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Biomedical subjects

J Dorman

Publications and source records attributed to J Dorman.

16 recordsLinked to original sources

So you want to publish in JACH? How to avoid some potholes and pitfallls and make it into print.

Many college health professionals are intimidated at the thought of submitting an article to the Journal of American College Health. In this article, the editors provide details about the scope of the journal, describe types of articles it publishes, warn about common errors authors sometimes make in writing and submitting manuscripts for publication, and outline the steps in the review process.

Periodicals as Topic

The low prevalence of immunogenetic markers in Korean adult-onset IDDM patients.

OBJECTIVE: IDDM is an autoimmune disease that occurs among genetically susceptible individuals. In Asian populations, it is not uncommon for adult patients with NIDDM to eventually lose beta-cell function and develop IDDM. These individuals may be characterized by autoantibodies to GAD and high-risk HLA-DQ alleles, which are unlikely to be prevalent among patients with true NIDDM or in the general population. The objective of the present study was to evaluate and compare the prevalence of these immunogenetic markers in NIDDM patients and healthy nondiabetic individuals from Korea. RESEARCH DESIGN AND METHODS: The prevalences of anti-GAD antibodies and HLA-DQA1 and DQB1 alleles among 121 patients with newly diagnosed NIDDM identified from a population-based study in Yonchon, Korea, and 100 matched healthy control subjects were evaluated and compared. RESULTS: The overall prevalence of anti-GAD antibodies was 1.7% (2 of 121) in patients with previously undiagnosed NIDDM, whereas 1 of 100 control subjects had a positive test for antibodies. Among those who tested positive, titers of antibodies to GAD were not high. No statistically significant differences in the distributions of either mean levels of anti-GAD antibodies or DQA1 and DQB1 alleles were found comparing NIDDM patients with control subjects. Interestingly, the frequency of DQB1*non-Asp-57 and DQA1*Arg-52 alleles in the Korean adult control population was similar to that in the U.S. white population (DQB1*non-Asp-57: 0.431 vs. 0.475; DQA1*Arg-52: 0.492 vs. 0.463). CONCLUSIONS: The low prevalence of anti-GAD antibodies and HLA-DQA1 and DQB1 susceptibility alleles among recent-onset NIDDM patients, which was similar to observations in control subjects, suggests that diabetes in Korean adults is unlikely to have an autoimmune component to its pathogenesis.

Adult

HLA-DQ screening for risk assessment of insulin dependent diabetes in northern Italy.

Genetic markers may be used to improve the prediction of insulin-dependent diabetes mellitus (type 1) in individuals with islet autoantibodies. In order to develop a risk assessment strategy for the Lombardy region of northern Italy based on genetic and immunological markers, we analyzed HLA DQA1 and DQB1 alleles in 60 type 1 probands and their first-degree relatives and 65 unrelated control subjects from the same area using polymerase chain reaction (PCR) and oligonucleotide probes. The major risk haplotypes were DQA1 *0501-DQB1*0201 (39.1% of diabetic vs. 8.9% of non-diabetic haplotypes) and DQA1 *0301-DQB1*0302(20% of diabetic vs 7.1% of non-diabetic haplotypes). Stratified analysis showed DQA1*0102-DQB1*0502 also to be associated with type 1 susceptibility when found together with DQA1*0501-DQB1*0201 or DQA1*0301-DQB1*0302. One type 1 patient had the type 1-protective DQA1*0102-DQB1*0602 haplotype. Overall, 88% of patients and 20% of unrelated control subjects had either DQA1*0501-DQB1*0201 or DQA1*0301-DQB1*0302 in the absence of DQA1*0102-DQB1*0602. These data suggest that typing for markers identifying these three haplotypes in the Lombardy population will achieve a sensitivity of almost 90% and exclude 80% of children from subsequent islet autoantibody testing.

Adolescent

Plus ça change...?

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Health Care Reform

The history of psychosurgery.

Egas Moniz received the Nobel Prize for Medicine in 1949 for his discovery and popularization of the prefrontal lobotomy. This radical surgery was the product of the progression in our understanding of mental illness, the prevailing attitudes of the times, and the professional rivalry between psychiatrists and neurologists. The prefrontal lobotomy and its modifications, later to be referred to collectively as psychosurgery, offered hope to the mental illness that were previously thought to be incurable. Fueled by "miracle stories" from the popular press, this surgery was performed until the late 1960S. The following article chronicles the early days of psychosurgery, including the factors responsible for its inception and the different techniques used through the years.

History, 20th Century

Radical neck dissection: a subjective and objective evaluation of postoperative disability.

Nearly all patients who undergo radical neck dissection note significant morbidity if the XIth cranial nerve is sacrificed. Physicians can be misled to believe in a lower morbidity because the usual physical examination is unreliable in detecting weakness and because patients rarely persist in mentioning shoulder problems during follow-up visits. Eleven patients between the ages of 55 and 70, who had undergone unilateral neck dissection with sacrifice of the XIth cranial nerve, were given questionnaires and were objectively evaluated for strength and active range of motion on a Cybex II dynamometer. Eighty-two percent of patients experienced pain, 91% experienced weakness, and 91% experienced impairment on the affected side. Peak torque for the affected side ranged between 0 to 85% of the peak torque for the normal shoulder. Gravity-free active range of motions were 20 degrees to 162 degrees with 8 of 11 at 100 degrees or less. In all but two patients, the passive range of motion was limited by pain.

Accessory Nerve

Pharmacological activities of spirogermanium and other structurally related azaspiranes: effects on tumor cell and macrophage functions.

Spirogermanium is a germanium containing azaspirane which has been shown to have activity in experimental models of cancer and immune dysfunction. A series of analogs of the parent compound were synthesized and evaluated in a number of in vitro and in vivo biological assays to define the structure-activity relationships of this class of compounds relative to their potential therapeutic activities. In a colony-forming assay using HT-29 human colon carcinoma cells various analogs in which carbon replaced germanium (e.g. carbon) retained the potent cytotoxic activity in vitro seen with spirogermanium. Increased cytotoxic potency within the group of carbon containing analogs was directly related to increase in the length of the alkyl group(s) attached to the carbon atom opposite the azaspirane ring structure. DNA and protein synthesis by HT-29 cells was inhibited by these compounds. However, inhibition occurred only at supralethal concentrations or after long exposure times with the drug. None of the azaspiranes demonstrated in vivo anti-tumor activity against P388 leukemia or ADJ-PC6 plasmacytoma. The effect of these compounds on macrophage cell function was evaluated in vitro by their ability to modulate superoxide (O2-) production by macrophages. Spirogermanium inhibited the production of O2- by activated macrophages with an IC50 of 5 microM. Although macrophage viability did not appear to be decreased at the respective IC50 concentrations, the rank order potency for the analogs in the O2- production assay was directly proportional to that measured for their cytotoxic potency in the HT-29 colony formation assay. The results demonstrate that, within this class of compounds, (1) potent biological activity does not require the presence of germanium in the structure; (2) in vitro cytotoxic activity does not appear to be a direct result of the inhibition of macromolecular synthesis, and (3) macrophage function can be modulated in vitro at non-cytotoxic concentrations. These results are discussed in context with the reported anti-tumor activity of spirogermanium and the potential anti-arthritic and immunomodulatory activity of this class of compounds.

Animals

Why do children with diabetes die?

While the treatment of children with Type I diabetes mellitus has dramatically improved since the introduction of insulin in 1922, significant acute mortality still remains. To better ascertain the causes of death in younger children and adolescents with diabetes mellitus, a retrospective review was undertaken of diabetes associated mortality in the patient population followed at the Children's Hospital of Pittsburgh between the years 1950 and 1985. Fifty-five deaths were identified of which 20 occurred during the initial presentation of diabetes and 35 occurred between 2 months and 11 years following the diagnosis of diabetes mellitus. Diabetic ketoacidosis (DKA) was associated with 64% of the total mortality with 85% of the early onset and 54% of the late onset deaths being ketoacidosis related. Of these ketoacidosis associated deaths, cerebral edema was documented in 31%, or 20% of the total group mortality. Non ketoacidosis deaths in both early and late onset groups were caused by heterogeneous events. There were no deaths associated with the traditional late vascular complications of diabetes mellitus. Since diabetic ketoacidosis is a potentially preventable acute complication of diabetes mellitus and represented a predominant cause of mortality in these children, early recognition and prompt treatment might substantially reduce childhood mortality in patients with Type I diabetes mellitus.

Adolescent

Correlates of insulin antibodies in newly diagnosed children with insulin-dependent diabetes before insulin therapy.

Insulin antibodies, as measured by plasma radiolabeled insulin-binding capacity, were determined in 124 newly diagnosed insulin-dependent diabetic (IDDM) children before and after 1, 3, and 5 days of insulin therapy. Controls were 35 nondiabetic children with plasma insulin binding capacity of 1.0 +/- 0.7%. The patients were divided into three groups according to their plasma insulin-binding capacity. Group 1 (N = 79) had binding within two standard deviations (SD) of the control mean, group 2 (N = 20) had insulin binding 2-6 SD above controls, and group 3 (N = 25) showed insulin-binding capacity of more than 6 SD above the control mean. After exogenous insulin therapy, plasma 125I-insulin-binding capacity dropped significantly in both groups 2 and 3, concurrent with significant increases in plasma insulin levels. The three groups differed from each other in that patients in group 3 were significantly younger than in the other groups and clinically seemed to be more severely dehydrated, as reflected in their higher levels of serum urea nitrogen, plasma glucose, potassium, and elevated pulse rate. The three groups did not differ in respect to sex, HLA-DR antigens, Coxsackie-B antibody titers, islet cell cytoplasmic antibodies, immunoglobulin level, and C-peptide levels. Only two of 446 siblings of IDDM children showed elevated insulin binding, one of whom developed IDDM 6 wk later. The presence of an insulin-binding substance probably representing insulin antibodies in some cases of newly diagnosed IDDM suggests that autoimmunity in this disorder is not limited to the B-cell membrane and cytoplasm and lends further support to the heterogeneity of IDDM.

Adolescent

Hepatitis Bs antigen and liver cancer: A population based study in Kenya.

Peers and Linsell (1973) demonstrated a significant association between the incidence of primary liver cancer and ingested aflatoxin in a study in the Muranga district of Kenya. A study of hepatitis B antigen in the same district showed no significant differences between the low altitude area, with a relatively high incidence of primary liver cancer, and the high altitude area with a lower incidence of the tumour. Current evidence is more in favour of aflatoxin playing an important role in the aetiology of primary liver cancer but hepatitis B antigen may play an ancillary role.

Adolescent