Mesoporous SnO2@carbon core-shell nanostructures with superior electrochemical performance for lithium ion batteries.

SnO2@carbon nanostructure composites are prepared by a simple hydrothermal method. The composite exhibits unique structure, which consists of a mesoporous SnO2 core assembled of very small nanoparticles and a carbon shell with 10 nm thickness. The mesoporous SnO2@carbon core-shell nanostructures manifest superior electrochemical performance as an anode material for lithium ion batteries. The reversible specific capacity of the composite is about 908 mAh g(-1) for the first cycle and it can retain about 680 mAh g(-1) after 40 charge/discharge cycles at a current density of 0.3 C. Moreover, it shows excellent rate capability even at the high rate of 4.5 C. The enhanced performance was attributed to the mesoporous structure and a suitable carbon coating.

[Lectins in gastric carcinoma and precancerous lesions].

Three lectins (PNA, PHA, dBA) were used to study gastric carcinoma (66 cases), lymph node metastatic tumors (32), normal gastric mucosa (10), dysplasia (30), and intestinal metaplasia with gastritis (43). The intestinal metaplasia with quite abundant PHA and DBA receptors was closely related to gastric carcinoma. The positive rate of PHA receptors increased progressively in order of mild dysplasia, moderate dysplasia, severe dysplasia and gastric carcinoma. The distribution of PHA and PNA receptors was correlated with the histologic type and the degree of differentiation. 81.3% lymph node metastatic tumors produced cellular glycoconjugates, which differed in lectin binding profiles from those made by the cells in the respectively primary carcinoma. More PHA receptors were produced by the lymph node metastatic tumors than primary carcinoma.

Effect of selenium on aflatoxin hepatocarcinogenesis in the rat.

The effects of selenium (Na2SeO3) on aflatoxin B1 (AFB1)-induced hepatic neoplasia were studied in the rat. Putative preneoplastic foci and nodules composed of basophilic, eosinophilic, and clear cells developed early. Basophilic foci were seen first; in the later stages basophilic and eosinophilic nodules predominated. At each stage the AFB1 + Se groups showed fewer and smaller foci and nodules than the AFB1 - Se group. The number of foci in the AFB1 + 3 ppm Se group and their mean area were smaller than those in the 6 ppm Se + AFB1 group. At the end of the experiment hepatocellular carcinoma (HCC) was found in 11/18 rats (61%) of the AFB1 - Se group. HCC was not found in either of the groups given AFB1 + Se. We conclude that Se had an inhibitory effect on the initiation and promotion stages of AFB1-induced preneoplastic foci and nodules. Se also prevented progression of these nodules to HCC even after cessation of AFB1 administration. The inhibitory effect of Se at 3 ppm was greater than at 6 ppm. The 6 ppm Se group also showed evidence of toxicity.

[Evaluation of DNA content in gastric dysplasia and carcinoma by image cytometry].

In 30 cases of gastric dysplasia and 10 cases of gastric carcinoma, DNA content was studied by IBAS image analysis system. The mean DNA level increased steadily with the advance of histologic gradation, and the highest DNA content was observed in gastric carcinoma. No case of aneuploidy was found in mild dysplasia. In moderate dysplasia, aneuploid cells were occasionally encountered. Severe dysplasia had a lower percentage (4.48%), and gastric carcinoma was characterized by a high percentage of aneuploid cells (14.54%).

A study on the inhibition of aflatoxin B1 induced hepatocarcinogenesis by the Rhizopus delemar.

The effect of Rhizopus delemar on the carcinogenicity in rats of Aflatoxin B1 was studied. The Aflatoxin B1 was administered in free drinks to each male wistar rat at 126 micrograms per week such that a total dose of 3.40 mg was given over a period of 27 weeks. The culture abstract of Rhizopus delemar was added simultaneously to a group of these rats by mixing the Aflatoxin B1 solution. Animals were killed separately during 18th, 30th, 38th and 52nd week. Liver cell altered foci and neoplasms were qualified by using light microscopic and electromicroscopic morphology, by the morphometry and by the enzymic reactions. In the group of Aflatoxin B1 the incidence of hepatocellular carcinoma was 71%. In the group receiving Rhizopus delemar together with Aflatoxin B1, the hyperplastic foci and pathological enzymic foci were decreased at all times pointed and atd at termination, and in none of the rats had liver neoplasms appeared. The result of this experiment showed that the Rhizopus delemar has intensive capacity in inhibiting the toxic damage and carcinogenicity of the liver by the Aflatoxin B1, because it is not only able to postpone the appearance of altered foci and to control their development but also to accelerate their withdraw in advance. The Rhizopus delemar can be used as a feasible and efficacious means to control the intoxication of Aflatoxin B1.

[Cell kinetics in intestinal metaplasia and gastric carcinoma].

48 specimens of gastric mucosa, including those of normal mucosa, intestinal metaplasia, atypical hyperplasia and carcinoma, were studied with in vitro 3H-TdR double labeling autoradiographic technique. On the basis of cell kinetics, intestinal metaplasia might be divided into two types: Type A consisted of those cases in which the values of LI, Ts and Tc were approximately closer to those of normal mucosa. The labeling cells appeared in the lower two thirds of the intestinalized glands, including small intestinal type and the complete type of colonic intestinal metaplasia. In type B, the average values of LI were higher. Ts and Tc values approximated those found in carcinoma a. Type B consisted mostly of the incomplete type of colonic intestinal metaplasia. The above evidence suggests that type B intestinal metaplasia is precancerous.

Types of mucosal metaplasia in relation to the histogenesis of gastric carcinoma.

One hundred thirty-nine surgically resected stomachs and 16 stomachs obtained at necropsy in China were studied histochemically to evaluate the types and distribution of mucosal metaplasia in relation to benign and malignant disease. Three classes of mucin were distinguished: small-intestinal (N-acylated sialomucin); colonic (sulfated and O-acylated sialomucin); and gastric (neutral mucin). Small-intestinal type of metaplasia (SIM) occurred in 95% of instances of atrophic gastritis, 36% of cases of superficial gastritis, 60% of cases of gastric ulcers, and 39% of cases of duodenal ulcers. Colonic type of metaplasia (CIM) was less common and was found in only 11% of benign lesions. It was located in the antrum, particularly on the lesser curvature. Mucin was present in 66 of 84 carcinomas. The stomach tumors fell into three histochemical groups: colonic (acid mucin), 32; gastric (neutral mucin), 19; and mixed (acidic and neutral), 15. In 94% (30/32) of colonic type of gastric carcinoma, CIM was present. Thus, CIM is related to development of colonic type of gastric carcinoma, whereas SIM is a nonspecific reaction to mucosal damage.

The detection of serotonin and gastrin in gastric carcinoma.

It is believed that the immature precursor cells of gastric mucosa have multidirectional potency of differentiation and these cells can differentiate into both endocrine and nonendocrine tumor cells. Fifteen cases of surgically resected stomach with gastric nonendocrine carcinoma were studied by the three-layer immunoperoxidase method. Serotonin was found in five cases, gastrin in one case, and both serotonin and gastrin in three cases. Serotonin also was detected in the noncancerous mucosa in thirteen cases: ten showing positive cells in the antrum and seven in the body. Gastrin was found in the noncancerous mucosa in 13 cases: eight in the antrum, five in the body. In four cases, a few serotonin positive cells were found in glands showing intestinal metaplasia. No correlation was found between the endocrine tumor cells and the types of carcinoma. Because endocrine cells can be detected in general types of gastric carcinoma, these findings suggest that the different kinds of cancer cells (endocrine and nonendocrine) may have a common origin.