1,721,021 research outputs found
OSSITOCINA SINTETICA INTRAPARTUM : EFFETTI SULLA LATTOGENESI
No full textNumerose pratiche mediche e farmaci somministrati comunemente intrapartum sono stati sino ad ora associati a molteplici effetti avversi sull’equilibrio materno- neonatale, anche se in modo non univoco. In questa ricerca sono state considerate l’induzione del travaglio di parto con prostaglandine, la somministrazione di ossitocina sintetica e l’analgesia epidurale.
Attraverso uno studio osservazionale prospettico di coorte sono state analizzate 270 cartelle cliniche di puerpere sane da parto spontaneo a termine di gravidanza (dalla trentasettesima settimana di epoca gestazionale), con feto singolo. È stato valutato il momento di lattogenesi, escludendo chi non volesse o non potesse allattare al seno, o avesse subito ricoveri neonatali o fosse incorso in altre problematiche rilevanti.
Del campione totale il 44% ha richiesto la somministrazione ossitocica durante il travaglio per tempi più o meno lunghi, il 31% è stato indotto con prostaglandine, e più della metà delle donne (51,9%) è ricorsa ad analgesia epidurale.
Al 67% delle donne che hanno subito l’induzione ed al 62% delle donne sottoposte ad analgesia epidurale è stato necessario somministrare anche ossitocina per infusione endovenosa.
La galattogenesi si è verificata mediamente in terza giornata nell’intero campione esaminato, con un valore minimo di 1 ed un massimo di 6 giorni. La pluriparità si associa ad una curva di distribuzione di produzione del latte più anticipata rispetto alle donne al primo figlio. Pur essendo stato rilevato un ritardo nella lattogenesi in donne che avessero subito una qualunque delle procedure considerate, una significatività statistica (p <0,05) è stata evidenziata solo in due casi: nelle terzipare sottoposte ad ossitocina quasi per l’intera durata del travaglio in associazione all’analgesia, e nelle secondipare e terzipare indotte con prostaglandine a cui fosse stata somministrata ossitocina per più di due ore durante il travaglio.
L’aver subito una somministrazione di ossitocina in associazione all’epidurale porta quindi come conseguenza la stessa tempistica nella produzione del latte tra primipare e pluripare.
La maggiore età materna si correla con un diminuito ricorso a procedure mediche e con una riduzione dell’intervallo tra parto e montata lattea. Questo si spiega con il crescere della parità al crescere dell’età materna, e col diminuito rischio di subire procedure multiple nelle donne pluripare.
L’aspetto fondamentale che si deduce dallo studio è che il disagio e lo stress materno giocano una parte non secondaria nella ritardata produzione di latte. L’ipercortisolemia e l’importante attivazione del sistema ipotalamo- ipofisi- surrene fisiologicamente presenti in gravidanza esercitano un’inibizione nei confronti della prolattina e degli ormoni lattogenici. L’adrenalina e il cortisolo (ormoni dello stress) sono up- regolati dal progesterone, presente ad alti livelli fino al secondamento. Dopo il parto la drastica caduta del progesterone permette al sistema adrenergico di ritornare alla normalità, con una transitoria soppressione del CRH ipotalamico e un aumento di estrogeni, così da permettere l’azione di prolattina e ossitocina. Risulta quindi cruciale il calo di cortisolo nel postpartum per consentire la produzione di latte materno.
La medicalizzazione del parto, però, può creare uno stato di allerta, se la donna vive l’esperienza come una situazione allarmante. Questo mantiene un’attivazione prolungata del sistema adrenergico, con la permanenza in circolo di fattori che bloccano il rilascio di prolattina. Il fattore più facilmente osservabile in questo quadro è un ritardo nell’arrivo del latte. La medicalizzazione può quindi influire sulla ritardata lattogenesi, non tanto per effetto diretto dei farmaci, quanto per lo stimolo stressante al rilascio di adrenalina, che down- regola gli ormoni necessari alla produzione di latte.
Ulteriori studi condotti in modo prospettico sono necessari per stabilire l’esistenza di una relazione causale tra le procedure mediche intrapartum e la ritardata lattogenesi, in modo da confermare la tesi sostenuta dalla presente ricerca
Surface expression of alien hybrid IE/C antigens on the reticulum cell sarcoma of SJL/J mice
No full textImmunological and cytogenetic characterization of lymphocitic mouse leukemias after treatment with antineoplastic drugs
No full textNew antigenic specificities, not detectable on parental cells and transmissible after the drug withdrawal, have been induced in mouse lymphomas by a treatment with antineoplastic agents. Some surface properties and chromosome analysis of drug-altered cells have been studied
Serological demonstration of an allogeneic Ia.7 antigen on the cell surface of SJL/J-derived reticulum cell sarcomas
No full textThe reticulum cell sarcomas (RCS) of SJL/J mice are of particular interest since they readily induce the proliferation of syngeneic T-lymphocytes. Previous cellular studies examined the antigens on the RCS which stimulated this response and suggested that the tumor expressed allogeneic I-region-associated (Ia) antigens normally associated with the E alpha:E beta molecular complex (S. M. Wilbur and B. J. Bonavida, Exp. Med., 153: 501-513, 1981). These particular Ia glycoproteins are not expressed on normal SJL/J cells due to a defect in the E alpha polypeptide synthetic pathway. However, the E beta subunit is synthesized normally by these animals but remains intracellular. The SJL/J-derived RCS may circumvent this defect in E alpha subunit biosynthesis. The aberrant synthesis of this polypeptide is thought to allow membrane presentation of an intact pseudoallogeneic Ia glycoprotein which utilized the normally dormant E beta s polypeptide. In the present study, two monoclonal antibodies directed against the Ia.7 specificity of the E alpha chain (13/18, 14-4-4S) were used to examine more directly the expression of this polypeptide on the tumor. Surprisingly, neither antibody was effective against the RCS in a direct complement-mediated cytolysis assay. Nevertheless, the tumor was found to specifically adsorb lytic activity of both the monoclonal antibodies. In addition, both a cold-cell competition assay and indirect immunofluorescence corroborated the data and indicated that the RCS does express detectable levels of the Ia.7 antigen. Normal spleen cells and lipopolysaccharide B-derived blasts from SJL/J mice were found in all experiments to be devoid of any specific reactivity with these monoclonal antibodies. In addition, continued in vivo passage of transplantable RCS was found to cause down-modulation of the Ia.7 specificities on these tumors. Newer RCS transplantable lines, however, expressed demonstrable levels of this alloantigen in both cellular and serological assays. The observed down-modulation could explain the difficulties encountered in defining this specificity on long-term transplantable RCS. In conclusion, the present serological study corroborates the early cell-binding data. An Ia.7 antigen is shown to be expressed on the RCS, yet this specificity could not be detected on normal SJL/J cells
Inhibitory effect of somatostatin on human T lymphocytes proliferation
No full textSomatostatin (SOM) was originally described as a growth hormone release inhibiting factor, but SOM and its specific receptors (SOM-r) have been shown to be expressed on both normal and activated T and B lymphocytes and other immunocompetent cells. In the present study we have demonstrated that SOM strongly inhibits the proliferation of human T lymphocytes when stimulated by PHA, Con A or alloantigens. However, SOM was most effective when the T cells were stimulated by an alloantigen rather than a polyclonal activator such as PHA and ConA. Moreover, SOM strongly inhibited the expression of activation markers such as CD69 and CD25 that are expressed on T lymphocytes during alloantigen stimulation. SOM also inhibited both CD28 and CD2 mediated T cell proliferation. Whereas proliferation of T cells induced by the engagement of CD3 antigen using specific mAbs was only marginally affected. Our results would support the concept that in humans SOM plays a key role in the modulation of T cell activation by interfering with the antigen-independent pathways CD2 and CD28
Chemotherapy and immunotherapy of L1210 leukemic mice with antigenic tumor sublines
No full textTumor cells, treated in vivo with anticancer compounds, may acquire new antigenic specificities in addition to any original antigens associated with parental tumors. Treatment of mice carrying the parental leukemias L1210 Ha or L1210 Cr with leukemia cells antigenically altered by treatment with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (L1210 Ha/DTIC and L1210 Cr/DTIC, respectively) was essentially ineffective in prolonging the life span of the animals. However, synergic therapeutic activity was exhibited by administration of L1210 Ha/DTIC cells plus 1,3-bis(2-chloroethyl)-1-nitrosourea in the treatment of the moderately immunogenic L1210 Ha leukemia and by the combination of L1210 Cr/DTIC cells and lymphocytes immune to L1210 Cr/DTIC administered with 1,3-lymphocytes immune to L1210 Cr/DTIC administered with 1,3-bis(2-chloroethyl)-1-nitrosourea in the treatment of the low immunogenic L1210 Cr leukemia. Early and advanced L1210 Cr-bearing mice showed marked increases in survival time and a significant number of tumor-free survivors on treatment with cyclophosphamide followed by transfer of lymphocytes immune to L1210 Cr/DTIC cells. When parental tumor cells were used as the immunogen, the therapeutic effect was diminished. Thus, in the current investigation, although immunotherapy per se was essentially ineffective, the immunochemotherapeutic modalities used were successful in markedly increasing the survival time of leukemic animals and resulted in an incidence of cures
Vaccination of leukemic mice with viable drug-altered leukemic cells
No full textThe treatment in vivo with anti-tumour drugs can induce an antigenic alteration of L1210 leukemia resulting in the rejection of an inoculum of 10 X 10(6) viable cells in syngeneic mice. As drug-induced antigens appeared in excess of any pre-existing tumour-associated transplantation antigens (TATA), viable altered cells have been used to sensitize syngeneic animals. Experiments showed that viable altered cells elicited stronger anti-TATA reaction than X-inactivated parental cells, as measured by host survival to a challenge of L1210 leukemia. TATA immunogenicity of parental cells has been preminent, in the strain of animals used, to determine the sensitizing effectiveness of 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) cells. Host protection to an inoculum of parental tumours has been more proficient with the DTIC subline derived from highly immunogenic L1210Ha cells than from poorly immunogenic L1210Cr cells. Immunoprophylactic inocula, proper chemotherapeutic treatments and adoptive transfer of immune lymphocytes used in combination exerted a synergic host protection
Haematoporphyrin-treated murine lymphocytes: in vitro inhibition of DNA synthesis and light-mediated inactivation of cells responsible for GVHR
No full textIt has been known that haemoatoporphyrin derivative (Hpd) has a preferential distribution in tissues with high mitotic index. Furthermore, cytocidal activity of light activated Hpd within the cells has been exploited in the therapy of experimental and human cancer. It is reported here that maximum, long lasting, although reversible, inhibition of DNA synthesis was obtained in Hpd-treated lymphocytes. However, Hpd-treated lymphoid cells did not stimulate allogeneic lymphocytes in the primary mixed lymphocyte reaction (MLR) culture. Phytohaemagglutinin (PHA) stimulated murine lymphocytes treated with Hpd and exposed to laser light have shown higher susceptibility to lysis than resting, PHA unstimulated, lymphocytes. In vitro DBA/2 stimulated C57 lymphocytes, inoculated into X-irradiated BD2F1 mice, upon Hpd treatment followed by exposure to light, did not cause a lethal graft vs. host reaction (GVHR)
STUDIES OF THE EFFECT OF 2 PORPHYRINS ON THE LYMPHOHEMATOPOIETIC SYSTEM IN IRRADIATED MICE
No full text- …
