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Biomedical subjects

Sam Shuster

Publications and source records attributed to Sam Shuster.

9 recordsLinked to original sources
PubMed2006

Characterization of neuropeptide Y2 receptor protein expression in the mouse brain. I. Distribution in cell bodies and nerve terminals.

Neuropeptide Y (NPY), a 36-amino-acid peptide, mediates biological effects by activating Y1, Y2, Y5, and y6 receptors. NPY neurons innervate many brain regions, including the hypothalamus, where NPY is involved in regulation of a broad range of homeostatic functions. We examined, by immunohistochemistry with tyramide signal amplification, the expression of the NPY Y2 receptor (Y2R) in the mouse brain with a newly developed rabbit polyclonal antibody. Y2R immunoreactivity was specific with its absence in Y2R knockout (KO) mice and in adjacent sections following preadsorption with the immunogenic peptide (10(-5) M). Y2R-positive processes were located in many brain regions, including the olfactory bulb, some cortical areas, septum, basal forebrain, nucleus accumbens, amygdala, hippocampus, hypothalamus, substantia nigra compacta, locus coeruleus, and solitary tract nucleus. However, colchicine treatment was needed to detect Y2R-like immunoreactivity in cell bodies in many, but not all, areas. The densest distributions of cell bodies were located in the septum basal forebrain, including the bed nucleus, and amygdala, with lower density in the anterior olfactory nucleus, nucleus accumbens, caudal striatum, CA1, CA2, and CA3 hippocampal fields, preoptic nuclei lateral hypothalamus, and A13 DA cells. The widespread distribution of Y2R-positive cell bodies and fibers suggests that NPY signaling through the Y2R is common in the mouse brain. Localization of the Y2R suggests that it is mostly presynaptic, a view supported by its frequent absence in cell bodies in the normal mouse and its dramatic increase in cell bodies of colchicine-treated mice.

Animals↗
PubMed2006

NICE work: nice try.

Explore the source record for details and available documents.

Health Care Rationing↗
PubMed2005

Neuropeptide Y2 receptor protein is present in peptidergic and nonpeptidergic primary sensory neurons of the mouse.

The localization of the neuropeptide tyrosine (NPY) Y2 receptor (Y2R) protein was studied in mouse dorsal root ganglia (DRGs) and spinal cord, by using a recently developed rabbit anti-Y2R antibody and a sensitive immunohistochemical method. Y2R-like immunoreactivity (-LI) was observed in about 10% of the small/medium-sized lumbar DRG neurons. Among these, about 44% were calcitonin gene-related peptide-immunoreactive, and about 38% bound isolectin B4. In the dorsal horn of the spinal cord, an intense Y2R-LI was seen in the most superficial layers, mostly restricted to laminae I-II. This immunoreactivity was completely abolished by dorsal rhizotomy. Y2R-L1 was also detected on the skin, more abundantly in hairy than glabrous skin. Specificity experiments showed complete disappearance of the Y2R-LI described above after incubation with antibody preadsorbed with the immunogenic peptide. Furthermore, Y2R-LI was also absent in a Y2R knockout mouse. These results demonstrate that the NPY Y2R is associated mainly with both peptidergic and nonpeptidergic small, presumably nociceptive, neurons projecting to the superficial layers of the dorsal horn. The results also support a role for this receptor and NPY in pain mechanisms.

Animals↗
PubMed2005

Treatment and prophylaxis of seborrheic dermatitis of the scalp with antipityrosporal 1% ciclopirox shampoo.

OBJECTIVE: To demonstrate the efficacy, safety, and tolerance of ciclopirox shampoo for treatment and prophylaxis of seborrheic dermatitis of the scalp. DESIGN: Multicenter, randomized, double-blind, vehicle-controlled study. After treatment with ciclopirox shampoo once or twice weekly or vehicle for 4 weeks (study segment A), responders were randomized to a 12-week prophylactic study arm (segment B). SETTING: Forty-five medical centers in Germany (n = 19), France (n = 15), the United Kingdom (n = 8), and Austria (n = 3). Patients A total of 1000 patients with stable or exacerbating seborrheic dermatitis of the scalp. Interventions A total of 949 patients were randomized to receive ciclopirox treatment once or twice weekly or vehicle for 4 weeks. Thereafter, 428 responders received either ciclopirox prophylaxis once weekly or every 2 weeks or vehicle for 3 months. MAIN OUTCOME MEASURES: Primary and secondary: response of "effectively treated" and "cured," with investigators and patients rating acceptability and tolerance. RESULTS: Ciclopirox twice and once weekly produced response rates of 57.9% and 45.4%, respectively, compared with 31.6% for vehicle. Relapses occurred in 14.7% of patients using prophylactic ciclopirox once weekly, 22.1% of those in the prophylactic group shampooing once every 2 weeks, and 35.5% in the vehicle group. The few adverse events were evenly distributed among groups. Local tolerance and cosmetic acceptability were "good" in more than 85% of subjects. CONCLUSIONS: Seborrheic dermatitis of the scalp responds well to 1% ciclopirox shampoo once or twice weekly for 4 weeks. A low relapse rate is maintained by once-weekly shampooing or shampooing once every 2 weeks. These treatments are safe and well-tolerated.

Adult↗
PubMed2005

Osteoporosis, a unitary hypothesis of collagen loss in skin and bone.

Progress in osteoporosis has been stultified by repetitive, statistic-driven studies and catechistic reviews; in the absence of concept and hypothesis research is aimless, and the trivial associations it continually reveals, has led to the cul-de-sac of multifactorialism. A return to hypothesis-led research which seeks major causal defects and the conclusive therapies that arise from them is essential. The hypothesis proposed evolved from research into the mechanism of senile purpura. This predicted a causal loss of skin collagen that was contrary to contemporary opinion, but was confirmed when collagen was expressed absolutely, instead as a percentage or ratio: women have less collagen than men and it decreases by 1% a year in exposed and unexposed skin. Corticosteroids (which also produce shear purpura) reduce skin collagen and androgen and virilism increase it; growth hormone produces the greatest increase, and there is a decrease in hypopituitarism. All these changes in skin collagen correspond to changes in bone density, and the circumstances are too various for coincidence. This led to the hypothesis that the changes found in skin collagen also occur in bone collagen, leading to the associated changes in bone density; thus a loss of collagen in skin and bones with aging is the causal counterpart to loss of bone density in senile osteoporosis. If this is correct then, as with aging, androgen and virilisation, corticosteroids, growth hormone and hypopituitarism, changes in bone density should correspond to systemic changes in skin collagen. This correspondence is found to occur in osteogenesis imperfecta and Ehlers-Danlos syndrome, two genetically discrete families of disordered collagen production, and other situations, e.g., scurvy and homocystinuria. A primary loss of collagen in osteoporotic bones is an essential prediction of the hypothesis; in fact this loss is well established but, inexplicably, it has been assumed to be secondary to the bone loss. Because of the comparable changes in skin and bones, the hypothesis implies that skin collagen could be used to predict the state of the bones and their response to treatment. It also implies androgen should be an effective treatment of osteoporosis, and growth hormone even more effective (likewise, of course, skin aging). More importantly, skin collagen and the production of collagen by skin fibroblasts could be used for the assay and industrial development of more potent, if not less toxic treatments and prevention of loss of bone (and skin) substance.

Bone and Bones↗
PubMed2005

Two new XPD patients compound heterozygous for the same mutation demonstrate diverse clinical features.

Xeroderma pigmentosum (XP) and Cockayne syndrome (CS) are both rare autosomal recessive disorders with defects in DNA repair. They are usually distinct both clinically and genetically but in rare cases, patients exhibit the clinical characteristics of both diseases concurrently. We report two new phenotypically distinct cases of XP with additional features of CS (xeroderma pigmentosum and Cockayne syndrome crossover syndrome (XP/CS)) carrying an identical mutation (G47R) in the XPD gene within the N terminus of the protein. Both patients had clinical features of XP and CS but only one fulfilled most criteria for diagnosing CS. Unusually, patient 1 developed early skin cancer, in contrast to patient 2, who never developed any malignancies. Cells from both these patients have repair defects typical of xeroderma pigmentosum complementation group D (XPD) cells, but also had the phenotype of uncontrolled DNA breakage found specifically in XPD/CS cells and similarly reduced levels of TFIIH. Despite these similarities between our two patients, their clinical features are quite different and the clinical severity correlates with other cellular responses to ultraviolet irradiation.

Adult↗