85 research outputs found
Topological Sectors and Measures on Moduli Space in Quantum Yang-Mills on a Riemann Surface
Previous path integral treatments of Yang-Mills on a Riemann surface
automatically sum over principal fiber bundles of all possible topological
types in computing quantum expectations. This paper extends the path integral
formulation to treat separately each topological sector. The formulation is
sufficiently explicit to calculate Wilson line expectations exactly. Further,
it suggests two new measures on the moduli space of flat connections, one of
which proves to agree with the small-volume limit of the Yang-Mills measure.
\copyright {\em 1996 American Institute of Physics.}Comment: 13 pages, Latex (v. 2.09), figure available on request, revised to
add 2 new references, clarify exposition, fix typos. Version to appear in J.
Math. Phys., Spring 199
Energy in Yang-Mills on a Riemann Surface
Sengupta's lower bound for the Yang-Mills action on smooth connections on a
bundle over a Riemann surface generalizes to the space of connections whose
action is finite. In this larger space the inequality can always be saturated.
The Yang-Mills critical sets correspond to critical sets of the energy action
on a space of paths. This may shed light on Atiyah and Bott's conjecture
concerning Morse theory for the space of connections modulo gauge
transformations.Comment: 7 pages, 2 figures, Latex2e with epsfig, submitted to Journal of
Mathematical Physic
A Rigorous Path Integral for Supersymmetric Quantum Mechanics and the Heat Kernel
In a rigorous construction of the path integral for supersymmetric quantum
mechanics on a Riemann manifold, based on B\"ar and Pf\"affle's use of
piecewise geodesic paths, the kernel of the time evolution operator is the heat
kernel for the Laplacian on forms. The path integral is approximated by the
integral of a form on the space of piecewise geodesic paths which is the
pullback by a natural section of Mathai and Quillen's Thom form of a bundle
over this space.
In the case of closed paths, the bundle is the tangent space to the space of
geodesic paths, and the integral of this form passes in the limit to the
supertrace of the heat kernel.Comment: 14 pages, LaTeX, no fig
The Use of Rodent Models to Investigate Host-Bacteria Interactions Related to Periodontal Diseases
Even though animal models have limitations they are often superior to in vitro or clinical studies in addressing mechanistic questions and serve as an essential link between hypotheses and human patients. Periodontal disease can be viewed as a process that involves four major stages: bacterial colonization, invasion, induction of a destructive host response in connective tissue and a repair process that reduces the extent of tissue breakdown. Animal studies should be evaluated in terms of their capacity to test specific hypotheses rather than their fidelity to all aspects of periodontal disease initiation and progression. Thus, each of the models described below can be adapted to test discrete components of these four major steps, but not all of them. This review describes five different animal models that are appropriate for examining components of host-bacteria interactions that can lead to breakdown of hard and soft connective tissue or conditions that limit its repair as follows: the mouse calvarial model, murine oral gavage models with or without adoptive transfer of human lymphocytes, rat ligature model and rat Aggregatibacter actinomycetemcomitans feeding model
Bacterial Infection Increases Periodontal Bone Loss in Diabetic Rats Through Enhanced Apoptosis
Periodontal disease is the most common osteolytic disease in humans and is significantly increased by diabetes mellitus. We tested the hypothesis that bacterial infection induces bone loss in diabetic animals through a mechanism that involves enhanced apoptosis. Type II diabetic rats were inoculated with Aggregatibacter actinomycetemcomitans and treated with a caspase-3 inhibitor, ZDEVD-FMK, or vehicle alone. Apoptotic cells were measured with TUNEL; osteoblasts and bone area were measured in H&E sections. New bone formation was assessed by labeling with fluorescent dyes and by osteocalcin mRNA levels. Osteoclast number, eroded bone surface, and new bone formation were measured by tartrate-resistant acid phosphatase staining. Immunohistochemistry was performed with an antibody against tumor necrosis factor-α. Bacterial infection doubled the number of tumor necrosis factor-αâexpressing cells and increased apoptotic cells adjacent to bone 10-fold (P \u3c 0.05). Treatment with caspase inhibitor blocked apoptosis, increased the number of osteoclasts, and eroded bone surface (P \u3c 0.05); yet, inhibition of apoptosis resulted in significantly greater net bone area because of an increase in new bone formation, osteoblast numbers, and an increase in bone coupling. Thus, bacterial infection in diabetic rats stimulates periodontitis, in part through enhanced apoptosis of osteoblastic cells that reduces osseous coupling through a caspase-3âdependent mechanism. Diabetes is a chronic inflammatory disease characterized by hyperglycemia that affects 26 million Americans.1 Diabetes has several complications, such as cardiovascular, renal, microvascular, and periodontal diseases. Periodontal disease is one of the most common forms of osteolytic bone disease and one of the most frequent complications of the diabetes.2 Recent research suggests that the relationship between periodontitis and diabetes is reciprocal.3, 4 People with diabetes are more susceptible to periodontitis, and periodontitis may affect serum glucose levels and contribute to progression of diabetes.5 Diabetes may contribute to periodontitis because of its effect on inflammation.6, 7 Despite being triggered by bacterial infection, periodontal bone loss is tied to the inflammatory host response, which leads to the generation of prostaglandins and cytokines that stimulate osteoclastogenesis and periodontal bone loss.8 Several of the detrimental aspects of periodontal disease have recently been shown to be mediated by elevated levels of tumor necrosis factor-α (TNF-α).9, 10 TNF-α is a proinflammatory cytokine produced by leukocytes and other cell types.11 Enhanced TNF-α levels have been directly linked to cellular changes in diabetic retinopathy, deficits in wound healing, and diabetes-enhanced periodontitis.12, 13, 14 Some of the detrimental effects of diabetes-enhanced TNF-α levels may be because of the induction of cell death by triggering caspase activity. Caspases are a family of cysteine proteases that can act as either initiators (caspases 2, 8, and 9) or executioners (caspases 3, 6, and 7) of apoptosis.15 Caspase-3 appears to play a central role in bacteria and lipopolysaccharide-mediated apoptosis.16, 17 In addition, it has been shown that TNF-α can stimulate the expression of several pro-apoptotic genes, many of which are regulated by the pro-apoptotic transcription factor, forkhead box-O1 (FOXO1).18 The functional role of apoptosis in pathological processes can be studied with caspase inhibitors, which are small peptides that block the activity of well-defined caspases.19 These inhibitors have been used in animal models to attenuate cell death and diminish tissue damage in ischemic conditions, sepsis, and other pathological processes.20, 21 Other studies using caspase inhibitors have shown that part of the detrimental effect of diabetes on healing after infection is the result of increased fibroblast or osteoblast apoptosis.16, 22 To understand how diabetes may affect periodontal bone loss through apoptosis, we used a caspase-3/7 inhibitor in a type 2 Goto-Kakizaki (GK) diabetic rat model of periodontal disease induced by bacterial infection. The aim of this study was to determine how apoptosis of osteoblasts contributed to periodontal bone loss by its effect on bone formation in diabetic animals
A.ActinomycetemcomitansâInduced Periodontal Disease Promotes Systemic and Local Responses in Rat Periodontium
Aim
To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. Material & Methods
Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNFâα in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. Results
An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p \u3c 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p \u3c 0.05). TNFâα expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNFâα expression in the connective tissue (p \u3c 0.05). PMN recruitment significantly increased after Aa infection (p \u3c 0.05). Aa also increased the number of CD8+ T cells (p \u3c 0.05), but not CD4+ T cells or regulatory T cells (Tregs) (p \u3e 0.05). Conclusion
Aa infection stimulated a local response that increased numbers of PMNs and TNFâα expression in the junctional epithelium and loss of attachment. Both TNFâα expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNFâα in the connective tissue, osteoclast numbers and CD8+ T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction
Surveillance for Anthrax Cases Associated with Contaminated Letters, New Jersey, Delaware, and Pennsylvania, 2001
In October 2001, two inhalational anthrax and four cutaneous anthrax cases, resulting from the processing of Bacillus anthracisâcontaining envelopes at a New Jersey mail facility, were identified. Subsequently, we initiated stimulated passive hospital-based and enhanced passive surveillance for anthrax-compatible syndromes. From October 24 to December 17, 2001, hospitals reported 240,160 visits and 7,109 intensive-care unit admissions in the surveillance area (population 6.7 million persons). Following a change to reporting criteria on November 8, the average of possible inhalational anthrax reports decreased 83% from 18 to 3 per day; the proportion of reports requiring follow-up increased from 37% (105/286) to 41% (47/116). Clinical follow-up was conducted on 214 of 464 possible inhalational anthrax patients and 98 possible cutaneous anthrax patients; 49 had additional laboratory testing. No additional cases were identified. To verify the limited scope of the outbreak, surveillance was essential, though labor-intensive. The flexibility of the system allowed interim evaluation, thus improving surveillance efficiency
Hundred Years of Gravity and Accelerated Frames: The Deepest Insights of Einstein and Yang-Mills
- âŠ