Evaluation of an Online Training Course for Childcare Providers Participating in the CACFP Infant Feeding Program.

INTRODUCTION: The Child and Adult Care Food Program (CACFP) provides reimbursement for meals and snacks offered in participating centers and issues nutrition standards, including guidelines for feeding infants in childcare settings. Offering training to childcare providers participating in the CACFP is necessary to ensure compliance with nutrition standards in childcare settings. METHODS: A State Department of Education and University Extension system collaborated to develop an online nutrition training course for childcare providers. Providers (n = 57) participated in the course on CACFP nutrition standards related to feeding infants (0-12 months of age). Thirty-two of 57 participants completed both pre- and post-training surveys that were used to assess changes in knowledge and confidence concerning infant feeding standards. Paired t-tests and Wilcoxon signed-rank tests were conducted to assess differences in survey responses before and after the course. RESULTS: Self-confidence and knowledge of providers related to infant feeding were significantly increased after completion of the training course (p < 0.001). More participants reported their sites were likely to respond to infants showing they were hungry or full than before the course (44.4% vs. 75.7%, respectively). Participant feedback indicated the online asynchronous course was convenient, useful, and topics were relevant to training needs. DISCUSSION: The online course was feasible and effective for providing training on CACFP guidelines for childcare providers. Feedback from participants can be adapted and used for future training programs to further improve the course and delivery methods and efficiently reach a broad audience of childcare providers.

Peptide-mediated targeted delivery of SOX9 nanoparticles into astrocytes ameliorates ischemic brain injury.

Astrocytes are highly activated following brain injuries, and their activation influences neuronal survival. Additionally, SOX9 expression is known to increase in reactive astrocytes. However, the role of SOX9 in activated astrocytes following ischemic brain damage has not been clearly elucidated yet. Therefore, in the present study, we investigated the role of SOX9 in reactive astrocytes using a poly-lactic-co-glycolic acid (PLGA) nanoparticle plasmid delivery system in a photothrombotic stroke animal model. We designed PLGA nanoparticles to exclusively enhance SOX9 gene expression in glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes. Our observations indicate that PLGA nanoparticles encapsulated with GFAP:SOX9:tdTOM reduce ischemia-induced neurological deficits and infarct volume through the prostaglandin D2 pathway. Thus, the astrocyte-targeting PLGA nanoparticle plasmid delivery system provides a potential opportunity for stroke treatment. Since the only effective treatment currently available is reinstating the blood supply, cell-specific gene therapy using PLGA nanoparticles will open a new therapeutic paradigm for brain injury patients in the future.

Examining Predictors of Nutritional Risk among Older Adults: A Needs Assessment.

Older adults are the fastest growing population in the United States. This group is at risk for developing chronic diseases resulting from high nutritional risk. The objective of this study was to assess nutritional risks and their key predictors among older adults. In this cross-sectional study, the Dietary Screening Tool, the Nutrition Self-efficacy Scale, food security, perceived health, and sociodemographics were measured. A total of 475, English-speaking adults, 50 years of age or older, residing in Maryland and attending senior congregate sites, participated in the study (urban n = 215, rural n = 260). Results showed 88.8% of participants were classified as being nutritionally 'at risk' or 'possible' risk. Higher education level, higher nutrition self-efficacy, and food security were significant predictors associated with lower nutritional risk among older adults. Implementing suitable and effective nutrition interventions requires assessing diet and identifying the needs specific to older adult populations. Utilizing appropriate screening tools is an important step in improving overall diets and may reduce barriers to adopting healthy eating behaviors in this population.

PINK1 siRNA-loaded poly(lactic-co-glycolic acid) nanoparticles provide neuroprotection in a mouse model of photothrombosis-induced ischemic stroke.

PTEN-induced kinase 1 (PINK1) is a well-known critical marker in the pathway for mitophagy regulation as well as mitochondrial dysfunction. Evidence suggests that mitochondrial dynamics and mitophagy flux play an important role in the development of brain damage from stroke pathogenesis. In this study, we propose a treatment strategy using nanoparticles that can control PINK1. We used a murine photothrombotic ischemic stroke (PTS) model in which clogging of blood vessels is induced with Rose Bengal (RB) to cause brain damage. We targeted PINK1 with poly(lactic-co-glycolic acid) (PLGA)-based nanoparticles loaded with PINK1 siRNA (PINK1 NPs). After characterizing siRNA loading in the nanoparticles, we assessed the efficacy of PINK1 NPs in mice with PTS using immunohistochemistry, 1% 2,3,5-triphenyltetrazolium chloride staining, measurement of motor dysfunction, and Western blot. PINK1 was highly expressed in microglia 24 h after PTS induction. PINK1 siRNA treatment increased phagocytic activity, migration, and expression of an anti-inflammatory state in microglia. In addition, the PLGA nanoparticles were selectively taken up by microglia and specifically regulated PINK1 expression in those cells. Treatment with PINK1 NPs prior to stroke induction reduced expression of mitophagy-inducing factors, infarct volume, and motor dysfunction in mice with photothrombotic ischemia. Experiments with PINK1-knockout mice and microglia depletion with PLX3397 confirmed a decrease in stroke-induced infarct volume and behavioral dysfunction. Application of nanoparticles for PINK1 inhibition attenuates RB-induced photothrombotic ischemic injury by inhibiting microglia responses, suggesting that a nanomedical approach targeting the PINK1 pathway may provide a therapeutic avenue for stroke treatment.

One-year prevalence and clinical characteristics in chronic dizziness: The 2019-2020 Korean National Health and Nutrition Examination Survey.

Introduction: In this cross-sectional study, we investigated the 1-year prevalence and related factors in the general population with an experience of chronic dizziness. Methods: This study analyzed persons (n = 5,163) who respond to dizziness and nutrition questionnaire from participant of Korean National Health and Nutrition Examination Survey (KNHANES, 2019-2020). Results: Of individuals over 40 years, 25.3% of the general population (61.6% females) reported either dizziness or imbalance for the past year. Moreover, 4.8% of the patients reported they suffered from chronic dizziness or imbalance for more than 3 months. In multiple regression analysis, patients with chronic dizziness were older, females, had lower body mass index (BMI), had stress awareness, and had a history of tinnitus within 1 year (>5 min per episode). Relative to normal body weight, both overweight and mild obesity (obesity stages 1 and 2) were associated with a significantly lower risk of chronic dizziness. Overweight, obesity stage 1, and obesity stage 2 had odds ratios of 0.549 [95% confidence interval (CI), 0.332-0.910], 0.445 (95% CI, 0.273-0.727), and 0.234 (95% CI, 0.070-0.779), respectively. Conclusions: In this study, the prevalence of chronic dizziness in the general population was 4.8%. Our study demonstrated that overweight and mild obesity were independently associated with a lower risk of chronic dizziness in adults for the past year. Therefore, the optimal BMI for patients with dizziness should be defined and managed according to an integrated care pathway.

Oxygenated Water Increases Seizure Threshold in Various Rodent Seizure Models.

Oxygenated water (OW) contains more oxygen than normal drinking water. It may induce oxygen enrichment in the blood and reduce oxidative stress. Hypoxia and oxidative stress could be involved in epilepsy. We aimed to examine the effects of OW-treated vs. control on four rodent models of epilepsy: (1) prenatal betamethasone priming with postnatal N-methyl-D-aspartate (NMDA)-triggered spasm, (2) no prenatal betamethasone, (3) repetitive kainate injection, and (4) intraperitoneal pilocarpine. We evaluated, in (1) and (2), the latency to onset and the total number of spasms; (3) the number of kainate injections required to induce epileptic seizures; (4) spontaneous recurrent seizures (SRS) (numbers and duration). In model (1), the OW-treated group showed significantly increased latency to onset and a decreased total number of spasms; in (2), OW completely inhibited spasms; in (3), the OW-treated group showed a significantly decreased number of injections required to induce epileptic seizures; and in (4), in the OW-treated group, the duration of a single SRS was significantly reduced. In summary, OW may increase the seizure threshold. Although the underlying mechanism remains unclear, OW may provide an adjunctive alternative for patients with refractory epilepsy.

Antitumor Potential of Sericite Treatment Mediated by Cell Cycle Arrest in Triple-Negative MDA-MB231 Breast Cancer Cells.

Breast cancer is the most common cancer and the leading cause of cancer-related mortality among females worldwide. Triple-negative breast cancer (TNBC) accounts for about 10-15% of all breast cancers and is usually more aggressive and has a poorer prognosis. Sericite has been known to have antitumor and immune-stimulatory effects. Although the chemopreventive potential of sericite has been demonstrated in other cancers, its molecular pathways in TNBC still require investigation. Thus, in the present study, the antitumor mechanism of sericite against MDA-MB231 breast cancer cells was examined in vitro and in an in vivo xenograft mouse model. Sericite treatment reduced cell proliferation and cell proliferation marker proliferating cell nuclear antigen (PCNA) in MDA-MB231 cells. It also decreased the total cell number and arrested cells in the G0/G1 phase of the cell cycle with an increase in the phosphorylation of P53 and upregulation of cell cycle regulatory proteins P21 and P16. In addition, sericite treatment also induced apoptosis signaling, which was evident by the upregulation of apoptotic protein markers cleaved caspases 3 and 9. A reduction in reactive oxygen species (ROS), NADPH oxidase 4 (NOX4), p22phox, and heat shock proteins (HSPs) was also observed. Similar results were obtained in vivo with significantly reduced tumor volume in sericite-administered mice. Collectively, these findings suggest that sericite has antitumor potential based on its property to induce cell cycle arrest and apoptotic cell death and therefore could serve as a potential therapeutic agent and crucial candidate in anticancer drug development for TNBC.

Cannabidiol exerts anti-proliferative activity via a cannabinoid receptor 2-dependent mechanism in human colorectal cancer cells.

Colorectal cancer is the third leading cause of cancer incidence and mortality in the United States. Cannabidiol (CBD), the second most abundant phytocannabinoid in Cannabis sativa, has potential use in cancer treatment on the basis of many studies showing its anti-cancer activity in diverse types of cancer, including colon cancer. However, its mechanism of action is not yet fully understood. In the current study, we observed CBD to repress viability of different human colorectal cancer cells in a dose-dependent manner. CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6. CBD further increased caspase 3/7 activity and cleaved poly(ADP-ribose) polymerase, and elevated expression of endoplasmic reticulum (ER) stress proteins including binding immunoglobulin protein (BiP), inositol-requiring enzyme 1α (IRE1α), phosphorylated eukaryotic initiation factor 2α (eIF2α), activating transcription factor 3 (ATF3), and ATF4. We found that CBD repressed cell viability and induced apoptotic cell death through a mechanism dependent on cannabinoid receptor type 2 (CB2), but not on CB1, transient receptor potential vanilloid, or peroxisome proliferator-activated receptor gamma. Anti-proliferative activity was also observed for other non-psychoactive cannabinoid derivatives including cannabidivarin (CBDV), cannabigerol (CBG), cannabicyclol (CBL), and cannabigerovarin (CBGV). Our data indicate that CBD and its derivatives could be promising agents for the prevention of human colorectal cancer.

Permethrin inhibits tube formation and viability of endothelial cells.

BACKGROUND: Exposure to environmental chemicals has been linked with endothelial dysfunction, which is a leading cause of human diseases, including atherosclerosis. Permethrin is a frequently used synthetic pyrethroid insecticide for which longer exposure may cause toxicity in several types of tissues and the development of metabolic diseases, including atherosclerosis, obesity and diabetes. The present study was designed to evaluate the potential adverse effect of permethrin on the function and activity of human endothelial cells. RESULTS: Permethrin was found to repress migration and tube formation by human umbilical vein endothelial cells (HUVECs) in a dose-dependent manner, as well as to significantly repress their viability after 24 and 48 h of treatment. Furthermore, increased reactive oxygen species (ROS) production was observed in cells treated with permethrin, and the permethrin-induced repression of cell viability was ROS-dependent. Permethrin did not influence apoptosis, necrosis or mitochondrial membrane potential in HUVECs. CONCLUSION: The results of the present study suggest that permethrin represses angiogenesis and viability through ROS-dependent and cell growth-, apoptosis- and necrosis-independent means. © 2022 Society of Chemical Industry.

Home-delivered meal programme participants may be at greater risk of malnutrition without the meal programme.

OBJECTIVES: (1) To examine total quality of foods consumed on the day a home-delivered meal (HDM) of the Older Americans Act Nutrition Program (OAANSP) was served, and when a HDM was not served; and (2) to estimate proportion of HDM participants and non-participants meeting the daily average recommendations for guidance-based foods and nutrients. DESIGN: Cross-sectional study. SETTING: Data were obtained from the national 2015-2017 Outcomes Evaluation Study of HDM participants in the USA. PARTICIPANTS: Adults aged 67 years and older (n 1227), 620 HDM recipients and 607 matching non-participants examined in three groups: (1) meal recipients who received a HDM on the day of the 24-h dietary recall; (2) no-meal recipients who did not receive a HDM on the day of the recall and (3) matching HDM non-participants. RESULTS: Healthy Eating Index (HEI)-2010 scores of HDM participants were significantly lower on the day the meal was not received compared with when a meal was received (52·5 v. 63·4, P < 0·0001). There was no significant difference in the total HEI-2010 scores of HDM meal recipients and HDM non-participants. Despite the meal, less than 20 % of HDM participants and non-participants met the 2010-Diet Guidelines for Americans recommended average daily intake for fruit, vegetables, dairy, protein foods and solid fats. CONCLUSION: HDM participants' diet quality is poorer when they do not receive a meal putting them at increased risk of malnutrition. Expanding the OAANSP to offer meals on weekends and/or to include more than one meal/d is recommended to improve the diet of this vulnerable population.

Protective Effects of ShcA Protein Silencing for Photothrombotic Cerebral Infarction.

Reactive oxygen species (ROS) exacerbate stroke-induced cell damage. We found that ShcA, a protein that regulates ROS, is highly expressed in a Rose Bengal photothrombosis model. We investigated whether ShcA is essential for mitophagy in ROS-induced cellular damage and determined whether ROS exacerbate mitochondrial dysfunction via ShcA protein expression. Ischemic stroke was generated by Rose Bengal photothrombosis in mice. To silence ShcA protein expression in the mouse brain, ShcA-targeting siRNA-encapsulated nanoparticles were intrathecally injected into the cisterna magna. Upon staining with antibodies against ShcA counterpart caspase-3 or NeuN, we found that the ShcA protein expression was increased in apoptotic neurons. In addition, mitochondrial dysfunction and excessive mitophagy were evident in photothrombotic stroke tissue. Infarct volumes were significantly reduced, and neurological deficits were diminished in the ShcA siRNA nanoparticle-treated group, compared with the negative control siRNA nanoparticle-treated group. We confirmed that the reduction of ShcA expression by nanoparticle treatment rescued the expression of genes, associated with mitochondrial dynamics and mitophagy mediation in a stroke model. This study suggests that the regulation of ShcA protein expression can be a therapeutic target for reducing brain damage with mitochondrial dysfunction caused by thrombotic infarction.

Preventive Effects of Neuroprotective Agents in a Neonatal Rat of Photothrombotic Stroke Model.

Neonatal ischemic stroke has a higher incidence than childhood stroke. Seizures are the first sign for the need for clinical assessment in neonates, but many questions remain regarding treatments and follow-up modalities. In the absence of a known pathophysiological mechanism, only supportive care is currently provided. Stroke-induced microglia activation and neuroinflammation are believed to play a central role in the pathological progression of neonatal ischemic stroke. We induced a photothrombotic infarction with Rose Bengal in neonatal rats to investigate the effects of pre- and post-treatment with Aspirin (ASA), Clopidogrel (Clop), and Coenzyme Q10 (CoQ10), which are known for their neuroprotective effects in adult stroke. Pre-stroke medication ameliorates cerebral ischemic injury and reduces infarct volume by reducing microglia activation, cellular reactive oxygen species (ROS) production, and cytokine release. Post-stroke administration of ASA, Clop, and CoQ10 increased motor function and reduced the volume of infarction, and the statistical evidence was stronger than that seen in the pre-stroke treatment. In this study, we demonstrated that ASA, Clop, and CoQ10 treatment before and after the stroke reduced the scope of stroke lesions and increased behavioral activity. It suggests that ASA, Clop, and CoQ10 medication could significantly have neuroprotective effects in the neonates who have suffered strokes.

miRNA 146a-5p-loaded poly(d,l-lactic-co-glycolic acid) nanoparticles impair pain behaviors by inhibiting multiple inflammatory pathways in microglia.

Aims: We investigated whether miRNA (miR) 146a-5p-loaded nanoparticles (NPs) can attenuate neuropathic pain behaviors in the rat spinal nerve ligation-induced neuropathic pain model by inhibiting activation of the NF-κB and p38 MAPK pathways in spinal microglia. Materials & methods: After NP preparation, miR NPs were assessed for their physical characteristics and then injected intrathecally into the spinal cords of rat spinal nerve ligation rats to test their analgesic effects. Results: miR NPs reduced pain behaviors for 11 days by negatively regulating the inflammatory response in spinal microglia. Conclusion: The anti-inflammatory effects of miR 146a-5p along with nanoparticle-based materials make miR NPs promising tools for treating neuropathic pain.

Relationships of Obesity-Related Behavior Patterns With Socioeconomic Status and Acculturation in Korean American Women.

There is limited understanding about the obesity-related behaviors of diet, physical activity, and sedentary behavior in Korean American women. The purpose of this study was to cluster obesity-related behavior patterns of Korean American women and to examine group differences in acculturation, socioeconomic status (SES), and body mass index (BMI). A secondary analysis from a cross-sectional study was conducted using two-step cluster analysis for clustering groups. A total of 137 Korean American women (M age = 42.7 years, SD = 3.9 years; MBMI = 23.1 kg/m2, SD = 3.1 kg/m2; 47.7% BMI ⩾ 23 kg/m2) participated. Three clusters were identified: healthy lifestyle, unhealthy lifestyle, and low physical activity but healthy diet group. The unhealthy lifestyle group was more likely to have high acculturation compared with other groups (p = .03). SES and BMI were not significantly different between groups. Further intervention is needed to improve obesity-related behaviors of acculturated Korean American women.

Pink1-Mediated Chondrocytic Mitophagy Contributes to Cartilage Degeneration in Osteoarthritis.

Cartilage loss is a central event in the pathogenesis of osteoarthritis (OA), though other than mechanical loading, the biochemical mechanisms underlying OA pathology remain poorly elucidated. We investigated the role of Pink1-mediated mitophagy in mitochondrial fission, a crucial process in OA pathogenesis. We used a monosodium iodoacetate (MIA)-induced rodent model of OA, which inhibits the activity of articular chondrocytes, leading to disruption of glycolytic energy metabolism and eventual cell death. The OA rat cartilage exhibits significant induction of autophagy-related proteins LC3B and p62, similar to human osteoarthritic cartilage. Moreover, expression of Pink1 and Parkin proteins were also increased in OA. Here, we confirm that Pink1-mediated mitophagy leads to cell death in chondrocytes following MIA treatment, while deficiency in Pink1 expression was associated with decreased cartilage damage and pain behaviors in MIA-induced OA. Finally, we found that autophagy and mitophagy-related genes are highly expressed in human osteoarthritic cartilage. These results indicate that OA is a degenerative condition associated with mitophagy, and suggest that targeting the Pink1 pathway may provide a therapeutic avenue for OA treatment.

Far-Infrared-Emitting Sericite Board Upregulates Endothelial Nitric Oxide Synthase Activity through Increasing Biosynthesis of Tetrahydrobiopterin in Endothelial Cells.

Far-infrared ray (FIR) therapy has been reported to exert beneficial effects on cardiovascular function by elevating endothelial nitric oxide synthesis (eNOS) activity and nitric oxide (NO) production. Tetrahydrobiopterin (BH4) is a key determinant of eNOS-dependent NO synthesis in vascular endothelial cells. However, whether BH4 synthesis is associated with the effects of FIR on eNOS/NO production has not yet been investigated. In this study, we investigated the effects of FIR on BH4-dependent eNOS/NO production and vascular function. We used FIR-emitting sericite boards as an experimental material and placed human umbilical vein endothelial cells (HUVECs) and Sprague-Dawley rats on the boards with or without FIR irradiation and then evaluated vascular relaxation by detecting NO generation, BH4 synthesis, and Akt/eNOS activation. Our results showed that FIR radiation significantly enhanced Akt/eNOS phosphorylation and NO production in human endothelial cells and aorta tissues. FIR can also induce BH4 storage by elevating levels of enzymes (e.g., guanosine triphosphate cyclohydrolase-1, 6-pyruvoyl tetrahydrobiopterin synthase, sepiapterin reductase, and dihydrofolate reductase), which ultimately results in NO production. These results indicate that FIR upregulated eNOS-dependent NO generation via BH4 synthesis and Akt phosphorylation, which contributes to the regulation of vascular function. This might develop potential clinical application of FIR to treat vascular diseases by augmenting the BH4/NO pathway.

Analgesic Effect of Toll-like Receptor 4 Antagonistic Peptide 2 on Mechanical Allodynia Induced with Spinal Nerve Ligation in Rats.

Neuroinflammation is one of the key mechanisms of neuropathic pain, which is primarily mediated by the Toll-like receptor 4 (TLR4) signaling pathways in microglia. Therefore, TLR4 may be a reasonable target for treatment of neuropathic pain. Here, we examined the analgesic effect of TLR4 antagonistic peptide 2 (TAP2) on neuropathic pain induced by spinal nerve ligation in rats. When lipopolysaccharide (LPS)-stimulated BV2 microglia cells were treated with TAP2 (10 µM), the mRNA levels of proinflammatory mediators, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS), were markedly decreased by 54-83% as determined by quantitative PCR (qPCR) analysis. Furthermore, when TAP2 (25 nmol in 20 µL PBS) was intrathecally administered to the spinal nerve ligation-induced rats on day 3 after surgery, the mechanical allodynia was markedly decreased for approximately 2 weeks in von Frey filament tests, with a reduction in microglial activation. On immunohistochemical and qPCR analyses, both the level of reactive oxygen species and the gene expression of the proinflammatory mediators, such as TNF-α, IL-1ß, IL-6, COX-2, and iNOS, were significantly decreased in the ipsilateral spinal dorsal horn. Finally, the analgesic effect of TAP2 was reproduced in rats with monoiodoacetate-induced osteoarthritic pain. The findings of the present study suggest that TAP2 efficiently mitigates neuropathic pain behavior by suppressing microglial activation, followed by downregulation of neuropathic pain-related factors, such as reactive oxygen species and proinflammatory molecules. Therefore, it may be useful as a new analgesic for treatment of neuropathic pain.

Blood Pressure Variability Is Associated With White Matter Lesion Growth in Intracranial Atherosclerosis.

BACKGROUND: High blood pressure variability (BPV) is associated with recurrent stroke. We investigated the association between BPV, new ischemic lesions (NILs), and white matter lesion (WML) growth in patients with ischemic stroke due to intracranial atherosclerosis (ICAS). METHODS: This study was performed as a post-hoc analysis of the STABLE-ICAS trial, which enrolled subacute ischemic stroke patients with symptomatic ICAS (>50% stenosis) and hypertension. BPV was measured at the office (visit by visit) and at home (day by day). Patients were divided into 3 groups (tertiles) according to their home BPV. WML growth and the occurrence of NILs were compared among the 3 groups. Multivariable analyses were performed to identify the independent risk factors of WML growth and NILs. RESULTS: Of the 111 enrolled patients, 69 patients (67.6%) demonstrated WML growth and 15 patients (13.7%) had NILs. Patients with higher BPV demonstrated a more WML growth (50% vs. 61.8% vs. 83.8; P = 0.02, by tertiles) and more NILs (5.4% vs. 5.4% vs. 29.7%; P = 0.002, by tertiles). In multivariable analyses, old age [odds ratio (OR) = 1.052 (95% confidence interval (CI) = 1.005-1.101); P = 0.03] and home BPV [OR = 1.149 (95% CI = 1.013-1.304); P = 0.02] were independently associated with WML growth. Low mean diastolic blood pressure [OR = 0.913 (95% CI = 0.874-0.984); P = 0.02] and high home BPV [OR = 1.287 (95% CI = 1.086-1.526); P = 0.004] were independently associated with NILs at follow-up. CONCLUSIONS: High BPV is associated with WML growth and NIL in ischemic stroke patients with symptomatic ICAS. BPV monitoring at home may be helpful.

Use of microcatheters for suction thrombectomy of acute distal occlusions.

We report our initial experience of using a microcatheter for contact aspiration of acute distal occlusions for recanalization. Endovascular technique and a case using Excelsior XT-27 microcatheter are presented. After manual suction within distal middle cerebral artery segments using a 50-ml syringe, instant and complete recanalization was obtained. Microcatheter suction thrombectomy using a 50-ml syringe can be considered a feasible treatment option for acute distal small artery occlusions.