Acta Neuropathol (Berl) 2006 Jun; 111(6): 510-8 (Read article online)

Oshima K, Akiyama H, Tsuchiya K, Kondo H, Haga C, Shimomura Y, Iseki E, Uchikado H, Kato M, Niizato K, Arai H

Cerebral amyloid angiopathy (CAA) is a manifestation of amyloid beta-protein (Abeta) accumulation in the elderly as well as in patients with Alzheimer's disease (AD). Two types of CAA have been noted, based on the type of vasculature in which Abeta is deposited: cerebral capillary amyloid angiopathy (capCAA) and non-capCAA. Non-capCAA is a common form of CAA that consists of Abeta deposited in arteries and arterioles. Recent information on Abeta metabolism in the brain suggests that non-capCAA is associated with Abeta secretion into the cerebrospinal fluid via the perivascular space, whereas capCAA is associated with Abeta removal to blood plasma via the capillary endothelium. Abeta40, a major and relatively soluble Abeta isoform, is deposited predominantly in non-capCAA, and Abeta42, which is insoluble and associated more closely than Abeta40 with AD, is deposited predominantly in capCAA. Studying small areas of microscopic size within a given cortical region, we found an inverse association of capCAA and senile plaques. We also found a relative paucity of tau pathology in the small areas with abundant capCAA compared with the small areas with abundant senile plaques within a cortical region with the same cytoarchitecture. We suppose that both capCAA and senile plaques indicate high Abeta42 in the neuropil but that only Abeta42 in the form of insoluble deposits in senile plaques promotes tau abnormality.

Brain Res Bull 2006 May 31; 69(6): 626-30 (Read article online)

Long KD, Mastropaolo J, Rosse RB, Manaye KF, Deutsch SI

Abnormalities of NMDA receptor-mediated neurotransmission are involved in the pathophysiology of schizophrenia, Alzheimer's disease, substance abuse and seizure disorders. The NMDA receptor is implicated in schizophrenia because phencyclidine (PCP), a noncompetitive NMDA receptor antagonist, binds to a hydrophobic domain within the channel, precipitating a schizophreniform psychosis in susceptible persons. Pharmacological, environmental, and genetic variables alter NMDA receptor-mediated neurotransmission. Inbred mouse strains differ in their sensitivity to some of the behavioral effects of MK-801 (dizocilpine), a PCP analogue. The NMDA receptor complex in the BALB/c strain could reflect a unique stoichiometric combination of receptor subunits resulting in a higher proportion of the channels in the open configuration, a higher affinity of MK-801 for its hydrophobic channel domain, and/or a combination of the above. The BALB/c mouse strain, "stressed" mice, and behavioral consequences of MK-801 administration represent models of altered glutamatergic neural transmission. We were interested in examining the effect of stress on the modulatory properties of d-serine and sarcosine. d-Serine is a naturally occurring glycine agonist that modulates the ability of l-glutamate to influence the opening of the NMDA receptor-associated ionophore, and sarcosine is a naturally occurring glycine reuptake inhibitor. The data suggest that 24h after stress, d-serine and sarcosine interact synergistically to reduce MK-801's ability to antagonize electrically precipitated tonic hindlimb extension. Under conditions of stress, modulatory effects of d-serine and sarcosine on the antiseizure effect of MK-801 are observed that are not apparent in the nonstress condition. The results could be relevant to the development of glycinergic interventions for the treatment of neuropsychiatric disorders.

Arch Intern Med 2006 May 22; 166(10): 1115-20 (Read article online)

Wang L, Larson EB, Bowen JD, van Belle G

BACKGROUND: The association of physical function with progression to dementia has not been well investigated. We aimed to determine whether physical function is associated with incident dementia and Alzheimer disease (AD). METHODS: We performed a prospective cohort study of 2288 persons 65 years and older without dementia. Patients were enrolled from 1994 to 1996 and followed up through October 2003. Main outcome measures included incident dementia and AD. RESULTS: During follow-up 319 participants developed dementia (221 had AD). The age-specific incidence rate of dementia was 53.1 per 1000 person-years for participants who scored lower on a performance-based physical function test at baseline (10 points). A 1-point lower performance-based physical function score was associated with an increased risk of dementia (hazard ratio, 1.08; 95% confidence interval, 1.03-1.13; P<.001), an increased risk of AD (hazard ratio, 1.06; 95% confidence interval, 1.01-1.12; P = .01), and an increased rate of decline in the Cognitive Ability Screening Instrument scores (0.11 point per year; 95% confidence interval, 0.08-0.14; P<.001) after adjusting for age, sex, years of education, baseline cognitive function, APOE epsilon4 allele, family history of AD, depression, coronary heart disease, and cerebrovascular disease. CONCLUSIONS: Lower levels of physical performance were associated with an increased risk of dementia and AD. The study suggests that poor physical function may precede the onset of dementia and AD and higher levels of physical function may be associated with a delayed onset.

Brain Res Bull 2006 May 31; 69(6): 669-79 (Read article online)

Hernández-Espinosa D, Jennifer Morton A

Calcineurin (CaN) is a Ca(2+)- and calmodulin-dependent protein serine-threonine phosphatase that is thought to play an important role in the neuronal response to changes in the intracellular Ca(2+) concentration. CaN has been implicated in numerous physiological processes including learning and memory. Decreases in CaN expression are thought to be responsible for some of the pathological features seen in brain ischemia, Down's syndrome and Alzheimer's disease. In this study, we examined the possibility of CaN playing a role in the progressive neurological phenotype of the R6/2 mouse of Huntington's disease. We studied the effects of the CaN inhibitors cyclosporin A and FK506 on the progressive neurological phenotype in the R6/2 mouse. We found that an immunosuppressive dose of both drugs dramatically accelerated the main features of the neurological phenotype in R6/2 mice. This was unlikely to be due solely to the immunosuppressive action of these drugs, since treatment with cyclophosphamide, an immunosuppressant drug with a mechanism of action that is not mediated via CaN, did not have deleterious effects on the R6/2 mouse. If anything, cyclophosphamide improved the neurological symptoms in the R6/2 mice. Together, our data suggest a central role for CaN in the deleterious phenotype of the R6/2 mouse. Treatments aimed at preventing the loss of CaN or stimulating its function may be beneficial in the treatment of HD.

Nucleic Acids Res 2006; 34(9): 2736-50 (Read article online)

Kim JH, Yang CK, Stallcup MR

The coiled-coil coactivator (CoCoA) is a transcriptional coactivator for nuclear receptors and enhances nuclear receptor function by the interaction with the bHLH-PAS domain (AD3) of p160 coactivators. The C-terminal activation domain (AD) of CoCoA possesses strong transactivation activity and is required for the coactivator function of CoCoA with nuclear receptors. To understand how CoCoA AD transmits its activating signal to the transcription machinery, we defined specific subregions, amino acid motifs and protein binding partners involved in the function of CoCoA AD. The minimal transcriptional AD was mapped to approximately 91 C-terminal amino acids and consists of acidic, serine/proline-rich and phenylalanine-rich subdomains. Transcriptional activation by the CoCoA AD was p300-dependent, and p300 interacted physically and functionally with CoCoA AD and was recruited to a promoter by the interaction with CoCoA AD. The FYDVASAF motif in the CoCoA AD was critical for the transcriptional activity of CoCoA AD, the interaction of CoCoA with p300, the coactivator function of CoCoA for estrogen receptor alpha and GRIP1 and the transcriptional synergy among coactivators GRIP1, CARM1, p300 and CoCoA. Taken together these data extend our understanding of the mechanism of downstream signaling by the essential C-terminal AD of the nuclear receptor coactivator CoCoA; they indicate that p300 is a functionally important interaction partner of CoCoA AD and that their interaction potentiates transcriptional activation by the p160 coactivator complex.

Biosci Biotechnol Biochem 2006 May; 70(5): 1242-5 (Read article online)

Kobayashi-Hattori K, Watanabe T, Kimura K, Sugita-Konishi Y

We investigated the change in renal mdr1b mRNA expression in offspring exposed to tributyltin chloride (TBTC) via the placenta and lactation or via lactation, using the real-time reverse transcription-polymerase chain reaction. Pregnant ICR mice were given water containing TBTC (0, 15, and 50 mug/ml) ad libitum from the start of pregnancy to weaning or from parturition to weaning. Exposure via the placenta and lactation significantly reduced the renal mdr1b level in offspring. Exposure to TBTC through the mother might impair the exclusion system of toxic compounds in offspring.

Mol Cell Biochem 2006 May 23; (Read article online)

Lin Y, Liu L, Li Z, Qiao J, Wu L, Tang W, Zheng X, Chen X, Yan Z, Tian W

Musculoskeletal tissues regeneration requires rapid expansion of seeding cells both in vitro and in vivo while maintaining their multilineage differentiation ability. Human adipose-derived stem cells (ASCs) are considered to contain multipotent mesenchymal stem cells. Monolayer cultures of human ASCs were isolated from human lipoaspirates and passaged 3 times and then infected with replication-incompetent adenoviral vectors carrying green fluorescent protein (Ad/GFP) genes. Then, Ad/GFP infected human ASCs were transferred to osteogenic, chondrogenic, adipogenic, and myogenic medium. The morphological characterization of induced cells was observed using phase-contrast microscopy and fluorescence microscopy. The expression of marker proteins or genes was measured by immunocytochemical and RT-PCR analysis. Osteopontin (OPN), and osteocalcin (OCN) were positive in osteogenic lineages, aggrecan and SOX9 were positive in chondrogenic ones, peroxisome proliferator-activated receptor (PPAR-gamma2) and lipoprotein lipase (LPL) were positive in adipogenic ones, and myogenin and myod1 was positive in myogenic ones. At the same time, the results of fluorescence microscopic imaging proved that the high level of GFP expression during ASCs differentiation maintained stable nearly 2 months. So the exogenous GFP and multilineage potential of human ASCs had no severe influences on each other. Since the human ASCs can be easily obtained and abundant, it is proposed that they may be promising candidate cells for further studies on tissue engineering. Imaging with expression of GFP facilitates the research on ASCs physiological behavior and application in tissue engineering during differentiation both in vitro and in vivo.

N Z Med J 2006; 119(1234): U1976 (Read article online)

Weatherall M, Arnold T

Nocturia is a common bothersome condition. An ad hoc group of interested clinicians from a variety of backgrounds has developed draft guidelines for the assessment and management of this condition in primary care in New Zealand. The guidelines propose four steps in the assessment and management: clinical evaluation; simple investigations; assignment of a provisional diagnosis; and management based on the provisional diagnosis. For nocturnal polyuria-associated nocturia, the draft guidelines recommend that: lifestyle measures should be used as part of the management; if a patient complaining of nocturia has other features of overactive bladder, then bladder retraining and/or anticholinergics can be used; hypnosedatives should not be used to treat nocturia in older adults because of the increased risk of falls; loop diuretics given in the afternoon should be considered for the treatment; and desmopressin can be considered in the management of nocturnal polyuria associated nocturia but that it should be used cautiously in people aged over 65 because of the risk of hyponatraemia. A draft algorithm based on international guidelines is presented.

ANS Adv Nurs Sci 2006 Apr-Jun; 29(2): 152-60 (Read article online)

Sorrell JM

Healthcare professionals may see prolonging life and use of scarce resources as futile if the quality of life of persons with Alzheimer's disease is deemed to be poor. Thus, nurses and other healthcare providers need to question traditional assumptions of quality of life. This article presents a phenomenological study of ethical concerns related to quality of life as described by persons with Alzheimer's disease, family caregivers, and professional caregivers. The theme of "Creating a Quality of Life Through Connected Lives" calls forth an ethics of respect for the individual experience and its connecting relationships.

Acta Neuropathol (Berl) 2006 Jun; 111(6): 519-528 (Read article online)

Pugliese M, Geloso MC, Carrasco JL, Mascort J, Michetti F, Mahy N

Like humans, canines develop with aging beta-amyloid (Abeta) plaques and a progressive cognitive deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer's disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Abeta plaque maturation and its relationship with cognitive deficit. The aim of the present investigation was to study the link between the diffuse Abeta plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100beta) overexpression in the process was also investigated. Abeta plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe cognitive deficit. A correlation between canine graded cognitive deficit, diffuse plaque maturation, and S100beta (-) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Abeta deposition in Alzheimer's disease.

Radiol Med (Torino) 2006 May 25; (Read article online)

Sbarzaglia P, Lovato L, Buttazzi K, Russo V, Renzulli M, La Palombara C, Fattori R

Acute aortic dissection continues to be one of the most catastrophic cardiovascular events. While there is a general consensus on immediate surgical repair when the ascending aorta is involved, the optimal treatment strategy for type B aortic dissection (B-AD) remains controversial. Recently, endovascular treatment with percutaneous stent-graft implantation, originally used for aortic aneurysm exclusion, has acquired an important role in the treatment of B-AD. Imaging techniques such as computed tomography (CT), magnetic resonance imaging (MRI) and angiography have a fundamental role in the search for the anatomic details necessary to tailor the stent graft and in evaluating the most suitable anatomy for stent graft. Transesophageal echocardiography is fundamental during the procedure to monitor the correct release of the stent graft and evaluate the result of the procedure expressed by immediate thrombosis out of the stent-graft. Again, imaging techniques, more notably CT, have a fundamental role in the postoperative followup after stent-graft placement. The risk of endoleaks may compromise the result of endovascular repair and increase the risk of aortic rupture. Several reports and a few trials attesting to technical feasibility and safety of stent-graft implantation procedures for B-AD have been reported so far. Also, a randomised trial comparing type B aortic stent-graft placement with medical therapy is currently underway. According to the investigators, new therapeutic indications are likely to emerge also in uncomplicated B-AD.

Ann Neurol 2006 May 22; 59(6): 952-962 (Read article online)

Forman MS, Farmer J, Johnson JK, Clark CM, Arnold SE, Coslett HB, Chatterjee A, Hurtig HI, Karlawish JH, Rosen HJ, Van Deerlin V, Lee VM, Miller BL, Trojanowski JQ, Grossman M

OBJECTIVE: Frontotemporal lobar degeneration (FTLD) is characterized by impairments in social, behavioral, and/or language function, but postmortem studies indicate that multiple neuropathological entities lead to FTLD. This study assessed whether specific clinical features predict the underlying pathology. METHODS: A clinicopathological correlation was performed on 90 consecutive patients with a pathological diagnosis of frontotemporal dementia and was compared with an additional 24 cases accrued during the same time period with a clinical diagnosis of FTLD, but with pathology not typically associated with frontotemporal dementia. RESULTS: Postmortem examination showed multiple pathologies including tauopathies (46%), FTLD with ubiquitin-positive inclusions (29%), and Alzheimer's disease (17%). The pathological groups manifested some distinct demographic, clinical, and neuropsychological features, although these attributes showed only a statistical association with the underlying pathology. FTLD with ubiquitin-positive inclusions was more likely to present with both social and language dysfunction, and motor neuron disease was more likely to emerge in these patients. Tauopathies were more commonly associated with an extrapyramidal disorder. Alzheimer's disease was associated with relatively greater deficits in memory and executive function. INTERPRETATION: Clinical and neuropsychological features contribute to delineating the spectrum of pathology underlying a patient diagnosed with FTLD, but biomarkers are needed that, together with the clinical phenotype, can predict the underlying neuropathology. Ann Neurol 2006;59:952-962.

Neurology 2006 May 23; 66(10): 1506-10 (Read article online)

Kulstad JJ, Green PS, Cook DG, Watson GS, Reger MA, Baker LD, Plymate SR, Asthana S, Rhoads K, Mehta PD, Craft S

BACKGROUND: Hyperinsulinemia and insulin resistance are risk factors for memory impairment and Alzheimer disease (AD). Insulin regulates levels of the amyloid beta-peptide (Abeta) in vitro in neuronal cultures and in vivo in the CSF of normal older adults. OBJECTIVE: To determine whether insulin affected plasma Abeta levels and whether such effects differed for patients with AD compared with normal older adults. METHODS: Fifty-nine patients with AD and 50 healthy older adults each received infusions of saline and of insulin (1.0 mU.kg(-1).min(-1)) with accompanying dextrose to maintain euglycemia. A subset of participants (19 AD, 12 normal) received two additional conditions, in which insulin was infused at a lower (0.33 mU.kg(-1).min(-1)) and higher (1.67 mU.kg(-1).min(-1)) rate. Plasma insulin and Abeta were measured after 120 minutes of infusion. RESULTS: Adults with AD had higher plasma insulin vs normal adults at the two higher infusion rates, despite receiving comparable amounts of insulin. For normal adults, insulin reduced plasma Abeta levels at the middle (1.0 mU.kg(-1).min(-1)) dose, with attenuated effects at lower and higher doses. In contrast, for patients with AD, insulin raised plasma Abeta levels at the two higher doses (1.0 and 1.67 mU.kg(-1).min(-1)). CONCLUSIONS: These results suggest that patients with Alzheimer disease (AD) have reduced insulin clearance and insulin-provoked plasma amyloid beta-peptide (Abeta) elevation. Abnormal regulation of peripheral Abeta by insulin may contribute to AD risk.

Circulation 2006 May 22; (Read article online)

Maekawa N, Abe JI, Shishido T, Itoh S, Ding B, Sharma VK, Sheu SS, Blaxall BC, Berk BC

BACKGROUND: Pharmacological and genetic studies indicate that the Na(+)-H(+) exchanger isoform 1 (NHE1) plays a critical role in myocardial ischemia and reperfusion (I/R) injury. We found that p90 ribosomal S6 kinase (RSK) phosphorylated serine 703 of NHE1, stimulating 14-3-3 binding and NHE1 activity. Therefore, we hypothesized that inhibiting RSK in cardiomyocytes would prevent NHE1 activation and decrease I/R-mediated injury. METHODS AND RESULTS: To examine the role of RSK in vivo, we generated transgenic mice with cardiac-specific overexpression of dominant negative RSK (DN-RSK-TG). DN-RSK-TG hearts demonstrated normal basal cardiac function and morphology. However, myocardial infarction (left coronary artery occlusion for 45 minutes) in DN-RSK-TG hearts was significantly reduced at 24 hours of reperfusion from 46.9+/-5.6% area at risk in nontransgenic littermate controls to 26.0+/-4.2% in DN-RSK-TG (P<0.01). Cardiomyocyte apoptosis was significantly reduced after I/R in DN-RSK (0.9+/-0.2%) compared with nontransgenic littermate controls (6.2+/-2.6%). Importantly, activation of RSK and interaction of 14-3-3 with NHE1, necessary for agonist-stimulated NHE1 activity, were increased by I/R and inhibited by 70% in DN-RSK-TG (P<0.01). Next, we transduced rat neonatal cardiomyocytes with adenovirus-expressing DN-RSK (Ad.DN-RSK) and measured NHE1 activity. The baseline rate of pH recovery in acid-loaded cells was equal in cells expressing LacZ or DN-RSK. However, NHE1 activation by 100 micromol/L H2O2 was significantly inhibited in cells expressing DN-RSK (0.16+/-0.02 pH units/min) compared with Ad.LacZ (0.49+/-0.13 pH units/min). Apoptosis induced by 12 hours of anoxia followed by 24 hours' reoxygenation was significantly reduced in cells expressing Ad.DN-RSK (18.6+/-2.0%) compared with Ad.LacZ (29.3+/-5.4%). CONCLUSIONS: In summary, RSK is a novel regulator of cardiac NHE1 activity by phosphorylating NHE1 serine 703 and a new pathological mediator of I/R injury in the heart.

Neurochem Res 2006 May 23; (Read article online)

Pomara N, Hernando RT, de la Pena CB, Sidtis JJ, Cooper TB, Ferris S

The glucocorticoid receptor (GR) antagonist mifepristone (RU-486) has been reported to increase early morning plasma ACTH/cortisol in diverse non-demented populations. This pilot study examined the cortisol response to RU 486 in patients with Alzheimer's disease (AD), a condition associated with abnormalities in various aspects of the hypothalamic-pituitary-adrenal (HPA) axis. Nine AD subjects were randomized in a placebo-controlled parallel study: 4 in the placebo group and 5 in the RU 486 group. Subjects received oral doses of RU 486 (200 mg) or placebo daily for 6-weeks. Morning plasma cortisol was determined at baseline, at 12 h following the first study drug dose, and weekly thereafter. RU 486 resulted in a significant increase in cortisol levels [F(1,6)=65.32; P<0.001]. The magnitude of this increase grew over the course of the study [F(1,6)=63.17; P<0.001], was not related to cortisol suppression after dexamethasone and appeared greater than that reported in the literature in younger populations in response to the same drug regimen. However, further studies with age-matched controls should be done to determine possible AD related changes in this response.

J Psychiatr Res 2006 May 19; (Read article online)

Ruano D, Macedo A, Soares MJ, Valente J, Azevedo MH, Hutz MH, Gama CS, Lobato MI, Belmonte-de-Abreu P, Goodman AB, Pato C, Saraiva MJ, Heutink P, Palha JA

It has been proposed that schizophrenia results from an environmental insult in genetically predisposed individuals. Environmental factors capable of modulating transcriptional activity and their carriers could link the genetic and environmental components of schizophrenia. Among these is transthyretin (TTR), a major carrier of thyroid hormones and retinol-binding protein (RBP). Retinoids and thyroid hormones regulate the expression of several genes, both during development and in the adult brain. Decreased TTR levels have been reported in the cerebrospinal fluid of patients with depression and Alzheimer's disease, and the absence of TTR influences behavior in mice. DNA variants capable of altering TTR ability to carry its ligands, either due to reduced transcription of the gene or to structural modifications of the protein, may influence development of the central nervous system and behavior. In the present study we searched for variants in the regulatory and coding regions of the TTR gene, and measured circulating levels of TTR and RBP. We found a novel single nucleotide polymorphism (SNP), ss46566417, 18 bp upstream of exon 4. Neither this SNP nor the previously described rs1800458 were found associated with schizophrenia. In addition, serum TTR and RBP levels did not differ between mentally healthy and schizophrenic individuals. In conclusion, our data does not support an involvement of the TTR gene in the pathophysiology of schizophrenia.

Neurology 2006 May 23; 66(10): 1523-6 (Read article online)

Charlton RA, Morris RG, Nitkunan A, Markus HS

BACKGROUND: Interpretation of treatment trials in vascular dementia is confounded by the presence of coexistent Alzheimer disease (AD) pathology. The younger onset genetic disease cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) offers a model of pure vascular dementia, in which such confounding is unlikely. To validate CADASIL's use as a model it is important to show it results in a similar cognitive impairment. METHODS: The same neuropsychological assessment was administered to patients with CADASIL (n = 34, 14 of whom had had stroke), sporadic small vessel disease (SVD) presenting with lacunar stroke and having confluent leukoaraiosis (n = 54), and healthy controls (n = 25). RESULTS: A similar pattern of neuropsychological impairment was seen in the two diseases, with prominent early executive dysfunction. Patients with CADASIL and SVD performed worse than controls on Trails switching test (CADASIL p = 0.006; SVD p < 0.001), and on verbal fluency test (CADASIL p = 0.015; SVD p = 0.004). The SVD group also performed worse on immediate (p = 0.050) and delayed (p = 0.049) memory. When only patients with CADASIL with stroke were included in analysis with SVD subjects, all of whom had had stroke, a very similar cognitive profile was seen. The only difference was on verbal fluency, where CADASIL subjects performed worse (p = 0.044). CONCLUSION: Patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and small vessel disease show a similar pattern of cognitive deficits. This suggests that CADASIL provides a model of pure vascular dementia relevant for sporadic small vessel disease vascular dementia.

Dement Geriatr Cogn Disord 2006 May 23; 22(1): 108-120 (Read article online)

Irish M, Cunningham CJ, Walsh JB, Coakley D, Lawlor BA, Robertson IH, Coen RF

The enhancing effect of music on autobiographical memory recall in mild Alzheimer's disease individuals (n = 10; Mini-Mental State Examination score >17/30) and healthy elderly matched individuals (n = 10; Mini-Mental State Examination score 25-30) was investigated. Using a repeated-measures design, each participant was seen on two occasions: once in music condition (Vivaldi's 'Spring' movement from 'The Four Seasons') and once in silence condition, with order counterbalanced. Considerable improvement was found for Alzheimer individuals' recall on the Autobiographical Memory Interview in the music condition, with an interaction for condition by group (p < 0.005). There were no differences in terms of overall arousal using galvanic skin response recordings or attentional errors during the Sustained Attention to Response Task. A significant reduction in state anxiety was found on the State Trait Anxiety Inventory in the music condition (p < 0.001), suggesting anxiety reduction as a potential mechanism underlying the enhancing effect of music on autobiographical memory recall. Copyright (c) 2006 S. Karger AG, Basel.

J Chem Ecol 2006 May 23; (Read article online)

Shaw RA, Villalba JJ, Provenza FD

In grazing systems, forage availability is a function of herbivore density, which can influence an animal's ability to be selective. In turn, the influence of food availability on selectivity has the potential to influence plant biodiversity. We hypothesized that the ability of herbivores to mix toxin-containing foods in their diets is a function of the availability of nontoxic foods and the nutritional characteristics of the toxin-containing foods. We evaluated this hypothesis in two trials simulating different diet qualities (high-quality foods in trial 1, low-quality foods in trial 2). Within each trial, the four treatment groups were offered with different amounts of nutritious, familiar foods-10, 30, 50, and 70% of ad libitum intake-but were offered with ad libitum access to toxin-containing foods. Each lamb was presented with five foods, including three toxin-containing unfamiliar foods (terpenes, tannins, and oxalates) and two nutritious familiar foods (alfalfa and barley). In trial 1, as the availability of nutritious familiar foods decreased, animals ate more of all three toxin-containing foods. As the availability of nutritious alternatives increased, the pattern of selection shifted from terpenes to tannins and oxalates. In trial 2, animals also ate more toxins as the availability of nutritious alternatives decreased, but their pattern of diet mixing changed. Low availability of nutritious alternatives resulted in the animals eating more oxalates. During preference tests when all five foods were offered ad libitum, animals fed with 10, 30, 50, and 70% of ad libitum intake from trial 1 ate 49, 47, 41, and 38% of the three toxin-containing foods, respectively. The lower diet quality in trial 2 affected intake of the toxin-containing foods such that animals fed with 10, 30, 50, and 70% of ad libitum intake ate 37, 36, 29, and 27%, respectively, of the three toxin-containing foods. Thus, the quality of toxin-containing foods and the availability of nutritious alternatives interacted to modify the pattern of diet mixing by lambs.

Ann Urol (Paris) 2006 Apr; 40(2): 139-48 (Read article online)

Makhoul B, Yatim M, Guinard J, Fourcade RO

Obtaining a precise percutaneous calyceal puncture gave way to the development of percutaneous nephrolithotomy, one of the first micro-invasive techniques described in urology. Both radiologist and urologist can perform puncture, sometimes in a collaborative effort. However, being followed by a true surgical procedure, it should be done in the O.R; perfect knowledge of the procedure is mandatory for every urologist. Standard guidance uses a fluoroscopic C-arm device, only able to guide the needle precisely towards the apex of the chosen calyx. Moving the C-arm with cephalad tilting will provide 3-D imaging. Ultrasound guidance is an alternative, but might be difficult with non dilated upper tract. CT guidance and retrograde puncture are rarely used. The access is to be adapted according to the patient (adult or child), type of stone (single or multiple access), or kidney position (eutopic or ectopic). Direct ad stable puncture entering the apex of the chosen calyx is a pre-requisite for easy and efficient subsequent nephrolithotomy.