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Biomedical subjects

Jonathan Newmark

Publications and source records attributed to Jonathan Newmark.

9 recordsLinked to original sources
PubMed2007

Vitamin D and Parkinson's disease--a hypothesis.

Parkinson's disease (PD), a common disease of the elderly, is a movement disorder characterized by tremor, akinesia, and loss of postural reflexes, leading to immobility and frequent falls. It results from selective loss (death) of dopaminergic neurons in the substantia nigra region of the brain, largely developed prior to clinical diagnosis, and continuous after diagnosis, despite use of current therapeutic modalities. In PD in the United States the cause and mechanism of continued neuron cell death in the substantia nigra is currently unknown. We hypothesize, based upon several lines of evidence, that documented chronically inadequate vitamin D intake in the United States, particularly in the northern states and particularly in the elderly, is a significant factor in the pathogenesis of PD. This hypothesis implies that dietary aid for prevention and therapy for PD is possible.

Calcitriol↗
PubMed2007

Nerve agents.

BACKGROUND: Nerve agents, the deadliest of the classic chemical warfare agents, primarily function as acetylcholinesterase inhibitors and cause a rapidly progressive cholinergic crisis. Originally developed for battlefield use, they have been used in terrorist attacks and are considered threats to the civilian population. REVIEW SUMMARY: The pathophysiology and clinical presentation of acute nerve agent poisoning are summarized and acute treatment protocols reviewed. Timely support and antidotal treatment are crucial and may be lifesaving. Pyridostigmine bromide, recently approved by the Food and Drug Administration as a pretreatment for soman poisoning, forms part of battlefield doctrine but is unlikely to be used in the civilian sector. Aside from that, civilian recommendations for acute therapy derive, with only minor modifications, from military doctrine. CONCLUSION: Neurologists should familiarize themselves with the pathophysiology and treatment principles for the syndromes caused by nerve agents, not only to assist with the hospital care of these patients but also to serve as resources to their local medical communities in preparation for chemical terrorism. Because nerve agents injure the nervous system, nonneurologists have a right to expect neurologists to have mastered these principles.

Animals↗
PubMed2006

Sulfur mustard-induced neutropenia: treatment with granulocyte colony-stimulating factor.

Although best known as a blistering agent, sulfur mustard (HD) can also induce neutropenia in exposed individuals, increasing their susceptibility to infection. Granulocyte colony-stimulating factor (G-CSF) and pegylated G-CSF (peg-G-CSF) have been approved by the U.S. Food and Drug Administration as hematopoietic growth factors to treat chemotherapy-induced neutropenia. The goal of this study was to determine the effectiveness of G-CSF and peg-G-CSF in ameliorating HD-induced neutropenia. African green monkeys (Chlorocebus aethiops) were challenged with HD and, at 1, 3, 5, or 7 days after exposure, G-CSF therapy (10 microg/kg per day for 21 days) was initiated. Peg-G-CSF (300 microg/kg, single treatment) was similarly tested, with treatment given at 3 days after exposure. Untreated HD-exposed animals recovered from neutropenia 28 days after exposure, whereas G-CSF- or peg-G-CSF-treated animals recovered 8 to 19 days after exposure (p < 0.05). These results indicate that G-CSF or peg-G-CSF may provide Food and Drug Administration-approved treatments that will reduce the duration of HD-induced neutropenia.

Animals↗
PubMed2005

Nerve agents.

Nerve agents cause a rapidly fatal cholinergic crisis, but rapid, appropriate antidotal treatment saves lives. Survivors of nerve-agent poisoning generally are healthy, unlike survivors of some other chemical agent attacks. Neurologists can assist first responders and mass casualty planners materially by serving as resources for information on nerve agents and the syndromes they cause. They also can help their communities by reinforcing that treatment for nerve-agent poisoning is effective.

Animals↗
PubMed2004

The birth of nerve agent warfare: lessons from Syed Abbas Foroutan.

The author reviewed Farsi-language articles published recently by Dr. Syed Abbas Foroutan, which constitute the only firsthand clinical descriptions of battlefield nerve agent casualties in the world literature, and the author compares his comments with US and North Atlantic Treaty Organization (NATO) chemical casualty care doctrine. Foroutan's lessons learned reassure us that a robust medical evacuation system, coupled with timely and appropriate medical care of nerve agent poisoning, will save many more lives on future battlefields.

Antidotes↗
PubMed2004

Therapy for nerve agent poisoning.

Neurologists need to familiarize themselves with nerve agents, the most toxic of the chemical warfare agents. Their mode of action lies within the nervous system, and nonneurologists will look to neurologists for expert advice on therapy. These agents cause rapid-onset cholinergic crisis amenable to prompt treatment with specific antidotes. Experience on the battlefield and in terrorist attacks demonstrates that therapy saves lives.

Antidotes↗
PubMed2004

Nerve agents: pathophysiology and treatment of poisoning.

Nerve agents, the deadliest of the classical chemical warfare agents, primarily function as acetylcholinesterase inhibitors and cause a rapidly progressive cholinergic crisis. Because of the speed of onset of the syndrome, treatment must be rendered emergently and will most likely be performed by first responders. Neurologists should be familiar with the pathophysiology and treatment of syndromes caused by nerve agents, not only to assist with the hospital care of these patients but also to serve as resources to their local medical communities in preparation for chemical terrorism.

Antidotes↗
PubMed2003

Nerve agent attacks on children: diagnosis and management.

Nerve agents (NAs) are the most lethal chemical weapons. We review the pathophysiology and management of NA poisoning of children. NAs cause cholinergic crisis. Children may manifest signs of cholinergic poisoning differently than adults. Children may be less likely to manifest miosis and glandular secretions. They may present with neurologic derangements alone. The goals of treatment should be to limit additional exposure, to provide respiratory support, and to prevent neurologic morbidity. Autoinjectors are optimal delivery vehicles for intramuscular antidotes and are likely to be used in civilian prehospital care. Antidotes include anticholinergics, oximes, and benzodiazepines. Several medications may be available within each class of antidotes. Clinicians will select an antidote based on the status of the individual victim, the accessibility of supportive care, and the availability of the drug. Atropine is well-tolerated and high doses may be required. The oxime pralidoxime chloride has a longer half-life in children. Currently, diazepam is the standard NA anticonvulsant. Midazolam may be the most effective intramuscular anticonvulsant after NA exposure, but, despite its efficacy, it is not an approved agent for seizures. Supportive care and long-term complications are summarized.

Anticonvulsants↗