In vivo EMG biofeedback in violin and viola pedagogy

In vivo EMG biofeedback was found to be an effective pedagogical tool for removing unwanted left-hand tension in nine violin and viola players. Improvement occurred rapidly and persisted throughout a 5-month follow-up period. Further studies will be necessary to assess the effect of biofeedback independent of placebo effects. The brevity of the method and the magnitude of improvement warrant further investigation.     

Modification of testicular and thyroid function by chronic exposure to short photoperiod: a comparison in four rodent species

Exposure of male Syrian hamsters (Mesocricetus auratus) for 10 weeks to short photoperiod (SP) providing 10 hr light: 14 hr darkness (10:14 LD) produced a significant reduction in the weights of the reproductive organs, plasma thyroxine (T4) levels and free T4 index (FT4I) compared to the values of animals exposed to long photoperiod (LP, 14:10 LD). C57bl male house mice (Mus musculus) kept in SP (10:14 LD) had reproductive organ weights equivalent to those of mice kept in long days (14:10 LD) and lower T3 uptake (T3U) values. Male gerbils (Meriones unguiculatus) exposed to 13 weeks of SP (10:14 LD) had lower body weights, testes and seminal vesicle weights and higher T3U values compared to LP (14:10 LD) controls. However, no effect was seen on plasma T4 and triiodothyronine (T3) values nor the FT4I and free T3 index (FT3I). White-footed male mice (Peromyscus leucopus) exposed to SP (8:16 LD) had significantly lower testes and seminal vesicle weights while plasma T4 and T3 levels were unaffected. Snell strain house mice (Mus musculus) exposed to SP (8:16 LD) had normal reproductive organ weights compared to the values of LP-exposed (16:8 LD) control animals. However, there was a significant depression in T3 and in the FT3I in the SP animals.     

Syntheses of (Z)-and (E)-4-amino-2-(trifluoromethyl)-2-butenoic acid and their inactivation of gamma-aminobutyric acid aminotransferase.

(Z)- and (E)-4-amino-2-(trifluoromethyl)-2-butenoic acid (4 and 5, respectively) were synthesized and investigated as potential mechanism-based inactivators of gamma-aminobutyric acid aminotransferase (GABA-AT) in a continuing effort to map the active site of this enzyme. The core alpha-trifluoromethyl-alpha,beta-unsaturated ester moiety was prepared via a Reformatsky/reductive elimination coupling of the key intermediates tert-butyl 2,2-dichloro-3,3,3-trifluoropropionate and N,N-bis(tert-butoxy-carbonyl)glycinal. Both 4 and 5 inhibited GABA-AT in a time-dependent manner, but displayed non-pseudo-first-order inactivation kinetics; initially, the inactivation rate increased with time. Further investigation demonstrated that the actual inactivator is generated enzymatically from 4 or 5. This inactivating species is released from the active site prior to inactivation, and as a result, 4 and 5 cannot be defined as mechanism-based inactivators. Furthermore, 4 and 5 are alternate substrates for GABA-AT, transaminated by the enzyme with Km values of 0.74 and 20.5 mM, respectively. Transamination occurs approximately 276 and 305 times per inactivation event for 4 and 5, respectively. The enzyme also catalyzes the elimination of the fluoride ion from 4 and 5. A mechanism to account for these observations is proposed.     

Pharmakogenetik der oralen Antikoagulation mit Cumarinen

The recent identification of VKORC1 has made important contributions to our understanding of the vitamin K cycle. The VKORC1 enzyme was shown to be the molecular target of coumarin drugs. Mutations and polymorphisms in coding and noncoding regions of the VKORC1 gene have been shown to cause both a partial to total coumarin resistance and coumarin sensitivity. Availability of molecular diagnostics (VKORC1, CYP2C9) and drug monitoring by HCPLC (determination of coumarin, vitamin K, and vitamin K epoxide levels) is helpful for detecting hereditary and acquired factors influencing coumarin therapy. In the future, these tools may be instrumental in designing individualized oral anticoagulation therapy regimens.     

Phosphorylation of lens membranes with a cyclic AMP-dependent protein kinase purified from the bovine lens

We report the phosphorylation of lens membranes with a cAMP-dependent protein kinase isolated from bovine lenses. The holoenzyme was eluted from DEAE agarose at less than 100 mM NaCl and from gel filtration columns with a relative molecular weight of 180 000. The regulatory subunit was identified with the affinity label 8-azido-[32P]cAMP. Four focusing variants with relative molecular weights of 49 000 were seen on two-dimensional gels. The catalytic subunit was purified approx. 5000-fold and migrated at 42 000 Mr on SDS gels. Based on these observations, the enzyme is classified as a Type I cAMP-dependent protein kinase. Purified lens plasma membranes were incubated with the holoenzyme or its catalytic subunit in the presence of 32P-labeled ATP. Several membrane proteins, including the major lens membrane polypeptide, MP26, were shown to be substrates for the kinase in this reaction. MP26 appears to be the major component of intercellular junctions in the lens. Studies with protease treatments on labeled membranes appeared to localize the phosphorylation sites to the cytoplasmic side of the membrane.     

A Simple Survival Model for Combined Action of Two Damaging Agents

The aim of this study was mathematical formalization of the development of two damage processes in response to the combined action of two different damaging agents. The model allows to obtain the parametric family of distributions for the life-span when the organism's death is due to joint effect of two damage processes. Differing by their probabilistic meaning the notions of a priori (M (t)) and a posteriori (M(y)) conditional mean contributions of each damage process to the final effect of combined injury are introduced. The formulas permitting to compute the M and M values on the basis of survival data parametric analysis are given.     

Hypophysiotropic neurons in the goldfish hypothalamus demonstrated by retrograde transport of horseradish peroxidase

Summary The horseradish-peroxidase (HRP) technique was used to visualize the cell bodies of axons projecting to the goldfish pituitary. Following intravenous injections of HRP, HRP reaction products were observed in axons of the rostral pars distalis, proximal pars distalis, neurointermediate lobe, pituitary stalk and in axons coursing from the pituitary into the hypothalamus. HRP-labelled cells in the brain were localized in two regions only — the nucleus preopticus (NPO) pars magnocellularis and pars parvocellularis, and the nucleus lateralis tuberis (NLT) of the hypothalamus. These observations suggest that the NPO and NLT are the source of the neurosecretory innervation of the goldfish pituitary.     

Attachment of blastocysts to lens capsule: A model system for trophoblast-epithelial cell interaction on a natural basement membrane

Summary The bovine lens capsule has previously been shown to provide an optimal surface for the examination of epithelial cell interaction with a basement membrane. This native substrate has been used to investigate some initial aspects of attachment of mouse blastocysts and trophoblastic cellular outgrowth. Mouse blastocysts were presented to the cell-free humoral side of the anterior lens capsule, incubated for 72 h, and examined by scanning and transmission electron microscopy. Blastocysts hatch and attach from their zonae pellucidae by 30 h. Trophoblastic cells proliferate rapidly in a coronal direction, display extensive surface microvilli, and advance by the extension of numerous filipodia, many of which terminate with bulbous projections. These projections were shown by transmission electron microscopy to contain numerous vacuoles and polysomes. To simulate further the initial blastocyst-uterine interaction, a suspension of lens epithelial cells was introduced to the capsule and permitted to form a monolayer prior to the addition of the blastocysts. At 72 h the monolayer of lens cells remained intact. We observed that: a) lens cells appear to recede from the advancing trophoblastic cells, and b) trophoblastic cells extend beneath the monolayer of lens cells and thereby dislodge the cells from the lens capsule substrate. No infiltration of the capsule by the advancing trophoblastic cells was observed. The lens capsule appears to offer a promising system for the study of trophoblast-epithelial cell interaction on a natural basement membrane.     

Genetische Aspekte bei Spermatogenesestörungen

The cause for infertility which affects about 10–15% of all couples may be found in approximately half of the cases in the male partners who usually exhibit reduced sperm counts in the ejaculate (i.e. oligozoospermia or azoospermia). The clinically most relevant genetic causes of spermatogenic failure are chromosomal aberrations including Klinefelter’s syndrome and Y chromosomal microdeletions of the AZF loci. Aside from the full clinical picture of cystic fibrosis, mutations in the CFTR gene can cause an isolated obstructive azoospermia without spermatogenic impairment. Genetic investigations should depend on the results of andrological examinations. Chromosomal aberrations are detected more frequently with decreasing sperm counts, where autosomes (e.g. translocations) are predominantly involved in men with oligozoospermia whereas in 10–15% azoospermia is caused by Klinefelter’s syndrome. Classical AZF deletions are found only in men with severe oligospermia or azoospermia and have a prognostic value. In contrast to men with AZFc deletions, carriers of complete AZFa and AZFb deletions have virtually no chance for testicular sperm extraction and a testicular biopsy is not advised. Rare cases of male infertility may be caused by specific syndromes or sperm defects (e.g. globozoospermia and disorders of ciliary structure).