Postsurgical, chronic, nonprogressive, cutaneous ulcers: a possible variant of pyoderma gangrenosum associated with diabetes mellitus

Two patients developed persistent ulcers on the trunk after cutaneous surgery. Both had "chemical" diabetes mellitus. Bacteriologic and histopathologic studies of the ulcers were not revealing of cause. The characteristics of the ulcers are described, and are contrasted with typical lesions of pyoderma gangrenosum and Meleney's postoperative progressive synergistic bacterial gangrene. We believe these patients had variant lesions of pyoderma gangrenosum.     

Changes in the N- and C-terminal sequences of the murine R7 Gag-tMos protein affect brain lesion induction

Our preliminary studies suggested that the novel gag-truncated mos (tmos) open reading frame (ORF) of R7, a spontaneous deletion mutant of Moloney murine sarcoma virus 124 (MoMuSV124), may be responsible for R7's unique ability to induce brain lesions in all R7-injected mice. However, when we replaced the gag-tmos ORF with either the MoMuSV124 or the homologous myeloproliferative sarcoma virus env-mos gene, we found that both recombinant viruses also induced brain lesions in all injected mice. Although these studies suggested that the critical determinants for brain lesion induction may reside in the tmos sequence common to all three viruses, they did not demonstrate if the N-terminus of Mos was dispensable for this activity. By inserting the FLAG sequence at the 3' end of the R7 gag-tmos ORF, we demonstrated that R7 does synthesize a Gag-tMos fusion protein. Using R7 gag deletion mutants with and without the FLAG sequence, we further demonstrated that (i) deletion of the entire gag sequence abolished R7's transforming activity; (ii) the ability of the virus to transform cultured NIH/3T3 cells was significantly reduced only when most of gag was deleted; (iii) the ability of the virus to induce brain lesions was inversely proportional to the extent of its gag deletions; and (iv) the insertion of FLAG at the Mos C-terminus did not reduce the in vitro transforming activity of the FLAG-tagged viruses but did reduce their ability to induce brain lesions. Thus, we have demonstrated that altering the N- or C-terminus of the R7 Gag-tMos fusion protein can affect disease manifestation.     

Small-cell carcinoma of the cervix: fourteen years of experience at a single institution using a combined-modality regimen of involved-field irradiation and platinum-based combination chemotherapy.

PURPOSE: To determine the efficacy and toxicity of a combined-modality regimen of irradiation with platinum-based combination chemotherapy in small-cell carcinoma of the cervix (SCCC). PATIENTS AND METHODS: Thirty-four patients with SCCC were seen and treated at the British Columbia Cancer Agency between May 1988 and November 2002. Two protocols were used, SMCC (May 1988 to December 1995) and SMCC2 (January 1996 to November 2002). Both protocols used cisplatin, etoposide, and involved-field irradiation (essentially pelvis plus or minus para-aortics) with concurrent chemotherapy. In addition, SMCC2 included carboplatin and paclitaxel, and the para-aortics were irradiated routinely. RESULTS: Thirty-one patients received either SMCC (n = 17) or SMCC2 (n = 14), and three patients did not (disease too extensive, n = 1; patient refusal, n = 1; and alternative regimen, n = 1). For the 31 patients treated on one of the protocols, the 3-year overall and failure-free survival (FFS) rates were 60% and 57%, respectively. The results were equivalent for SMCC and SMCC2. Radiologic stage was the only independent predictor for FFS (80% at 3 years for stage I and II patients v 38% at 3 years for stage III and IV patients). Distant failure (28%) was the most common cause of failure, with local failure occurring in 13% of patients. The switch to SMCC2 did not improve efficacy but did lessen the toxicity. CONCLUSION: SCCC can be successfully treated in approximately 55% of patients with a combination of irradiation and platinum-based chemotherapy. Disease extent predicts for chance of curability.     

Protein metabolism in patients with chronic renal failure: role of uremia and dialysis

Individuals with chronic renal failure (CRF) have a high prevalence of protein-energy malnutrition. There are many causes for this condition, chief among which is probably reduced nutrient intake from anorexia. In nondialyzed patients with CRF, energy intake is often below the recommended amounts; in maintenance dialysis patients, both dietary protein and energy intake are often below their needs. Although a number of studies indicate that rats with CRF have increased protein catabolism in comparison to control animals, more recent evidence suggests that increased catabolism in CRF rats is largely if not entirely due to acidemia, particularly if these animals are compared to pair-fed control rats. Studies in humans with advanced CRF also indicate that acidemia can cause protein catabolism. Indeed, nitrogen balance studies and amino acid uptake and release and isotopic kinetic studies indicate that in nondialyzed individuals with CRF, who are not acidemic, both their ability to conserve body protein when they ingest low protein diets and their dietary protein requirements appear to be normal. For patients undergoing maintenance hemodialysis or chronic peritoneal dialysis, dietary protein requirements appear to be increased. The increased need for protein is due, in part, to the losses into dialysate of such biologically valuable nitrogenous compounds as amino acids, peptides, and proteins. However, the sum of the dietary protein needs for CRF patients (of about 0.60 g/kg/day) and the dialysis losses of amino acids, peptides and proteins do not equal the apparent dietary protein requirements for most maintenance dialysis patients. This discrepancy may be due to a chronic state of catabolism in the clinically stable maintenance dialysis patient that is not present in the clinically stable nondialyzed individual who has advanced CRF. Possible causes for such a low grade catabolic state include resistance to anabolic hormones (for example, insulin, IGF-1) and a chronic inflammatory state associated with increased levels of pro-inflammatory cytokines.     

A man with osteoblastic metastasis and hypocalcaemia

We report a case of an 80-year-old man with osteoblastic metastases from advanced carcinoma of the prostate presenting with a grand mal seizure resulting from severe hypocalcaemia. He had low serum phosphate and ionised calcium levels, elevated serum skeletal alkaline phosphatase and intact parathormone levels. 99mTc radioisotope bone scan revealed a "super bone scan" suggestive of osteomalacia. The serum 1, 25-dihydroxycholecalciferol level was unexpectedly elevated. The biochemical abnormalities persisted despite high dose calcium replacement, but improved with supraphysiological doses of 1,25 (OH)2 vitamin D3 (Rocaltrol) therapy. We hypothesise that the hypocalcaemia in this patient was due to vitamin D resistance secondary to a humoral factor secreted by the tumour.     

抗补体蛋白对大鼠局灶脑缺血损伤的作用

0　引言　近年来脑缺血损伤的早期炎症受到重视 .有学者观察到在人脑梗塞部位白细胞集聚 ,临床预后与梗塞部位的白细胞数量有关 ,白细胞多者预后差 [1 ] .还有文献描述了大鼠持续性脑缺血损伤中的多形核中性细胞反应的时间过程 ,收稿日期 :1999-0 3 -2 6;　修回日期 :1999-0 5 -13基金项目 :国家自然科学基金资助项目 ( 3 9170 3 15 ) ;全军医药卫生科研基金资助项目 ( 92 5 0 5 2 )作者简介 :刘　立 ( 195 8-) ,男 (汉族 ) ,江苏省无锡市人 .副教授 ,博士 .Tel.( 0 2 9) 3 3 74819缺血 30 min就可以观察到多形核中性细胞于缺血部位的微血…