Synthesizing two-fingered grippers for positioning and identifying objects.

Most industrial grippers now in use are two-fingered. Among them the parallel-jaw gripper is the simplest. It can partially remove the pose uncertainty of an object through grasping, such as the orientation uncertainty. This paper addresses a new type of grippers with the finger configuration of four circles instead of two parallel lines. It has a number of important advantages. Especially, it achieves form-closure and confines the object to a locally unique pose, so as to remove the pose uncertainty completely. It allows the gripped object to reach this pose freely without loss of required friction in the direction perpendicular to the grasping plane. More information can be acquired for identifying the object and its grasp mode. As a result the identification can be performed at one grasp. The key parameter of a symmetric four-pin gripper is the distance (span) between two pin centers on each finger, which depends upon the object shape and impacts the closure property, Based on a new approach to the grasp geometry, selection and limitations of the span are illustrated.

Autoimmunity to munc-18 in Rasmussen's encephalitis.

Rasmussen's encephalitis (RE) is a rare disease of the central nervous system characterized by severe epileptic seizures, progressive degeneration of a single cerebral hemisphere, and autoimmunity directed against glutamate receptor subunit, GluR3. We report here the identification of high-titer autoantibodies directed against munc-18 in the serum of a single patient with RE previously shown to have anti-GluR3 antibodies. Munc-18 is an intracellular protein residing in presynaptic terminals, which is required for secretion of neurotransmitters. These findings are consistent with the possibility of intermolecular epitope spreading between GluR3, a postsynaptic cell surface protein, and munc-18, a presynaptic intracellular protein. Immune attack on these two proteins, which participate at distinct steps of synaptic transmission, could act in an additive or synergistic manner to impair synaptic function and lead to seizures and neuronal death.

A general dynamic force distribution algorithm for multifingered grasping.

A general dynamic force distribution (DFD) algorithm for multifingered grasping is presented. Based on the convexity and cone property of contact constraints, the optimal internal force is defined. Determination of the contact force is divided into two phases: (1) determine the direction of the optimal internal force during grasp planning and (2) determine the manipulation force and compensation factor during task manipulation. The total computation cost consists of off-line numerical iterations and on-line analytical computations. Only the latter is related to the real-time control. The algorithm can directly deal with the nonlinear and/or coupled constraints and well overcome the temporal discontinuity.

CLN3 defines a novel antiapoptotic pathway operative in neurodegeneration and mediated by ceramide.

Juvenile neuronal ceroid lipofuscinosis or Batten disease (JNCL) is a neurodegenerative disorder characterized by blindness, seizures, cognitive decline and early death. Brain atrophy and retinitis pigmentosa ensue because of neuronal and photoreceptor apoptosis. The CLN3 gene defective in JNCL encodes a novel 438 amino acid protein. Most affected genes harbor a deletion resulting in a truncated protein. CLN3 overexpression in NT2 cells enhances growth, reverses growth inhibition induced by serum starvation and protects from apoptosis induced by vincristine, staurosporine, and etoposide but not from death caused by ceramide. CLN3 modulates endogenous and vincristine-activated ceramide, and therefore suppresses apoptosis by impacting generation of ceramide.

Novel polypeptide toxins with crab lethality from the sea anemone Anemonia erythraea.

The sea anemone Anemonia erythraea was found to contain polypeptide toxins with crab lethality as well as hemolysins. Three polypeptide toxins (AETX I, II and III) were isolated by gel filtration on Sephadex G-50 and reverse-phase HPLC on TSKgel ODS-120T. A geographic variation in toxin composition was suggested. The LD50 against crabs of AETX I, II and III were estimated to be 2.2, 0.53 and 0.28 microg/kg, respectively, but none of the toxins showed lethality in mice. The amino acid sequences of the three toxins were deduced from sequencings of the whole molecules and their enzymatic fragments. Amino acid analyses and molecular mass determinations supported the accuracy of the deduced sequences. AETX I, comprising 47 amino acid residues including 6 half-Cys residues, is an analog of sea anemone type I toxins. On the other hand, AETX II and III, which are highly homologous with each other, are quite distinct from the known sea anemone polypeptide toxins in that they are composed of 59 residues including 10 half-Cys residues. Interestingly, both toxins have sequence similarities with neurotoxins isolated from the Brazilian 'armed' spider Phoneutria nigriventer.

Upregulation of Bcl-2 and elevation of ceramide in Batten disease.

The late infantile and juvenile variants of Batten disease are genetically distinct neurodegenerative disorders. Hallmarks of Batten disease include cognitive and motor decline, seizures and blindness due to retinitis pigmentosa. Recently, the CLN3 gene responsible for the juvenile variant has been cloned. Also, apoptosis was proven to be the mechanism by which neurons and photoreceptors die. This paper provides mechanistic support for the occurrence of apoptosis in this disease: There was marked upregulation of Bcl-2 in brain from the late infantile and juvenile types at the protein and RNA levels both by immunocytochemistry and by Northern blot analysis; there were also a 42% to 197% increase in brain ceramide determinations in brains from three patients with the juvenile type and three patients with the late infantile type. Double immunolabeling of brain sections for apoptosis and Bcl-2 supported a protective role for Bcl-2 in the juvenile form of Batten disease. These results raise the possibility that the intact CLN3 gene is normally antiapoptotic, and that it could be an upstream regulator of ceramide.

A common mutation site in the beta-galactosidase gene originates in Puerto Rico.

Several mutation sites have been found in the beta-galactosidase gene of patients with GM1 gangliosidosis. In a previous report we found a common point mutation site in American patients with GM1 gangliosidosis resulting in a 208Arg --> Cys amino acid substitution. From the patients' family history, we suggested that this mutation may have come to South and North America via Puerto Rico. Four new patients with infantile GM1 gangliosidosis have been analyzed with allele-specific hybridization. Two siblings from Puerto Rico of Spanish ancestry are homozygous for this mutation. Another patient also from Puerto Rico is heterozygous for this allele, and another black patient does not have this mutation. These results support our initial hypothesis that this mutation has probably arisen in Puerto Rico.

Role of subunit-9 of mitochondrial ATP synthase in Batten disease.

The role of subunit-9 of mitochondrial ATP synthase in Batten disease was defined by characterizing the expression of genes encoding this protein in human tissues. Two genetically distinct neuronal ceroid-lipofuscinoses (NCL) comprise Batten disease: the late-infantile (LINCL) and juvenile (JNCL) types. We tested cell lines and tissues from both types of patients, along with normal controls. Differences in expression between diseased and normal samples were found for both mRNA and protein. Antibody staining of subunit-9 protein was detected in LINCL and JNCL tissues, and in 6 LINCL and 4 of 5 JNCL fibroblast lines. No immunoreactivity was seen in fibroblasts from obligate carriers, normal controls, and 6 other storage disease controls, with the exception of faint staining in Niemann-Pick, type C cells. There was an appreciable difference in staining pattern in both tissue sections and fibroblasts between LINCL and JNCL. Three subunit-9 transcripts (Hum1, Hum2, and Hum3) were specifically detected in NCL and normal human tissue from heart, liver, brain, muscle, and pancreas. Transcriptional regulation of subunit-9 genes was found to be altered in Batten disease. Pseudogenes related to each of the subunit-9 genes were isolated. Sequence analysis of cDNAs spanning the protein-coding regions of the Hum1, Hum2, and Hum3 genes showed conclusively that the primary defect(s) causing NCL are not mutations in the protein-coding regions of the 3 known subunit-9 genes.

Mutations in acid beta-galactosidase cause GM1-gangliosidosis in American patients.

We describe four new mutations in the beta-galactosidase gene. These are the first mutations causing infantile and juvenile GM1-gangliosidosis to be described in American patients. Cell lines from two patients with juvenile and from six patients with infantile GM1-gangliosidosis were analyzed. Northern blot analysis showed the acid beta-galactosidase message to be of normal size and quantity in two juvenile and four infantile cases and of normal size but reduced quantity in two infantile cases. The mutations are distinct from the Japanese mutations. All are point mutations leading to amino acid substitutions: Lys577-->Arg, Arg590-->His, and Glu632-->Gly. The fourth mutation, Arg208-->Cys, accounts for 10 of 16 possible alleles. Two infantile cases from Puerto Rico of Spanish ancestry are homozygous for this mutation, suggesting that this allele may have come to South America and North America via Puerto Rico. That these mutations cause clinical disease was confirmed by marked reduction in catalytic activity of the mutant proteins in the Cos-1 cell expression system.

A serologically confirmed, case-control study, of a large outbreak of hepatitis A in China, associated with consumption of clams.

A matched and serologically confirmed case-control study was carried out to investigate the source of an outbreak of acute hepatitis involving 290,000 cases in the suburbs of Shanghai, in January 1988. A total of 132 patients with acute hepatitis from six different hospitals were chosen as cases and the same number of control patients without hepatitis were matched for gender, age, admission date and area of residence. Serum specimens from both case and control patients were detected for specific anti-hepatitis A (HA) IgM antibody and a questionnaire was used to investigate probable risk factors related to the outbreak. The positive rate of anti-HA IgM was 98.48% in the case group and only 0.76% in the control, indicating that the infection was caused by HA virus. The results revealed that the source and mode of transmission were due to the consumption of contaminated and inadequately cooked clams (Anadara subcrenata lischke). There was a highly positive dose-response relationship between the odds ratio of contracting HA and the quantity or frequency of clam consumption. The odds ratios of acquiring HA from clams were up to 62.4-63.4 by both group stratification and multiple unconditional logistic regression analyses.

Chang-Ning epidemiological study of children's health: I: Passive smoking and children's respiratory diseases.

The effects of household exposure to cigarette smoke on hospitalization and incidence of respiratory illness were examined among 2227 children at Chang-Ning District, Shanghai Municipality, People's Republic of China. The passive smoking quantity was estimated by total daily cigarette consumption of family members and number of cigarettes smoked in the home. No mothers who smoked were found. A significant dose-response relationship of passive smoking to hospitalization for respiratory illness during the children's first 18 months of life was found, for which no confounding factors were discovered. The incidence density ratio of hospitalization for respiratory illness was 2.1 for children living in families including people who smoked 20 or more cigarettes a day compared with those living in non-smoking families. The children appeared to be more vulnerable in the first six months of life than in the 7-18 month period, and those with lower birth weight and the artificially fed were more susceptible. The cumulative incidence of bronchitis or pneumonia increased significantly with increasing cigarette smoking of family members, which persisted when sex, birthweight, nursery care, father's education, coal for cooking, and adult cases with chronic respiratory disease were taken into account. Family smoking status was not found to be significantly associated with the incidence of asthma, whooping cough, sinusitis and measles.