Sociodemographic, psychological, and clinical characteristics associated with health service (non-)use for mental disorders in adolescents and young adults from the general population.

Most adolescents and young adults who experience psychological distress do not seek professional help. This study aims to enhance the understanding of sociodemographic, psychological, and clinical characteristics associated with the underuse of health services by adolescents and young adults with mental disorders. Data from a cross-sectional, epidemiological study with a population-based sample (N = 1180 participants, 14-21 years old) were used. Participants completed a fully standardized, computer-assisted diagnostic interview (DIA-X-5/D-CIDI) administered by trained clinical interviewers to assess lifetime mental disorders according to DSM-5 as well as lifetime health service use for mental health problems, and completed self-report questionnaires to assess various psychological variables (e.g., stigma). Predictors of health service use were examined using univariate and multiple logistic regression analyses, data were weighted for age and sex to improve representativeness Of n = 597 participants with any lifetime mental disorder, 32.4% [95% CI 28.4; 36.7] had ever used any health services because of a mental health, psychosomatic, or substance use problem. Even less had received psychotherapeutic or pharmacological treatment (Cognitive Behavioral Therapy: 12.1% [9.5; 15.2]; other psychotherapy: 10.7% [8.4; 13.7]; medication: 5.4% [3.7; 7.8]). High education was associated with less health service use (low/ middle/ other vs. high education: 53.8% vs. 26.9%; OR = 0.26, p < .001). In the multiple regression model, stigma toward mental disorders was the single psychological variable associated with a reduced likelihood of using health services (OR = 0.69 [0.52; 0.90], p < .01). These findings draw attention to the treatment gap for mental disorders during adolescence and highlight related factors to be addressed in public health contexts.

Cell swelling and ion redistribution assessed with intrinsic optical signals.

Cell volume changes are associated with alterations of intrinsic optical signals (IOS). In submerged brain slices in vitro, afferent stimulation induces an increase in light transmission. As assessed by measurement of the largely membrane impermeant ion tetramethylammonium (TMA) in the extracellular space, these IOS correlate with the extent and time course of the change of the extracellular space size. They have a high signal to noise ratio and allow measurements of IOS changes in the order of a few percent. Under conditions of reduced net KCl uptake (low Cl solution) a directed spatial buffer mechanism (K syphoning) can be demonstrated in the neocortex with widening of the extracellular space in superficial layers associated with a reduced light transmission and an increase of extracellular K concentration. The nature of the IOS under pathophysiological conditions is less clear. Spreading depressions first cause an increase of light transmission, then a decrease. Such a decrease has also been observed following application of NMDA where it was associated with structural damage. Pharmacological analyses suggest that under physiological conditions changes of extracellular space size are mainly caused by astrocytic volume changes while with strong stimuli and under pathophysiological conditions also neuronal swelling occurs. With reflected light usually signals opposite to those observed with transmitted light are seen. Recording of IOS from interface slices gives very complex signals since under these conditions an increase of light transmission has been reported to be superimposed by a decrease of the signal due to mechanical lensing effects of the slice surface. Depending on the method of measurement and the exact conditions, several mechanisms may contribute to IOS. Under well defined conditions IOS are a useful supplementary tool to monitor changes of extracellular volume both in space and time.

A novel role of vasopressin in the brain: modulation of activity-dependent water flux in the neocortex.

The brain contains an intrinsic vasopressin fiber system the function of which is unknown. It has been demonstrated recently that astrocytes express high levels of a water channel, aquaporin-4 (AQP4). Because vasopressin is known to regulate aquaporin expression and translocation in kidney collecting ducts and thereby control water reabsorption, we hypothesized that vasopressin might serve a similar function in the brain. By recording intrinsic optical signals in an acute cortical slice preparation we showed that evoked neuronal activity generates a radial water flux in the neocortex. The rapid onset and high capacity of this flux suggest that it is mediated through the AQP4-containing astrocytic syncytium that spans the entire thickness of the neocortical mantle. Vasopressin and vasopressin receptor V1a agonists were found to facilitate this flux. V1a antagonists blocked the facilitatory effect of vasopressin and reduced the water flux even in the absence of any exogenous agonist. V2 agonists or antagonists had no effect. These data suggest that vasopressin and V1a receptors play a crucial role in the regulation of brain water and ion homeostasis, most probably by modulating aquaporin-mediated water flux through astrocyte plasma membranes.

Basal membrane-depleted scar in lesioned CNS: characteristics and relationships with regenerating axons.

The lesion scar formed after CNS injury is an impediment to axonal regeneration and leads to growth arrest or misrouting of sprouting axons. Our previous study showed that pharmacological reduction of basal membrane formation within the scar can overcome this scar impermeability [Stichel C. C. et al. (1999) Eur. J. Neurosci. 11, 632-646]. The aim of the present study was to characterize the basal membrane-depleted scar and to analyse its relationships with penetrating axons. The experiments comprised two groups of animals in which the left postcommissural fornix was transected; in addition, one group received a local immediate injection of the collagen IV-reducing agent dipyridyl, while the other group received an injection of phosphate-buffered saline. Immunohistochemical methods were used to characterize scar formation and scar-axon relationships. Animals receiving dipyridyl showed reduction of collagen IV-immunopositive basal membrane in the lesion center, which was accompanied by: (i) a decrease in laminin, as well as chondroitin and heparan sulfate proteoglycan, deposition in the lesion center; (ii) an increase in chondroitin and keratan sulfate proteoglycan expression in the perilesional area; (iii) a typical activation pattern of astrocytes and microglia/macrophages; (iv) axons regenerating through this modified scar were closely associated with various glial cell types and crossed a prominent chondroitin/keratan sulfate proteoglycan matrix. Our results suggest that neither the formation of a reactive astroglial network nor the accumulation of microglia/macrophages or the deposition of chondroitin and keratan sulfate proteoglycans in the perilesional area represent a barrier to regrowing axons. The present approach demonstrates that the lesion-induced basal membrane itself is the primary determinant of scar impermeability.

Inhibition of collagen IV deposition promotes regeneration of injured CNS axons.

Scarring impedes axon regrowth across the lesion site and is one major extrinsic constraint to effective regeneration in the adult mammalian central nervous system. In the present study we determined whether specific biochemical or immunochemical modulation of one major component of the scar, the basal membrane (BM), would provide a means to stimulate axon regeneration in the mechanically transected postcommissural fornix of the adult rat. Basal membrane developed within the first 2 weeks after transection in spatiotemporal coincidence with the abrupt growth arrest of spontaneously regrowing axons. Local injection of anticollagen IV antibodies or alpha, alpha'-dipyridyl, an inhibitor of collagen triple helix formation and synthesis, significantly reduced lesion-induced BM deposition. This treatment allowed massive axon elongation across the lesion site. Anterograde tracing provided unequivocal evidence that regenerating axons follow their original pathway, reinnervate the appropriate target, the mammillary body, and become remyelinated with compact myelin. Presynaptic electrophysiological recordings of regenerated fibre tracts showed recovery to nearly normal conduction properties. Our results indicate that lesion-induced BM is an impediment for successful axonal regeneration and its reduction is a prerequisite and sufficient condition for regrowing axons to cross the lesion site.

Purification and structures of branched blood-group-B-active glycosphingolipids from human erythrocyte membranes.

Three different variants of complex, branched, highly blood-group-B-active glycosphingolipids (B-III, B-IV, and B-V) have been isolated from human erythrocytes by means of partition of their membranes in n-butanol/phosphate buffer, subsequent removal of nonpolar lipids and proteins by several steps of phase distribution, acetone or sodium acetate precipitation, peracetylation and repeated fractionation of all crude extracts by silicic acid and ion exchange column chromatography. Finally, peracetylated B-glycolipid fractions were purified to homogeneity by preparative silica gel high-performance thin-layer chromatography. Their structures were elucidated by gas chromatographical sugar analysis, by combined gas chromatography/mass spectrometry of partially methylated alditol acetates for the identification of glycosidic linkages, and by fast atom bombardment and electron impact mass spectrometry of the undegraded, permethylated substances in order to establish the molecular mass, sugar sequence, type of oligosaccharide chain, position of hexosyl branching points, number of N-acetyllatosamine units, as well as sphingosine and fatty acid patterns of the ceramide residues. 360-MHz 1H nuclear magnetic resonance spectroscopy in (2H)dimethylsulfoxide of deuterium-exchanged native B-III and B-IV identified all carbohydrate components, their sites of attachment, the anomeric nature of their glycosidic linkages and the sequential arrangement within the oligosaccharide chain. Furthermore, it established the nature of branching points within the carbohydrate sequence, and assigned the different typical saccharide branches to either the position 2 versus 3, or position 3 versus 6 of the 2,3-disubstituted or 3,6-disubstituted galactoses. The nature of the anomeric linkages and branching points of B-V was based upon the series of NMR data obtained from the B-I--B-IV analogues. All results thus establish the following structures: (formula; see text)

[Men with female karyotypes]. / [Männer mit weiblichen Karyotyp.

Hypotheses concerning phenotypic males with a female karyotype (46,XX males) are discussed. This peculiar chromosomal anomaly may be explained either by a mutation of autosomal sex determining genes or by a translocation of Y chromosomal genes to an X chromosome or an autosome. Recent studies concerning the H-Y antigen indicate that mosaicism with cell lines containing a Y chromosome may not be made responsible for phenotypic males with a 46,XX karyotype.

Relationship between sperm count, serum gonadotropins and testosterone levels in normo-, oligo- and azoospermia.

In 92 men with normozoospermia (greater than 40 X 10(6)/ml), 105 with slight oligozoospermia (greater than 10 X 10(6)/ml), 100 with severe oligozoospermia (less than 10 X 10(6)/ml) and 56 with azoospermia, serum testosterone, LH and FSH were measured radioimmunologically. With an increasing degree of reduction of spermatozoa, a decreasing testosterone level and increasing LH and FSH levels could be demonstrated. In normozoospermia, between 40 and 140 X 10(6)/ml, a direct correlation was found between FSH and sperm count, and, in the group between 40 and 100 X 10(6)/ml, a direct correlation between T and sperm count. A disturbed LH:T balance is often observed which beside decreased serum T levels demonstrates a testicular deficiency in androgen production.

C1q precipitins in human seminal plasma.

Seminal plasma was tested against purified C1q by double diffusion. Precipitation reactions were frequently observed in the seminal plasma of patients with normozoospermia and patients with azoospermia; most of these reactions were not due to soluble immune complexes binding to C1q. A factor resistant to DNAse and RNAse (mol wt: 25,000--150,000 daltons) was found to precipitate C1q. Its discovery adds to the list of substances which may interfere in C1q precipitation tests.

Testosterone levels and gonadotrophins in Klinefelter's patients treated with injections of mesterolone cipionate.

Hormone levels were measured in patients with Klinefelter's syndrome after treatment with 100 mg mesterolone cipionate (twice monthly). There was no difference in plasma testosterone and FSH levels in treated and untreated patients. The basal and maximum LH levels were lower, but remained raised. The urinary excretion of testosterone as measured by liquid gaschromatography was higher in treated patients after treatment was discontinued.-From these results it is concluded that in spite of reported decreases of plasma testosterone during therapy with mesterolone cipionate this drug does not lead to severe impairment of the endogenous hormone production after discontinuing treatment.

Seminal proteins in patients with agglomerations of spermatozoa.

Seminal proteins (IgA, IgG, albumin) were measured in normozoospermic patients and in patients with normozoospermia associated with agglomerations of spermatozoa. The type of agglomeration was not taken into account. A slight yet significant increase in seminal IgA was detected in patients with agglomerations whereas the other proteins remained unchanged. By testing seminal plasma against C1q by double diffusion it was shown that many patients of both groups had nonimmune C1q precipitins. The significance of such precipitins in semen is not known.

Excretion of urinary testosterone in Klinefelter's syndrome.

The urinary testosterone excretion in 55 patients with Klinefelter's syndrome was determined by gas-chromatographic methods. The mean testosterone level in the group of Klinefelter patients was significantly decreased (15.7 mug/24 hrs) compared with the excretion by 30 normal men (44.1 mug/24 hrs). An age dependency of excretion levles was not obvious in chromatin-positive men when compared to healthy subjects. A correlation between testosterone excretion and configuration types seemed to be probable by reason of observations and statistical values. Average testosterone excretion increased with increasing normalization of body proportions. Gynecomastia was noticed in 56% of those examined. With increasing severity of gynecomastia the mean testosterone levels decreased. A correlation between beard and body hair, which was decreased in almost all subjects, and testosterone excreiton was not visible. With diminishing mean testosterone excretion an increase of osteoporosis seemed to be probable. A statistically significant difference was found when comparing patients who never had ejaculations with those who had regular libido and ejaculations. Klinefelter patients who had not succeeded in completing school or an occupational education showed a significantly decreased testosterone level as compared with others who had a profession.