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E Sanna

Publications and source records attributed to E Sanna.

At least 37 records · Page 2Linked to original sources

Characterization of the electrophysiological and pharmacological effects of 4-iodo-2,6-diisopropylphenol, a propofol analogue devoid of sedative-anaesthetic properties.

1. Several derivatives and analogues of the general anaesthetic 2,6-diisopropylphenol (propofol) have been recently synthesised with the aim of exploring the structure-activity relationships. 2. In the present study, the effects of one such compound, 4-iodo-2,6-diisopropylphenol (4-I-Pro), on gamma-aminobutyric acid type A (GABA(A)) receptors in vitro were compared with its in vivo effects in rodents. Human GABA(A) receptors were expressed in Xenopus oocytes, and the actions of 4-I-Pro on receptor function were compared with those of propofol by two-electrode voltage-clamp recording. 3. Similar to propofol, 4-I-Pro directly activated Cl- currents in the absence of GABA at all combinations of receptor subunits tested. However, the efficacy of 4-I-Pro in inducing direct activation of alpha1beta2gamma2S receptors was markedly less than that of propofol. 4. Similarly to propofol, 4-I-Pro potentiated in a concentration-dependent manner GABA-evoked Cl- currents measured at different GABA(A) receptor constructs. 5. As expected, intraperitoneal injection of propofol induced sedation, ataxia, and loss of the righting reflex in rats. In contrast, administration of 4-I-Pro failed to produce any of these behavioural effects. 6. Administration of 4-I-Pro to rats reduced in a dose-dependent manner the incidence of tonic-clonic seizures induced by pentylenetetrazol and induced an anticonflict effect as measured in the Vogel test. 7. Microdialysis revealed that, like propofol, administration of 4-I-Pro reduced acetylcholine release in the hippocampus of freely moving rats. 8. These results demonstrate that para-substitution of the phenol ring of propofol with iodine yields a compound that exhibits anticonvulsant and anticonflict effects, but is devoid of sedative-hypnotic and anaesthetic properties. Thus, 4-I-Pro possesses pharmacological characteristics more similar to anxiolytic and anticonvulsant drugs than to general anaesthetics.

Acetylcholine↗

2-Phenyl-imidazo[1,2-a]pyridine derivatives as ligands for peripheral benzodiazepine receptors: stimulation of neurosteroid synthesis and anticonflict action in rats.

Selective activation of peripheral benzodiazepine receptors (PBRs) in adrenal cells and brain oligodendrocytes promotes steroidogenesis. Three 2-phenyl-imidazo[1,2-a]pyridine derivatives (CB 34, CB 50 and CB 54) have now been investigated with regard to their selectivity for PBRs and their ability to stimulate central and peripheral steroidogenesis in rats. The three CB compounds (10(-10)-10(-4) M) potently inhibited the binding of the PBR ligand [3H]-PK 11195 to brain and ovary membranes in vitro, without substantially affecting [3H]-flunitrazepam binding to central benzodiazepine receptors. These compounds (10(-7)-10(-4) M) also had little or no marked effects on GABA-evoked Cl- currents in voltage-clamped Xenopus oocytes expressing human alpha1beta2gamma2S GABA(A) receptors. In addition, they failed to affect ligands binding to GABA(B), D1/D2 dopamine, muscarinic acetylcholine, N-methyl-D-aspartic acid and opiate receptors. Intraperitoneal administration of CB compounds (3-50 mg kg(-1)) induced a dose-dependent increase in the concentrations of neuroactive steroids in plasma and brain. The brain concentrations of pregnenolone, progesterone, allopregnanolone and allotetrahydrodeoxycorticosterone (THDOC) showed maximal increases in 96+/-3, 126+/-14, 110+/-12 and 70+/-13% above control, respectively, 30 to 60 min after injection of CB 34 (25 mg kg(-1)). CB 34 also increased the brain concentrations of neuroactive steroids in adrenalectomized-orchiectomized rats, although to a lesser extent than in sham-operated animals, suggesting that CB compounds stimulate brain steroidogenesis independently of their effects on peripheral tissues. The increase in brain and plasma neurosteroid content induced by CB 34 was associated with a marked anticonflict effect in the Vogel test. Our results indicate that the three CB compounds tested are specific and potent agonists at peripheral benzodiazepine receptors, and that they stimulate steroidogenesis in both the brain and periphery.

Adrenalectomy↗

Proviral DNA in the brains of goats infected with caprine arthritis-encephalitis virus.

Archive paraffin wax-embedded sections of brain from goats and kids naturally infected with caprine arthritis-encephalitis virus (CAEV) were examined. Severe leucoencephalitis was present, with infiltration of lymphocytes, plasma cells and macrophages into the white matter, meninges and choroid plexus. On both CAEV-positive and negative (control) tissues, in-situ polymerase chain reactions were used to amplify a DNA sequence specific to the proviral Pol region. In the infected tissues, strong hybridization signals were observed, mainly located in macrophages, microglial cells, astrocytes and oligodendrocytes, and in the ependymal epithelium and choroid plexus. Positive areas were also found in the spinal cord in endothelial cells of small blood vessels. Some neurons showed a positive reaction.

Animals↗

Molecular and neurochemical evaluation of the effects of etizolam on GABAA receptors under normal and stress conditions.

The thienobenzodiazepine derivative etizolam (CAS 40054-69-1, 6-(o-chlorophenyl)-8-ethyl-1-methyl-4H-s-triazolo-(3,4-c)thienol(1 ,4) diazepine) is a potent anxiolytic with a pharmacological profile similar to that of classical benzodiazepines. In order to rationalize the therapeutic use of etizolam, its pharmacodynamics properties on GABAA receptors were investigated by a comparative study with other ligands on human recombinant GABAA as well as rat brain native receptors. Etizolam inhibited in a concentration-dependent manner [3H]flunitrazepam (CAS 1622-62-4) binding to rat cortical membranes, with an affinity of 4.5 nmol/l greater than that of alprazolam (CAS 28981-97-7) (7.9 nmol/l). Ethizolam enhanced GABA-induced Cl- currents in oocytes expressing human cloned GABAA receptors. With alpha 1 beta 2 gamma 2S subunit combination, etizolam produced a 73% increase in GABA-induced currents with an EC50 of 92 nmol/l. At the same receptor type, alprazolam showed a higher degree of potentiation and potency (98%, EC50 56 nmol/l). At alpha 2 beta 2 gamma 2S or alpha 3 beta 2 gamma 2S subunit constructs, the effects of etizolam were similar to those of alprazolam. Flumazenil (CAS 78755-81-4) completely blocked both etizolam and alprazolam effects on GABA-induced currents. Etizolam, administered i.p., was uneffective in changing ex vivo t-[35S]butylbicyclophosphorothionate ([35S]-TBPS) binding to rat cerebral cortex, whereas alprazolam and abecarnil (CAS 111841-85-1) significantly reduced this parameter. However, etizolam similarly to abecarnil and alprazolam, antagonized isoniazid-induced increase (61%) in [35S]-TBPS binding to rat cortical membranes. Further, etizolam inhibited in a dose-dependent manner basal acetylcholine release from both hippocampus and prefrontal cortex, and reversed foot-shock-induced increase of basal acetylcholine release to a control level. Altogether, these results suggest that etizolam may have a reduced intrinsic activity, at least at specific subpopulations of GABAA receptors. This property, together with the pharmacokinetic indication of a short-acting drug, may characterize etizolam as a ligand endowed with less side-effects typical of full agonits such as diazepam (CAS 439-14-5) and alprazolam. Finally, given its marked efficacy under conditions of GABAergic deficit, etizolam may represent a possible drug of choice with reduced liability to produce tolerance and dependence after long-term treatment of anxiety and stress syndromes.

Acetylcholine↗

Comparison of blood lead levels in three groups of Sardinian children.

This paper reports blood lead levels in children from three Sardinian municipalities: Portoscuso, Iglesias, and Sestu. Portoscuso, chosen as the control area, is located about 2 km from one of the most important industrial complexes of the island. Iglesias was once an important zinc-lead mining centre. Sestu is a semi-urban centre located about 10 km from Cagliari (the islands's capital), and may be considered unexposed to lead pollution. Blood lead concentration was evaluated in heparinized venous blood samples by graphite furnace atomic absorption spectrophotometry. Children living in Portoscuso show a higher mean of blood lead levels (8.43 micrograms/dl) as compared to that of children of the same age living in Iglesias (6.92 micrograms/dl) and Sestu (5.71 micrograms/dl). By the Bonferroni t-tests procedure these mean differences appear to be statistically significant. The mean of PbB levels obtained in this investigation for children from Portoscuso showed a decrease of 33.62% with respect to that reported in a previous investigation carried out in 1987 (12.7 micrograms/dl).

Adolescent↗

Propofol analogues. Synthesis, relationships between structure and affinity at GABAA receptor in rat brain, and differential electrophysiological profile at recombinant human GABAA receptors.

A number of propofol (2,6-diisopropylphenol) congeners and derivatives were synthesized and their in vitro capability to affect GABAA receptors determined by the inhibition of the specific [35S]-tert-butylbicyclophosphorothionate ([35S]TBPS) binding to rat whole brain membranes. Introduction of halogen (Cl, Br, and I) and benzoyl substituents in the para position of the phenyl group resulted in ligands with higher potency at inhibiting [35S]TBPS binding. A quantitative structure-affinity relationship (QSAR) study demonstrated that affinity is enhanced by increases in lipophilicity of the ligand whereas affinity is adversely affected by increases in size of the substituent para to the phenolic hydroxyl group. Consistent with the displacement of [35S]TBPS and with the activation of GABAA receptors, we demonstrate that ligands displaying high affinity (i.e., 2-4, and 8) are able to increase GABA-stimulated chloride currents in oocytes expressing human GABAA receptors and to directly activate chloride currents in an electrophysiological assay. Among them, compound 4 showed a rather peculiar profile in the electrophysiological examination with cloned alpha1beta2gamma2 GABAA receptors. Indeed, compared to propofol, it displayed a much greater efficacy at potentiating GABA-elicited chloride currents, but a much lower efficacy at producing a direct activation of the chloride channel in the absence of GABA. This behavior may give to compound 4 pharmacological properties that are more similar to anxiolytic and anticonvulsant drugs than to those of general anesthetics.

Anesthetics, Intravenous↗

Inclusion complexation of propofol with 2-hydroxypropyl-beta-cyclodextrin. Physicochemical, nuclear magnetic resonance spectroscopic studies, and anesthetic properties in rat. trapani@ippo.uniba.it.

An aqueous formulations of propofol 1 can be prepared by solubilizing it in the presence of 2-hydroxypropyl-beta-cyclodextrin (HP-beta-CD). This is potentially useful for parenteral administration of the drug. The aqueous solubility of 1 linearly increased as a function of HP-beta-CD concentration and showed features of an AL type diagram. Thermodynamic parameters were obtained by using the temperature dependence of the stability constant at temperatures of between 25 and 37 degrees C. The results indicate that complex formation is enthalpically, rather than entropically, driven and that it may involve van der Waals (dispersive) forces, rather than hydrophobic interactions. The structure of the inclusion complex propofol/HP-beta-CD was investigated in D2O, using 1H and 13C NMR spectroscopy. These studies revealed that the whole aromatic ring, as well as part of the isopropyl groups of the guest molecule, is located inside the HP-beta-CD cavity, while the hydroxy group is located at the rim of the wider cavity end. The geometrical features of the inclusion complex 1-HP-beta-CD are confirmed by 1D NOE difference spectra and molecular modeling experiments. The anesthetic activity in rat was investigated, and it was found that there are significant differences in induction time and sleeping time between 1 solubilized in the presence of HP-beta-CD and the formulation currently used (Diprivan), which is a 1% w/v oil/water emulsion.

2-Hydroxypropyl-beta-cyclodextrin↗

Functional changes in rat nigral GABA(A) receptors induced by degeneration of the striatonigral GABAergic pathway: an electrophysiological study of receptors incorporated into Xenopus oocytes.

Expression of rat brain gamma-aminobutyric acid type A (GABA(A)) receptors in Xenopus laevis oocytes can be achieved by injection of the oocytes with synaptosomes. This approach has now been applied to evaluate changes in the function of nigral GABA(A) receptors after degeneration of the striatonigral GABAergic pathway induced by the unilateral infusion of kainic acid into the rat striatum. Ten days after striatal injection, synaptosomal membranes were prepared from the substantia nigra and introduced into oocytes. Nigral GABA(A) receptors incorporated into the oocyte cell membrane were then characterized electrophysiologically under voltage-clamp conditions. The maximal amplitude of GABA-induced Cl- currents in oocytes injected with synaptosomes from denervated substantia nigra was twice that observed in oocytes injected with synaptosomes from control substantia nigra. The concentration of GABA required for the half-maximal response did not differ between the two groups of oocytes. In addition, the potentiation of GABA-induced currents by the benzodiazepine diazepam (1 microM) and the steroid derivative allopregnanolone (3 microM) was increased by approximately 65 and 60%, respectively, in oocytes injected with synaptosomes from denervated substantia nigra compared with those injected with control synaptosomes. The concentrations of diazepam and allopregnanolone giving half-maximal responses were not affected by denervation. In contrast, the inhibitory effects of the benzodiazepine receptor inverse agonists FG 7142 (10 microM) and 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylic acid ethyl ester (1 microM) were reduced by 48 and 38%, respectively, after denervation. These results indicate that the up-regulation of nigral GABA(A) receptors induced by degeneration of the striatonigral GABAergic pathway is associated with an increased efficacy of positive allosteric modulators, such as benzodiazepines and steroids, and with a reduced efficacy of negative allosteric modulators such as beta-carbolines.

Animals↗

Synthesis and binding affinity of 2-phenylimidazo[1,2-alpha]pyridine derivatives for both central and peripheral benzodiazepine receptors. A new series of high-affinity and selective ligands for the peripheral type.

A number of 6-substituted or 6,8-disubstituted alkyl 2-phenylimidazo[1,2-alpha]pyridine-3-carboxylates 5a-h, -acetates 5i-s, 6a-g, and -propionates 5t, 6h and of N,N-dialkyl-2-phenylimidazo[1,2-alpha]pyridine-3-carboxamides 7a-d,-acetamides 7e-t or -propionamide 7u were prepared following new synthetic methods, and their affinities for both the central (CBR) and the peripheral (PBR) benzodiazepine receptors evaluated. The compounds of the ester series displayed low affinity for both receptor types. Conversely, most of N,N-dialkyl(2-phenylimidazo[1,2-alpha]pyridin-3-yl)acetamides 7e-t proved to possess high affinity and selectivity for CBR or PBR depending on the nature of substituents at C(6)- and/or C(8) on the heterocyclic ring system. In particular, the 6-substituted compounds 7f-n displayed ratios of IC50 values (IC50(CBR)/IC50(PBR)) ranging from 0.32 (7m) to 232 (7k), while the 6,8-disubstituted compounds 7o-t were more than 1000-fold more selective for PBR versus CBR. Compounds 7f,m were examined in several different benzodiazepine receptor subtypes. Expression of specific GABAA, receptor subunit assemblies in Xenopus oocytes was utilized to evaluate functionally both the efficacy and potency of the positive modulation of GABA-evoked Cl- currents by 7f and 7m in comparison with Zolpidem. The rank order of potencies of these drugs was 7f (EC50 = 3.2 x 10(-8) M) > Zolpidem (EC50 = 3.6 x 10(-8) M) > 7m (EC50 = 2.2 x 10(-7) M). The actions of these compounds were also tested on alpha 2 beta 2 gamma 2s, receptors. However, the EC50 of these compounds was increased, compared to alpha 1 beta 2 gamma 2s receptors, by 30-, 4-, and 5-fold for 7m, 7f, and Zolpidem, respectively. Finally, these compounds were almost completely devoid of activity at receptors containing the alpha 5 subunit.

Animals↗

Modulation of 6-hydroxydopamine oxidation by various proteins.

The spontaneous autoxidation of the neurotoxin 6-hydroxydopamine proceeds by a free radical chain reaction involving the superoxide anion radical and produces the corresponding chromogen 6-hydroxydopamine quinone and hydrogen peroxide. The rate of this reaction is increased in the presence of ceruloplasmin and peroxidase, and reduced by superoxide dismutase, catalase, and DT-diaphorase. We report some explanations of why these proteins may increase or reduce the rate of autoxidation of 6-hydroxydopamine.

Animals↗

Differential subunit dependence of the actions of the general anesthetics alphaxalone and etomidate at gamma-aminobutyric acid type A receptors expressed in Xenopus laevis oocytes.

The effects of subunit composition of the gamma-aminobutyric acid (GABA) type A receptor on the multiple actions of the general anesthetics alphaxalone and etomidate were investigated. The abilities of the two drugs to activate directly Cl- currents and to modulate GABA-evoked Cl- currents mediated by human recombinant GABA(A) receptors composed of alpha1, gamma2S, and either beta1, beta2, or beta3 subunit expressed in Xenopus laevis oocytes were compared. Both alphaxalone and etomidate evoked Cl currents in alpha1 beta1 gamma2S, alpha1 beta2 gamma2S, and alpha1 beta3 gamma2S receptors, an action that was blocked by both SR 95531 and picrotoxin. However, although maximal current activation by alphaxalone varied only slightly with the specific beta subunit isoform present, the efficacy of etomidate showed a rank order of beta3 > beta2 >>> beta1. In addition, beta1 homomeric receptors were markedly activated by etomidate but not by alphaxalone. Conversely, receptors consisting of alpha1 and gamma2S subunits were markedly activated by alphaxalone but not by etomidate. The modulatory effect of alphaxalone was also not markedly influenced by the beta-specific subunit isoform, whereas the modulatory efficacy of etomidate showed a rank order of beta3 > beta2 >> beta1. These results further demonstrate that the actions of general anesthetics at GABA(A) receptors are influenced by receptor subunit composition, and they suggest that the effects of alphaxalone and etomidate are mediated by different binding sites on the receptor complex.

Anesthetics↗

Biochemical evaluations of the effects of loreclezole and propofol on the GABAA receptor in rat brain.

The effects of loreclezole on the function of the gamma-aminobutyric acid type A (GABAA) receptor complex in rat cerebral cortical membrane preparations were compared with those of propofol and diazepam. Loreclezole and propofol modulated [3H]muscimol binding and t-[35S]butylbicyclophosphorothionate ([35S]TBPS) binding to washed and unwashed membranes with potencies and efficacies greater than those of diazepam. Loreclezole and propofol enhanced [3H]flunitrazepam binding to washed membranes with efficacies lower than those of GABA and muscimol. Both loreclezole and propofol showed biphasic effects on [35S]TBPS binding to washed membranes: at low concentrations (5 to 10 microM), both drugs, with different efficacies, enhanced [35S]TBPS binding whereas, at higher concentrations (30 to 100 microM), they inhibited this biochemical parameter. In contrast, diazepam enhanced [35S]TBPS binding to washed membranes at all concentrations tested. The combination of loreclezole with GABA, at a concentration (0.3 microM) that only slightly increased [35S]TBPS binding to washed membranes, reversed the increase in binding elicited by loreclezole (5 to 10 microM) and significantly potentiated the inhibitory effect exerted by higher concentrations (30 to 100 microM) of this drug. Similar effects were observed with the combination of GABA and propofol. However, GABA had no effect on the enhancement of [35S]TBPS binding induced by diazepam. The ability of GABA to reverse and potentiate the effects of loreclezole and propofol on [35S]TBPS binding to washed membranes was shared by pentobarbital (200 microM) and alphaxalone (3 microM). These anesthetics showed greater efficacies in combination with pentobarbital (200 microM) and alphaxalone (3 microM). These anesthetics showed greater efficacies in combination with propofol than with loreclezole. These results suggest that, unlike diazepam, loreclezole and propofol may activate the receptor-associated Cl- channel in the absence of GABA. Furthermore, the difference in the pharmacological profiles of loreclezole and propofol may result from their different effectiveness in activating the receptor Cl- channel directly.

Anesthetics↗

Direct activation of GABAA receptors by loreclezole, an anticonvulsant drug with selectivity for the beta-subunit.

Loreclezole, an anticonvulsant and antiepileptic compound, potentiates gamma-aminobutyric acid (GABA) type A receptor function, by interacting with a specific allosteric modulatory site on receptor beta-subunits. A similar selectivity for GABAA receptor beta-subunits is apparent for the direct activation of receptor-operated Cl- channels, by the general anesthetics propofol and pentobarbital. The ability of loreclezole to activate GABAA receptors directly has now been compared, biochemically and electrophysiologically, with that of propofol. In well-washed rat cortical membranes (devoid of endogenous GABA), loreclezole and propofol increased t-[35S]butylbicyclophosphorothionate ([35S]TBPS) binding by up to 28% (at 5 microM) and 80% (at 10 microM), respectively. Higher concentrations (50-100 microM) of both compounds inhibited [35S]TBPS binding with great efficacy, an effect mimicked by GABA. In contrast, the benzodiazepine diazepam increased [35S]TBPS binding, but failed to inhibit this parameter, even at high concentrations. At concentrations of 50-100 microM, loreclezole induced inward Cl- currents in the absence of GABA, in Xenopus oocytes expressing human recombinant GABAA receptors, comprised of alpha 1-, beta 2- and gamma 2S-subunits. At 100 microM, the current evoked by loreclezole was 26% of that induced by 5 microM GABA. The current evoked by 100 microM propofol was 98% of that induced by 5 microM GABA. Currents induced by loreclezole, like those evoked by propofol, were potentiated by diazepam in a flumazenil-sensitive manner and blocked by either bicuculline or picrotoxin. These data suggest that loreclezole shares, with propofol, an agonistic action at GABAA receptors containing the beta 2-subunit and that the different efficacies of the two compounds in this regard, may underlie the difference in their pharmacological profiles. The failure of loreclezole to activate GABAA receptors containing the beta 1-subunit may be responsible for its lack of hypnotic effect.

Animals↗

Expression of native GABAA receptors in Xenopus oocytes injected with rat brain synaptosomes.

Oocytes from the frog Xenopus laevis were shown recently to express native nicotinic acetylcholine receptors after injection with purified Torpedo electroplaque membrane vesicles. Injection of Xenopus oocytes with rat cortical or nigral synaptosomes has now been shown to result in the expression of gamma-aminobutyric acid type A (GABAA) receptor-mediated Cl- currents. Electrophysiological characterization of the responses of these receptors to GABA and other agents revealed that they were incorporated into the oocyte membrane and that they retained their original pharmacological properties, such as sensitivity to Cl- channel blockers, benzodiazepines, and general anesthetics. These results suggest that this approach to the expression of heterologous proteins in Xenopus oocytes may facilitate the study of native synaptic proteins derived from brain tissue.

Anesthetics↗

Proconflict effect of carbon dioxide inhalation in rats.

The effect of brief inhalation of carbon dioxide (CO2) was studied in a conflict situation (Vogel test) in the rat. This treatment, which inhibits gamma-aminobutyric acid (GABA)-mediated transmission in rat brain and induces anxiety and panic attacks in humans, elicited a proconflict effect. Exposure of rats for 1 min to CO2 decreased by approximately 40% the number of licking periods in the test. This effect was abolished by prior administration of alprazolam (0.5 mg per kilogram of body mass, i.p.). Although these results may support a role for GABA-mediated transmission in the anxiogenic effect of CO2 inhalation, the possibility that different neurotransmitters other than GABA are involved in the action of CO2 can not be ruled out.

Administration, Inhalation↗

Actions of the general anesthetic propofol on recombinant human GABAA receptors: influence of receptor subunits.

The intravenous general anesthetic 2,6-diisopropylphenol (propofol) potentiates GABAA receptor function, but the precise mechanisms and specificity of this action are still unclear. To study the influence of receptor subunit composition on the action of propofol, 18 different combinations of cloned cDNAs coding for human brain subunit isoforms of the GABAA receptor, as well as mRNAs from mouse brain, were expressed in Xenopus oocytes, and effects of this anesthetic were investigated by the voltage-clamp technique. We found that low concentrations (1-10 microM) of propofol dramatically potentiated GABA-evoked Cl- currents in all GABAA receptor constructs tested. This action did not require specific subunits but was correlated inversely with the GABA sensitivity of each receptor construct. Larger concentrations (10-25 microM) of propofol produced direct activation of Cl- currents, and this action was dependent on the expression of the beta-subunit of the GABAA receptor and did not correlate with the GABA sensitivity of the receptors. These results suggest that propofol exerts a dual effect on GABAA receptors: a positive modulation of the GABA-mediated action on GABAA receptors that is not influenced by the receptor subunit composition, and a specific interaction with the beta-subunit that directly activates the GABAA receptor-coupled Cl- channel.

Animals↗

Polymorphism of palmar main line terminations as an indicator of relationships among Sardinian linguistic groups of males.

Palmar main line modal types were used to calculate distance coefficients between Sardinian linguistic groups of males. By using correlation matrix analyses of the coefficients, we then determined whether or not the dermatoglyphic traits could reliably identify the biological relationships on the basis of the linguistic backgrounds of these groups. With Sanghvi's (X2)1/2 and by using palmar main lines both singly and together, we calculated dermatoglyphic distance matrices. Mantel tests of matrix correspondence showed that, by using C and D lines singly or all palmar main lines together, statistical significance between dermatoglyphic and linguistic distances can be obtained, even when the effect of geography is removed; there is no statistically significant correspondence between geographic and dermatoglyphic distance matrices, even when the effect of language is removed. Considering the historical and linguistic background, the results obtained by means of the Mantel test procedure, and the present dermatoglyphic differences in Sardinian linguistic groups of males, we can hypothesize that these groups were already genetically differentiated before the Romance languages and their respective dialects developed.

Dermatoglyphics↗