Wan Omar A et al. (2001) Malays J Med Sci "Epidemiological screening of lymphatic filariasis among immigrants using dipstick colloidal dye immunoassay."

Sulaiman O, Wan Omar A, Yusof S, Ismail G, Fatmah MS, Rahmah N, Khairul AA

[Malays J Med Sci, 2001]

We have recently reported that a dipstick colloidal dye immunoassay (DIA) that detect parasite antigens in human serum is sensitive and specific for the diagnosis of active infection of lymphatic filariasis. Rabbit polyclonal antibodies (RbBmCAg) labelled with a commercial dye, palanil navy blue was used to detect filarial antigenemia among Indonesian and Bangladeshi immigrant workers (N= 630) at oil palm estates at Hulu Trengganu District, Peninsular Malaysia. Microfilaremia with Brugia malayi were detected in 51 (8.10 %) individuals, of which 42 (6.67 %) were among the Indonesians and 9 (1.98 %) among the Bangladeshis. Microfilaremia with Wuchereria bancrofti were detected in 33 (5.24 %) individuals of which 15 (2.38 %) were among the Indonesians and 18 (2.86 %) among the Bangladeshis workers. The DIA detected 96 (15.24 %) antigenemic cases which comprise of all the microfilaremic cases and 15 (2.38 %) amicrofilaremic cases. The amicrofilaremic cases with filarial antigenemia consisted of 9 (1. 43 %) Indonesians and 6 (0.95%) Bangladeshis. We have used 6 ul of the RbBmCAg and diluted (1:10) patients' sera per dipstick which make the DIA reagent conservative. The DIA is a rapid test and can be read in approximate 2 hours.. Additionally, coloured dots developed in the DIA can be qualitatively assessed visually for intensity. The DIA does not require sophisticated equipment or radioactivity, and therefore suitable for field application.

Shen Q et al. (2009) Mol Cell Biol "Adenine nucleotide translocator cooperates with core cell death machinery to promote apoptosis in Caenorhabditis elegans."

Yang C, Xu Z, Xiao H, Gao Z, Qin F, Shen Q, Cui J

[Mol Cell Biol, 2009]

In Caenorhabditis elegans, the central cell-killing process is essentially controlled by the interplay of four apoptotic factors: EGL-1/BH3-only protein, CED-9/Bcl2, CED-4/Apaf1, and CED-3/caspase. In cells destined to die, EGL-1 binds to CED-9 and results in the release of CED-4 from the mitochondrion-tethered CED-9-CED-4 complex to the perinucleus, which facilitates processing of the CED-3 caspase to cause apoptosis. However, whether additional factors exist to regulate the cell-killing process remains largely unknown. We have identified here WAN-1, the C. elegans ortholog of mammalian adenine nucleotide translocator, as an important cell death regulator. Genetic inactivation of wan-1 significantly suppressed both somatic and germ line cell deaths in C. elegans. Consistently, chemical inhibition of WAN-1 activity also caused strong reduction of germ line apoptosis. WAN-1 localizes to mitochondria and can form complex with both CED-4 and CED-9. Importantly, the cell death initiator EGL-1 can disrupt the interaction between CED-9 and WAN-1. In addition, overexpression of WAN-1 induced ectopic cell killing dependently on the core cell death pathway. These findings suggest that WAN-1 is involved in the central cell-killing process and cooperates with the core cell death machinery to promote programmed cell death in C. elegans.

Uebel, Celja J. et al. (2021) MicroPubl Biol

Manage, Kevin I., Uebel, Celja J., Phillips, Carolyn M.

[MicroPubl Biol, 2021]

Multiple condensates occupy the perinuclear space of C. elegans germ cells, where they coordinate RNA surveillance to ensure proper gene expression (Lev and Rechavi 2020; Sundby et al. 2021). The most well-studied of these condensates are P granules, phase-separated germ granules required for maintenance of germ cell identity and fertility (Kawasaki et al. 1998; Updike et al. 2014). P granule morphology and localization is well documented in C. elegans development (Strome et al. 1982). Adjacent to P granules are Mutator foci, which are nucleated by MUT-16 and required for the amplification of small interfering RNAs (siRNAs) to create a robust and heritable silencing signal (Phillips et al. 2012). During development, faint Mutator foci are occasionally seen in the P4 germline blastomere of 30-cell embryos, but are most robust and numerous in the Z2 and Z3 progenitor germ cells (PGCs) of 100-cell embryos (Uebel et al. 2020). A third germline condensate, Z granules, are situated between P granules and Mutator foci and facilitate transgenerational epigenetic inheritance of silencing signals. Z granule components ZNFX-1 and WAGO-4 colocalize with P granules in early embryos, but begin to de-mix from P granules in the Z2/Z3 PGCs to form separate Z granule condensates (Wan et al. 2018). Lastly, recently discovered SIMR foci also intimately localize within this cluster of germline granules. SIMR-1, a key component of SIMR foci, is a Tudor domain protein that mediates production of secondary siRNAs for piwi-interacting RNA (piRNA)-targeted mRNAs (Manage et al. 2020). While P granule, Z granule, and Mutator foci localization through embryonic development has been previously described, the embryonic appearance of SIMR foci is not known.

Quartey MO et al. (2021) Sci Rep "The A(1-38) peptide is a negative regulator of the A(1-42) peptide implicated in Alzheimer disease progression."

Pennington PR, Heistad RM, Nyarko JNK, Barnes JR, Bolanos MAC, Parsons MP, Knudsen KJ, De Carvalho CE, Leary SC, Mousseau DD, Buttigieg J, Maley JM, Quartey MO

[Sci Rep, 2021]

The pool of -Amyloid (A) length variants detected in preclinical and clinical Alzheimer disease (AD) samples suggests a diversity of roles for A peptides. We examined how a naturally occurring variant, e.g. A(1-38), interacts with the AD-related variant, A(1-42), and the predominant physiological variant, A(1-40). Atomic force microscopy, Thioflavin T fluorescence, circular dichroism, dynamic light scattering, and surface plasmon resonance reveal that A(1-38) interacts differently with A(1-40) and A(1-42) and, in general, A(1-38) interferes with the conversion of A(1-42) to a -sheet-rich aggregate. Functionally, A(1-38) reverses the negative impact of A(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an A(1-42) phenotype in Caenorhabditis elegans. A(1-38) also reverses any loss of MTT conversion induced by A(1-40) and A(1-42) in HT-22 hippocampal neurons and APOE 4-positive human fibroblasts, although the combination of A(1-38) and A(1-42) inhibits MTT conversion in APOE 4-negative fibroblasts. A greater ratio of soluble A(1-42)/A(1-38) [and A(1-42)/A(1-40)] in autopsied brain extracts correlates with an earlier age-at-death in males (but not females) with a diagnosis of AD. These results suggest that A(1-38) is capable of physically counteracting, potentially in a sex-dependent manner, the neuropathological effects of the AD-relevant A(1-42).

Tangrodchanapong T et al. (2020) Front Pharmacol "Frondoside A Attenuates Amyloid- Proteotoxicity in Transgenic Caenorhabditis elegans by Suppressing Its Formation."

Tangrodchanapong T, Sobhon P, Meemon K

[Front Pharmacol, 2020]

Oligomeric assembly of Amyloid- (A) is the main toxic species that contribute to early cognitive impairment in Alzheimer's patients. Therefore, drugs that reduce the formation of A oligomers could halt the disease progression. In this study, by using transgenic <i>Caenorhabditis elegans</i> model of Alzheimer's disease, we investigated the effects of frondoside A, a well-known sea cucumber <i>Cucumaria frondosa</i> saponin with anti-cancer activity, on A aggregation and proteotoxicity. The results showed that frondoside A at a low concentration of 1 M significantly delayed the worm paralysis caused by A aggregation as compared with control group. In addition, the number of A plaque deposits in transgenic worm tissues was significantly decreased. Frondoside A was more effective in these activities than ginsenoside-Rg3, a comparable ginseng saponin. Immunoblot analysis revealed that the level of small oligomers as well as various high molecular weights of A species in the transgenic <i>C. elegans</i> were significantly reduced upon treatment with frondoside A, whereas the level of A monomers was not altered. This suggested that frondoside A may primarily reduce the level of small oligomeric forms, the most toxic species of A. Frondoside A also protected the worms from oxidative stress and rescued chemotaxis dysfunction in a transgenic strain whose neurons express A. Taken together, these data suggested that low dose of frondoside A could protect against A-induced toxicity by primarily suppressing the formation of A oligomers. Thus, the molecular mechanism of how frondoside A exerts its anti-A aggregation should be studied and elucidated in the future.

Yue-E H et al. (2016) Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi "[Meta regression analysis of five heavy metal biotoxicity effects onCaenorhabditis elegans]."

Yue-E H, Chao-Pin L, Nan Z

[Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi, 2016]

OBJECTIVE: To evaluate five heavy metal biotoxicity effects on Caenorhabditis elegans with Meta regression analysis. METHODS: The data were collected from the following electronic databases&#65306;PubMed, Web of Science, EBSCO, the Chinese Biomedical Database, Chinese National Knowledge Infrastructure, Wan Fang (Chinese) Databases and so on, and all updated through January 2004 to December 2014. A literature review was made on articles about Cd, Hg, Pb, As and Cr toxicity effects on C. elegans, and the data was extracted from figure information by Scan It software. A Meta regression model was built by stata12.0 software, using toxicity indices such as the dependent variables, and different metals, concentrations, exposure time, and development stages of C. elegans as independent variables. RESULTS:The study articles asociated with heavy metal biotoxicity effects on C. elegans were selected out, 10 studies of Cu, 12 studies of Cr, 12 studies of Pb, 12 studies of Cd, 3 studies of As and 14 studies of Hg. The mortality of toxicities of 5 heavy metals on C. elegans ranked Hg > Pb > Cr> Cd>As; the biotoxicity of the indexes of body size based on development, generational time based on reproductive toxicity, body bend frequencies, and head thrash frequencies based on neurotoxicity ranked Hg > Pb > Cr > Cd; the biotoxicity ranked Hg > Pb > Cr> Cd>As by LC50 indexes of toxicities of 5 heavy metals on C. elegans. The sensitivity analysis proved that the Meta regression model was reliable. CONCLUSIONS: The biotoxicities on C. elegans of Hg and Pb are stronger than Cr, Cd and As.

Viney ME et al. (2004) Naturwissenschaften "Is dauer pheromone of Caenorhabditis elegans really a pheromone?"

Viney ME, Franks NR

[Naturwissenschaften, 2004]

Animals respond to signals and cues in their environment. The difference between a signal (e.g. a pheromone) and a cue (e.g. a waste product) is that the information content of a signal is subject to natural selection, whereas that of a cue is not. The model free-living nematode Caenorhabditis elegans forms an alternative developmental morph (the dauer larva) in response to a so-called 'dauer pheromone', produced by all worms. We suggest that the production of 'dauer pheromone' has no fitness advantage for an individual worm and therefore we propose that 'dauer pheromone' is not a signal, but a cue. Thus, it should not be called a pheromone.

Schaeffer JM et al. (1990) J Antibiot (Tokyo) "Cochlioquinone A, a nematocidal agent which competes for specific [3H]ivermectin binding sites."

Williamson JM, Schaeffer JM, Bergstrom AR, Liesch JM, Goetz MA, Frazier EG

[J Antibiot (Tokyo), 1990]

Cochlioquinone A, isolated from the fungus Helminthosporium sativum, was found to have nematocidal activity. Cochlioquinone A is a competitive inhibitor of specific [3H]ivermectin binding suggesting that cochlioquinone A and ivermectin interact with the same membrane receptor.

Desta IT et al. (2016) J Lab Autom "Detecting and Trapping of a Single C. elegans Worm in a Microfluidic Chip for Automated Microplate Dispensing."

Giakoumidis N, Mustafa N, AlGharibeh N, Orozaliev A, Al-Sharif A, Song YA, Desta IT, Gunsalus KC

[J Lab Autom, 2016]

Microfluidic devices offer new technical possibilities for a precise manipulation of Caenorhabditis elegans due to the comparable length scale. C. elegans is a small, free-living nematode worm that is a popular model system for genetic, genomic, and high-throughput experimental studies of animal development and neurobiology. In this paper, we demonstrate a microfluidic system in polydimethylsiloxane (PDMS) for dispensing of a single C. elegans worm into a 96-well plate. It consists of two PDMS layers, a flow and a control layer. Using five microfluidic pneumatic valves in the control layer, a single worm is trapped upon optical detection with a pair of optical fibers integrated perpendicular to the constriction channel and then dispensed into a microplate well with a dispensing tip attached to a robotic handling system. Due to its simple design and facile fabrication, we expect that our microfluidic chip can be expanded to a multiplexed dispensation system of C. elegans worms for high-throughput drug screening.

Ailion M et al. (2017) Curr Biol "Genetics: Master Regulator or Master of Disguise?"

Malik HS, Ailion M

[Curr Biol, 2017]

The pha-1 gene of Caenorhabditis elegans was originally heralded as a master regulator of organ differentiation. A new study suggests instead that pha-1 actually serves no role in development and instead is a component of a selfish genetic element.