Biomedical subjects

M Luciano

Publications and source records attributed to M Luciano.

5 recordsLinked to original sources

PubMed2025

Multi-Polygenic prediction of Frailty and its Trajectories highlights Chronic Pain, Rheumatoid Arthritis, and Educational Attainment pathways.

Frailty is a complex ageing-related trait with a growing evidence base for genetic influence. While a single polygenic score (PGS) for frailty has shown predictive value, few studies have examined the joint effect of multiple genetic risks. This study used a multi-polygenic score (MPS) approach to evaluate the combined and relative contributions of 26 PGSs to frailty, measured via the Frailty Index (FI), in two UK cohorts aged 65 and older: the English Longitudinal Study of Ageing (ELSA) and the Lothian Birth Cohort 1936 (LBC1936). Using elastic net regression with repeated cross-validation, we identified chronic pain and depressive symptoms PGSs as the strongest risk predictors of cross-sectional frailty status, while educational attainment, parental longevity, and rheumatoid arthritis PGSs were protective. Compared to single PGS models, MPS models provided improved prediction of frailty levels, explaining up to 4.7% of variance in frailty status - an improvement over the best single PGS (2.5%). To assess whether PGSs also predicted longitudinal frailty progression, we applied generalized additive mixed models (GAMMs) to model age-related trajectories. In ELSA, five PGSs (chronic pain, depressive symptoms, rheumatoid arthritis, educational attainment, and parental death) significantly interacted with age, influencing the rate of frailty change. In LBC1936, consistent though weaker effects were observed for chronic pain and education PGSs. These findings show that polygenic liability shapes both frailty levels and trajectories in later life. Our results support the use of multi-trait genomic models to improve risk prediction and understanding of frailty's complex aetiology.

Journal Article↗

PubMed1991

[Suprapubic bladder ultrasonography and urinary cytology: indications and limits in the follow-up of superficial bladder tumors].

139 patients underwent urinary cytology and bladder sonography in follow-up of superficial bladder cancer (Ta G1-3) alternatively or at the same time of cystoscopy. Medium follow-up was 27.2 mos. In 7.91% there was progression to T1 o T2 but no case escaped this protocol. In 9% urinary cytology and bladder sonography were both falsely negative: tumors were smaller than 0.5 cm and low grade. In 76 patients with Tar bladder cystoscopy rate was 1/5.2 mos. before this study and 1/7.2 mos. after this study. In our opinion this protocol reveals the recurrence of superficial bladder tumor, reduce cystoscopy rate with no risk of ignored progression.

Carcinoma in Situ↗

PubMed1984

Pancreatic immunoreactive somatostatin and diabetes mellitus.

Pancreatic secretions were collected during endoscopic retrograde cholangiopancreatography from 15 subjects without pancreatic, biliary, or hepatic diseases, 11 patients with non-insulin-dependent diabetes, and 11 patients with insulin-dependent diabetes. Pancreatic secretion was stimulated by the intravenous administration of one unit of secretin per kilogram of body weight. Immunoreactive somatostatin (IRS) in the pancreatic juice of the nondiabetic subjects ranged from 43 to 97 pg/ml, in non-insulin-dependent diabetics from 5 to 3872, and in the insulin-dependent diabetics from 0 to 2093. IRS in insulin-dependent diabetics under good plasma glucose control ranged from 0 to 281 pg/ml, compared to those under poor control who ranged from 518 to 2093 pg/ml. These results indicate that IRS in pancreatic juice is higher in poorly controlled insulin-dependent diabetics than in well controlled insulin-dependent diabetics and nondiabetics. Whether these changes in IRS are purely secondary phenomena or play some pathogenetic role in the disturbed metabolism of diabetes remains to be proven. The chromatographic profile of IRS in pancreatic juice on both gel filtration and high-performance liquid chromatography has indicated that these IRS moieties represent somatostatin 14 and somatostatin 28.

Adult↗

PubMed1981

In vivo and in vitro release of ACTH by synthetic CRF.

The 41-residue corticotropin releasing factor (CRF) was synthesized by the solid phase method. The synthetic CRF and arginine vasopressin (AVP) were examined for ACTH releasing activity and effects on the release of 5 other pituitary hormones in vivo and in vitro. Injection of the CRF into pharmacologically blocked rats increased plasma corticosterone levels in a dose-related manner. The minimum effective dose was 1.6 x 10(-12) mol/100 g body weight. CRF also significantly stimulated release of ACTH-like immunoreactivity in a dose-related manner from rat pituitary quarters beginning at a concentration of 10(-9) M. AVP, a peptide known to have CRF activity, exhibited slightly lower corticotropin releasing activity than the CRF at equimolar dose levels. Secretion of other pituitary hormones was not appreciably altered by either the CRF or AVP.

Adrenocorticotropic Hormone↗

PubMed1980

Naltrexone reduces weight gain, alters "beta-endorphin", and reduces insulin output from pancreatic islets of genetically obese mice.

Naltrexone, an opiate antagonist, was administered to young obese (ob/ob) and lean mice for five weeks. Animals had continuous access to food and received 10 mg/kg SC twice daily with equivalent volumes of saline given to controls. The effects on body weight, and pituitary and plasma levels of beta-endorphin-like material were measured. Naltrexone-injected obese animals gained weight more slowly over the first three weeks while the weight gain of lean animals was not affected by naltrexone. Plasma levels of beta-endorphin were shown to be significantly higher in untreated ob/ob mice and this difference increased with age (4-20 weeks). With naltrexone treatment, plasma levels in +/? mice rose and exceeded those in ob/ob. Saline treatment appeared to be a stress, and pituitary beta-endorphins rose 4-6 fold in ob/ob compared with +/?. While naltrexone reduced the levels of ob/ob pituitary towards normal, no effect on beta-endorphin levels in pituitary of lean mice was obtained. In vitro studies of effects of the opiate antagonists, naloxone, on insulin secretion by isolated islets provided additional evidence of resistance of lean mice to naloxone relative to ob/ob. (IRI secretion fell only in naloxone treated ob/ob islets). These observations support the contention that this form of genetic obesity is characterized by elevated endogenous opiate levels and an increased sensitivity to opiate antagonists such as naltrexone or naloxone.

Animals↗