Mechanisms of remembering the past and imagining the future--new data from autobiographical memory tasks in a lifespan approach.

We investigated the episodic/semantic distinction in remembering the past and imagining the future and explored cognitive mechanisms predicting events' specificity throughout the lifespan. Eighty-three 6- to 81-year-old participants, divided into 5 age groups, underwent past, present and future episodic (events' evocation) and semantic (self-descriptions) autobiographical tasks and a complementary cognitive test battery (executive functions, working and episodic memory). The main results showed age effects on episodic events' evocation indicating an inverted U function (i.e., developmental progression from 6 to 21years and aging decline). By contrast, age effects were slighter on self-descriptions while self-defining events' evocation increased with age. Furthermore, age effects on episodic events' evocation were mainly mediated by age effects on cognitive functions and personal semantics. These new findings indicate a developmental and aging episodic/semantic distinction for both remembering the past and imagining the future, and suggest that above similarities, these abilities could have a fundamentally different basis.

[Comparison of foetal and neonatal mortality of monochorionic monoamniotic and monochorionic biamniotic twin pregnancies]. / Comparaison de la mortalité fœtale et néonatale des grossesses gémellaires monochoriales monoamniotiques et monochoriales biamniotiques.

OBJECTIVES: To compare the mortality of monochorionic-monoamniotic (MCMA) and monochorionic-biamniotic (MCBA) twin pregnancies, from 14weeks of gestation to 28th day of life, before and after exclusion of major congenital malformations. METHODS: We conducted a retrospective cohort study in two level 3 maternity units of the Hospices civils de Lyon (France) including all patients with a monochorionic twin pregnancy between January 2013 and December 2020. We excluded TRAP sequences and conjoined twins. RESULTS: A total of 38 MCMA and 658 MCBA pregnancies were included. We showed an increase in overall mortality in the MCMA group compared to the MCBA group (31.6% versus 16.4%, P=0.03) even after exclusion of major congenital malformations (20.3% versus 9.5%, P=0.01). The main cause of mortality found in the MCMA group was the occurrence of unexpected IUGR. CONCLUSIONS: MCMA pregnancies have a higher foetal and neonatal mortality rate than MCBA pregnancies even after exclusion of congenital malformations related to the occurrence of unexpected MFIU.

Identification of a novel type of glucose dehydrogenase involved in the mineral weathering ability of Collimonas pratensis strain PMB3(1).

The exact molecular mechanisms as well as the genes involved in the mineral weathering (MW) process by bacteria remain poorly characterized. To date, a single type of glucose dehydrogenase (GDH) depending on a particular co-factor named pyrroloquinoline quinone (PQQ) is known. These enzymes allow the production of gluconic acid through the oxidation of glucose. However, it remains to be determined how bacteria missing PQQ-dependent GDH and/or the related pqq biogenesis genes weather minerals. In this study, we considered the very effective mineral weathering bacterial strain PMB3(1) of Collimonas pratensis. Genome analysis revealed that it does not possess the PQQ-based system. The use of random mutagenesis, gene complementation and functional assays allowed us to identify mutants impacted in their ability to weather mineral. Among them, three mutants were strongly altered on their acidification and biotite weathering abilities (58% to 75% of reduction compared to WT) and did not produce gluconic acid. The characterization of the genomic regions allowed noticeably to the identification of a Glucose/Methanol/Choline oxidoreductase. This region appeared very conserved among collimonads and related genera. This study represents the first demonstration of the implication of a PQQ-independent GDH in the mineral weathering process and explains how Collimonas weather minerals.

Potent inhibition of HIV-1 infectivity in macrophages and lymphocytes by a novel CCR5 antagonist.

The chemokine receptors CXCR4 and CCR5 have recently been shown to act as coreceptors, in concert with CD4, for human immunodeficiency virus-type 1 (HIV-1) infection. RANTES and other chemokines that interact with CCR5 and block infection of peripheral blood mononuclear cell cultures inhibit infection of primary macrophages inefficiently at best. If used to treat HIV-1-infected individuals, these chemokines could fail to influence HIV replication in nonlymphocyte compartments while promoting unwanted inflammatory side effects. A derivative of RANTES that was created by chemical modification of the amino terminus, aminooxypentane (AOP)-RANTES, did not induce chemotaxis and was a subnanomolar antagonist of CCR5 function in monocytes. It potently inhibited infection of diverse cell types (including macrophages and lymphocytes) by nonsyncytium-inducing, macrophage-tropic HIV-1 strains. Thus, activation of cells by chemokines is not a prerequisite for the inhibition of viral uptake and replication. Chemokine receptor antagonists like AOP-RANTES that achieve full receptor occupancy at nanomolar concentrations are strong candidates for the therapy of HIV-1-infected individuals.

[Radiosurgery of cerebral arteriovenous malformations: a prescription algorithm]. / Radiochirurgie des malformations artérioveineuses cérébrales : élaboration d'un algorithme de prescription.

PURPOSE: To study prognostic factors of obliteration and risk factors of brain radiation necrosis in order to propose an algorithm for radiosurgery prescription for cerebral arteriovenous malformations (cAVM). MATERIAL AND METHODS: One hundred and seventy-nine patients were analysed. Radiosurgery delivered 6 or 10 MV X-rays by arc therapy in 84% of cases, or by fixed field in 16% of cases using two different micro-multileaf collimators (micro-MLC). Follow-up consisted of screening radiation necrosis by MRI every 6 months, and assessing local control by arteriography every 2 years. Obliteration was defined as at least 95% reduction of cAVM volume. Cox proportional hazard model was used to evaluate the local control and the appearance of radiation necrosis over time. RESULTS: Local control rate was 82.7% with the mean follow-up of 3.1 years (0.5-11). Significant prognostic factors were: simple nidus (RR=2.8, p<0.0001), number of embolizations before radiosurgery below 4 (RR=2.9, p<0.0001), prescribed dose to the periphery of at least 18 Gy (RR=2, p=0.0002), nidus volume below8cm(3) (RR=1.9, p=0.0002), and number of table positions below six (RR=1.4, p=0.05). Radiation necrosis rate was 11.2% with a mean time to onset of 18 months. Significant predictive factors were: fixed field versus arc therapy (according to MLC RR=9.1, p<0.0001, and RR=15.1, p=0.01), age below 30 years (RR=2.5, p=0.04), depth of cAVM greater than or equal to 7 cm (RR=7.6, p=0.008), and volume of brain tissue covered by the 12 Gy isodose (V12 Gy) of at least 11 cm(3) (RR=7.8, p=0.05). CONCLUSION: A radiosurgery prescription algorithm taking into account the prescribed dose to the periphery (> or = 18 Gy) and reduction of V12 Gy was elaborated from these data.

Pediatric neurolisteriosis: A diagnosis to consider even in the absence of immunodeficiency.

Neurolisteriosis is known to affect vulnerable groups, for example neonates or children with immunodeficiency. This is a key point of the current clinical guidelines regarding pediatric meningitis. We report a rare case of neurolisteriosis in an immunocompetent infant, without the typical signs of listeriosis, which led to a delay in administering the appropriate antibiotherapy. This case illustrates the clinical heterogeneity of neurolisteriosis and the relevance of appropriate polymerase chain reaction (PCR) tests when the clinical presentation differs from the current guidelines. This case also reminds us that raw or unpasteurized milk-based food products pose a risk even in immunocompetent infants or children.

[A survey of the management of unruptured intracranial aneurysms as practised by French neuroradiological and neurosurgical teams]. / Prise en charge des anévrismes intracrâniens non rompus. Enquête de pratique des équipes neurochirurgicales et neuroradiologiques françaises.

BACKGROUND: The lack of consensus in the management of unruptured intracranial aneurysms (UIA) has resulted in a variety of different clinical practices. The aim of this study is to analyze these different practices. METHODS: A questionnaire concerning the management of UIA was mailed out to French neurosurgeons (NS) and neuroradiologists (NR). Eighteen responses from 17 teams of NS and 23 responses from 19 teams of NR were included in our analysis. RESULTS: In making a therapeutic decision, about three-quarters of both NR and NS take into account the age of the patient and all of our responders except one consider the aneurysm's morphology, especially its size and neck structure. Pinpointing the location of the aneurysm is an important factor for 61% of NR and 40% of NS. Information concerning the risk of aneurysm rupture and the risks of treatment is routinely given to the patient orally and, sometimes, in writing. The follow-up of UIA treated by NR usually consists of one X-ray angiography and several MR angiographic (MRA) films taken over a period of at least five years and, sometimes, for the rest of the patient's life (22%). The follow-up after surgical treatment mainly comprises X-ray angiography for a limited period of time-usually from five to ten years. The follow-up of untreated aneurysms is usually by either MRA or angioCT. For most NR, the duration of follow-up is long and, sometimes, unlimited. For NS, the duration is more difficult to pinpoint: the response was indeterminate in 28 and 33% gave no response at all. If the first screening tests negative, 44% of NS and 61% of NR propose a repeat screening. CONCLUSION: Given the differences in the management of UIA as revealed by this survey, a multidisciplinary approach that combines the various clinical practices may be the best way forward.

[MRI findings in a case of prolonged status epilepticus]. / Suivi iconographique d'un etat de mal epileptique prolonge.

We report the MR imaging findings in a 20 year old woman with status epilepticus of more than 3 months duration following an episode of lymphocytic meningitis. Repeated MR examinations showed progressive symmetrical cortical lesions, followed by subcortical and basal ganglia lesions which evolved to cortical laminar necrosis and hemorrhagic necrosis with eventual subcortical cerebral atrophy. This case has similarities with animal status epilepticus models. Biological investigations were all negative. This suggests that the brain lesions may be related to the prolonged status epilepticus.

Total chemical synthesis and high-resolution crystal structure of the potent anti-HIV protein AOP-RANTES.

BACKGROUND: RANTES is a CC-type chemokine protein that acts as a chemoattractant for several kinds of leukocytes, playing an important pro-inflammatory role. Entry of human immunodeficiency virus-1 (HIV-1) into cells depends on the chemokine receptor CCR5. RANTES binds CCR5 and inhibits HIV-1 entry into peripheral blood cells. Interaction with chemokine receptors involves a distinct set of residues at the amino terminus of RANTES. This finding was utilized in the development of a chemically modified aminooxypentane derivative of RANTES, AOP-RANTES, that was originally produced from the recombinant protein using semisynthetic methods. RESULTS: AOP-RANTES has been produced by a novel total chemical synthesis that provides efficient, direct access to large amounts of this anti-HIV protein analog. The crystal structure of chemically synthesized AOP-RANTES has been solved and refined at 1.6 A resolution. The protein is a dimer, with the amino-terminal pentane oxime moiety clearly defined. CONCLUSIONS: Total chemical synthesis of AOP-RANTES provides a convenient method of producing the multi-milligram quantities of this protein needed to investigate the molecular basis of receptor binding and antiviral activity. This work provides the first truly high-resolution structure of a RANTES protein, although the structure of RANTES was known from previous nuclear magnetic resonance (NMR) determinations.

[Neuroimaging of hereditary hemorrhagic telangiectasia]. / Neuroradiologie de la maladie de Rendu Osler.

Hereditary Hemorrhagic telangiectasia is an autosomal dominant vascular disorder with high penetrance and variable expressivity. Most cases are caused by mutations in the endoglin gene on chromosome 9 (HHT type 1) or the activin receptor-like kinase 1 gene on chromosome 12 (HHT type 2). HHT is characterized by mucocutaneous telangiectases and visceral arteriovenous malformations (AVMs). Neurological complications occur in 8 to 10% of the patients. Brain ischemia or abscess are often associated with pulmonary arteriovenous fistula. Cerebral or spinal arteriovenous malformations are frequent but have a lower risk of haemorrhage than sporadic AVMs and routine screening should not be practiced in adult patients. Routine screening should be discussed for children with a familial history of cerebral haemorrhage and/or HHT type 1.

[Risks and responsibilities in diagnostic and interventional radiology. Ethical and medicolegal considerations]. / Risques et responsabilités en radiologie diagnostique et interventionnelle. Aspects éthiques et médico-légaux.

Medical risk management has one main purpose: to ensure the safety of care. The law of March 2002 has generated a true cultural revolution. The radiologist is involved with new and difficult areas of medical liability due to technical advances, the increasing number of imaging techniques, the increasing complexity of imaging techniques, their efficiency and the need for multidisciplinary approach. Imaging recommendations requiring increasing levels of technical and clinical skills. The radiologist is liable with regards to the indications of imaging studies, and also with regards to informed consent. The prevention of medicolegal problems is achieved by competency, which must be combined to good liability insurance and ongoing vigilance supported by appropriate continuous medical education.

Multiple mechanisms of regulation of the inositol 1,4,5-trisphosphate receptor by calcium.

Ca2+ mobilisation by inositol 1,4,5-trisphosphate (InsP3) is a complex phenomenon which involves positive and negative feedback regulation by cytosolic Ca2+. It has been shown that Ca2+ increased the affinity of [3H]-InsP3 binding to liver membranes and inhibited [3H]-InsP3 binding to cerebellar membranes. We investigated the effects of Ca2+ on the [3H]-InsP3 binding to receptor solubilised and rapidly purified by immunoprecipitation. The InsP3 binding to the purified liver receptor was insensitive to the addition of Ca2+, indicating that Ca2+ did not interact directly with the receptor. The loss of the Ca2+ effect on liver receptor affinity was reproduced by alkaline treatment of liver membranes, which is known to extract the peripheral membrane proteins. This suggests that Ca2+ regulates the liver InsP3 receptor by interacting with a membrane-associated protein. Ca2+ inhibited the binding of [3H]-InsP3 to purified cerebellar receptors as was found with the membrane fraction. The treatment of the purified cerebellar receptor with media of high ionic strength or at alkaline pH did not abolish the effect of Ca2+ on the receptor. This indicates that the inhibitory effect of Ca2+ on [3H]-InsP3 binding to cerebellar membranes occurs either via direct interaction with the receptor or via an integral protein strongly associated with the receptor. In conclusion, the mechanisms of regulation of InsP3-induced Ca2+ release by Ca2+ involve different molecular support in cerebellum and in liver. This may reflect different regulation dependent on the receptor type.

Vasospasm after subarachnoid hemorrhage: interest in diffusion-weighted MR imaging.

BACKGROUND AND PURPOSE: Vasospasm secondary to subarachnoid hemorrhage (SAH) is responsible for severe ischemic complications. Although effective, angioplasty must be performed at a very early stage to produce any clinical recovery. Diagnostic investigations to assess arterial narrowing (transcranial Doppler, angiography) or cerebral perfusion (xenon CT, single-photon emission CT) do not provide evidence of the extent of parenchymal ischemia. In stroke, diffusion-weighted MR imaging (DWI) appears to be the most sensitive procedure to detect cerebral ischemia. We studied asymptomatic vasospasm in patients with aneurysmal SAH to assess whether DWI provides predictive markers of silent ischemic lesions and/or progression toward symptomatic ischemia. METHODS: Seven asymptomatic vasospasm patients (average blood velocity rates >120 cm/s), 3 patients with symptomatic vasospasm, and 4 patients with SAH but without vasospasm were studied at regular intervals by DWI, and their apparent diffusion coefficients (ADCs) were calculated. RESULTS: All patients with vasospasm including those without symptoms presented abnormalities on DWI with a reduction of the ADC prevalently in the white matter. No such abnormalities were observed in patients without vasospasm. The abnormalities on DWI resolved completely in 4 of the 7 patients, with no parenchymal lesion. Resolution was partial in 3 patients whose white matter still presented residual round, focal ischemic lesions. CONCLUSIONS: Being able to correlate abnormalities on DWI with parenchymal involvement in asymptomatic patients would be of considerable clinical significance. It is hoped that larger studies will be undertaken to determine whether the ADC has a reversibility threshold, because this would facilitate patient management.

A characterization of the nonstructural protein from which the virus-specified tubules in epizootic haemorrhagic disease virus-infected cells are composed.

The complete nucleotide sequence of segment 6 of epizootic haemorrhagic disease virus serotype 2 (Alberta) which encodes nonstructural protein NS1 was determined from a cDNA clone containing a full-length copy of the gene. The gene was found to be 1806 bp in length, constituted by one open reading frame of 1656 bp which is flanked by 5' and 3' noncoding regions of 32 and 118 bp, respectively. The conserved 5' and 3' terminal hexanucleotide sequences were identical to those of BTV-10. The 5' noncoding nucleotide sequences of cognate genome segments 4, 6 and 8 were found to be highly conserved in EHDV-2 and BTV-10. The 3' noncoding regions are less conserved but share common characteristics. The predicted EHDV-2 NS1 gene product, a 552 amino acid polypeptide, is predominantly hydrophobic and has a net charge of +5 at neutral pH. Comparison to its BTV-10 counterpart revealed a high degree of homology. Regions of high amino acid similarity were shown to correlate with hydrophobic domains on the proteins whilst regions of lower amino acid similarity corresponded with the hydrophilic domains. Thirteen conserved cysteine residues of which the majority occurred in hydrophobic regions with more than 80% amino acid similarity were identified.

Narcolepsy associated with arteriovenous malformation of the diencephalon.

Narcolepsy associated with localized brain lesions is rare, and few reports of well-documented cases have been published. We describe the case of a 20-year-old male (HLA DQw1 negative) who fulfilled clinical and polygraphic criteria of symptomatic narcolepsy. Narcolepsy in this patient was associated with an arteriovenous malformation involving the structures around the third ventricle. Clinical symptoms improved after embolization and radiosurgery. These findings support the hypothesis that lesions in the vicinity of the third ventricle can cause symptomatic narcolepsy.

Ligand-binding affinity of the type 1 and 2 inositol 1,4,5-trisphosphate receptors: effect of the membrane environment.

The inositol 1,4,5-trisphosphate (InsP3) receptor is essential for Ca2+ release from intracellular stores. There are three InsP3 receptor types which are targets for several types of regulation. Ca2+, phosphorylation, and protein-protein interactions may contribute to the complex pattern of the Ca2+ signal in stimulated cells. Furthermore, the 3 receptor types could have different affinities for InsP3. We compared the affinities of the type 1 receptor from the cerebellum with the liver type 2 receptor both in their membrane environment and after isolation by immunoprecipitation. Measurements of [3H]InsP3 binding in a cytosol-like medium revealed that the Kd of the liver receptor (45 +/- 5 nM, N = 14) was higher than the Kd of the cerebellar receptor (28 +/- 3 nM, N = 9). Solubilization and immunopurification of the liver InsP3 receptor resulted in a 10-fold increase in its affinity for InsP3. The affinity of the cerebellar receptor did not change under these conditions. Therefore, the extraction of the liver and the cerebellar receptors from their membrane environments induced an inversion of their relative affinities. Treatment of liver membranes with low concentrations of detergents also increased the affinity for InsP3 binding. These data indicate that the type 1 and the type 2 InsP3 receptors have different affinities for InsP3 and that the properties of the type 2 receptor are strongly regulated by hydrophobic interactions within its membrane environment.

Changes in lung and systemic oxidant and antioxidant activity after smoke inhalation.

We determined the oxidant activity in lung airways, parenchyma, and systemic tissues in response to smoke inhalation, comparing lipid peroxidation with physiologic and histologic change. Adult sheep were given a controlled amount of cooled smoke from burned cotton toweling, containing a uniform particle diameter of 3-4 microns. The mean peak carboxyhemoglobin was 45 +/- 4%. Animals were monitored unanesthetized for 24 h and killed. Severe respiratory failure was noted, as a result of airways mucosal ulceration, submucosal edema, and atelectasis, along with increased airways fluid, but minimal alveolar edema. Airway fluid malondialdehyde (MDA) content was threefold greater than plasma. However, airways mucosa and lung parenchymal tissue, lipid peroxidation, and oxidized glutathione were not increased, suggesting the only direct oxidant activity was present only at the airways surface. Other factors besides oxidants are likely to be involved in the lung injury. However, a marked systemic oxidant stress was noted as evidenced by a significant increase in liver tissue MDA and decrease in reduced glutathione and catalase activity. The tissue oxidant stress also corresponded with a 75% increase in systemic oxygen consumption and an increase in soft tissue vascular permeability. We conclude that: 1) the only direct lung oxidant stress after smoke was noted in airways fluid, while lung tissue lipid peroxidation was not seen despite severe airways injury and atelectasis, and 2) major systemic physiologic changes, as evidenced by increased systemic oxygen demands and systemic microvascular permeability are seen with smoke exposure in addition to evidence of systemic tissue oxidant stress. The likely source of the oxidant activity was a smoke-induced systemic inflammation.

Comparison of plasma reduced glutathione and oxidized glutathione with lung and liver tissue oxidant and antioxidant activity during acute inflammation.

We determined whether plasma levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) accurately reflect the tissue GSH and GSSG levels in lung and liver during a progressive acute inflammation-induced increased oxidant activity. We also determined whether plasma GSH also reflected other antioxidant defenses. Male Wistar rats (n = 38) were given intraperitoneal zymosan (.75 mg/g body weight) producing an acute progressive peritonitis and generalized inflammation. Animals were resuscitated then killed at 4 or 24 h. Plasma and tissue levels of GSH, GSSG, vitamin C, alpha-tocopherol, and catalase were measured. Conjugated dienes and malondialdehyde were used as tissue markers of lipid peroxidation. We found lung and liver tissue GSH to be decreased significantly at 4 h while GSSG was increased. Lipid peroxidation was also present in the lung. At 24 h, GSH remained decreased in liver and GSSG remained increased in lung along with the lipid peroxides conjugated dienes and malondialdehyde. In addition, overall antioxidant defenses were decreased in both lung and liver. Plasma GSH remained decreased at 24 h corresponding with the decrease in liver GSH as well as the decrease in other plasma and tissue antioxidants. However, plasma GSSG levels were not significantly increased, at any time point, indicating plasma GSSG does not accurately reflect tissue oxidant activity.

Alpha-tocopherol attenuates lung edema and lipid peroxidation caused by acute zymosan-induced peritonitis.

BACKGROUND: Inflammation-induced disease as seen with trauma and infection can lead to increased lung oxidant activity resulting in cell membrane lipid peroxidation. Acute zymosan-induced peritonitis in rats produces lung inflammation, edema, and lipid peroxidation. We determined whether administered alpha-tocopherol (vitamin E), the key antioxidant protection against cell membrane lipid peroxidation, would improve this process. METHODS: Male Wistar rats were given 0.75 mg/kg of intraperitoneal zymosan, volume resuscitated, monitored, and killed at 4 or 24 hours. Lung histologic changes and levels of conjugated dienes, a marker of lipid peroxidation, were used to monitor injury. The levels of vitamin E, vitamin C, and catalase were used to monitor antioxidant defenses. The effect of administering alpha-tocopherol (50 mg/kg) by gavage immediately after zymosan on the degree of the lung injury was then determined. RESULTS: Twenty-four hours after zymosan was administered, the vitamin E levels in plasma were significantly decreased, but lung tissue vitamin E levels were maintained, whereas tissue catalase and vitamin E levels decreased. Lung tissue-conjugated diene levels, alveolar edema, and neutrophil count were significantly increased. alpha-Tocopherol treatment increased the postzymosan plasma vitamin E levels by 50%. Lung tissue vitamin E levels did not increase; however, the degree of lung injury and lipid peroxidation was significantly attenuated. Tissue catalase levels were also maintained. CONCLUSIONS: We conclude that alpha-tocopherol given at the onset of a progressing inflammatory injury can protect the lung from oxidant damage and attenuate the degree of lung injury.

Effect of increasing the tidal volume of smoke breaths on smoke-induced lung dysfunction.

We determined the effect of a graded increase in lung exposure to a toxic smoke by increasing smoke tidal volume (VT) or the number of smoke breaths. Sheep were anesthetized and then insufflated with cooled cotton toweling smoke; VT was 5, 10, or 20 ml/kg, and smoke breaths were varied from 12 to 48. The smoke had a uniform particle size (3 +/- 0.4 microns diam). Peak carboxyhemoglobin levels varied from 8 +/- 2 to 45 +/- 4% in the lowest to highest exposure groups, respectively. Animals were monitored unanesthetized for 24 h, and then they were killed. Oxygenation (ratio of arterial PO2 to fraction of inspire O2) decreased from 480 +/- 21 to 200 Torr, and compliance decreased by approximately 50% in the highest smoke exposure groups, whereas only a modest decrease in oxygenation and no compliance changes were seen with lesser exposures. A moderate tracheobronchitis, some atelectasis, and no alveolar edema were noted in the lower smoke exposure groups, whereas severe tracheobronchitis, airway edema, and alveolar atelectasis were observed in the highest exposure group. Only modest alveolar flooding was noted. Impaired oxygenation and anatomic injury correlated best with the total smoke delivered (r = 0.59). Increasing VT from 5 to 20 ml/kg did not increase airway or alveolar injury if the total smoke mass delivered was maintained constant. The degree of impaired oxygenation did not correlate with measured lung water (r = 0.27) or lung lymph flow (r = 0.31).