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1.
Lymphology ; 56(1): 13-26, 2023.
Article in English | MEDLINE | ID: mdl-38019876

ABSTRACT

The aim of this pilot study was to investigate the effects of defocused and radial shock wave therapy, mesotherapy, and kinesio taping on pain, circumferences of lower limbs, echographic/ elastosonographic pattern of subcutaneous adipose tissue (SAT), and quality of life in patients with lipedema. Fifteen women affected by lower limb lipedema in stage II were treated with shock wave therapy, mesotherapy, and kinesio taping on thighs and legs (eight sessions, twice a week). The primary outcome was pain, as assessed by Numeric Rating Scale (NRS). Secondary outcomes included the limb circumferences measurements, the SF-12 Health Survey for quality of life, the International Classification of Functioning (ICF) for disability, and echographic/ elastosonographic changes of SAT. Significant reductions of pain and circumference measurements were seen in patients at each follow up. This was associated with significant reduction of thickness, echographic pattern improvement, and increased elasticity of SAT, with consequent positive impact on the quality of life and disability reported by the patients. The results demonstrate improved clinical and functional ultrasound findings in patients affected by lipedema in the early stages of lower limbs, and this combination therapy needs to be investigated in larger populations at multiple centers to confirm the findings.


Subject(s)
Extracorporeal Shockwave Therapy , Lipedema , Mesotherapy , Humans , Female , Lipedema/therapy , Pilot Projects , Quality of Life , Pain
2.
Neurobiol Dis ; 70: 117-26, 2014 Oct.
Article in English | MEDLINE | ID: mdl-24969023

ABSTRACT

In this study we show that postnatal development of cerebellar granule neurons (GNs) is defective in Npc1(-/-) mice. Compared to age-matched wild-type littermates, there is an accelerated disappearance of the external granule layer (EGL) in these mice. This is due to a premature exit from the cell cycle of GN precursors residing at the level of the EGL. As a consequence, the size of cerebellar lobules of these mice displays a 20%-25% reduction compared to that of age-matched wild-type mice. This size reduction is detectable at post-natal day 28 (PN28), when cerebellar GN development is completed while signs of neuronal atrophy are not yet apparent. Based on the analysis of EGL thickness and the determination of proliferating GN fractions at increasing developmental times (PN8-PN14), we trace the onset of this GN developmental defect during the second postnatal week. We also show that during this developmental time Shh transcripts undergo a significant reduction in Npc1(-/-) mice compared to age-matched wild-type mice. In light of the mitogenic activity of Shh on GNs, this observation further supports the presence of defective GN proliferation in Npc1(-/-) mice. A single injection of hydroxypropyl-ß-cyclodextrin at PN7 rescues this defect, restoring the normal patterns of granule neuron proliferation and cerebellar lobule size. To our knowledge, these findings identify a novel developmental defect that was underappreciated in previous studies. This defect was probably overlooked because Npc1 loss-of-function does not affect cerebellar foliation and causes the internal granule layer and molecular layer to decrease proportionally, giving rise to a normally appearing, yet harmoniously smaller, cerebellum.


Subject(s)
Cerebellum/drug effects , Cerebellum/growth & development , Neurons/drug effects , Neuroprotective Agents/pharmacology , Proteins/metabolism , beta-Cyclodextrins/pharmacology , 2-Hydroxypropyl-beta-cyclodextrin , Animals , Apoptosis/drug effects , Apoptosis/physiology , Cell Cycle/drug effects , Cell Cycle/physiology , Cerebellum/physiopathology , Hedgehog Proteins/metabolism , Intracellular Signaling Peptides and Proteins , Mice, Inbred BALB C , Mice, Knockout , Mitosis/drug effects , Mitosis/physiology , Neurogenesis/drug effects , Neurogenesis/physiology , Neurons/physiology , Niemann-Pick C1 Protein , Organ Size , Proteins/genetics , RNA, Messenger/metabolism
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