Vascular flow patterns of hepatic tumors in contrast-enhanced 3-dimensional fusion ultrasonography using plane shift and opacity control modes.

OBJECTIVE: This study was conducted to determine whether contrast-enhanced 3-dimensional (3D) fusion ultrasonography with combined use of the plane shift and opacity control modes can serve as a useful tool for identifying the vascular characteristics of hepatic tumors in 3D perspective. METHODS: Contrast-enhanced 3D fusion ultrasonography was performed in 31 patients with hepatic tumors after the intravenous injection of contrast media. The shapes, courses, and distributions of tumor vessels, displayed in 3D perspective, were examined to identify the characteristic vascular flow patterns of various tumors. Images before and after contrast media administration were compared for evaluation of the effectiveness of contrast enhancement with regard to tumor diameter for various types of tumors. The images were interpreted in a blinded manner by 3 physicians specializing in abdominal ultrasonography, and vascular flow patterns were determined on the basis of consensus. RESULTS: The characteristic vascular flow patterns observed in hepatocellular carcinomas are reticular flow within the tumor and flow showing a ringlike distribution surrounding the tumor. Metastatic tumors show a vascular flow pattern running between adjacent tumor nodules, and hemangiomas show localized nodular flow at the tumor margins. Contrast enhancement was found to be useful for showing the vascular flow patterns in small hepatocellular carcinomas and hemangiomas. CONCLUSIONS: Contrast-enhanced 3D fusion ultrasonography makes it possible to display images combining the plane shift and opacity control modes to show tumor vessels, including minute vascular flow within hepatic tumors, in 3D perspective and to identify tumor-specific vascular flow patterns.     

Perception of hunger and satiety induced by 2-deoxy-D-glucose in anorexia nervosa and bulimia nervosa

The effect of intracellular glucopenia induced by 2-deoxy-D-glucose (2-DG) on changes in hunger ratings, blood glucose, plasms cortisol, and prolactin levels were examined in six female patients with primary anorexia nervosa, three patients with bulimia nervosa, and six age-and sex-matched volunteers. In the normal subjects, hunger ratings obtained by the linear visual analog technique increased significantly at 60 minutes after 2-DG infusion and remained elevated. In Patients with anorexia nervosa, however, hunger ratins paradoxically decreased significantly at 90 minutes. In normal subjects, the ingestion of a 20-minute lunch relieved hunger, but neither the anorexic patients nor bulimic patients felt satiety even after food intake. These results suggest that the perception of hunger induced by 2-DG in anorexia nervosa and that of satiety in anorexia nervosa and bulimia nervosa are disturbed.     

Comparison of long-term prognosis of laparoscopy-assisted gastrectomy and conventional open gastrectomy with special reference to D2 lymph node dissection

Background

Laparoscopy-assisted gastrectomy (LAG) is becoming widely used for early gastric cancer. However, how the curability and long-term prognosis of LAG and open gastrectomy (OG) for early and advanced gastric cancer compare remains unclear. This study assessed short- and long-term outcomes after LAG with lymph node dissection in early and advanced gastric cancer.

Methods

A total of 332 patients who underwent LAG or OG for early and advanced gastric cancer from January 2001 through December 2010 were reviewed retrospectively. The mean operating time, estimated mean blood loss, number of dissected lymph nodes, and survival rates were compared between LAG and OG for early and advanced gastric cancer.

Results

Overall, 47.6% (158/332) of patients underwent LAG; D1, D1+ lymph node dissection was carried out in 77.2%, with D2 dissection in 22.8%. Only one patient required conversion to OG. Comparing LAG and OG with D1, D1+ lymph node dissection for early gastric cancer (EGC), mean operating time was significantly longer, estimated mean blood loss was significantly smaller, and the average number of retrieved lymph nodes was significantly greater with LAG. The rate of specific postoperative morbidity was 17.2% for LAG patients and 25.0% for OG patients, with no postoperative mortality. Survival and recurrence rates were not significantly different. Comparing LAG and OG with D2 lymph node dissection for advanced gastric cancer (AGC), mean operating time was significantly longer and estimated mean blood loss was significantly smaller with LAG, while the average number of retrieved lymph nodes, specific postoperative morbidity and mortality, and survival and recurrence rates were not significantly different.

Conclusions

LAG with D1, D1+ lymph node dissection for EGC is safe and equivalent to open gastrectomy in curability. Moreover, LAG with D2 lymph node dissection for AGC is comparable to OG with D2 lymph node dissection with regard to short- and long-term results.     

Decreased serum levels of epidermal growth factor in adult subjects with high-functioning autism.

BACKGROUND: The neurobiological basis for autism remains poorly understood. Given the role of growth factors in brain development, we hypothesized that epidermal growth factor (EGF) may play a role in the pathophysiology of autism. In this study, we examined whether serum levels of EGF are altered in adult subjects with high-functioning autism. METHODS: We measured serum levels of EGF in the 17 male subjects with high-functioning autism and 18 age-matched healthy male subjects. RESULTS: The serum levels of EGF in the subjects with high-functioning autism (72.4 +/- 102.8 pg/mL [mean +/- SD]) were significantly lower (Mann-Whitney U = 22.0, p < .001) than those of normal control subjects (322.3 +/- 122.0 pg/mL [mean +/- SD]). However, there were no correlations between serum EGF levels and clinical variables in the subjects with autism. CONCLUSIONS: This study suggests that decreased levels of EGF might be implicated in the pathophysiology of high-functioning autism.     

A case of WHIM syndrome associated with diabetes and hypothyroidism

Abstract: The WHIM syndrome is a rare immunological disorder characterized by warts, hypogammaglobulinemia, infections, and myelokathexis. We hypothesized that immunological or genetic mechanisms may link WHIM syndrome and type 1 diabetes. We report that the young girl with WHIM syndrome developed diabetes and transient hypothyroidism. A nonsense mutation (C→T) truncating the CXC chemokine receptor 4 (CXCR4) C-terminal cytoplasmic tail domain occurred at nucleotide position 1000(R334X) of the CXCR4 gene in one allele of the patient was identified, and the person was diagnosed as having WHIM syndrome. Recent observation suggested that the CXCR4, a G-protein-coupled receptor with a unique ligand, CXCL12, might be involved in the pathogenesis for type 1 diabetes. Taken into consideration the concurrent prevalence of the two disorders and the speculated common pathogenesis associated with the CXCR4, our patient may enable us to understand the genetic damage related to accelerated apoptosis.     

Cumulative effects of chromosome aberrations and sister chromatid exchanges in rat liver induced in vivo by heterocyclic amines

Cumulative effects of chromosome aberrations and sister chromatidexchanges (SCEs) were studied in hepatocytes of F344 rats exposedin vivo to 2-amino-3-methylimidazo[4,5-fIquinoline (IQ) at dosesof 12.5,25 or 50 mg/kg body wt/day or 2-nitro-3-methylimidazo[4,5-f quinoline (nitro-IQ) at doses of 12.5, 25 or 50 mg/kg bodywt/day. Hepatocytes were isolated 24 h after 1, 7,14 or 28 repeateddoses (once a day) by gastric intubation and allowed to proliferatein Williams' medium E supplemented with epidermal growth factor.Cells were fixed after a culture period of 48 h. Multiple treatmentwith IQ or nitro-IQ induced significant chromosome aberrationstime- and dose-dependently, the maximum frequency of chromosomeaberrations in metaphase cells being 39 and 33% respectively,while that in controls was 1.1%. Single treatment with IQ ornitro-IQ induced significant SCEs dose-dependently, the maximumfrequency being 0.83 and 0.79 per chromosome respectively, whilethe control value was 0.51. Multiple treatment with nitro-IQinduced significant SCEs to a plateau level of 0.90 per chromosome.Cytogenetic damage in the liver by IQ was greater than thatby nitro-IQ. These results show that this assay of chromosomeaberrations and SCEs in rat liver in vivo without partial hepatectomyor mitogen treatment in vivo is a sensitive method for evaluatingthe cumulative tumor-initiating activities of carcinogenic heterocyclicamines at low doses and should be useful for the detection ofunknown hepatocarcinogens.     

Proton Beam Therapy for Patients with Esophageal Carcinoma

Fifteen patients with esophageal carcinoma (superficial, sixcases; advanced, nine cases) were treated with 250 MeV protonbeam irradiation with or without external x-ray irradiation(12 MV linear accelerator) from October, 1985, to May, 1991.Eleven patients were initially treated with x-ray at doses of16.2-50.4 (mean 42.5) Gy, followed by proton beam at doses of30.0-52.9 (mean 37.6) Gy. The other four patients were treatedwith proton beam alone at total doses of 75.0-88.5 (mean 81.4)Gy. The mean total dose for the 15 patients was 80.4 Gy. Asa result, the primary tumor lesions of all 15 patients disappearedand complete responses were obtained. Approximately four tofive months later, nine of the 15 patients developed esophagealulcer formations at the circumferences of their primary lesions.The ulcerations were healed, however, by conservative management.There was no evidence of local recurrence throughout the observationson six cases of superficial carcinoma. Among nine advanced carcinomapatients, three relapsed into esophageal carcinoma. Recurrenceswere observed eight, 16 and 44 months, respectively, after thetreatment. Ten of the 15 patients died, but eight died of otherdiseases. Three of four cases at autopsy did not show any cancercells in irradiated primary lesions. Four of the 15 patientslived for over five years. The results suggest that a high doseof irradiation delivered by a well-defined proton field couldresult in improved local control and long-term survival in esophagealcarcinoma without undue risk of injury to primary and adjacentorgans.     

Inhibition of 1,2-Dimethylhydrazine-induced Oxidative DNA Damage by Green Tea Extract in Rat

Following subcutaneous injection of 1,2-dimethylhydrazine (DMH), which is carcinogenic to rat colon and liver, to Sprague-Dawley rats, a significant increase of 8-hydroxydeoxyguanosine (8-OHdG) was observed in the DNA of colonic mucosa and liver. The 8-OHdG formation reached the maximal level at about 24 h after the DMH injection. On the other hand, no increase of 8-OHdG was observed in the DNA of the kidney. Drinking green tea extract (GTE) for ten days prior to the DMH injection significantly inhibited the formation of 8-OHdG in the colon. These findings demonstrate that DMH causes oxidative damage to the DNA of its target organ, and that GTE protects colonic mucosa from this oxidative damage.