Febrile state, bloody diarrhea and megacolon

We report about a forty year old female patient with severe bloody diarrhoea and fever over a period of 14 days due to an infection with Salmonella enteritidis. X-ray of the abdomen showed a toxic megacolon. With the diagnosis of an infectious colitis we started therapy with ciprofloxacin i/v. The toxic megacolon progressed despite intensive care and parenteral nutrition. Additionally the patient received metronidazole i/v and in combination with a roll technique in bed in the knee-elbow-position the leucocytosis and the megacolon decreased. A toxic megacolon is in about 3% associated with an infection with Salmonella enteritidis. It is essentially diagnosed by X-ray. Patients should receive intensive care, and because of the high mortality rate an interdisciplinary management is required. The article discusses the major differential diagnosis of the toxic megacolon, as well as the pathogenesis and therapy of Salmonella ent, infection. In case of an infection with Salmonella ent. physicians should acknowledge the possibility of development of a toxic megacolon.     

Are stereotaxic breast biopsies adequate?

BACKGROUND: Stereotaxic core breast biopsy (SCBB) has been proposed as a cost-effective and reliable method of evaluating mammographic lesions. This study evaluates an initial experience with SCBB and assesses the adequacy of the biopsy specimens obtained. METHODS: Two hundred forty-one SCBB were performed on 221 patients during 13 months by four radiologists. Mammograms were assigned a suspicion index on a scale of 1 to 5. One pathologist performed a blinded retrospective review of all SCBB specimens and assigned an adequacy score based on the quality and amount of the tissue present. RESULTS: The majority of SCBB were ordered by general surgeons (67%). A suspicion index score of 3 was assigned to 74% of lesion specimens. Twelve percent of specimens were malignant. Overall SCBB adequacy (score > or = 2) was 77%. Adequacy was present in 74% of benign biopsy specimens as compared with 100% of malignant specimens (p < 0.005). Only 62% of specimens reported as benign without specific features were adequate. There were no differences in adequacy between individual radiologists or during the study period. CONCLUSIONS: SCBB is largely used by surgeons to assess indeterminate mammographic lesions. One of four benign specimens was inadequate. Benign SCBB specimens must be interpreted with caution.     

Fine mapping of the dyskeratosis congenita locus in Xq28

Dyskeratosis congenita (DC) is characterised by reticulate skin pigmentation, mucosal leucoplakia, and nail dystrophy. Bone marrow failure occurs in 50% of patients and is the principal cause of early mortality. In the majority of families the pattern of inheritance of DC is compatible with an X linked recessive trait. The locus for the X linked recessive form of DC has been linked to Xq28. We have now extended our earlier studies by investigating five families with additional Xq28 polymorphic markers; analysis of recombination events in these families has located the DC1 locus between GABRA3 and DXS1108, an interval of approximately 4 Mb.     

Fatal varicella-zoster encephalitis; a rare complication of herpes zoster

In a 82-year-old woman varicella zoster encephalitis was diagnosed, a rare complication of shingles. The case was remarkable for its rapid and fatal course in a patient without an underlying disease. At autopsy, the histological picture of an acute haemorrhagic encephalitis was seen, also a rare finding.     

Activation of the genetically defined m1 muscarinic receptor potentiates N-methyl-D-aspartate (NMDA) receptor currents in hippocampal pyramidal cells

Evidence suggests that cholinergic input to the hippocampus plays an important role in learning and memory and that degeneration of cholinergic terminals in the hippocampus may contribute to the memory loss associated with Alzheimer's disease. One of the more prominent effects of cholinergic agonists on hippocampal physiology is the potentiation of N-methyl-D-aspartate (NMDA)-receptor currents by muscarinic agonists. Here, we employ traditional pharmacological reagents as well as m1-toxin, an m1 antagonist with unprecedented selectivity, to demonstrate that this potentiation of NMDA-receptor currents in hippocampal CA1 pyramidal cells is mediated by the genetically defined m1 muscarinic receptor. Furthermore, we demonstrate the colocalization of the m1 muscarinic receptor and the NR1a NMDA receptor subunit at the electron microscopic level, indicating a spatial relationship that would allow for physiological interactions between these two receptors. This work demonstrates that the m1-muscarinic receptor gene product modulates excitatory synaptic transmission, and it has important implications in the study of learning and memory as well as the design of drugs to treat neurodegenerative diseases such as Alzheimer's.     

Requirement of protein synthesis for group I mGluR-mediated induction of epileptiform discharges

Picrotoxin (50 microM) elicited rhythmic synchronized bursting in CA3 pyramidal cells in guinea pig hippocampal slices. Addition of the selective group I metabotropic glutamate receptor (mGluR) agonist (S)-3,5-dihydroxyphenylglycine (25 microM) elicited an increase in burst frequency. This was soon followed by a slowly progressive increase in burst duration (BD), converting the brief 250-520 ms picrotoxin-induced synchronized bursts into prolonged discharges of 1-5 s in duration. BD was significantly increased within 60 min and reached a maximum after 2-2.5 h of agonist exposure. The protein synthesis inhibitors anisomycin (15 microM) or cycloheximide (25 microM) significantly impeded the mGluR-mediated development of the prolonged bursts; 90-120 min of agonist application failed to elicit the expected burst prolongation. By contrast, the mGluR-mediated enhancement of burst frequency progressed unimpeded. Furthermore, protein synthesis inhibitors had no significant effect on the frequency or duration of fully developed mGluR-induced prolonged discharges. These results suggest that the group I mGluR-mediated prolongation of synchronized bursts has a protein synthesis-dependent mechanism.     

The phylogeny of the wrist

BACKGROUND: Long-term results on LASIK are not available to date. We therefore evaluated the predictability, stability and complication rate after LASIK in moderate--to-high myopia. PATIENTS AND METHODS: We treated 70 eyes (41 patients) using the Automatic Corneal Shaper and the Keracor 116 excimer laser. Patients were followed for 1, 6, 12 and 24 months. Spectacle refraction, visual acuity, rate of retreatment, and patient satisfaction were evaluated. RESULTS: At 24 months the results were as follows: Myopia -5 to -9.9 D (n = 18): 94% within 1 D; regression between 1 and 12 (12 and 24) months > 1 D in 6% (6%); uncorrected acuity 20/40 or better in 83%; no loss of 2 ore more lines of visual acuity; 89% highly satisfied. Myopia -10 to -14.9 D (n = 12): 88% within 1 D; regression between 1 and 12 (12 and 24) months > 1 D in 20% (0%); uncorrected acuity 20/40 or better in 72%; 4% lost 2 or more lines of visual acuity; 96% highly satisfied. Myopia -15 to -29 D (n = 22): 33% within 1 D; regression between 1 and 12 (12 and 24) months > 1 D in 41% (18%); uncorrected acuity 20/40 or better in 7%; no loss of 2 or more lines of visual acuity; 67% highly satisfied. CONCLUSION: LASIK is an accurate, effective and stable procedure for correcting myopia of -5 to -10 D. Results are less precise in myopia up to -15 D, and some visual loss occurs in a number of patients. In myopia > -15 D, results are not satisfactory because of poor accuracy and low stability.     

Characterization of the mechanism of action of tachykinins in rat striatal cholinergic interneurons

Plasma membranes of neutrophil cells contain the redox component of the O2(-)-generating NADPH oxidase complex, namely a heterodimeric flavocytochrome b consisting of an alpha subunit of 22 kDa and a beta subunit of 85-105 kDa of a glycoprotein nature. The NADPH oxidase is dormant in resting neutrophils. When neutrophils are exposed to a variety of particulate or soluble stimuli, the oxidase becomes activated, due to the assembly on the membrane-bound flavocytochrome b of three cytosolic factors, p47phox, p67phox and Rac 2 (or Rac 1). The effect of phenylarsine oxide (PAO), which reacts specifically with vicinal and neighbouring thiol groups in proteins, was assayed on the NADPH oxidase activity of bovine neutrophils, elicited after activation of the oxidase in a cell-free system consisting of plasma membranes and cytosol from resting neutrophils, GTP[S], ATP and arachidonic acid; the effect of PAO on the oxidase activation itself was measured independently. PAO preferentially inhibited oxidase activation rather than the elicited oxidase activity, and inhibition resulted from binding of PAO to the membrane component of the cell-free system. To determine the PAO-binding protein responsible for the loss of oxidase activation, we used photoaffinity labeling with a tritiated azido derivative of PAO, 4-[N-(4-azido-2-nitrophenyl)amino-[3H]acetamido]phenylarsine oxide, ([3H]azido-PAO). Photoirradiation of plasma membranes from resting neutrophils in the presence of [3H]azido-PAO resulted in the prominent labeling of a protein of 85-105 kDa whose migration on SDS/PAGE coincided with that of the beta subunit of flavocytochrome b as identified by immunoreaction. Upon deglycosylation, the photolabeled band at 85-105 kDa was shifted to 50-60 kDa as was the immunodetected beta subunit. Similar results were obtained with isolated flavocytochrome b in liposomes. Photoaffinity labeling of the beta subunit of the membrane-bound flavocytochrome b or the isolated flavocytochrome b in liposomes resulted in abolition of oxidase activation in the reconstituted cell-free system. Incorporation of [3H]azido-PAO into flavocytochrome b was negligible when photoaffinity labeling was performed on neutrophil membranes that had been previously activated. The results suggest that the beta subunit of flavocytochrome contains two target sites for PAO which are accessible in resting neutrophils, but not in activated neutrophils.