Monoamine oxidase A genotype, childhood adversity, and criminal behavior in an incarcerated sample.

BACKGROUND: A number of studies have found a functional variable number tandem repeat polymorphism in the upstream regulatory region of the monoamine oxidase A gene (MAOA-uVNTR) interacts with childhood adversity to increase risk for antisocial behavior. Several studies have also reported null findings. METHODS: Here, we examine the association between MAOA-uVNTR genotype, childhood adversity, and criminal activity in a sample of 99 male volunteers who were incarcerated in a large city jail in the Southern United States. MAOA-uVNTR genotypes were obtained from DNA extracted from buccal swabs. Criminal activity in the year before incarceration and childhood adversity were measured with self-report surveys. Violent arrest rates and property arrest rates were quantified with official records of arrest and accounted for periods of incarceration in local and state correctional facilities. RESULTS: The low expressing allele of the MAOA-uVNTR genotype (MAOAL) interacted with abuse to predict self-reports of less serious criminal and delinquent behavior and had a direct association with serious criminal activity. MAOAL genotype interacted with parental criminality to predict self-reports of serious criminal behavior, property arrest rates, and violent arrest rates. CONCLUSION: The findings suggest that crime prevention efforts may be improved through attention to the neurodevelopmental consequence of gene-by-environment interactions.

Population data for DXS6800, DXS101 and DXS8377 loci from Buenos Aires (Argentina).

The X-chromosomal short tandem repeats (X-STRs) DXS6800, DXS101 and DXS8377 were analysed in a population sample from Buenos Aires (Argentina) using a polymerase chain reaction (PCR) multiplex approach with fluorescent detection. We present allele frequencies for these loci in a population comprising 113 women and 99 men. The Hardy-Weinberg equilibrium (HWE) was tested in the female sample and no significant deviations were observed. The homogeneity of allele frequencies of men and women was compared by the Fisher's exact test and showed similar distributions. Linkage disequilibrium (LD) tests were performed in males for all pairs of loci and no significant associations were detected. Parameters of forensic interest were also estimated.

Removal of urothelium affects bladder contractility and release of ATP but not release of NO in rat urinary bladder.

BACKGROUND: The objective of our work was to investigate both the contractile function and the release of ATP and NO from strips of bladder tissue after removal of the urothelium. METHODS: The method of removal was a gentle swabbing motion rather than a sharp surgical cutting to separate the urothelium from the smooth muscle. The contractile response and ATP and NO release were measured in intact as well as on swabbed preparations. The removal of the urothelial layer was affirmed microscopically. RESULTS: After the swabbing, the smaller contractions were evoked by electrical as well as by chemical stimulation (50 microM carbachol or 50 microM alpha, beta meATP). Electrical stimulation, carbachol and substance P (5 microM) evoked lower release of ATP in the swabbed strips than in intact strips. Although release of NO evoked by electrical stimulation or substance P was not changed, release of NO evoked by carbachol was significantly less in the swabbed preparations. CONCLUSION: Since swabbing removes only the urothelium, the presence of the suburothelial layer may explain the difference between our findings and those of others who found an increase in contractility. Evoked release of ATP is reduced in swabbed strips, indicating that ATP derives solely from the urothelium. On the other hand, electrical stimulation and substance P evoke identical degrees of NO release in both intact and swabbed preparations, suggesting that NO can be released from the suburothelium. Conversely, carbachol-induced release of NO is lower in swabbed strips, implying that the cholinergic receptors (muscarinic or nicotinic) are located in the upper layer of the urothelium.

Necrophagous caterpillars provide human mtDNA evidence.

Decomposition of large mammalian carcasses is greatly accelerated through the action of insects. Specialized feeders capable of digesting keratin and collagen found in skin, hair, and tendons and ligaments are attracted to corpses in late stages of dry decomposition and include Tinea pellionella, the casemaking clothes moth, and Tineola bisselliella, the webbing clothes moth (Lepidoptera; Tineidae). Until now, details of the caterpillar behavior as necrophagous insects were vague. Here, we detail the behavior of each species and document the incorporation of human hair into the portable larval shelters constructed by the caterpillars of T. pellionella. Hair of the decedent used as building material for caterpillar shelters provided enough starting template to amplify and sequence the HVI and HVII sections of the control region (mtDNA) of the decedent.

Botulinum toxin type A normalizes alterations in urothelial ATP and NO release induced by chronic spinal cord injury.

The purpose of this paper was to simultaneously examine changes in urothelial ATP and NO release in normal and spinal cord injured animals as well as in spinal cord injured animals treated with botulinum toxin type A (BoNT-A). Furthermore we correlated changes in transmitter release with functional changes in bladder contraction frequency, and determined the effects of BoNT-A on bladder efferent nerve function. Normal and spinal cord injured rat bladders were injected on day 0 with either vehicle (saline containing bovine serum albumin) or BoNT-A. On day 2, in vitro neurotransmitter release and bladder strip contractility studies as well as in vivo cystometrographic studies were conducted. Resting ATP release was significantly enhanced following spinal cord injury (i.e. 57% increase, p<0.05) and was unaffected by BoNT-A treatment. SCI increased hypoosmotic evoked urothelial ATP release by 377% (p<0.05). BoNT-A treatment reduced evoked ATP release in SCI bladders by 83% (p<0.05). In contrast, hypoosmotic stimulation induced NO release was significantly inhibited following SCI (i.e. 50%, p<0.05) but recovered in SCI rats treated with BoNT-A (i.e. 195% increase in NO release in SCI-BTX-treated rats compared to SCI controls, p<0.01). Changes in urothelial transmitter release coincided with a significant decrease in non-voiding bladder contraction frequency (i.e. 71%, p<0.05) in SCI-BTX rats compared to SCI rats. While no difference was measured between neurally evoked contractile amplitude between SCI and SCI-BTX animals, atropine (1 microM) inhibited contractile amplitude to a greater extent (i.e. 76%, p<0.05) in the SCI-BTX group compared to the SCI group. We hypothesize that alterations in the ratio of excitatory (i.e. ATP) and inhibitory (i.e. NO) urothelial transmitters promote bladder hyperactivity in rat bladders following SCI that can be reversed, to a large extent, by treatment with BoNT-A.

Receptor activated bladder and spinal ATP release in neurally intact and chronic spinal cord injured rats.

Neurally intact (NI) rats and chronic spinal cord injured (SCI) rats were studied to determine how activation of mechanosensory or cholinergic receptors in the bladder urothelium evokes ATP release from afferent terminals in the bladder as well as in the spinal cord. Spinal cord transection was performed at the T(9)-T(10) level 2-3 weeks prior to the experiment and a microdialysis fiber was inserted in the L(6)-S(1) lumbosacral spinal cord one day before the experiments. Mechanically evoked (i.e. 10 cm/W bladder pressure) ATP release into the bladder lumen was approximately 6.5-fold higher in SCI compared to NI rats (p<0.05). Intravesical carbachol (CCh) induced a significantly greater release of ATP in the bladder from SCI as compared to NI rats (3424.32+/-1255.57 pmol/ml versus 613.74+/-470.44 pmol/ml, respectively, p<0.05). However, ATP release in NI or SCI rats to intravesical CCh was not affected by the muscarinic antagonist atropine (Atr). Spinal release of ATP to bladder stimulation with 10 cm/W pressure was five-fold higher in SCI compared to NI rats (p<0.05). CCh also induced a significantly greater release of spinal ATP in SCI rats compared to controls (4.3+/-0.9 pmol versus 0.90+/-0.15 pmol, p<0.05). Surprisingly, the percent inhibitory effect of Atr on CCh-induced ATP release was less pronounced in SCI as compared to NI rats (49% versus 89%, respectively). SCI induces a dramatic increase in intravesical pressure and cholinergic receptor evoked bladder and spinal ATP release. Muscarinic receptors do not mediate intravesical CCh-induced ATP release into the bladder lumen in NI or SCI rats. In NI rats sensory muscarinic receptors are the predominant mechanism by which CCh induces ATP release from primary afferents within the lumbosacral spinal cord. Following SCI, however, nicotinic or purinergic receptor mechanisms become active, as evidenced by the fact that Atr was only partially effective in inhibiting CCh-induced spinal ATP release.

Typing of the locus DYS19 from DNA derived from fingernail clippings using PCR Concert rapid purification system.

DNA extracted from the fingernails of female victims of a violent or aggressive act may assist in the identification of the male. Sometimes with the current autosomal STR loci, however, the victim's profile may mask the perpetrator's DNA profile or the perpetrator's DNA may be substantially lower in quantity than that of the victim's DNA. Thus, under these conditions, no characterization is possible. In this paper, an alternative DNA extraction procedure was employed, and the application of an STR locus residing on the Y chromosome DYS19 was typed to allow for genetic characterization of the perpetrator in such cases.