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1

Fatemi, S. Hossein, Teri J. Reutiman, and Timothy D. Folsom. "The role of lithium in modulation of brain genes: relevance for aetiology and treatment of bipolar disorder." Biochemical Society Transactions 37, no. 5 (September 21, 2009): 1090–95. http://dx.doi.org/10.1042/bst0371090.

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Bipolar disorder is a debilitating disorder of the brain with a lifetime prevalence of 1.0% for bipolar I, 1.1% for bipolar II disorder and 2.4–4.7% for subthreshold bipolar disorder. Medications, including lithium, have demonstrated efficacy in the treatment of bipolar disorder, but their molecular targets and mode of action are largely unknown. A few studies have begun to shed light on potential targets of lithium treatment that may be involved in lithium's therapeutic effect. We have recently conducted a microarray study of rat frontal cortex following chronic treatment (21 days) with lithium. Chronic treatment with lithium led to a significant (at least 1.5-fold) down-regulation of 151 genes and up-regulation of 57 genes. We discuss our results in the context of previous microarray studies involving lithium and gene-association studies to identify key genes associated with chronic lithium treatment. A number of genes associated with bipolar disorder, including Comt (catechol-O-methyltransferase), Vapa (vesicle-associated membrane protein-associated protein A), Dtnb (dystrobrevin β) and Pkd1 (polycystic kidney disease 1), were significantly altered in our microarray dataset along with genes associated with synaptic transmission, apoptosis and transport among other functions.
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2

McClements, Michelle E., Federica Staurenghi, Meike Visel, John G. Flannery, Robert E. MacLaren, and Jasmina Cehajic-Kapetanovic. "AAV Induced Expression of Human Rod and Cone Opsin in Bipolar Cells of a Mouse Model of Retinal Degeneration." BioMed Research International 2021 (February 9, 2021): 1–8. http://dx.doi.org/10.1155/2021/4014797.

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Vision loss caused by inherited retinal degeneration affects millions of people worldwide, and clinical trials involving gene supplementation strategies are ongoing for select forms of the disease. When early therapeutic intervention is not possible and patients suffer complete loss of their photoreceptor cells, there is an opportunity for vision restoration techniques, including optogenetic therapy. This therapy provides expression of light-sensitive molecules to surviving cell types of the retina, enabling light perception through residual neuronal pathways. To this end, the bipolar cells make an obvious optogenetic target to enable upstream processing of visual signal in the retina. However, while AAV transduction of the bipolar cells has been described, the expression of human opsins in these cell types within a model of retinal degeneration (rd1) has been less successful. In this study, we have expanded the optogenetic toolkit and shown successful expression of human rhodopsin driven by an ON-bipolar cell promoter (Grm6) in the rd1 mouse model using modified AAV capsids (AAV2.4YF, AAV8.BP2, and AAV2.7m8) delivered via intraocular injection. We also show the first presentation of ectopic expression of human cone opsin in the bipolar cells of rd1 mice. These data provide evidence of an expansion of the optogenetic toolkit with the potential to restore useful visual function, setting the stage for future trials in human patients.
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3

Park, MiYoun, JiYoung Ahn, YeonJin Choi, MyeungNam Kim, and JungYeon Lee. "The safety and efficacy of a combined diode laser and bipolar radiofrequency compared with combined infrared light and bipolar radiofrequency for skin rejuvenation." Indian Journal of Dermatology, Venereology, and Leprology 78, no. 2 (2012): 146. http://dx.doi.org/10.4103/0378-6323.93630.

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4

Wadhwa, Ridhima, Riya Gupta, and Pawan K. Maurya. "Oxidative Stress and Accelerated Aging in Neurodegenerative and Neuropsychiatric Disorder." Current Pharmaceutical Design 24, no. 40 (March 15, 2019): 4711–25. http://dx.doi.org/10.2174/1381612825666190115121018.

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Background: Neurodegenerative diseases are becoming more and more common in today’s world. As people are continuously being exposed to exogenous factors like UV radiations, gamma rays, X-Rays, environmental pollutants and heavy metals, the cases of increased oxidative damage are increasing. Even though some amount of oxidative damage occurs in all metabolic reactions but their increase from the normal level in organisms causes neurodegenerative diseases. These neurodegenerative disorders like Alzeimers, Parkinsons disease and neuropsychiatric disorders such as schizophrenia, bipolar, depression are caused due to the decline in physiological and psychological functions caused by ROS and RNS. These ROS and RNS are formed as the result of excess oxidative damage in the system. Methods: The following article goes into detail explaining all the effects caused by excess oxidative damage like ROS/RNS formation and telomere shortening. Further, it explains the pathways of neurodegenerative diseases and neuropsychiatric diseases. This article also sheds light on the effective treatments of such disorders by changing lifestyle and activating antioxidant pathways. Conclusion: It is clear that neurodegenerative diseases are caused due to excess oxidative stress and alter the functioning of the central nervous system. The central nervous system undergoes neurodegenerative or neuropsychiatric changes.
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5

Carta, MG, V. Ruggiero, F. Sancassiani, F. Cutrano, AR Manca, M. Peri, A. Fais, and E. Cacace. "The Use of Antidepressants in the Long-Term Treatment Should not Improve the Impact of Fibromyalgia on Quality of Life." Clinical Practice & Epidemiology in Mental Health 9, no. 1 (July 12, 2013): 120–24. http://dx.doi.org/10.2174/1745017901309010120.

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Background: Antidepressant (AD) drugs are effective in the short term treatment of fibromyalgia (FM). It may be useful to study the long-term impact of AD on patients with FM. Methods: One-year follow-up study on 23 females with FM divided into groups on AD (ADg-N=7), and not taking AD (NADg-N=11). Evaluation at t1 and at the end (t2) with the Fibromyalgia Impact Questionnaire (FIQ); at t2 with: SCID-IV; Mood Disorder Questionnaire (MDQ); Short Form-12; Hamilton Depression Rating Scale (HAM-D); Functioning Assessment Short Test (FAST) Results: After a year the AD group showed a worst impact of the disease by FIQ (p=0.017), worsened quality of life by SF-12 (p<0.01), and disability linked to bipolar symptoms by FAST (p=0.05). About 40% of the sample was screened positive at MDQ without difference in the two groups. The patients who recovered from a depressive episode did not differ between ADg and NADg (20% vs 33.3%), and were fewer than expected from the literature (40-60%). The HAM-D score at the end of the trial was worse in the ADg (p<0.03). Limitations: Observational research on few patients, not specifically designed to test the hypothesis. The results have a heuristic value only. Discussion: The results should be read in the light of the high prevalence of patients screened positive for Bipolar Disorders and of the well-known poor response of the mood symptoms to antidepressants in Bipolar Depression. The deterioration in the long-term management of FM patients following AD treatments suggests the need for new and robust studies.
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6

Smith, Rachel N., Amruta S. Agharkar, and Eric B. Gonzales. "A review of creatine supplementation in age-related diseases: more than a supplement for athletes." F1000Research 3 (September 15, 2014): 222. http://dx.doi.org/10.12688/f1000research.5218.1.

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Creatine is an endogenous compound synthesized from arginine, glycine and methionine. This dietary supplement can be acquired from food sources such as meat and fish, along with athlete supplement powders. Since the majority of creatine is stored in skeletal muscle, dietary creatine supplementation has traditionally been important for athletes and bodybuilders to increase the power, strength, and mass of the skeletal muscle. However, new uses for creatine have emerged suggesting that it may be important in preventing or delaying the onset of neurodegenerative diseases associated with aging. On average, 30% of muscle mass is lost by age 80, while muscular weakness remains a vital cause for loss of independence in the elderly population. In light of these new roles of creatine, the dietary supplement’s usage has been studied to determine its efficacy in treating congestive heart failure, gyrate atrophy, insulin insensitivity, cancer, and high cholesterol. In relation to the brain, creatine has been shown to have antioxidant properties, reduce mental fatigue, protect the brain from neurotoxicity, and improve facets/components of neurological disorders like depression and bipolar disorder. The combination of these benefits has made creatine a leading candidate in the fight against age-related diseases, such as Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, long-term memory impairments associated with the progression of Alzheimer’s disease, and stroke. In this review, we explore the normal mechanisms by which creatine is produced and its necessary physiology, while paying special attention to the importance of creatine supplementation in improving diseases and disorders associated with brain aging and outlining the clinical trials involving creatine to treat these diseases.
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7

Wanot, Bartosz, Barbara Szczygieł, Wojciech Wanot, and Mariana Magerčiaková. "DEPRESSION - TYPES AND TREATMENT OF DEPRESSION." Scientific Journal of Polonia University 32, no. 1 (April 3, 2019): 121–30. http://dx.doi.org/10.23856/3216.

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The key symptom of depression is lowering the mood, but this is not the only sign of depression. Depression is a disease in which the symptoms reach various intensities and occur in many configurations. We distinguish the following types of depression: reactive, endogenous, neurotic, anankastic, agitated, large and small, morning (subclinical and subliminal), seasonal, masked, psychotic, postpartum, drug resistant, in children and adolescents, in the elderly, involutional, organic , in bipolar disorder, dysthymia, depression and anxiety, and in somatic diseases. Psychotherapy is now a popular and effective method of treating depression. The effects of treatment after the use of antidepressants appear only after a few weeks from the beginning of therapy. Old-generation medicines: these are tricyclic antidepressants (TLPDs), inhibitors of neuromediator reuptake and monoamine oxidase enzyme (IMAO) inhibitors. The new generation of drugs is distinguished by selective serotonin reuptake inhibitors (SSRIs), selective serotonin and noradrenaline reuptake inhibitors (SNRIs), four-ring drugs, noradrenaline reuptake inhibitors, selective reversible MAO inhibitors, and drugs with other mechanisms of action. Phototherapy (treatment of light) is currently a widely accepted method of winter depression therapy. Other treatments for depression include electroconvulsive therapy and transcranial magnetic stimulation.
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8

Oriolo, G., A. Brugués, J. M. Goikolea, and L. Pintor. "Lamotrigine induced DRESS syndrome in bipolar disorder: Multiple snares behind a potentially life-threatening adverse reaction." European Psychiatry 33, S1 (March 2016): S616. http://dx.doi.org/10.1016/j.eurpsy.2016.01.2304.

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BackgroundLamotrigine is widely used to prevent bipolar depression. Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) is a rare, potentially life-threatening adverse effect. The long latency between drug exposure and disease onset, added to the high variability of its clinical presentation, can increase the risk of misdiagnosis lamotrigine withdrawal delay.ObjectiveTo highlight potential risk factors that can be related to a worse clinical onset and evolution of lamotrigine-induced DRESS syndrome.MethodsWe report the case of a 25-year-old-man, with a type I bipolar disorder, treated with lithium and lamotrigine 50 mg per day during the first 13 days of treatment, progressively increase up to 200 mg. Thirty-five days after the treatment initiation, a pruritic rash appeared in his upper arms, and scabies infestation was diagnosed. After 72 hours, the patient required urgent hospitalization due to hemodynamic instability.ResultsOn admission, facial edema and erythrodermia were involving 70 to 80% of the body surface. DRESS diagnosis due to lamotrigine was made following RegiSCAR criteria (Table 1). Psychiatric medication was stopped and DRESS treatment established. Complete recovery without recurrence was achieved after 2 months.ConclusionsThe lamotrigine up titration faster than recommended may have facilitated the DRESS syndrome reaction. Moreover, the latency between lamotrigine introduction and the rash onset could have increased the possibilities of misdiagnosis. In light of this, physicians need to consider at least the last 3 months treatment history when assessing a rash, as the delay of DRESS syndrome diagnosis can fastly lead to a fatal event.Table not available.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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9

Lan, Yi-Feng Carol, Diane C. Zelman, and Wen-Tao Chao. "Angry characters and frightened souls: Patients and family explanatory models of bipolar disorder in Taiwan." Transcultural Psychiatry 55, no. 3 (March 19, 2018): 317–38. http://dx.doi.org/10.1177/1363461518761924.

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Bipolar disorder (BD) affects a significant proportion of Taiwanese individuals (Weissman et al., 1996; Yang, Yeh, & Hwu, 2012). Psychotropic medications are typically the mainstay of treatment for BD, and there is an abundance of international research on biological etiology and medication options. However, there is comparatively little research on psychosocial aspects of BD, including how it is understood and managed within families. As culture provides the context in which psychiatric disease is managed, there is a need to identify distinct Chinese psychosocial perspectives that might shed light on intervention options. This research explored how Taiwanese patients and family members comprehend and cope with BD. A sample of 42 participants, including 20 Taiwanese patients diagnosed with Bipolar Disorder-I (BD-I) for at least 4 years, and 22 family members, participated in separate interviews on explanatory models of illness. Qualitative thematic analysis focused on features that were distinct from those in current Western research literature. Five themes were identified that represented Taiwanese conceptualizations of BD, notions of etiology, views regarding treatment, and the difficulties in managing the disorder. Participants used Chinese language terms and descriptions of BD that reflected greater concerns about irritability, anger, and family conflict than about other symptoms, and participants also emphasized characterological trait descriptions of the condition. Their responses reflected their acceptance of lifelong family responsibility for caretaking, clashing beliefs regarding biomedical versus traditional Chinese medical and spiritual models of etiology and cure, profound concerns about the effects of psychiatric medication on the liver and kidney systems, and a focus on stress rather than genetic or biological models of etiology.
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10

Liu, Zhuolin, Kazuhiro Kurokawa, Furu Zhang, John J. Lee, and Donald T. Miller. "Imaging and quantifying ganglion cells and other transparent neurons in the living human retina." Proceedings of the National Academy of Sciences 114, no. 48 (November 14, 2017): 12803–8. http://dx.doi.org/10.1073/pnas.1711734114.

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Ganglion cells (GCs) are fundamental to retinal neural circuitry, processing photoreceptor signals for transmission to the brain via their axons. However, much remains unknown about their role in vision and their vulnerability to disease leading to blindness. A major bottleneck has been our inability to observe GCs and their degeneration in the living human eye. Despite two decades of development of optical technologies to image cells in the living human retina, GCs remain elusive due to their high optical translucency. Failure of conventional imaging—using predominately singly scattered light—to reveal GCs has led to a focus on multiply-scattered, fluorescence, two-photon, and phase imaging techniques to enhance GC contrast. Here, we show that singly scattered light actually carries substantial information that reveals GC somas, axons, and other retinal neurons and permits their quantitative analysis. We perform morphometry on GC layer somas, including projection of GCs onto photoreceptors and identification of the primary GC subtypes, even beneath nerve fibers. We obtained singly scattered images by: (i) marrying adaptive optics to optical coherence tomography to avoid optical blurring of the eye; (ii) performing 3D subcellular image registration to avoid motion blur; and (iii) using organelle motility inside somas as an intrinsic contrast agent. Moreover, through-focus imaging offers the potential to spatially map individual GCs to underlying amacrine, bipolar, horizontal, photoreceptor, and retinal pigment epithelium cells, thus exposing the anatomical substrate for neural processing of visual information. This imaging modality is also a tool for improving clinical diagnosis and assessing treatment of retinal disease.
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11

Yurko, Ronald, Max G’Sell, Kathryn Roeder, and Bernie Devlin. "A selective inference approach for false discovery rate control using multiomics covariates yields insights into disease risk." Proceedings of the National Academy of Sciences 117, no. 26 (June 10, 2020): 15028–35. http://dx.doi.org/10.1073/pnas.1918862117.

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To correct for a large number of hypothesis tests, most researchers rely on simple multiple testing corrections. Yet, new methodologies of selective inference could potentially improve power while retaining statistical guarantees, especially those that enable exploration of test statistics using auxiliary information (covariates) to weight hypothesis tests for association. We explore one such method, adaptiveP-value thresholding (AdaPT), in the framework of genome-wide association studies (GWAS) and gene expression/coexpression studies, with particular emphasis on schizophrenia (SCZ). Selected SCZ GWAS associationPvalues play the role of the primary data for AdaPT; single-nucleotide polymorphisms (SNPs) are selected because they are gene expression quantitative trait loci (eQTLs). This natural pairing of SNPs and genes allow us to map the following covariate values to these pairs: GWAS statistics from genetically correlated bipolar disorder, the effect size of SNP genotypes on gene expression, and gene–gene coexpression, captured by subnetwork (module) membership. In all, 24 covariates per SNP/gene pair were included in the AdaPT analysis using flexible gradient boosted trees. We demonstrate a substantial increase in power to detect SCZ associations using gene expression information from the developing human prefrontal cortex. We interpret these results in light of recent theories about the polygenic nature of SCZ. Importantly, our entire process for identifying enrichment and creating features with independent complementary data sources can be implemented in many different high-throughput settings to ultimately improve power.
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12

Grzywacz, Anna, Małgorzata Ryder, Iwona Małecka, and Jolanta Chmielowiec. "The current state of research on psychiatric genetics in Poland and the world: A report covering recent years." Postępy Higieny i Medycyny Doświadczalnej 72 (January 12, 2018): 1–12. http://dx.doi.org/10.5604/01.3001.0010.7979.

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The aim of this article was to review the results of research carried out in recent years in relation to genetic studies in psychiatry. The authors’ focus is on the selected disorders, with particular emphasis on the reports from Poland. For this purpose, the most often mentioned studies describing genes and biomarkers involved in psychiatry were selected. Genetic polymorphisms were described in relation to schizophrenia, alcoholism, addiction to psychoactive substances, autistic spectrum, unipolar depression and bipolar disorder, eating disorders and other psychiatric disorders. Characterizing the impact of inheritance factors on the processes in the central nervous system, it can be observed that some biological mechanisms forms associations with tested genetic variants and this combination is linked with the risk of mental disorders. To understand the role of psychiatric genetics, surveys which join genotype and phenotype associations (endophenotype) are essential. It seems important to study and search for associations of genes polymorphisms and biomarkers with mental and psychiatric disorders in order to better understanding the biological basis of the disease and more effective treatment of patients. In many cases, the variability analysis of selected genes sheds new light on understanding the etiology of diseases and mental disorders. Genetics is a powerful technique which allows us to study the impact of the inherited variance on changes in mental state, even without having prior knowledge about biological changes.
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13

Evrensel, Alper, and Nevzat Tarhan. "Inflammation Biomarkers in Psychiatry." Current Psychiatry Research and Reviews 16, no. 2 (December 7, 2020): 78–85. http://dx.doi.org/10.2174/2666082216999200625115701.

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Introduction: There has long been a need for diagnostic, theragnostic, and prognostic biomarkers for psychiatric disorders. Biomarkers help in reducing ambiguity and arbitrariness and increase objectivity. In this context, many candidates for hormonal, immunological, serological, and neuroimaging markers have been proposed, but none of these marker candidates alone nor a biomarker panel has been approved for any disease. The fact that almost all psychiatric disorders are heterogeneous makes this process challenging. However, strong biomarker candidates have been identified, especially in light of the large number of clinical and preclinical studies conducted within the last five years. Objective: The aim of this article was to compile and discuss the current information on immune biomarkers in major psychiatric disorders, such as schizophrenia, depression, bipolar disorder, and anxiety disorders. Methods: In this study, respected scientific databases were searched using key terms related to the subject, and the related literature was examined in detail. Results: There are many relationships between psychiatric disorders and immune system parameters. Evidence also suggests that neuroinflammation is involved in the etiopathogenesis of psychiatric disorders. Markers, such as proinflammatory cytokines, tumor necrosis factor alpha, and C-reactive protein have been associated with psychiatric disorders in numerous studies. Conclusions: The neuroinflammation hypothesis has an important place in the etiopathogenesis of psychiatric disorders. Uncertainty remains as to whether neuroinflammation is a cause or consequence of psychiatric disorders. Some researchers have indicated that intestinal microbiota composition disorders and dysbiosis are sources of neuroinflammation. Immune marker studies are of great importance in terms of eliminating this uncertainty and overcoming diagnostic and treatment difficulties in the clinic. In this review, biomarker studies on psychiatric disorders were examined from the viewpoint of the immune system and discussed in light of the current studies.
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14

Chen, Bo, Bogale Aredo, Yi Ding, Xin Zhong, Yuanfei Zhu, Cynthia X. Zhao, Ashwani Kumar, et al. "Forward genetic analysis using OCT screening identifiesSfxn3mutations leading to progressive outer retinal degeneration in mice." Proceedings of the National Academy of Sciences 117, no. 23 (May 26, 2020): 12931–42. http://dx.doi.org/10.1073/pnas.1921224117.

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Retinal disease and loss of vision can result from any disruption of the complex pathways controlling retinal development and homeostasis. Forward genetics provides an excellent tool to find, in an unbiased manner, genes that are essential to these processes. UsingN-ethyl-N-nitrosourea mutagenesis in mice in combination with a screening protocol using optical coherence tomography (OCT) and automated meiotic mapping, we identified 11 mutations presumably causative of retinal phenotypes in genes previously known to be essential for retinal integrity. In addition, we found multiple statistically significant gene-phenotype associations that have not been reported previously and decided to target one of these genes,Sfxn3(encoding sideroflexin-3), using CRISPR/Cas9 technology. We demonstrate, using OCT, light microscopy, and electroretinography, that twoSfxn3−/−mouse lines developed progressive and severe outer retinal degeneration. Electron microscopy showed thinning of the retinal pigment epithelium and disruption of the external limiting membrane. Using single-cell RNA sequencing of retinal cells isolated from C57BL/6J mice, we demonstrate thatSfxn3is expressed in several bipolar cell subtypes, retinal ganglion cells, and some amacrine cell subtypes but not significantly in Müller cells or photoreceptors. In situ hybridization confirmed these findings. Furthermore, pathway analysis suggests that Sfxn3 may be associated with synaptic homeostasis. Importantly, electron microscopy analysis showed disruption of synapses and synaptic ribbons in the outer plexiform layer ofSfxn3−/−mice. Our work describes a previously unknown requirement forSfxn3in retinal function.
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Pangestiningsih, Tri Wahyu, Woro Danur Wendo, Yulfia Nelymalik Selan, Filphin Adolfin Amalo, Nemay Anggadewi Ndaong, and Victor Lenda. "Histological Features of Catecholaminergic Neuron in Substantia Nigra Induced by Paraquat Dichloride (1,1-dimethyl-4,4 bipyridinium) in Wistar Rat as A Model of Parkinson Disease." Indonesian Journal of Biotechnology 19, no. 1 (December 31, 2015): 91. http://dx.doi.org/10.22146/ijbiotech.8638.

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Paraquat dichloride has been used by farmers as a herbicide to kill the grass. On the other hand, paraquatdichloride is harmful if enters to the body, causing Parkinson’s disease, since it is disrupting dopamineproduction in the substantia nigra pars compacta or dopamine pathways Nigro striatal pathway. The studywas done to fi nd out the histological changes of catecholaminergic neurons and Nigro striatal pathway causedby paraquat dichloride treatment in Wistar rats as a model of Parkinson’s disease.Twenty-two Wistar rats 3,5 months old were divided into 4 groups, 5 rats each. Group I (control group)were injected with aquabidest, while groups II, III, and IV were injected intraperitoneally with paraquatdichloride in aquabidest, with the dosage 5 , 10 and 15 mg/kg bw respectively. The rats were injected onceper week for 6 weeks. Three days after the last injection, the rats were anesthetized using xylasin (2 mg/kg)and ketamine (20 mg/kg) intramuscularly, and then were intracardiac perfused using physiological saline asprerinse solution, followed by 10% buffered formalin solution as a fi xative. After animals were fi xed, the brainswere removed and embedded in paraffi n block and cut in 12 μm thickness for immunohistochemistry stainingusing tyrosine hydroxylase antibody. The results of staining then were observed under light microscope andanalyzed descriptively.The results showed that the catecholaminergic neurons were distributed in the substantia nigrapars compacta in all treatment groups, however, the cell density were found decreased only in group IV.Catecholaminergic neurons appear in the bipolar and multipolar form, while dopamine ‘Nigro striatal pathway’was found exist in all treatment groups. From our study, histologycally the decreased of catecholaminergicneurons is only found in rats that received paraquat dichloride in dose 15 mg/kg bw for 6 weeks.
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16

Magnusson, Andres, and Timo Partonen. "The Diagnosis, Symptomatology, and Epidemiology of Seasonal Affective Disorder." CNS Spectrums 10, no. 8 (August 2005): 625–34. http://dx.doi.org/10.1017/s1092852900019593.

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AbstractThe operational criteria for seasonal affective disorder (SAD) have undergone several changes since first proposed in 1984. SAD is currently included as a specifier of either bipolar or recurrent major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The International Classification of Diseases, Tenth Edition has provisional diagnostic criteria for SAD. The most characteristic quality of SAD is that the symptoms usually present during winter and remit in the spring. Furthermore, the symptoms tend to remit when the patients are exposed to daylight or bright light therapy. The cognitive and emotional symptoms are as in other types of depression but the vegetative symptoms are the reverse of classic depressive vegetative symptoms, namely increased sleep and increased appetite. SAD is a common condition, but the exact prevalence rates vary between different studies and countries and is consistently found to be more common in women and in youth. SAD probably possibly occurs in children although not as commonly as in young adults. Some studies have found that certain ethnic groups who live at high northern latitudes may have adapted to the long arctic winter.
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17

Connors, Michael H., Lena Quinto, and Henry Brodaty. "Longitudinal outcomes of patients with pseudodementia: a systematic review." Psychological Medicine 49, no. 5 (October 15, 2018): 727–37. http://dx.doi.org/10.1017/s0033291718002829.

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AbstractDepression and a number of other psychiatric conditions can impair cognition and give the appearance of neurodegenerative disease. Collectively, this group of disorders is known as ‘pseudodementia’ and are important to identify given their potential reversibility with treatment. Despite considerable interest historically, the longitudinal outcomes of patients with pseudodementia remain unclear. We conducted a systematic review of longitudinal studies of pseudodementia. Bibliographic databases were searched using a wide range of search terms. Two reviewers independently assessed papers for inclusion, rated study quality, and extracted data. The search identified 18 studies with follow-up varying from several weeks to 18 years. Overall, 284 patients were studied, including 238 patients with depression, 18 with conversion disorder, 14 with psychosis, and 11 with bipolar disorder. Irrespective of diagnosis, 33% developed irreversible dementia at follow-up, 53% no longer met criteria for dementia, and 15% were lost to follow-up. Considerable variability was identified, with younger age at baseline, but not follow-up duration, associated with better outcomes. ECT and pharmacological interventions were also reported to be beneficial, though findings were limited by the poor quality of the studies. Overall, the findings suggest that pseudodementia may confer an increased risk of irreversible dementia in older patients. The findings also indicate, however, that a significant proportion improve, while many remain burdened with their psychiatric condition, independent of organic dementia. The findings support the clinical value of the construct and the need for its re-examination in light of developments in neuroimaging, genomics, other investigative tools, and trial methodology.
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18

Li, P. P., Z. Y. Cao, J. G. Dong, L. H. Zhang, H. Jia, N. Liu, S. H. Li, Z. M. Hao, S. Q. Gu, and X. Y. Wang. "First Report of Bipolaris papendorfii Causing Corn Leaf Spot in China." Plant Disease 97, no. 11 (November 2013): 1506. http://dx.doi.org/10.1094/pdis-02-13-0203-pdn.

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Corn is the most important cereal crop in China, with over 34.94 million ha being cultivated in the country annually. However, fungal diseases are a major limiting factor in corn production. In August 2012, 20 ha of corn fields in Anhui Province were found to be heavily infected by fungi. The margin of the lesion was achlorotic, and the middle was yellowish white or off-white, which was similar to the corn Curvalaria leaf spot. The oval lesions were approximately 5 to 7 mm. Lesion tissue was removed from the border between symptomatic and healthy tissue. The surface was sterilized in 75% ethanol for 30 s and 0.1% HgCl2 for 1 min, after which the sample was washed three times in sterile distilled water. The isolate was purified and subcultured on potato dextrose agar (PDA) at 25 ± 2°C. The initial color of the colony was light brown, turning dark brown after being cultured for 7 days. The conidia were boat-shaped or inverted pear-shaped and were clearly bent to one side. The cells of both ends were slightly lighter and respectively ranged from 34.5 to 44.0 μm and 12.0 to 21.0 μm away from the base, with the second cell as the widest. The majority conidia had three or four false septates; isolates produced light brown to medium brown conidiophore, scattered or clustered, often branching, and exhibited bending. These morphological characteristics matched with the description of Bipolaris papendorfii reported by Zhang (3). A pathogenicity test was conducted with the two isolates on each of the 36 corns by spraying 2 ml spore suspension (106 conidia/ml). For the control treatment, 36 corns were inoculated with an equal volume of sterilized water. Inoculated plants were placed in a greenhouse from 29 to 33°C and 95% relative humidity. The typical 5 to 7 mm oval lesions were observed 7 days after inoculation, except on the control samples. Three replications of 36 corns were used for each treatment. The isolate was consistently 100% reisolated from the diseased tissue according to Koch's postulate. The isolate was found to be morphologically similar to B. papendorfii. Preliminary morphological identification of the fungus was confirmed by PCR assay using genomic DNA extracted from the mycelium of a 7-day-old culture on PDA at 25 ± 2°C. A 550-bp amplified region of the internal transcribed spacer (ITS) of rDNA was generated using ITS1 (5′-TCCGTAGGTGAACCTGCGG-3′) and ITS4 (5′-TCCTCCGCTTATTGATATGC-3′) universal primers (1). The ITS region (GenBank Accession No. KC592365) was then sequenced by Sangon Biotech (Shanghai, China), and displayed 99% nucleotide similarity with the rDNA-ITS of B. papendorfii (JQ753972.1) separately after BLASTn research in GenBank. Based on the symptoms, fungal morphology, ITS sequence, and pathogenicity testing, this fungus was identified as B. papendorfii. The pathogen could reportedly infect tobacco and cotton (2). To our knowledge, this is the first study to report that B. papendorfii can infect corn in China. This report will establish a foundation for the further study of B. papendorfii to address the disease effectively. Further studies will be conducted to determine the incidence of the disease and the severity of damage caused by B. papendorfii as well as determine a possible mode for controlling the spread of the disease. References: (1) Y. J. Cao et al. Chin. J. Trop. Crops 31:1098, 2010. (2) H. Deng et al. Mycosystema 21:327, 2002. (3) T. Y. Zhang. Chin. Fungi Chi. 30:21, 2010.
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Choi, Hannah, Lei Zhang, Mark S. Cembrowski, Carl F. Sabottke, Alexander L. Markowitz, Daniel A. Butts, William L. Kath, Joshua H. Singer, and Hermann Riecke. "Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina." Journal of Neurophysiology 112, no. 6 (September 15, 2014): 1491–504. http://dx.doi.org/10.1152/jn.00437.2014.

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In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. We tested and confirmed this hypothesis experimentally by recording from AIIs in a slice preparation of rd1 retina. Additionally, recordings from ganglion cells in a whole mount preparation of rd1 retina demonstrated that activity in AIIs was propagated unchanged to elicit bursts of action potentials in ganglion cells. We conclude that oscillations are not an emergent property of a degenerated retinal network. Rather, they arise largely from the intrinsic properties of a single retinal interneuron, the AII amacrine cell.
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20

Szuromi, Phil. "Bipolar light-emitting junctions." Science 356, no. 6343 (June 15, 2017): 1135.7–1136. http://dx.doi.org/10.1126/science.356.6343.1135-g.

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Araki, Yasuo, Takeshi Terao, Nobuhiko Hoaki, Yumei Wang, and Shinjiro Goto. "Bipolar temperaments and light." Journal of Affective Disorders 136, no. 3 (February 2012): 740–42. http://dx.doi.org/10.1016/j.jad.2011.09.050.

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22

Vu, A. L., M. M. Dee, R. J. Gualandi, S. Huff, J. Zale, K. D. Gwinn, and B. H. Ownley. "First Report of Leaf Spot Caused by Bipolaris spicifera on Switchgrass in the United States." Plant Disease 95, no. 9 (September 2011): 1191. http://dx.doi.org/10.1094/pdis-10-10-0774.

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Light-to-dark brown leaf spots and general chlorosis were observed on ‘Alamo’ switchgrass (Panicum virgatum L.) grown in ornamental plantings on the campus of the University of Tennessee in Knoxville in December 2007. Disease distribution was patchy, infecting ~10% of plants. Patches had mild to severely infected plants with stunting in areas of severe infection. Symptomatic leaf tissue was surface sterilized, air dried on sterile filter paper, and plated on 2% water agar amended with 10 mg/liter of rifampicin (Sigma-Aldrich, St. Louis, MO) and 10 μl/liter of 2.4 EC Danitol miticide (Valent Chemical, Walnut Creek, CA). Plates were incubated at 26°C in darkness for 5 days. A sporulating, dematiaceous mitosporic fungus was observed and transferred to potato dextrose agar (PDA). Conidiophores were single, light brown, multiseptate, mostly straight, polytretic, geniculate, and sympodial. Conidia were 17.5 × 12 (22) to 30 × 14 (12.5) μm, oval, light brown, and distoseptate, with one to three septa and a flattened hilum on the basal cell. Conidia germinated from both poles. The causal agent was identified as Bipolaris spicifera (Bainier) Subram. Morphological features were as described for B. spicifera (2). Pathogenicity studies were conducted with 5-week-old ‘Alamo’ switchgrass plants grown from surface-sterilized seed in 9 × 9-cm pots containing 50% ProMix Potting and Seeding Mix (Premier Tech Horticulture, Rivière-du-Loup, Québec, Canada) and 50% Turface ProLeague (Profile Products, Buffalo Grove, IL) (vol/vol). Ten replicate pots with ~20 plants each were sprayed with a spore suspension of 4.5 × 106 spores/ml of sterile water prepared from 6-day-old cultures grown on PDA. Plants were subjected to high humidity for 45 h then incubated at 25/20°C with a 12-h photoperiod in a growth chamber. Leaf spot symptoms similar to the original disease appeared on plants in each of the 10 replicate pots 6 days postinoculation. Lesions were excised from leaves, surface sterilized, plated on water agar, and the resulting cultures were again identified as B. spicifera. The internal transcribed spacer (ITS) region of ribosomal DNA from the original isolate used for inoculation and the reisolated culture recovered from plants in the pathogenicity studies were amplified with PCR using primers ITS4 and ITS5 (3). PCR amplicons of ~560 bp were obtained from both isolates and sequenced. Amplicon sequences were identical and the sequence was submitted to GenBank (Accession No. HQ015445). The DNA sequence had 100% homology to the ITS sequence of B. spicifera strain NRRL 47508 (GenBank Accession No. GU183125.1) that had been isolated from sorghum seed. To our knowledge, leaf spot caused by B. spicifera has not been described on switchgrass (1). B. spicifera can be seedborne and has been reported on turfgrass seed exported from the United States to Korea (2). As switchgrass is transitioned from a prairie grass to a biofuels crop planted in large acreages, disease incidences and severities will likely increase, necessitating rapid disease identification and cost effective management strategies. References: (1) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ , 4 August 2010. (2) H.-M. Koo et al. Plant Pathol. J. 19:133, 2003. (3) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds, Academic Press, San Diego, 1990.
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23

Milenkovic, Vladimir M., Evan H. Stanton, Caroline Nothdurfter, Rainer Rupprecht, and Christian H. Wetzel. "The Role of Chemokines in the Pathophysiology of Major Depressive Disorder." International Journal of Molecular Sciences 20, no. 9 (May 9, 2019): 2283. http://dx.doi.org/10.3390/ijms20092283.

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Major depressive disorder (MDD) is a debilitating condition, whose high prevalence and multisymptomatic nature set its standing as a leading contributor to global disability. To better understand this psychiatric disease, various pathophysiological mechanisms have been proposed, including changes in monoaminergic neurotransmission, imbalance of excitatory and inhibitory signaling in the brain, hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, and abnormalities in normal neurogenesis. While previous findings led to a deeper understanding of the disease, the pathogenesis of MDD has not yet been elucidated. Accumulating evidence has confirmed the association between chronic inflammation and MDD, which is manifested by increased levels of the C-reactive protein, as well as pro-inflammatory cytokines, such as Interleukin 1 beta, Interleukin 6, and the Tumor necrosis factor alpha. Furthermore, recent findings have implicated a related family of cytokines with chemotactic properties, known collectively as chemokines, in many neuroimmune processes relevant to psychiatric disorders. Chemokines are small (8–12 kDa) chemotactic cytokines, which are known to play roles in direct chemotaxis induction, leukocyte and macrophage migration, and inflammatory response propagation. The inflammatory chemokines possess the ability to induce migration of immune cells to the infection site, whereas their homeostatic chemokine counterparts are responsible for recruiting cells for their repair and maintenance. To further support the role of chemokines as central elements to healthy bodily function, recent studies suggest that these proteins demonstrate novel, brain-specific mechanisms including the modulation of neuroendocrine functions, chemotaxis, cell adhesion, and neuroinflammation. Elevated levels of chemokines in patient-derived serum have been detected in individuals diagnosed with major depressive disorder, bipolar disorder, and schizophrenia. Furthermore, despite the considerable heterogeneity of experimental samples and methodologies, existing biomarker studies have clearly demonstrated the important role of chemokines in the pathophysiology of psychiatric disorders. The purpose of this review is to summarize the data from contemporary experimental and clinical studies, and to evaluate available evidence for the role of chemokines in the central nervous system (CNS) under physiological and pathophysiological conditions. In light of recent results, chemokines could be considered as possible peripheral markers of psychiatric disorders, and/or targets for treating depressive disorders.
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Gnasekaran, Pavallekoodi, Maziah Mahmood, and Sreeramanan Subramaniam. "Ultrastructure study of Vanda Kasem's Delight orchid's protocorm-like body." Horticultura Brasileira 34, no. 3 (September 2016): 333–39. http://dx.doi.org/10.1590/s0102-05362016003005.

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ABSTRACT Growing orchids has been classified as an international business since it covers 8% of the world floriculture trade. Thus, large-scale micropropagation of orchid using tissue culture techniques and improvement of some essential traits, such as resistances to various diseases and pests, and tolerances to environmental stresses, such as low temperatures and low light intensities, via genetic engineering acknowledged the orchids as one of the top ten cut flowers. Protocorm-like bodies (PLBs) are excellent explants for clonal propagation, artificial seeds development and genetic engineering since they are organized and easily regenerable somatic embryos that propagate rapidly. Vanda Kasem's Delight hybrid orchid's PLBs derived from shoot tip culture were examined in order to understand the fundamental ultrastructure of PLB. Examination of the cross sections of PLB revealed that PLB is made of a discrete bipolar structure that contains anterior and posterior meristems. Actively dividing meristem cells and outer layer lined by several rows of small and isodiametric cells with a dense cytoplasm and a prominent nucleus were also observed via cytological studies. Scanning Electron Microscope investigations revealed that the surface of PLBs is occupied by vertically positioned branched trichome appendages and regularly spaced stomatal openings with two guard cells. Organelles such as mitochondria of various sizes, shapes and biconvex chloroplast in the cytoplasm were revealed by Transmission Electron Microscope analysis. Hence, inheriting actively dividing cells, and bestowed with elements related to transpiration, photosynthesis and energy synthesizing power house makes PLB a suitable explant for micropropagation and genetic engineering studies.
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Heisler-Taylor, Tyler, Richard Wan, Elizabeth G. Urbanski, Sumaya Hamadmad, Mohd Hussain Shah, Hailey Wilson, Julie Racine, and Colleen M. Cebulla. "Multimodal imaging and functional analysis of the chick NMDA retinal damage model." PLOS ONE 16, no. 9 (September 7, 2021): e0257148. http://dx.doi.org/10.1371/journal.pone.0257148.

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Objectives The chick is rapidly becoming a standardized preclinical model in vision research to study mechanisms of ocular disease. We seek to comprehensively evaluate the N-methyl-D-aspartate (NMDA) model of excitotoxic retinal damage using multimodal imaging, functional, and histologic approaches in NMDA-damaged, vehicle-treated, and undamaged chicks. Methods Chicks were either left undamaged in both eyes or were injected with NMDA in the left eye and saline (vehicle) in the right eye. TUNEL assay was performed on chicks to assess levels of retinal cell death one day post-injection of NMDA or saline and on age-matched untreated chicks. Spectral domain optical coherence tomography (SD-OCT) was performed weekly on chicks and age-matched controls day 1 (D1) up to D28 post-injection. Light adapted electroretinograms (ERG) were performed alongside SD-OCT measurements on post-injection chicks along with age-matched untreated controls. Results Untreated and vehicle-treated eyes had no TUNEL positive cells while NMDA-treated eyes accumulated large numbers of TUNEL positive cells in the Inner Nuclear Layer (INL), but not other layers, at D1 post injection. Significant inner retina swelling or edema was found on SD-OCT imaging at D1 post-injection which resolved at subsequent timepoints. Both the INL and the inner plexiform layer significantly thinned by one-week post-injection and did not recover for the duration of the measurements. On ERG, NMDA-treated eyes had significantly reduced amplitudes of all parameters at D1 with all metrics improving over time. The b-wave, oscillatory potentials, and ON/OFF bipolar responses were the most affected with at least 70% reduction immediately after damage compared to the fellow eye control. Conclusion This study establishes a normative baseline on the retinal health and gross functional ability as well as intraocular pressures of undamaged, vehicle-treated, and NMDA-damaged chicks to provide a standard for comparing therapeutic treatment studies in this important animal model.
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26

Vu, A. L., M. M. Dee, J. Zale, K. D. Gwinn, and B. H. Ownley. "First Report of Leaf Spot caused by Bipolaris oryzae on Switchgrass in Tennessee." Plant Disease 97, no. 12 (December 2013): 1654. http://dx.doi.org/10.1094/pdis-01-13-0070-pdn.

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Knowledge of pathogens in switchgrass, a potential biofuels crop, is limited. In December 2007, dark brown to black irregularly shaped foliar spots were observed on ‘Alamo’ switchgrass (Panicum virgatum L.) on the campus of the University of Tennessee. Symptomatic leaf samples were surface-sterilized (95% ethanol, 1 min; 20% commercial bleach, 3 min; 95% ethanol, 1 min), rinsed in sterile water, air-dried, and plated on 2% water agar amended with 3.45 mg fenpropathrin/liter (Danitol 2.4 EC, Valent Chemical, Walnut Creek, CA) and 10 mg/liter rifampicin (Sigma-Aldrich, St. Louis, MO). A sparsely sporulating, dematiaceous mitosporic fungus was observed. Fungal plugs were transferred to surface-sterilized detached ‘Alamo’ leaves on sterile filter paper in a moist chamber to increase spore production. Conidia were ovate, oblong, mostly straight to slightly curved, and light to olive-brown with 3 to 10 septa. Conidial dimensions were 12.5 to 17 × 27.5 to 95 (average 14.5 × 72) μm. Conidiophores were light brown, single, multiseptate, and geniculate. Conidial production was polytretic. Morphological characteristics and disease symptoms were similar to those described for Bipolaris oryzae (Breda de Haan) Shoemaker (2). Disease assays were done with 6-week-old ‘Alamo’ switchgrass grown from seed scarified with 60% sulfuric acid and surface-sterilized in 50% bleach. Nine 9 × 9-cm square pots with approximately 20 plants per pot were inoculated with a mycelial slurry (due to low spore production) prepared from cultures grown on potato dextrose agar for 7 days. Cultures were flooded with sterile water and rubbed gently to loosen mycelium. Two additional pots were inoculated with sterile water and subjected to the same conditions to serve as controls. Plants were exposed to high humidity by enclosure in a plastic bag for 72 h. Bags were removed, and plants were incubated at 25/20°C with 50 to 60% relative humidity. During the disease assay, plants were kept in a growth chamber with a 12-h photoperiod of fluorescent and incandescent lighting. Foliar leaf spot symptoms appeared 5 to 14 days post-inoculation for eight of nine replicates. Control plants had no symptoms. Symptomatic leaf tissue was processed and plated as described above. The original fungal isolate and the pathogen recovered in the disease assay were identified using internal transcribed spacer (ITS) region sequences. The ITS region of rDNA was amplified with PCR and primer pairs ITS4 and ITS5 (4). PCR amplicons of 553 bp were sequenced, and sequences from the original isolate and the reisolated pathogen were identical (GenBank Accession No. JQ237248). The sequence had 100% nucleotide identity to B. oryzae from switchgrass in Mississippi (GU222690, GU222691, GU222692, and GU222693) and New York (JF693908). Leaf spot caused by B. oryzae on switchgrass has also been described in North Dakota (1) and was seedborne in Mississippi (3). To our knowledge, this is the first report of B. oryzae from switchgrass in Tennessee. References: (1) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/, 28 June 2012. (2) J. M. Krupinsky et al. Can. J. Plant Pathol. 26:371, 2004. (3) M. Tomaso-Peterson and C. J. Balbalian. Plant Dis. 94:643, 2010. (4) T. J. White et al. Pages 315-322 in: PCR Protocols: a Guide to Methods and Applications. M. A. Innis et al. (eds), Acad. Press, San Diego, 1990.
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27

Clark, Richard, and Scott Chambers. "Disease overview – Bipolar disorder." Drugs in Context 4 (2007): 1–11. http://dx.doi.org/10.7573/dic.212206.

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Lachinov, A. N., O. A. Selezneva, I. L. Valeeva, and M. G. Zolotukhin. "Bipolar absorption of light in polyarylenephthalides." Journal of Applied Spectroscopy 51, no. 5 (November 1989): 1199–202. http://dx.doi.org/10.1007/bf00664984.

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29

Ünal, F., E. B. Turgay, A. F. Yıldırım, and C. Yüksel. "First Report of Leaf Blotch on Sorghum Caused by Bipolaris spicifera in Turkey." Plant Disease 95, no. 4 (April 2011): 495. http://dx.doi.org/10.1094/pdis-01-10-0037.

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In July 2009, a leaf blotch disease was observed on sorghum in Sakarya Province, Turkey. Disease incidence and severity were rated at 45% and 25 to 75%, respectively. Typical symptoms included elliptical, straw-colored, necrotic lesions with darker margins. The lesions eventually coalesced, resulting in drying of leaves. A fungus was isolated from the lesions on potato dextrose agar (PDA) incubated under near ultraviolet light for 12 h daily at 22°C for 2 weeks. Flexuous conidiophores of the fungus were solitary or produced in small groups. They were geniculate with numerous well-defined scars, medium to dark brown, ≥300 μm long, and 4 to 9 μm thick. Five to eight or more conidia were produced on the apices of the conidiophores. The conidia were straight, oblong or cylindrical, rounded at the ends, golden brown at maturity except for a small area just above the dark scar, pseudoseptate, and 20 to 31 × 7.5 to 12.5 μm (1). The causal fungus was identified as Bipolaris spicifera (Bain) Subram. (teleomorph Cochliobolus spicifer Nelson). The identification was confirmed with specific PCR primers (Bipol-1 F: 5′-CAGTTGCAATCAGCGTCAGT-3′, R: 5′-AAGACAAAAACGCCCAACAC-3′, Bipol-2 F: 5′-GTGTTGGGCGTTTTTGTCTT-3′, R: 5′-CCTACCTGATCCGAGGTCAA-3′, Bipol-3 F: 5′-GATGAAGAACGCAGCGAAAT-3′, R: 5′-AAGACAAAAACGCCCAACAC-3′). These primers were designed by the authors using Primer3 primer design software and sequences of B. spicifera found in GenBank. PCR products were amplified from nuclear DNA of the cultured fungus and were sequenced after cleaning with a Beckman 8000 CEQ DNA sequencer. Sequences amplified using Bipol-1 and Bipol-2 showed 99 to 100% similarity with B. spicifera sequences from GenBank. The DNA sequence amplified using Bipol-2 was deposited in GenBank (Accession No. HQ538774). B. spicifera has been reported previously as pathogenic in Africa, North and South America, Asia, Australia, Oceania, and the West Indies on Agrostis, Avena, Cymbopogon, Cynodon, Dactylis, Desmostachya, Eleusine, Holcus, Hordeum, Oryza, Panicum, Pennisetum, Phleum, Poa, Saccharum, Sorghum, Triticum, and Zea spp. (3). Pathogenicity tests were conducted on sorghum (Sorghum bicolor (L.) Moench) and Sorghum × sudangrass hybrid cultivars. From PDA cultures, conidia were collected in sterile distilled water with a concentration of 3% Tween 20. Twenty-five plants (five per pot) were inoculated by spraying the conidia (105 ml–1) onto 21-day-old plants, which were then maintained at 25 ± 2°C in a greenhouse following 48 h in a humid chamber. The test was repeated once. Control plants were sprayed with sterile distilled water. Typical symptoms (2) were obtained from all inoculated plants 7 days after inoculation. No symptoms developed on the control plants. The pathogen was reisolated from inoculated leaves to fulfill Koch's postulates. To our knowledge, this is the first report of B. spicifera on sorghum in Turkey. References: (1) M. B. Ellis. Dematiaceous Hyphomycetes. Commonwealth Mycological Institute, Kew, Surrey, England, 1971. (2) H. Koo et al. Plant Pathol. J. 19:133, 2003. (3) A. Sivanesan. Mycologia Papers 158:1, 1987.
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Milla-Navarro, Santiago, Ariadna Diaz-Tahoces, Isabel Ortuño-Lizarán, Eduardo Fernández, Nicolás Cuenca, Francisco Germain, and Pedro de la Villa. "Visual Disfunction due to the Selective Effect of Glutamate Agonists on Retinal Cells." International Journal of Molecular Sciences 22, no. 12 (June 10, 2021): 6245. http://dx.doi.org/10.3390/ijms22126245.

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One of the causes of nervous system degeneration is an excess of glutamate released upon several diseases. Glutamate analogs, like N-methyl-DL-aspartate (NMDA) and kainic acid (KA), have been shown to induce experimental retinal neurotoxicity. Previous results have shown that NMDA/KA neurotoxicity induces significant changes in the full field electroretinogram response, a thinning on the inner retinal layers, and retinal ganglion cell death. However, not all types of retinal neurons experience the same degree of injury in response to the excitotoxic stimulus. The goal of the present work is to address the effect of intraocular injection of different doses of NMDA/KA on the structure and function of several types of retinal cells and their functionality. To globally analyze the effect of glutamate receptor activation in the retina after the intraocular injection of excitotoxic agents, a combination of histological, electrophysiological, and functional tools has been employed to assess the changes in the retinal structure and function. Retinal excitotoxicity caused by the intraocular injection of a mixture of NMDA/KA causes a harmful effect characterized by a great loss of bipolar, amacrine, and retinal ganglion cells, as well as the degeneration of the inner retina. This process leads to a loss of retinal cell functionality characterized by an impairment of light sensitivity and visual acuity, with a strong effect on the retinal OFF pathway. The structural and functional injury suffered by the retina suggests the importance of the glutamate receptors expressed by different types of retinal cells. The effect of glutamate agonists on the OFF pathway represents one of the main findings of the study, as the evaluation of the retinal lesions caused by excitotoxicity could be specifically explored using tests that evaluate the OFF pathway.
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31

Figliola, Suzanne S., N. D. Camper, and W. H. Ridings. "Potential Biological Control Agents for Goosegrass (Eleusine indica)." Weed Science 36, no. 6 (November 1988): 830–35. http://dx.doi.org/10.1017/s0043174500075913.

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Two leaf-spotting pathogens, [Bipolaris setariae(Saw.)] and [Piricularia grisea(Cke.) Sacc.], were isolated from severely infected goosegrass plants. Pathogenicity tests conducted at 28 C showed that both fungi were 100% effective in infecting goosegrass when given a 72-h dew period. Dew period temperature and duration requirements were tested by inoculating 2-week-old plants with conidial suspensions of each fungus and incubating them in dew chambers (100% relative humidity). Disease index increased as dew period duration increased for both fungi and at all temperatures tested. Infection occurred at all temperatures with an optimum of 24 to 28 C forB. setariaeand 28 C forP. grisea. In host range tests, representative plants of the Fabaceae, Malvaceae, Poaceae, and Solanaceae were inoculated with suspensions of either 20 000 or 60 000 spores/ml of each fungus and placed in growth chambers at 28 C. Infection was limited to members of the Poaceae. Sorghum showed a hypersensitive response toB. setariae. Both cultivars of corn developed light symptoms in response to both fungi at 20 000 and 60 000 spores/ml.
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32

Jawad, Ali SM. "Behçet’s disease and bipolar disorder." Journal of the Royal College of Physicians of Edinburgh 49, no. 2 (2019): 171–74. http://dx.doi.org/10.4997/jrcpe.2019.221.

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Swartz, Holly A., and Andrea Fagiolini. "Cardiovascular Disease and Bipolar Disorder." Journal of Clinical Psychiatry 73, no. 12 (December 15, 2012): 1563–65. http://dx.doi.org/10.4088/jcp.12ac08227.

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34

Cotovio, G., J. B. Barahona-Corrêa, R. Ribeiro, S. Senova, and A. J. Oliveira-Maia. "Neuroanatomy of secondary bipolar disease." European Neuropsychopharmacology 26 (October 2016): S487. http://dx.doi.org/10.1016/s0924-977x(16)31496-1.

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35

&NA;. "Bipolar Disease and Drug Abuse." Emergency Medicine News 25, no. 7 (July 2003): 12. http://dx.doi.org/10.1097/00132981-200307000-00010.

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36

Greener, Mark. "Genetic insights into bipolar disease." Progress in Neurology and Psychiatry 12, no. 1 (January 2008): 12–13. http://dx.doi.org/10.1002/pnp.55.

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37

Feng, M., N. Holonyak, and W. Hafez. "Light-emitting transistor: Light emission from InGaP/GaAs heterojunction bipolar transistors." Applied Physics Letters 84, no. 1 (January 5, 2004): 151–53. http://dx.doi.org/10.1063/1.1637950.

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38

Pratt, R. G. "An Excised-Leaf Inoculation Technique for Evaluating Host-Pathogen Interactions and Quantitative Resistance of Bermudagrass Genotypes to Dematiaceous Hyphomycetes." Phytopathology® 93, no. 12 (December 2003): 1565–71. http://dx.doi.org/10.1094/phyto.2003.93.12.1565.

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Excised leaves of bermudagrass were inoculated with mycelium of isolates of Bipolaris, Exserohilum, Curvularia, and Drechslera spp. in water agar plates to evaluate differences in susceptibility of leaf tissue, virulence of pathogens, and quantitative resistance of bermudagrass genotypes. Isolates of nine species of pathogens induced similar symptoms of light- to dark-brown necrosis and bordering chlorosis in excised leaves that were not distinct for individual species or genera. Severity of symptoms induced by most isolates increased progressively from younger to older leaves. Within and across leaf positions, numerous significant differences in virulence of isolates within fungal species and between species were observed. Among 40 randomly selected bermudagrass genotypes, a continuous quantitative gradient was observed for mean scores of disease severity in excised leaves inoculated with E. rostratum. Numerous significant differences were observed within this gradient, and severity of symptoms in the most susceptible genotypes was approximately double that in the most resistant. When intact foliage of genotypes from the resistant and susceptible extremes of the gradient was inoculated with spores of E. rostratum, corresponding differences in severity of symptoms and significant (P = 0.05) correlations between results with excised leaves and intact foliage were observed. However, the range of differences in disease severity between genotypes was more narrow in intact foliage than in excised leaves. Results indicate that the excised leaf inoculation technique can be used to evaluate the relative resistance of bermudagrass genotypes to E. rostratum for use in programs to breed for quantitative host resistance.
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39

Eggers, Erika D., Reece E. Mazade, and Justin S. Klein. "Inhibition to retinal rod bipolar cells is regulated by light levels." Journal of Neurophysiology 110, no. 1 (July 1, 2013): 153–61. http://dx.doi.org/10.1152/jn.00872.2012.

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The retina responds to a wide range of light stimuli by adaptation of retinal signaling to background light intensity and the use of two different photoreceptors: rods that sense dim light and cones that sense bright light. Rods signal to rod bipolar cells that receive significant inhibition from amacrine cells in the dark, especially from a rod bipolar cell-activated GABAergic amacrine cell. This inhibition modulates the output of rod bipolar cells onto downstream neurons. However, it was not clear how the inhibition of rod bipolar cells changes when rod signaling is limited by an adapting background light and cone signaling becomes dominant. We found that both light-evoked and spontaneous rod bipolar cell inhibition significantly decrease with light adaptation. This suggests a global decrease in the activity of amacrine cells that provide input to rod bipolar cells with light adaptation. However, inhibition to rod bipolar cells is also limited by GABAergic connections between amacrine cells, which decrease GABAergic input to rod bipolar cells. When we removed this serial inhibition, the light-evoked inhibition to rod bipolar cells remained after light adaptation. These results suggest that decreased inhibition to rod bipolar cells after light adaptation is due to decreased rod pathway activity as well as an active increase in inhibition between amacrine cells. Together these serve to limit rod bipolar cell inhibition after light adaptation, when the rod pathway is inactive and modulation of the signal is not required. This suggests an efficiency mechanism in the retina to limit unnecessary signaling.
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40

Vu, A. L., M. M. Dee, K. D. Gwinn, and B. H. Ownley. "First Report of Spot Blotch and Common Root Rot Caused by Bipolaris sorokiniana on Switchgrass in Tennessee." Plant Disease 95, no. 9 (September 2011): 1195. http://dx.doi.org/10.1094/pdis-12-10-0880.

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Light-to-dark brown, irregular-shaped leaf spots, chlorosis, necrotic roots, and severe stunting were observed on ‘Alamo’ switchgrass (Panicum virgatum L.) grown on the campus of the University of Tennessee in December 2007. Symptomatic leaf and root samples were surface sterilized, air dried on sterile filter paper, and plated on 2% water agar amended with 10 mg/liter of rifampicin (Sigma-Aldrich, St. Louis, MO) and 10 μl/liter of 2,4 EC Danitol miticide (Valent Chemical, Walnut Creek, CA). Plates were incubated at 25°C in darkness for 4 days. A sporulating, dematiaceous mitosporic fungus was noted and transferred to potato dextrose agar (PDA). Conidia were ovate, oblong, mostly straight, and olive to brown with three to nine septa. Conidial dimensions were 12.5 × 27.5 (17.5) to 20 × 77.5 (57) μm. Conidia were produced on single, light brown, multiseptate conidiophores that were polytretic, geniculate, and sympodial. Morphological features were as described for Bipolaris sorokiniana (Sacc.) Shoemaker (teleomorph = Cochliobolus sativus) (2,3). Disease assays were conducted with 5-week-old ‘Alamo’ switchgrass grown from surface-sterilized seed. Ten 9 × 9-cm2 with ~20 switchgrass seedlings were sprayed with 2.4 × 105 spores/ml of sterile water. Plants were subjected to high humidity created by enclosure in a plastic bag for 45 h. The bag was removed and plants were incubated at 25/20°C with 50 to 60% relative humidity. During the incubation, plants were maintained in growth chamber with a 12-h photoperiod of fluorescent and incandescent lighting. Foliar leaf spot symptoms appeared 6 to 10 days postinoculation for plants in all 10 replicates and necrotic lesions were observed on roots. Foliar lesions and diseased roots were surface sterilized, plated on water agar, and resultant fungal colonies were identified as B. sorokiniana. The internal transcribed spacer (ITS) and mitochondrial small subunit (SSU) regions of ribosomal DNA from the original isolate, and the isolate recovered from plants in the pathogenicity assay, were amplified with PCR, with primer pairs ITS4 and ITS5 and NMS1 and NMS2. PCR amplicons of ~551 and 571 bp were obtained with the two primer pairs, respectively. Both amplicons were obtained from both isolates and sequenced. Amplicon sequences from the original isolate and re-isolate were identical and the sequences were submitted to GenBank (Accession Nos. HQ611957 and HQ611958). The ITS sequences had 98% homology to 23 B. sorokiniana isolates, including B. sorokiniana strain DSM 62608 (GenBank Accession No. EF187908); SSU sequences had 99% homology to Cochliobolus sativus isolate AFTOL-ID 271 (GenBank Accession No. FJ190589). Spot blotch caused by B. sorokiniana has been reported on switchgrass in Iowa, Nebraska, Pennsylvania, and Virginia (1). To our knowledge, this is the first report of B. sorokiniana causing spot blotch or common root rot of switchgrass in Tennessee, which extends the current known distribution of these diseases. More recently, we isolated B. sorokiniana from switchgrass seed received from commercial sources in the United States, indicating a seedborne transmission. References: (1) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ , 15 November 2010. (2) R. F. Nyvall and J. A. Percich. Plant Dis. 83:936, 1999. (3) A. Sivanesan and P. Holliday. CMI Descr. Pathog. Fungi bact. 71:701, 1981.
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41

Ducharme, Simon, Annemiek Dols, Robert Laforce, Emma Devenney, Fiona Kumfor, Jan van den Stock, Caroline Dallaire-Théroux, et al. "Recommendations to distinguish behavioural variant frontotemporal dementia from psychiatric disorders." Brain 143, no. 6 (March 4, 2020): 1632–50. http://dx.doi.org/10.1093/brain/awaa018.

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Abstract The behavioural variant of frontotemporal dementia (bvFTD) is a frequent cause of early-onset dementia. The diagnosis of bvFTD remains challenging because of the limited accuracy of neuroimaging in the early disease stages and the absence of molecular biomarkers, and therefore relies predominantly on clinical assessment. BvFTD shows significant symptomatic overlap with non-degenerative primary psychiatric disorders including major depressive disorder, bipolar disorder, schizophrenia, obsessive-compulsive disorder, autism spectrum disorders and even personality disorders. To date, ∼50% of patients with bvFTD receive a prior psychiatric diagnosis, and average diagnostic delay is up to 5–6 years from symptom onset. It is also not uncommon for patients with primary psychiatric disorders to be wrongly diagnosed with bvFTD. The Neuropsychiatric International Consortium for Frontotemporal Dementia was recently established to determine the current best clinical practice and set up an international collaboration to share a common dataset for future research. The goal of the present paper was to review the existing literature on the diagnosis of bvFTD and its differential diagnosis with primary psychiatric disorders to provide consensus recommendations on the clinical assessment. A systematic literature search with a narrative review was performed to determine all bvFTD-related diagnostic evidence for the following topics: bvFTD history taking, psychiatric assessment, clinical scales, physical and neurological examination, bedside cognitive tests, neuropsychological assessment, social cognition, structural neuroimaging, functional neuroimaging, CSF and genetic testing. For each topic, responsible team members proposed a set of minimal requirements, optimal clinical recommendations, and tools requiring further research or those that should be developed. Recommendations were listed if they reached a ≥ 85% expert consensus based on an online survey among all consortium participants. New recommendations include performing at least one formal social cognition test in the standard neuropsychological battery for bvFTD. We emphasize the importance of 3D-T1 brain MRI with a standardized review protocol including validated visual atrophy rating scales, and to consider volumetric analyses if available. We clarify the role of 18F-fluorodeoxyglucose PET for the exclusion of bvFTD when normal, whereas non-specific regional metabolism abnormalities should not be over-interpreted in the case of a psychiatric differential diagnosis. We highlight the potential role of serum or CSF neurofilament light chain to differentiate bvFTD from primary psychiatric disorders. Finally, based on the increasing literature and clinical experience, the consortium determined that screening for C9orf72 mutation should be performed in all possible/probable bvFTD cases or suspected cases with strong psychiatric features.
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42

Yorguner Kupeli, Nese, Necati Serkut Bulut, Gresa Carkaxhiu Bulut, Emel Kurt, and Kaan Kora. "Efficacy of bright light therapy in bipolar depression." Psychiatry Research 260 (February 2018): 432–38. http://dx.doi.org/10.1016/j.psychres.2017.12.020.

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43

Lamberg, Lynne. "Let There Be Light in Depression, Bipolar Illness." Psychiatric News 44, no. 22 (November 20, 2009): 22–32. http://dx.doi.org/10.1176/pn.44.22.psychnews_44_22_028.

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44

Zagorski, Nick. "Blue Light–Blocking Glasses May Reduce Bipolar Mania." Psychiatric News 51, no. 16 (August 19, 2016): 1. http://dx.doi.org/10.1176/appi.pn.2016.8a24.

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45

Zagorski, Nick. "Adjunctive Light Therapy Found Effective for Bipolar Depression." Psychiatric News 52, no. 24 (December 15, 2017): 1. http://dx.doi.org/10.1176/appi.pn.2017.pp10b3.

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46

Ding, J., and Y. Yang. "Small Angle Light Scattering from Bipolar Nematic Droplets." Molecular Crystals and Liquid Crystals Science and Technology. Section A. Molecular Crystals and Liquid Crystals 257, no. 1 (December 1994): 63–87. http://dx.doi.org/10.1080/10587259408033765.

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47

Feng, M., N. Holonyak, and R. Chan. "Quantum-well-base heterojunction bipolar light-emitting transistor." Applied Physics Letters 84, no. 11 (March 15, 2004): 1952–54. http://dx.doi.org/10.1063/1.1669071.

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48

Canavan, N., and G. Sachs. "Antidepressants in Bipolar Disorder: STEP into the Light." MD Conference Express 8, no. 3 (October 1, 2008): 24–25. http://dx.doi.org/10.1177/155989770800800318.

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49

Yook, Kyoung Soo, and Jun Yeob Lee. "Bipolar Host Materials for Organic Light-Emitting Diodes." Chemical Record 16, no. 1 (November 23, 2015): 159–72. http://dx.doi.org/10.1002/tcr.201500221.

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50

Engmann, Birk. "Bipolar Affective Disorder and Parkinson's Disease." Case Reports in Medicine 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/154165.

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Little is known about comorbidities of bipolar disorder such as Parkinson's disease. A case history and a literature survey indicate that bipolar disorder is linked with or influences Parkinson's disease and vice versa. Underlying mechanisms are poorly understood, and, more importantly, no treatment options are established in such double diagnoses. The few data in comorbid Parkinson cases seem to point to a rapid cycling pattern of bipolar symptoms. With regard to therapeutic intervention, the literature supports pramipexole for treatment of both Parkinson and depressive symptoms in bipolar depression. Lithium, the mood stabilizer of choice for treating manic states, is problematical for use in Parkinson patients because of its side effects. Valproate might be an alternative, especially for treatment of rapid cycling.
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