Mcdonalddrew6387
In breast cancer, radiotherapy is an essential component of the treatment. However, indications of irradiation of the internal mammary chain and axillary area are debatables. Axillary recurrence in patients with invasive breast carcinoma remains an issue. Currently, the substitution of axillary lymph node dissection by sentinel node biopsy leads to revisit the role of axillary irradiation. Breast irradiation including level I, II and III might decrease the risk of axillary recurrence.
A literature search was performed in PubMed and the Cochrane library to identify articles publishing data regarding dose-volume analysis of axillary levels in breast irradiation aiming to determine the potential therapeutic implications.
Eleven articles were retained. A total of 375 treatment plans were analyzed. The results concerning the irradiation technique, initial dose prescribed to breast, delineated volumes and dose received at axillary levels were heterogeneous. The average dose delivered to axilla levels I-III with 3D-conformal radiotherapy using standard fields were between 24Gy and 43.5Gy, 3Gy and 32.5Gy and between 1.0Gy and 20.5Gy respectively. The average doses delivered to axilla levels I-III with 3D-conformal radiotherapy using high tangential fields were between 38Gy and 49.7Gy, 11Gy and 47.1Gy and 5Gy 38.7Gy, 32.1Gy and 5Gy (result available for only one study) respectively. Finally, the average doses delivered to axilla levels I-III with intensity modulated radiation therapy were between 14.5Gy and 42.6Gy, 3.4Gy and 35Gy and between 1.2Gy and 25.5Gy respectively.
Incidental axillary dose seems insufficient to be therapeutic regardless of the irradiation technique. There are meaningful differences between intensity modulated radiation therapy and 3D-conformal radiotherapy.
Incidental axillary dose seems insufficient to be therapeutic regardless of the irradiation technique. There are meaningful differences between intensity modulated radiation therapy and 3D-conformal radiotherapy.
The intrinsically photosensitive retinal ganglion cells (ipRGCs) signal environmental light, with axons projected to the midbrain that control pupil size and circadian rhythms. Selleckchem Leukadherin-1 Post-illumination pupil response (PIPR), a sustained pupil constriction after short-wavelength light stimulation, is an indirect measure of ipRGC activity. Here, we measured the PIPR in young adults with various refractive errors using a custom-made optical system.
PIPR was measured on myopic (-3.50 ± 1.82 D, n = 20) and non-myopic (+0.28 ± 0.23 D, n = 19) participants (mean age, 23.36 ± 3.06 years). The right eye was dilated and presented with long-wavelength (red, 625 nm, 3.68 × 10
photons/cm
/s) and short-wavelength (blue, 470 nm, 3.24 × 10
photons/cm
/s) 1 s and 5 s pulses of light, and the consensual response was measured in the left eye for 60 s following light offset. The 6 s and 30 s PIPR and early and late area under the curve (AUC) for 1 and 5 s stimuli were calculated.
For most subjects, the 6 s and 30 s PIPR were significantly lower (p < 0.001), and the early and late AUC were significantly larger for 1 s blue light compared to red light (p < 0.001), suggesting a strong ipRGC response. The 5 s blue stimulation induced a slightly stronger melanopsin response, compared to 1 s stimulation with the same wavelength. However, none of the PIPR metrics were different between myopes and non-myopes for either stimulus duration (p > 0.05).
We confirm previous research that there is no effect of refractive error on the PIPR.
We confirm previous research that there is no effect of refractive error on the PIPR.Actinomyces and related genera are grampositive bacilli, opportunistic pathogens, which have been mainly involved in endogenous infections. However, due to the complexity in identifying them for most clinical laboratories, there is scant knowledge about their real clinical significance. In this work, 166 isolates of 13 different species of Actinomyces/Actinotignum species recovered from clinical samples of patients treated in a university hospital were studied. The identification was performed by MALDI-TOF MS and molecular identification. MALDI-TOF MS identified 91.57% of the isolates (152/166) at the species level using a score ≥ 1.7 and 3.61% (6/166) of the isolates were identified only at the gender level with a score ≥ 1.5. MALDI-TOF MS did not yield reliable identification results for 4.82% (8/166) of the isolates. Actinomyces/Actinotignum species were isolated from soft tissue (n 47), urine samples (n 35), head / neck abscesses (n 19), genital abscesses (n 11), blood samples (n 10), breast abscesses (n 8), osteoarticular samples (n 6), abdominal/ascitic fluids (n 3), abdominal abscesses (n 5), sputum/BAL (n 4), brain abscesses (n 3), and others (n 15). The results obtained from the statistical analysis showed a high differential frequency (> 2) for the location/species association urine/A. schaalii/sanguinis; brain abscesses/A. europaeus; osteoarticular samples/A. urogenitalis; abdominal abscesses/ A. turicensis; respiratory samples/A. naeslundii/viscosus. This information provides a greater understanding of the clinical and epidemiological relevance of these species. The pathogenic role of Actinomyces spp. will be increasingly revealed as these microorganisms could be recognized thanks to prolonged culture and the advances in identification technology facilitated by MALDI-TOF MS.
Aminoacyl-tRNA synthetase-interacting multifunctional protein 1 (AIMP1) is a non-catalytic component of the multi-tRNA synthetase complex that catalyzes the ligation of amino acids to their correct tRNAs. Bi-allelic truncating variants in the AIMP1 gene have been associated with hypomyelinating leukodystrophy-3 (HLD3; MIM 260600), which is characterized by hypomyelination, microcephaly, seizures and decreased life expectancy. Although peripheral nerve involvement has been assumed for HLD3, no compelling evidence is available to date.
The case was a first-born Filipino male. He showed profound developmental delay, failure to thrive, and spasticity in his limbs. At three months of age he developed refractory epilepsy. Serial magnetic resonance imaging (MRIs) showed profound myelination delay and progressive cerebral atrophy. He showed abnormal nerve conduction studies. Genetic testing revealed a homozygous pathogenic variant in the AIMP1 gene (NM_004757.3 c.115C>T p.Gln39*). The parents were heterozygous for the same variant.
