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COVID-19 is a pandemic disease in which most patients have pulmonary symptoms. However, several cases of CNS involvement associated with COVID-19 have been reported. Acute necrotizing encephalopathy of childhood (ANEC) is a rare CNS complication of viral infections such as influenza, herpes virus, and COVID-19, leading to high mortality and morbidity rates. Several cases of COVID-19-associated acute necrotizing encephalopathy (ANE) have been reported since March 2020 in adults, with just a few cases in pediatrics. This article reports a 5-month-old child who presented with seizures, with the final diagnosis of ANE as a complication of COVID-19. MRI findings of ANEC, as reported in most COVID-19-associated ANEC case reports, involve bilateral, symmetric, multifocal lesions in the central thalami. Moreover, the brainstem, cerebral white matter, and cerebellum could be affected. The prognosis of COVID-19-associated ANE is poor, leading to neurologic dysfunction or mortality. COVID-19-associated ANE cases must be reported, especially in pediatrics, with detailed clinical history, laboratory data, and radiologic findings to introduce diagnostic criteria, prognosis, and a management protocol. [ABSTRACT FROM AUTHOR]

Cerebral stroke is a serious clinical condition in which oxidative stress, inflammation, necrosis, apoptosis, and autophagy play important roles in its pathogenesis. This study investigated the neuroprotective and healing effects of calcium dobesilate (CD) on cerebral hypoxia/reperfusion injury in rats. Forty Wistar albino male rats, each weighing 300–350 g, were separated into the Control group (no surgery and no pharmacological agent was administered); Sham-A group (only surgery was performed); DBL-A group (surgery was performed and CD 100 mg/kg/day was administered intraperitoneally for 3 days); Sham-C group (only surgery was performed); and DBL-C group (surgery was performed and 100 mg/kg/day CD was administered intraperitoneally for 10 days). Under sedation anesthesia, the bilateral common carotid arteries of all rats except the Control group were clipped for 30 min. After 4 h, the CD was given to the relevant groups, and then, all subjects were euthanized at scheduled times. The brain of each animal was removed for histopathological (hematoxylin and eosin staining), immunohistochemical (beclin-1, anti-MHC class II and anti-CD-68 staining), and biochemical (TNF, IL-1β, IL-6, caspase-3, GSH/GSSG, malondialdehyde, protein carbonyl, LC3II/LC3I, and beclin-1 levels) evaluations. It was observed that CD could reduce necrosis and mitigate polarization of microglia to the M1 phenotype, autophagy, free oxygen radicals, protein carbonylation, lipid peroxidation, IL-1β, IL6, TNF, caspase-3, beclin-1, and LC3II/LC3I levels in acute and chronic periods of hypoxia/reperfusion injury. From these results, it was observed that CD treatment could reduce neuronal necrosis and create anti-inflammatory, anti-edema, anti-oxidant, anti-apoptotic, and anti-autophagic effects in hypoxia/reperfusion injury in rats. [ABSTRACT FROM AUTHOR]

Objectives Methadone is a kind of opioid that is used to reduce the pain of addicts who decide to withdraw drugs. Sometimes due to a lack of appropriate cautions, this drug will be accessible to children, and poisoning might occur. Methadone poisoning usually presents with the loss of consciousness and pinpoint pupils. Herein, we present two cases of delayed hypoxic encephalopathy that had been poisoned by methadone. Case Presentation The first case was a 4-year-old female patient who firstly presented with nausea and vomiting; then, the case was discharged; however, 1 week later, the case was returned with the loss of consciousness and poisoning by methadone confirmed in her urine. Again 2 weeks later, the case returned to the hospital, developing weakness of limbs, slurred speech, and abnormal movement of her limbs. The second case was an 11-year-old female patient who was admitted to an intensive care unit due to the loss of consciousness and methadone poisoning. After providing supporting care, she was discharged but returned to the hospital 5 days later. She developed weakness of limbs, abnormal movement of tongue and extremities, and slurred speech. In their last admission, the magnetic resonance imaging of the patients revealed hypoxic damage in the basal ganglia; therefore, delayed hypoxic encephalopathy was confirmed. Conclusion Patients with methadone poisoning should be observed for at least 1 and a half months after poisoning. Moreover, parents should notice that in the case of observing abnormal neurologic manifestations bring their child as soon as possible to a hospital to prevent irreversible damage to the brain. [ABSTRACT FROM AUTHOR]

• Isolated triad findings will no longer by default be classified as caused by SBS/AHT. • Revival shaking attempts will be considered as a benevolent action, not as abuse. • The number of innocent caregivers who are currently considered as lying perpetrators, will decrease. • Presumed innocence and the rule of law will prevail. During the 1980′s a sudden life-lessness attack in a very young infant was described as "near-SIDS", and a caregiver who observed and tried to revive the infant was considered to be reliable and honourable. If, after the later acceptance of the traditional shaken baby theory, bilateral thin subdural hemorrhages (SDH) and retinal hemorrhages (RH) are detected after a lifelessness attack such a reliable caregiver has by default been transformed into an unreliable perpetrator of violent shaking. In 2016, the term "near-SIDS" was – via "apparent life-threatening event" (ALTE) − replaced by "brief resolved unexplained event" (BRUE). We suggest that such a life-threatening event is not always brief, and not always resolved. Based on a neglected hypoxia theory from 2004 we suggest as a hypothesis that a prolonged episode of apnea can result in brain hypoxia, brain edema, SDH, RH and increased intracranial pressure. The new hypothesis includes two new concepts: Prolonged Non-fatal Unexplained Event (PNUE) and Prolonged Fatal Unexplained Event (PFUE) which together with the hypoxia theory might explain why these two separate diagnoses have been conflated into one, viz. shaken baby syndrome (SBS). We suggest a study design that might corroborate or falsify the hypothesis, and if our hypothesis is corroborated, current "unreliable perpetrators" could be re-established as reliable resuscitators. [ABSTRACT FROM AUTHOR]

Survivors of an out-of-hospital cardiac arrest are at a high risk of mortality and morbidity especially when there is resultant global hypoxic brain injury. In these situations, the patient's degree of neurologic recovery may be uncertain and family decision making is often difficult. Decision making may also be complicated by the age of the patient and one's underlying cultural and spiritual beliefs stressing the importance of patient- and family-centered care. In this article, this clinical case demonstrates the challenges in decision making and highlights the importance of communication among the health care team and the family to align the patient's goals, values, and preferences in light of a poor neurological prognosis. [ABSTRACT FROM AUTHOR]

Rationale: Delayed post-hypoxic leukoencephalopathy (DPHL) is usually an overlooked condition, which arises as a result of a multitude of reversible and irreversible conditions. Patient's Concern: A 50-year-old female with a history of epilepsy, who developed DPHL 12 days after respiratory failure secondary to barbiturate toxicity. Diagnosis: DPHL on magnetic resonance imaging of the brain. Interventions: Mechanical ventilation was initiated for respiratory failure and hemodialysis for barbiturate toxicity. Outcomes: The patient developed akinetic mutism due to infirmity and had a residual disability, which led to permanent dependency. Lessons: The diagnosis of DPHL is often delayed or missed, given the rarity of this condition and its inconsistent clinical symptomatology. Diagnostic delay can be avoided by early recognition of the classical "delayed onset" symptoms. [ABSTRACT FROM AUTHOR]

Background: Trombley-Brennan terminal tissue injury (TB-TTI), also known as skin failure, was first identified in 2009 among critically ill adults receiving palliative care. Identification of this skin injury can be misinterpreted as a pressure ulcer. However, this phenomenon is now accepted as an early sign of impending death among critically ill adults.Clinical Findings: This case study describes TB-TTI in a terminally ill infant in a neonatal intensive care unit evidenced by intact, 2-cm oval skin discoloration on the lateral side of both knees with rapid progression in size.Primary Diagnosis: TB-TTI was identified on the day of death in an infant with a primary diagnosis of hypoxic-ischemic encephalopathy born at 32 weeks' gestation.Interventions: The neonatal intensive care unit (NICU) team mobilized the NICU advanced care team, institution's ethical council, and "Team Lavender" to provide infant comfort measures and emotional support to the family and care givers.Outcomes: Infant death occurred 8 hours after TB-TTI was identified.Practice Recommendations: To our knowledge, this case study of TB-TTI in a terminally ill neonate in the NICU has not been previously described in the neonatal or pediatric population. Early recognition of the phenomenon can enable the healthcare team to provide timely emotional, spiritual, and psychosocial support to the family and allow time to "be present" with the infant at "end of life." Future work should explore additional signs of TB-TTI and the occurrence rate. [ABSTRACT FROM AUTHOR]

Perinatal hypoxia is still one of the greatest threats to the newborn child, even in developed countries. However, there is a lack of works which summarize up-to-date information about that huge topic. Our review covers a broader spectrum of recent results from studies on mechanisms leading to hypoxia-induced injury. It also resumes possible primary causes and observed behavioral outcomes of perinatal hypoxia. In this review, we recognize two types of hypoxia, according to the localization of its primary cause: environmental and placental. Later we analyze possible pathways of prenatal hypoxia-induced injury including gene expression changes, glutaminergic excitatory damage (and a role of NMDA receptors in it), oxidative stress with ROS and RNS production, inflammation and apoptosis. Moreover, we focus on the impact of these pathophysiological changes on the structure and development of the brain, especially on its regions: corpus striatum and hippocampus. These brain changes of the offspring lead to impairments in their postnatal growth and sensorimotor development, and in their motor functions, activity, emotionality and learning ability in adulthood. Later we compare various animal models used to investigate the impact of prenatal and postnatal injury (hypoxic, ischemic or combinatory) on living organisms, and show their advantages and limitations. [ABSTRACT FROM AUTHOR]

Brain tissue oxygenation (rSO2) measured by near-infrared spectroscopy (NIRS) is lower in hemodialysis patients than in the healthy population and is associated with cognitive dysfunction. The involved mechanisms are not known. We conducted this study to identify the factors that influence the rSO2 values in endstage renal disease (ESRD) patients and to describe rSO2 changes during hemodialysis. We included a cohort of ESRD patients hemodialyzed in our institution. We recorded rSO2 using INVOS 5100C oximetry system (Medtronic, Essex, U.K.) and analyzed changes in basic laboratory values and hemodynamic fluctuations. Baseline rSO2 was lower in patients with heart failure (45.2±8.3 % vs. 54.1±7.8 %, p=0.006) and was significantly linked to higher red cell distribution width (RDW) (r=-0.53, p=0.001) and higher BNP level (r=-0.45, p=0.01). The rSO2 value decreased in first 15 min of hemodialysis, this decrease correlated with drop in white blood count during the same period (r=0.43, p=0.02 in 10 min, r=0.43, p=0.02 in 20 min). Lower rSO2 values in patients with heart failure and higher RDW suggest that hemodynamic instability combined with vascular changes probably leads to worse cerebral oxygenation in these patients. Decrease of rSO2 in 15th minute of hemodialysis accompanied with a significant drop in leukocyte count could be explained by complement activation. [ABSTRACT FROM AUTHOR]

We investigated if transcriptional responses are consistent with the arrest of synaptic activity in the anoxic turtle (Trachemys scripta) brain. Thirty-nine genes of key receptors, transporters, enzymes and regulatory proteins of inhibitory and excitatory neurotransmission were partially cloned and their expression in telencephalon of 21 °C- and 5 °C-acclimated normoxic, anoxic (24 h at 21 °C; 1 and 14 days at 5 °C) and reoxygenated (24 h at 21 °C; 13 days at 5 °C) turtles quantified by real-time RT-PCR. Gene expression was largely sustained with anoxia at 21 °C and 5 °C. However, the changes in gene expression that did occur were congruous with the decline in glutamatergic activity and the increase in GABAergic activity observed at cellular and whole organism levels. Moreover, at 21 °C, the alterations in gene expression with anoxia induced a distinct gene expression pattern compared to normoxia and reoxygenation. Strikingly, acclimation from 21 °C to 5 °C in normoxia effectuated substantial transcriptional responses. Most prominently, 56% of the excitatory neurotransmission genes were down-regulated, including most of the ones encoding the subunits composing excitatory N -methyl- d -aspartate (NMDA) and 3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) glutamate receptors. By contrast, only 26% of the inhibitory neurotransmission genes were down-regulated. Consequently, the gene expression pattern of 5 °C normoxic turtles was statistically distinct compared to that of 21 °C normoxic turtles. Overall, this study highlights that key transcriptional responses are consonant with the synaptic arrest that occurs in the anoxic turtle brain. In addition, the findings reveal that transcriptional remodelling induced by decreased temperature may serve to precondition the turtle brain for winter anoxia. [ABSTRACT FROM AUTHOR]

Sirtuin 3 (SIRT3) mediates cellular resistance toward various forms of stress. SIRT3 expression in the developing brain, especially its localization in various glial cell types, has not been fully explored. This study aimed to determine SIRT3 expression in the brain of neonatal rats subjected to hypoxia. By immunohistochemistry, immunofluorescence and Western blotting, we show here that SIRT3 expression in the periventricular white matter was up-regulated in hypoxia group compared with the control group at the corresponding time points. Intense SIRT3 expression was detected in microglia at early time points after hypoxia whose cell number was increased with reduced ramifications in hypoxia group compared with the control group. Furthermore, SIRT3 immunoreactivity was obviously enhanced at 24 h, 3 and 7d, but was declined at 14d after hypoxia so that SIRT3 expression between the two groups was comparable. SIRT3 immunofluorescence was also localized in astrocytes labeled with GFAP which was augmented at different time points in hypoxia group. GPAP positive astrocytes exhibited long extending processes being most pronounced at 3d. SIRT3 was moderately expressed at 24 h, 3 and 7d, but was markedly increased at 14d after hypoxia. Moderate SIRT3 expression was also localized in oligodendrocytes labeled with CNPase in the control group. The incidence of CNPase positive oligodendrocytes showing colocalization of SIRT3 increased significantly at 24 h, 3 and 7d after hypoxia. In conclusion, SIRT3 expression was differentially up-regulated in all three major glial cell types following hypoxia. It is suggested that increased SIRT3 expression in the respective glial cell types following hypoxia is involved in different signaling pathways that protect against hypoxic stress in the developing brain. [ABSTRACT FROM AUTHOR]

While normal oxygen saturation is commonly thought to be a marker of normal oxygenation, cutaneous saturation does not account for the sufficiency of oxygen within each cell or that of the system overall. Rather, cutaneous oximetry simply defines the saturation of haemoglobin (Hb) with oxygen in a pulsatile vessel. Assessment of sufficiency is best determined by measurement of the amount of oxygen left over following aerobic respiration. This left over oxygen is 'stored' on Hb in the venous compartment and can be calculated as the venous oxygen content. We hypothesize that the development of a venous oxygen content or saturation reference range in a group of well, uninjured very preterm newborns and subsequent application, in a randomised trial, with a structural, functional and molecular outcome will resolve the method for assessment of oxygen sufficiency in preterms by demonstrating both clinical safety and effectiveness. This method could be subsequently used for titration of supplemental oxygen. [ABSTRACT FROM AUTHOR]

Electronic fetal monitoring (EFM) is the recommended method of intrapartum fetal surveillance for high-risk pregnancies. The cardiotocogram (CTG) trace forms a central piece of documentary evidence in medico-legal cases related to intrapartum hypoxia and birth asphyxia. Cardiotocography was introduced in 1960s as a screening tool with the view to reduce fetal hypoxic brain injury and cerebral palsy rates. However, its positive predictive value for intrapartum fetal hypoxia is as low as 30%, with false positive rate of around 60%. Since its introduction in obstetric practice there has been an increase in intrapartum caesarean section and operative delivery rates, but there has been no demonstrable reduction in occurrence of cerebral palsy or intrapartum fetal deaths. The low specificity of CTG for detection of fetal hypoxia therefore necessitates confirmatory tests such as fetal scalp blood sampling (FBS) or analysis of fetal electrocardiography. The National Institute for Health and Clinical Excellence (NICE) recommends continuous intrapartum fetal monitoring with CTG for high-risk pregnancies and storing the CTG electronically for at least 25 years for medicolegal purposes. It is mandatory that all healthcare professionals who are responsible for the care of women in labour are adequately trained and assessed on pathophysiology of fetal heart rate (FHR) changes in labour to improve interpretation of CTG and avoid adverse maternal and/or fetal outcomes. Confidential enquiries into intrapartum morbidity and deaths have shown that the four main contributors to poor perinatal outcomes are – an inability to interpret CTG by the health professionals, a failure to incorporate the overall clinical condition, a failure to communicate or escalate, and delay in taking appropriate action. In this article we discuss three cases, two of which led to adverse perinatal outcomes. The key learning points and risk management issues relevant to the cases are also discussed. [ABSTRACT FROM AUTHOR]

Tumour hypoxia leads to radio and chemotherapy resistance among cancer patients. The aim of this paper is to formulate a hypothesis on the heterogeneity of hypoxia in solid tumours. Tumour vasculature is known to be significantly variable. The great structural and functional abnormalities of tumour microcirculation cause spatial and temporal heterogeneity in its perfusion. Tumours have constantly been under the influence of pulsatile blood perfusion with variable pressure that initiates inhomogeneous erythrocyte deformation and following impact on oxygen disorder release from red blood cells into plasma within the blood vessel. Furthermore, stochastically released oxygen in tumour vessel, plasma and interstitial fluid may lead to heterogeneity of hypoxia. Under the influence of increased heterogeneity of hemodynamic force, the oxygen molecules dissolved in blood plasma are inclined to form nanobubbles (NBs) in tumour vessels. Considering the fact that tumour interstitial fluid pressure is increased compared to normal tissues, we assume that oxygen NBs may burst under the impact of shear stress. During the course of mechanochemical reaction, when a nanobubble (NB) bursts, both reactive oxygen species and ions form in various charged states. In consequence of a chain reaction, free radical oxygen molecules bind to proteins and lipids, thus reducing oxygen molecules in a chaotic manner within the tumour. The proposed hypothesis should be used as a methodical approach based on the simultaneous ultrasound imaging diagnostic techniques and therapy, regarding the mechanochemical effect on NB conglomerates with drugs in the tumour. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Infantile spasms is diagnosed late even by expert pediatricians. Late diagnosis (later than 3 weeks) can have a negative effect on the long-term prognosis. We aimed to investigate infantile spasms treated with intravenous methylprednisolone pulse. MATERIALS & METHODS: In this case series study, 20 infants with infantile spasms in 17-Shahrivar Hospital, Rasht, Iran were enrolled. Drugs were administered based on Mytinger protocol that included 3 days of methylprednisolone pulse and 56 days of oral prednisolone. The control of spasms and the omission of hypsarrhythmia in infants follow-up were the primary and secondary outcomes, respectively. Remission was indicated if the caregivers mentioned no spasms or >50% decrease regarding drug initiation for at least 5 consecutive days and the electroencephalography during sleep period noted the omission of hypsarrhythmia. RESULTS: Eleven female (55%) and 9 male (45%) patients with the mean age of 4.95±1.39 months were enrolled. Mean rapid remission was noted as 4.41±1.50 days. Twelve patients (60%) noted early remission. seizure was controlled in 3(15%) patients completely after 24 months. Five (25%) occasional seizures were noted controlled by routine anticonvulsant drugs after 24 months and 12 (60%) no response was mentioned. Most of the patients (65%) had cryptogenic etiology for infantile spasms. Uncontrolled seizure was mentioned after initial remission. CONCLUSION: Methyl prednisolone is an appropriate drug based on easy administering, low cost, and its accessibility. [ABSTRACT FROM AUTHOR]

In tissues with elastic properties, an edema causes a raised tissue pressure and therefore a diminished blood flow. The authors assume that an increased tissue pressure due to local and/or relapsing edema may be the cause for incomplete necrosis (e.g. demyelinated lesions) or seldom complete necrosis in the brain. Newly forming demyelinating lesions seldom show small tissue bands with normal appearing myelin sheaths in the immediate vicinity of precursor lesions (Baló type of MS). The small myelinated bands are the result of a "protected zone" on the edge of previous demyelinated lesions. The authors explain this protected zone with two arguments. Firstly, the resorptive granulation tissue of more or less older lesions is relatively rich in capillaries. These capillaries may act as an energy reservoir that can nourish not only the plaque, but also a narrow adjacent myelinated tissue band by diffusion, even if the capillary blood flow in this tissue band is limited due to the greater tissue pressure of a new developing lesion in the neighborhood. Secondly, another protective mechanism may act simultaneously: older or more sclerosed lesions and small adherent bands of myelinated tissue with them may swell less in cases of an edema than in normal tissue. The hardening of the older lesions is caused by proliferated fiber-forming astrocytes in the sense of scarring. In an area with an increased tissue pressure, the capillaries are less compressed in a sclerosed lesion than in regions of normal grey and white matter. In addition, the adherent myelinated tissue band closest to the edge of a hardened plaque is better protected against swelling and compression than the further away tissue. Theoretically, this protection zone is comparable with protected blood vessels in the Haversian canals or the medullary spaces of bones. Both theses of protecting mechanisms at the edges of demyelinated lesions support the assumption of a hypoxic causation principle of demyelinating lesions in Baló's concentric sclerosis and multiple sclerosis. [ABSTRACT FROM AUTHOR]

Occupational deaths are work-related deaths and usually occur in the work place of an individual. A case of occupational death in a female factory worker has been described, where the saree she was wearing accidentally got entangled in the moving belt and caused ligature strangulation. She was unconscious throughout indicating bilateral occlusion of the carotids and died a day after the incident. The authors have described the correlation between the distribution of the injuries on the body and the manner a saree is worn. Investigation of the workplace revealed that the place where she was standing was located between two machines, and the space was inadequate for normal movement. Some suggestions have been offered which may decrease the incidences of occupational ligature strangulation due to entanglement of dress materials in the moving machineries. [ABSTRACT FROM AUTHOR]

Sepsis is a leading cause of morbidity and mortality for infants and children in the United States and is associated with peripheral and central nervous system dysfunction including encephalopathy and paresis. Sepsis-associated encephalopathy (SAE) may be underdiagnosed in children, but the exact incidence is not known because of variable criteria for its diagnosis, which require a high index of suspicion and exclusion of other confounding factors. Neuroimaging and cerebrospinal fluid analysis are often normal. Electroencephalography may correlate with the severity of encephalopathy. Intensive care unit--acquired weakness due to critical illness neuropathy or myopathy develops later, and resolution of weakness is gradual. Difficulty weaning from the ventilator is an early sign. Electroencephalography may be helpful in identifying SAE once other causes of encephalopathy have been ruled out. However, the lack of consensus on the definition of SAE and sparse pediatric data limit the specific evidence-based recommendations, which can be made for the assessment and treatment of this disorder in the emergency department. [ABSTRACT FROM AUTHOR]

Objective The purpose of this study was to determine the effects of different inspired oxygen fractions (Fi o 2 ) on average and peak power capacity during consecutive jumps to assess the effectiveness of a hypoxic explosive-strength program. Methods Eight physically active subjects (aged 33.62 ± 4.07 years; height, 1.77 ± 0.05 m; weight, 74.38 ± 6.86 kg) completed a Bosco jump test, consisting of a series of 15-second “all-out” jumps with 3 minutes of recovery, performed in a normoxia condition (N [Fi o 2 = 21%]) and in two hypoxic conditions: moderate hypoxia (MH [Fi o 2 16.5% o 2 ]) and high hypoxia (HH [13.5% o 2 ]). A force platform provided the average and the maximal power output (W) generated during consecutive jumps. Measurements were also taken of lactate, creatine kinase, arterial oxygen saturation, and perceived exertion using the Borg fatigue scale. Results The average power outputs throughout the entire sets were similar between N (3187 ± 46) and MH (3184 ± 15; P > .05), but slightly greater with HH (3285 ± 43) compared with N ( P < .05). Values for lactate during N (7.5 ± 3.0), MH (7.7 ± 4.0), and HH (7.9 ± 3.0; P > .05), and for creatine kinase (values before, 69.8 ± 15; and 24 hours after in N [79.4 ± 15.60], MH [85.2 ± 26.7], and HH [84.3 ± 47.2]; P > .05) were similar for all conditions. Only during exercise in hypoxia were moderate and severe hypoxemia induced as the sets increased and Fi o 2 was lower ( P < .05). At the same time, the perceived exertion reported by subjects was substantially higher at HH (8.9 ± 1.1) than at N (7.1 ± 1.9; P < .05). Conclusions Jumping power output was not negatively affected by mild or high hypoxia in comparison with normoxia during an anaerobic workout despite having higher hypoxemia and a greater perception of exertion. [ABSTRACT FROM AUTHOR]

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Patients with chronic obstructive pulmonary disease (COPD) present many neurological disorders of unknown origin. Although hypoxemia has long been thought to be responsible, several studies have shown evidence of neuronal damage and dysfunction even in non-hypoxemic patients with COPD. Adaptive mechanisms protect the brain from hypoxia: when arterial oxygen tension (PaO 2 ) decreases, the cerebral blood flow (CBF) increases, ensuring continuously adequate oxygen delivery to the brain. However, this mechanism is abolished during non-rapid eye movement (NREM) sleep. Any drop in PaO 2 during NREM sleep is therefore not compensated by increased CBF, causing decreased cerebral oxygen delivery with subsequent brain hypoxia. Patients with may therefore be exposed to neuronal damage during this critical time. This mechanism is of vital importance for patients with COPD because of the potentially deleterious cortical effects. Nocturnal desaturation is quite frequent in COPD and affects approximately one out of two patients who are not hypoxemic during wakefulness. Although the prevalence of NREM sleep desaturation has never been specifically assessed in COPD, current data suggest that at least half of the nocturnal desaturation in desaturating patients occurs during NREM sleep. This review presents the rationale for the hypothesis that nocturnal desaturation during NREM sleep promotes neuronal damage and dysfunction in COPD. [ABSTRACT FROM AUTHOR]

Objective Seizures in neonates are very different from those of older children and adults. The aim of this study was to determine the etiology, clinical presentation, and outcome of seizures in hospitalized neonates of Besat Hospital, Hamadan, Iran. Material & Methods In this retrospective study, we evaluated all neonates with seizures (aged 0-28 days) admitted to the Besat hospital, Hamadan, over a period of three years from September 2008 to September 2011. The data were obtained from hospital records and analyzed using SPSS 12. Results Seizures were reported in 102/1112 (9.1%) neonatal admissions. Among neonates with seizures, 57% were male and 23.5% were preterm. The mean birth weight was 2936±677 grams and the mean gestational age was 37.60±1.94 weeks. 16.7% of them were LBW and 2.9% VLBW. In terms of seizure type, subtle seizures were observed in 38.2%, tonic in 29.4%, clonic in 26.4%, and myoclonic in 5.9% of cases. The main diagnosis in neonates with seizures included hypoxic-ischemic encephalopathy (HIE) (34.3%), infections (24.4%), intracranial hemorrhage (6.9%), hypoglycemia (5.9%), hypocalcemia (2.9%), inborn error of metabolism (1%), and unknown cause (24.5%). The mortality rate was 14.7%. Conclusion Neonatal seizures indicate a significant underlying disease. HIE was the most common cause of neonatal seizures in our study. Therefore, efforts should be made to improve care during childbirth. [ABSTRACT FROM AUTHOR]

Highlights: [•] Improved quadratic TFDs with lag-independent kernels to characterize HRV signals. [•] Instantaneous frequency based HRV features for the detection of perinatal hypoxia. [•] The proposed TFD can enhance the ability of resulted features for hypoxia detection. [ABSTRACT FROM AUTHOR]

The brain of fish plays an important role in regulating growth and adapting to environmental changes. However, few studies have been performed to address the changes in gene expression profiles in fish brains under hypoxic stress. In the present study, silver carp (Hypophthalmichthys molitrix) were kept under hypoxic experimental conditions by using the method of natural oxygen consumption, which resulted in a significant decrease in malondialdehyde (MDA) and glutathione (GSH) content and superoxide dismutase (SOD) activity in the brain. In addition, RNA sequencing (RNA-Seq) was performed to analyze transcriptional regulation in the brains of silver carp under normoxia (control group), hypoxia, semi-asphyxia, and asphyxia conditions. The results of KEGG enrichment pathway analysis showed that the immune system, such as antigen processing and presentation, natural killer cell-mediated cytotoxicity, was enriched in the hypoxia group; the nervous system (e.g., "glutamatergic synapse"), signal transduction (e.g., "calcium signaling pathway"; "foxo signaling pathway"), and signaling molecules and interactions (e.g., "neuroactive ligand-receptor interaction") were enriched in the semi-asphyxia group; and signaling molecules and interactions (e.g., "neuroactive ligand–receptor interaction") were enriched in the asphyxia group. These results provide novel insights into the molecular regulatory mechanism of the fish brain coping with hypoxia stress. [Display omitted] • Hypoxia might cause brain of silver carp oxidative stress. • "neuroactive ligand-receptor interaction" pathway might play an important role in brain of silver carp under hypoxia. • Hypoxia stress might damage the immune system and nervous system in the brain tissue of the silver carp. [ABSTRACT FROM AUTHOR]

Objectives: Given that reliable markers for early ischemic brain damage are lacking, we set out to test whether pimonidazole can be used as a reliable tool in the quantification of hypoxic insults, at early time points following experimental stroke. Methods: We have used semi-quantitative Western blotting detection of pimonidazole adducts in a rat model of reversible middle cerebral artery occlusion (MCAO), treated with remote post-conditioning. Results: First, we demonstrated that a linear relationship exist between pimonidazole binding in the ischemic hemisphere and duration of ischemia, in animals subjected to 5, 15, 30, or 60 minutes of occlusion followed by 120 minutes of reflow. Then we showed a significant reduction in pimonidazole binding in the infarcted hemisphere, when rats with 60 minutes of MCAO, immediately after establishment of cerebral reflow, had 3×15 minutes intermittent hind limb ischemia followed by 24-hour survival. We analysed the middle cerebral arteries from animals with 60 minutes of MCAO and early remote postconditioning, followed by 30 minutes, 24, or 48 hours of reflow. At 24 hours of reflow increases in phosphorylated protein kinase C-alpha with concomitantly increased levels of p38 phosphorylation were observed. Conclusions: Our investigation demonstrates that pimonidazole can be used for quantifying ischemic impact in stroke, even after very short survival times. It furthermore shows that early remote postconditioning reduces ischemic damage, probably through hyperpolarization and reduced reflow vasospasm in the conduit middle cerebral arteries. [ABSTRACT FROM AUTHOR]

Objective: To elucidate the magnitude of global cerebral oxygenation impairment, using cerebral oxygenation indices and S-100β protein as potential markers, during off-pump coronary artery bypass grafting (OPCAB). Design: Prospective cohort study. Setting: Tertiary cardiac center. Participants: Thirty-five patients undergoing OPCAB. Interventions: Jugular bulb and arterial blood samples for cerebral oxygenation indices (arterial oxygen and carbon dioxide partial pressures, jugular bulb oxygen saturation, arterial-jugular bulb oxygen content, arterial-jugular carbon dioxide partial pressure, brain oxygen extraction ratio, and estimated respiratory quotient) and S-100β protein determination were collected at anesthesia induction; anterior, inferior, and posterior wall anastomoses; after sternal closure; and 6 hours postoperatively. Concomitant hemodynamic data were obtained. The S-100β determination was extended to 12 and 24 hours postoperatively. Measurements and Main Results: Heart positioning for the target vessel exposure induced significant hemodynamic deterioration (p < 0.001). Although cerebral oxygenation indices were influenced adversely by a low-cardiac-output state mainly during vertical heart dislocation (p < 0.001), they remained within normal limits. Hemodynamic and cerebral oxygenation statuses reverted to baseline within 6 hours postoperatively. Similarly, S-100β jugular bulb and arterial protein levels presented a gradual increase, which peaked by the end of surgery (means, 0.54 and 0.62 μg/L, respectively; p < 0.001) and then decreased by the first postoperative day. Jugular bulb-arterial S-100β levels were maximized during posterior wall anastomosis (0.098 μg/L; p < 0.01). Conclusion: Although exposure of the 3 main coronary arteries during OPCAB promotes derangement of the cerebral oxygen indices and S-100β release, this seems to be transient, remains within the near-normal range, and is reversible almost completely 6 hours postoperatively. [Copyright &y& Elsevier]

Summary: Transplantation of human umbilical cord blood (hUCB) cells is a potential approach for the treatment of perinatal hypoxic-ischemic brain injury. Neurological and motor deficits resulting from the brain lesion are ameliorated upon transplantation. The molecular mechanisms underlying these improvements are currently being unravelled. One parameter identified as part of the beneficial effects of hUCB cells is the reduction of brain inflammation. It is, however, unclear whether the modulation of brain inflammation is due to local or systemic effects of hUCB cells. In this study, the effects of hUCB cell transplantation in a model of perinatal hypoxic-ischemic brain injury were investigated at the systemic level by measurement of serum levels of pro-inflammatory cytokines by multiplex bead arrays. Two days after induction of the brain damage, levels of the pro-inflammatory cytokines Interleukin-1α (IL-1α), Interleukin-1β (IL-1β), and Tumor necrosis factor α (TNFα) were increased in the serum of rats. Application of hUCB cells, in turn, correlated with a reduced elevation of serum levels of these pro-inflammatory cytokines. This decrease was accompanied by a reduced expression of CD68, a marker protein of activated microglia/macrophages in the brain. Therefore, systemic modulation of the immune response by hUCB cells could represent one possible mechanism of how these cells might mediate their beneficial effects. Creation of a regenerative environment with reduced inflammation might account for the functional regeneration observed upon hUCB cell treatment in lesioned animals. [Copyright &y& Elsevier]

The management of patients with traumatic brain injury has evolved in the last several years, due to the introduction of new, invasive monitoring devices. The ability to monitor parameters other than measurements related to pressures has generated substantial interest. Brain tissue oxygenation monitoring has been consistently shown to provide prognostic information, as indicated by poor prognosis associated with low brain tissue oxygen values. Furthermore, various physiologic manipulations, including increasing the PaO2, have been associated with an increase in brain tissue oxygenation. Whether brain-oxygenation-guided therapy results in improvement in outcomes is debatable. Retrospective studies suggest benefit, while prospective studies have shown a higher intensity of therapeutic interventions with no outcome differences. Data from high quality randomized trials are necessary to determine if brain-oxygenation-guided therapy is beneficial. An oxygen challenge (transient increase in FIO2 to 0.6 up to 1.0) to assess the responsiveness of the monitoring and ascertain the presence of technical malfunction is an accepted practice. [ABSTRACT FROM AUTHOR]

Objective Developmental impairment is a common problem in children health that occurs in approximately 5-10% of the childhood population. The aim of this study was to determine the etiologic yield of subspecialists' evaluation of young children with developmental disability. Materials & Methods All children aged between 2 months and 5 years referred over a 15-month period to Hamadan University of Medical Sciences subspecialty services for initial evaluation of a suspected developmental Disability, were enrolled in the present study. Diagnostic yield was determined after the completion of clinical assessments and laboratory tests requested by the evaluating physician. Results A total of 198 children (129 boys and 69 girls) were eligible for our study. 108 children had global developmental delay and 90 children had isolated developmental delay. Approximately ¼ of all patients did not have any specific etiology for developmental disability. Cerebral palsy (CP) was the most common clinical syndrome in all patients (41.4%). Hypoxic ischemic encephalopathy (13.8%), brain dysgenesis (13%), genetic disorder (13%), and neurodegenerative diseases (11%) were determined in more than one half of all children with global developmental disability. in our study, "developmental speech delay" was the common cause of isolated speech delay. Conclusion Determination of an underlying etiology is an essential part of specialty evaluation of young children with developmental disability. The results of this study were similar closely to the results of other studies. [ABSTRACT FROM AUTHOR]

Background: Cerebral hypoxia-ischemia remains a complication in children with congenital heart disease. Near-infrared spectroscopy can be utilized at the bedside to detect cerebral hypoxia-ischemia. This study aimed to calibrate and validate an advanced technology near-infrared cerebral oximeter for use in children with congenital heart disease. Methods: After institutional review board approval and parental consent, 100 children less than 12 years and less than 40 kg were enrolled. Phase I (calibration) measured arterial and jugular venous saturation (SaO2, SjO2) by co-oximetry simultaneously with device signals to calibrate an algorithm to determine regional cerebral saturation against a weighted average cerebral saturation (0.7 SjO2 + 0.3 SaO2). Phase II (validation) evaluated regional cerebral saturation from the algorithm against the weighted average cerebral saturation by correlation, bias, precision, and ARoot Mean Square assessed by linear regression and Bland-Altman analysis. Results: Of 100 patients, 86 were evaluable consisting of 7 neonates, 44 infants, and 35 children of whom 55% were female, 79% Caucasian, and 41% with cyanotic disease. The SaO2 and regional cerebral saturation ranged from 34% to 100% and 34% to 91%, respectively. There were no significant differences in subject characteristics between phases. For the entire cohort, ARMS, bias, precision, and correlation coefficient were 5.4%, 0.5%, 5.39%, and 0.88, respectively. Age, skin color, and hematocrit did not affect these values. Conclusions: This cerebral oximeter accurately measures the absolute value of cerebral saturation in children over a wide range of oxygenation and subject characteristics, offering advantages in assessment of cerebral hypoxia-ischemia in congenital heart disease. [ABSTRACT FROM AUTHOR]

The article focuses on the impact of environmental noise on cerebral oxygenation. Twenty-four premature infants born less than 32 weeks' gestational age were tapped by the authors for their study and they were first observed between 2 and 48 hours of life, once again on day of life 7 and every seven days thereafter. They found that there was no significant change in cerebral oxygen saturation values for peak sound levels 5 decibels above the average ambient sound level.

Abstract: Introduction: The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear, but one of the possible underlying mechanisms is the alteration of the cerebral microvascular function. The aim of the present work was to test whether cerebral vasomotor reactivity is impaired in patients with severe sepsis. Methods: Patients fulfilling the criteria of clinical sepsis and showing at least 2 organ dysfunctions were included (n = 16). Nonseptic healthy persons without previous diseases affecting cerebral vasoreactivity served as controls (n = 16). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15, and 20 minutes after intravenous administration of 15 mg/kg acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity [CVR]) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity [CRC]) were compared among the groups. Results: Absolute blood flow velocities after administration of the vasodilator drug did not differ between control and septic patients. Assessment of the time course of the vasomotor reaction showed that patients with sepsis reacted in a similar fashion to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that there was no difference in vasodilatory ability between septic and healthy subjects (CRC controls, 54.8% ± 11.1%; CRC sepsis-associated encephalopathy, 61.1% ± 34.4%; P = .49). Conclusions: We conclude that cerebrovascular reactivity is not impaired in patients with severe sepsis. It is conceivable that cerebral vasoreactivity may be differently involved at different severity stages of the septic process. [Copyright &y& Elsevier]

Abstract: Treatment of subclinical seizures in newborn HIE remains a contentious issue, especially in light of potential adverse effects of aggressive use of anticonvulsants. We report on the association of subclinical seizures with changes in cerebral oxygenation in an infant with HIE. Our results show that subclinical seizures of longer durations and with associated autonomic disturbance (increased blood pressure) are more likely to be associated with fluctuation in cerebral oxygenation, with some seizures resulting in cerebral hypoxia. Future studies should aim to delineate the effects of subclinical seizure and anticonvulsant treatment on cerebral oxygenation, and their relationships to developmental outcome. Level of cerebral oxygenation may play a role in refining anti-convulsant treatment and management of subclinical seizures in newborns. [Copyright &y& Elsevier]

Abstract: Basal ganglia injury (BGI) is a type of perinatal hypoxic-ischemic (H-I) brain injury. Both malfunctions of glutamatergic and dopaminergic pathways in striatum were suggested to contribute to BGI. In current study, we investigated the imaging profile of glutamate (Glx) levels by proton magnetic resonance spectroscopy (1H-MRS), and the expression of dopamine D2 receptors (D2R) and dopamine transporter (DAT) by immunohistochemical staining in a newborn piglet model of H-I brain injury. We found that the number of striatal D2R positive neurons decreased following H-I brain injury, and the decrease in positive neuron number was consistent with the degree of striatum. Following H-I brain insult, the number of striatal DAT positive neurons and glutamate level were simultaneously increased initially, followed by a gradual decline toward control level. There was a positive correlation between the changes in striatal DAT positive neurons and glutamate level following H-I brain insults in newborn piglets. Our findings suggest that following H-I brain insult, striatal D2R positive neurons decreased due to neuron death; straital DAT initially increased to compensate for dopamine uptake; and glutamatergic and dopaminergic systems in striatum may act in an interdependent way in the striatum of newborn piglets. [Copyright &y& Elsevier]

Purpose: Near infrared spectroscopy measures tissue oxygenation even when there is complete cessation of blood flow. We evaluated near infrared spectroscopy to diagnose testicular torsion and blindly compared its accuracy with that of Doppler ultrasound. We also compared it by immunohistochemical evaluation of hypoxia and cell viability. Material and Methods: Rats were randomized to 4 groups, including group 1—720-degree unilateral torsion, group 2—360-degree unilateral torsion, group 4—sham operation and group 4—720-degree unilateral torsion followed by surgical torsion reduction at minute 180. Near infrared spectroscopy and Doppler ultrasound were done blindly at minutes 0, 5, 30, 60, 180 and 400. All torsed and contralateral testicles were excised for pathological examination using hypoxia inducible factor-α for hypoxia and the TUNEL test for apoptosis. We compared all groups with the contralateral testis and the sham operated group. Results: All blinded, near infrared spectroscopy measurements correctly identified the torsed testis after minute 5. Median oxygen saturation in groups 1 and 2 was significantly different compared to that in the sham operated group after minute 5. In group 4 near infrared spectroscopy detected detorsion with the loss of a significant oxygen saturation difference between the affected and the contralateral testicle after detorsion. At minute 400 median oxygen saturation in group 4 was not statistically different compared to that in the sham operated group (p = 0.09) but it was significantly different compared to that in groups 1 and 2 (p <0.001). In each torsed testis oxygen saturation was at least 18.75% lower than in the contralateral testis. In groups 1 and 2 hypoxia inducible factor-α staining in torsed testicles was significantly greater than that in the contralateral organ and the sham operated group. In group 4 hypoxia inducible factor-α staining after detorsion was significantly decreased compared to that in groups 1 and 2. There was no significant difference in the apoptotic index between the experimental and the contralateral testis or the sham operated group. Conclusions: Near infrared spectroscopy is as effective but quicker than Doppler ultrasound for detecting testicular torsion without a radiologist. Near infrared spectroscopy accurately reveals oxygen saturation, which is more vital than blood flow, on which Doppler ultrasound focuses. [ABSTRACT FROM AUTHOR]

Abstract: Transtracheal jet ventilation is a technique for ventilation of apnoeic lungs. This article outlines the indications, equipment required, insertion technique and complications of transtracheal jet ventilation. It can be used electively to aid management of the difficult airway and for laryngeal surgery. It also has a vital role in the management of the ‘can''t intubate – can'' ventilate’ scenario. Death and hypoxic brain damage under anaesthesia are fortunately rare, but most commonly occur as a result of problems with tracheal intubation. No patient should suffer hypoxic brain damage without an attempt at transtracheal ventilation being made. [Copyright &y& Elsevier]

Abstract: Breath hold divers are faced with two main physiological challenges: pressure induced compression and extended time without breathing, exposing them to extremes of hypoxia/hypercapnia. Current world records are 214m for depth and 11:35min for duration. Hypoxic loss of consciousness is frequently observed during competitions. The major physiological components of the diving response that occurs during breath holding are peripheral vasoconstriction, bradycardia, decreased cardiac output, increased cerebral and myocardial blood flow, increased blood pressure, splenic contraction and preserved O2 delivery to the brain and the heart. Sympathetic nervous activity is exceptionally engaged at the end of voluntary breath holds. We hypothesize that these adaptations to extended cessation of breathing ending with extreme hypoxia can be used as a model of brain survival response during conditions involving profound brain deoxygenation and in some instances reduced brain perfusion. [Copyright &y& Elsevier]

Summary: Background: Hypoxia is the original signal to promote angiogenesis in ischaemic tissues. However, hypoxia-induced angiogenesis usually cannot compensate for the ischaemic injury in surgery, resulting in tissue necrosis. Mimic hypoxia may be an option to improve angiogenesis for the purpose of preventing or reducing necrosis. In this study, the authors explored the feasibility of applying hypoxic mimic – deferoxamine (DFO) to the treatment of ischaemic random skin flaps. Methods: Ischaemic random skin flap models were developed in 18 nude mice using a cutaneous marking technique. The mice were divided into a DFO-treated group and a control group. Vascular endothelial growth factor (VEGF) protein level, vessel density and flap survival rate were evaluated on the seventh postoperative day. In vitro, both VEGF mRNA expression and protein level were investigated in endothelial cells and fibroblasts under DFO, hypoxia and normoxia conditions. The (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to study the impact of DFO-induced VEGF up-regulation on endothelial cell viability after severe hypoxia injury. Results: The flap survival rate, vessel density and VEGF level in the DFO group are significantly higher than in the control group. In vitro, DFO-induced increase in VEGF mRNA expression translated into 2.3- and 5.8-fold increases in VEGF protein secretion in DFO-conditioned media of endothelial cells and fibroblasts, respectively. The MTT assay showed that the cell viability both in the DFO group and in the VEGF group was significantly higher than in the control group. Conclusion: VEGF praracrine and autocrine secretion in fibroblasts and in endothelial cells play an important role in DFO-induced angiogenesis, which improves ischaemic flap survival. DFO-induced VEGF autocrine secretion also protects endothelial cells from severe hypoxia injury. [ABSTRACT FROM AUTHOR]

Abstract: A combination of multiple injury types are typically involved in combat-related head injuries. Innovations in firearms, has led to new types of brain injuries from which we are able to learn much about how the brain responds to trauma. Traumatic brain injury is physical injury to brain tissue that temporarily or permanently impairs brain function. Initial treatment consists of ensuring a reliable airway and maintaining adequate ventilation, oxygenation, and blood pressure. Neurosurgical damage control includes early intracranial pressure control; cerebral blood flow preservation; and prevention of secondary cerebral injury from hypoxia, hypotension, and hyperthemia. Evacuation to the nearest neurosurgeon, avoiding diagnostic delays, and initiating cerebral resuscitation allow for the best chance for ultimate functional recovery. [Copyright &y& Elsevier]

Abstract: Background: Improvements in perinatal care have resulted in increased survival of infants born prematurely, however neurological damage due to ischaemic infarction of the periventricular white matter is a problem of enormous medical, social and economic importance. Such vascular insult leads to destruction of the periventricular white matter, termed periventricular leukomalacia (PVL). This abnormality is the leading cause of significant morbidity in the survivors of premature birth. Magnetic Resonance Imaging (MRI) is perhaps the only imaging modality, which can accurately detect and quantify periventricular leukomalacia. Methods: Magnetic Resonance Imaging was carried out in 45 children in the age group of 4 weeks to 8 years, with history of premature birth and perinatal hypoxia. These children had neurological deficits ranging from cortical blindness, spastic diplegia, spastic quadriplegia to severe mental retardation. The procedure was carried out on a 1.5 Tesla (Siemens Magnetom Avanto) MR system using available protocols for imaging the paediatric brain. Result: The study revealed that MR imaging could accurately identify areas of ischaemic infarction of the periventricular white matter both in the early as well as in the late stages. The pattern of abnormalities detected on MRI of the brain in these patients can be considered specific for PVL in the clinical background of premature birth and perinatal hypoxia. Conclusion: MRI is the ideal imaging modality to detect, quantify and accurately map the areas of brain affected by this hypoxicischaemic process. It is presently the gold standard for evaluating the neuroparenchyma in those with perinatal hypoxia. Advanced MR techniques like Diffusion Weighted Imaging (DWI), Proton MR Spectroscopy and DTI have shown great promise in our understanding of the pathophysiology and anatomic considerations of this disease process. [Copyright &y& Elsevier]

Abstract: The present study evaluates the toxicity from sub-chronic administration of CoCl2 (12.5mgcobaltkg−1 BW for 7 days) to male Sprague-Dawley rats in view of the beneficial effects of CoCl2 in animals and for developing efficacious therapeutic regimen in humans. 32 rats weighing 200±25g were used for all experiments. Blood was collected for hematological and biochemical analysis and various organs were dissected after perfusion of animals under anesthesia for other analyses. Mean feed consumption and feed conversion efficiency values were comparable across all study groups; however, hematological analysis depicted a significant increase in hemoglobin, hematocrit and RBC in the entire cobalt-supplemented groups, which are a component of its beneficial effect. There was a significant increase in monocytes, granulocytes and WBC after 1 and 24h, which were comparable with control after 7 days. Other biochemical analyses also showed no change with respect to control. Though the metal content increased significantly in liver initially (1 and 24h) after treatment, it was equivalent to control after 7 days. Moreover, histopathological analysis revealed no evidence of changes that could be attributed to cobalt pretreatment. It is therefore reasonable to conclude that the present study supports further use of the present dose of CoCl2, which was found to be nontoxic. [ABSTRACT FROM AUTHOR]

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Copyright of Radiologia Brasileira is the property of Radiologia Brasileira and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: We explored the possibility that hypoxia-inducible factor-1α (HIF-1α) might contribute to the therapeutic effect of neural stem cell (NSC) transplantation in cerebral ischemia. The relative efficacy of modified NSC to promote behavioral recovery was investigated in a rat model of stroke induced by a transient middle cerebral artery occlusion (MCAO). A recombinant adenovirus (Ad-HIF-1α) was engineered to express HIF-1α. Control NSC infected with control adenovirus (NSC-Ad), recombinant adenovirus Ad-HIF-1α, or NSC infected by Ad-HIF-1α (NSC-Ad-HIF-1α), were used for intraventricular transplantion into rat brain 24 hours after MCAO. Neurological deficits were assessed over 4 weeks using the modified neurological severity scale (NSS) score. Long-term in vivo expression of HIF-1α was demonstrated by Western blotting and immunocytochemistry, and derivatives of nestin-positive transplanted cells contributed to both neuronal (neurofilament-positive) and astroglial (glial fibrillary acidic protein-positive) lineages. All animals showed functional improvement. Improvement was accelerated in animals receiving either NSC-Ad or Ad-HIF-1α, while improvement at all times between 7 days and 28 days post MCAO was significantly greater in animals transplanted with NSC-Ad-HIF-1α than for other treated animals. NSC-Ad-HIF-1α cells also increased the number of factor VIII-positive cells in the region of ischemic injury, indicating that HIF-1α expression can promote angiogenesis. Gene-modified NSC expressing HIF-1α have therapeutic potential in ischemic stroke. [Copyright &y& Elsevier]

Abstract: Over 700,000 babies are born in the UK each year. Most of them do not require intervention to make the transition from intrauterine to extrauterine life but approximately 10% require some assistance to begin breathing at birth and about 1% require active resuscitation. Training of those attending deliveries may help decrease the incidence of adverse outcomes. All personnel attending deliveries should be trained in neonatal resuscitation. [Copyright &y& Elsevier]

Summary: The high prevalence of sleep-disordered breathing (SDB) in hypertensive patients has been well studied. However, regular screening of SDB in these patients is not performed routinely as the diagnostic procedures are both time-consuming and labour-intensive. Overnight portable device screening is useful, but is sometimes not acceptable for asymptomatic SDB patients. We evaluated the usefulness of daytime 30-min recording with a portable recording device during pulse wave velocity (PWV) measurement sessions as a screening method for detection of asymptomatic SDB in hypertensive patients. Eighty-one hypertensive patients underwent 30-min daytime screening session using a Type III portable recording device during PWV measurement. Each screening session was followed by full overnight Level I polysomnography (PSG). The screening session included recordings of airflow (mouth–nose), chest movement, oximetry, and electrocardiography. The correlation coefficient between respiratory disturbance index (RDI) by screening session and apnea–hypopnea index (AHI) by PSG was 0.64. Using AHI ≥30 as diagnostic of severe SDB, 47 of 80 patients had the disorder based on PSG results. Using an RDI cut-off value of 22, the sensitivity and specificity for detection of severe SDB were 86.1% and 64.5%, respectively. Daytime 30-min recording with a portable device for apnea detection during PWV recording is useful for screening of asymptomatic severe SDB in hypertensive patients. [Copyright &y& Elsevier]

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