Anticonvulsant Activity of Extracts of Diospyros Fischeri Stem Bark

Evaluation of extracts of Diospyros fischeri Gurke (Ebenaceae), which is used traditionally for the treatment of epilepsy shows that the aqueous extract of the tem bark has no effect againstpicrotoxin induced convulsions in mice. However, an 80% ethanol extract of the bark caused dose-dependent suppression of convulsions induced by 10 mg/kg body wt picrotoxin, at doses between 100–3200 mg/kg body wt. Petroleum ether, 1:1 dichloromethane:methanol, and methanol extracts also suppressed picrotoxin-induced convulsions, but had a slightly lower inhibitory effect. The petroleum ether extract was the most active, but all were less active than the ethanol extract. Unlike phenobarbitone, which at 50 mg/kg body wt completely suppressed convulsions induced by 10 mg/kg body wt picrotoxin, none of the plant extracts completely suppressed convulsions in the mice. These results support the traditional uses of D.fischeri for the treatment of epilepsy. Given the seemingly innocuous nature of the extracts more work is suggested to ascertain their clinical application.     

胰胆管十二指肠乳头X线解剖与胆囊切除后胆源性腹痛

为研究胆管十二指肠乳头部的Ｘ线解剖与胆囊切除后胆源性腹痛发生间的关系，回顾性研究胆囊切除后胆源性腹痛连续ＥＲＣＲ检查７６例，术前病变为胆囊结石，慢性胆囊炎，胆管胰腺未发现病变。     

Overexpression of p53 in hepatocellular carcinomas: A clinicopathological and prognostic correlation

Abstract Overexpression of the p53 tumour suppressor gene is one of the most common abnormalities in primary human cancers and appears to be a result of point mutation within a highly conserved region of the gene with subsequent encoding for a mutant, more stable protein. In this study, 71 surgically resected hepatocellular carcinomas (HCC) were examined to study the expression of the p53 gene, its relation with clinicopathological parameters and its prognostic significance. Using immunohistochemical detection for mutant p53 protein with monoclonal antibody PAb1801, p53 overexpression was found in 22 tumours (31%) but in none of the non-tumorous liver specimens. Overexpression of p53 was more frequent in tumours with poor cellular differentiation ( P = 0.01), in tumours > 5 cm in diameter ( P = 0.05), and in those with giant cells present ( P = 0.03) and, less significantly, of massive type of Eggel's classification ( P = 0.06). It did not have any significant correlation with hepatitis B or C status, background liver disease or serum α-fetoprotein levels, nor was it related to tumour invasiveness (venous permeation, direct liver invasion and tumour microsatellite formation). In addition, the presence of p53 mutant protein did not influence tumour recurrence or patients' survival rates. The data suggested that p53 mutation in HCC was associated with a later stage of oncogenesis. However, it was not apparently related to tumour invasiveness/aggressiveness and prognosis.     

The Laugier–Hunziker syndrome

Laugier and Hunziker described a syndrome consisting of asymptomatic benign areas of hyperpigmentation affecting the lips, buccal mucosa and, in 50%, the fingernails. We report a 67-year-old woman with the clinical features of Laugier-Hunziker syndrome in association with vulval pigmentation. Histology, immunohistochemistry and electron microscopy from the various areas of pigmentation on the body confirmed the benign nature of the pigmentation. We review potential causes of oral and genital pigmentation, and suggest an expansion of the original syndrome described by Laugier and Hunziker to include more widespread areas of benign hyperpigmentation, which may associated.     

Ranitidine 300 mg twice daily and 150 mg four-times daily are effective in healing erosive oesophagitis.

BACKGROUND: Ranitidine 150 mg q.d.s. is the currently recommended dosage in the United States for the treatment of erosive oesophagitis. To determine whether a higher dose of ranitidine administered less frequently would also be effective in healing erosive oesophagitis, we compared ranitidine 300 mg b.d. with ranitidine 150 mg q.d.s. in the treatment of erosive oesophagitis. METHODS: This multicentre, double- blind, randomized, placebo-controlled study conducted in the United States compared two dosages of ranitidine in 772 patients with endoscopically diagnosed erosive oesophagitis. Patients were treated with ranitidine 300 mg b.d., ranitidine 150 mg q.d.s. or placebo for up to 12 weeks. Endoscopies were repeated after 4, 8 and 12 weeks of treatment. RESULTS: Ranitidine 300 mg b.d. was significantly more effective than placebo in healing erosive oesophagitis at weeks 8 and 12 (51 vs. 36% and 66 vs. 52%, respectively; P < or = 0.004). Significantly higher healing rates were also achieved with ranitidine 150 mg q.d.s. compared with placebo at 4, 8 and 12 weeks (37 vs. 21%, 62 vs. 36% and 77 vs. 52%, respectively; P < 0.001). Healing rates were significantly higher with ranitidine 150 mg q.d.s. than with ranitidine 300 mg b.d. at all scheduled endoscopies (P < or = 0.041). CONCLUSIONS: Ranitidine 300 mg b.d. is effective in healing erosive oesophagitis and may be appropriate as an alternative dosage regimen to ranitidine 150 mg q.d.s. in some patients with erosive oesophagitis.     

Proteoglycan metabolism in normal and inflammatory human macrophages

To study proteoglycan metabolism in inflammatory macrophages, primary cultures of human macrophages were cultured in the absence and presence of bacterial lipopolysaccharide (LPS). When exposed to [35S]sulfate, the cells incorporated the label almost exclusively into chondroitin sulfate proteoglycan (CSPG), which was recovered from the culture medium and the cell layer. Cells stimulated with LPS secreted approximately three times more [35]CSPG into the culture medium than control cells. Furthermore, cell adhesion was also found to promote proteoglycan secretion; when nonadherent monocytic cells were induced to adhere, the release of proteoglycan increased two times. The increased secretion seen in LPS-stimulated macrophages was partly due to increased biosynthesis, but was mostly due to increased sorting of CSPG to the secretory pathway. Only about 20% of the CSPG synthesized in unstimulated cells was secreted, whereas the corresponding figure in LPS-treated cells was 35%. In both cell types, the remaining [35S]CSPG was degraded, probably in the lysosomes. The degradation was a two-step process. First, the [35S]CSPG was rapidly cleaved to yield free glycosaminoglycan (GAG) chains (t1/2 = 15 to 30 minutes). Secondly, the GAG chains were completely depolymerized (t1/2 = 2 to 3 hours). Neither resting nor LPS-stimulated cells sorted CSPG to intracellular storage, as is evident in many hematopoietic cells. The LPS-treated cells synthesized [35S]CSPG of smaller molecular size than did control cells, with GAG chains of approximate molecular mass of 12 kD versus 16 kD in control cells. No difference was seen in the disaccharide composition of the GAG chains; both LPS-stimulated and unstimulated cells expressed a mixture of 80% to 90% chondroitin 4-sulfate and 10% to 20% chondroitin 4,6-disulfate. N-terminal sequence and Northern blot analysis indicate that the core protein of the CSPG secreted by human macrophages is serglycin.