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Recent and historical evidence is consistent with the view that atherosclerosis is an infectious disease or microbial toxicosis impacted by genetics and behavior. Because small bacterial-like particles, also known as nanobacteria have been detected in kidney stones, kidney and liver cyst fluids, and can form a calcium apatite coat we posited that this agent is present in calcified human atherosclerotic plaques. Carotid and aortic atherosclerotic plaques and blood samples collected at autopsy were examined for nanobacteria- like structures by light microscopy (hematoxylin-eosin and a calcium-specific von Kossa staining), immuno-gold labeling for transmission electron microscopy (TEM) for specific nanobacterial antigens, and propagation from homogenized, filtered specimens in culture medium. Nanobacterial antigens were identified in situby immuno-TEM in 9 of 14 plaque specimens, but none of the normal carotid or aortic tissue (5 specimens). Nanobacteria-like particles were propagated from 26 of 42 sclerotic aorta and carotid samples and were confirmed by dot immunoblot, light microscopy and TEM. [3H]L-aspartic acid was incorporated into high molecular weight compounds of demineralized particles. PCR amplification of 16S rDNA sequences from the particles was unsuccessful by traditional protocols. Identification of nanobacteria-like particles at the lesion supports, but does not by itself prove the hypothesis that these agents contribute to the pathogenesis of atherosclerosis, especially vascular calcifications.

Recent and historical evidence is consistent with the view that atherosclerosis is an infectious disease or microbial toxicosis impacted by genetics and behavior. Because small bacterial-like particles, also known as nanobacteria have been detected in kidney stones, kidney and liver cyst fluids, and can form a calcium apatite coat we posited that this agent is present in calcified human atherosclerotic plaques. Carotid and aortic atherosclerotic plaques and blood samples collected at autopsy were examined for nanobacteria-like structures by light microscopy (hematoxylin-eosin and a calcium-specific von Kossa staining), immuno-gold labeling for transmission electron microscopy (TEM) for specific nanobacterial antigens, and propagation from homogenized, filtered specimens in culture medium. Nanobacterial antigens were identified in situby immuno-TEM in 9 of 14 plaque specimens, but none of the normal carotid or aortic tissue (5 specimens). Nanobacteria-like particles were propagated from 26 of 42 sclerotic aorta and carotid samples and were confirmed by dot immunoblot, light microscopy and TEM. [3H]L-aspartic acid was incorporated into high molecular weight compounds of demineralized particles. PCR amplification of 16S rDNA sequences from the particles was unsuccessful by traditional protocols. Identification of nanobacteria-like particles at the lesion supports, but does not by itself prove the hypothesis that these agents contribute to the pathogenesis of atherosclerosis, especially vascular calcifications.

The effects of glucocorticoids on acute pancreatitis (AP) have remained contradictory. The aim of this study was to investigate the time courses of the effects of the exogenous glucocorticoid agonists dexamethasone (DEX) and hydrocortisone (HYD) and a glucocorticoid antagonist (RU-38486) and to characterize the local and systemic responses in AP in rats. The glucocorticoid antagonist and agonists were administered just before AP induction. Serum amylase activity determinations, IL-6 bioassays, pancreatic weight/body weight ratio measurements, and survival analysis were performed. Liver and lung injuries were assessed via neutrophil leukocyte infiltration in myeloperoxidase (MPO) assays, tissue adenosine triphosphate (ATP) level determinations, and histology. In the glucocorticoid agonist groups, the survival rate increased, while the serum amylase level, the IL-6 activity, and the pancreatic weight/body weight ratio decreased significantly as compared with the control and RU-treated groups. AP resulted in significant decreases in tissue ATP levels in both the liver and the lung. In the DEX- or HYD-treated groups, the liver ATP levels were significantly elevated, while both the liver and the lung MPO levels were attenuated as compared with the AP and RU-treated groups. These results suggest that glucocorticoids may play important roles in mitigating the progression of the inflammatory reaction during the early phases of AP.

To analyze the data on patients operated on for pulmonary tuberculosis (TB) with (Group I) or without (Group II) a correct TB diagnosis and preoperative anti-TB treatment.

Purpose: Chronic over distention may lead to enterocystoplasty rupture. It is hypothesized that pressure induced microvascular derangement and subsequent ischemia of the enterocystoplasty intestinal patch may have a role in this process. We describe distention induced microcirculatory alterations in a chronic rat model of enterocystoplasty using intravital video microscopy. Materials and Methods: Microcirculation in the muscle layer of the intact bladder and intestine, and in the enterocystoplasty 90 days after surgery were examined at greater and less than urethral sphincter closure pressure. Microcirculatory changes were recorded during stepwise increments of intraluminal pressure up to 80 mm. Hg or when 20 mm. Hg was continuously maintained for 60 minutes. Results: The enterocystoplasty components of intestine and bladder displayed baseline microcirculatory characteristics similar to those observed in the intact organs. As evidenced by microcirculatory flow and functional capillary density measurements in the intact intestine and the ileal portion of enterocystoplasty, intraluminal pressure elevation to greater than 25 or 30 mm. Hg significantly compromised capillary perfusion by approximately 50% and 75%, respectively. Lower intraluminal pressure did not cause microcirculatory disturbance even when maintained for a longer period. In the intact bladder and bladder portion of enterocystoplasty only pressure increases to greater than 80 mm. Hg affected tissue perfusion. Conclusions: Intravital microscopy in the augmented rat bladder is a sensitive and suitable means of assessing clinically relevant microcirculatory changes. These experiments demonstrate the significance of distention induced microcirculatory impairment in the intact bowel and the intestinal site of enterocystoplasty even at less than urethral closure pressure.