Stimulation of protein phosphatase activity by insulin and growth factors in 3T3 cells.

Incubation of Swiss mouse 3T3-D1 cells with physiological concentrations of insulin resulted in a rapid and transient activation of protein phosphatase activity as measured by using [32P]phosphorylase a as substrate. Activation reached a maximum level (140% of control value) within 5 min of addition and returned to control levels within 20 min. The effect of insulin was dose-dependent with half-maximal activation occurring at approximately 5 nM insulin. This activity could be completely inhibited by addition of the heat-stable protein inhibitor 2, which suggests the presence of an activated type-1 phosphatase. Similar effects on phosphatase activity were seen when epidermal growth factor and platelet-derived growth factor were tested. These results suggest that some of the intracellular effects caused by insulin and growth factors are mediated through the activation of a protein phosphatase.     

Complete excision of acoustic neurinoma. Preservation of the facial nerve and hearing

Using microtechniques, total removal of acoustic neuromas with facial nerve preservation is possible today in most cases. The next barrier of operative treatment is hearing preservation which is routinely attempted, with the help of intraoperative brainstem auditory evoked responses monitoring. The present series deals with 176 operations performed sub-occipitally in 159 patients from 1970 up to 1985. Twelve patients were operated upon 29 times. According to the W.T. Koos classification, there were 16 type II, 39 type III and 121 type IV neuromas. Ten patients died postoperatively. In seven of these, death was related to surgery, in two it was caused by respiratory failure. In the last patient unexplained sudden death occurred. 169 patients had no facial weakness preoperatively, in 158 of these the facial nerve was anatomically preserved (93.5%). Facial nerve function was judged by evaluation of function of face at least 12 months after operation. Up to 36 months after surgery, a good facial result may be expected in cases where the facial nerve was macroscopically spared at completion of removal. Functional results have been reviewed in 151 patients according to the J.W. House's International Evaluation System, with an excellent or good result in 66 (44%), fair in 65 (43%), bad or poor in 20 (13%). The anatomical preservation of the cochlear nerve could be achieved in 80 patients of the group of 169 in whom the auditory function had not been damaged by a previous operation. In fact, the auditory function preservation could be reasonably attempted in 79 patients: showing a hearing loss below 70 dB on tone audiometry, whatever may be the result of speech discrimination score. 59 patients (75%) of this later group had their auditory nerve preserved, 14 (18%) showed preserved hearing function postoperatively, 10 of these with a speech discrimination score over 50%. Two of these showed an improvement of preoperative hearing, two others showed a total recovery of hearing function after removal.     

Carbon monoxide production in ventilated premature infants weighing less than 1500 g.

Mean pulmonary excretion rate of carbon monoxide in 13 premature babies on ventilators was significantly higher (p less than 0.001) than that of 19 healthy infants born at full term. This correlated with carboxyhaemoglobin concentrations in blood, indicating that the premature infants on ventilators produced abnormally large amounts of bilirubin.     

Nationales Reanimationsregister

Within the scope of the symposium “Rescue Medicine in Germany” (held at the Reisensburg near Ulm in 2002), the need for a standardized data acquisition set for prehospital cardiac arrest patients was identified. Therefore, the working group “Emergency Medicine” of the German Society of Anesthesiology and Intensive Care Medicine (DGAI) created a nationwide data acquisition system for primary medical care in prehospital cardiac arrest patients treated with cardiopulmonary resuscitation procedures. The system is in full accordance with the “Utstein style.” Integration of this data acquisition system, for example into the “Dortmund protocol,” is providing a standardized data web base of all acquired prehospital data analyze and to compare processing and structural quality. As additional modules for this nationwide data web base system, an inhospital module “further clinical treatment” and a “long-term follow-up” module are currently in the developmental process.     

Microtubule-associated protein tau is required for axonal neurite elaboration by neuroblastoma cells.

NB2a/d1 neuroblastoma cells constitutively express multiple isoforms of the microtubule-associated protein tau and incorporate this protein into the axonal neurites elaborated during serum deprivation. To examine whether or not tau played an essential role in axonal outgrowth, cells cultured in serum-free medium were treated at 24 h intervals with antisense- and sense-oriented cDNA oligonucleotides (25 or 36 mers that span or are upstream of tau initiation codon) and were simultaneously serum deprived. Oligonucleotide uptake was confirmed by determination of intracellular levels of radiolabeled oligonucleotides. Treatment for 48 h with tau antisense oligonucleotides reversibly inhibited the expression of tau and the number of neurite-bearing cells compared with treatment with sense oligonucleotides. By contrast, tubulin expression was not affected. When cells were treated with antisense oligonucleotide simultaneously with serum deprivation, the initial outgrowth of neurites was unaffected, but continued neurite elongation was prevented. By contrast, neurite outgrowth at 4 h was inhibited when cells were pretreated with tau antisense 24 h before serum deprivation. Furthermore, intracellular delivery of anti-tau antiserum prevented neurite outgrowth and, in cells that had previously been deprived of serum for 24 h, induced retraction of existing neurites. These findings indicate that both the initiation and the continued outgrowth of neurites are dependent on tau and that pre-existing cytoplasmic pools of tau can mediate initial neuritogenesis.     

Hematopoietic turnover index in reactive and neoplastic bone marrow lesions: quantification by apoptosis and PCNA labeling

 In order to determine the dynamics of hematopoietic cell turnover, proliferative activity and incidence of apoptosis (programmed cell death) were evaluated in bone marrow trephine biopsies. Selection of patients (20 in each group) included in addition to a control group, idiopathic thrombocytopenia (ITP), reactive thrombocytosis (TH), secondary polycythemia-smokers' polyglobuly (PG), primary (essential-hemorrhagic) thrombocythemia (PTH), polycythemia vera (PV), and finally acute myeloid leukemia (AML). Apoptosis was demonstrated by the in situ end-labeling technique (ISEL) and proliferative activity by applying the monoclonal antibody PC10 raised against proliferating cell nuclear antigen (PCNA). To assess dynamic features of hematopoiesis, an index was calculated consisting of the ratio between PCNA-positive nuclei and the apoptotic cell fraction. This factor was termed the hematopoietic turnover index (HTI). Morphometric analysis revealed that the HTI was significantly increased in AML and PV. According to cell culture studies both disorders are characterized by either a prevalent proliferation of the myeloid or erythroid cell mass. On the other hand, PG, PTH, and TH showed no relevant enhancement of this index in comparison to the control specimen. In vitro experiment results are in keeping with the finding that PG and PTH are not associated with a significant expansion of the erythroid lineage (CFU-E). Similar to ITP and TH, in PTH megakaryocyte proliferation (CFU-MEG) is the predominant feature of cell turnover. Differences between PTH and TH are in line with the reduced in vitro formation of CFU-MEG in the latter disorder. In conclusion, our in situ study on turnover rates of the bone marrow in various neoplastic and reactive lesions extends previous experimental data on hematopoietic cell kinetics. Received: 10 March 1997 / Accepted: 18 May 1997