Financial effect of clinical decisions: case study of a dialysis center

This paper explores, in the isolated guinea-pig ileum, the effects of temperature on the acute development of opioid dependence and on the precipitation of the abstinence response, using as reference the effect of temperature on the response to a standard nicotine concentration. Additionally, the influence of temperature on acute morphine neurodepression was examined. Three experimental groups were included. In the first, the bath temperature was adjusted and maintained along the experimental session (2.5 h) at one of the following values: 28, 32, 36 or 40 degrees C. In the second, the different values of bath temperature were applied only during the period of morphine exposure before testing the abstinence response at 36 degrees C. In the third, all segments were initially incubated at 36 degrees C for 1 h, and afterwards, abstinence and the nicotine response were elicited at the different temperatures mentioned. In all the series, a single challenge naloxone dose (3.1, 10, 31, 100, 316, 1000 or 3160 nM) was administered after 1h of morphine and complete naloxone concentration-response curves were obtained. The abstinence response was expressed as a percentage of the nicotine reference response. All segments showed robust nicotine responses at all the experimental protocols tested indicating that, at the temperature range studied, the contractile mechanisms were impaired. This study showed that changes in bath temperature modify the magnitude of acute morphine neurodepression, and of the abstinence response but did no affect the development of acute opioid dependence. These data, along with several lines of evidence, strongly suggest that acute neurodepression, the development of opiate dependence and antagonist-precipitated abstinence are separable. Results are discussed on the basis of drug-receptor interactions.     

Biochemical mediators of meningeal inflammatory response to group B streptococcus in the newborn piglet model

The meningeal inflammatory response to a heat-killed mutant unencapsulated strain of type III group B Streptococcus (GBS) was studied in a newborn piglet model. GBS (10(9) colony-forming unit equivalents) or saline (control) was inoculated intraventricularly. Serial cerebrospinal fluid measurements were done at baseline and over the course of the next 24 h for cytochemical changes and production of tumor necrosis factor (TNF) and prostaglandins. In separate experiments, we defined the time course of early changes during the first 6 h and dose response relationship over a range of inocula 10(6) to 10(9) colony-forming unit equivalents. The intraventricular inoculation of the heat-killed unencapsulated GBS induced marked leukocytosis and increased protein by 6 h. These changes were preceded by a several hundredfold increase in TNF (maximum at 2 h) and prostaglandins (maximum at 2-4 h). The early and sharp rise in TNF suggests its pivotal role in initiating the inflammatory cascade. The magnitude of the inflammatory response increased with increasing bacterial dose over the range studied. To study the effect of encapsulation of GBS in the induction of meningeal inflammation, we compared the response to the unencapsulated mutant strain with that to the encapsulated parent strain. The encapsulated strain produced much smaller inflammatory changes, and only with high doses of bacteria. The GBS cell wall appeared to be the primary bacterial product triggering inflammation. Intraventricular injection of the heat-killed unencapsulated GBS with exposed cell wall can serve as a valid model for studying neonatal meningitis.     

Restricted mandibular opening complicating intraoral galeal flap reconstruction and radiotherapy: case report

The delto-pectoral flap has been used to repair burned scar in the faciocervical region for some years. However, its limited size restricts its application. Furthermore, direct transfer of the flap may result in a swelling and inexpressive face and the donor site needs skin grafting. To avoid the above disadvantages, we have tried pre-expansion of the flap. In this article, the authors report the experiences in the application of the method to eighteen cases, including the surgical procedure, the applied anatomy, and typical cases as well. Also included in the article are the comparison between various therapies to the burned scar of the face, the key points for successful pre-expansion of the delto-pectoral flap, accurately maintaining the desired position. The method has been proved to have many advantages and can be widely applied.     

The granulomatous response in murine Schistosomiasis mansoni does not switch to Th1 in IL-4-deficient C57BL/6 mice

IL-4 plays an important role in polarizing inflammation toward a Th2 response. It remains uncertain, however, whether IL-4 also serves to prevent expression of Th1 inflammation. Therefore, using a genetically pure C57BL/6 IL-4-deficient mouse, we studied the role of IL-4 in regulating the production of IFN-gamma and Th1 inflammation in the granulomas of mice infected with Schistosoma mansoni. In contrast to normal animals, IL-4 mutant mice generated smaller liver granulomas that contained fewer eosinophils and no mast cells. Collagenase-dispersed granuloma cells were analyzed by flow cytometry and cultured in vitro to measure cytokine and Ig production. Compared with control granuloma cells, IL-4-/- cells secreted only small quantities of IL-5 and IL-10. Also, there was impaired expression of the IL-4-dependent molecules IgE and IgG1 as well as B cell surface class II and CD23. Yet the granulomas of IL-4 -/- animals produced little IFN-gamma, IgG2a, or other molecules associated with Th1 inflammation even after Ag or anti-CD3 stimulation. Splenocytes from IL-4 -/- animals stimulated with schistosome Ag also failed to produce a Th1 response. Our data show that most aspects of the Th2 response in murine schistosomiasis are highly dependent on IL-4 production. But in the absence of IL-4, neither the natural local granulomatous response to schistosome ova nor the systemic response to soluble egg Ag switches to the type 1 phenotype. Thus the production of IL-4 early in the inflammatory response is not the only factor preventing Th1 expression in inflammation.     

Quantitative measurements of desmin and vimentin immunostains and cell density in leiomyomas and leiomyosarcomas

The distinction between benign and malignant smooth muscle tumours relying on histological features such as the mitotic index and pleomorphism remains a generally acknowledged difficulty in modern pathology. A cell image processor was therefore used to quantitatively assess the desmin and vimentin immunostain in 39 smooth muscle tumours which included 26 benign (leiomyomas) and 13 malignant (leiomyosarcomas) cases. The 13 leiomyosarcomas were primary (non-recurrent and non-metastatic). Ploidy level and cell density were also assessed on each of these 39 tumours by means of the computer-assisted microscopic analysis of 5-microns thick Feulgen-stained histological sections. The results show that while neither the ploidy level determination nor the quantitative assessment of the vimentin immunostain made it possible to distinguish between leiomyomas and leiomyosarcomas, cell density determination and the quantitative assessment of the desmin immunostain enabled such a distinction to be made. Indeed, the leiomyomas exhibited a much higher level of desmin positivity than the leiomyosarcomas, as did diploid tumours as compared to the aneuploid (benign or malignant) ones. Furthermore, the leiomyoma group exhibited a significantly lower mean cell density value than the leiomyosarcoma group. The present study further confirms the lack of relationship between ploidy level and cytological malignancy in smooth muscle tumours.