HANDdata - first-person dataset including proximity and kinematics measurements from reach-to-grasp actions.

HANDdata is a dataset designed to provide hand kinematics and proximity vision data during reach to grasp actions of non-virtual objects, specifically tailored for autonomous grasping of a robotic hand, and with particular attention to the reaching phase. Thus, we sought to capture target object characteristics from radar and time-of-flight proximity sensors, as well as details of the reach-to-grasp action by looking at wrist and fingers kinematics, and at hand-object interaction main events. We structured the data collection as a sequence of static and grasping tasks, organized by increasing levels of complexity. HANDdata is a first-person, reach-to-grasp dataset that includes almost 6000 human-object interactions from 29 healthy adults, with 10 standardized objects of 5 different shapes and 2 kinds of materials. We believe that such data collection can be of value for researchers interested in autonomous grasping robots for healthcare and industrial applications, as well as for those interested in radar-based computer vision and in basic aspects of sensorimotor control and manipulation.

Characterization of the mechanisms by which gelatinase A, neutrophil collagenase, and membrane-type metalloproteinase MMP-14 recognize collagen I and enzymatically process the two alpha-chains.

The turnover of native collagen has been ascribed to different members of the matrix metalloproteinase (MMP) family. Here, the mechanisms by which neutrophil collagenase (MMP-8), gelatinase A (MMP-2), and the ectodomain of MT1-MMP (ectMMP-14) degrade fibrillar collagen were examined. In particular, the hydrolysis of type I collagen at 37 degrees C was investigated to identify functional differences in the processing of the two alpha-chain types of fibrillar collagen. Thermodynamic and kinetic parameters were used for a quantitative comparison of the binding, unwinding, and hydrolysis of triple helical collagen. We demonstrate that the MMP family has developed at least two distinct mechanisms for collagen unwinding and cleavage. MMP-8 and ectMMP-14 display a similar mechanism (although with different catalytic parameters), which is characterized by binding (likely through the hemopexin-like domain) and cleavage of alpha-1 and/or alpha-2 chains without distinguishing between them and keeping the gross conformation of the triple helix (at least during the first cleavage step). On the other hand, MMP-2 binds preferentially the alpha-1 chains (likely through the fibronectin-like domain, which is not present in MMP-8 and ectMMP-14), grossly altering the whole triple helical arrangement of the collagen molecule and cleaving preferentially the alpha-2 chain. These distinctive mechanisms underly a drastically different mode of interaction with triple helical fibrillar collagen I, according to which the MMP domain is involved in binding. These findings can be related to the different role exerted by these MMPs on collagen homeostasis in the extracellular matrix.

The p53 codon 72 arg/arg homozygous women in central Italy are at increased risk for HPV infections.

BACKGROUND: The oncoprotein E6 binds to and degrades the p53 tumor suppressor protein, with different efficacy depending on the p53 codon 72 (arg/pro) polymorphism. The arg/arg allele has been shown to increase the risk for cervical cancer. MATERIALS AND METHODS: Fifty-eight women infected with HPV and 32 normal controls were analyzed by restriction fragment length polymorphism to detect arg/arg or arg/pro alleles. RESULTS: The allele frequencies in HPV-positive women were: arg/arg 47/58 (81%); arg/pro 9/58 (15.5%) and pro/pro 2/58 (3.4%), while those in controls were: arg/arg 19/32 (59%); arg/pro 10/32 (31.2%) and pro/pro 3/32 (9.3%) (Fisher's exact test, p = 0.068). The risk of having HSIL in arg/arg homozygous patients had odds ratio (OR) = 1.33 (95% CI 1.12-1.58, p = 0.628). Women with the arg/arg phenotype were at significantly increased risk for HPV infection; OR = 2.93 (95% CI 1.11-7.66, p = 0.028). Being homozygous arg/arg also substantially increased the risk of HR-HPV infection, with OR = 3.84 (95% CI 0.71-20.57, p = 0.128), whereas heterozygosity for arg/pro was protective against HR-HPV; OR = 0.186 (95% CI 0.03-1.04, p = 0.074). Allele frequencies in women with different HPV types were not significantly different, however (p = 0.174). CONCLUSION: These data suggest that arg/arg homozygous patients are at increased risk for HR-HPV infections.

Comparison of DNA sequencing and Roche Linear array in human papillomavirus (HPV) genotyping.

BACKGROUND: Human papillomavirus (HPV) is the etiological agent of cervical cancer. HPV genotyping is important to determine the presence of high-risk types. Recently, a new HPV genotyping method, the Roche Linear array genotyping test, was introduced and is compared here with a sequencing-based HPV genotyping system. MATERIALS AND METHODS: A series of 102 women (age range 30-55 years) shown to be HPV DNA-positive by PCR were typed by sequencing and the Linear array genotyping assay. RESULTS: The sequence analysis revealed the presence of 80 single high-risk types and 22 single low-risk types. With the Linear array, single infections were found in 46 cases, double infections in 37 cases, triple infections in 12 cases, and more than three in 6 cases. One case positive by sequencing gave a negative result by Linear array. Altogether, a concordant single genotype was found in 93 (91.2%) out of the 102 cases and the single-type concordance between the two assays was significant (Spearman rho = 0.849, p = 0.0001; intraclass correlation coefficient (ICC) (ICC = 0.924, 95% CI 0.888-0.949) (p = 0.0001). The majority of the disparate results were due to the detection of multiple types by the Linear array. CONCLUSION: The Roche Linear array is a highly accurate assay for HPV genotyping. This is particularly true in the presence of multiple infections which DNA sequencing is unable to resolve.

Role of apoptosis in intracranial aneurysm rupture.

OBJECT: Mechanisms involved in the rupture of intracranial aneurysms remain unclear, and the literature on apoptosis in these lesions is extremely limited. The hypothesis that apoptosis may reduce aneurysm wall resistance, thus contributing to its rupture, warrants investigation. The authors in this study focused on the comparative evaluation of apoptosis in ruptured and unruptured intracranial aneurysms. Peripheral arteries in patients harboring the aneurysms and in a group of controls were also analyzed. METHODS: Between September 1999 and February 2002, specimens from 27 intracranial aneurysms were studied. In 13 of these patients apoptosis was also evaluated in specimens of the middle meningeal artery (MMA) and the superficial temporal artery (STA). The terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique was used to study apoptosis via optical microscopy; electron microscopy evaluation was performed as well. Apoptotic cell levels were related to patient age and sex, aneurysm volume and shape, and surgical timing. Significant differences in apoptosis were observed when comparing ruptured and unruptured aneurysms. High levels of apoptosis were found in 88% of ruptured aneurysms and in only 10% of unruptured lesions (p < 0.001). Elevated apoptosis levels were also detected in all MMA and STA specimens obtained in patients harboring ruptured aneurysms, whereas absent or very low apoptosis levels were observed in MMA and STA specimens from patients with unruptured aneurysms. A significant correlation between aneurysm shape and apoptosis was found. CONCLUSIONS: In this series, aneurysm rupture appeared to be more related to elevated apoptosis levels than to the volume of the aneurysm sac. Data in this study could open the field to investigations clarifying the causes of aneurysm enlargement and rupture.

Beta-catenin accumulates in intercalated disks of hypertrophic cardiomyopathic hearts.

OBJECTIVE: To evaluate whether cardiomyocyte membrane structure and cell/extracellular matrix adhesion alterations perturb the cadherin/catenin complex in the hypertrophic cardiomyopathy (HCM). METHODS: Hypertrophic cardiomyopathic hamster (UM-X7.1 strain) and human hearts were studied by light and electron microscopy, Northern and Western blot analyses and immunohistochemistry. RESULTS: Intercalated disks are disorganized in both hamster and human cardiomyopathic hearts; beta-catenin is increased and accumulated in intercalated disks depriving cardiomyocyte nuclei of fundamental signals. The accumulation of beta-catenin is post-translationally regulated by an increased Wnt expression, a simultaneous decrease in glycogen synthase kinase 3beta (GSK3beta) expression and a different expression pattern of adenomatous polyposis coli (APC) isoforms. CONCLUSION: The reorganization of cell/cell adhesion in cardiomyopathic hearts is mainly contributed by the cadherin/catenin system, which is differently regulated to sustain cell structural rather than signalling needs causing considerable consequences in the determination of cardiomyocyte phenotype and clinical outcome. The accumulation of beta-catenin in intercalated disks could concur to increase myocardial wall stiffness and left ventricular end-diastolic pressure (LVEDP) in hypertrophic cardiomyopathic hamster and human hearts.

Identification of a new missense mutation in the mtDNA of hereditary hypertrophic, but not dilated cardiomyopathic hamsters.

The cardiomyopathic hamster is characterized by a naturally occurring deletion in the delta-sarcoglycan gene generating either the hypertrophic or the dilatative phenotype of cardiomyopathy. This evidence suggests that other genetic or environmental factors might concur to the pathogenesis of cardiomyopathy. The aim of the present study was to investigate on the possibility that other genes are involved in the pathogenesis of hamster cardiomyopathy. For this purpose, a series of genes of cardiomyopathic and healthy hamsters were compared by the differential display technique. The hamster cytochrome c oxidase mitochondrial subunit III (COIII) gene has been sequenced and identified as the gene upregulated in brain and skeletal muscle. The gene sequencing and restriction analysis demonstrated that a missense mutation is present in the COIII gene of hamsters exhibiting hypertrophic cardiomyopathy while no mutations were present in dilatative cardiomyopathic hamsters. The mutation was heteroplasmic and the heteroplasmy level was increased with age in skeletal muscle and heart. The ultrastructural analysis of cardiac tissue showed severe damage in the mitochondrial structure of hypertrophic but not dilatative hamster hearts. These results suggest that the pathogenesis of the cardiac damage in hypertrophic cardiomyopathic hamster may be sustained by multiple mutations exerting a cumulative effect on both structure and function of cardiac muscle.

Retinoic acid inhibits fibronectin and laminin synthesis and cell migration of human pleural mesothelioma in vitro.

The effects of retinoic acid (RA) on cell replication, fibronectin and laminin synthesis, integrin expression and haptotactic migration of three mesothelioma cell cultures of different histotype, one epithelioid, one fibromatous and one biphasic, were evaluated. Cell growth was not affected by RA, while RA treatment decreased the synthesis of fibronectin and laminin and inhibited the migration of all three mesotheliomas on substrates of fibronectin and laminin; on the contrary, the expression of some integrins was not significantly modified by RA. These data indicate that RA may lead to a decrease of mesothelioma cell local invasion; this can correlate with a modification induced by RA on mesothelioma tumor progression in vivo.