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Biomedical subjects

Michael S Turner

Publications and source records attributed to Michael S Turner.

11 recordsLinked to original sources
PubMed2007

Quarks and the cosmos.

Cosmology is in the midst of a period of revolutionary discovery, propelled by bold ideas from particle physics and by technological advances from gigapixel charge-coupled device cameras to peta-scale computing. The basic features of the universe have now been determined: It is 13.7 billion years old, spatially flat, and expanding at an accelerating rate; it is composed of atoms (4%), exotic dark matter (20%), and dark energy (76%); and there is evidence that galaxies and other structures were seeded by quantum fluctuations. Although we know much about the universe, we understand far less. Poised to dramatically advance our understanding of both the universe and the laws that govern it, cosmology is on the verge of a golden age.

Journal Article↗
PubMed2005

Dorsal rhizotomy.

Explore the source record for details and available documents.

Cerebral Palsy↗
PubMed2003

Intrathecal baclofen withdrawal mimicking sepsis.

Baclofen (Lioresal) is a drug of choice to treat spasticity and is increasingly being administered intrathecally via an implantable pump in cases refractory to oral therapy. Emergency physicians will likely treat patients with baclofen withdrawal or overdose as this treatment becomes more widespread. The syndrome of baclofen withdrawal presents with altered mental status, fever, tachycardia, hypertension or hypotension, seizures, and rebound spasticity, and may be fatal if not treated appropriately. Baclofen withdrawal may mimic other diseases including sepsis, meningitis, autonomic dysreflexia, malignant hyperthermia, or neuroleptic malignant syndrome. Treatment consists of supportive care, reinstitution of baclofen, benzodiazepines, and diagnosis and eventual repair of intrathecal pump and catheter malfunction.

Baclofen↗
PubMed2003

Mucins in gastrointestinal cancers.

The mucin family has been under study by molecular biologists, biochemists, pathologists and immunologists interested in cancer because of the role these molecules can play in the diagnosis and treatment of cancer. Immense knowledge has been accumulated, but the high speed of progress in the laboratory has not been matched by the progress towards applying this knowledge in the clinic. For example, specific knowledge of cancer-associated changes in the expression and glycosylation of various mucins, which can aid in the diagnosis as well as prognosis of GI cancers, has not yet led to the use of a panel of anti-mucin antibodies as a standard diagnostic tool. Similarly, many more opportunities exist for using mucin-based therapies than are currently being considered in the clinic. This chapter aimed to highlight some of these opportunities and to interest clinician scientists in exploring them in the near future.

Cancer Vaccines↗
PubMed2002

Abrupt withdrawal from intrathecal baclofen: recognition and management of a potentially life-threatening syndrome.

OBJECTIVE: To suggest guidelines for the prevention, recognition, and management of a life-threatening syndrome (high fever, altered mental status, profound muscular rigidity that sometimes progressed to fatal rhabdomyolysis) in patients who experience the abrupt withdrawal of intrathecal baclofen (ITB) therapy. DESIGN: Retrospective literature and safety-file review. SETTING: Expert panel drawn from physiatry, neurology, and neurosurgery. PARTICIPANTS: Experienced users of ITB therapy in the pediatric and adult populations in the United States. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: We reviewed literature reports, MedWatch reports to the US Food and Drug Administration, and our own experiences. We critically analyzed patient management and drug therapy in the context of the pharmacology of baclofen and other antispastic agents. RESULTS: An abrupt reduction in gamma-aminobutyric acid(B) (GABA) agonist activity in the central nervous system can cause the ITB withdrawal syndrome, which is clinically and pathophysiologically distinct from autonomic dysreflexia, malignant hyperthermia, and neuroleptic-malignant syndrome. ITB withdrawal evolves over 1 to 3 days, but may become fulminant if not recognized and treated early. The syndrome can be interrupted by the restoration of ITB therapy. However, supportive measures and high-dose benzodiazepine infusion may be life saving in the interval before ITB therapy is resumed. Dantrolene infusion may relieve muscle rigidity but does not reverse the other manifestations of GABAergic agonist withdrawal. CONCLUSIONS: Most episodes of severe ITB withdrawal were preventable. Patients at risk can be identified and educated prospectively and given medication for emergency use. Treatment with GABAergic agonist drugs may prevent potentially fatal sequelae.

Anti-Anxiety Agents↗
PubMed2002

Alterations in responses of ventral pallidal neurons to excitatory amino acids after long-term dopamine depletion.

The present study explored the possibility that excitatory amino acid (EAA) sensitivity within the ventral pallidum (VP) is altered by long-term removal of dopamine (DA). Electrophysiological experiments were conducted in chloral hydrate-anesthetized rats 21 to 28 days after they received unilateral substantia nigra injections of the dopaminergic toxin 6-hydroxydopamine (6-OHDA). VP neurons increased firing at low microiontophoretic ejection currents of the EAA agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA); however, high currents decreased action potential amplitude and rapidly caused cessation of neuronal firing. These responses likely reflected the induction of depolarization block for they were reversed by coiontophoresis of the hyperpolarizing transmitter gamma-aminobutyric acid (GABA) at ejection current levels that normally suppressed firing. The ability of NMDA and AMPA to induce such inactivation was greater in the VP of 6-OHDA-lesioned hemispheres, but unchanged in reserpinized rats, verifying that the alterations in responding to NMDA were the result of chronic, rather than acute, DA removal. The adaptations do not appear to be the consequence of a diminished GABAergic tone for the ability of bicuculline to increase firing (due to blocking a tonic GABAergic input) was not changed. However, low ejection currents of GABA that were insufficient to alter firing rate greatly attenuated the ability of NMDA to induce an apparent depolarization inactivation when coiontophoresed with NMDA onto VP neurons of the lesioned, but not the unlesioned, hemisphere. These studies show that chronic DA removal altered the EAA-induced amplitude-decreasing (i.e., the apparent depolarization inactivation) effects in VP neurons in the absence of a decrease in GABAergic tone.

Action Potentials↗