Biosynthesis of a cyclic tautomer of (3-methylmaleyl)acetone from 4-hydroxy-3,5-dimethylbenzoate by Pseudomonas sp. HH35 but not by Rhodococcus rhodochrous N75

Vitamin E is one of the most important lipid-soluble antioxidant nutrients. Severe vitamin E deficiency can have a profound effect on the central nervous system. Cystic fibrosis, chronic cholestatic liver disease, abetalipoproteinemia, short bowel syndrome, isolated vitamin E deficiency syndrome and other malabsorption syndromes all may cause varying degrees of neurologic deficits due to related vitamin deficiencies. The classic abnormalities in vitamin E deficiency progress from hyporeflexia, ataxia, limitations in upward gaze and strabismus to long-tract defects, profound muscle weakness and visual field constriction. Patients with severe, prolonged deficiency may develop complete blindness, dementia and cardiac arrhythmias. Treatment must be tailored to the underlying cause of vitamin E deficiency and may include oral or parenteral vitamin supplementation. The more advanced the deficits, the more limited the response to therapy. Therefore, a good neurologic examination and periodic serum vitamin E levels are essential in patients at risk of vitamin E deficiency.     

The creation of a legal-standards basis for the economic validation of nature-preserving activities in health resorts

In patients with pulmonary tuberculosis, intestinal dysbacteriosis has clinical and bacteriological features characterized by the short-age of bifidobacteria (in 88-92%), by changes in the composition of Escherichia coli strains (in 38-42%), by the presence of Candida (in 58-62%), Proteus in half the patients, and by associated dysbacteriosis. Most (75%) patients show Stage III-IV intestinal dysbiosis formed after 3-4 months of continuous chemotherapy. There is a direct relationship between the magnitude of dysbiotic disorders and the duration of chemotherapy.     

CT reconstruction of an unusual chronic posttraumatic aneurysm of the thoracic aorta

Chronic traumatic aneurysm of the thoracic aorta is an unusual occurrence. Previously, arteriography was performed on all patients seen in our institution with this entity to allow confirmation of the diagnosis and anatomic delineation for operation. A case of chronic traumatic aneurysm of the distal descending aorta discovered on a routine chest roentgenogram and evaluated with chest computed tomographic scanning with three-dimensional reconstruction is presented. It is our belief that not all thoracic aneurysms require arteriography, and improved methods of computed tomographic scanning allow adequate diagnosis and anatomic delineation with decreased morbidity and cost.     

Ceramide selectively decreases tau levels in differentiated PC12 cells through modulation of calpain I

Ceramide has been recently proposed to be a signal mediator in several important physiological processes including apoptosis, cellular growth, and differentiation. Because the microtubule-associated protein tau plays an important role in the establishment and maintenance of neuronal morphology, the effects of ceramide on tau were examined. Treatment of differentiated PC12 cells with the cell-permeable ceramide derivative N-acetylsphingosine (C2) resulted in a significant reduction in tau levels. Significant decreases in tau levels were also observed when the cells were treated with another ceramide derivative, N-hexanoylsphingosine (C6). In addition, C2 treatment increased the levels of a calpain-derived spectrin breakdown product but did not alter the levels of two cytoskeletal proteins, alpha-actin and alpha-tubulin. Because both tau and spectrin are proteolyzed in vitro by the calcium-activated cysteine protease calpain, the effects of ceramide analogues on the activity of this protease were examined. Treatment of PC12 cells with C2 enhanced calcium-stimulated proteolytic activity significantly, as revealed by monitoring the hydrolysis of the membrane-permeable calpain-selective fluorescence probe N-succinyl-L-leucyl-L-leucyl-L-valyl-L-tyrosine-7-amido-4-methylcoumarin . This activity increase was not due to a direct effect of C2 on calpains, because C2 did not alter the activities of purified calpain I or II. In addition, C2 treatment of PC12 cells resulted in a significant increase in the levels of calpain I and, to a lesser extent, the levels of calpastatin (an endogenous calpain inhibitor protein), whereas the levels of calpain II were not changed. Moreover, treatment of the cells with the synthetic calpain-specific inhibitor N-carbobenzoxy-L-leucyl-L-leucyl-L-tyrosine diazomethyl ketone blocked the C2-induced decreases in tau levels. These results indicate that tau levels are regulated in response to a physiological factor and, thus, have implications for ceramide-mediated changes in normal and pathological neuronal processes.     

Effects of pancreatic polypeptide amylin on ulceration and acid gastric secretion

The effects of the pancreatic polypeptide amyline on ulceration and acid gastric secretion were studied in rat experiments. Pyloric ligation was used as a model of ulceration. Amyline administration caused significantly less gastric mucosal damage in response to pyloric ligation. The severity of gastric mucosal damage averaged 47 +/- 13 mm2 in the control group and 25 +/- 11 mm2 (p < 0.005). The rate of acid gastric secretion in the animals whose pylorus had been ligated as judged by the pH of gastric content was significantly higher than that in the controls (2.87 +/- 0.22 and 2.34 +/- 0.17 (p = 0.05). It is concluded that amyline has a noticeable effect on the gastric mucosa. It is suggested that suppressed acid gastric secretion, i.e. reduced influence of aggressive agents on the gastric mucosa, is a mechanism of antiulcerative action of the peptide.