk factors for coagulation disorders. We describe the homozygous mutation of the fibrinogen alpha chain gene and additional heterozygous mutation of the protein C gene in a male infant who showed prolonged umbilical bleeding after birth. On examination, the plasma fibrinogen was undetectable, and the activity and antigen level of protein C were reduced. The patient showed no fibrinogen Aalpha chain as well as Bbeta and gamma chains by Western blotting. The sequencing analysis showed the homozygous deletion of 1238 bases from intron 3 at position 2008 to intron 4 at position 3245 in the fibrinogen alpha chain gene. Both parents were heterozygous carriers of this mutation. In this patient, an additional mutation was also detected in the protein C gene: the heterozygous deletion of exon 7 at position 6161-6163 or 6164-6166, resulting the deletion of one amino acid (Lys150 or 151). His mother was also a carrier of this mutation. As the simultaneous mutation of the fibrinogen alpha chain and protein C genes has not been previously reported, the influence of the interaction between these two mutations on the clinical manifestations of this patient should be carefully monitored for a long period.     

Endothelin activates the dihydropyridine-sensitive, voltage-dependent Ca2+ channel in vascular smooth muscle.

Endothelin is a potent endothelium-derived vasoconstrictor peptide recently characterized from porcine and human vascular endothelial cells. Here we provide evidence that endothelin activates the dihydropyridine-sensitive, voltage-dependent Ca2+ channel in porcine coronary artery smooth muscle. The vasoconstrictor action of endothelin is efficiently antagonized by low doses of the dihydropyridine Ca2+-channel blocker nicardipine. Endothelin augments the Ca2+-induced contraction in a high-K+ depolarizing solution, markedly enhances high-threshold Ca2+-channel current on the whole-cell patch clamp recording, and causes a sustained increase in the intracellular Ca2+ that is largely dependent on extracellular Ca2+. These findings suggest that endothelin exerts its vasoconstrictor effect by either directly or indirectly activating the voltage-dependent Ca2+ channel.