Assessing forest availability for wood supply in Europe.

The quantification of forests available for wood supply (FAWS) is essential for decision-making with regard to the maintenance and enhancement of forest resources and their contribution to the global carbon cycle. The provision of harmonized forest statistics is necessary for the development of forest associated policies and to support decision-making. Based on the National Forest Inventory (NFI) data from 13 European countries, we quantify and compare the areas and aboveground dry biomass (AGB) of FAWS and forest not available for wood supply (FNAWS) according to national and reference definitions by determining the restrictions and associated thresholds considered at country level to classify forests as FAWS or FNAWS. FAWS represent between 75 and 95 % of forest area and AGB for most of the countries in this study. Economic restrictions are the main factor limiting the availability of forests for wood supply, accounting for 67 % of the total FNAWS area and 56 % of the total FNAWS AGB, followed by environmental restrictions. Profitability, slope and accessibility as economic restrictions, and protected areas as environmental restrictions are the factors most frequently considered to distinguish between FAWS and FNAWS. With respect to the area of FNAWS associated with each type of restriction, an overlap among the restrictions of 13.7 % was identified. For most countries, the differences in the FNAWS areas and AGB estimates between national and reference definitions ranged from 0 to 5 %. These results highlight the applicability and reliability of a FAWS reference definition for most of the European countries studied, thereby facilitating a consistent approach to assess forests available for supply for the purpose of international reporting.

Cytochrome c depletion upon expression of Bcl-XS.

We have shown previously that Bcl-XS causes acute cell death in 3T3 cells without activating caspases (Fridman, J. S., Benedict, M. A., and Maybaum, J. (1999) Cancer Res. 59, 5999-6004). In this study, we determined that the explanation for lack of caspase activation is the cellular depletion of cytochrome c. Electron microscopy revealed gross structural changes in the mitochondria of Bcl-XS-expressing cells; however, cytochrome c was not detected in cytosolic fractions from these cells. Surprisingly, it was determined that cellular cytochrome c levels decreased as Bcl-XS expression levels increased. Experiments performed to eliminate other possible explanations for the lack of caspase activation showed that these 3T3 cells have a functional cytoplasmic apoptosome, a complex of proteins that form a functional trigger capable of activating the proximal caspase in an apoptotic pathway Chinnaiyan, A. M. (1999) Neoplasia 1, 5-15, as cytosolic extracts from these cells were capable of cleaving pro-caspase-9. These cells were also able to release cytochrome c from their mitochondria after appropriate stimulation, other than Bcl-XS expression (i.e. withdrawal from serum for 24 h), and initiate a cell death that is inhibited by a dominant negative caspase-9. We conclude that lack of caspase activation is due to a Bcl-XS-induced depletion of active cytochrome c, a phenomenon that represents an alternative cell death effector pathway and/or a novel mechanism for regulating caspase activation.

bcl-X(S)-induced cell death in 3T3 cells does not require or induce caspase activation.

Using a tetracycline-regulated expression system, we have shown that expression of bcl-X(s) is sufficient to induce acute cell death in 3T3 cells, and that the manner in which these cells die is both morphologically and biochemically different from Fas/CD95-induced apoptosis. bcl-X(s) expression causes loss of the inner mitochondrial membrane potential (deltapsim) but does not induce caspase activation. Loss of viability, as determined by mitochondrial function and ethidium bromide exclusion, was not inhibited by the broad-spectrum caspase inhibitor zVAD-fmk or by expression of a dominant negative caspase 9 (9DN). However, zVAD-fmk was efficacious in inhibiting cell death triggered by an activating anti-Fas/CD95 antibody. In addition, bcl-X(s) does not possess the 5th and 6th alpha-helices (thought to be the membrane-spanning domains in bcl-2, bcl-X(L), and bax) and, therefore, should not be able to form membrane channels, thus eliminating this possible mechanism of action. The finding that bcl-X(s) kills 3T3 cells without caspase activation, along with the absence of membrane spanning domains in bcl-X(s), may, therefore, represent a novel cell death pathway for the pro-death bcl-2 family members.

Models to Assess the Risk of Snow and Wind Damage in Pine, Spruce, and Birch Forests in Sweden.

/ Each year damage to forests caused by snow and wind causes high economic losses. In Sweden, approximately 4 million m3 are damaged annually by snow and wind, roughly corresponding to a value of US$150 million, and in Europe, the damage amounts to hundreds of millions of US dollars each year. To help to reduce these losses, tools for risk assessment within forest management have been developed. Predictions were developed of the risk of damage from snow and wind to Scots pine (Pinus sylvestris L.), Norway spruce [Picea abies (L.) Karst.] and Birch (Betula spp. L.) plots using tree, stand, and site characteristics. The data were obtained from 6756 permanent sample plots within the Swedish National Forest Inventory, which were inventoried twice at five-year intervals between 1983 and 1992. Input data for model development used measurements from the first inventory of tree characteristics for the largest sample tree, stand, and site data, and records of snow and wind damage from the second inventory. Models were developed for three different regions for pine- and spruce-dominated sites, while models for the whole country were developed for birch sites. In general the estimated proportion of damaged plots was highly overestimated (31.7%-56.2%), compared with the observed proportion of 3.4%-11.9%. The models for Norway spruce comprising tree, stand, and site data show the best predictability of damaged plots, with 60.6%-67.6% of plots correctly classified. It is concluded that the models developed can be used to detect sites with a high probability of damage from snow and wind, and thus be used as tools to reduce future damage and costs in practical forestry.KEY WORDS: Birch; Norway spruce; Risk assessment; Risk management; Scots pine; Silviculturehttp://link.springer-ny.com/link/service/journals/00267/bibs/24n2p209.html

A caspase-resistant form of Bcl-X(L), but not wild type Bcl-X(L), promotes clonogenic survival after ionizing radiation.

Bcl-2 and Bcl-X(L) belong to a family of proteins overexpressed in a variety of human cancers which inhibit apoptosis in response to a number of stimuli including chemotherapeutic agents and ionizing radiation. To better understand the role of these polypeptides in modulating the response of cancer cells to ionizing radiation we used cell lines that were engineered to overexpress the two polypeptides. Although Bcl-2 and Bcl-X(L) overexpression resulted in inhibition of radiation-induced apoptosis, it did not result in enhanced clonogenic survival. Consistent with this was the observation that Bcl-2 and Bcl-X(L) protected cells from DNA fragmentation, loss of mitochondrial membrane potential, and caspase activation for up to 72 hours after irradiation. Beyond 72 hours, there was a rapid loss in the ability of Bcl-2 and Bcl-X(L) to inhibit these markers of apoptosis. When Bcl-X(L) was analyzed at 72 hours after irradiation and beyond, a rapid accumulation of a 16-kDa form of Bcl-X(L) was observed. To test the hypothesis that cleavage of the 29-kDa form of Bcl-X(L) by caspases to a 16-kDa polypeptide results in its inability to inhibit apoptosis beyond 72 hours, we constructed a cell line that overexpressed a caspase-resistant form of Bcl-X(L) (Bcl-X(L)-deltaloop). Cells overexpressing Bcl-X(L)-deltaloop were resistant to apoptosis beyond 72 hours after irradiation and did not contain the 16-kDa form at these time points. In addition, Bcl-X(L)-deltaloop overexpression resulted in enhanced clonogenic survival compared with control or Bcl-X(L) overexpressing cells. These results provide a molecular basis for the observation that expression of Bcl-2 or Bcl-X(L) is not a prognostic marker of tumor response to cancer therapy.

Expression of Bcl-XS alters cytokinetics and decreases clonogenic survival in K12 rat colon carcinoma cells.

bcl-XS, a member of the bcl-2 family, has been shown to induce and/or sensitize some cells to undergo programmed cell death, and to negate the anti-apoptotic activity of bcl-XL and bcl-2 by mechanisms which are still uncertain. To help understand these mechanisms we have established stable derivatives of the K12 rat colon carcinoma cell line that express bcl-XS in a tetracycline-regulated manner, using an autoregulatory retroviral cassette. When bcl-XS expression is induced, we observe two phenotypic responses. A small fraction of cells appear to undergo spontaneous apoptosis while the majority of cells undergo a form of cytostasis. In the latter case, the cells stop dividing (or divide a limited number of times at a retarded rate) and swell to many times their original size. These cells can take on a ghostlike appearance and subsequently detach from the culture plates and die or they may remain intact in a hindered state of proliferation. Doubling times were calculated to be 31.4 h in the presence of tetracycline and 50.4 h without tetracycline, bcl-XS expression also causes dramatic alterations in the cell cycle distribution of K12 cells manifesting as a substantial decrease (approximately 50%) in the fraction of S phase cells with a concomitant increase in the G1 population. Continuous expression of bcl-XS, at levels approximately equal to that of bcl-XL, decreased the viability of K12 cells as demonstrated by a log decline in clonogenic survival. This decrease occurred without considerable apoptosis or a compensatory increase in the level of bcl-XL. None of these phenotypes were present in control cells expressing beta-galactosidase in a similar retroviral cassette. These observations demonstrate that bcl-XS can have substantial cytokinetic effects under circumstances that produce relatively little apoptosis.

Male pseudohermaphroditism due to a homozygous missense mutation of the luteinizing hormone receptor gene.

Leydig cell hypoplasia is a rare autosomal recessive condition that interferes with normal development of male external genitalia in 46,XY individuals. We have studied two Leydig cell hypoplasia patients (siblings born to consanguineous parents), and found them to be homozygous for a missense mutation (Ala593Pro) in the sixth transmembrane domain of the luteinizing hormone (LH) receptor gene. In vitro expression studies showed that this mutated receptor binds human choriogonadotropin with a normal KD, but the ligand binding does not result in increased production of cAMP. We conclude that a homozygous LH receptor gene mutation underlies the syndrome of autosomal recessive congenital Leydig cell hypoplasia in this family. These results have implications for the understanding of the development of the male genitalia.

Neurometrics: computer-assisted differential diagnosis of brain dysfunctions.

Normative developmental equations provide reliable descriptors of brain electrical activity in people 6 to 90 years old. Healthy persons display only chance deviations beyond predicted ranges. Patients with neurological impairment, subtle cognitive dysfunctions, or psychiatric disorders (including dementia and primary depression) show a high incidence of abnormal values. The magnitude of the deviations increases with clinical severity. Different disorders are characterized by distinctive profiles of abnormal values of brain electrical features. Computerized differential classification of some of these disorders can be achieved with high accuracy. Such classification, providing objective corroboration of brain dysfunctions, may be a useful adjunct to psychiatric diagnosis, which relies primarily on subjective clinical impressions. These methods may provide independent criteria for diagnostic validity, evaluations of treatment efficacy, and more individualized therapy.

Response threshold determination of the brain stem auditory evoked response: a comparison of the phase versus magnitude derived from the fast Fourier transform.

An ensemble of 10 groups of brain stem evoked responses (BAERs), each consisting of 200 sweeps, was collected for different intensity levels and for a no-stimulus condition. A fast Fourier transform was calculated for the separate groups, which permitted a phase variance to be derived. The phase variance was compared to the magnitude value for selected frequency components making up the BAER. It was found that the phase variance was a better predictor of signal than magnitude. The superiority of prediction by phase results from intersubject variation being smaller for phase compared to magnitude.

Application of phase spectral analysis for brain stem auditory evoked potential detection in normal subjects and patients with posterior fossa tumors.

A statistical test of the brain stem auditory-evoked potential (BAEP) detection is presented. The data were collected by averaging groups of 200 sweeps in order to obtain a set of group averages. The synchrony measure (SM), which represents the degree of reproducibility for group averages, is used as a statistical measure and is calculated from the phase variance for selected Fourier components of the group averages. The sensitivity of the test was demonstrated on 375 normal BAEPs with different stimulus intensities (45, 60, 75 dB SL) from both the ipsilateral and contralateral recordings, and on 82 BAEP recordings in the absence of stimulus. In all 375 cases of normal BAEPs the SM exceeds the threshold level while in the absence of stimulation the SM was below the threshold level. The clinical usefulness of the test was demonstrated on 22 patients with tumors of the posterior fossa. The absence of the BAEP was detected in 21 patients. In 12 out of 13 patients with lateralized tumors (acoustic neuromas), absence of the BAEP was noted for stimulation of the affected ear.

Normative values for brain stem auditory evoked potentials obtained by digital filtering and automatic peak detection.

A BAEP test which uses constant, high level click stimulation was developed for preliminary screening of patients with known or suspected problems in auditory information processing. Digital filtering and automatic peak detection were employed to aid in the analysis of BAEP component latencies. The results of 148 BAEP tests allowed us to select a set of normative measures: absolute peak latency, interpeak latency and left-right peak latency difference. The set of threshold values was developed for selected BAEP measures, in order to evaluate test results.

Application of digital filtering and automatic peak detection to brain stem auditory evoked potential.

A method to establish optimal parameters for automatic analysis of the BAEP was proposed. Spectral analysis of a set of BAEP trial averages yields criteria for the selection of the optimal bandwidth for digital filtering, establishes a lower limit for the number of averaged responses required for accurate determination of BAEP wave shape and permits accurate estimation of the amplitude and latency of BAEP peaks. Estimation of phase variance proved to be an effective procedure for selection of the optimal frequency band for automatic peak detection. Complete representation of the BAEP should include unfiltered and digitally filtered signals, an accuracy estimate of the filtered signal, and computer peak detection. High stability of detected peak latency values, as a result of using a digital filter with optimal parameters, will allow a reduction in the number of responses which must be averaged to obtain an accurate estimate of BAEP morphology. This should be of particular value where closely spaced serial observations are desirable, as in intra-operative monitoring. Procedures analogous to those described herein should permit reduction of the sample size required for accurate estimation of the morphology of far-field somatosensory evoked potentials, and for cortical potentials evoked by any stimulus modality. The consequent increase in the speed with which reliable measurements can be obtained can be expected to increase the practical application of all evoked potential techniques.

Effects of probenecid on blood levels and tissue distribution of ampicillin in fowls and turkeys.

The effect of probenecid (a benzoic acid derivative which competitively inhibits active secretion of weak organic acids by the renal tubules) on serum ampicillin concentrations and the distribution of ampicillin in body organs was examined in fowls and turkeys. An aqueous solution of probenecid coadministered intramuscularly, at 200 mg/kg, with sodium ampicillin solution, at 25 mg/kg, resulted in peak serum antibiotic concentration of 16.5 microgram/ml. A similar dose of ampicillin administered alone produced a peak level of 4.6 microgram/ml. Subcutaneous injections of sodium ampicillin at 25 mg/kg with aqueous probenecid at 200 mg/kg resulted in a peak serum ampicillin concentration (12.8 microgram/ml) three times as high as the peak produced by the subcutaneous injection of ampicillin alone at 50 mg/kg (4.2 microgram/ml). The elimination half-life (t 1/2) of the drug (30 min) was increased to 1.5 hr by coadministration of probenecid parenterally, and serum antibiotic levels greater than or equal to 5.0 microgram/ml were maintained during 3 hours. Ampicillin seemed to be poorly absorbed from the gastrointestinal tract of fowls. A single oral bolus administration of ampicillin trihydrate aqueous suspension produced a peak of 0.6 microgram/ml, and coadministrations of aqueous probenecid suspension at 20, 50, and 100 mg/kg respectively produced peaks of 0.9, 1.25, and 1.5 microgram/ml. During 4 and 5 days, when ampicillin was added to the drinking water at rates of 200 and 50 mg/liter, serum ampicillin levels were rather low (peaks of 0.20 and 0.12 microgram/ml, respectively), and although these levels were increased by 50% with the coadministration of probenecid they were considered to be of limited clinical value for treating systemic bacterial infections. Probenecid did not change the distribution of ampicillin in the organs.