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Biomedical subjects

K Robbins

Publications and source records attributed to K Robbins.

At least 19 recordsLinked to original sources
PubMed2001

Early thyrotoxic thyroiditis after radiotherapy for tonsillar carcinoma.

Thyroiditis with hyperthyroidism is a recognized early complication of intrathyroidal irridiation by orally ingested radiolabeled iodine I 131, but has seldom been described following external delivery of radiotherapy to the thyroid bed. We treated a man who was initially seen with a clinical picture suggestive of hyperthyroidism after receiving a course of radiotherapy for tonsillar carcinoma. Laboratory studies and thyroidal radioiodine uptake confirmed the diagnosis of thyrotoxic thyroiditis, having onset within 2 weeks of completion of the course of radiotherapy. The literature concerning thyroiditis and thyroid function following external beam radiotherapy is reviewed. Because several of the clinical features of thyrotoxic thyroiditis may resemble those resulting from the cancer under treatment or complications of its therapy, we recommend evaluation of thyroid function at the conclusion of the course of radiotherapy and 2 weeks thereafter to exclude this self-limited and treatable cause of weight loss.

Carcinoma, Squamous Cell↗
PubMed2001

Primary care physicians' experience with mental health consultation.

A total of 684 primary care physicians in Wisconsin participated in a survey designed to explore their experiences of consulting with and referring patients to mental health care professionals. The respondents indicated that they had only moderate access to mental health care professionals, and even less access when a patient was covered by Medicare or Medicaid or had no insurance. Physicians in group practices that included at least one mental health professional reported having better access to care than those in practices that did not include mental health services. Perceived access to mental health care services was not related to community size or to a managed care setting.

Communication↗
PubMed2000

Human immunodeficiency virus (HIV) subtype surveillance of African-born persons at risk for group O and group N HIV infections in the United States.

A population-based surveillance registry was used to identify human immunodeficiency virus (HIV)-infected persons in the United States at increased risk for group O and group N infections (those born in or near African countries where group O infection has been reported). Of 155 eligible subjects, 37 gave samples. By phylogenetic and serologic analysis, 32 were infected with group M (16 with subtype A, 5 with B, 7 with C, and 1 each with subtypes D, F2, G, and recombinant A/J) and 2 with group O but none with group N virus. For 3, samples could not be typed by serology or amplified by polymerase chain reaction using group M-, O-, or N-specific primers. In the United States, group O HIV infection is uncommon; no case of group N infection was found. African-born persons may have HIV strains typical of their birth country. Ongoing subtype surveillance may allow early identification of novel or emerging HIV strains.

Adult↗
PubMed2000

The Cochrane Library: a resource for current reviews of clinical evidence.

The Cochrane Library is a tool for physicians and other health care practitioners seeking evidence to inform their decisions. The systematic reviews provide a high-quality synthesis of the current literature, saving time for busy people. To make the library more user-friendly, the collaboration plans to produce a consumer summary for each topic in the Database of Systematic Reviews and a cancer library aimed at the general public. In contrast to some of the questionable health-related resources on the Web, the Cochrane Library is an authoritative reference that can help physicians with everyday treatment decisions. The collaboration's commitment to keeping its resources up to date through vigorous support of reviewers should ensure that it remains a valuable Internet tool for physicians.

Databases as Topic↗
PubMed1999

Two outbreaks of multidrug-resistant Salmonella serotype typhimurium DT104 infections linked to raw-milk cheese in Northern California.

CONTEXT: Salmonella serotype Typhimurium definitive type 104 (DT104), with resistance to 5 drugs (ampicillin, chloramphenicol, streptomycin, sulfonamides, and tetracycline), has emerged as the most common multidrug-resistant Salmonella strain in the United States. However, illnesses resulting from this strain have not been associated definitively with a source in this country. OBJECTIVE: To determine the source of 2 outbreaks of Salmonella Typhimurium DT104. DESIGN: Matched case-control study conducted between March 24 and April 5, 1997 (outbreak 1), enhanced surveillance for new cases dating from February 1, 1997 (outbreak 2), and environmental and laboratory investigations. SETTING AND PARTICIPANTS: The case-control study included residents of 2 adjacent counties in northern California infected with the outbreak strain of Salmonella Typhimurium var Copenhagen and age-matched controls. For enhanced surveillance, a case was defined as Salmonella Typhimurium infection in a person exposed to fresh Mexican-style cheese. MAIN OUTCOME MEASURES: Risk factors for infection and source of implicated food. RESULTS: Outbreak 1 peaked in February 1997; 31 patients were confirmed by culture as having Salmonella Typhimurium var Copenhagen infection, isolates of which showed indistinguishable pulsed-field gel electrophoresis (PFGE) patterns. The outbreak strain was phage type DT104 with the 5-drug resistance pattern. Sixteen cases and 25 controls were enrolled in the case-control study; 15 of 16 Salmonella Typhimurium var Copenhagen cases compared with 14 of 24 matched controls reported eating unpasteurized Mexican-style cheese, (matched odds ratio, 7.9; 95% confidence interval, 1.1-354.9). Enhanced surveillance uncovered outbreak 2, which peaked in April 1997 and was caused by a non-Copenhagen variant of Salmonella Typhimurium. During outbreak 2, Salmonella Typhimurium was isolated from 79 persons who ate fresh Mexican-style cheese from street vendors and from cheese samples and raw milk. The PFGE pattern of the milk isolate matched 1 of the 3 patterns recovered from patients; all strains were phage type DT104b with the 5-drug resistance pattern. CONCLUSION: Raw-milk products pose a risk for multidrug-resistant Salmonella Typhimurium DT104 infections.

Adolescent↗
PubMed1998

Time course of ADCw changes in ischemic stroke: beyond the human eye!

BACKGROUND AND PURPOSE: Using newly developed computerized image analysis, we studied the heterogeneity of apparent diffusion coefficient of water (ADCw) values in human ischemic stroke within 10 hours of onset. METHODS: Echo-planar trace diffusion-weighted images from 9 patients with focal cortical ischemic stroke were obtained within 10 hours of symptom onset. An Iterative Self-Organizing Data Analysis (ISODATA) clustering algorithm was implemented to segment different tissue types with a series of DW images. ADCw maps were calculated from 4 DW images on a pixel-by-pixel basis. The segmented zones within the lesion were characterized as low, pseudonormal, or high, expressed as a ratio of the mean+/-SD of ADCw of contralateral noninvolved tissue. RESULTS: The average ADCW in the ischemic stroke region within 10 hours of onset was significantly depressed compared with homologous contralateral tissue (626.6+/-76.8 versus 842.9+/-60.4x10(-6) mm2/s; P<0.0001). Nevertheless, ISODATA segmentation yielded multiple zones within the stroke region that were characterized as low, pseudonormal, and high. The mean proportion of low:pseudonormal:high was 72%:20%:8%. CONCLUSIONS: Despite low average ADCW, computer-assisted segmentation of DW MRI detected heterogeneous zones within ischemic lesions corresponding to low, pseudonormal, and high ADCw not visible to the human eye. This supports acute elevation of ADCw in human ischemic stroke and, accordingly, different temporal rates of tissue evolution toward infarction.

Acute Disease↗
PubMed1998

Phase III trial of modulation of cisplatin/fluorouracil chemotherapy by interferon alfa-2b in patients with recurrent or metastatic head and neck cancer. Head and Neck Interferon Cooperative Study Group.

PURPOSE: In preclinical experiments, interferon alfa modulates the anticancer activity of fluorouracil (5-FU) and cisplatin (CDDP). To test this effect clinically in patients with recurrent or metastatic head and neck cancer (RMHNC), a multicenter randomized controlled trial with CDDP and 5-FU with or without interferon alfa-2b (IFNalpha) was performed. PATIENTS AND METHODS: Eligible patients had histologically confirmed RMHNC; a good performance status; measurable disease; adequate bone marrow, hepatic, and renal function; no prior chemotherapy for recurrent or metastatic disease; only one chemotherapy regimen administered with previous local therapy; and a treatment-free interval of at least 3 months following previous local therapy. Patients were randomized and stratified according to treatment center, and prior radiotherapy and chemotherapy. The treatment regimen consisted of CDDP 100 mg/m2 on day 1 and 5-FU 1,000 mg/m2/d by continuous infusion for 96 hours (days 1 to 4), without (arm A) or with (arm B) IFNg alpha 3 x 10(6) U/d subcutaneously on days 1 to 5. Cycles were repeated every 21 days. RESULTS: One hundred twenty-two patients were entered on each arm. The response rate (RR) was similar in both arms (arm A: complete response [CR] 10.7%, partial response [PR] 36.4%; arm B: CR 6.8%, PR 31.6%) (.70 < P < .50). There was no difference in median survival between the two arms (arm A 6.3 months v arm B 6.0 months; P = .49). Anorexia, fever, leukopenia, and thrombocytopenia grade III to IV were significantly more frequent in the IFNalpha arm. CONCLUSION: Modulation of CDDP and 5-FU with IFNalpha as used in this study does not improve the RR or the median survival in patients with RMHNC. Patients on both study arms had a poor prognosis, which indicates the need for novel therapies.

Adult↗
PubMed1994

Anti-immunoglobulin E treatment decreases worm burden and egg production in Schistosoma mansoni-infected normal and interferon gamma knockout mice.

The immunoglobulin E (IgE) response is generally considered an essential component of the host defense against parasitic helminths such as Schistosoma mansoni. In contrast, work on antischistosome vaccines suggests that interferon gamma (IFN-gamma) is the critical immune mediator for vaccine-induced immunity to the parasite. In this study, the total IgE response to a primary S. mansoni infection was suppressed by anti-IgE treatment in both normal mice and in mice with defective IFN genes (gene knockout [GKO]). Reduction of the IgE response resulted in decreased worm burden and a decrease in the number of eggs produced per worm in both normal and GKO mice. Whereas anti-IgE treatment also resulted in reduced hepatosplenomegaly, granulomas around existing schistosome eggs showed normal cellularity. Serum interleukin 4 levels fell in response to the reduction in serum IgE as well. The data suggest that IgE plays a detrimental, rather than beneficial, role for the host in schistosomiasis. Furthermore, the absence of IFN-gamma was found to be of little consequence to the host-response to adults or eggs in a primary schistosome infection.

Animals↗
PubMed1994

Reference accuracy in the dermatologic literature.

BACKGROUND: The reference list is an important part of a scientific article. To be useful it must be accurate. OBJECTIVE: The purpose of this study was to evaluate the accuracy of references in the dermatologic literature. METHODS: We randomly selected 240 references (60 per journal) from the Archives of Dermatology, the British Journal of Dermatology, this Journal, and the Journal of Investigative Dermatology and checked them against the original articles. RESULTS: The overall rate of citation error (the information identifying the source) was 41%, and the quotation error (inconsistency between the statement referenced and the original source) was 35%. Only 36% of references were free of error. CONCLUSION: This study shows that the rate of citation and quotation errors is unacceptably high in the dermatologic literature, which significantly diminishes the value of the reference list.

Bibliometrics↗
PubMed1994

Immunological effects of insulin-like growth factor-I--enhancement of immunoglobulin synthesis.

In addition to its activity as a metabolic hormone and a regulator of somatic growth, insulin-like growth factor-I (IGF-I) has cytokine-like activities on lymphoid cells. A 14-day infusion of recombinant human (rh)IGF-I increased lymphocyte numbers in all the peripheral lymphoid organs examined. This increase was apparent for up to 3 weeks following cessation of hormone treatment. A second administration of rhIGF-I, given when the lymphocyte numbers in the rhIGF-I-treated mice had returned to control values, resulted in similar increases in the peripheral T and B cell populations. This increase in lymphocyte numbers had functional significance, since rhIGF-I-treated mice produced elevated antibody titres following primary or secondary antigen challenge compared with controls. In addition, when rhIGF-I-treated mice were immunized with a suboptimal dose of antigen they produced antibody titres which were equivalent to those generated by immunization with optimal doses of antigen. When examined in vitro, addition of rhIGF-I alone to cultures of splenocytes from antigen-primed mice stimulated immunoglobulin synthesis. These studies suggest that IGF-I produced locally by thymic and bone marrow stromal cells may be a natural component of B and T cell lymphopoiesis.

Animals↗
PubMed1994

Administration of an anti-IgE antibody inhibits CD23 expression and IgE production in vivo.

High IgE responder BDF1 mice were immunized intraperitoneally (i.p.) with dinitrophenol4 (DNP4)-ovalbumin (OVA) in alum concomitant with intravenous (i.v.) administration of an anti-IgE monoclonal antibody (mAb). IgE levels were undetectable in mice treated with the anti-IgE antibody, whereas mice treated with isotype-matched irrelevant mAb had IgE levels comparable to that of untreated, immunized mice. Subsequent antigen challenges with DNP4-OVA, either at weekly or monthly intervals, failed to evoke an IgE response for greater than 2 months in mice treated with anti-IgE during the primary sensitization, even though the terminal half-life of the anti-IgE antibody was 7 days. This inhibition was specific for DNP4-OVA since the DNP4-OVA-suppressed mice were able to respond to keyhole limpet haemocyanin (KLH). To investigate the effects of antibody treatment at the cellular level, passive transfer experiments were performed. The primary DNP-specific IgE response of adoptive transfer recipient mice was the same whether the donor cells were from mice treated with IgG or anti-IgE. Transfer of enriched T- or B-cell populations indicated that T-cell help was not compromised by administration of the anti-IgE mAb. However, splenocytes from the anti-IgE-treated mice failed to synthesize IgE in vitro, and flow cytometric analysis of B cells from anti-IgE-treated mice showed a dose-dependent decrease in CD23+ cells following antibody treatment, which correlated with decreased serum IgE levels. Taken together, the results of these studies suggest that anti-IgE treatment suppresses IgE responses via effects on B cells rather than T cells, possibly through effects on CD23-dependent pathways.

Animals↗
PubMed1993

Human IgE receptor alpha-chain IgG chimera blocks passive cutaneous anaphylaxis reaction in vivo.

Cross-linking of the high affinity IgE receptor (Fc epsilon RI) expressed on mast cells and basophils is essential for triggering anaphylaxis in vivo. Previously, other investigators have tried to produce competitive inhibitors using IgE peptide analogues and anti-IgE antibodies with limited success. To create a novel specific inhibitor of IgE that can block binding of IgE to Fc epsilon RI without the capacity to stimulate degranulation, we made an Fc epsilon RI-IgG immunoadhesin. The Fc epsilon RI-IgG was constructed by gene fusion of the extracellular portion of the human alpha-chain of Fc epsilon RI, which contains the high affinity binding site for IgE, with a truncated human IgG1 H chain C region. The Fc epsilon RI-IgG recognizes both human and murine IgE. Coincubation of Fc epsilon RI-IgG with murine IgE prevented sensitization of RBL-2H3 cells and the subsequent histamine release in response to anti-IgE. Similarly, when the Fc epsilon RI-IgG was preincubated with equimolar concentrations of either hyperimmune mouse sera or purified mouse IgE, it completely blocked the passive cutaneous anaphylaxis reaction in rats. Furthermore, i.v. administration of Fc epsilon RI-IgG following intracutaneous injection of serum from DNP-immunized mice was able to block the passive cutaneous anaphylaxis reaction in a time-dependent fashion. These results demonstrate that Fc epsilon RI-IgG is a potent inhibitor of IgE binding to intracutaneous mast cells in vivo and may prove clinically useful for the treatment of IgE-mediated disease.

Amino Acid Sequence↗
PubMed1993

Activin induces cell death in hepatocytes in vivo and in vitro.

While studying endocrine responses to activin in female rats, we discovered that activin caused a marked reduction in liver mass. The regressed livers exhibited no gross signs of necrosis or infarction, but histopathological evaluation revealed extensive cell death in the centrilobular regions. The dying cells appeared to fragment into structures resembling apoptotic bodies. Liver mass and histological appearance were restored after cessation of activin infusion, indicating that on an organ level, this effect was reversible. To determine whether the effects observed in vivo were caused by direct actions on the liver, we then tested activin on isolated hepatocytes in serum-free medium. Under these conditions, activin caused many hepatocytes to undergo fragmentation, which was accompanied by a loss of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-reducing activity, an index of viability. We compared the effects of activin with those of transforming growth factor-beta because activin is structurally related to transforming growth factor-beta and because transforming growth factor-beta has been shown previously to induce cell death in hepatocytes. Both proteins caused cell death of comparable magnitude, as defined by the extent of loss of MTT-reducing activity, but transforming growth factor-beta was active at one tenth of the effective activin concentrations. A neutralizing monoclonal antibody to transforming growth factor-beta blocked the response to transforming growth factor-beta but had no effect on the response to activin. Conversely, follistatin, an activin-binding protein, blocked the response to activin but not to transforming growth factor-beta. Inhibin, which antagonizes the effects of activin in many systems, had little effect on the response to activin. Activin and transforming growth factor-beta differed in their onset of action; exposure to transforming growth factor-beta for only 1 hr induced a maximal response, whereas maximal response to activin required its continuous presence for 24 hr. These results show a novel effect of activin on cell death in hepatocytes in vivo and in vitro, suggesting that activin may have a previously unrecognized role in regulating hepatic function.

Activins↗
PubMed1993

Insulin-like growth factor-1 stimulation of lymphopoiesis.

We show that treatment of adult mice with recombinant human insulin-like growth factor 1 (rhIGF-1) induces striking modifications in lymphocyte number and function. 9-mo-old male mice received rhIGF-1 (4 mg/kg per d) or its excipient by subcutaneous infusion from osmotic minipumps for 7 or 14 d. Mice were weighed daily and bled at sacrifice; the spleen and thymus were harvested and single cell suspensions were made for analysis of cell phenotype and cell number. The responses of splenocytes to mitogens (concanavalin A, lipopolysaccharide, and pokeweed mitogen), alloantigens and dinitrophenyl ovalbumin were measured. After either 7 or 14 d of treatment, rhIGF-1 had an overall whole-body anabolic effect, resulting in increased body and organ weights with prominent increases in the weight of the spleen and thymus. Furthermore, the rhIGF-1 treated mice were normoglycemic but had reduced blood urea nitrogens, again reflecting the anabolic activity of rhIGF-1. The increased spleen and thymus weights were associated with a large increase in the number of lymphocytes in both organs. In addition to an increase in T cells, specifically CD4+ T cells, a dramatic increase in splenic B cells was also observed. This increase was accompanied by an enhanced responsiveness to dinitrophenyl ovalbumin resulting in increased immunoglobulin production. However, despite the increases in cellularity, there was a decrease in the in vitro responses of spleen cells to mitogens after 7 d of rhIGF-1 treatment. In contrast, treatment with rhIGF-1 for 14 d increased both the cell number and mitogenic responses of splenocytes suggesting that some time is required for the cells populating the peripheral organs to gain mitogenic responsiveness. It is clear from these data that rhIGF-1, at doses that have whole-body anabolic activity, can expand cell number in lymphoid tissue in a normal adult mouse. These dual effects of rhIGF-1, of increasing lymphocyte number and activity, indicate that, in a normal adult animal, rhIGF-1 can cause major changes in lymphoid tissues that are of potential benefit to the functioning of the immune system.

Animals↗