Astrocyte focal adhesion kinase reduces passive stress coping by inhibiting ciliary neurotrophic factor only in female mice.

Astrocytes have been implicated in stress responses and produce ciliary neurotrophic factor (CNTF), which we have shown in the mouse medial amygdala (MeA) to promote passive stress coping response only in females. Pharmacological inhibition of focal adhesion kinase (FAK) upregulates CNTF expression. Here, we found that inducible knockout of FAK in astrocytes or systemic treatment with an FAK inhibitor increased passive coping behavior, i.e., immobility, in an acute forced swim stress test in female, but not male, mice. Strikingly, four weeks of chronic unpredictable stress (CUS) did not further increase passive coping in female astrocytic FAK knockout mice, whereas it exacerbated it in female wildtype mice and male mice of both genotypes. These data suggest that astrocyte FAK inhibition is required for chronic stress-induced passive coping in females. Indeed, CUS reduced phospho-FAK and increased CNTF in the female MeA. Progesterone treatment after ovariectomy activated amygdala FAK and alleviated ovariectomy-induced passive coping in wildtype, but not astrocytic FAK knockout females. This suggests that progesterone-mediated activation of FAK in astrocytes reduces female stress responses. Finally, astrocytic FAK knockout or FAK inhibitor treatment increased CNTF expression in the MeA of both sexes, although not in the hippocampus. As mentioned, MeA CNTF promotes stress responses only in females, which may explain the female-specific role of astrocytic FAK inhibition. Together, this study reveals a novel female-specific progesterone-astrocytic FAK pathway that counteracts CNTF-mediated stress responses and points to opportunities for developing treatments for stress-related disorders in women.

Sales to Apparently Intoxicated Customers in Three States With Different Histories of Responsible Beverage Service Training.

OBJECTIVE: Most states prohibit sales of alcohol to customers who are apparently intoxicated, and many require training in responsible beverage service (RBS), with the aim of reducing driving while intoxicated (DWI) and other harms. Sales to apparently intoxicated patrons were assessed in onsite alcohol sales establishments and compared across three states. METHOD: A sample of 180 licensed onsite alcohol establishments was selected in California (n = 60), New Mexico (n = 60), and Washington State (n = 60). States had different RBS training histories, content, and procedures. Research confederates, trained to feign cues of intoxication, visited each establishment twice. The pseudo-intoxicated patron (PP) ordered an alcoholic beverage while displaying intoxication cues. Sale of alcohol was the primary outcome. RESULTS: At 179 establishments assessed, PPs were served alcohol during 56.5% of 356 visits (35.6% of establishments served and 22.6% did not serve at both visits). Alcohol sales were less frequent in New Mexico (47.9% of visits; odds ratio [OR] = 0.374, p = .008) and Washington State (49.6%; OR = 0.387, p = .012) than in California (72.0%). Servers less consistently refused service at both visits (6.8%) in California than New Mexico (33.9%) or Washington (27.1%), χ2(4, n = 177) = 16.72, p = .002. Alcohol sales were higher when intoxication cues were less obvious (p < .001). CONCLUSIONS: Overservice of alcohol to apparently intoxicated customers was frequent and likely elevated risk of DWI and other harms. The lower sales in New Mexico and Washington than California may show that a policy approach prohibiting sales to intoxicated customers combined with well-established RBS training can reduce overservice. Further efforts are needed to reduce overservice.

Female-specific role of ciliary neurotrophic factor in the medial amygdala in promoting stress responses.

Ciliary neurotrophic factor (CNTF) is produced by astrocytes which have been implicated in regulating stress responses. We found that CNTF in the medial amygdala (MeA) promotes despair or passive coping, i.e., immobility in an acute forced swim stress, in female mice, while having no effect in males. Neutralizing CNTF antibody injected into the MeA of wildtype females reduced activation of downstream STAT3 (Y705) 24 and 48 h later. In concert, the antibody reduced immobility in the swim test in females and only after MeA injection, but not when injected in the central or basolateral amygdala. Antibody injected into the male MeA did not affect immobility. These data reveal a unique role of CNTF in female MeA in promoting despair or passive coping behavior. Moreover, 4 weeks of chronic unpredictable stress (CUS) increased immobility in the swim test and reduced sucrose preference in wildtype CNTF+/+, but not CNTF-/- littermate, females. Following CUS, 10 min of restraint stress increased plasma corticosterone levels only in CNTF+/+ females. In males, the CUS effects were present in both genotypes. Further, CUS increased CNTF expression in the MeA of female, but not male, mice. CUS did not alter CNTF in the female hippocampus, hypothalamus and bed nucleus of stria terminalis. This suggests that MeA CNTF has a female-specific role in promoting CUS-induced despair or passive coping, behavioral anhedonia and neuroendocrine responses. Compared to CNTF+/+ mice, CNTF-/- mice did not show differences in CUS-induced anxiety-like behavior and sensorimotor gating function as measured by elevated T-Maze, open field and pre-pulse inhibition of the acoustic startle response. Together, this study reveals a novel CNTF-mediated female-specific mechanism in stress responses and points to opportunities for developing treatments for stress-related disorders in women.

The effects of a novel inhibitor of tumor necrosis factor (TNF) alpha on prepulse inhibition and microglial activation in two distinct rodent models of schizophrenia.

Increased neuroinflammation has been shown in individuals diagnosed with schizophrenia (SCHZ). This study evaluated a novel immune modulator (PD2024) that targets the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) to alleviate sensorimotor gating deficits and microglial activation employing two different rodent models of SCHZ. In Experiment 1, rats were neonatally treated with saline or the dopamine D2-like agonist quinpirole (NQ; 1 mg/kg) from postnatal day (P) 1-21 which produces increases of dopamine D2 receptor sensitivity throughout the animal's lifetime. In Experiment 2, rats were neonatally treated with saline or the immune system stimulant polyinosinic:polycytidylic acid (Poly I:C) from P5-7. Neonatal Poly I:C treatment mimics immune system activation associated with SCHZ. In both experiments, rats were raised to P30 and administered a control diet or a novel TNFα inhibitor PD2024 (10 mg/kg) in the diet from P30 until P67. At P45-46 and from P60-67, animals were behaviorally tested on auditory sensorimotor gating as measured through prepulse inhibition (PPI). NQ or Poly I:C treatment resulted in PPI deficits, and PD2024 treatment alleviated PPI deficits in both models. Results also revealed that increased hippocampal and prefrontal cortex microglial activation produced by neonatal Poly I:C was significantly reduced to control levels by PD2024. In addition, a separate group of animals neonatally treated with saline or Poly I:C from P5-7 demonstrated increased TNFα protein levels in the hippocampus but not prefrontal cortex, verifying increased TNFα in the brain produced by Poly I:C. Results from this study suggests that that brain TNFα is a viable pharmacological target to treat the neuroinflammation known to be associated with SCHZ.

The adenosine A(2A) receptor agonist CGS 21680 alleviates auditory sensorimotor gating deficits and increases in accumbal CREB in rats neonatally treated with quinpirole.

RATIONALE AND OBJECTIVE: The adenosine A(2A) receptor forms a mutually inhibitory heteromer with the dopamine D2 receptor, and A(2A) agonists decrease D2 signaling. This study analyzed whether an adenosine A(2A) agonist would alleviate deficits in sensorimotor gating and increases in cyclic-AMP response element binding protein (CREB) in the nucleus accumbens (NAc) in the neonatal quinpirole model of schizophrenia (SZ). METHODS: Male and female Sprague-Dawley rats were neonatally treated with saline (NS) or quinpirole HCl (NQ; 1 mg/kg) from postnatal days (P) 1-21. Animals were raised to P44 and behaviorally tested on auditory sensorimotor gating as measured through prepulse inhibition (PPI) from P44 to P48. Approximately 15 min before each session, animals were given an ip administration of saline or the adenosine A(2A) agonist CGS 21680 (0.03 or 0.09 mg/kg). One day after PPI was complete on P49, animals were administered a locomotor activity test in the open field after saline or CGS 21680 treatment, respectively. On P50, the nucleus accumbens (NAc) was evaluated for CREB protein. RESULTS: NQ-treated rats demonstrated a deficit in PPI that was alleviated to control levels by either dose of CGS 21680. The 0.03 mg/kg dose of CGS 21680 increased startle amplitude in males. The 0.09 mg/kg dose of CGS 21680 resulted in an overall decrease in locomotor activity. NQ treatment significantly increased NAc CREB that was attenuated to control levels by either dose of CGS 21680. CONCLUSIONS: This study revealed that an adenosine A(2A) receptor agonist was effective to alleviate PPI deficits in the NQ model of SZ in both male and female rats.

Ciliary neurotrophic factor is a key sex-specific regulator of depressive-like behavior in mice.

Ciliary neurotrophic factor (CNTF) is produced by astrocytes and promotes neurogenesis and neuroprotection. Little is known about the role of CNTF in affective behavior. We investigated whether CNTF affects depressive- and anxiety-like behavior in adult mice as tested in the forced swim, sucrose preference and elevated-T maze tests. Female wild type CNTF+/+ mice more readily developed behavioral despair with increased immobility time and decreased latency to immobility in the forced swim test than male CNTF+/+ littermates. The lack of CNTF in CNTF-/- mice had an opposite effect on depressive-like behavior in female mice (reduced immobility time and increased sucrose preference) vs. male mice (increased immobility time). Female wildtype mice expressed more CNTF in the amygdala than male mice. Ovariectomy increased CNTF expression, as well as immobility time, which was significantly reduced in CNTF-/- mice, suggesting that CNTF mediates overiectomy-induced immobility time, possibly in the amygdala. Progesterone but not 17-ß estradiol inhibited CNTF expression in cultured C6 astroglioma cells. Progesterone treatment also reduced CNTF expression in the amygdala and decreased immobility time in female CNTF+/+ but not in CNTF-/- mice. Castration did not alter CNTF expression in males nor their behavior. Lastly, there were no effects of CNTF on the elevated T-maze, a behavioral test of anxiety, suggesting that a different mechanism may underlie anxiety-like behavior. This study reveals a novel CNTF-mediated mechanism in stress-induced depressive-like behavior and points to opportunities for sex-specific treatments for depression, e.g. progesterone in females and CNTF-stimulating drugs in males.

Effects of Environmental Enrichment on Nicotine Sensitization in Rats Neonatally Treated with Quinpirole: Analyses of Glial Cell Line-Derived Neurotrophic Factor and Implications towards Schizophrenia.

The current study analyzed the effects of environmental enrichment versus isolation housing on the behavioral sensitization to nicotine in the neonatal quinpirole (NQ; dopamine D2-like agonist) model of dopamine D2 receptor supersensitivity, a rodent model of schizophrenia. NQ treatment in rats increases dopamine D2 receptor sensitivity throughout the animal's lifetime, consistent with schizophrenia. Animals were administered NQ (1 mg/kg) or saline (NS) from postnatal day (P)1 to P21, weaned, and immediately placed into enriched housing or isolated in wire cages throughout the experiment. Rats were behaviorally sensitized to nicotine (0.5 mg/kg base) or saline every consecutive day from P38 to P45, and brain tissue was harvested at P46. Results revealed that neither housing condition reduced nicotine sensitization in NQ rats, whereas enrichment reduced sensitization to nicotine in NS-treated animals. The nucleus accumbens (NAcc) was analyzed for glial cell line-derived neurotrophic factor (GDNF), a neurotrophin important in dopamine plasticity. Results were complex, and revealed that NAcc GDNF was increased in animals given nicotine, regardless of housing condition. Further, enrichment increased GDNF in NQ rats regardless of adolescent drug treatment and in NS-treated rats given nicotine, but did not increase GDNF in NS-treated controls compared to the isolated housing condition. This study demonstrates that environmental experience has a prominent impact on the behavioral and the neural plasticity NAcc response to nicotine in adolescence.

A study of selected factors affecting efficacy of compost tea against several fungal pathogens of potato.

AIM: To investigate selected factors of two nonaerated compost teas (NCT) and mechanisms that influence the restriction of several fungal potato pathogens. METHODS AND RESULTS: Two NCTs, made from either commercial compost, (CCT) or vineyard compost (VCT), were tested for their ability to suppress potato pathogens. The VCT was more suppressive than CCT to mycelial growth of Alternaria solani and Rhizoctonia solani isolate 299, but not for R. solani isolate 422. Metagenomic studies of microbial diversity revealed that the CCT had higher fungal and bacterial diversity and richness than the VCT. Use of CCT significantly reduced lesion area of Alternaria alternata on detached leaves, however, a gum adjuvant did not lead to significantly greater control. Scanning microscopy showed that the spatial distribution of microbes from the CCT was altered with gum addition, to resemble what may have been a microbial biofilm. CONCLUSION: We confirmed that each NCT could suppress the mycelial growth of selected potato pathogens in culture, and CCT reduced A. alternata lesions on detached leaves. Factors including concentration, microbial communities and physio-chemical properties could not be consistently linked to NCT efficacy. SIGNIFICANCE AND IMPACT OF THE STUDY: This study particularly highlights the application of scanning microscopy to study the interaction between pathogens and putative NCT microbes on foliar surfaces. This adds insight to mechanisms of NCT efficacy, along with physico-chemical and microbial characterization of the teas. This study shows the potential for the use of NCTs as a crop protection tool of low-cost which could be of particular benefit in smallholder agriculture.

The effects of nicotine in the neonatal quinpirole rodent model of psychosis: Neural plasticity mechanisms and nicotinic receptor changes.

Neonatal quinpirole (NQ) treatment to rats increases dopamine D2 receptor sensitivity persistent throughout the animal's lifetime. In Experiment 1, we analyzed the role of α7 and α4ß2 nicotinic receptors (nAChRs) in nicotine behavioral sensitization and on the brain-derived neurotrophic factor (BDNF) response to nicotine in NQ- and neonatally saline (NS)-treated rats. In Experiment 2, we analyzed changes in α7 and α4ß2 nAChR density in the nucleus accumbens (NAcc) and dorsal striatum in NQ and NS animals sensitized to nicotine. Male and female Sprague-Dawley rats were neonatally treated with quinpirole (1mg/kg) or saline from postnatal days (P)1-21. Animals were given ip injections of either saline or nicotine (0.5mg/kg free base) every second day from P33 to P49 and tested on behavioral sensitization. Before each injection, animals were ip administered the α7 nAChR antagonist methyllycaconitine (MLA; 2 or 4mg/kg) or the α4ß2 nAChR antagonist dihydro beta erythroidine (DhßE; 1 or 3mg/kg). Results revealed NQ enhanced nicotine sensitization that was blocked by DhßE. MLA blocked the enhanced nicotine sensitization in NQ animals, but did not block nicotine sensitization. NQ enhanced the NAcc BDNF response to nicotine which was blocked by both antagonists. In Experiment 2, NQ enhanced nicotine sensitization and enhanced α4ß2, but not α7, nAChR upregulation in the NAcc. These results suggest a relationship between accumbal BDNF and α4ß2 nAChRs and their role in the behavioral response to nicotine in the NQ model which has relevance to schizophrenia, a behavioral disorder with high rates of tobacco smoking.

Genome Editing in Large Animals.

Genome editing in large animals has tremendous practical applications, from more accurate models for medical research through improved animal welfare and production efficiency. Although genetic modification in large animals has a 30 year history, until recently technical issues limited its utility. The original methods - pronuclear injection and integrating viruses - were plagued with problems associated with low efficiency, silencing, poor regulation of gene expression, and variability associated with random integration. With the advent of site specific nucleases such as TALEN and CRISPR/Cas9, precision editing became possible. When used on their own, these can be used to truncate or knockout genes through non-homologous end joining (NHEJ) with relatively high efficiency. When used with a template containing desired gene edits, these can be used to allow insertion of any desired changes to the genome through homologous recombination (HR) with substantially lower efficiency. Consideration must be given to the issues of marker sets and off-target effects. Somatic cell nuclear transfer is most commonly used to create animals from gene edited cells, but direct zygote injection and use of spermatogonial stem cells are alternatives under development. In developing gene editing projects, priority must be given to understanding the potential for off-target or unexpected effects of planned edits, which have been common in the past. Because of the increasing technical sophistication with which it can be accomplished, genome editing is poised to revolutionize large animal genetics, but attention must be paid to the underlying biology in order to maximize benefit.

Activation of 5-HT1A receptors in the paragigantocellularis lateralis decreases shivering during cooling in the conscious piglet.

Activation of 5-HT(1A) receptors in the medullary raphé decreases sympathetic outflow to thermoregulatory mechanisms, including brown adipose tissue (BAT), thermogenesis, and peripheral vasoconstriction when these mechanisms are previously activated with leptin, prostaglandins, or cooling. These same mechanisms are also inhibited during rapid eye movement (REM) sleep. It is not known whether shivering is also modulated by medullary raphé neurons. We previously showed in the conscious piglet that activation of 5-HT(1A) receptors with 8-OH-DPAT (DPAT) in the paragigantocellularis lateralis (PGCL), a medullary region lateral to the midline raphé that contains 5-HT neurons, decreases heart rate, body temperature and muscle activity during non-rapid eye movement (NREM) sleep. We therefore hypothesized that activation of 5-HT(1A) receptors in the PGCL would also attenuate shivering and peripheral vasoconstriction during cooling. During REM sleep in a cool environment, shivering, carbon dioxide production, and body temperature decreased, and ear capillary blood flow and ear skin temperature increased. Shivering associated with rapid cooling was attenuated after dialysis of DPAT into the PGCL. In animals maintained in a continuously cool environment, dialysis of DPAT into the PGCL attenuated shivering and decreased body temperature, but there were no significant increases in ear capillary blood flow or ear skin temperature. We conclude that both naturally occurring REM sleep and exogenous activation of 5-HT(1A) receptors in the PGCL are associated with a suspension of shivering during cooling. Our data are consistent with the hypothesis that 5-HT neurons in the PGCL facilitate oscillating spinal motor circuits involved in shivering but are less involved in modulating sympathetically mediated thermoregulatory mechanisms.

Effect of intense lifestyle modification and cardiac rehabilitation on psychosocial cardiovascular disease risk factors and quality of life.

This study examined the effect of the Ornish Program for Reversing Heart Disease and cardiac rehabilitation (CR) on psychosocial risk factors and quality of life in patients with confirmed coronary artery disease. Participants had previously undergone a revascularization procedure. The 84 patients self-selected to participate in the Ornish Program for Reversing Heart Disease (n = 507 28), CR (n = 28), or a control group (n = 28). Twelve psychosocial risk factors and quality of life variables were collected from all three groups at baseline, 3 months, and 6 months. At 3 and 6 months, Ornish group participants demonstrated significant improvements in all 12 outcome measures. The rehabilitation group improved in 7 of the 12, and the control group showed significant improvements in 6 of the variables. Intensive lifestyle modification programs significantly affect psychosocial risk factors and quality of life.

Inhibition of serotonergic neurons in the nucleus paragigantocellularis lateralis fragments sleep and decreases rapid eye movement sleep in the piglet: implications for sudden infant death syndrome.

Serotonergic receptor binding is altered in the medullary serotonergic nuclei, including the paragigantocellularis lateralis (PGCL), in many infants who die of sudden infant death syndrome (SIDS). The PGCL receives inputs from many sites in the caudal brainstem and projects to the spinal cord and to more rostral areas important for arousal and vigilance. We have shown previously that local unilateral nonspecific neuronal inhibition in this region with GABA(A) agonists disrupts sleep architecture. We hypothesized that specifically inhibiting serotonergic activity in the PGCL would result in less sleep and heightened vigilance. We analyzed sleep before and after unilaterally dialyzing the 5-HT1A agonist (+/-)-8-hydroxy-2-(dipropylamino)-tetralin (8-OH-DPAT) into the juxtafacial PGCL in conscious newborn piglets. 8-OH-DPAT dialysis resulted in fragmented sleep with an increase in the number and a decrease in the duration of bouts of nonrapid eye movement (NREM) sleep and a marked decrease in amount of rapid eye movement (REM) sleep. After 8-OH-DPAT dialysis, there were decreases in body movements, including shivering, during NREM sleep; body temperature and heart rate also decreased. The effects of 8-OH-DPAT were blocked by local pretreatment with N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexane-carboxamide, a selective 5-HT1A antagonist. Destruction of serotonergic neurons with 5,7-DHT resulted in fragmented sleep and eliminated the effects of subsequent 8-OH-DPAT dialysis on REM but not the effects on body temperature or heart rate. We conclude that neurons expressing 5-HT1A autoreceptors in the juxtafacial PGCL are involved in regulating or modulating sleep. Abnormalities in the function of these neurons may alter sleep homeostasis and contribute to the etiology of SIDS.

Omnidirectional reflector using nanoporous SiO2 as a low-refractive-index material.

Triple-layer omnidirectional reflectors (ODRs) consisting of a semiconductor, a quarter-wavelength transparent dielectric layer, and a metal have high reflectivities for all angles of incidence. Internal ODRs (ambient material's refractive index n >> 1.0) are demonstrated that incorporate nanoporous SiO2, a low-refractive-index material (n = 1.23), as well as dense SiO2 (n = 1.46). GaP and Ag serve as the semiconductor and the metal layer, respectively. Reflectivity measurements, including angular dependence, are presented. Calculated angle-integrated TE and TM reflectivities for ODRs employing nanoporous SiO2 are R(int)/TE = 99.9% and R(int)/TM = 98.9%, respectively, indicating the high potential of the ODRs for low-loss waveguide structures.

The influence of an intense cardiovascular disease risk factor modification program.

In an effort to make intensive lifestyle modification programs more accessible to patients with cardiovascular disease, the Ornish Program was offered at eight independent medical centers located across the United States. The purpose of this study was to determine if one of these independent sites was able to replicate outcomes produced by the original Ornish Program. Fifty program participants from six different cohorts provided baseline, 3- and 12-month data consisting of blood lipids, body fat, blood pressure, anginal pain, quality of life, stress, depression, social support, and hostility. A pooled analysis showed significant reductions in almost all physiological and psychosocial variables with most reductions persisting for at least 12 months. These findings suggest that cardiovascular disease patients who choose to participate in an independent, intensive lifestyle modification program can experience significant improvements in both physiological and psychosocial cardiovascular disease risk factors.

Aspects of the pathology and etiology of 'drippy gill' disease of the cultivated mushroom Agaricus bisporus.

Agaricus bisporus sporocarps exhibiting characteristic 'drippy gill' symptoms from a natural outbreak were examined. Discrete bacterial droplets on the hymenial lamellae often coalesced to form ribbons of bacterial ooze. Longitudinal splits on the stipe were lined with a similar bacterial ooze. Bacteria isolated from both the hymenium and stipe were identified as Pseudomonas agarici, and were confirmed to be the causal organism by satisfying Koch's postulates. By light and transmission electron microscopy, the causal bacteria were found to colonize the extrahyphal spaces and degrade the extracellular matrix within affected sporocarps. Degradation of the extracellular matrix was shown to reduce the integrity of the sporocarp, and result in stipe splitting and hymenium disruption. In artificial inoculations of the pileus, bacteria were shown to exist predominantly in sporocarp tissue below the point of inoculation and above affected areas of the hymenium, indicating an approximately vertical passage through the sporocarp via the extracellular spaces. The dissolution of the extracellular matrix, and the observed failure of the bacterium to produce a toxin active against A. bisporus, allow the bacteria to pass through protective membranes unnoticed, and infect the stipe and hymenium prior to veil break. These observations dispel previous assumptions of intrahyphal existence and transmission. In the few instances in which the bacteria were observed to be intrahyphal, the host fungal cell wall was often broken, suggesting intrahyphal existence was opportunistic rather than obligatory. The taxonomic position of a bacterium isolated previously from sporocarps exhibiting symptoms similar to those of drippy gill was determined by examining the biochemical and nutritional profiles of the bacterium, and comparing them with other Pseudomonas agarici isolates.

Comparative genomics of BCG vaccines by whole-genome DNA microarray.

Bacille Calmette-Guérin (BCG) vaccines are live attenuated strains of Mycobacterium bovis administered to prevent tuberculosis. To better understand the differences between M. tuberculosis, M. bovis, and the various BCG daughter strains, their genomic compositions were studied by performing comparative hybridization experiments on a DNA microarray. Regions deleted from BCG vaccines relative to the virulent M. tuberculosis H37Rv reference strain were confirmed by sequencing across the missing segment of the H37Rv genome. Eleven regions (encompassing 91 open reading frames) of H37Rv were found that were absent from one or more virulent strains of M. bovis. Five additional regions representing 38 open reading frames were present in M. bovis but absent from some or all BCG strains; this is evidence for the ongoing evolution of BCG strains since their original derivation. A precise understanding of the genetic differences between closely related Mycobacteria suggests rational approaches to the design of improved diagnostics and vaccines.

[Extracorporeal membrane oxygenation in neonatology: review of the use of the method]. / Extracorporalis membránoxigenizáció az újszülöttgyógyászatban: áttekintés a módszer alkalmazásáról.

Extracorporeal life support and extracorporeal membrane oxygenation characterize the use of mechanical devices for temporary support of heart and lung function. The mechanical circuit consists of a blood pump (heart), membrane oxygenator (lung: which accomplishes both carbon dioxide removal and oxygen delivery), heat exchanger and a servo-control module. Venous blood is drained from the right atrium through the right internal jugular vein, and returned oxygenated through either the right common carotid artery (venoarterial bypass), or into a large vein (venovenous bypass). All patients treated must be free of coagulopathies, as all patients are anticoagulated. Neonatal candidates should be older than 34 weeks gestational age and weigh more than 2000 grams. As of March, 1997 twenty six patients have been treated with extracorporeal life support at Tulane Medical Center with an overall survival rate of 62%. Twelve neonates with either meconium aspiration or pneumonia have been treated with a 100% survival. Six children with congenital diaphragmatic hernia have been unsuccessfully treated.