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Biomedical subjects

V Braun

Publications and source records attributed to V Braun.

At least 91 records · Page 5Linked to original sources
PubMed1997

Colicin U, a novel colicin produced by Shigella boydii.

A novel colicin, designated colicin U, was found in two Shigella boydii strains of serovars 1 and 8. Colicin U was active against bacterial strains of the genera Escherichia and Shigella. Plasmid pColU (7.3 kb) of the colicinogenic strain S. boydii M592 (serovar 8) was sequenced, and three colicin genes were identified. The colicin U activity gene, cua, encodes a protein of 619 amino acids (Mr, 66,289); the immunity gene, cui, encodes a protein of 174 amino acids (Mr, 20,688); and the lytic protein gene, cul, encodes a polypeptide of 45 amino acids (Mr, 4,672). Colicin U displays sequence similarities to various colicins. The N-terminal sequence of 130 amino acids has 54% identity to the N-terminal sequence of bacteriocin 28b produced by Serratia marcescens. Furthermore, the N-terminal 36 amino acids have striking sequence identity (83%) to colicin A. Although the C-terminal pore-forming sequence of colicin U shows the highest degree of identity (73%) to the pore-forming C-terminal sequence of colicin B, the immunity protein, which interacts with the same region, displays a higher degree of sequence similarity to the immunity protein of colicin A (45%) than to the immunity protein of colicin B (30.5%). Immunity specificity is probably conferred by a short sequence from residues 571 to residue 599 of colicin U; this sequence is not similar to that of colicin B. We showed that binding of colicin U to sensitive cells is mediated by the OmpA protein, the OmpF porin, and core lipopolysaccharide. Uptake of colicin U was dependent on the TolA, -B, -Q, and -R proteins. pColU is homologous to plasmid pSB41 (4.1 kb) except for the colicin genes on pColU. pSB41 and pColU coexist in S. boydii strains and can be cotransformed into Escherichia coli, and both plasmids are homologous to pColE1.

Amino Acid Sequence↗
PubMed1997

Pesticin displays muramidase activity.

Pesticin of Yersinia pestis is the only bacteriocin that converts sensitive cells to stable spheroplasts. The amino acid sequence of pesticin as derived from the nucleotide sequence shows no similarity to those of any of the bacteriocins. The unique properties of pesticin prompted an investigation of its mode of action. Since the pesticin plasmid does not encode a lysis protein for release of pesticin into the culture medium, pesticin was isolated from cells and purified to electrophoretic homogeneity. Highly purified pesticin degraded murein and murein glycan strands lacking the peptide side chains to products that were similar to those obtained by lysozyme, as revealed by high-resolution high-pressure liquid chromatography. After reduction of the murein degradation products with tritium-labeled sodium borohydride, acid hydrolysis, and separation of the products by thin-layer chromatography, radiolabeled muraminitol was identified. This indicates that pesticin is a muramidase, and not an N-acetyl-glucosaminidase, that converts cells into stable spheroplasts by slowly degrading murein.

Bacteriocins↗
PubMed1997

Avoidance of iron toxicity through regulation of bacterial iron transport.

Under oxic conditions and at pH 7, ferric iron is insoluble, and complex formation of Fe3+ with ligands is required to supply cells with iron. Bacteria and fungi synthesize and secrete low-molecular-weight compounds, termed siderophores, that bind Fe3+. Certain human pathogens take up iron from human transferrin, lactoferrin, hemoglobin, and heme. The ferric siderophores are actively transported into bacterial cells by highly specific transport systems. In Gram-negative bacteria, the ferric siderophores and iron released from the host proteins are actively transported across the outer membrane (OM). The electrochemical potential of the cytoplasmic membrane (CM) energizes transport across the outer membrane, which requires an energy-transducing device, consisting of the proteins TonB, ExbB and ExbD, from the CM to the OM. Active transport across the CM is energized by ATP hydrolysis. Transport is regulated at the level of gene transcription. In Gram-negative bacteria, this is controlled by the Fur protein, in most gram-positive bacteria, by the DtxR protein. Fur and DtxR act as repressors when loaded with Fe2+. In the cytoplasm, iron is released from the siderophores by reduction to Fe2+, and the siderophores are either inactivated or secreted. The intracellular iron is built into heme and non-heme iron proteins, and a small proportion is incorporated into bacterioferritin, but most of the iron is present in a poorly defined state. Iron overload results in iron toxicity, mainly due to the formation of hydroxyl radicals that strongly react with all kinds of biomolecules, of which DNA damage has the most deleterious consequences.

Bacteria↗
PubMed1997

[Significance of distal motor latency after carpal tunnel operation].

Motor distal latency (MDL) is one of the most important parameters in the electrodiagnosis of carpal tunnel syndrome (CTS). In a retrospective study of 1816 open surgical decompressions for CTS, a total of 612 postoperative motor nerve conduction measurements on 485 hands could be evaluated. In patients with good or satisfactory results after carpal tunnel release, an average improvement of MDL of 1.0 ms after 9-13 days, and of 2.2 ms after 1 year and longer was found. The individual motor nerve conduction improvement was in close correlation with the extent of preoperative prolongation of the MDL. Whereas relief of symptoms can be noted almost immediately, prolonged latencies often do not return to normal, even when the study is done a year later. Of the 10 patients with persisting symptoms, four had a new postoperative impairment of MDL, and also four had a marked improvement, whereas it remained unchanged in two. Patients with severe recurrent CTS presented in 11 out of 31 cases with an improved MDL from 0.3 ms to 3.0 ms in comparison to the initial preoperative evaluation; in 6 hands MDL was unchanged, further prolongation up to 2.0 ms was seen in 6 cases and marked worsening with new loss of motor response had to be noted in 8 hands at repeat electrodiagnosis. In 33 cases of postoperative reflex sympathetic dystrophy, an improvement of MDL from 0.3 ms to 3.3 ms (mean 1.7 ms) was observed in 22 hands and dissolution of a preexisting motor conduction block in three others, whereas two remained unchanged (without motor response) and an electrophysiological impairment was found only in six hands. Three of them presented with a further prolongation of MDL from 0.3 to 1.0 ms and a new loss of response was noted in the remaining three. In conclusion, postoperative motor nerve conduction studies may assess a favorable course following carpal tunnel release. However, they are often not helpful when surgical results are unsatisfactory, and indication for repeat surgical decompression should be based merely on clinical symptoms.

Carpal Tunnel Syndrome↗
PubMed1996

Definition of the single integration site of the pathogenicity locus in Clostridium difficile.

We determined the nucleotide sequence 3.8 kb upstream and 5.2 kb downstream of the toxin genes A and B of Clostridium difficile. Nine ORFs were discovered. Based on PCR-directed approaches, two were attributed to the pathogenicity locus (PaLoc). The other seven were found in every C. difficile isolate obtained from the human gastrointestinal tract, respectless of their toxinogenicity. The ORFs cdu1 and cdu2/2' upstream of the PaLoc displayed similarity to repressors of Gram-positive bacteria (cdu1), and to an Na+/H+ antiporter described for Enterococcus hirae (cdu2/2'). Downstream of the locus a putative ABC transporter (cdd2-4) was identified. With a set of three paired primers used in polymerase chain reactions we succeeded in delineating the PaLoc. Sequencing of the appropriate stretch of DNA in C. difficile VPI10463 and four additional toxinogenic strains proved a high conservation of the borders of the PaLoc in all these strains. Our data define the locus as a distinct genetic element. Comparing the sequences of five toxinogenic and five non-toxinogenic strains the integration site of the PaLoc was defined. This showed that a stretch of 115 bp found in non-toxinogenic strains is replaced by the 19-kb locus in toxinogenic strains. Analysis of the boundary sequences showed that the locus is obviously not a mobile genetic element by itself. Instead we propose that it is the independent pathogenic part of a more extended genetic element associated with virulence. The 115 bp of non-toxinogenic strains replaced by the locus in toxinogenic strains carry the putative transcription terminator of the cdu1, a predicted repressor protein. A possible polar effect of the loss of this terminator on transcription of the TcdABCDE genes is discussed. Such an effect would explain the unidirectional insertion of the PaLoc at a single site of the C. difficile genome and might give a rationale for the development of the disease which is induced after antibiotical treatment.

ATP-Binding Cassette Transporters↗
PubMed1996

Colicin M is inactivated during import by its immunity protein.

Colicin M (Cma) displays a unique activity that interferes with murein and O-antigen biosynthesis through inhibition of lipid-carrier regeneration. Immunity is conferred by a specific immunity protein (Cmi) that inhibits the action of colicin M in the periplasm. The subcellular location of Cmi was determined by constructing hybrid proteins between Cmi and the TEM-beta-lactamase (BlaM), which confers resistance to ampicillin only when it is translocated across the cytoplasmic membrane with the aid of Cmi. The smallest Cmi'-BlaM hybrid that conferred resistance to 50 micrograms/ml ampicillin contained 19 amino acid residues of Cmi; cells expressing Cmi'-BlaM with only five N-terminal Cmi residues were ampicillin sensitive. These results support a model in which the hydrophobic sequence of Cmi comprising residues 3-23 serves to translocate residues 24-117 of Cmi into the periplasm and anchors Cmi to the cytoplasmic membrane. Residues 8-23 are integrated in the cytoplasmic membrane and are not involved in Cma recognition. This model was further tested by replacing residues 1-23 of Cmi by the hydrophobic amino acid sequence 1-42 of the penicillin binding protein 3 (PBP3). In vivo, PBP3'-'Cmi was as active as Cmi, demonstrating that translocation and anchoring of Cmi is not sequence-specific. Substitution of the 23 N-terminal residues of Cmi by the cleavable signal peptide of BlaM resulted in an active BlaM'-'Cmi hybrid protein. The immunity conferred by BlaM'-'Cmi was high, but not as high as that associated with Cmi and PBP3'-'Cmi, demonstrating that soluble Cmi lacking its membrane anchor is still active, but immobilization in the cytoplasmic membrane, the target site of Cma, increases its efficiency. Cmi delta 1-23 remained in the cytoplasm and conferred no immunity. We propose that the immunity protein inactivates colicin M in the periplasm before Cma can reach its target in the cytoplasmic membrane.

Amino Acid Sequence↗
PubMed1996

Surface signaling in transcriptional regulation of the ferric citrate transport system of Escherichia coli: mutational analysis of the alternative sigma factor FecI supports its essential role in fec transport gene transcription.

Ferric citrate induces transcription of the ferric citrate transport genes (fec) in escherichia coli by binding to the outer membrane receptor protein FecA without entering the cell. The signal elicited by ferric citrate crosses the outer membrane via TonB, ExbB, and ExbD. FecR transmits the signal across the cytoplasmic membrane and activates FecI located in the cytoplasm. FecI belongs to a subgroup of sigma factors that respond to extracytoplasmic stimuli. Chromosomal insertion and deletion mutations were generated in fecI; the resulting mutants were totally devoid of FecA production and fecB-lacZ expression. Iron starvation did not derepress fec transport gene transcription in fecI mutants. Missense point mutations were generated in the predicted helix-turn-helix motif of FecI to examine its role in transcription initiation. Replacement of glutamate by alanine (E141A) at the third position in the first helix reduced the residual activity of FecI in the absence of ferric citrate to 30% of the wild-type level, but induced fec transcription almost normally n the presence of ferric citrate. Mutant FecI(K145E) displayed 156% of the activity of wild-type FecI in the absence of ferric citrate and conferred full induction by ferric citrate. Mutant FecI(K155E), which has a mutation in the second helix, showed 9% of the wild-type activity in the presence of ferric citrate and 78% in the absence of ferric citrate. The reduced activity of FecI(K155E) was also shown in vitro by DNA binding assays with cell lysates; in gel retardation experiments FecI(K155E) reduced the electrophoretic mobility of fecA promoter-containing DNA less than did wild-type FecI. fecI is not autoregulated, as demonstrated by the lack of FecI-induced fecI-lacZ expression in vivo and by the lack of specific fecI transcription in vitro. Instead, formation of fecI mRNA requires sigma 70. We conclude that transcription of the fec transport genes is regulated by FecI, which responds to ferric citrate via FecR. fecI and fecR co-transcription is inhibited by the iron-loaded Fur repressor, which then results in a low level of transcription of the fec transport genes.

Amino Acid Sequence↗
PubMed1996

Influence of blood supply, thermal and mechanical traumata on hearing function in an animal model.

Even with modern neurosurgical techniques preservation of functional hearing in acoustic neurinoma surgery is still impossible in a large number of cases. Due to the necessity of averaging the brainstem auditory evoked potentials (BAEP) this monitoring is not a real time measurement. Therefore the surgeon cannot be sure which manipulation during the tumour dissection has caused the loss of the BAEPs. The direct monitoring of the cochlear nerve (CNAP) may warn the surgeon earlier. But it is not able to explain, which manipulation has caused the worsening of the potentials. A loss of the waves after coagulation of a vessel next to the cochlear nerve may be the result of the heat or of the disturbance of the blood supply. Potentially harmful to cochlear nerve function may be the interruption of inner ear blood supply, thermal or mechanical traumata. Experimental studies are rare to nonexistent. We therefore tested selectively each trauma for its influence on the BAEPs in an animal model. In New Zealand rabbits a lateral craniectomy of the posterior fossa was performed. Care was taken not to retract the cerebellum or to open the inner ear system, because both factors might disturb the BAEPs. Each step of the operation was followed by BAEP recording. After reaching the internal auditory canal, the cerebellopontine angle of 6 animals was exposed to heated water with definitive increasing temperature. The BAEPs did not react significantly until 71 degrees C was reached and protein coagulation started. In the second group, the internal auditory artery of 6 rabbits was compressed with a microdissector for 3 minutes. Subsequently the BAEPs disappeared in all animals. In the last group a constant pressure of 10 g was applied to 6 cochlear nerves for 1 minute consistently causing the loss of the BAEPs. The results are statistically significant (p = 0.03). We therefore concluded that the blood supply of the inner ear is of the upmost importance for cochlear nerve function. Mechanical manipulation should be minimized whereas thermal traumatization of the nerve is only critical when the nerve itself is coagulated.

Animals↗
PubMed1996

Results of DREZ coagulations for pain related to plexus lesions, spinal cord injuries and postherpetic neuralgia.

The results of 58 dorsal root entry zone (DREZ) thermocoagulation procedures in 51 patients are reported. The postoperative analgesic effect was judged by the patients as being good (more than 75% pain reduction), fair (25-75% pain reduction) or poor (less than 25% pain reduction). Of the 14 patients who underwent surgery for pain due to cervical root avulsion, 10 (77%) had permanently good (8) or fair (2) pain relief after a mean follow up period of 76 months, another 2 (15%) experienced recurrence to the preoperative level (initially 1 good, 1 fair) after more than 2 and 4 years, respectively. Twenty two paraplegics were operated upon, 3 of whom twice, for intractable pain. After a mean observation time of 54 months, continuing pain relief was reported by 12 (55%) patients (11 good, 1 fair), and one (initially fair) had recurrent pain after 8 months. All 3 (early) re-operations remain successful for an average period of 75 months. Poor results were seen especially in cases of associated spinal cord cysts (5 out of 7), despite combined drainage, and in patients with diffuse pain distribution (5 out of 6). Continuous marked improvement for longer periods (mean follow up: 52 months) after DREZ lesions was reported only by 2 out of 10 patients with postherpetic neuralgia (12 procedures) and by 1 out of 5 with painful states due to radiation-induced brachial plexopathy (2), previous surgery (2) and malignant tumour infiltration of the brachial plexus (1). Three patients died postoperatively due to acute cardiac failure (2) and pulmonary embolism (1). Major complications, especially permanent gait disturbances were observed in 6 patients (12%) following primary procedures and in 2 out of 7 patients after re-operations, most of them suffering from postherpetic neuralgia. Minor neurological deficits were noted in 9 cases (18%). DREZ lesions revealed to be an effective procedure in patients with pain related to root avulsion and paraplegia. In contrast, it seems to be less successful for painful states due to other plexus lesions or postherpetic neuralgia.

Adult↗
PubMed1996

Reconstruction of the spinal accessory nerve with an anastomosis to the dorsal C3 branch: technical note.

Most lesions of the spinal accessory nerve are of traumatic origin. If the proximal part is sectioned next to its exit from the cranial base, the reconstruction might be difficult. In such a case, one option is intracranial identification of the spinal accessory nerve and transdural interposition of a graft to its distal stump. Cerebrospinal fluid leaks or infections, caudal nerve palsies, or even spinal neurological deficits are possible complications. From more than 70 patients who underwent selective peripheral denervations for the treatment of spasmodic torticollis in our department, we have learned that the dorsal C1-C6 branches can be sectioned without any functional impairment. The dorsal C2 and C3 branches have diameters comparable to that of the spinal accessory nerve. They contain between 600 and 700 myelinated fibers per square millimeter. Therefore, they seem to be ideal proximal donors for the reconstruction of a severed motor nerve. They may be used in patients with peripheral nerve injuries in the craniocervical region, if other possibilities are not suitable.

Accessory Nerve↗
PubMed1996

Energy-coupled transport across the outer membrane of Escherichia coli: ExbB binds ExbD and TonB in vitro, and leucine 132 in the periplasmic region and aspartate 25 in the transmembrane region are important for ExbD activity.

Ferric siderophores, vitamin B12, and group B colicins are taken up through the outer membranes of Escherichia coli cells by an energy-coupled process. Energy from the cytoplasmic membrane is transferred to the outer membrane with the aid of the Ton system, consisting of the proteins TonB, ExbB, and ExbD. In this paper we describe two point mutations which inactivate ExbD. One mutation close to the N-terminal end of ExbD is located in the cytoplasmic membrane, and the other mutation close to the C-terminal end is located in the periplasm. E. coli CHO3, carrying a chromosomal exbD mutation in which leucine at position 132 was replaced by glutamine, was devoid of all Ton-related activities. A plasmid-encoded ExbD derivative, in which aspartate at position 25, the only changed amino acid in the predicted membrane-spanning region of ExbD, was replaced by asparagine, failed to restore the Ton activities of strain CHO3 and negatively complemented ExbD+ strains, indicating an interaction of this mutated ExbD with wild-type ExbD or with another component. This component was shown to be ExbB. ExbB that was labeled with 6 histidine residues at its C-terminal end and that bound to a nickel-nitrilotriacetic acid agarose column retained ExbD and TonB specifically; both were eluted with the ExbB labeled with 6 histidine residues, demonstrating interaction of ExbB with ExbD and TonB. These data further support the concept that TonB, ExbB, and ExbD form a complex in which the energized conformation of TonB opens the channels in the outer membrane receptor proteins.

Amino Acid Sequence↗
PubMed1996

Ferric rhizoferrin uptake into Morganella morganii: characterization of genes involved in the uptake of a polyhydroxycarboxylate siderophore.

Iron uptake in Morganella morganii, mediated by the fungal siderophore rhizoferrin, was studied. A Mud1 insertion mutant devoid of growth on ferric rhizoferrin was complemented by a chromosomal DNA fragment of M. morganii that encoded an outer membrane protein and a periplasmic protein named RumA and RumB (for rhizoferrin uptake into Morganella spp.), respectively. rumA and rumB have the same transcription polarity and are probably cotranscribed from an iron-regulated promoter upstream of rumA. A predicted Fur regulatory sequence upstream of rumA was confirmed by the Fur titration assay. At the N terminus of RumA, a putative TonB box contains a proline residue that inactivates TonB-dependent receptors and colicins when introduced at the same position into TonB boxes of Escherichia coli. Analysis of a 10-kb sequence flanking rumA and rumB on both sides revealed seven additional open reading frames for which no role in ferric rhizoferrin uptake could be discerned. Thus, rumA and rumB, both essential for transport of this siderophore, form an isolated operon. Additional genes required for ferric rhizoferrin translocation across the cytoplasmic membrane must map at sites distinct from rumA and rumB. Transport studies revealed that both 55Fe3+ and [3H]ketorhizoferrin are incorporated by M. morganii, demonstrating that rhizoferrin serves as a true iron carrier.

Amino Acid Sequence↗
PubMed1996

Properties of the FhuA channel in the Escherichia coli outer membrane after deletion of FhuA portions within and outside the predicted gating loop.

Escherichia coli transports Fe3+ as a ferrichrome complex through the outer membrane in an energy-dependent process mediated by the FhuA protein. A FhuA deletion derivative lacking residues 322 to 355 (FhuA delta322-355) forms a permanently open channel through which ferrichrome diffused. This finding led to the concept that the FhuA protein forms a closed channel that is opened by input of energy derived from the electrochemical potential across the cytoplasmic membrane, mediated by the Ton system. In this study, we constructed various FhuA derivatives containing deletions inside and outside the gating loop. FhuA delta322-336 bound ferrichrome and displayed a residual Ton-dependent ferrichrome transport activity. FhuA delta335-355 no longer bound ferrichrome but supported ferrichrome diffusion through the outer membrane in the absence of the Ton system. FhuA delta335-355 rendered cells sensitive to sodium dodecyl sulfate and supported diffusion of maltotetraose and maltopentaose in a lamB mutant lacking the maltodextrin-specific channel in the outer membrane. Cells expressing FhuA delta70-223, which has a large deletion outside the gating loop, were highly sensitive to sodium dodecyl sulfate and grew on maltodextrins but showed only weak ferrichrome uptake, suggesting formation of a nonspecific pore through the outer membrane. FhuA delta457-479 supported Ton-dependent uptake of ferrichrome. None of these FhuA deletion derivatives formed pores in black lipid membranes with a stable single-channel conductance. Rather, the conductance displayed a high degree of current noise, indicating a substantial influence of the deletions on the conformation of the FhuA protein. FhuA also supports infection by the phages T1, T5, and phi80 and renders cells sensitive to albomycin and colicin M. Cells expressing FhuA delta322-336 were sensitive to albomycin and colicin M but were only weakly sensitive to T5 and phi480 and insensitive to T1. Cells expressing FhuA delta335-355 were resistant to all FhuA ligands. These results indicate different structural requirements within the gating loop for the various FhuA ligands. Cells expressing FhuA delta457-479 displayed a strongly reduced sensitivity to all FhuA ligands, while cells expressing FhuA delta70-223 were rather sensitive to all FhuA ligands except albomycin, to which they were nearly resistant. It is concluded that residues 335 to 355 mainly determine the properties of the gate with regard to FhuA permeability and ligand binding.

Anti-Bacterial Agents↗
PubMed1996

Periplasmic location of the pesticin immunity protein suggests inactivation of pesticin in the periplasm.

The pesticin activity and immunity genes on plasmid pPCP1 of Yersinia pestis were sequenced. They encoded proteins of 40 kDa (pesticin) and 16 kDa (immunity protein); the latter was found in the periplasm. The location of the immunity protein suggests that imported pesticin is inactivated in the periplasm before it hydrolyzes murein. Pesticin contains a TonB box close to the N-terminal end that is identical to the TonB box of colicin B. The DNA sequences flanking the pesticin determinant were highly homologous to those flanking the colicin 10 determinant. It is proposed that through these highly homologous DNA sequences, genes encoding bacteriocins may be exchanged between plasmids by recombination. In the case of pesticin, recombination may have destroyed the lysis gene, of which only a rudimentary fragment exists on pPCP1.

Amino Acid Sequence↗
PubMed1996

Suprascapular nerve entrapment: experience with 28 cases.

Suprascapular nerve entrapment (SNE) in the suprascapular notch is a rare entity that must be considered in the differential diagnosis of radicular pain, as well as that of shoulder discomfort. Over a period of 10 years (1985-1995), the authors treated 28 cases of SNE in 27 patients by surgical decompression of the nerve. One patient underwent operation bilaterally within 5 years. Five patients presented with a history of trauma to the shoulder region. In three patients, a ganglion cyst was the origin of the nerve lesion. In 16 patients, the nerve problem was primarily related to athletic activities. Eight of these patients were professional volleyball players. In the remaining three patients, there was no relationship between the nerve lesion and trauma or athletic activities. Twenty-one patients (22 cases) complained of pain located over the suprascapular notch. Seventeen patients had paresis and atrophy of both the supraspinatus (SS) and infraspinatus (IS) muscles. In 10 patients only the IS muscle was involved. One patient exhibited a sensory deficit over the posterior portion of the shoulder. Electromyography was performed in all cases. The mean follow-up period in the 25 cases (24 patients) that could be evaluated was 20.8 months (range 3-70 months). Nineteen of 22 cases with preoperative pain could be evaluated. Sixteen of these patients were completely free of pain after surgery and three patients found their pain had improved. Motor function in the SS muscle improved in 86.7% and motor function in the IS muscle in 70.8% of cases. Atrophy of the SS muscle resolved in 80.7% and atrophy of the IS muscle in 50% of cases. Surgical treatment of SNE is indicated after failed conservative treatment and in cases of atrophy of the SS and IS muscles. The authors recommend the posterior approach, which minimizes risks and complications and produces good postoperative results.

Adolescent↗
PubMed1996

[Cavernoma. Indications for surgical removal and outcome].

Between July 1990 and October 1994 26 patients were operated on for 26 intracranial and 2 intraorbital cavernous hemangiomas. We found seizures in 62% of our patients, focal neurological deficits and unspecific complains (like headache or dizziness) in 19% each. The average follow-up period was 12 months, 24 patients could be included in this study. 12/14 patients of the seizure group improved, 10/14 reported a complete relieve of their epilepsy. All 5 patients with focal deficits improved, among them 2 with no residual deficit. Finally 3/5 patients with unspecific complains improved, 2/5 remained unchanged. The functional morbidity was 4% (one slight aphasic syndrome), we did not have any mortality. Therefore we conclude that a neurosurgical treatment is indicated in any case of cavernous hemangioma with focal deficits or intractable epilepsy. The operation should also be considered in patients with supressed seizures by anti-convulsants, if the malformation is not located in an eloquent area. Due to the risk of spontaneous bleeding (comparable to incidental aneurysms), the indication for a neurosurgical treatment mainly depends on the location of the cavernoma in cases of its accidental discovery.

Adolescent↗
PubMed1995

Transcription of the region encoding the ferric dicitrate-transport system in Escherichia coli: similarity between promoters for fecA and for extracytoplasmic function sigma factors.

We have analyzed the molecular mechanism of regulation of the ferric dicitrate transport system in Escherichia coli (Ec), by studying the transcription of the regulatory and structural genes under various environmental conditions, and by determining the location of their transcriptional start points and promoter regions. We report here that the main species observed in Northern hybridization analyses were a 2.5-kb mRNA, encoded by the outer membrane protein receptor gene fecA, and a 1.5-kb mRNA encoded by a region including the fecIR genes. The synthesis of the 2.5-kb fecA mRNA is regulated by both citrate and iron. Furthermore, transcription of fecA is dependent on the presence of FecI. The promoter region for the fecA mRNA, a likely site of action for FecI, is not related to the consensus promoter region for sigma 70 RNA polymerase in Ec K-12. However, it shows greatest similarity with promoters of genes regulated by a new sub-family of sigma factors, i.e., the extracytoplasmic function (ECF) sigma factors, which are associated with the expression of genes involved in extracytoplasmic functions, suggesting that FecI may act as a specialized sigma factor. We also show that the fecB,C,D,E transport genes are linked in operon fashion to fecA. Since the levels of the fecB,C,D,E RNAs are extremely low, as compared to the level of fecA mRNA, it is likely that processing from the 3' end must occur and stop near the end of fecA where a hairpin structure is located.

Base Sequence↗