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1.
OTO Open ; 7(1): e46, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-36998554

RESUMO

Objective: Adipose stem cells (ASCs) have been shown in many preclinical studies to be potent suppressors of the immune system. Prior studies suggest that ASCs may promote cancer progression and wound healing. However, clinical studies investigating the effects of native, or fat-grafted adipose tissue on cancer recurrence have generated mixed results. We investigated whether adipose content in reconstructive free flaps for oral squamous cell carcinoma (OSCC) is associated with disease recurrence and/or reduction in wound complications. Study Design: Retrospective chart review. Setting: Academic medical center. Methods: We performed a review of 55 patients undergoing free flap reconstruction for OSCC over a 14-month period. Using texture analysis software, we measured the relative free flap fat volume (FFFV) in postoperative computed tomography scans and compared fat volume with patient survival, recurrence, and wound healing complications. Results: We report no difference in mean FFFV between patients with or without recurrence: 13.47 cm3 in cancer-free survivors and 17.99 cm3 in cases that recurred (p = .56). Two-year recurrence-free survival in patients with high and low FFFV was 61.0% and 59.1%, respectively (p = .917). Although only 9 patients had wound healing complications, we found no trend in the incidence of wound healing complications between patients with high versus low FFFV. Conclusion: FFFV is not associated with recurrence or wound healing in patients undergoing free flap reconstruction for OSCC, suggesting adipose content should not be of concern to the reconstructive surgeon.

2.
J Neuroophthalmol ; 43(1): 55-62, 2023 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-36166790

RESUMO

BACKGROUND: Radiologic findings of intracranial hypertension (RAD-IH) are common in idiopathic intracranial hypertension (IIH) patients. Paralleling the increasing rates of obesity, the burden of IIH is growing. Urgent neuro-ophthalmology consultations for possible IIH in patients with incidentally detected RAD-IH are increasing, with many patients receiving unnecessary lumbar punctures (LPs) and treatments. This retrospective observational study aimed to determine the prevalence of neuro-ophthalmology consultations for RAD-IH, rate of funduscopic examination by referring providers, prevalence of papilledema, outcomes after neuro-ophthalmic evaluation, and rates of misdiagnosis. METHODS: Records of 1,262 consecutive new patients seen in one neuro-ophthalmology clinic from January 2019 to January 2020 were reviewed. We identified patients who were: 1) referred with concern for IIH because of findings of RAD-IH; 2) referred for "papilledema"; 3) referred with a diagnosis of IIH; and 4) referred for spontaneous cranial cerebrospinal fluid (CSF) leaks. In addition to basic demographic profiles for all groups, detailed information was collected for patients referred solely for RAD-IH, including referral patterns, prior history of IIH, previous LPs, prior medical or surgical treatment(s), risk factors for increased intracranial pressure (ICP), presenting symptoms, radiologic features observed on neuroimaging, and final disposition. When available, the neuroimaging was reviewed by an expert neuroradiologist. RESULTS: Of 1,262 consecutive new patients, 66 (5%) were referred specifically for RAD-IH; most referrals came from neurologists (58%); 8/66 (12%) patients had papilledema; 16/66 (24%) patients had prior LP and 13/66 (20%) were already treated based on MRI findings; and 22/66 (33%) patients had ≤2 RAD-IH. Only 34/66 (52%) of patients referred for RAD-IH had prior funduscopic examinations. We confirmed papilledema in 26/82 (32%) patients referred for "papilledema." Only 29/83 (35%) patients referred with a diagnosis of IIH had active papilledema, and 3/16 (19%) patients with spontaneous CSF leaks had papilledema. In total, 247/1,262 (20%) new patients were referred to our clinic over 1 year with concern for IIH, among whom only 66 (27%) were confirmed to have active IIH with papilledema. CONCLUSIONS: One in 5 new patient referrals seen in our neuro-ophthalmology clinic were referred because of concern for increased ICP, but only 1/4 had active papilledema. Most patients referred for isolated RAD-IH do not have papilledema, many having undergone unnecessary LPs and treatments. The burden of these "rule-out IIH" consultations is overwhelming and will only continue to increase with the concurrent rise of obesity and IIH, straining the already limited neuro-ophthalmologic resources available in the US.


Assuntos
Hipertensão Intracraniana , Papiledema , Pseudotumor Cerebral , Humanos , Pseudotumor Cerebral/complicações , Pseudotumor Cerebral/diagnóstico , Pseudotumor Cerebral/epidemiologia , Lipopolissacarídeos , Hipertensão Intracraniana/diagnóstico , Papiledema/diagnóstico , Papiledema/epidemiologia , Papiledema/etiologia , Obesidade/complicações , Neuroimagem , Vazamento de Líquido Cefalorraquidiano/diagnóstico , Estudos Retrospectivos
3.
Radiol Case Rep ; 15(8): 1331-1334, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32612734

RESUMO

We present the appearance of brain capillary telangiectasia on 3.0T magnetic resonance imaging (MRI) perfusion. A 42-year-old female presented with intermittent left arm weakness and paresthesia. Initial 1.5T MRI obtained 2 months after presentation demonstrated a 6 mm right caudate head lesion with ring-like enhancement, and no significant surrounding edema or mass effect. On gradient echo there was mild associated susceptibility artifact. Follow-up 3.0T MRI demonstrated increased blooming on 3.0T imaging relative to prior 1.5T imaging. The lesion also demonstrated increased blood volume on dynamic susceptibility contrast perfusion. Given these imaging findings and interval stability, a definitive imaging diagnosis of capillary telangiectasia was made. Recognition of the MRI findings of capillary telangiectasia is imperative to avoid misdiagnosis and prevent unnecessary intervention.

4.
PLoS One ; 7(12): e52056, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23284867

RESUMO

Alzheimer's disease (AD) is a devastating neurodegenerative condition with no known cure. While current therapies target late-stage amyloid formation and cholinergic tone, to date, these strategies have proven ineffective at preventing disease progression. The reasons for this may be varied, and could reflect late intervention, or, that earlier pathogenic mechanisms have been overlooked and permitted to accelerate the disease process. One such example would include synaptic pathology, the disease component strongly associated with cognitive impairment. Dysregulated Ca(2+) homeostasis may be one of the critical factors driving synaptic dysfunction. One of the earliest pathophysiological indicators in mutant presenilin (PS) AD mice is increased intracellular Ca(2+) signaling, predominantly through the ER-localized inositol triphosphate (IP(3)) and ryanodine receptors (RyR). In particular, the RyR-mediated Ca(2+) upregulation within synaptic compartments is associated with altered synaptic homeostasis and network depression at early (presymptomatic) AD stages. Here, we offer an alternative approach to AD therapeutics by stabilizing early pathogenic mechanisms associated with synaptic abnormalities. We targeted the RyR as a means to prevent disease progression, and sub-chronically treated AD mouse models (4-weeks) with a novel formulation of the RyR inhibitor, dantrolene. Using 2-photon Ca(2+) imaging and patch clamp recordings, we demonstrate that dantrolene treatment fully normalizes ER Ca(2+) signaling within somatic and dendritic compartments in early and later-stage AD mice in hippocampal slices. Additionally, the elevated RyR2 levels in AD mice are restored to control levels with dantrolene treatment, as are synaptic transmission and synaptic plasticity. Aß deposition within the cortex and hippocampus is also reduced in dantrolene-treated AD mice. In this study, we highlight the pivotal role of Ca(2+) aberrations in AD, and propose a novel strategy to preserve synaptic function, and thereby cognitive function, in early AD patients.


Assuntos
Doença de Alzheimer/metabolismo , Retículo Endoplasmático/metabolismo , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Doença de Alzheimer/prevenção & controle , Peptídeos beta-Amiloides/metabolismo , Animais , Cálcio/metabolismo , Sinalização do Cálcio/efeitos dos fármacos , Dantroleno/farmacologia , Modelos Animais de Doenças , Retículo Endoplasmático/efeitos dos fármacos , Feminino , Hipocampo/metabolismo , Masculino , Camundongos , Camundongos Transgênicos , Plasticidade Neuronal/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Transmissão Sináptica/efeitos dos fármacos
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