Effect of CT fluoroscopy-guided transpulmonary radiofrequency ablation of liver tumours on the lung.

OBJECTIVE: We retrospectively evaluated the effect of transpulmonary radiofrequency ablation (RFA) of liver tumours on the lung. METHODS: 16 patients (10 males and 6 females; mean age, 65.2 years) with 16 liver tumours (mean diameter 1.5 cm) underwent transpulmonary RFA under CT fluoroscopic guidance. The tumours were either hepatocellular carcinoma (n=14) or liver metastasis (n=12). All 16 liver tumours were undetectable with ultrasonography. The pulmonary function values at 3 months after transpulmonary RFA were compared with baseline (i.e. values before RFA). RESULTS: In 8 of 16 sessions, minor pulmonary complications occurred, including small pneumothorax (n=8) and small pleural effusion (n=1). In two sessions, major pulmonary complications occurred, including pneumothorax requiring a chest tube (n=2). These chest tubes were removed at 4 and 6 days, and these patients were discharged 7 and 10 days after RFA, respectively, without any sequelae. The pulmonary function values we evaluated were forced expiratory volume in 1 s (FEV1.0) and vital capacity (VC). The mean values of FEV1.0 before and 3 months after RFA were 2.55 l and 2.59 l, respectively; the mean values of VC before and 3 months after RFA were 3.20 l and 3.27 l, respectively. These pulmonary values did not show any significant worsening (p=0.393 and 0.255 for FEV1.0 and VC, respectively). CONCLUSION: There was no significant lung injury causing a fatal or intractable complication after transpulmonary RFA of liver tumours.

Hepatitis C virus NS4 protein impairs the Th1 polarization of immature dendritic cells.

Dendritic cells (DCs) in chronic hepatitis C patients display impaired function, although the details remain unclear. To investigate the hepatitis C virus (HCV) protein that has the most impact on DC function, we compared five recombinant proteins and seven HCV protein genes in modulating DC phenotype and function. Immature DCs (iDCs) were established from healthy donor peripheral blood monocytes with granulocyte-macrophage colony stimulating factor (GM-CSF) and IL-4. Lipopolysaccharide was used to establish mature DCs (mDCs). Cells were then pulsed with HCV recombinant proteins or transfected with HCV plasmids and subsequently assayed for cell surface marker expression by flow cytometry. For cytokine and proliferative T-cell response analysis, DCs were cultured with autologous CD4 T cells and tuberculin purified protein derivative (PPD). Mean fluorescent intensity of CD86 was reduced in HCV protein-pulsed iDCs. Proliferative T-cell responses and Th1 cytokine concentrations were reduced with HCV nonstructural proteins (NS), particularly with HCV NS4. HCV nonstructural proteins, particularly NS4, change the iDC phenotype and reduce antigen-specific T-cell stimulatory function with Th1 cytokine reductions.

Histidine induces lipolysis through sympathetic nerve in white adipose tissue.

BACKGROUND: Hypothalamic neuronal histamine has been shown to increase lipolysis in white adipose tissue. The present study aimed to clarify whether peripheral loading with L-histidine, a precursor of neuronal histamine, may affect lipid metabolism in adipose tissue. MATERIALS AND METHODS: The in vivo microdialysis study was used to assess lipolysis in rat epididymal adipose tissue by measuring the release of glycerol in response to administration of L-histidine. In addition, electrophysiological measurements were performed to record changes in activity of sympathetic nerve innervating adipose tissue following histidine treatment. RESULTS: Sequential administration of isoproterenol, a beta-adrenoceptor agonist, through the microdialysis cannula at concentrations of 10(-)8 to 10(-6) M increased the glycerol concentration in the dialysate dose-dependently (P < 0.05). Intraperitoneal administration of L-histidine at a dosage of 0.35 mmol kg(-1) also increased the glycerol concentration compared to that of phosphate buffered saline (P < 0.05). Concomitantly, the administration of histidine increased the serum concentration of free fatty acid compared to control treatment (P < 0.05). The accelerating effects of histidine on lipolysis were mimicked by the infusion of 10(2) nmol rat(-1) L-histamine into the third cerebroventricle (P < 0.05). Electrophysiological measurement demonstrated that administration of histidine at a dosage of 0.35 mmol kg(-1) increased the activity of efferent sympathetic nerve, innervating adipose tissue more than the infusion of phosphate buffered saline (P < 0.05). CONCLUSION: The present results indicate that histidine accelerates lipolysis in white adipose tissue through activation of the sympathetic nerve. The regulation of lipolysis may therefore involve histamine neurons in the brain, probably through the conversion of L-histidine to histamine in the hypothalamus.

[A case of severe adult measles pneumonia--efficacy of combination of steroid pulse therapy, high-dose vitamin A and gamma globulins].

A 33 year-old female was admitted with facial, trunk and limb eruptions, conjunctiva intrahemorrhage, Koplik's spots in the pharynx and severe hypoxemia after fever and upper respiratory tract symptom. Infiltrative shadow of the whole right lung was seen on chest radiography. Fine crackles were seen in the lower left lung and in the whole right lung. Severe inflammation and liver dysfunction were indicated by blood test. Measles antibody IgM was high. The abnormal interstitial shadows were confirmed in greater detail by chest computed tomography. Her condition was diagnosed as measles pneumonia. A combination therapy with steroid pulse, high dose vitamin A, and gamma globulin was started, after which the patient gradually improved, indicating the effectiveness of this combination therapy for severe adult measles pneumonia.

Regional fat deposition in the legs is useful as a presumptive marker of antiatherogenesity in Japanese.

To examine the pathological role of regional fat deposition in development of metabolic and cardiovascular disorders, regional fat distribution was evaluated using metabolites and hormones as measures of obesity-related disorders. The subjects enrolled were 100 sex-matched inpatients, who were admitted, regardless of their body mass index values, for further examination of unusual results from periodic medical screening tests, and for examination of obesity-induced complications and treatment of obesity. Body fat distribution was analyzed using dual energy X-ray absorptiometry (DEXA). Analysis of parameters regarding fat distribution showed that gender was one of the determinants affecting correlation between fat distribution and metabolites of fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), total cholesterol (TC), or triglyceride (TG). However, regardless of gender, both leg trunk fat (L/Tr) and arm trunk fat (A/Tr) ratios negatively correlated with a total body fat (% total fat) ratio, whereas the intercept value of female regression line in L/Tr was greater than that in males, but not in A/Tr. Percentage total fat, L/Tr, and A/Tr in males correlated significantly with FPG, TC, TG, low-density lipoprotein (LDL), very low density lipoprotein (VLDL), atherogenic index (A.I.), and apoB/A1 only low density lipoprotein (LDL) was significantly correlated solely to L/Tr and A/Tr. These results indicate that regional fat distribution in males may not be a major determinant for development of metabolic disorders in obese patients. Unlike male regional fat distribution, female L/Tr correlated significantly not only with TC, TG, and LDL, but also with FPG and HbA1c, although both of the latter 2 glucose-related parameters in males showed no correlation with any parameters of fat deposition. The remaining female parameters of fasting plasma insulin, VLDL, A.I., and ApoB/A1 correlated with each of the three parameters of fat deposition, as similarly shown in males. The powerful and negative correlation was thus evident, particularly in females, between leg fat deposition and parameters of glucose and lipid metabolites. The resulting information provides a novel insight that regional fat deposition at the legs is useful as a marker for metabolic and cardiovascular disorders associated with obesity.

Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta.

Dynamic involvement of hypothalamic histamine in ingestive behavior and thermogenesis induced by interleukin-1 beta (IL-1 beta) was examined in rats. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta decreased food and water intake and elevated body temperature. However, depletion of neuronal histamine induced by intraperitoneal injection of 160 mumol/rat alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the suppressive effect on drinking, and enhanced the elevating effect on rectal temperature. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta increased hypothalamic histamine turnover rate. The same dose of IL-1 beta also increased activity of HDC and histamine-N-methyltransferase (HMT). These results suggest that IL-1 beta may stimulate synthesis and release of hypothalamic histamine in presynaptic terminals by activation of HDC and facilitate degradation of extracellular histamine by activation of MHT. These changes in the dynamics of hypothalamic histamine modulate IL-1 beta-induced ingestive behavior and body temperature.

Allergic granulomatosis and angiitis with severe cardiac disease: a case in which cardiac function was extremely improved by long-term steroid therapy.

A 38-year-old man with a history of bronchial asthma developed marked eosinophilia, mononeuritis multiplex and transient pulmonary infiltration. Pathological findings from the lung and nerve biopsy were helpful in determining the diagnosis as allergic granulomatosis and angiitis (AGA). Echocardiogram indicated dilation of the left ventricle with impaired systolic contraction. Coronary arteriography demonstrated significant stenosis only in the peripheral segment of the circumflex artery. After 1 year of corticosteroid therapy, echocardiogram revealed improvement of left ventricular contractility evaluated by ejection fraction (from 28% to 67%). To our knowledge, no previous reports have described amelioration of severe cardiac lesions during long-term steroid treatment in patients with AGA.