Miracle-dz/UniFAR-FTUs huggingface dataset:
The Association Between Fruit and Vegetable Intake, Knowledge of the Recommendations, and Health Information Seeking Within Adults in the U.S. Mainland and in Puerto Rico

Health information correlates of fruit and vegetable intake and of knowledge of the fruit and vegetable recommendations were examined using bivariate and multivariate regressions with data from the 2007–2008 U.S. National Cancer Institute's Health Information National Trends Survey in the United States and in Puerto Rico. Residents from Puerto Rico had the lowest reported fruit and vegetable intake and the lowest knowledge of the recommended servings of fruits and vegetables to maintain good health, compared with U.S. Hispanics, non-Hispanic Whites, and Blacks. Sixty-seven percent of Puerto Rican residents and 62% of U.S. Hispanics reported never seeking information on health or medical topics. In multivariate analysis, those who never sought information on health or medical topics reported significantly lower fruit and vegetable intake (coefficient = −0.24; 95% CI [−0.38, −0.09]), and were less likely to know the fruit and vegetable recommendations (OR = 0.32; 95% CI [0.20, 0.52]), compared with those who obtained information from their health care providers. Health promotion initiatives in the United States and Puerto Rico have invested in mass media campaigns to increase consumption of and knowledge about fruit and vegetables, but populations with the lowest intake are less likely to seek information. Strategies must be multipronged to address institutional, economic, and behavioral constraints of populations who do not seek out health information from any sources.
Cochlear Implant–Evoked Cortical Activation in Children With Cochlear Nerve Deficiency

Objective To report the results of cochlear implant-elicited cortical auditory evoked potentials (eCAEP) in children with cochlear nerve deficiency (CND). Study Design Case control series. Setting Tertiary academic referral center. Patients Seven children with CND that have a cochlear implant in their affected ear. Four children without CND served as controls. Intervention(s) eCAEPs were elicited by activation of individual cochlear implant electrodes. Main Outcome Measure(s) Onset responses (P1-N1-P2 complex). Results Three of 7 CND children demonstrated eCAEP responses across a broad range of electrodes despite having limited or no open set speech perception abilities using their implants. Two of these children had eCAEPs that were characterized by substantial variability in latency, amplitude, and number of electrodes with identifiable responses. The remaining 4 ears with CND and poor speech perception had multiphasic responses that are inconsistent with eCAEPs. Non-CND ears with excellent speech perception abilities demonstrated robust responses on all electrodes stimulated. Conclusion Abent eCAEP responses were indicative of poor open-set speech perception skills in all cases. However, eCAEP onset responses were measurable in some children with imaging evidence of CND, indicating probable cochlear nerve hypoplasia rather than aplasia. That some children with CND and poor speech perception had robust eCAEPs in some instances makes this particular measure of limited use for predicting good speech perception outcomes after cochlear implantation in these children. The origin of multiphasic responses remains to be determined but may be of somatosensory origin in some instances.
Upper motor neuron lesions in stroke patients do not induce anterograde transneuronal degeneration in spinal anterior horn cells.

BACKGROUND AND PURPOSE To determine whether upper motor neuron lesions in stroke can cause transneuronal degeneration of lower motor neurons, we assessed spinal anterior horn cells in patients dying with poststroke hemiplegia. METHODS Subjects were four stroke patients with severe left hemiplegia and four age-matched control subjects who died of nonneurological disease. After histological processing and staining, cytoarchitectonic assessment was made of all neurons in the ventral horns of the 4th lumbar segment of the spinal cord according to cell diameter and topography. RESULTS In the four stroke patients, no differences were seen in anterior horn cell populations or diameter and size distribution patterns between affected and unaffected sides or between these patients and the control subjects. CONCLUSIONS The present quantitative analysis provides no evidence of anterograde transneuronal degeneration of lower motor neurons after upper motor neuron damage in stroke patients.
Asthma symptoms in obese adults: The challenge of achieving asthma control

The association between asthma and obesity is well-described, but not straightforward, and according to current guidelines asthma control is more difficult to achieve in obese patients. The currently available studies evaluating response to pharmacological asthma therapy in obese patients show that these patients have an altered, in general less favorable, response to both reliever and controller medication compared to normal weight patients. However, at present, the limited available evidence precludes evidence-based recommendations. The ‘obesity-related asthma’ phenotype has different characteristics, including association with atopy and type of airway inflammation, compared to ‘classic’ asthma. Furthermore, weight loss in patients with this phenotype leads to an improvement in symptoms, lung function, and airway responsiveness, as well as a reduction in medication utilization and hospital admissions. Obese patients, who present with symptoms suggesting a diagnosis of asthma, may have a distinct phenotype or a disease mimicking asthma, likely to have a potentially higher remission rate. And by that, our approach to this group of patients should combine pharmacologic and non-pharmacologic therapies, including exercise, weight loss and dietary interventions, instead of primarily focusing on disease control by stepping up asthma therapy.
Detailed Comparative Anatomy of the Extrinsic Cardiac Nerve Plexus and Postnatal Reorganization of the Cardiac Position and Innervation in the Great Apes: Orangutans, Gorillas, and Chimpanzees

To speculate how the extrinsic cardiac nerve plexus (ECNP) evolves phyletically and ontogenetically within the primate lineage, we conducted a comparative anatomical study of the ECNP, including an imaging examination in the great apes using 20 sides from 11 bodies from three species and a range of postnatal stages from newborns to mature adults. Although the position of the middle cervical ganglion (MG) in the great apes tended to be relatively lower than that in humans, the morphology of the ECNP in adult great apes was almost consistent with that in adult humans but essentially different from that in the lesser apes or gibbons. Therefore, the well‐argued anatomical question of when did the MG acquire communicating branches with the spinal cervical nerves and appear constantly in all sympathetic cardiac nerves during primate evolution is clearly considered to be after the great apes and gibbons split. Moreover, a horizontal four‐chambered heart and a lifted cardiac apex with a relatively large volume in newborn great apes rapidly changed its position downward, as seen in humans during postnatal growth and was associated with a reduction in the hepatic volume by imaging diagnosis and gross anatomy. In addition, our observation using a range of postnatal stages exhibits that two sympathetic ganglia, the middle cervical and cervicothoracic ganglia, differed between the early and later postnatal stages. Anat Rec, 2012. © 2011 Wiley Periodicals, Inc.
Two Consecutive Clusters of Toxic Anterior Segment Syndrome

Purpose To present clinical findings and etiologic investigation of two consecutive clusters of toxic anterior segment syndrome (TASS) after uncomplicated phacoemulsification cataract surgery. Case Report At the Veterans Affairs Northern Indiana Health Care System Fort Wayne campus, 11 consecutive patients on two separate days in 2011 underwent clear corneal incision phacoemulsification cataract surgery by the same surgeon. On the first postoperative day, all patients had 1+ to 2+ diffuse limbus to limbus stromal edema and 2+ to 4+ anterior chamber white blood cells. Five eyes had inflammatory plaques on the surface of the intraocular implant, six had fibrin, three had hypopyon, and one had inflammatory debris “puff ball. ” Visual acuity ranged 20/70 to 20/400. Treatment included moxifloxacin four times a day, diclofenac four times a day, and prednisolone acetate 1% every 1 to 2 hours. In all patients, active inflammation and corneal edema resolved within 6 weeks, and visual outcome was 20/20. Cataract surgery was paused for 5 months after the first cluster of TASS and then immediately paused again after restarting because of a second cluster. Although no specific causes were identified, etiologic investigation resulted in the implementation of multiple changes. The changes included new replacement surgical instruments, disposable irrigation/aspirator tip and handle, risk of residue on reusable instruments minimized, preservative-free medications used when available, ophthalmic ointment eliminated, manufacturers’ recommendations followed exactly, and eye instruments processed separately. Toxic anterior segment syndrome did not occur when surgery resumed 11 months after the last cluster. Conclusions There are multiple possible etiologies of TASS. However, as in our clusters, specific causes are often not identified. Thorough review of all steps in surgery, processing of equipment and preparation of injectable solutions and materials, and adoption of best practices can prevent additional cases of TASS. Prompt diagnosis and treatment of TASS are extremely important because this leads to a desirable outcome.
Retinoic acid biosynthesis and metabolism

Metabolic activation of retinol into the hormone retinoic acid and metabolism of retinoic acid entail essential aspects of retinoid biology that seem interdependent with functions of retinoid bind‐ ing‐proteins. Cellular retinol binding protein and cellular retinoic acid binding protein enjoy widespread expression and, where expressed, their li‐ ganded forms represent the major physiological forms of retinol and retinoic acid, respectively. These retinoid binding proteins may protect cells from the amphipathic properties of retinoids and protect the structurally sensitive retinoids from the cellular milieu. Starting from the perspective that the enzymes most likely to metabolize retinoids in vivo might recognize the major forms of retinoids that occur in vivo, several laboratories have produced results that support a model of retinoid metabolism with prominent roles for the cellular retinoid binding proteins. In this model, liganded cellular retinoid binding proteins serve as substrates for the metabolism of some retinoids (retinol, retinoic acid), restricting access to those enzymes that recognize both the binding protein and the retinoid. Other retinoids (3,4‐didehydroretinol, 4‐oxo‐retinoic acid) liganded to binding‐proteins have their metabolism arrested. In its unliganded form, at least one retinoid binding protein (cellular retinol binding protein) serves as a retinoid concentration‐sensitive modulator of enzymes that catalyze retinol metabolism. This review will describe the model and the intrinsic relationships among retinoid‐specific enzymes and retinoid binding proteins. —Napoli, J. L. Retinoic acid biosynthesis and metabolism. FASEBJ. 10,993‐1001 (1996)
Staging in the onset of DSM-IV alcohol symptoms in adolescents: survival/ hazard analyses.

OBJECTIVE This research examined staging in the time to onset of DSM-IV alcohol symptoms in adolescents. Consistent staging in the onset of symptoms provides important tests of the construct validity of diagnostic systems, and aids the development of early case identification strategies. METHOD The Structured Clinical Interview for the DSM (SCID), adapted to assess DSM-IV alcohol abuse and dependence symptoms, was used to determine time to symptom onset in 102 male and 97 female adolescent drinkers with and without alcohol use disorders. The sample provided a broad range of drinking practices and alcohol-related problems. Symptom onset patterns were examined using survival-hazard analyses. RESULTS Survival and hazard data suggested three stages of alcohol problems distinguished by time to onset: heavy and heedless drinking with associated social and role obligation problems, psychological dependence, and withdrawal. This three-stage model fit both the male and female data, and described staging patterns in 70% of the subjects. CONCLUSIONS The symptom onset model suggested a first stage of adolescent alcohol symptoms characterized by heavy and heedless drinking with associated interpersonal and role obligation problems. The data did not support the construct validity of DSM-IV alcohol abuse when applied to adolescents, and suggested staging among DSM-IV alcohol dependence symptoms. Implications for the diagnosis and early identification of adolescent alcohol problems are discussed.
Insecticide susceptibilities in populations of two rice planthoppers, Nilaparvata lugens and Sogatella furcifera, immigrating into Japan in the period 2005-2012.

BACKGROUND The brown planthopper Nilaparvata lugens and the whitebacked planthopper Sogatella furcifera are both important pests on rice throughout Asia. The major cause of recent outbreaks is thought to be the development of insecticide resistance. Thus, the authors monitored insecticide susceptibilities in populations of these two insects immigrating into Japan in the period 2005-2012. Ten insecticides were tested, including members of the organophosphate, carbamate, pyrethroid, neonicotinoid and phenylpyrazole groups. RESULTS The LD50 values of N. lugens against imidacloprid increased from 2005 (0.7 µg g(-1)) to 2012 (98.5 µg g(-1)). The resistance ratio (LD50 value in 2012/baseline LD50 value in 1992) was 615.5. In contrast, LD50 values of N. lugens against fipronil were <1.0 µg g(-1) up to 2012, suggesting that N. lugens had developed no insecticide resistance to this insecticide. However, S. furcifera exhibited resistance against fipronil up to 2012. Except for the case of malathion, the resistances of N. lugens against members of the organophosphate and carbamate groups were closely similar in the period 2005-2012 to earlier determinations in 1984 and 1985. CONCLUSION Species-specific insecticide resistance (imidacloprid resistance in N. lugens and fipronil resistance in S. furcifera) is ongoing in populations of the two planthoppers immigrating into Japan.
The expression of E-cadherin-catenin complex in adenoid cystic carcinoma of salivary glands.

OBJECTIVE The aim of this study was to investigate the expression of the E-cadherin-catenin (E-cad-cat) complex in human salivary adenoid cystic carcinoma (ACC) and determine the effects of E-cad-cat expression on tumor differentiation, metastasis, and invasion, as well as its clinical significance. METHODS The expression of adhesion molecules, which included E-cadherin, alpha-catenin, and beta-catenin, on 10 cases of normal salivary glands, and 50 cases of human salivary ACC were investigated by immunohistochemistry. RESULTS Strong and stable expression of E-cad-cat complex showed in normal salivary glands tissues. However, weaker expression and even complete absence, of the positive signals were shown on all ACC cases. Coexpression of E-cad-cat were detected in 29 (58%) of the 50 ACC specimens. Positive staining of E-cad-cat complex were detected in 7 (39%) of the 18 ACC primary sites that had aggressive phenotype of nerve and vasculature. CONCLUSION Strong positive signals of E-cad-cat complex are shown in normal salivary glands, and the down-regulated expression were observed in ACC cases. The expression of E-cad-cat complex is associated with a more aggressive phenotype on nerve and vasculature. No association with various histopathologic subtypes was found. However, absent or low E-cad expression was observed more frequently in solid carcinomas than in cribriform or tubular carcinomas. Down-regulation of E-cad-cat complex may be associated with canceration of normal salivary glands. The expression levels of E-cad-cat were positively correlated to the differentiation of ACC tumor cells.
Association of Serotonin Transporter Promoter Gene Polymorphism (5-HTTLPR) With Depression in Costa Rican Schizophrenic Patients

Abstract: Depression and suicidal behavior are frequently observed in patients with schizophrenia. The serotonin transporter protein regulates serotonergic signaling at synapses and is encoded by a single gene (SLC6A4; Locus Link ID: 6532), located at 17q11.1-q12 with two polymorphic variants (the short and the long allele). The short allele of serotonin transporter gene has been associated with depression and suicidality in individuals who suffered negative life events and with depression in individuals with chronic psychosis. Subjects were recruited from a genetic study of schizophrenia conducted in Costa Rica. The authors replicated their previous research, using a more narrow phenotype (only schizophrenic subjects) and a more ethnically homogenous sample (only Costa Rican schizophrenic individuals who were not included in the previous study). The authors hypothesized that subjects with at least one copy of the serotonin transporter promoter gene polymorphism (5-HTTLPR) “s” allele would have a greater history of lifetime depression and suicidability rate than those who had an “l/l” genotype. The authors analyzed 155 subjects with a DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) diagnosis of schizophrenia (73% male, age at interview 38.3, SD = 11.23). The genotype distribution was “ss” 58 (37%), “sl” 69 (45%), and “ll” 28 (18%). In the secondary analysis, the authors explored association of the “s” allele with lifetime history of suicide behavior in 173 subjects (18 more subjects than primary analysis because schizophrenic individuals were included regardless of history of depression). The authors found that subjects carrying at least one short allele had a significant increased lifetime risk for depressive syndromes (χ2 = 5.4, df = 1, P = 0.02; odds ratio [OR] = 2.7, 95% confidence interval [CI] = 1.15–6.3). No association was found for suicidal behavior in the same sample (χ2 = 0.928, P = 0.629). In conclusion, the genotype at the 5-HTTLPR promoter polymorphic locus increases the risk of developing major depression but not suicidal behavior during the course of the schizophrenia in these patients. Due to the small sample size, these results should be followed by definitive replication.
Role of mTOR in the degradation of IRS‐1: Regulation of PP2A activity

We have investigated the role of PI 3‐kinase and mTOR in the degradation of IRS‐1 induced by insulin. Inhibition of mTOR with rapamycin resulted in approximately 50% inhibition of the insulin‐induced degradation of IRS‐1. In contrast, inhibition of PI‐3 kinase, an upstream activator of mTOR, leads to a complete block of the insulin‐induced degradation. Inhibition of either PI‐3 kinase or mTOR prevented the mobility shift in IRS‐1 in response to insulin, a shift that is caused by Ser/Thr phosphorylation. These results indicate that insulin stimulates PI 3‐kinase‐mediated degradation of IRS‐1 via both mTOR‐dependent and ‐independent pathways. Platelet‐derived growth factor (PDGF) stimulation leads to a lower level of degradation, but significant phosphorylation of IRS‐1. Both the degradation and phosphorylation of IRS‐1 in response to PDGF are completely inhibited by rapamycin, suggesting that PDGF stimulates IRS‐1 degradation principally via the mTOR‐dependent pathway. Inhibition of the serine/threonine phosphatase PP2A with okadaic acid also induced the phosphorylation and degradation of IRS‐1. IRS‐1 phosphorylation and degradation in response to okadaic acid were not inhibited by rapamycin, suggesting that the action of mTOR in the degradation of IRS‐1 results from inhibition of PP2A. Consistent with this, treatment of cells with rapamycin stimulated PP2A activity. While the role of mTOR in the phosphorylation of IRS‐1 appears to proceed primarily through the regulation of PP2A, we also provide evidence that the regulation of p70S6 kinase phosphorylation requires the direct activity of mTOR. J. Cell. Biochem. 85: 304–314, 2002. © 2002 Wiley‐Liss, Inc.
Carprofen simultaneously reduces progression of morphological changes in cartilage and subchondral bone in experimental dog osteoarthritis.

OBJECTIVE To examine the effect of a nonsteroidal antiinflammatory drug, carprofen, on the structure and metabolism of cartilage and subchondral bone in the experimental osteoarthritic (OA) canine model. METHODS Experimental Groups 1 and 2 received a sectioning of the anterior cruciate ligament (ACL) of the right stifle joint, and were administered carprofen (2.2 and 4.4 mg/kg/twice daily/po, respectively) for 8 weeks beginning 4 weeks postsurgery. Group 3 received ACL sectioning and no treatment. Group 4 was composed of unoperated normal dogs. Cartilage macroscopic lesions were assessed, and their histological severity was graded. Specimens of subchondral bones were fixed, decalcified, and stained with hematoxylin/eosin. The level of metalloprotease (MMP) activity in cartilage was measured. Osteoblast cells were prepared from the subchondral bone. The level of synthesis of osteoblast biomarkers (osteocalcin, alkaline phosphatase), as well as urokinase plasminogen activator (uPA) activity and insulin-like growth factor (IGF-1) in the culture medium, was estimated. RESULTS Carprofen treatment decreased the width of osteophytes (p < 0.01), the size of cartilage lesions, and the histologic severity of cartilage lesions (p < 0.008). There was no difference in the levels of MMP activity in cartilage between OA and carprofen treated groups. In OA dogs, the subchondral bone plate was thinner and was the site of an extensive remodeling process with numerous lacunae. Dogs treated with carprofen showed a marked decrease in the remodeling activity with normal plate thickness, and subchondral bone morphology resembling that of normal dogs. Osteoblasts from untreated OA dogs showed slightly higher alkaline phosphatase activities and osteocalcin release that reverted back to normal upon carprofen treatment. Moreover, uPA activity and IGF-1 levels were increased in OA dogs and were significantly reduced in carprofen treated dogs. CONCLUSION Under therapeutic conditions, treatment with carprofen could reduce the progression of early structural changes in experimental OA. Carprofen treatment also delays and/or prevents the abnormal metabolism of subchondral osteoblasts in this model. The hypothesis of a possible link between the protective effect of carprofen and its effect on subchondral bone is of interest in the context of therapeutic intervention.