The Molecular and Crystal Structures of Phosphinoborane and Dimethylsulfoxide-Boron Trifluoride

Thesis (Ph.D.)--Boston Universit

Spectroscopic studies of Lewis acid‐base complexes. III: Vibrational frequencies, assignments and normal coordinate analyses for isotopic varieties of phosphine borane and trifluorophosphine borane

Vibrational spectra of the two Lewis complexes, phosphine borane, PH 3 BH 3 , and trifluoro‐phosphine borane, PF 3 BH 3 , have been investigated for several isotopic species preserving C 3 v symmetry. New assignments are proposed and substantiated by normal coordinate analyses formulated in the compliance constant basis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/91113/1/1250020208_ftp.pd

Episode 71: Booked Solid: The History of USC Press

For nearly 80 years, the University of South Carolina Press has been publishing books — more than 1,000 and counting — on topics ranging from the history of the Palmetto State to literary figures, cuisine and much more. Pull up a reading chair and learn more about the Press came to be.https://scholarcommons.sc.edu/rememberingthedays/1070/thumbnail.jp

Levodopa-Induced Dyskinesia Is Associated with Increased Thyrotropin Releasing Hormone in the Dorsal Striatum of Hemi-Parkinsonian Rats

Background Dyskinesias associated with involuntary movements and painful muscle contractions are a common and severe complication of standard levodopa (L-DOPA, L-3,4-dihydroxyphenylalanine) therapy for Parkinson's disease. Pathologic neuroplasticity leading to hyper-responsive dopamine receptor signaling in the sensorimotor striatum is thought to underlie this currently untreatable condition. Methodology/Principal Findings Quantitative real-time polymerase chain reaction (PCR) was employed to evaluate the molecular changes associated with L-DOPA-induced dyskinesias in Parkinson's disease. With this technique, we determined that thyrotropin releasing hormone (TRH) was greatly increased in the dopamine-depleted striatum of hemi-parkinsonian rats that developed abnormal movements in response to L-DOPA therapy, relative to the levels measured in the contralateral non-dopamine-depleted striatum, and in the striatum of non-dyskinetic control rats. ProTRH immunostaining suggested that TRH peptide levels were almost absent in the dopamine-depleted striatum of control rats that did not develop dyskinesias, but in the dyskinetic rats, proTRH immunostaining was dramatically up-regulated in the striatum, particularly in the sensorimotor striatum. This up-regulation of TRH peptide affected striatal medium spiny neurons of both the direct and indirect pathways, as well as neurons in striosomes. Conclusions/Significance TRH is not known to be a key striatal neuromodulator, but intrastriatal injection of TRH in experimental animals can induce abnormal movements, apparently through increasing dopamine release. Our finding of a dramatic and selective up-regulation of TRH expression in the sensorimotor striatum of dyskinetic rat models suggests a TRH-mediated regulatory mechanism that may underlie the pathologic neuroplasticity driving dopamine hyper-responsivity in Parkinson's disease.Morris K. Udall Center for Excellence in Parkinson’s Research at MGH/MITNational Institutes of Health (U.S.) (NIH NS38372)American Parkinson Disease Association, Inc.University of Alabama at BirminghamMassachusetts General HospitalNational Institute of Diabetes and Digestive and Kidney Diseases (U.S.) (NIDDK/NIH grant R01 DK58148)National Institute of Neurological Disorders and Stroke (U.S.) (R01 NINDS/NIH grant NS045231)Stanley H. and Sheila G. Sydney FundMichael J. Fox Foundation for Parkinson's Researc

Healthy ageing, appetite, frailty and sarcopenia: a brief overview

In many societies the population is getting older, such that in some western countries it is expected that those over 80 years of age will make up 30% of the population (1-2). In the modern era, due to improved health and better medical support/treatment, many people may spend as many years retired as they did working. Unfortunately, as one ages, the burden of disease increases (2.9 million people in England have >1 long-term condition), longevity is compromised by disability; therefore the drive must be to add life to years rather than just years to life. When people live long, the media often asks “what is the success associated with longevity or successful (healthy) ageing?” Is it a success to live a long life, or is successful ageing the key? Healthy ageing, is defined as a state, where the effect of frailty, sarcopenia, disease and disability have been minimised. Farpour et al (3) discuss the effect that aging has on Iranian people, and Liang et al discuss the findings of a systematic review looking at traditional Chinese’ medicine and subhealth (4), which could be aligned to prefrailty. In 2015 the WHO defined Health as “a state of complex physical, mental and social well-being and not merely absence of disease” (5). Healthy ageing was also defined as “the process of developing and maintaining the functional ability that enables well-being in older age”. Rowe and Khan (1987) commented that to age successfully one must avoid disease, remain engaged with life and maintain a high level of physical and cognitive function (6). Healthy ageing is, therefore, a complex interplay between physical, cognitive and social factors, and perhaps is dependent on how we individually respond to the internal and external forces at play (table 1). The definition of what is normal and what is abnormal is fraught with difficulty; what is acceptable and what is not? There is a risk that where normative parameters (for younger adults) are exceeded there will be a medicalisation of “older age”! What ultimately matters is the preservation of functional ability, which the majority (75%) of very old people are able to do and live relatively independent lives (6). This paper will discuss the interdependency between healthy ageing, appetite, frailty and sarcopenia and their impact on functional ability