Depression and quality of life in living related renal transplantation.

BACKGROUND: More than other operations on the body, organ transplantation has a psychological resonance relating to the self and body image representation, both in donors and in recipients. In the medical literature there are many psychopathological patterns related to ESRD and to the changes in psychologic assessment and lifestyle after transplantation. Similar changes have been found in living donors. METHODS: Forty-eight donor-recipient couples were evaluated before and 4 months after transplantation, using clinical interview, according to the DSM IV TR criteria; The structured Interview for renal transplantation, both for recipients and for donors; psychodiagnostic tests: mini-mental state; Hamilton Rating Scale for Depression; Hamilton Anxiety Scale; Self-Rating Anxiety Scale; Short-Form 36 Health Survey Questionnaire. RESULTS: Comparisons by paired Students t tests showed a significant Hamilton depression variation among recipients, with improvement in the gained score and reduction of depressive symptom (Hamilton score >7) frequency from 45.8% to 32%, and a decreased proportion of patients with a score >18 from 16.4% to 0%. There was no significant Hamilton Depression variation among donors, but there was somehow a reduction in depressive symptom frequency (Hamilton score >7) from 37.5% to 33.3% and a decrease among >18 scores from 12.6% to 0% patients. CONCLUSIONS: Living donor kidney transplantation did not adversely affect the lives of donors and significantly improved many aspects of the lives of recipients. However, physical and psychological aspects may be impaired by living donation. Careful donor selection, with appropriate pretransplantation psychiatric consulting, allows those with a normal life quality to donate without consequence to their physical or psychological status.

Effects of medetomidine on intestinal and colonic motility in the dog.

The motor responses of the jejunum and colon to stimulation of alpha 2-adrenoceptors by medetomidine and clonidine were investigated in four dogs. In fasting dogs, medetomidine, at a dose rate of 30 micrograms/kg i.v., disrupted the migrating myoelectric complex (MMC) pattern of the small intestine for about 2 h. Similar, but shorter-lasting effects were also induced by clonidine (30 micrograms/kg i.v.) on the jejunum. The administration of alpha 2-agonists inhibited colonic motility in fasting dogs, although medetomidine-induced inhibition was preceded by a short period of increased muscle tone. All these effects were reversed by the alpha 2-antagonists atipamezole (0.15 mg/kg i.v.) and yohimbine (0.20 mg/kg i.v.). In fed dogs, medetomidine (30 micrograms/kg i.v.) induced a strong increase of the tone on the proximal colon, while the activity of the medium and distal colon was completely suppressed. Yohimbine (0.50 mg/kg i.v.) immediately restored the activity of the colon and induced a propagated giant contraction and defaecation by the animal. These data confirm the importance of alpha 2-adrenergic receptors in the control of intestinal and colonic motility in the dog.

Effects of CGRP in different models of mouse ear inflammation.

The anti-inflammatory activity of calcitonin gene-related peptide (CGRP) has been studied in cutaneous inflammation induced by croton oil (CO), arachidonic acid (AA), tetradecanoylphorbol acetate (TPA) or cantharidin (CA). Our results show that mouse ear inflammation induced by CO, AA or TPA is decreased by topical administration of CGRP, whereas that induced by CA is not affected. The dose-response and temporal analysis of CGRP effect show that the maximal activity is present at the dose of 30 pmol/ear and when administered 30 min after the irritating agent. Moreover, pretreatment with capsaicin is able to mimic the anti-inflammatory effect of exogenous CGRP, while simultaneous administration of CGRP and capsaicin produces a reduced response. Our results suggest that CGRP released from sensory.

Protective effects of calcitonin gene-related peptide in different experimental models of gastric ulcers.

Intravenous administration of calcitonin gene-related peptide (CGRP) prevented in a dose-dependent manner reserpine-induced gastric mucosal damage, but failed to affect the lesions produced by ethanol administration. In pylorus-ligated rats, CGRP significantly reduced gastric volume, total acid and peptic activity output as well as ulcer formation. These protective effects of CGRP were not present when rats were pretreated with cysteamine. Our data suggest that CGRP exerts its antisecretory and antiulcer activity, at least in part, by interfering with somatostatin transmission.

Assignment of the human heterogeneous nuclear ribonucleoprotein A1 gene (HNRPA1) to chromosome 12q13.1 by cDNA competitive in situ hybridization.

Heterogeneous nuclear ribonucleoprotein (HNRP) core protein A1 is a major component of mammalian HNRP particles. The human HNRP A1 protein was shown to be encoded by a 4.6-kb gene, split into 10 exons, belonging to a multigene family of about 30 A1-specific sequences per haploid genome, many of which correspond to pseudogenes of the processed type. Here we report the mapping of the human HNRPA1 gene to band 12q13.1. Localization was performed by nonisotopic in situ hybridization using a phage genomic clone that contains the active HNRPA1 gene as well as 13.5-kb flanking sequences. To suppress hybridization to pseudogene sequences, unlabeled HNRPA1 cDNA was added in excess over the probe to the hybridization mixture.

In situ hybridization to cytogenetic bands of yeast artificial chromosomes covering 50% of human Xq24-Xq28 DNA.

From the collection described by Abidi et al., 102 yeast artificial chromosomes (YACs) with human DNA inserts more than 300 kb in length were assigned to chromosomal band positions on early metaphase chromosomes by in situ hybridization using the biotin-avidin method. All the YACs hybridized within the Xq24-Xqter region, supporting the origin of the vast majority of the YACs from single human X-chromosomal sites. With assignments precise to +/- 0.5 bands, YACs were distributed among cytogenetic bands to roughly equal extents. Thus, there is no gross bias in the cloning of DNA from different bands into large YACs. To test band assignments further, hybridizations were carried out blind, and band positions were then compared with (1) probe localizations in cases in which a reported location was present in one of the YACs; (2) cross-hybridization of a labeled YAC with others in the collection; and (3) hybridization to a panel of DNAs from a series of hybrid cells containing Xq DNA truncated at various regions. Of 31 cases in which YACs contained a probe with a previously reported location, 28 in situ assignments were in agreement, and 14 other assignments, including one of the three discordant with probe localization, were confirmed by YAC cross-hybridization studies. Results with a group of nine YACs were further confirmed with a panel of somatic cell hybrid DNAs from that region. Five YACs hybridized both to Xq25 and to a second site (four in Xq27 and one in Xq28), suggestive of some duplication of DNA of the hybrid cell and perhaps in normal X chromosomes. The in situ assignments are thus sufficient to place YACs easily and systematically within bins of about 7-10 Mb and to detect some possible anomalies. Furthermore, on the basis of expectations for random cloning of DNA in YACs, the assigned YACs probably cover more than 50% of the total Xq24-Xq28 region. This provides one way to initiate the assembly of YAC contigs over extended chromosomal regions.

Effects of salmon calcitonin on plasma renin activity and systolic blood pressure in the rat.

Salmon calcitonin, centrally injected, increased plasma renin activity and blood pressure in rats. It is possible that the peptide through an action on the central serotonergic tone stimulated plasma renin activity with subsequent enhancement of blood pressure. Conversely, peripheral administration of the peptide increased plasma renin activity but did not cause changes in blood pressure. Probably, the enhancement of renin may be a physiological response to the renal activity of calcitonin; however, this activity does not seem to involve urinary prostaglandins.

Prevention of compensatory ovarian hypertrophy by local treatment of the ovary with 6-OHDA.

The possible role of a neural mechanism involved in the development of compensatory ovarian hypertrophy has been studied. A new technique, the use of a special plastic capsule, has been developed to allow chronic local treatment of the ovary. Local treatment of one of the ovaries with 6-hydroxydopamine (6-OHDA) resulted in a weight increase in the other ovary. In the unilaterally ovariectomized rat the local application of 6-OHDA on the ovary blocked the development of compensatory ovarian hypertrophy. Local treatment of the ovary with dopamine (DA) did not interfere with the compensatory ovarian growth of the other ovary. Data suggest that intact adrenergic afferent and efferent neural elements of the ovary are required for the development of compensatory ovarian hypertrophy.