The value of middle phalangeal hair as an anthropometric marker: A review of the literature.

Middle phalangeal hair (MPH) is a trait frequently examined in anthropological studies throughout the 20th century. MPH is found on the back of the middle segment of the fingers, excluding the thumb. Typically, researchers examined the presence and absence of hair in various populations, and described it in terms of age, ancestry, and sex. Recently MPH has been examined as a potential anthropometric indicator of: androgen levels, androgen-related side effects in women, gene homozygosity, and disease resistance. Given the potential value of this marker, the present paper provides a comprehensive overview of MPH and its associated characteristics (i.e., ethnicity, sex, age, and hormonal variations) and presents new data on the reliability of MPH assessment. Findings suggest that ethnicity, sex, and age need to be controlled in any studies examining MPH and its relationship with other variables. Two measures of MPH (i.e., presence/absence of MPH and actual hair count) are both acceptable to use in MPH assessment; and the use of a hand lens to examine MPH provides high reliability when MPH is assessed by expert raters. However, researchers should avoid participant self-assessment. Future avenues for research are suggested (e.g., measurement issues and studies on hormonal correlates in women). MPH could be useful in research or for clinical purposes as a possible non-invasive indicator of hormone levels or hormonal sensitivity, or of predisposition toward androgen-related or gene-homozygosity-related health issues or behaviors.

Dexamethasone potentiates the stimulatory effect of insulin-like growth factor-I on collagen production in cultured human fibroblasts.

We examined the effects of insulin-like growth factor-I (IGF-I) and dexamethasone on the production of collagen by cultures of human infant foreskin fibroblasts, and the interaction between these two factors. IGF-I at 500 ng/ml maximally increased collagen accumulation fourfold. Collagen was increased twofold relative to total protein production. Dexamethasone at a concentration of 1 mumol/l reduced collagen production by between 25% and 40% in unstimulated cells and those cultured with up to 100 ng IGF-I/ml. However, dexamethasone did potentiate collagen production in cells stimulated with 250 ng IGF-I/ml. This potentiation was independent of any effects of IGF-I or dexamethasone on prostaglandin (PG)E2 production. Transforming growth factor-beta (TGF-beta) is also a potent stimulator of collagen formation. However, no potentiation of TGF-beta-stimulated collagen production by dexamethasone was apparent. The mechanism by which dexamethasone potentiates IGF-I-stimulated collagen production was investigated. Dexamethasone treatment increased IGF-I binding to the type 1 IGF receptor without altering the binding affinity. Dexamethasone also attenuated the secretion of IGF-binding proteins by IGF-I-maintained cells.

Tumour necrosis factor alpha, interferon gamma and dexamethasone regulate IGF-I-maintained collagen production in cultured human fibroblasts.

We examined the effects of tumour necrosis factor alpha (TNF alpha) and interferon gamma (IFN gamma) on the production of collagen by human infant foreskin fibroblasts. Collagen synthesis was maintained in the presence of IGF-I so that cytokine effects could be examined in the absence of serum. TNF alpha inhibited IGF-I-maintained collagen production in a dose-dependent manner. Maximal suppression of 50% was attained at a concentration of 7.5 ng/ml. IFN gamma also suppressed collagen accumulation in IGF-I-maintained cells, with a maximal inhibition to 55% at 375 U/ml. The rate of collagen formation relative to total protein production for secreted proteins was calculated. This value decreased from 10.3% for IGF-I-cultured cells to 6.2% and 8.4% with the inclusion of TNF alpha and IFN gamma respectively, indicating that inhibition was selective for collagen. TNF alpha (5 ng/ml) and IFN gamma (250 U/ml) together suppressed IGF-I-maintained collagen production to approximately 35%, with a decrease from 10.3% to 2.9% in collagen production relative to total protein. The inclusion of a serum-free period prior to the addition of TNF alpha to the cultures resulted in a further inhibition to 15% of control. This increase in inhibition was not seen if dexamethasone was present in the serum-free period prior to cytokine addition. These data showed that IGF-I-maintained collagen formation is suppressed by the proinflammatory cytokines TNF alpha and IFN gamma, and that these interactions are influenced by dexamethasone. Proinflammatory cytokines interact in a complex manner with other serum factors to modulate IGF-I-stimulated extracellular matrix production and may have important roles in regulating tissue repair.

Role of NMDA glutamate receptors in regulating D2 dopamine-dependent Fos induction in the rat striatopallidal pathway.

Acute administration of reserpine induces Fos expression in striatopallidal neurons, an effect blocked by pretreatment with the D2 dopamine agonist quinpirole. Pretreatment with the NMDA antagonists (+)MK-801 or CPP attenuated reserpine-mediated striatal Fos induction whereas pretreatment with ketamine or the inactive isomer (-)MK-801 did not. These results support a role of NMDA glutamate receptors in regulating the activity of the striatopallidal pathway.

Polyacrylamide gel electrophoresis of human salivary histidine-rich-polypeptides.

A method of polyacrylamide gel electrophoresis for examining histidine-rich-polypeptides in human saliva is described. Comparison is made to several commonly used electrophoretic techniques. The described method allows for the resolution of seven histidine-rich-polypeptide fractions and is convenient and quite reproducible.

Mitral valve prolapse. Echocardiographic changes during pregnancy.

Mitral valve prolapse (MVP) has been reported to be the most common cardiac disorder in reproductive-age women. The purposes of this prospective investigation were to determine the effect of pregnancy on cardiac function in women thought to have MVP and to determine whether any such changes would adversely affect pregnancy outcome. During a recent three-year period, 43 (1.2%) of 3,582 pregnant women followed in our clinic had a prior diagnosis of MVP without any other cardiac disorder. On closer evaluation, only 21 women (0.6%) had a previous echocardiogram suggestive of MVP. Serial echocardiograms in these women revealed that pregnancy caused either no change or an improvement in the valve prolapse. No cardiac complications were present, and perinatal outcomes were favorable. MVP may be less pronounced during pregnancy, and an echocardiogram late in gestation seems worthwhile to confirm the diagnosis before delivery.

Effect of matrix depleting agents on the expression of chondrocyte metabolism by equine chondrocytes.

This study was carried out to investigate the effect of two enzymes (collagenase and chondroitinase) and two cytokines/metabolites (interleukin-1beta and retinoic acid) of known catabolic activity on the expression of cartilage metabolism/phenotype in equine articular cartilage. Articular cartilage explants from 11 horses (5-13 years old) were treated for 48 h and assayed for total sulphated glycosaminoglycan (GAG), the incorporation of 35S-sulphate, collagen degradation and mRNA expression of the proteoglycans collagen II, collagen IIA, collagen III, collagen IX, collagen X, collagen XI and glyceraldehyde-3-phosphate (GAPDH). Purified collagenase and retinoic acid were responsible for increased GAG loss from the tissues. Chondroitinase, responsible for catalysing the elimination of glucuronate residues from chondroitin A, B and C (Chondroitinase ABC) and retinoic acid treatment induced an inhibition of proteoglycan synthesis, whereas collagenase treatment did not. Collagenase activity was correlated with increased appearance of the CB11B epitope and type II collagen denaturation. By RT-PCR there was evidence of expression of altered collagen type IIA in purified collagenase treated tissues.

Ageing of equine articular cartilage: structure and composition of aggrecan and decorin.

In order to identify the pathological processes involved in the destruction of articular cartilage in arthritic diseases, it is first necessary to characterise the normal homeostasis of cartilage in a healthy joint. In particular, normal age-related changes in the biochemistry of cartilage complicate any comparisons that are made between diseased and healthy tissue. There are, however, no reports in the literature detailing the influence of ageing on the biochemistry of proteoglycans in equine articular cartilage. This study addresses the absence of such information by investigating the structure of aggrecan and decorin extracted from a wide age-range of full thickness equine tissue. The total glycosaminoglycan content of articular cartilage from the metacarpophalangeal joint remained relatively constant throughout life. In contrast, specific components such as hyaluronan increased in concentration with advancing age as did the content of a structural epitope present on keratan sulphate chains. There were also significant age-related changes in the sulphation pattern of chondroitin sulphate chains. The structure of the large aggregating proteoglycan (aggrecan) became more heterogeneous in size with increasing age and each of the subspecies of aggrecan identified in the extracts was shown to carry a hyaluronan binding region (G1) domain. All subspecies of aggrecan also expressed specific epitopes to keratan sulphate, chondroitin-4-sulphate and chondroitin-6-sulphate glycosaminoglycan chains. The structure of the small nonaggregating proteoglycan decorin and the aggrecan stabilising molecule link protein were demonstrated to be similar in size and charge to that reported for other species.

Nitric oxide inhibits aggrecan degradation in explant cultures of equine articular cartilage.

Arthroses are debilitating diseases of articular joints which result in erosion of the cartilage extracellular matrix. Nitric oxide (NO) is a major component of the inflammatory response, and has been implicated as a mediator of some of the effects of the proinflammatory cytokine, interleukin-1 (IL-1). In this study, we investigated the role of NO in the regulation of proteoglycan degradation in equine articular cartilage. NO fully mediated the suppressive effect of IL-1 on proteoglycan synthesis. However, NO was also antagonistic to proteoglycan degradation, irrespective of whether degradation was initiated by 10 ng/ml IL-1 or 1 micromol/l all-trans retinoic acid (RA) which (unlike IL-1) does not elevate NO production. This was confirmed using the NO donor 2,2'-(hydroxynitrosohydrazono) bis-ethanamine (DETA-NONOate) and the iNOS inhibitor L-N5-iminoethyl ornithine (dihydrochloride) (L-NIO). The G1 fragments of aggrecan were detected in the media and extracts of cartilage explant cultures treated with all-trans RA, DETA-NONOate and L-NIO. The presence of exogenous NO in culture resulted in a decrease in the appearance of the 'aggrecanase' cleavage epitope. Therefore, changes in the appearance of the G1 fragment expressing the 'aggrecanase' cleavage epitope in the media emulated the glycosaminoglycan loss from the tissue. These results lend further support to the hypothesis that NO has an anticatabolic role in equine cartilage proteoglycan degradation, and suggest that this may be mediated by the regulation of 'aggrecanase' activity. Therefore, any pharmacological intervention using NO as a target must take into account both its catabolic and anticatabolic roles in joint tissue turnover.

Effect of low-viscosity resins on the performance of dental adhesives.

PURPOSE: To determine whether the use of low-viscosity intermediate resins (LVR) reduces microleakage of dental adhesive systems. MATERIALS AND METHODS: Wedge-shaped Class V cavities were prepared in sound extracted molars. Occlusal margins were in enamel and gingival margins were in dentin/cementum. Five adhesive systems (All-Bond 2, Clearfil Liner Bond 2, OptiBond, Prime & Bond and Scotchbond Multi-Purpose) were applied to the preparations strictly according to manufacturers' directions on one side of the tooth and with the addition of LVR (OptiBond FL Adhesive or Protect Liner F) on the other. All cavities were restored with Z100 resin composite. Specimens were then stored in water at 37 degrees C for 24 hours, thermocycled 800x, stained with silver nitrate, sectioned, and evaluated for leakage. Marginal penetration of silver nitrate was scored on 0-3 scale. RESULTS: Statistical analysis (Kruskal-Wallis non-parametric ANOVA) revealed a significant difference (P < 0.0001) in leakage at dentin margins. Multiple pairwise comparisons of control groups revealed considerable overlapping between groups, but with a trend toward less leakage by OptiBond and Clearfil Liner Bond 2. Leakage of Scotchbond Multi-Purpose was significantly reduced when Protect Liner F was used.

Evaluation of translocator protein quantification as a tool for characterising macrophage burden in human carotid atherosclerosis.

Macrophage presence within atherosclerotic plaque is a feature of instability and a risk factor for plaque rupture and clinical events. Activated macrophages express high levels of the translocator protein/peripheral benzodiazepine receptor (TSPO/PBR). In this study, we investigated the potential for quantifying plaque inflammation by targeting this receptor. TSPO expression and distribution in the plaque were quantified using radioligand binding assays and autoradiography. We show that cultured human macrophages expressed 20 times more TSPO than cultured human vascular smooth muscle cells (VSMCs), the other abundant cell type in plaque. The TSPO ligands [3H](R)-1-(2-chlorophenyl)-N-methyl-(1-methylpropyl)-3-isoquinoline carboxamide ([3H](R)-PK11195) and [3H]N-(2,5-dimethoxybenzyl)-N-(5-fluoro-2-phenoxyphenyl)acetamide ([3H]-DAA1106) bound to the same sites in human carotid atherosclerotic plaques in vitro, and demonstrated significant correlation with macrophage-rich regions. In conclusion, our data indicate that radioisotope-labelled DAA1106 has the potential to quantify the macrophage content of atherosclerotic plaque.

The effect of harmine and other monoamine oxidase inhibitors on N-acetyltransferase activity.

Prior studies indicate that the monoamine oxidase inhibitors (MAOI) harmine and iproniazide inhibit N-acetyltransferase activity from liver. In this report we have demonstrated that harmine and harmaline are potent inhibitors of N-acetyltransferase, purified from hamster and rat liver. However, other MAOI such as deprenyl, clorgyline, methysergide, cyproheptadine, phenelzine, pargyline, methyltryptamine and tranylcypromine have either no effect, or only trivial effects on N-acetyltransferase. There is no correlation between a compound's properties as an MAO and N-acetyltransferase inhibitor. One must consider the inhibitory effect of harmine and harmaline on both MAO and N-acetyltransferase when evaluating the effects of these compounds on physiological processes.

Effect of increased pancreatic islet norepinephrine, dopamine and serotonin concentration on insulin secretion in the golden hamster.

The purpose of this study was to determine if increased concentrations of pancreatic islet norepinephrine, dopamine, or serotonin after insulin secretion. Golden hamsters received intraperitoneal injections of the norepinephrine precursor DL-threo-dihydroxyphenylserine, the dopamine precursor L-3,4-dihydroxyphenylalanine, or the serotonin precursor 5-hydroxytryptophan with and without pretreatment of the hamsters with the monoamine oxidase inhibitor tranylcypromine. Administration of the monoamine precursors to animals pretreated with tranylcypromine resulted in a mean increase in plasma glucose of 192% and a mean decrease in plasma insulin of 58%. Using a collagenase isolation technique, islets from control and treated animals were evaluated for monoamine content and insulin secretory capacity. The monoamine concentrations in control islets, in mumol/kg wet weight, were: norepinephrine 42 +/- 8; dopamine 8 +/- 2; and serotonin 26 +/- 9. Administration of the appropriate precursor to control hamsters resulted in a 1.9-fold (norepinephrine), 6-fold (dopamine), and 22-fold (serotonin) increase in monoamines. There was no alteration in the glucose (16.3 mmol/l)-stimulated in vitro insulin secretion from islets obtained from these hamsters. Administration of the precursors to hamsters pretreated with tranylcypromine resulted in a 3.5-fold (norepinephrine), 22-fold (dopamine), and 59-fold (serotonin) increase in monoamines. Glucose-stimulated in vitro insulin secretion from islets obtained from these hamstes was completely blocked. This study suggest that high concentrations of norepinephrine, dopamine, and serotonin in the pancreatic islets can decrease glucose-stimulated insulin secretion.

Age-related effects of TGF-beta on proteoglycan synthesis in equine articular cartilage.

The synthesis of proteoglycans was measured in normal equine articular cartilage of ages 9 months to 20 years and the effect of TGF-beta1 on this activity was investigated. The rate of incorporation of [(35)S]Na(2)SO(4) decreased with age as did the responsiveness of the tissue to the growth factor. The enhanced synthesis of proteoglycan induced at all ages by TGF-beta1 was down-regulated by IL-1 beta and retinoic acid. The expression of mRNA for TGF-beta1, 2, and 3 was also measured, and although the level of TGF-beta1 was highest at all ages, the expression of each growth factor decreased with age.

IL-1 beta induces the degradation of equine articular cartilage by a mechanism that is not mediated by nitric oxide.

Proteoglycan degradation was induced in young equine articular cartilage explants cultured for eight days in the presence of 50 ng/ml recombinant human interleukin-1 beta. Degradation was initiated after 6 hours of exposure to the cytokine. This was accompanied by an induction of nitric oxide synthesis and a decrease in the incorporation of [36S]sulphate into the glycosaminoglycan chains of proteoglycans. The addition of 1mM N-iminoethyl-L-ornithine (an inhibitor of nitric oxide synthase) to the explant cultures in the presence of rhIL-1 beta suppressed the synthesis of NO and restored proteoglycan synthesis to control levels. However, treatment of explants with LNIO did not overcome proteoglycan degradation. These results indicate that although IL1 beta regulates both proteoglycan synthesis and degradation in equine cartilage explants, only the inhibition of proteoglycan synthesis is mediated by nitric oxide.

The G1 domain of aggrecan released from porcine articular cartilage forms stable complexes with hyaluronan/link protein.

OBJECTIVE: To raise peptide antibodies recognizing the C-terminal amino acid sequence in the G1 domain of porcine aggrecan, generated by the action of either aggrecanase or neutral metalloproteinase(s), in rabbits and to use them to investigate the release of aggrecan from porcine articular cartilage. METHOD: An explant culture system was used to investigate the release of the G1 domain of aggrecan from porcine articular cartilage treated with retinoic acid or interleukin 1beta and to study how the activity of these agents is modified by the proteinase inhibitor, batimastat (BB94). RESULTS: Retinoic acid and interleukin 1beta induced both enzyme activities and the release of the G1 domain into the culture medium. Proteinase activity was significantly reduced when the tissue was incubated in the presence of BB94. The functional properties of the enzyme-generated G1 domain were studied using large-pore, agarose/polyacrylamide gel electrophoresis, and it was shown to interact with hyaluronan and link protein. CONCLUSIONS: The results show that there must be a mechanism for removing a functional G1 domain from aggrecan during tissue turnover using this culture system.