More than 40 specialists from Afghanistan, Armenia, Kazakhstan, Kyrgyzstan and Tajikistan completed a training seminar on advanced explosive ordnance disposal on April 20, 2016 in Dushanbe, organized by the OSCE Office in Tajikistan as a part of a multi-year project.

The course, which covered levels one and two of the explosive ordnance disposal curriculum outlined in International Mine Action Standards, was held at the Lyaur Field Training Centre of Tajikistan’s Ministry of Defence. The participants came from national armed forces, national mine action co-ordination authorities and civilian agencies which are directly engaged in addressing explosive hazards threats.

“The second explosive ordnance disposal training cycle is particularly significant as it introduces the mentorship approach to training whereby junior instructors – graduates of the first training cycle implemented in years 2014 and 2015 - are providing training shoulder-to-shoulder with their United States Army Central colleagues to the students from Central Asian and Afghanistan,” said Scott Kearin, Acting Head of the OSCE Office in Tajikistan.

U.S. Ambassador to Tajikistan Elisabeth Millard highlighted the leadership that the Ministry of Defense of Tajikistan has shown in hosting this series of training events. She said: “The need for competent explosive ordnance disposal specialists and trainers is critical for removing landmines and explosive remnants of war that threaten safety and stability in Tajikistan and surrounding countries.” She praised the Tajik Ministry of Defence for hosting a train-the-trainer program that allows them to lead humanitarian mine action programmes in the wider region.

Muhabbat Ibrohimzoda, Director of the Tajikistan National Mine Action Centre, said: “Tajikistan recognizes the present-day threats of explosive hazards and the need to address these challenges throughout the region and on a global level.”

Two separate courses – for Russian speaking and Tajik-Dari speaking groups of students - were facilitated by the OSCE Office in partnership with the United States Army Central and supported by the U.S. Embassy’s Office for Military Co-operation in Dushanbe. They were financed by the U.S. State Department’s Office of Weapons Removal and Abatement.

Since 2009, the OSCE has been supporting the development of co-operative mechanisms on a technical level among states in Central Asia and Afghanistan to address concerns and challenges stemming from explosive hazards.

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The use of DNA to self-assemble nanoscale objects has scaled up in both structure size and complexity, as well as the quantity produced.

Disney reopening Pixar Place, an 'Incredibles' meet-and-greet at Hollywood Studios in May.

DNA-testing company 23andMe (Nasdaq: ME), once an industry leader that attracted millions of customers, including rapper Snoop Dogg and investor Warren Buffett, has announced significant cuts to its operations, with plans to lay off 200 employees or roughly 40% of its workforce. The company also said it will discontinue development of its therapeutic programs. Here’s what to know about the latest development and what led up to it.

Board exodus

The latest move comes as the company looks to stabilize after facing significant challenges, including the resignation of all seven independent board members in October.

Data breach

Last year, 23andMe suffered a massive data breach when hackers accessed the personal information of 6.9 million users. The incident led to a class-action lawsuit, which, in September, 23andMe agreed to settle for $30 million.

The problem with SPACs

In 2021, 23andMe went public through a merger with a special purpose acquisition company, or SPAC. It later expanded into drug-discovery and weight-loss sectors. However, as DNA test kit sales declined, so did its financial health. By fiscal 2023, it reported a $312 million net loss, with its stock down 98% since going public, currently at about $4 after a reverse stock split in October 2024.

Separate reports have found that things have often not ended well for companies that took advantage of the pandemic-era SPAC boom, which led to billions in losses for investors and a number of bankruptcies for companies.

What’s next for 23andMe and its employees?

The layoffs are expected to result in $12 million in severance, termination, and transition-related costs and are part of a broader plan to streamline the business and achieve annual cost savings of $35 million.

The company says it is exploring various strategic options for its therapeutic programs, including potential licensing agreements and the sale of assets in its development pipeline.

“We are taking these difficult but necessary actions as we restructure 23andMe and focus on the long-term success of our core consumer business and research partnerships,” said Anne Wojcicki, cofounder, CEO, and chair of the board, in a statement.

Shares of 23andMe were up almost 6% to $4.87 on the news, which was announced late yesterday. The stock is down more than 73% year to date.

Location: Electronic Resource- 

Location: Engineering Library- TP248.25.N35S77 2015

Assyrian Heritage DNA Project

Turmoil at 23andMe, and a lawsuit alleging that GEDmatch shares data with Facebook, highlights how far your genetic information could travel without your consent.

A breakthrough enzyme aims to resolve a persistent DNA artifact that has challenged forensic analysis for decades.

Thankfully the young boy manages to return safely to his family after police interfered when the boy's sister and father chased the alleged kidnapper down in a high-speed chase.

Artasia Viges, 24, is facing multiple charges after police said she lied about her son being kidnapped after she left him unattended on a major roadway.

Our young people are being kidnapped by culture, and many are quitting church. But you can reach youth like Ethan by supporting the many Amazing Facts resources and events designed to help them find freedom in Christ. Will you support faith-building conferences and materials that lead others to God’s kingdom? Thank you!

Listen to O'Brien's conversation from 2009 with Eleanor Wachtel. O'Brien died on July 27, 2024 at the age of 93.

Dancing really is all about the bass and is it too late for fusion?

Farming fish lose their fertilizer and inoculation against misinformation.

If they survive the winners’ curse, Little Mix could prove an interesting prospect.

Zvyšování daní nebo hromadné výpovědi lékařů ve slovenských nemocnicích se premiér Robert Fico snažil zametat pod koberec, jak jen to bylo možné, a dělal všechno pro to, aby odlákal pozornost veřejnosti k něčemu jinému. Nakonec přestal experimentovat a vrátil se k osvědčené klasice „za to můžou ostatní“. V tomto případě za to můžou ostatní politické strany, kterých je prostě moc.

The oldest DNA ever retrieved, preserved in sediments in northern Greenland, reveals that Arctic and temperate species once commingled in an ecosystem unlike anything that exists today.

"Customers must be able to reevaluate their willingness to have their genome data shared outside the original intent.”

The post Patronis Questions DNA Testing Companies’ User Confidentiality appeared first on Shark Tank.

Mitochondria are specialized compartments that produce requisite ATP to fuel cellular functions and serve as centers of metabolite processing, cellular signaling, and apoptosis. To accomplish these roles, mitochondria rely on the genetic information in their small genome (mitochondrial DNA) and the nucleus. A growing appreciation for mitochondria's role in a myriad of human diseases, including inherited genetic disorders, degenerative diseases, inflammation, and cancer, has fueled the study of biochemical mechanisms that control mitochondrial function. The mitochondrial transcriptional machinery is different from nuclear machinery. The in vitro re-constituted transcriptional complexes of Saccharomyces cerevisiae (yeast) and humans, aided with high-resolution structures and biochemical characterizations, have provided a deeper understanding of the mechanism and regulation of mitochondrial DNA transcription. In this review, we will discuss recent advances in the structure and mechanism of mitochondrial transcription initiation. We will follow up with recent discoveries and formative findings regarding the regulatory events that control mitochondrial DNA transcription, focusing on those involved in cross-talk between the mitochondria and nucleus.

RecQ family helicases are highly conserved from bacteria to humans and have essential roles in maintaining genome stability. Mutations in three human RecQ helicases cause severe diseases with the main features of premature aging and cancer predisposition. Most RecQ helicases shared a conserved domain arrangement which comprises a helicase core, an RecQ C-terminal domain, and an auxiliary element helicase and RNaseD C-terminal (HRDC) domain, the functions of which are poorly understood. In this study, we systematically characterized the roles of the HRDC domain in E. coli RecQ in various DNA transactions by single-molecule FRET. We found that RecQ repetitively unwinds the 3'-partial duplex and fork DNA with a moderate processivity and periodically patrols on the ssDNA in the 5'-partial duplex by translocation. The HRDC domain significantly suppresses RecQ activities in the above transactions. In sharp contrast, the HRDC domain is essential for the deep and long-time unfolding of the G4 DNA structure by RecQ. Based on the observations that the HRDC domain dynamically switches between RecA core- and ssDNA-binding modes after RecQ association with DNA, we proposed a model to explain the modulation mechanism of the HRDC domain. Our findings not only provide new insights into the activities of RecQ on different substrates but also highlight the novel functions of the HRDC domain in DNA metabolisms.

Bacterial low-copy-number plasmids require partition (par) systems to ensure their stable inheritance by daughter cells. In general, these systems consist of three components: a centromeric DNA sequence, a centromere-binding protein and a nucleotide hydrolase that polymerizes and functions as a motor. Type III systems, however, segregate plasmids using three proteins: the FtsZ/tubulin-like GTPase TubZ, the centromere-binding protein TubR and the MerR-like transcriptional regulator TubY. Although the TubZ filament is sufficient to transport the TubR-centromere complex in vitro, TubY is still necessary for the stable maintenance of the plasmid. TubY contains an N-terminal DNA-binding helix-turn-helix motif and a C-terminal coiled-coil followed by a cluster of lysine residues. This study determined the crystal structure of the C-terminal domain of TubY from the Bacillus cereus pXO1-like plasmid and showed that it forms a tetrameric parallel four-helix bundle that differs from the typical MerR family proteins with a dimeric anti-parallel coiled-coil. Biochemical analyses revealed that the C-terminal tail with the conserved lysine cluster helps TubY to stably associate with the TubR-centromere complex as well as to nonspecifically bind DNA. Furthermore, this C-terminal tail forms an amphipathic helix in the presence of lipids but must oligomerize to localize the protein to the membrane in vivo. Taken together, these data suggest that TubY is a component of the nucleoprotein complex within the partitioning machinery, and that lipid membranes act as mediators of type III systems.

We have observed overexpression of PACS-1, a cytosolic sorting protein in primary cervical tumors. Absence of exonic mutations and overexpression at the RNA level suggested a transcriptional and/or posttranscriptional regulation. University of California Santa Cruz genome browser analysis of PACS-1 micro RNAs (miR), revealed two 8-base target sequences at the 3' terminus for hsa-miR-34a and hsa-miR-449a. Quantitative RT-PCR and Northern blotting studies showed reduced or loss of expression of the two microRNAs in cervical cancer cell lines and primary tumors, indicating dysregulation of these two microRNAs in cervical cancer. Loss of PACS-1 with siRNA or exogenous expression of hsa-miR-34a or hsa-miR-449a in HeLa and SiHa cervical cancer cell lines resulted in DNA damage response, S-phase cell cycle arrest, and reduction in cell growth. Furthermore, the siRNA studies showed that loss of PACS-1 expression was accompanied by increased nuclear γH2AX expression, Lys382-p53 acetylation, and genomic instability. PACS-1 re-expression through LNA-hsa-anti-miR-34a or -449a or through PACS-1 cDNA transfection led to the reversal of DNA damage response and restoration of cell growth. Release of cells post 24-h serum starvation showed PACS-1 nuclear localization at G1-S phase of the cell cycle. Our results therefore indicate that the loss of hsa-miR-34a and hsa-miR-449a expression in cervical cancer leads to overexpression of PACS-1 and suppression of DNA damage response, resulting in the development of chemo-resistant tumors.

Mitochondrial DNA (mtDNA) encodes proteins and RNAs that support the functions of mitochondria and thereby numerous physiological processes. Mutations of mtDNA can cause mitochondrial diseases and are implicated in aging. The mtDNA within cells is organized into nucleoids within the mitochondrial matrix, but how mtDNA nucleoids are formed and regulated within cells remains incompletely resolved. Visualization of mtDNA within cells is a powerful means by which mechanistic insight can be gained. Manipulation of the amount and sequence of mtDNA within cells is important experimentally and for developing therapeutic interventions to treat mitochondrial disease. This review details recent developments and opportunities for improvements in the experimental tools and techniques that can be used to visualize, quantify, and manipulate the properties of mtDNA within cells.

In nucleotide excision repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genome by concerted dual incisions bracketing the lesion, followed by gap filling and ligation. So far, two dual-incision patterns have been discovered: the prokaryotic type, which removes the damage in 11–13-nucleotide-long oligomers, and the eukaryotic type, which removes the damage in 24–32-nucleotide-long oligomers. However, a recent study reported that the UvrC protein of Mycobacterium tuberculosis removes damage in a manner analogous to yeast and humans in a 25-mer oligonucleotide arising from incisions at 15 nt from the 3´ end and 9 nt from the 5´ end flanking the damage. To test this model, we used the in vivo excision assay and the excision repair sequencing genome-wide repair mapping method developed in our laboratory to determine the repair pattern and genome-wide repair map of Mycobacterium smegmatis. We find that M. smegmatis, which possesses homologs of the Escherichia coli uvrA, uvrB, and uvrC genes, removes cyclobutane pyrimidine dimers from the genome in a manner identical to the prokaryotic pattern by incising 7 nt 5´ and 3 or 4 nt 3´ to the photoproduct, and performs transcription-coupled repair in a manner similar to E. coli.

The faithful segregation, or “partition,” of many low-copy number bacterial plasmids is driven by plasmid-encoded ATPases that are represented by the P1 plasmid ParA protein. ParA binds to the bacterial nucleoid via an ATP-dependent nonspecific DNA (nsDNA)-binding activity, which is essential for partition. ParA also has a site-specific DNA-binding activity to the par operator (parOP), which requires either ATP or ADP, and which is essential for it to act as a transcriptional repressor but is dispensable for partition. Here we examine how DNA binding by ParA contributes to the relative distribution of its plasmid partition and repressor activities, using a ParA with an alanine substitution at Arg351, a residue previously predicted to participate in site-specific DNA binding. In vivo, the parAR351A allele is compromised for partition, but its repressor activity is dramatically improved so that it behaves as a “super-repressor.” In vitro, ParAR351A binds and hydrolyzes ATP, and undergoes a specific conformational change required for nsDNA binding, but its nsDNA-binding activity is significantly damaged. This defect in turn significantly reduces the assembly and stability of partition complexes formed by the interaction of ParA with ParB, the centromere-binding protein, and DNA. In contrast, the R351A change shows only a mild defect in site-specific DNA binding. We conclude that the partition defect is due to altered nsDNA binding kinetics and affinity for the bacterial chromosome. Furthermore, the super-repressor phenotype is explained by an increased pool of non-nucleoid bound ParA that is competent to bind parOP and repress transcription.

DNA polymerase from bacteriophage T7 undergoes large, substrate-induced conformational changes that are thought to account for high replication fidelity, but prior studies were adversely affected by mutations required to construct a Cys-lite variant needed for site-specific fluorescence labeling. Here we have optimized the direct incorporation of a fluorescent un-natural amino acid, (7-hydroxy-4-coumarin-yl)-ethylglycine, using orthogonal amber suppression machinery in Escherichia coli. MS methods verify that the unnatural amino acid is only incorporated at one position with minimal background. We show that the single fluorophore provides a signal to detect nucleotide-induced conformational changes through equilibrium and stopped-flow kinetic measurements of correct nucleotide binding and incorporation. Pre-steady-state chemical quench methods show that the kinetics and fidelity of DNA replication catalyzed by the labeled enzyme are largely unaffected by the unnatural amino acid. These advances enable rigorous analysis to establish the kinetic and mechanistic basis for high-fidelity DNA replication.

In eukaryotic DNA replication, DNA polymerase ε (Polε) is responsible for leading strand synthesis, whereas DNA polymerases α and δ synthesize the lagging strand. The human Polε (hPolε) holoenzyme is comprised of the catalytic p261 subunit and the noncatalytic p59, p17, and p12 small subunits. So far, the contribution of the noncatalytic subunits to hPolε function is not well understood. Using pre-steady-state kinetic methods, we established a minimal kinetic mechanism for DNA polymerization and editing catalyzed by the hPolε holoenzyme. Compared with the 140-kDa N-terminal catalytic fragment of p261 (p261N), which we kinetically characterized in our earlier studies, the presence of the p261 C-terminal domain (p261C) and the three small subunits increased the DNA binding affinity and the base substitution fidelity. Although the small subunits enhanced correct nucleotide incorporation efficiency, there was a wide range of rate constants when incorporating a correct nucleotide over a single-base mismatch. Surprisingly, the 3'→5' exonuclease activity of the hPolε holoenzyme was significantly slower than that of p261N when editing both matched and mismatched DNA substrates. This suggests that the presence of p261C and the three small subunits regulates the 3'→5' exonuclease activity of the hPolε holoenzyme. Together, the 3'→5' exonuclease activity and the variable mismatch extension activity modulate the overall fidelity of the hPolε holoenzyme by up to 3 orders of magnitude. Thus, the presence of p261C and the three noncatalytic subunits optimizes the dual enzymatic activities of the catalytic p261 subunit and makes the hPolε holoenzyme an efficient and faithful replicative DNA polymerase.

The origin recognition complex (ORC), composed of six subunits, ORC1–6, binds to origins of replication as a ring-shaped heterohexameric ATPase that is believed to be essential to recruit and load MCM2–7, the minichromosome maintenance protein complex, around DNA and initiate DNA replication. We previously reported the creation of viable cancer cell lines that lacked detectable ORC1 or ORC2 protein without a reduction in the number of origins firing. Here, using CRISPR-Cas9–mediated mutations, we report that human HCT116 colon cancer cells also survive when ORC5 protein expression is abolished via a mutation in the initiator ATG of the ORC5 gene. Even if an internal methionine is used to produce an undetectable, N terminally deleted ORC5, the protein would lack 80% of the AAA+ ATPase domain, including the Walker A motif. The ORC5-depleted cells show normal chromatin binding of MCM2–7 and initiate replication from a similar number of origins as WT cells. In addition, we introduced a second mutation in ORC2 in the ORC5 mutant cells, rendering both ORC5 and ORC2 proteins undetectable in the same cells and destabilizing the ORC1, ORC3, and ORC4 proteins. Yet the double mutant cells grow, recruit MCM2–7 normally to chromatin, and initiate DNA replication with normal number of origins. Thus, in these selected cancer cells, either a crippled ORC lacking ORC2 and ORC5 and present at minimal levels on the chromatin can recruit and load enough MCM2–7 to initiate DNA replication, or human cell lines can sometimes recruit MCM2–7 to origins independent of ORC.

Timely repair of DNA double-strand breaks (DSBs) is essential to maintaining genomic integrity and preventing illnesses induced by genetic abnormalities. We previously demonstrated that the E3 ubiquitin ligase SMURF2 plays a critical tumor suppressing role via its interaction with RNF20 (ring finger protein 20) in shaping chromatin landscape and preserving genomic stability. However, the mechanism that mobilizes SMURF2 in response to DNA damage remains unclear. Using biochemical approaches and MS analysis, we show that upon the onset of the DNA-damage response, SMURF2 becomes phosphorylated at Ser384 by ataxia telangiectasia mutated (ATM) serine/threonine kinase, and this phosphorylation is required for its interaction with RNF20. We demonstrate that a SMURF2 mutant with an S384A substitution has reduced capacity to ubiquitinate RNF20 while promoting Smad3 ubiquitination unabatedly. More importantly, mouse embryonic fibroblasts expressing the SMURF2 S384A mutant show a weakened ability to sustain the DSB response compared with those expressing WT SMURF2 following etoposide treatment. These data indicate that SMURF2-mediated RNF20 ubiquitination and degradation controlled by ataxia telangiectasia mutated–induced phosphorylation at Ser384 constitutes a negative feedback loop that regulates DSB repair.

Is it possible to meet the world's seemingly infinite demand for data storage while also caring for the natural environment? Biomedical researcher Keolu Fox and professional surfer and scientist Cliff Kapono believe that Indigenous knowledge combined with the science of genetics may offer such a solution: using the DNA of plant cells (like those found in sugar cane) as mini data warehouses. Learn more about the incredible potential of this technology — and how it could help foster ecosystem resilience in a high-tech world.

Cochlear hair cells (HCs) sense sound waves and allow us to hear. Loss of HCs will cause irreversible sensorineural hearing loss. It is well known that DNA damage repair plays a critical role in protecting cells in many organs. However, how HCs respond to DNA damage and how defective DNA damage repair contributes to hearing loss remain elusive. In this study, we showed that cisplatin induced DNA damage in outer hair cells (OHCs) and promoted OHC loss, leading to hearing loss in mice of either sex. Cisplatin induced the expression of Brca1, a DNA damage repair factor, in OHCs. Deficiency of Brca1 induced OHC and hearing loss, and further promoted cisplatin-induced DNA damage in OHCs, accelerating OHC loss. This study provides the first in vivo evidence demonstrating that cisplatin mainly induces DNA damage in OHCs and that BRCA1 promotes repair of DNA damage in OHCs and prevents hearing loss. Our findings not only demonstrate that DNA damage–inducing agent generates DNA damage in postmitotic HCs but also suggest that DNA repair factors, like BRCA1, protect postmitotic HCs from DNA damage–induced cell death and hearing loss.

Researchers recently identified James Fitzjames, a captain on the ill-fated HMS Erebus that went looking for the Northwest Passage in 1845

New research has revealed that the mysterious white substance found alongside three ancient mummies was once a soft cheese called kefir

The notorious predators, nicknamed the “Man-Eaters of Tsavo,” terrorized railway workers in Kenya for roughly nine months

The baby boy’s recovered genome suggests he’s related to a famous Ice Age population

A new study has shattered historians' long-held assumptions about some of the people who died in Mount Vesuvius' eruption in 79 C.E.

Quebec provincial police have confirmed that the body found in a Montreal nature park on Oct. 30 was that of kidnapping victim and cryptocurrency influencer Kevin Mirshahi.

Mosquitoes take blood meals from a diverse range of host animals and their host associations vary by species. Characterizing these associations is an important element of the transmission dynamics of mosquito-vectored pathogens. To characterize mosquito host associations, various molecular techniques have been developed, which are collectively referred to as blood meal analysis. DNA barcoding has diverse biological applications and is well-suited to mosquito blood meal analysis. The standard DNA barcoding marker for animals is a 5' fragment of the cytochrome c oxidase I (COI) gene. A major advantage of this marker is its taxonomic coverage in DNA sequence reference databases, making it feasible to identify a wider range of mosquito host species than with any other gene. However, the COI gene contains high sequence variation at potential priming sites between vertebrate orders. Coupled with the need for primer sequences to be mismatched with mosquito priming sites so that annealing to mosquito DNA is inhibited, it can be difficult to design primers suitable for blood meal analysis applications. Several primers are available that perform well in mosquito blood meal analysis, annealing to priming sites for most vertebrate host taxa, but not to those of mosquitoes. Because priming site sequence variation among vertebrate taxa can cause amplification to fail, a hierarchical approach to DNA barcoding-based blood meal analysis can be applied. In such an approach, no single primer set is expected to be effective for 100% of potential host species. If amplification fails in the initial reaction, a subsequent reaction is attempted with primers that anneal to different priming sites, and so on, until amplification is successful.

Mosquito species vary in their host associations. Although some species are relative generalists, most specialize, to varying extents, on particular types of host animals. Mosquito host associations are among the most important factors that influence the transmission dynamics of mosquito-vectored pathogens, and understanding these associations can provide insight on how such pathogens move within ecosystems. Characterization of the host associations of mosquito species requires applying blood meal analysis to the largest possible sample size of mosquito blood meals. Processing large samples of mosquito blood meals can be time-consuming, especially when chain-termination sequencing is used, necessitating individual processing of each specimen. Various methods and commercially available kits and products are available for extracting DNA from mosquito blood meals. The hot sodium hydroxide and Tris (HotSHOT) method is a rapid and inexpensive method of DNA extraction that is compatible with the recovery of DNA from mosquito blood meals preserved on QIAcard Flinders Technology Associates (FTA) Classic Cards (FTA cards). FTA cards allow nucleic acids found in blood meals to be preserved easily, even in field conditions. DNA prepared using this method is suitable for polymerase chain reaction (PCR)-based blood meal analysis.

In a political twist almost no one saw coming, on the morning of November 23, 2019, Devendra Fadnavis took oath as the Maharashtra Chief Minister for a second term.

A day after the political row over a routine check of Shiv Sena (BT) chief Uddhav Thackeray's luggage, the BJP today posted a video of airport security frisking Maharashtra Deputy Chief Minister Devendra Fadnavis' bags and took a dig at Mr Thackeray

A day after the political row over a routine check of Shiv Sena (BT) chief Uddhav Thackeray's luggage, the BJP today posted a video of airport security frisking Maharashtra Deputy Chief Minister Devendra Fadnavis' bags and took a dig at Mr Thackeray

Recent DNA findings from Pompeii reveal complex ancestry and social diversity, challenging earlier assumptions about family structures and cultural roles in the ancient city. Analysing skeletal remains has shown that some groups presumed to be family members were not biologically related, while traditional gender roles were also re-evaluated. This research highlights the cosmopolitan nature of Pompeii’s society and opens a new chapter in understanding life before the eruption of Mount Vesuvius.

Atlas Biomed's website is no longer active and the phone number listed is dead as well.

Three men, including a suspect in the kidnapping of American national Elliot Onil Eastman, were killed in an encounter in Kabasalan, Zamboanga Sibugay yesterday.