Advances in the prenatal diagnosis of hematologic diseases

Prenatal diagnosis of hematologic diseases can now be performed with fetal blood, fetal amniotic fluid cell DNA, and fetal chorionic villi DNA. Some hemoglobinopathies can be detected by all three methods, and the choice will depend on the available obstetric and laboratory techniques, as well as the time of presentation of the pregnancy. Hopefully, further development of molecular probes and techniques will soon expand these options to all of the globin disorders. Detection of coagulation disorders in utero currently requires samples of pure fetal blood. Gene cloning is accomplished for some (factor IX and antithrombin III) and is underway for others (factor VIII), and further investigation is necessary to determine whether deficiencies in these gene products are due to gene deletion or to mutant genes linked to polymorphic restriction enzyme sites of diagnostic use. Thus, molecular biology may be applied to prenatal diagnosis of the clotting problems, but this has not yet been accomplished. Disorders affecting the number and/or function of erythrocytes, leukocytes, and platelets can be diagnosed by analysis of fetal blood. Blood samples will continue to be required until more is known about the molecular biology of hematopoiesis. Syndromes that can be diagnosed by chromosome studies should be revealed in cultures of amniotic fluid cells, fetal blood lymphocytes, and chorionic villi cells. Cultured cells can be examined for karyotypes, Y-chromatin, spontaneous or induced chromosome breakage, DNA repair, SCEs, and translocations. The techniques for culturing amniotic cells and fetal blood white cells are established, and those for growing cells from chorionic villi are improving rapidly. Direct preparations of cells from villi only may suffice for some of the above analyses. The study of hematologic disease in utero has thus come full circle, from the use of amniotic cells to determine the sex in X-linked disorders, to fetal blood sampling for the analysis of gene products, then back to amniocentesis for DNA, and now earlier in gestation to chorionic villi. All of this has occurred in less than ten years, and it is anticipated that developments in the next ten years will be equally dramatic. The future should bring all prenatal testing into the first trimester, use molecular probes, and provide for both early diagnosis and early treatment of genetic hematologic disease.     

The use of mineral trioxide aggregate in one-visit apexification treatment: a prospective study

AIM: To assess the outcome of apexification using mineral trioxide aggregate (MTA). METHODOLOGY: Fifty-seven teeth with open apices on 50 patients referred for root canal treatment received an apexification procedure in one appointment with MTA by the same operator. Patients were recalled at 6 months, 12 months and every year thereafter. Blind to the treatment record, two examiners assessed the pre-treatment, post-treatment and control radiographs of the study patients in a dark room using a magnifier. Each apex visible on the radiographs was scored with the periapical index (PAI), and the size of the apical lesion was measured. The presence of an apical bridge was also noted. Kappa-Cohen test was used for examiners calibration. The paired t-test was used for statistical analysis of apical healing. RESULTS: Forty-three cases were included with at least 12 months follow-up. When considering the PAI score and the decrease in size of the apical lesion, healing occurred in 81% of cases. CONCLUSION: Apexification in one step using an apical plug of MTA can be considered a predictable treatment, and may be an alternative to the use of calcium hydroxide.     

口蹄疫患者的护理1例

0　引言　口蹄疫是由口蹄疫病毒引起的一种人、畜共患的急性传染病 ,主要先流行于偶蹄动物如猪、牛、羊等 ,人与患病动物密切接触而感染 ,以小儿发病为多 .现将我科收治的 1例患儿护理体会报告如下 .1　病例介绍　患者 ,男性 ,3岁 ,因发热 4d,疱疹 2 d入院 .患儿于 4d前因饮用未煮的鲜牛奶后出现发热 ,体温 38.5℃左右 ,伴恶心、呕吐 ,病后 2 d口腔粘膜、舌、手、足底部出现红色斑丘疹 .查体 :体温 38.2℃ ,双手掌、指间、双足底及趾间可见散在的丘疹及疱疹 ,疹间皮肤正常 ,口腔粘膜及舌面、舌缘可见较密集红色粘膜疹 ,疹间皮肤正常 .血常规…     

5-HT2C Receptor Desensitization Moderates Anxiety in 5-HTT Deficient Mice: From Behavioral to Cellular Evidence

Background:

Desensitization and blockade of 5-HT_2C receptors (5-HT_2CR) have long been thought to be central in the therapeutic action of antidepressant drugs. However, besides behavioral pharmacology studies, there is little in vivo data documenting antidepressant-induced 5-HT_2CR desensitization in specific brain areas.

Methods:

Mice lacking the 5-HT reuptake carrier (5-HTT^-/-) were used to model the consequences of chronic 5-HT reuptake inhibition with antidepressant drugs. The effect of this mutation on 5-HT_2CR was evaluated at the behavioral (social interaction, novelty-suppressed feeding, and 5-HT_2CR–induced hypolocomotion tests), the neurochemical, and the cellular (RT-qPCR, mRNA editing, and c-fos–induced expression) levels.

Results:

Although 5-HTT^-/- mice had an anxiogenic profile in the novelty-suppressed feeding test, they displayed less 5-HT_2CR–mediated anxiety in response to the agonist m-chlorophenylpiperazine in the social interaction test. In addition, 5-HT2CR–mediated inhibition of a stress-induced increase in 5-HT turnover, measured in various brain areas, was markedly reduced in 5-HTT^-/- mutants. These indices of tolerance to 5-HT_2CR stimulation were associated neither with altered levels of 5-HT_2CR protein and mRNA nor with changes in pre-mRNA editing in the frontal cortex. However, basal c-fos mRNA production in cells expressing 5-HT_2CR was higher in 5-HTT^-/- mutants, suggesting an altered basal activity of these cells following sustained 5-HT reuptake carrier inactivation. Furthermore, the increased c-fos mRNA expression in 5-HT_2CR–like immune-positive cortical cells observed in wild-type mice treated acutely with the 5-HT_2CR agonist RO-60,0175 was absent in 5-HTT^-/- mutants.

Conclusions:

Such blunted responsiveness of the 5-HT_2CR system, observed at the cell signaling level, probably contributes to the moderation of the anxiety phenotype in 5-HTT^-/- mice.