scholarly journals Acute Injection of Omega-3 Triglyceride Emulsion Provides Very Similar Protection as Hypothermia in a Neonatal Mouse Model of Hypoxic-Ischemic Brain Injury

2021 ◽  
Vol 11 ◽  
Author(s):  
Denny Joseph Manual Kollareth ◽  
Hylde Zirpoli ◽  
Vadim S. Ten ◽  
Richard J. Deckelbaum
Keyword(s):  
Rectal Temperature ◽  
Infarct Volume ◽  
Tertiary Care ◽  
Acute Administration ◽  
Omega 3 ◽  
Ischemic Brain ◽  
Neonatal Mice ◽  
Tertiary Care Centers ◽  
Acute Injection ◽  
The Brain

Therapeutic hypothermia (HT) is a currently accepted treatment for neonatal asphyxia and is a promising strategy in adult stroke therapy. We previously reported that acute administration of docosahexaenoic acid (DHA) triglyceride emulsion (tri-DHA) protects against hypoxic-ischemic (HI) injury in neonatal mice. We questioned if co-treatment with HT and tri-DHA would achieve synergic effects in protecting the brain from HI injury. Neonatal mice (10-day old) subjected to HI injury were placed in temperature-controlled chambers for 4 h of either HT (rectal temperature 31–32°C) or normothermia (NT, rectal temperature 37°C). Mice were treated with tri-DHA (0.375 g tri-DHA/kg bw, two injections) before and 1 h after initiation of HT. We observed that HT, beginning immediately after HI injury, reduced brain infarct volume similarly to tri-DHA treatment (~50%). Further, HT delayed 2 h post-HI injury provided neuroprotection (% infarct volume: 31.4 ± 4.1 vs. 18.8 ± 4.6 HT), while 4 h delayed HT did not protect against HI insult (% infarct volume: 30.7 ± 5.0 vs. 31.3 ± 5.6 HT). HT plus tri-DHA combination treatment beginning at 0 or 2 h after HI injury did not further reduce infarct volumes compared to HT alone. Our results indicate that HT offers similar degrees of neuroprotection against HI injury compared to tri-DHA treatment. HT can only be provided in tertiary care centers, requires intense monitoring and can have adverse effects. In contrast, tri-DHA treatment may be advantageous in providing a feasible and effective strategy in patients after HI injury.

scholarly journals Ghrelin reduces cerebral ischemic injury in rats by reducing M1 microglia/macrophages

2022 ◽  
Vol 66 (1) ◽  
Author(s):  
Rong Tian ◽  
Gengsheng Mao
Keyword(s):  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Infarct Volume ◽  
Neurological Function ◽  
Tunel Staining ◽  
Triphenyltetrazolium Chloride ◽  
Ischemic Brain ◽  
Tnf Α ◽  
Ischemic Brain Tissue ◽  
The Brain

The purpose of this study was to investigate the effect of Ghrelin on the polarization of microglia/ macrophages after cerebral ischemia (CI) in rats. 60 wild-type SD rats were randomly divided into sham group, CI group, CI+Ghrelin group, 20 rats in each group. The modified Longa suture method was used to establish the middle cerebral artery occlusion (MCAO) model in rats. Before surgery, Ghrelin was injected subcutaneously (100μg/kg, twice a day) for 4 consecutive weeks. After modeling, neurological function scores were performed with three behavioral experiments: mNSS score, Corner test, and Rotarod test, to evaluate the recovery of neurological function after Ghrelin treatment. At the same time, the brain tissues were collected and stained with 2,3,5-triphenyltetrazolium chloride (TTC) to detect the cerebral infarct volume. RT-qPCR was used to detect the expression of TNF-α and IL-1β in the ischemic brain tissue, and the TUNEL staining was used to detect the apoptosis of brain tissue. Flow cytometry was used to detect the percentage of M1 type microglia/macrophages which were isolated by trypsin digestion of fresh cerebral cortex. Then, the Western blotting and immunofluorescence method were used to detect the phosphorylation level of AKT (P-AKT) and AKT. Compared with the CI group, the neurological function of the rats in the CI+Ghrelin group was dramatically improved, and the cerebral infarction area was dramatically reduced. At the same time, the expression of TNF-α and IL-1β in the ischemic brain tissue of rats in the CI+Ghrelin group decreased, and the apoptotic cells in the brain tissue also decreased. Compared with the CI treatment group, the activation of M1 microglia/macrophages in the cortex of the ischemic side of the infarct and the peri-infarct area in the CI+Ghrelin group was dramatically inhibited. At the same time, the ratio of P-AKT/AKT of the brain tissue in the CI+Ghrelin group was dramatically higher than that of the CI group. In the rat cerebral ischemia model, Ghrelin can promote the repair of brain damage and the recovery of neurological function after ischemia. Its mechanism may be related to activating AKT to selectively reduce M1 microglia/macrophages, reducing inflammation and cell apoptosis in brain tissue.

Penetrating knife injury to the skull: A case report in pediatric neurosurgical care

Trauma ◽  
2016 ◽  
Vol 19 (4) ◽  
pp. 302-307
Author(s):  
Tene A Cage ◽  
Nader Sanai ◽  
Michael T Lawton ◽  
Kurtis I Auguste
Keyword(s):  
Pediatric Population ◽  
Tertiary Care ◽  
Interdisciplinary Team ◽  
Brain Parenchyma ◽  
Cerebral Vasculature ◽  
Local Trauma ◽  
Tertiary Care Centers ◽  
Knife Injury ◽  
Neurologically Intact ◽  
The Brain

Isolated penetrating head injury in children is rare and is usually accidental. Each case is unique since the penetrating object and the trajectory through the brain parenchyma vary greatly among patients. We present a three-year-old girl who presented with a kitchen utility knife penetrating her left midface, skull, and brain abutting the anterior cerebral vasculature. Though the patient initially presented to a local trauma center, there were no pediatric nor vascular neurosurgeons on staff. Thus, she was transferred to our tertiary facility for definitive surgical management. A pediatric and vascular neurosurgeon worked together to remove the knife safely and the underlying vasculature remained intact. Postoperatively, the patient did well and was neurologically intact. Though penetrating cranial injury is rare in the pediatric population, such complex cases of brain injury can be properly managed with good outcome by an interdisciplinary team of specialists in tertiary care centers and can result in an excellent surgical and functional outcome for the patient.

scholarly journals Lipopolysaccharide Worsens the Prognosis of Experimental Cerebral Ischemia via Interferon Gamma-Induced Protein 10 Recruit in the Acute Stage

2019 ◽  
Author(s):  
Ping Wang ◽  
Jiaqi ZHANG ◽  
Feifei GUO ◽  
Shuang Wang ◽  
Yi ZHANG ◽  
...  
Keyword(s):  
Brain Injury ◽  
Interferon Gamma ◽  
Infarct Volume ◽  
Brain Homogenate ◽  
Acute Stage ◽  
Male Rats ◽  
Ischemic Brain Injury ◽  
Ppi Network ◽  
Ischemic Brain ◽  
The Brain

Abstract Background: Infection is an important clinical complication facing stroke-patients and triples the risk of death within 30 days post-stroke via mechanisms which are poorly understood. Aims: We tried to explore the mechanisms that inflammation caused by infections aggravated the ischemic brain injury after middle cerebral artery occlusion (MCAO). Methods: We used lipopolysaccharide (LPS) as systemic inflammatory stimuli to explore the mechanisms of aggravated ischemic brain injury after Sprague-Dawley male rats subjected to MCAO.Brain damage was evaluated by cerebral blood perfusion, Longa-5 scores, infarct volume and edema degree. Systemic cytokine responses and inflammatory changes in the plasma and brain were analyzed by ELISA kit, RT 2 Profiler TM PCR array, and quantitative real-time PCR.The differential genes were subjected to Gene Ontology enrichment analysis and Protein-Protein interaction (PPI) network construction. Results: LPS profoundly aggravated the brain damage after 24 hrs post-MCAO. At the acute stage (Ischemia/Reperfusion 90min/3h), the brain homogenate gene expression of Interleukin 6 (IL-6), Tumor necrosis factor a(TNF-a), Interleukin 1b(IL-1b)and Interferon Gamma-Induced Protein 10 (IP-10)was significantly up-regulated and the contents in plasma and brain homogenate were significantly increased in MCAO and MCAO+LPS group. IP-10 was the only gene with significant difference between MCAO and MCAO+LPS group, which was also in an important position with degrees of ³14 in PPI network. Conclusions: It was possible that trace LPS aggravated the ischemic brain injury by induction of excessive IP-10 secretion in the acute stage, leading to excessive inflammatory response, which consequently increased the infarct volume and edema degree 24 hrs post-MCAO.

scholarly journals Lipopolysaccharide worsens the prognosis of experimental cerebral ischemia via interferon gamma-induced protein 10 recruit in the acute stage

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Ping Wang ◽  
Jiaqi Zhang ◽  
Feifei Guo ◽  
Shuang Wang ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Interferon Gamma ◽  
Infarct Volume ◽  
Brain Homogenate ◽  
Acute Stage ◽  
Ischemic Brain Injury ◽  
Ppi Network ◽  
Ischemic Brain ◽  
The Brain

Abstract Background Infection is an important clinical complication facing stroke-patients and triples the risk of death within 30 days post-stroke via mechanisms which are poorly understood. Aims We tried to explore the mechanisms that inflammation caused by infections aggravated the ischemic brain injury after middle cerebral artery occlusion (MCAO). Methods We used lipopolysaccharide (LPS) as systemic inflammatory stimuli to explore the mechanisms of aggravated ischemic brain injury after Sprague-Dawley male rats subjected to MCAO. Brain damage was evaluated by cerebral blood perfusion, Longa-5 scores, infarct volume and edema degree. Systemic cytokine responses and inflammatory changes in the plasma and brain were analyzed by ELISA kit, RT2 Profiler™ PCR array, and quantitative real-time PCR. The differential genes were subjected to Gene Ontology enrichment analysis and protein–protein interaction (PPI) network construction. Results Lipopolysaccharide profoundly aggravated the brain damage after 24 h post-MCAO. At the acute stage (ischemia/reperfusion 90 min/3 h), the brain homogenate gene expression of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and Interferon gamma-induced protein 10 (IP-10) was significantly up-regulated and the contents in plasma and brain homogenate were significantly increased in MCAO and MCAO + LPS group. IP-10 was the only gene with significant difference between MCAO and MCAO + LPS group, which was also in an important position with degrees of ≥ 14 in PPI network. Conclusions It was possible that trace LPS aggravated the ischemic brain injury by induction of excessive IP-10 secretion in the acute stage, leading to excessive inflammatory response, which consequently increased the infarct volume and edema degree 24 h post-MCAO.

scholarly journals Chemokine Receptor Antagonist Peptide, Viral MIP-II, Protects the Brain against Focal Cerebral Ischemia in Mice

2001 ◽  
Vol 21 (12) ◽  
pp. 1430-1435 ◽  
Author(s):  
Shinya Takami ◽  
Masabumi Minami ◽  
Izumi Nagata ◽  
Shobu Namura ◽  
Masamichi Satoh
Keyword(s):  
Cerebral Ischemia ◽  
Chemokine Receptors ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Cortical Region ◽  
Dependent Manner ◽  
Ischemic Brain ◽  
Inflammatory Protein ◽  
The Brain ◽  
Macrophage Inflammatory Protein

The authors previously reported that mRNA for macrophage inflammatory protein-1α (MIP-1 α), a member of the CC chemokines, was expressed in glial cells after focal cerebral ischemia in rats. However, the function of chemokines in the ischemic brain remains unclear. Recently, viral macrophage inflammatory protein-II (vMIP-II), a chemokine analogue encoded by human herpesvirus-8 DNA, has been demonstrated to have antagonistic activity at several chemokine receptors. In the present study, the effects of vMIP-II and MIP-1α on ischemic brain injury were examined in mice to elucidate the roles of chemokines endogenously produced in the ischemic brain. Intracerebroventricular injection of vMIP-II (0.01–1 μg) reduced infarct volume in a dose-dependent manner when examined 48 hours after 1-hour middle cerebral artery occlusion followed by reperfusion. However, 1 μg MIP-1α increased infarct volume in the cortical region. These results supported the possibility that chemokines endogenously produced in the brain are involved in ischemic injury, and that chemokine receptors are potential targets for therapeutic intervention of stroke.

scholarly journals Lipopolysaccharide Worsens the Prognosis of Experimental Cerebral Ischemia via Interferon Gamma-Induced Protein 10 Recruit in the Acute Stage

2019 ◽  
Author(s):  
Ping Wang ◽  
Jiaqi Zhang ◽  
Feifei Guo ◽  
Shuang Wang ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Interferon Gamma ◽  
Infarct Volume ◽  
Brain Homogenate ◽  
Acute Stage ◽  
Ischemic Brain Injury ◽  
Ppi Network ◽  
Ischemic Brain ◽  
The Brain

Abstract Background: Infection is an important clinical complication facing stroke-patients and triples the risk of death within 30 days post-stroke via mechanisms which are poorly understood . Aims: We tried to explore the mechanisms that infections aggravated the ischemic brain injury after middle cerebral artery occlusion (MCAO). Methods: We used lipopolysaccharide (LPS) as systemic inflammatory stimuli to explore the mechanisms of aggravated ischemic brain injury after Sprague-Dawley male rats subjected to MCAO. Brain damage was evaluated by cerebral blood perfusion, Longa-5 scores, infarct volume and edema degree. Systemic cytokine responses and inflammatory changes in the plasma and brain were analyzed by ELISA kit, RT 2 Profiler TM PCR array, and quantitative real-time PCR.The differential genes were subjected to Gene Ontology enrichment analysis and Protein-protein interaction (PPI) network construction. Results: LPS profoundly aggravated the brain damage after 24 hrs post-MCAO . At the acute stage (Ischemia/ Reperfusion 90min/3h), the brain homogenate gene expression of Interleukin 6 (IL-6), Tumor necrosis factor a ( TNF- a ), Interleukin 1 b (IL-1 b ) and Interferon Gamma-Induced Protein 10 (IP-10) was significantly up-regulated and the contents in plasma and brain homogenate were significantly increased in MCAO and MCAO+LPS group. IP-10 was the only gene with significant difference between MCAO and MCAO+LPS group, which was also in an important position with degrees of ³ 14 in PPI network. Conclusions: It was possible that trace LPS aggravated the ischemic brain injury by induction of excessive IP-10 secretion in the acute stage, leading to excessive inflammatory response, which consequently increased the infarct volume and edema degree 24 hrs post-MCAO.

scholarly journals 124. Six-year Longitudinal Analysis of an Inpatient Infectious Diseases Telemedicine Service at a Community Hospital

2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S191-S192
Author(s):  
Nupur Gupta ◽  
Adit B Sanghvi ◽  
John Mellors ◽  
Rima Abdel-Massih
Keyword(s):  
Infectious Disease ◽  
Tertiary Care ◽  
Medical Officer ◽  
Rural Hospital ◽  
Hospital Length Of Stay ◽  
Observation Study ◽  
Patient Acuity ◽  
Telemedicine Service ◽  
Tertiary Care Centers ◽  
Over Time

Abstract Background Telemedicine (TM) has emerged as a viable solution to extend infectious disease (ID) expertise to communities without access to this specialty.1 TM allows clinicians in rural settings to connect with specialists at distant sites and provide the best care for their patients, often eliminating the need for hospital transfers. Here, we describe the experience from one of the longest standing inpatient Tele-ID consult services using live audio-video (AV) visits with the assistance of a telepresenter. Methods Longitudinal data were collected from a 126-bed rural hospital in Pennsylvania that had no access to ID consultation before 2014. Live AV consults during business hours began in 2014 and telephonic physician to physician consults were made available 24/7. All ID consult data were extracted from the hospital electronic health record between 2014 to 2019. Key outcomes assessed included the number of consult encounters, total hospital length of stay (LOS), discharges to home, transfer to tertiary care centers, and readmission rates at 30 days. Results Most consulted patients were Caucasians, and females with an average age of 64.7 years (Table 1). The number of unique consult encounters increased annually from 111 in 2014 to 469 in 2019 (Table 1). The Charlson Comorbidity Score and Elixhauser Comorbidity Index also increased each year beginning in 2016 (Table 1). By contrast, LOS decreased each year as did the 30-day readmission rate (Table 2). Most patients were not transferred (average 89.4% over 6 years) to tertiary care centers and more than half were discharged to home each year (Table 2). Conclusion This longitudinal 6-year observation study of an inpatient TM ID service at a rural hospital showed remarkable annual growth in consult encounters (total growth >400%). Despite increasing patient acuity, overall hospital LOS decreased over time (10.2 to 8.2 days). Patient transfers to tertiary care centers remained low (average 10.5% over 6 years) as did 30-day readmissions (average 16.3% over 6 years). The majority of patients were discharged to home (average 61.3% over 6 years). These findings show that a rural inpatient TM ID consult service can expand over time and is an effective alternative for hospitals without access to ID expertise. Disclosures John Mellors, MD, Abound Bio (Shareholder)Accelevir Diagnostics (Consultant)Co-Crystal Pharmaceuticals (Shareholder)Gilead (Consultant, Grant/Research Support)Merck (Consultant) Rima Abdel-Massih, MD, Infectious Disease Connect (Shareholder, Other Financial or Material Support, Chief Medical Officer)

scholarly journals Surgical outcome of primary intradural spinal arachnoid cysts: a series of 10 cases

2021 ◽  
Vol 57 (1) ◽  
Author(s):  
Essam Abdelhameed ◽  
Ahmed Ali Morsy
Keyword(s):  
Tertiary Care ◽  
Outer Wall ◽  
Arachnoid Cysts ◽  
Neurophysiological Monitoring ◽  
Japanese Orthopedic Association ◽  
Common Location ◽  
Before And After ◽  
Microsurgical Resection ◽  
Tertiary Care Centers ◽  
Intradural Arachnoid Cysts

Abstract Background Primary intradural spinal arachnoid cysts are rare pathologies of uncertain etiology and variable presentation from no symptoms to myelopathy or radiculopathy according to cord or root compression. MRI with diffusion and contrast differentiates them from many pathologies. There is a lot of debate regarding when to treat and how to treat such rare pathologies. Objective We present a series of 10 primary intradural arachnoid cysts and evaluate outcome after surgery. Methods This retrospective study includes patients having primary intradural spinal arachnoid cysts operated in two tertiary care centers from October 2012 till October 2019. Symptomatic cysts were subjected to microsurgical resection or outer wall excision and inner wall marsupialization under neurophysiological monitoring. The Japanese Orthopedic Association Score was used for clinical evaluation while MRI with contrast and diffusion was used for radiological evaluation before and after surgery. Results This series included 10 patients, 4 males and 6 females, with mean age of 40 years. Pain was the most common presentation. The most common location was dorsal thoracic region. Total excision was achieved in 2 cases and marsupialization in 8 cases. All symptoms improved either completely or partially after surgery. No neurological deterioration or recurrence was reported during the follow-up period in this series. Conclusion Treatment of symptomatic primary intradural spinal arachnoid cysts should be microsurgical resection, when the cyst is adherent to the cord, microscopic fenestration can be safe and effective.

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