Study of photodynamic treatment for P-388 lympho-leukemia in mice

Data are presented on the results of photodynamic treatment (PDT) of mice DBA2 with transplantable lympho-leukemia P-388. Different regimens of photosensitizer Dimegin and emission were used. Both intravenous PDT and in combination with local PDT should be recommended.     

叔丁基醚的制备

醇或酚与2当量叔丁基溴在0．1当量碳酸铅催化下,35～45℃搅拌1～2．25h,得相应的叔丁基醚,14例收率75％～96％。     

Prostate cancer associated with p53 and Rb deficiency arises from the stem/progenitor cell-enriched proximal region of prostatic ducts

Recently, we have shown that prostate epithelium-specific deficiency for p53 and Rb tumor suppressors leads to metastatic cancer, exhibiting features of both luminal and neuroendocrine differentiation. Using stage-by-stage evaluation of carcinogenesis in this model, we report that all malignant neoplasms arise from the proximal region of the prostatic ducts, the compartment highly enriched for prostatic stem/progenitor cells. In close similarity to reported properties of prostatic stem cells, the cells of the earliest neoplastic lesions express stem cell marker stem cell antigen 1 and are not sensitive to androgen withdrawal. Like a subset of normal cells located in the proximal region of prostatic ducts, the early neoplastic cells coexpress luminal epithelium markers cytokeratin 8, androgen receptor, and neuroendocrine markers synaptophysin and chromogranin A. Inactivation of p53 and Rb also takes place in the lineage-committed transit-amplifying and/or differentiated cells of the distal region of the prostatic ducts. However, the resulting prostatic intraepithelial neoplasms never progress to carcinoma by the time of mouse death. Interestingly, in an ectopic transplantation assay, early mutant cells derived from either region of the prostatic ducts are capable of forming neoplasms within 3 months. These findings indicate that p53 and Rb are critically important for the regulation of the prostatic stem cell compartment, the transformation in which may lead to particularly aggressive cancers in the context of microenvironment.     

Mouse models of prostate adenocarcinoma with the capacity to monitor spontaneous carcinogenesis by bioluminescence or fluorescence

The application of Cre/loxP technology has resulted in a new generation of conditional mouse models of prostate cancer. Here, we describe the improvement of the conditional Pten deletion model of prostate adenocarcinoma by combining it with either a conditional luciferase or enhanced green fluorescent protein reporter line. In these models, the recombination mechanism that inactivates the Pten alleles also activates the reporter gene. In the luciferase reporter model, the growth of the primary cancer can be followed noninvasively by bioluminescence imaging (BLI). Surgical castration of tumor-bearing animals leads to a reduced bioluminescence signal corresponding to tumor regression that is verified at necropsy. When castrated animals are maintained, the emergence of androgen depletion-independent cancer is detected using BLI at times varying from 7 to 28 weeks postcastration. The ability to monitor growth, regression, or relapse of the tumor with the use of BLI lead to the collection of tumors at different stages of development. By comparing the distribution of phenotypically distinct populations of epithelial cells in cancer tissues, we noted that the degree of hyperplasia of cells with neuroendocrine differentiation significantly increases in the recurrent cancer relative to the primary cancer, a characteristic which may parallel the appearance of a neuroendocrine phenotype in human androgen depletion-independent cancer. The enhanced green fluorescent protein model, at necropsy, can provide an opportunity to locate or assess tumor volume or to isolate enriched populations of cancer cells from tumor tissues via fluorescence-based technologies. These refined models should be useful in the elucidation of mechanisms of prostate cancer progression, and for the development of approaches to preclinical intervention.     

Consent Administrator Training to Reduce Disparities in Research Participation

Purpose: The aims for this paper are to summarize the current state of disparities in clinical research participation, discuss regulatory and interpersonal causes for these disparities, and to suggest an approach to address this problem by standardized training for consent administrators.
Organizing Construct: A program based on the Precede-Proceed model for training consent administrators is proposed and described.
Conclusions: The current process for informed consent for research is unstandardized and inadequate, and may contribute to racial and ethnic disparities. Researchers are urged to consider a formal training program for members of their research teams who will be obtaining participants' consent.
Clinical Relevance: An educational program for consent administrators may help to reduce disparities in research participation by improving communication between research staff and potential participants.     

Effect of bilateral destruction of the subretrofacial area on central inspiratory activity of the respiratory center and on the respiratory response to hypercapnia

Local bilateral destruction with 1 M glutamic acid of neuronal structures located between ventral surface of the medulla oblongata and the retrofacial nucleus (subretrofacial area) in rats increases the amplitude of pulses from the phrenic nerve and lowers respiratory rate. Hypercapnia does not affect the amplitude of phrenic nerve pulses but increases respiratory rate. It is suggested that the amplitude of central respiratory activity is regulated by the central chemoreceptors with participation of neuronal structures located in the subretrofacial area. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 5, pp. 491–493, May, 1997