Influence of Infraspinatus and Subscapularis Pathologies on Supraspinatus Muscle Atrophy - A Retrospective Cohort Study

@#Introduction:Many factors could affect the supraspinatus (SSP) muscle after tendon rupture. We aimed to determine how infraspinatus and subscapularis tendon problems affect supraspinatus muscle atrophy associated with tears, in a retrospective cohort study conducted in a tertiary-level centre. Materials and Methods:Fifty-eight patients with a fullthickness SSP tendon tear who fulfilled the inclusion criteria were enrolled in the study. They were evaluated for tear retraction, fatty degeneration, and other rotator cuff tendon pathologies. Supraspinatus muscle was assessed using the Goutallier classification, and its average area was also measured. Accompanying lesions of the subscapularis and infraspinatus tendons and degree of supraspinatus muscle atrophy were evaluated using magnetic resonance imaging. Results: Our results showed that supraspinatus tendon tears ranged between 3mm and 41mm, and the estimated average cross-sectional area of the SSP muscle was 247.6mm2. Any degree of infraspinatus tendon pathology, ranging from tendinosis to full-thickness tears, was significantly correlated with the SSP muscle area (P < 0.05). The subscapularis tendon pathologies did not show a similar correlation. The interobserver and intraobserver reliabilities of the measurements were graded as excellent. Conclusion: Impairment of any of the rotator cuff muscles may affect the other muscles inversely. Our study showed that all infraspinatus tendon pathologies and partial subscapularis tears affect and alter the SSP muscle belly. We suggest early intervention for supraspinatus tears to avoid further fatty degeneration, as muscle atrophy and fatty degeneration progress in combination with the accompanying lesions.

The NUMEN project: Heavy-Ion Double Charge Exchange reactions towards 0νββ NME determination / El proyecto NUMEN: reacciones de intercambio de cargas dobles de iones pesados hacia la determinación de 0νββ NME

Abstract NUMEN proposes cross sections measurements of Heavy-Ion double charge exchange reactions as an innovative tool to access the nuclear matrix elements, entering the expression of the life time of Neutrinoless double beta decay (0νββ). A key aspect of the projectis the use at INFN-Laboratori Nazionali del Sud (LNS) of the Superconducting Cyclotron (CS) for the acceleration of the required high resolution and low emittance heavy-ion beams and of MAGNEX large acceptance magnetic spectrometer for the detection of the ejectiles. The experimental measurements of double charge exchange reactions induced by heavy ions present a number of challenging aspects, since such reactions are characterized by very low cross sections. First experimental results give encouraging indication on the capability to access quantitative information towards the determination of the Nuclear Matrix Elements for 0νββ decay.

Resumen NUMEN propone mediciones de secciones eficaces de reacciones de intercambio de carga doble de iones pesados como una herramienta innovadora para acceder a los elementos de la matriz nuclear, entrando en la expresión del tiempo de vida de la desintegración beta doble sin neutrino (0νββ). Un aspecto clave del proyecto es el uso en INFN-Laboratori Nazionali del Sud (LNS) del ciclotrón superconductor (CS) para la aceleración de los haces de iones pesados de alta resolución y baja emitancia requeridos y del espectrómetro magnético de gran aceptación MAGNEX para la detección de los residuos eyectados. Las mediciones experimentales de reacciones de intercambio de carga doble inducidas por iones pesados presentan una serie de aspectos desafiantes, ya que tales reacciones se caracterizan por secciones eficaces muy bajas. Los primeros resultados experimentales dan una indicación alentadora sobre la capacidad de acceder a información cuantitativa para la determinación de los Elementos de la Matriz Nuclear para la descomposición de 0νββ.

GJB2 and mitochondrial A1555G gene mutations in nonsyndromic profound hearing loss and carrier frequencies in healthy individuals.

This study aimed to assess mutations in GJB2 gene (connexin 26), as well as A1555G mitochondrial mutation in both the patients with profound genetic nonsyndromic hearing loss and healthy controls. Ninety-five patients with profound hearing loss (>90 dB) and 67 healthy controls were included. All patients had genetic nonsyndromic hearing loss. Molecular analyses were performed for connexin 26 (35delG, M34T, L90P, R184P, delE120, 167delT, 235delC and IVS1+1 A-->G) mutations, and for mitochondrial A1555G mutation. Twenty-two connexin 26 mutations were found in 14.7% of the patients, which were 35delG, R184P, del120E and IVS1+1 A-->G. Mitochondrial A1555G mutation was not encountered. The most common GJB2 gene mutation was 35delG, which was followed by del120E, IVS1+1 A-->G and R184P, and 14.3% of the patients segregated with DFNB1. In consanguineous marriages, the most common mutation was 35delG. The carrier frequency for 35delG mutation was 1.4% in the controls. 35delG and del120E populations, seems the most common connexin 26 mutations that cause genetic nonsyndromic hearing loss in this country. Nonsyndromic hearing loss mostly shows DFNB1 form of segregation.