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Biomedical subjects

C Mueller

Publications and source records attributed to C Mueller.

At least 127 records · Page 7Linked to original sources
PubMed1995

Under-eating and over-eating concerns among adolescents.

462 adolescents were given a set of scales to determine their concerns about eating (under-eating or over-eating), and perceptions of family and peer intimacy, social support, self-esteem, depression and exercise. Although only 10% stated that they were "underweight" and 21% that they were "overweight", as many as 50% reported having eating concerns. As compared to those who did not have concerns about eating, those who were concerned about undereating felt that they had poorer relationships with their mothers and fathers, less social support, lower self-esteem and low levels of exercise. In contrast, those who were concerned about overeating perceived having an intimacy problem only with their fathers. Like those concerned about undereating, the group concerned about overeating also had lower self-esteem and low levels of exercise. But, unlike the under-eating concern group, the over-eating concern group scored higher on the depression scale.

Adolescent↗
PubMed1995

Cloning the gene for the heat shock response positive regulator (sigma 32 homolog) from Pseudomonas aeruginosa.

A 31 base pair synthetic oligonucleotide based on the genes for the Escherichia coli heat shock sigma factor (rpoH) and the Pseudomonas aeruginosa housekeeping sigma factor (rpoD) was employed in conjunction with the Tanaka et al. (K. Tanaka, T. Shiina, and H. Takahashi, 1988. Science (Washington, D.C.), 242: 1040-1042) RpoD box probe to identify the location of the rpoH gene in P. aeruginosa genomic digests. This gene was cloned into plasmid pGEM3Z(f+), sequenced, and found to share 67% nucleotide identity and 77% amino acid homology with the rpoH gene and its product (sigma 32) of E. coli. The plasmid containing the rpoH gene complemented the function of sigma 32 in an E. coli rpoH deletion mutant. Furthermore, this plasmid directed the synthesis of a 32-kDa protein in an E. coli S-30 in vitro transcription-translation system. Primer extension studies were used to identify the transcriptional start sites under control and heat-stressed (45 and 50 degrees C) conditions. Two promoter sites were identified having sequence homology to the E. coli sigma 70 and sigma 24 consensus sequences.

Amino Acid Sequence↗
PubMed1995

Regulation of medical foods: toward a rational policy.

Medical foods are enterally administered formulas used as complete or supplemental nutrition support in the treatment of diseases and clinical disorders of hospitalized or incapacitated adult patients. Because clinical trials have failed to demonstrate a consistent benefit of these products on morbidity and mortality rates, it has been difficult to reach consensus on their primary role. Are medical foods components of supportive care or should they be considered pharmacologic treatment? To date, the US Congress has defined medical foods, but the Food and Drug Administration has not developed regulatory statutes for them beyond those designed to ensure the sanitary manufacture of all processed foods. Before effective regulations can be developed, medical foods need to be defined further in order to distinguish them from each other and from other classes of nutritional products such as parenteral nutrients or infant formulas. Because we believe that the role of medical foods is in supportive care rather than pharmacologic therapy, we argue that these products should be subject to regulations similar to those that apply to conventional foods.

Enteral Nutrition↗
PubMed1995

Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates.

Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. These numbers gradually increased in the intra-islet infiltrates from day 14 through day 30 after adoptive transfer. Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. The effects of the observed enhanced TNF expression upon the pathogenesis of trIDDM are as yet unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Organizational response to adolescent HIV risk.

Using semi-structured interviews, the present study examined organizational responses to adolescent HIV risk in an urban Honolulu community. All 23 health, social service, and educational organizations studied have been impacted by HIV. However, the overall organizational response has been compartmentalized and limited. Recommendations concerning improved organizational responses are provided.

Adolescent↗
PubMed1995

Oculomotor abnormalities in Dyssynergia cerebellaris myoclonica.

In 1921 Ramsay-Hunt first described the syndrome of dyssynergia cerebellaris myoclonica (DCM), characterized by the clinical triad of action myoclonus, progressive ataxia and epilepsy with cognitive impairment, subsequently also referred to as the "Ramsay-Hunt syndrome". The cause of the symptoms of this rare degenerative syndrome (incidence: 500,000) is the impairment of a regulatory mechanism between nucleus dentatus, nucleus ruber and the bulbar olive. We present two sisters, aged 29 and 30 years, who were investigated for oculomotor abnormalities. The patients were diagnosed as having DCM according to clinical symptomatology, which was confirmed by neurophysiological and radiological findings. In both cases saccadic velocity was markedly reduced, whereas saccadic latency showed a significant increase. In addition, smooth pursuit eye-movements were abnormal and presented reduced gain. These findings suggest that pontine areas and the vestibulocerebellum also seem to be affected in DCM.

Adult↗
PubMed1994

GATA-4/5/6, a subfamily of three transcription factors transcribed in developing heart and gut.

We describe experiments which show that: 1) two previously identified members of the GATA family of transcription factors (both of which were originally called GATA-4) correspond to chicken cDNAs for two distinct factors (which we now refer to as cGATA-4 and cGATA-5); 2) another new member of this family corresponds to a third factor designated cGATA-6; 3) each of these mRNAs displays a differential expression pattern. The cGATA-5 gene is initially transcribed in the cardiac crescent prior to formation of the primordial heart tube. Following formation of the primitive heart, cGATA-5 transcripts are evident in both endocardium and myocardium as well as in other lateral plate derivatives. The cGATA-5 gene is also transcribed in the primitive embryonic gut and in late stage embryos is sequentially up-regulated in distinct segments of gastrointestinal epithelia as they undergo terminal differentiation. These studies thus provide novel insights into tissue-specific regulation by GATA-5, as well as into possibly overlapping regulatory functions for these three family members.

Animals↗
PubMed1994

Localized expression of mRNA for phagocyte-specific chemotactic cytokines in human periodontal infections.

In bacterial infections, mononuclear and polymorphonuclear phagocytes are key components of host defenses. Recent investigations have indicated that chemokines are able to recruit and activate phagocytes. In particular, interleukin-8 (IL-8) attracts polymorphonuclear leukocytes (PMNs), while monocyte chemoattractant protein-1 (MCP-1) is selective for cells of the monocyte/macrophage lineage. In this investigation, we analyzed the in situ expression of IL-8 and MCP-1 mRNAs in human periodontal infections. Specific mRNA was detected by in situ hybridization using 35S-labeled riboprobes in frozen tissue sections. Phagocytes (PMNs and macrophages) were specifically detected as elastase-positive or CD68+ cells by a three-stage immunoperoxidase technique. Results indicated that expression of phagocyte-specific cytokines was confined to selected tissue locations and, in general, paralleled phagocyte infiltration. In particular, IL-8 expression was maximal in the junctional epithelium adjacent to the infecting microorganisms; PMN infiltration was more prominent in the same area. MCP-1 was expressed in the chronic inflammatory infiltrate and along the basal layer of the oral epithelium. Cells of the monocyte/macrophage lineage were demonstrated to be present in the same areas. The observed expression pattern may be the most economic way to establish a cell-type-selective chemotactic gradient within the tissue that is able to effectively direct polymorphonuclear phagocyte migration toward the infecting microorganisms and modulate mononuclear phagocyte infiltration in the surrounding tissues. This process may optimize host defenses and contribute to containing leukocyte infiltration to the infected and inflamed area, thus limiting tissue damage.

Antigens, CD↗
PubMed1994

Expression of interleukin-8 gene in inflammatory bowel disease is related to the histological grade of active inflammation.

Interleukin-8 (IL-8) is a potent cytokine for recruitment and activation of neutrophils. To visualize its distribution in the intestinal mucosa and to understand better its possible role in the induction and promotion of inflammatory bowel disease, expression of the IL-8 gene was analyzed in resected bowel segments of 14 patients with active Crohn's disease or ulcerative colitis. In situ hybridization with IL-8 anti-sense RNA probes revealed strong and specific signals in the histologically affected mucosa. The number of cells expressing IL-8 gene correlated with the histological grade of active inflammation. In accordance with the characteristic histological signs of active disease, IL-8-expressing cells were diffusely distributed over the entire affected mucosa in patients with ulcerative colitis, whereas in patients with Crohn's disease, IL-8-expressing cells showed a focal distribution pattern. Cells expressing IL-8 were mainly located at the base of ulcers, in inflammatory exudates on mucosal surfaces, in crypt abscesses, and at the border of fistulae. Analysis of semi-serial sections pointed to macrophages, neutrophils, and epithelial cells as possible sources of this cytokine in active inflammatory bowel disease. We consistently failed to detect IL-8 messenger RNA in the mucosa of uninvolved bowel segments and in normal-appearing control mucosa of patients with colon cancer. In contrast, tissue specimens from two patients with acute appendicitis displayed IL-8-expressing cells in the mucosa. These results support the notion that IL-8 plays and important but nonspecific role in the pathogenesis of inflammatory bowel disease and that the production of IL-8 messenger RNA is restricted to areas with histological signs of inflammatory activity and mucosal destruction.

Adult↗
PubMed1993

Perforin and tumor necrosis factor alpha in the pathogenesis of experimental allergic encephalomyelitis: comparison of autoantigen induced and transferred disease in Lewis rats.

A cell-mediated cytotoxic reaction is believed to be involved in inflammatory lesion formation of experimental allergic encephalomyelitis (EAE). We compared EAE diseased animals which had either been immunized with myelin basic protein (MBP) or adoptively received MBP specific T-cell lines in order to study whether the different courses of disease induction are reflected by quantitative or qualitative differences in the expression of genes encoding putative mediators of tissue damage, i.e. TNF alpha, and the pore-forming protein perforin. With the appearance of signs of paralysis, both genes are induced in cells within the CNS lesions, whereas drastically reduced numbers of TNF alpha- and perforin gene-expressing cells are observed during recovery, despite the presence of high numbers of mononuclear cells in the CNS. Marked differences, however, exist in the gene expression profiles: during the phase of most severe clinical signs TNF alpha expressing cells are 2 to 3 times more frequent in transferred than immunized animals. In animals with MBP-induced EAE the number of perforin expressing cells represents only 1.6% of the IL2R gene expressing cells, while this fraction represents 25% in mice which received autoaggressive T cells. Thus, the presence of a high number of activated killer cells may accelerate tissue damage and progression of disease in passive EAE whereas in actively induced EAE activation of regulatory mechanisms induced by polyclonal activation after immunization may prevent generation of large amounts of activated cytotoxic T cells.

Animals↗
PubMed1993

Inhibition of angiogenesis by somatostatin and somatostatin-like compounds is structurally dependent.

We have previously demonstrated that somatostatin analogues SMS 201-995 and RC-160 inhibit angiogenesis using the chorioallantoic membrane (CAM) of the developing chicken embryo. In this study, we evaluated the ability of native somatostatin 14 and nine somatostatin analogues to inhibit angiogenesis. Two-millimeter methylcellulose disks containing 50 micrograms of somatostatin or somatostatin analogue were implanted on the CAM of 6- to 7-day-old shell-less chick embryos. Inhibition of blood vessel growth was visually assessed and graded in the region of the disk 24-36 hr following implementation. The analogues SMS 201-995 and RC-160 showed statistically significant inhibition of neovascularization when compared to native somatostatin 14. The amino acid homology comparison of the nine analogues revealed that individual differences in their abilities to inhibit angiogenesis may be structurally dependent.

Animals↗
PubMed1993

Differences in heavy chain amino acid sequences affecting the specificity of antibodies for variants of cytochrome c.

In a previous study [Goshorn et al. (1991) J. biol. Chem. 266, 2134-2142], several mAb specific for the same region on different cytochromes c were shown to have similar H or L chains. To determine the effect of differences in individual chains on antigenic variant specificity in the present study, chimeric mAb were prepared by recombining the H and L chains of mAb having the same or a different cytochrome c specificity. The H and L chains of two mAb to the region around residue 60 on horse cytochrome c (1F5.D1 and 2E5.G10) were functionally interchangeable even though the H chain differed by 11 amino acid residues in the complementarity-determining regions (CDR) and 15 amino acids overall in the variable regions. The L chains only differed by four amino acid residues in the CDR (five residues overall). Neither the H nor L chain of a mAb binding the same region of rat cytochrome c (6H2.B4) was functionally interchangeable with the chains of the two horse cytochrome c-specific mAb. The L chain of this mAb is very different from the other L chains which were derived from a different V kappa family, but the H chain is nearly as similar to the horse cytochrome c-specific H chains as they are to each other. Most of the differences occur in CDR3 and result from the use of a distinct DH segment. The results indicate that, in some cases, the specificity of a mAb for a particular variant of a protein Ag, at least in regard to the H chain, is determined by only a few amino acid differences. The differences in the sequences of the H chains of the three mAb in this study and in the structures of their specific Ag provide insight into a possible molecular basis for the specificity of these mAb.

Amino Acid Sequence↗
PubMed1993

The effect of cyclosporine treatment on the expression of genes encoding granzyme A and perforin in the infiltrate of mouse heart transplants.

Following activation of cytotoxic T cells and NK cells several genes encoding proteins putatively involved in cell-mediated cytotoxicity become expressed. The expression of genes encoding the cytotoxic T cell associated serine protease granzyme A and perforin was analyzed in cellular infiltrates of MHC mismatched (H-2d-->H-2k) heterotopic heart transplants both in immunosuppressed recipients treated with cyclosporine and in untreated recipients. Heart transplants were completely rejected by untreated animals on day 10 post-transplantation, whereas CsA treatment generally prolonged survival of the transplants beyond 30 days. In untreated recipients the number of granzyme A- and perforin-expressing cells in heart transplants increased from approximately 10 granzyme A-positive cells/mm2 and 1 perforin-positive cell/mm2 on day 2 posttransplantation to over 80 positive cells for both genes on day 5 posttransplantation. In contrast, these values remained always below 15 positive cells/mm2 for both genes between day 5 and day 30 posttransplantation in CsA-treated recipients. Comparison of the frequency of CD8+ T cells in the infiltrates showed that lower numbers of perforin and granzyme A-positive cells were mainly due to the immunosuppressive action of CsA rather than to reduced infiltration of transplants. The present study shows that expression of granzyme A and perforin gene can be used to discriminate between quiescent and activated cytotoxic cells also in immunosuppressed animals and further confirms that these can be used as sensitive markers for monitoring the fate of a transplant.

Animals↗
PubMed1993

Transient bilateral internuclear ophthalmoplegia after minor head-trauma.

Following minor occipital head-trauma, a six-year-old boy developed bilateral internuclear ophthalmoplegia (INO) as the only neurological sign. After having excluded all other possible aetiological causes by careful examination, including magnetic resonance imaging, the symptoms eventually were attributed to the trauma. The course of the INO was documented by electro-oculography. A saccades-training programme specially adapted to the boy's age was performed, and complete remission of the oculomotor symptoms occurred after one year.

Child↗
PubMed1993

Parenteral nutrition support of a patient with chronic mesenteric artery occlusive disease.

Vascular catastrophe resulting in a bowel infarction requiring massive resection is one of the most common indications for long-term total parenteral nutrition (TPN). The causes of mesenteric artery disease include embolic and thrombotic occlusions, nonocclusive mesenteric ischemia, and chronic mesenteric ischemia. This paper describes a case of a patient with chronic ischemia. The indication for TPN was intestinal angina limiting oral intake, not short-bowel syndrome as a result of bowel infarction and surgery. The patient had an extensive history of atherosclerotic disease and abdominal symptoms. Her nutritional status was maintained with TPN and oral intake as symptomatically tolerated. She eventually developed catheter sepsis. Her cardiopulmonary status deteriorated and she died. Progressive mesenteric ischemia and possible infarction may have contributed to her death. The patient had indicated she did not want surgery for a bowel infarction. She did consent to surgical correction of her disease, if feasible. Although TPN can maintain the nutritional and metabolic status of a patient with chronic mesenteric ischemia, the associated risk of catheter sepsis emphasizes the necessity for expedient treatment of the primary pathology.

Aged↗
PubMed1992

Cytokine pattern of Langerhans cells isolated from murine epidermal cell cultures.

In the present study we demonstrate that supernatants of highly enriched cultured Langerhans cells (cLC) display IL-1, IL-6, granulocyte/macrophage (GM)-CSF, and TNF-alpha, but no IL-2, IL-3, IL-4, and IFN-gamma activities. We further show that IL-6, GM-CSF, and TNF-alpha bioactivities can be specifically blocked in the presence of the respective neutralizing mAb. Concerning the IL-1 bioactivity, the combined use of anti-IL-1 alpha and anti-IL-1 beta mAb was needed to completely inhibit the proliferative response of the indicator cell line D10. One of the difficulties in studying the secretory potential of LC is that even highly enriched cLC are contaminated with keratinocytes (KC), which are known to be a rich source of cytokines. To overcome this problem we compared cytokine bioactivities in supernatants of cell cultures consisting of selected cLC:cKC ratios. These cell mixing experiments revealed that cLC are the major source of the IL-6 bioactivity, whereas IL-1, GM-CSF, and TNF-alpha are predominantly generated by cKC. In order to determine whether the cytokine bioactivities measured in supernatants of epidermal cell cultures are simply caused by an increased release or by de novo synthesis, we performed molecular biologic studies. Polymerase chain reaction analysis of cLC and cKC revealed that IL-1 beta and IL-6 transcripts are virtually limited to cLC, whereas IL-1 alpha, GM-CSF, and TNF-alpha messages are preferentially exhibited by cKC. mRNA coding for IL-2, IL-3, IL-4, and IFN-gamma could neither be amplified from cLC nor from cKC. Furthermore, the quantitative comparison of cytokine transcripts in cLC vs cKC using Northern blot analysis and mRNA detection on the single cell level using in situ hybridization confirmed that cLC generate IL-6, whereas cKC synthesize IL-1 alpha and GM-CSF. Taken together our results demonstrate that cultured murine LC synthesize and secrete IL-1 beta and IL-6, cytokines known to be important accessory molecules in T cell activation.

Animals↗
PubMed1992

Detection of transcripts for the receptor for macrophage colony-stimulating factor, c-fms, in murine osteoclasts.

Macrophage colony-stimulating factor (M-CSF), whose action is restricted to the cell populations of the mononuclear phagocyte system, has recently been found to be required for osteoclastogenesis and bone resorption. To investigate the cells involved in the action of M-CSF in these processes, expression of c-fms mRNA, encoding the M-CSF receptor, was studied by in situ hybridization. Paws from murine embryos and newborn mice, tibiae from 2-day-old animals, as well as isolated osteoclasts, were hybridized with a c-fms-specific RNA probe. In bone, c-fms mRNA was detected only in cells at the late stages of osteoclastogenesis and in mature osteoclasts. The findings strengthen the relation between osteoclasts and the mononuclear phagocyte system. Furthermore, they suggest that M-CSF acts directly on osteoclast precursors and on mature osteoclasts during osteoclastogenesis.

Animals↗