diff --git a/archive-covid-19/30 December, 2020.html b/archive-covid-19/30 December, 2020.html new file mode 100644 index 0000000..d380e40 --- /dev/null +++ b/archive-covid-19/30 December, 2020.html @@ -0,0 +1,185 @@ + +
+ + + ++People with pre-existing chronic health conditions are reportedly at high risk of getting the coronavirus disease (COVID-19) and of having a severe disease course but little data exist on rare diseases such as Primary Ciliary Dyskinesia (PCD). We studied risk and severity of SARS-CoV-2 infections among people with PCD using data from the COVID-PCD, a participatory study that collects data in real-time directly from people with PCD. Data was collected using online questionnaires. A baseline questionnaire collected information on demographic data, information about the PCD diagnosis and severity. A short weekly questionnaire collected information about current symptoms and incident SARS-CoV-2 infections. 578 people participated in the COVID-PCD by December 7, 2020, with a median number of follow-up weeks of 9 (interquartile range: 4-19 weeks). 256 (45%) of the participants had been tested for SARS-CoV-2 and 12 tested positive prior to study entry or during study follow up (2.1% of the total included population, 95% confidence interval (CI) 1.1-3.6%). 4 people tested positive during the study follow-up, corresponding to an incidence rate of 2.5 per 100 person-years (95% CI: 0.9-6.5). Overall, reported severity was mild with two reporting no symptoms, eight reporting mild symptoms, one reporting severe symptom without hospitalisation, and one reporting hospitalisation for 9 days. The study suggests that with careful personal protection, people with PCD do not seem to have an increased risk of infection with SARS-COV-2, nor an especially severe disease course. +
++SARS-CoV-2 Spike protein is critical for virus infection via engagement of ACE2, and amino acid variation in Spike is increasingly appreciated. Given both vaccines and therapeutics are designed around Wuhan-1 Spike, this raises the theoretical possibility of virus escape, particularly in immunocompromised individuals where prolonged viral replication occurs. Here we report chronic SARS-CoV-2 with reduced sensitivity to neutralising antibodies in an immune suppressed individual treated with convalescent plasma, generating whole genome ultradeep sequences by both short and long read technologies over 23 time points spanning 101 days. Although little change was observed in the overall viral population structure following two courses of remdesivir over the first 57 days, N501Y in Spike was transiently detected at day 55 and V157L in RdRp emerged. However, following convalescent plasma we observed large, dynamic virus population shifts, with the emergence of a dominant viral strain bearing D796H in S2 and 𝚫H69/𝚫V70 in the S1 N-terminal domain NTD of the Spike protein. As passively transferred serum antibodies diminished, viruses with the escape genotype diminished in frequency, before returning during a final, unsuccessful course of convalescent plasma. In vitro, the Spike escape double mutant bearing 𝚫H69/𝚫V70 and D796H conferred decreased sensitivity to convalescent plasma, whilst maintaining infectivity similar to wild type. D796H appeared to be the main contributor to decreased susceptibility, but incurred an infectivity defect. The 𝚫H69/𝚫V70 single mutant had two-fold higher infectivity compared to wild type and appeared to compensate for the reduced infectivity of D796H. Consistent with the observed mutations being outside the RBD, monoclonal antibodies targeting the RBD were not impacted by either or both mutations, but a non RBD binding monoclonal antibody was less potent against 𝚫H69/𝚫V70 and the double mutant. These data reveal strong selection on SARS-CoV-2 during convalescent plasma therapy associated with emergence of viral variants with reduced susceptibility to neutralising antibodies. +
++The expansion of the new coronavirus disease (COVID-19) triggered a renewed public interest in epidemiological models and on how parameters can be estimated from observed data. Here we investigated the relationship between average number of transmissions though time, the reproductive number Rt, and social distancing index as reported by mobile phone data service inloco, for Goias State, Brazil, between March and June 2020. We calculated Rt values using EpiEstim package in R-plataform for confirmed cases incidence curves. We found a correlation equal to -0.72 between Rt values for confirmed cases and isolation index at a time lag of 8 days. As the Rt values were paired with center of the moving window of 7 days, the delay matches the mean incubation period of the virus. Our findings reinforce that isolation index can be an effective surrogate for modeling and epidemiological analyses and, more importantly, can be an useful metrics for anticipating the need for early interventions, a critical issue in public health. +
++College campuses are highly vulnerable to infectious diseases outbreaks, and there is a mounting need to develop strategies that best mitigate their size and duration, particularly as colleges consider reopening their campuses in the midst of the COVID-19 pandemic. Towards addressing this need, we applied a stochastic transmission model to quantify the impact of university-level responses to past outbreaks on their campuses and used it to determine which control interventions are most effective. The model aims to simultaneously overcome three crucial issues: stochastic variation in small populations, missing or unobserved case data, and changes in disease transmission rates post-intervention. We tested the model and assessed various interventions using data from the 2014 and 2016 mumps outbreaks at Ohio State University and Harvard University, respectively. Our results suggest that universities should design more aggressive diagnostic procedures and stricter isolation policies to decrease infectious disease incidence on campus. Our model can be applied to data from other outbreaks in college campuses and similar small- population settings. +
+Dendritic Cell Vaccine to Prevent COVID-19 - Condition: COVID-19
Intervention: Biological: AV-COVID-19
Sponsors: Indonesia-MoH; Aivita Biomedical, Inc.; PT AIVITA Biomedika Indonesia; National Institute of Health Research and Development, Ministry of Health Republic of Indonesia; RSUP Dr. Kariadi Semarang, indonesia; Faculty of Medicine University of Diponegoro, Indonesia
Recruiting
Study on Safety and Clinical Efficacy of AZVUDINE in COVID-19 Patients (SARS-CoV-2 Infected) - Condition: COVID-19
Interventions: Drug: AZVUDINE; Drug: AZVUDINE placebo
Sponsors: HRH Holdngs Limited; GALZU INSTITUTE OF RESEARCH, TEACHING, SCIENCE AND APPLIED TECHNOLOGY, Brazil; SANTA CASA DE MISERICORDIA DE CAMPOS HOSPITAL (SCMCH), Brazil; UNIVERSIDADE ESTADUAL DO NORTE FLUMINENSE (UENF), Brazil
Not yet recruiting
Inhaled Ivermectin and COVID-19 - Condition: COVID-19
Intervention: Drug: Ivermectin Powder
Sponsor: Mansoura University
Not yet recruiting
AZD1222 Vaccine in Combination With rAd26-S, Recombinant Adenovirus Type 26 Component of Gam-COVID-Vac Vaccine, for the Prevention of COVID-19 - Condition: COVID-19
Interventions: Biological: AZD1222; Biological: rAd26-S
Sponsors: AstraZeneca; R-Pharm
Not yet recruiting
Study in Adults to Determine the Safety and Immunogenicity of AZD1222, a Non-replicating ChAdOx1 Vector Vaccine, Given in Combination With rAd26-S, Recombinant Adenovirus Type 26 Component of Gam-COVID-Vac Vaccine, for the Prevention of COVID-19. - Condition: COVID-19
Interventions: Biological: AZD1222; Biological: rAd26-S
Sponsors: R-Pharm; AstraZeneca
Not yet recruiting
Study to Investigate the Treatment Effect of Colchicine in Patients With COVID-19 - Condition: COVID-19
Interventions: Drug: Colchicine; Drug: Standard COVID-19 care
Sponsors: Ayub Teaching Hospital; Universidad de Murcia
Recruiting
Dendritic Cell Vaccine, AV-COVID-19, to Prevent COVID-19 Infection - Condition: COVID-19
Interventions: Biological: AV-COVID-19; Other: GM-CSF
Sponsors: Aivita Biomedical, Inc.; PT AIVITA Biomedika Indonesia; Indonesia Ministry of Health; National Institute of Health Research and Development, Ministry of Health Republic of Indonesia
Recruiting
Efficacy and Safety of hzVSF-v13 in Patients With COVID-19 Pneumonia - Condition: COVID-19
Interventions: Drug: hzVSF-v13; Drug: Placebo (Normal saline solution)
Sponsor: ImmuneMed, Inc.
Recruiting
Efficacy and Safety of hzVSFv13 in Patients With COVID-19 Pneumonia - Condition: COVID-19
Interventions: Drug: hzVSF-v13; Drug: Placebo (Normal saline solution)
Sponsor: ImmuneMed, Inc.
Not yet recruiting
Efficacy and Safety of hzVSF-v13 in Moderate to Severe Patients With COVID-19 Pneumonia - Condition: COVID-19
Interventions: Drug: hzVSF-v13; Drug: Placebo (Normal saline solution)
Sponsor: ImmuneMed, Inc.
Not yet recruiting
A Controlled Phase 2/3 Study of Adjuvanted Recombinant SARS-CoV-2 Trimeric S-protein Vaccine (SCB-2019) for the Prevention of COVID-19 - Condition: COVID-19
Interventions: Biological: AS03-adjuvanted SCB-2019 vaccine; Biological: Placebo; 0.9% saline
Sponsors: Clover Biopharmaceuticals AUS Pty Ltd; The Coalition for Epidemic Preparedness Innovations; International Vaccine Institute
Not yet recruiting
Evaluation of the Efficacy of High Doses of Methylprednisolone in SARS-CoV2 ( COVID-19) Pneumonia Patients - Condition: Covid19
Intervention: Drug: Methylprednisolone, Placebo
Sponsor: Azienda Unità Sanitaria Locale Reggio Emilia
Not yet recruiting
Risk of Infection of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), COVID-19, in a Massive Musical Show With Transmission Prevention Measures - Condition: COVID-19 (SARS-CoV-2)
Intervention: Behavioral: Participate in a massive musical event
Sponsors: Fundación FLS de Lucha Contra el Sida, las Enfermedades Infecciosas y la Promoción de la Salud y la Ciencia; Dr. Bonaventura Clotet Sala; Dr. Josep Mª LLibre Codina; Dr. Boris Revollo Barriga; Dra. Lidia Ruiz Tabuenca; Dr. Ignacio Blanco Guillermo; Dra. Andrea Alemany Ortiz; Dr. Roger Paredes Deiros
Active, not recruiting
Efficacy and Safety of Ivermectin for Treatment and Prophylaxis of COVID-19 Pandemic - Condition: Covid19
Interventions: Drug: Ivermectin; Drug: Hydroxychloroquine; Behavioral: personal protective Measures
Sponsor: Benha University
Completed
Effect of Dalcetrapib in Patients With Confirmed Mild to Moderate COVID-19 - Condition: Covid19
Interventions: Drug: Dalcetrapib; Other: Placebo
Sponsors: DalCor Pharmaceuticals; The Montreal Health Innovations Coordinating Center (MHICC); Covance
Not yet recruiting
Conus venom fractions inhibit the adhesion of Plasmodium falciparum erythrocyte membrane protein 1 domains to the host vascular receptors - Using high-throughput BioPlex assays, we determined that six fractions from the venom of Conus nux inhibit the adhesion of various recombinant PfEMP-1 protein domains (PF08_0106 CIDR1α3.1, PF11_0521 DBL2β3, and PFL0030c DBL3X and DBL5e) to their corresponding receptors (CD36, ICAM-1, and CSA, respectively). The protein domain-receptor interactions permit P. falciparum-infected erythrocytes (IE) to evade elimination in the spleen by adhering to the microvasculature in various organs including the...
Uncovering Flexible Active Site Conformations of SARS-CoV-2 3CL Proteases through Protease Pharmacophore Clusters and COVID-19 Drug Repurposing - The infectious SARS-CoV-2 causes COVID-19, which is now a global pandemic. Aiming for effective treatments, we focused on the key drug target, the viral 3C-like (3CL) protease. We modeled a big dataset with 42 SARS-CoV-2 3CL protease-ligand complex structures from ∼98.7% similar SARS-CoV 3CL protease with abundant complex structures. The diverse flexible active site conformations identified in the dataset were clustered into six protease pharmacophore clusters (PPCs). For the PPCs with distinct...
In silico analysis of phytochemicals as potential inhibitors of proteases involved in SARS-CoV-2 infection - In silico analysis of six phytochemicals, flabelliferin, marmelosin, piperine, ocimin, curcumin and leucoanthocyanin, along with three drug compounds, nelfinavir, remdesivir and hydroxychloroquine, as positive control against drug targets of one SARS-CoV-2 viral protease, COVID-19 main protease (SARS CoV-2 3CL(pro)/M(pro)), two coronavirus proteases, SARS-CoV main peptidase (SARS CoV M^(pro)), SARS-CoV main proteinase (SARS CoV 3CL^(pro)), and one human cellular transmembrane serine proteinase...
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling - Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has quickly spread worldwide and has affected more than 10 million individuals. A typical feature of COVID-19 is the suppression of type I and III interferon (IFN)-mediated antiviral immunity. However, the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive. Here, we reported that the SARS-CoV-2 membrane (M) protein inhibits the production of type I and III...
The potential mechanism of N-acetylcysteine in treating COVID-19 - N-Acetylcysteine (NAC) has been proposed and used to treat coronavirus disease 2019 (COVID-19). By reviewing the existing pathological studies of COVID-19, it was found that abundant mucus secretion, formation of a hyaline membrane (supportive of acute respiratory distress syndrome), and interstitial fibrous exudation may be important characteristics of COVID-19 and may be pathological targets of drug therapy. In addition, multiple extrapulmonary organ injuries in COVID-19 may be associated with...
The fight against human viruses: how NMR can help - CONCLUSION: Considering the NMR-based work conducted on different viruses, we believe that in the close future much more NMR efforts will be devoted to discover novel anti SARS-CoV-2 agents.
A Review of Treatment of Coronavirus Disease 2019 (COVID-19): Therapeutic Repurposing and Unmet Clinical Needs - For the initial phase of pandemic of coronavirus disease 2019 (COVID-19), repurposing drugs that in vitro inhibit severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) have been attempted with overlooked or overestimated efficacy owing to limited clinical evidence. Most early clinical trials have the defects of study design, small sample size, non-randomized design, or different timings of treatment initiation. However, well-designed studies on asymptomatic or mild, or pediatric cases of...
Remdesivir potently inhibits carboxylesterase-2 through covalent modifications: signifying strong drug-drug interactions - Remdesivir was recently approved to treat COVID-19. While this antiviral agent delivers clinical benefits, several safety concerns in many cases have been raised. This study reports that remdesivir at nanomolar concentrations inhibits carboxylesterase-2 (CES2) through covalent modifications. CES2 is a major drug-metabolizing enzyme. The combination of high potency with irreversible inhibition concludes that cautions must be exercised when remdesivir is used along with drugs hydrolyzed by CES2.
Might proton pump or sodium-hydrogen exchanger inhibitors be of value to ameliorate SARs-CoV-2 pathophysiology? - Discovering therapeutics for COVID-19 is a priority. Besides high-throughput screening of compounds, candidates might be identified based on their known mechanisms of action and current understanding of the SARs-CoV-2 life cycle. Using this approach, proton pump (PPIs) and sodium-hydrogen exchanger inhibitors (NHEIs) emerged, because of their potential to inhibit the release of extracellular vesicles (EVs; exosomes and/or microvesicles) that could promote disease progression, and to directly...
Targeting host cell proteases as a potential treatment strategy to limit the spread of SARS-CoV-2 in the respiratory tract - As the death toll of Coronavirus disease 19 (COVID-19) continues to rise worldwide, it is imperative to explore novel molecular mechanisms for targeting SARS-CoV-2. Rather than looking for drugs that directly interact with key viral proteins inhibiting its replication, an alternative and possibly add-on approach is to dismantle the host cell machinery that enables the virus to infect the host cell and spread from one cell to another. Excellent examples of such machinery are host cell proteases...
Spatial and temporal roles of SARS-CoV PL(pro) -A snapshot - SARS-CoV and SARS-CoV-2 encode four structural and accessory proteins (spike, envelope, membrane and nucleocapsid proteins) and two polyproteins (pp1a and pp1ab). The polyproteins are further cleaved by 3C-like cysteine protease (3CL^(pro) ) and papain-like protease (PL^(pro) ) into 16 nonstructural proteins (nsps). PL^(pro) is released from nsp3 through autocleavage, and then it cleaves the sites between nsp1/2, between nsp2/3 and between nsp3/4 with recognition motif of LXGG, and the sites in...
Heparin Inhibits Cellular Invasion by SARS-CoV-2: Structural Dependence of the Interaction of the Spike S1 Receptor-Binding Domain with Heparin - The dependence of development and homeostasis in animals on the interaction of hundreds of extracellular regulatory proteins with the peri- and extracellular glycosaminoglycan heparan sulfate (HS) is exploited by many microbial pathogens as a means of adherence and invasion. Heparin, a widely used anticoagulant drug, is structurally similar to HS and is a common experimental proxy. Exogenous heparin prevents infection by a range of viruses, including S-associated coronavirus isolate HSR1. Here,...
Therapeutic Approach Against 2019-nCoV by Inhibition of the ACE-2 receptor - The continued spread of the 2019 novel coronavirus (2019-nCoV) has prompted global concern. The formal name given to 2019-nCoV by the World Health Organization is COVID-19, while the International Committee on Taxonomy has named it severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Due to this viral attack, nations around the world have issued lockdown restrictions. Presently, there is no effective way to control the spread of 2019-nCoV, except through social distancing and hygienic...
Fostamatinib Inhibits Neutrophils Extracellular Traps Induced by COVID-19 Patient Plasma: A Potential Therapeutic - Neutrophil extracellular traps (NETs) contribute to immunothrombosis and have been associated with mortality in Coronavirus Disease 2019 (COVID-19). We stimulated donor neutrophils with plasma from patients with COVID-19 and demonstrate that R406 can abrogate the release of NETs. These data provide evidence for how fostamatinib may mitigate neutrophil-associated mechanisms contributing to COVID-19 immunopathogenesis.
Identification of Small Molecule Inhibitors of the Deubiquitinating Activity of the SARS-CoV-2 Papain-Like Protease: in silico Molecular Docking Studies and in vitro Enzymatic Activity Assay - COVID-19 is an ongoing pandemic caused by the SARS-CoV-2 virus with important political, socio-economic, and public health consequences. Inhibiting replication represents an important antiviral approach, and in this context two viral proteases, the SARS-CoV-2 main and papain-like proteases (PL^(pro)), which cleave pp1a and pp1ab polypeptides, are critical. Along with protease activity, the PL^(pro) possesses deubiquitinating activity, which is important in immune regulation. Naphthalene-based...
Covid 19 - Chewing Gum - - link
A traditional Chinese medicine composition for COVID-19 and/or influenza and preparation method thereof - - link
STOCHASTIC MODEL METHOD TO DETERMINE THE PROBABILITY OF TRANSMISSION OF NOVEL COVID-19 - The present invention is directed to a stochastic model method to assess the risk of spreading the disease and determine the probability of transmission of severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). - link
The use of human serum albumin (HSA) and Cannabigerol (CBG) as active ingredients in a composition for use in the treatment of Coronavirus (Covid-19) and its symptoms - - link
The use of human serum albumin (HSA) and Cannabigerol (CBG) as active ingredients in a composition for use in the treatment of Coronavirus (Covid-19) and its symptoms - - link
"AYURVEDIC PROPRIETARY MEDICINE FOR TREATMENT OF SEVERWE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2." - AbstractAyurvedic Proprietary Medicine for treatment of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)In one of the aspect of the present invention it is provided that Polyherbal combinations called Coufex (syrup) is prepared as Ayurvedic Proprietary Medicine , Aqueous Extracts Mixing with Sugar Syrup form the following herbal aqueous extract coriandrum sativum was used for the formulation of protek.Further another Polyherbal combination protek as syrup is prepared by the combining an aqueous extract of the medicinal herbs including Emblica officinalis, Terminalia chebula, Terminalia belerica, Aegle marmelos, Zingiber officinale, Ocimum sanctum, Adatoda zeylanica, Piper lingum, Andrographis panivulata, Coriandrum sativum, Tinospora cordiofolia, cuminum cyminum,piper nigrum was used for the formulation of Coufex. - link
제2형 중증급성호흡기증후군 코로나바이러스 감염 질환의 예방 또는 치료용 조성물 - 본 발명은 화학식 1로 표시되는 화합물, 또는 이의 약학적으로 허용가능한 염; 및 글루카곤 수용체 작용제(glucagon receptor agonist), 위 억제 펩타이드(gastric inhibitory peptide, GIP), 글루카곤-유사 펩타이드 1(glucagon-like peptide 1, GLP-1) 및 글루카곤 수용체/위 억제 펩타이드/글루카곤-유사 펩타이드 1(Glucagon/GIP/GLP-1) 삼중 완전 작용제(glucagon receptors, gastric inhibitory peptide and glucagon-like peptide 1 (Glucagon/GIP/GLP-1) triple full agonist)로 이루어진 군으로부터 선택된 1종 이상;을 포함하는 제2형 중증급성호흡기증후군 코로나바이러스 감염 질환 예방 또는 치료용 약학적 조성물을 제공한다. - link
Haptens, hapten conjugates, compositions thereof and method for their preparation and use - A method for performing a multiplexed diagnostic assay, such as for two or more different targets in a sample, is described. One embodiment comprised contacting the sample with two or more specific binding moieties that bind specifically to two or more different targets. The two or more specific binding moieties are conjugated to different haptens, and at least one of the haptens is an oxazole, a pyrazole, a thiazole, a nitroaryl compound other than dinitrophenyl, a benzofurazan, a triterpene, a urea, a thiourea, a rotenoid, a coumarin, a cyclolignan, a heterobiaryl, an azo aryl, or a benzodiazepine. The sample is contacted with two or more different anti-hapten antibodies that can be detected separately. The two or more different anti-hapten antibodies may be conjugated to different detectable labels. - link
SARS-CoV-2 RBD共轭纳米颗粒疫苗 - 本发明涉及免疫医学领域,具体而言,涉及一种SARS‑CoV‑2 RBD共轭纳米颗粒疫苗。该疫苗包含免疫原性复合物,所述免疫原性复合物包含:a)与SpyCatcher融合表达的载体蛋白自组装得到的纳米颗粒载体;b)与SpyTag融合表达的SARS‑CoV‑2病毒的RBD抗原;所述载体蛋白选自Ferritin、mi3和I53‑50;所述载体蛋白与所述抗原之间通过SpyCatcher‑SpyTag共价连接。 - link
Устройство электронного контроля и дистанционного управления аппарата искусственной вентиляции легких - Полезная модель относится к медицинской технике, а именно к устройствам для воздействия на дыхательную систему пациента смесью различных газов, в частности, к устройствам для проведения искусственной вентиляции легких (ИВЛ). Технический результат предлагаемой полезной модели заключается в решении технической проблемы, состоящей в необходимости расширения арсенала технических средств, предназначенных для электронного контроля и управления ИВЛ, путем реализации возможности дистанционного управления аппаратами ИВЛ в медицинских учреждениях, не оборудованных кабельными вычислительными сетями. Указанный технический результат достигается благодаря тому, что в известное устройство электронного контроля и дистанционного управления аппарата ИВЛ, содержащее центральный микроконтроллер, а также программно-аппаратные средства управления функциями доставки воздушной смеси пациенту и многоуровневой тревожной сигнализации об отклонениях от нормативных условий и технических неполадках в аппарате ИВЛ, введены связанные друг с другом микроконтроллер связи и дистанционного управления и радиомодем, выполненный с возможностью связи с точками доступа радиканальной сети, при этом центральный микроконтроллер устройства выполнен с дополнительными входом/выходом, которые связаны с управляющими выходом/входом микроконтроллера связи и дистанционного управления, а, в зависимости от типа применяемой в медицинском учреждении радиоканальной сети связи и передачи данных, радиомодем может быть выполнен в виде интерфейсного аудиомодуля Bluetooth 4.0 BLE, приемопередающего модуля Wi-Fi либо устройства "малого радиуса действия", работающего по технологии LoRa на нелицензируемых частотах мегагерцового диапазона, например, в диапазоне 868 МГц. 3 з.п. ф-лы, 1 ил. - link
The Plague Year - The mistakes and the struggles behind America’s coronavirus tragedy. - link
The Trümperdämmerung Is a Fitting End to 2020 - The President is careening through his final days in office with reckless disdain—for everything. - link
The Next Big Challenge: Trump-Proofing the Presidency - Trump’s departure will prompt cries of relief in many parts of the country, but there is now vital work to be done. - link
The Deep Origins of Latino Support for Trump - The leaders of the Hispanic Republican movement today haven’t felt such momentum for twenty years. - link
Can Wall Street’s Heaviest Hitter Step Up to the Plate on Climate Change? - More significant than BlackRock executives’s pledges is the firm’s continued inclusion of fossil-fuel companies in its index funds. - link
+What scientists have learned about the Covid-19 variants in the UK, South Africa, and now, the US. +
++A new, seemingly more contagious variety of SARS-CoV-2 — the virus that causes Covid-19 — that has been spreading rapidly in the United Kingdom has now been found in the United States. +
++On the evening of December 29, Colorado Gov. Jared Polis reported that the new strain, known as B.1.1.7 (we’ll call it the UK variant, for simplicity’s sake), was found in a male patient in his 20s with no history of travel, a sign that the virus is spreading locally. +
++“There is a lot we don’t know about this COVID-19 variant, but scientists in the United Kingdom are warning the world that it is significantly more contagious,” Polis said in a statement. +
++The evidence that this new strain spreads more easily between people is not rock solid, but it’s concerning enough to have forced dramatic action, like shutting down travel from the United Kingdom earlier this month. But it wasn’t enough: The variant has now been detected in Canada, Spain, Sweden, France, and Italy, among others. +
++At the moment, it doesn’t appear as though the new UK variant of SARS-CoV-2 is more dangerous in individuals. It doesn’t seem to make people sicker, nor is it more likely to kill them. “I think the key point is that there is no evidence now … that this virus is more pathogenic — creates more problems, more morbidity and mortality — than the previous virus,” Moncef Slaoui, the scientific lead for Operation Warp Speed, said during a December 21 press conference. +
++What it does appear to do, at least based on preliminary evidence, is spread more quickly among people. That alone is a problem: The coronavirus spreads fast enough as it is. Compounding concerns is that the UK variant echoes a similar story in South Africa, where a strain called 501.V2 has become the dominant version among new cases of the virus. Scientists are wondering whether that strain is more transmissible, too. +
++The virus has been continually changing its genetics through the course of the pandemic. That’s what RNA-based viruses like SARS-CoV-2 do — they mutate. Most of the time, the mutations mean nothing. But this time, something is different. +
++“I’ve spent a lot of time this year reminding people that mutations are normal,” molecular epidemiologist Emma Hodcroft, who works on a project called Nextstrain, said. For the entire pandemic, scientists the world over have been feeding Nextstrain sequences of the virus, and Hodcroft and her colleagues have been tracking its genetic changes closely. +
++In the past, mutations haven’t warranted big newspaper headlines. “I’m now finding myself singing a slightly different tune,” Hodcroft said. This time, there does seem to be evidence that the new strain is something worth being vigilant about. “We probably should consider taking some precautionary measures while we’re trying to find out more,” she added. +
++At the same time, Covid-19 is surging around the world, even without these new mutations. Scientists are still trying to figure out what these new variants of the coronavirus actually mean for the pandemic. It’s also unclear where else the UK variant may have already spread, aside from the countries where it has been detected. While it was only reported in the US this week, it could have been in the country for much longer. “The variant could already be in the United States without having been detected,” the US Centers for Disease Control and Prevention reported on December 22. +
++The good news is that we already know how to respond to these new variants: in the same way we’ve been responding to the pandemic overall. The virus still transmits primarily through viral-laden breaths in the air. Mask-wearing, social distancing, and good indoor ventilation are as critical as ever. +
++There’s a lot about this story that’s potentially very alarming or confusing. And the story is not yet complete, as scientists need more evidence to understand whether these new variants pose a new threat. +
++To add some clarity, here’s what researchers have learned so far. Let’s start with the basics. +
++Viral mutations. New strains. Increased transmission. It all sounds like scary science fiction. But to demystify things, and to understand why scientists are a little concerned about this new variant — and why most variants don’t faze them — it’s worth understanding how viruses mutate in the first place. +
++“Oftentimes, I think the word mutation in general conjures up a lot of things in people’s minds, like, you know, Ninja Turtles or X-Men or cancer, like zombie apocalypse-type stuff,” Angela Rasmussen, a virologist with Georgetown’s Center for Global Health Science and Security, said. “A mutation is just a lot more mundane than that.” +
++Viruses mutate because they’re constantly making copies of themselves in enormous numbers. To accomplish this, they have to hijack the hardware of a host cell that they infect. However, this process can be a bit sloppy. +
++Within a human body, a virus can replicate itself millions or billions of times, Hodcroft explains. If you were writing a draft of something millions of times on a computer, extremely quickly, you’d probably make some typos. That’s what’s happening with the viruses. “They make a typo” in their genetic code, she says. One letter of their ribonucleic acid (RNA) chain is replaced with another. +
++Viruses that use RNA as their genetic material, like SARS-CoV-2, are particularly vulnerable to mutations since the RNA molecule itself is more unstable than DNA. The process of copying RNA is also more prone to error. +
++These typos can be very useful for scientists because they happen at a regular rate, and are passed down through generations of the virus as it spreads through a community. Often, scientists can use these subtle changes to trace certain strains’ lineage and their spread through a population. +
++The majority of these typos are inconsequential when it comes to human health. “One typo, or even a few typos, doesn’t usually change how the virus works,” Hodcroft says. Some even harm the virus. “You’re much more likely to break it than to make it better” when it comes to mutations, she says. +
++But in rare instances, some mutations can give a virus an advantage, like allowing it to infect cells more readily or spread among people faster. Those mutant strains can then become dominant within a population. +
++That might be what we’re looking at here with the UK variant; this new strain may have accumulated typos that could make it more easily transmitted between people. +
++So why do scientists think this variant is more transmissible? +
++They don’t have this nailed down yet for sure, but four converging streams of evidence are all pointing in the same direction. “That’s making people feel like maybe there is something here to be worried about,” Hodcroft says. “Each one of these things on their own, I would say is not necessarily convincing.” But all together, they paint a concerning picture. +
++One is that in the areas of the UK where this new variant is spreading, it is accounting for a larger proportion of new cases. “What this implies is that this new variant is spreading better than other variants that are circulating in the same region,” she says. +
++++National testing data shows increased prevalence of the variant in positive cases over time. This is detected incidentally by the commonly used 3-gene PCR test because 69-70del leads to a negative signal. But this does not effect the results of the test. 7/
+— Muge Cevik (@mugecevik) December 21, 2020 +
h/t @The_Soup_Dragon pic.twitter.com/aPpAjjb35W +
+A second is that the increase didn’t co-occur with any overly obvious change in human behavior. “We don’t really have strong evidence that everyone in the southeast [UK where this variant is spreading] has just ripped their masks off and is, you know, totally violating restrictions,” she says. That said, it could be a coincidence. It could be just that people who happen to have contracted this variant have it are spreading it more often via their behavior. +
++After all, “this new variant has emerged at a time of the year when there has traditionally been increased family and social mixing,” according to the European Center for Disease Prevention and Control, which estimated that the transmissibility of the new variant has increased by 70 percent compared to prior versions of the virus. Both Rasmussen and Hodcroft say the 70 percent more transmissible figure is most likely an overestimate. A recent, not yet peer-reviewed study from the London School of Hygiene & Tropical Medicine used a mathematical model to estimate that the new strain may be 56 percent more infectious. +
++Third, there’s some early data about how this variant acts in Covid-19 patients. “There may be slightly higher viral loads in patients with the variants,” Hodcroft says, suggesting the virus has an easier time replicating in the body. (Viral load refers to the amount of virus in the patient. Rasmussen also cautions that viral load data is really sensitive to timing and when the patient was sampled in the course of the illness, so there needs to be more data to confirm this.) +
++Finally, the genetic changes in the UK variant mirror changes in the South African variant, which has also been associated with rising case numbers. That makes a plausible link: that this particular genetic change may be behind the increased transmissibility in both variants. +
++However, this is still short of definitive confirmation that the new variant is more transmissible. +
++According to Slaoui, figuring this out for certain would require laboratory animal testing to see how easily the virus can spread from one organism to another. But this testing can take several weeks. +
++In the face of that uncertainty, many urge caution. +
++Again, there’s still no evidence this new variant causes more severe disease. The evidence only points to increased transmissibility. But a more transmissible virus is still a concern. “In general, the more people get infected, the number of hospitalizations and deaths rise accordingly as a proportion of that number,” Hodcroft says. “So more cases is also bad news.” +
++The UK variant of SARS-CoV-2 actually contains 23 mutations in the genome of the virus. “We don’t really know what they do,” Rasmussen says. Individually, many of these mutations have already been seen in other strains of the virus around the world. But the combination of these changes in a single virus could be making the new variant more likely to spread. +
++However, scientists do think that some mutations may be more important than others, and there are several mechanisms by which mutations could make the virus more infectious. Those include: +
++
+
+
+One of the pathways scientists suspect may be at work stems from the N501Y mutation, where the amino acid asparagine is replaced by the amino acid tyrosine in the 501st position of the viral protein sequence. It’s one of several mutations in the virus’s spike protein in the UK variant, but N501Y is in the part of the spike that actually comes into direct contact with human cells. The same mutation has been found in the South African variant of SARS-CoV-2 that’s also quickly spreading. +
++Since the virus attaching to a host cell is critical to the virus’s reproduction, the virus’s spike protein is especially important — and delicate. +
++“If you were just making random changes in the lab, almost any change you make in that area would result in just a dead virus that can no longer get into the cell,” said Benjamin Neuman, a virologist at Texas A&M University Texarkana. “That fact that this thing is able to spread at all tells you that it’s at least as good as the original version. The fact that it’s spreading faster may indicate that it’s a little bit better at grabbing on to host cells, which is the first step of the entry process.” +
++But this particular N501Y mutation has already been detected in strains that have risen and fallen in other parts of the world over the course of the pandemic. So it may be that the other mutations coupled with N501Y are having some sort of compounding effect. And scientists still need to do more work to determine if this is actually what’s causing the rise of the new SARS-CoV-2 variant in the UK. Finding out the answer could help researchers come up with ways to counter this variety of the coronavirus. +
++Scientists don’t know exactly how the UK variant came to be. But there may be a clue. Hodcroft is struck by the sheer number of mutations in the UK variant — 23 in all — which makes her suspect it’s possible this variant arose in an immunocompromised person. “It’s an above-average number of mutations,” she says. +
++In most people, she explains, the immune system mounts a full-on assault on the virus, eliminating it in a matter of a couple of weeks. “In people that have compromised immune systems, though, there’s a very different dynamic,” she says. “So, for one thing, the virus could be in them for months instead of weeks.” That gives the virus more time to evolve, to accumulate mutations that might make it easier to thwart the immune system. +
++“It’s one scenario,” she says. “We may never know exactly what happened here.” +
++The basic truth: The more this virus spreads, the more chances there are for dangerous new variants to emerge. In any person — or animal, for that matter — the chance for a dangerous new variant to arise is rare. But rare things can happen when there are so many cases: more than 80 million confirmed cases worldwide. +
++Since viruses like SARS-CoV-2 are mutating and since Covid-19 has spread in so many people, it’s theoretically only a matter of time before a certain set of mutations align in a way to give the virus a boost. +
++To stop mutations, quite simply, we need to stop the spread of SARS-CoV-2 in general. For one, that helps us deal with the pandemic overall. But “that’s also conveniently how we get fewer emerging variants,” Rasmussen says. “If the virus isn’t replicating, it can’t mutate. And if it can’t mutate, the new variants can’t emerge.” +
++We fight the new variant as we would any variant of SARS-CoV-2: with masks, with social distancing, with good hand hygiene. “I don’t think people should be panicking,” Hodcroft says. “Lower case numbers, no matter what the variant, are better.” +
+++It’s already been said but if we actually follow protocol and have policies that support those protocols a new variant that is more transmissible would be combatted just as an older variant. So like worry less about mutants and more about masking and distancing and vaccination. +
+— K. Taylor, Ph.D., M.S. (@KYT_ThatsME) December 21, 2020 +
+Scientists have one more tool, though: genetic tracking. At Nextstrain, Hodcroft and her colleagues receive viral genetic sequences from all over the world to try to paint a real-time picture of transmission chains and keep tabs on how the virus is changing. But not every place in the world is providing the same amount of data. +
++The UK does a lot of viral sequencing, for instance. It was able to pick up on the new viral strain quickly because of that. In other locations around the globe, that might not have happened so fast. +
++“In the US, it’s a really spotty picture,” Hodcroft says when it comes to sequencing. “Some states have really invested in sequencing; some states haven’t. So for some states, we probably have a fair idea of what’s going on. In other states, we really don’t have many sequences.” +
++Overall, the CDC reports that the US has only sequenced 51,000 of the more than 17 million cases reported in the country. That’s 0.07 percent. In comparison, the UK aims to sequence 10,000 virus samples per week, and plans to increase that capacity further. (In addition: The UK sequences the genomes faster than the US, according to infectious disease researcher Trevor Bedford.) That lack of viral genetic testing creates a big blind spot in the US. The UK variant could have already arrived here undetected “given the small fraction of US infections that have been sequenced,” the CDC states. +
++More sequencing, overall, would lead to the faster detection of new strains and faster means to contain them if they were deemed problematic. +
++With new mutations, there is a concern that a new strain of SARS-CoV-2 could arise that would be different enough from previous versions such that prior exposures — whether through a vaccine or an infection — won’t offer protection. So, yes, it’s possible that the coronavirus could someday mutate in a way that would elude a vaccine or previous immunity. +
++Right now, though, scientists think this UK variant would still fall under the same umbrella of protection as earlier strains. If someone received a Covid-19 vaccine for an older generation of the virus, they would likely have protection against this one. +
++To explain why, it helps to understand how the immune system deals with viruses. When the human body detects a hostile foreign entity like a virus, it starts to produce antibodies (proteins that attach to the virus or to infected cells). Antibodies can then interfere with how the virus works. They can also flag the virus or virus-infected cells for destruction by other immune cells. +
+ ++The specific places where the antibodies attach to the virus are called epitopes, and most Covid-19 vaccines target epitopes on the virus’s spike protein (which is what the virus uses to attach to human cells and enter them). +
++“The good thing with the vaccine is that it induces an immune response against several epitopes that have been mapped around the spike protein,” Slaoui said. “The chances that one set of mutations would alter all those epitopes, I think, are extremely very low. The expectation, scientifically, is that these kinds of variations are unlikely to escape fully the protective response by the vaccine.” +
++More good news: Scientists at the University of Texas Medical Branch have announced (via a tweet) preliminary evidence that antibodies that neutralize the more common strain of the virus also neutralize a strain with the N501Y mutation (the one that impacts the part of the virus that comes into direct contact with human cells, as mentioned above). That suggests that an immune system primed — by a natural infection, at least — to fight the old variant can also fight one with this specific mutation. +
++++Some good news (and incredibly fast work) on one of the mutations scientists are worried about: N501Y.
+— Kai Kupferschmidt (@kakape) December 22, 2020 +
In these lab experiments serum from recovered #covid19 patients was just as good at neutralizing virus with the mutation as without it. https://t.co/SIxfo2x3qp +
+Texas A&M’s Neuman noted that there’s also evidence right now showing how well vaccines can protect against mutated forms of the virus in clinical trials. Many of the vaccines being administered were engineered to counter the earliest generations of SARS-CoV-2 but are still showing themselves to be highly effective against Covid-19 caused by more recent versions of the virus. +
++“All the tests are being done, all the papers being published, are being done with current strains, which have several mutations relative to [the first iterations of the virus], and it does still seem to be working,” Neuman said. +
++Covid-19 vaccine developers say they are keeping a close eye on these changes and testing to make sure their vaccines are still effective. “In terms of the new variant, Pfizer and BioNTech are monitoring SARS-CoV-2 sequence changes and the companies are working to generate data on how well serum from people immunized with [the Pfizer/BioNTech vaccine] may be able to neutralize the new strain,” said a Pfizer spokesperson via email. +
++And the new Covid-19 vaccines are well equipped to adapt. The two that have received emergency use authorizations from the Food and Drug Administration — the Pfizer/BioNTech vaccine and the Moderna vaccine — both use mRNA as their platform. These vaccines deliver the instructions for making the spike protein of SARS-CoV-2 to human cells. Those human cells then manufacture the component themselves, allowing the immune system to use it to prepare for an infection. One huge advantage of this approach is that the mRNA sequence can be altered quickly; the first such vaccines for Covid-19 were developed within days after the genetic sequence of the virus was posted online. +
++Could manufacturers like Moderna or Pfizer/BioNTech then retool their vaccines to target the new variants without going through the whole tedious clinical trial process again? +
++Possibly, according to Jesse Goodman, a former chief scientist at the FDA and a professor of medicine at Georgetown University. He told Vox that vaccines for new variants of the influenza virus are approved every year without large-scale trials. New versions of a Covid-19 vaccine to accommodate mutations similarly might not need another round of study in tens of thousands of people, but may require some testing to figure out dosing and immune response. With such a new virus and brand new vaccines, the regulations for these situations have not yet been laid out. +
++Short answer: yes. +
++The UK and South African variants are unlikely to be the last to make headlines. Coronavirus is constantly evolving. We should expect it to keep changing slightly. +
++“There will be new variants that emerge,” Rasmussen says. The thing is, with each new significant strain, scientists will have to do careful work to determine whether it’s more dangerous. +
++And there are some mutations we can perhaps even expect — if not in the coming weeks, over the next several years. +
++Recently, virology researchers at the Fred Hutch Cancer Research Center published a preprint (i.e., not yet peer-reviewed) study, looking at how a coronavirus that causes the common cold evolved from the 1980s onward. To accomplish that, they got old blood samples, which included antibodies that cling to this particular virus. They also reconstructed pieces of the cold virus from other eras. Basically, they wanted to see if older blood could still neutralize newer virus. If it couldn’t, that would indicate the virus has evolved over time to evade the immune system. +
++Here’s what the researchers found: “This other human coronavirus does indeed evolve over the course of multiple years to gradually escape human immunity,” Jesse Bloom, a virologist who co-authored the study, says. “So we think this suggests that there’s the potential for SARS-CoV-2 to do the same thing.” But Bloom stresses that this process takes years. It’s enough time to prepare, to monitor, and to potentially tweak vaccine formulations to keep up with the virus’s evolution. +
++It’s not like the virus can evolve into an entirely different beast. “It can mutate to maybe escape antibodies,” Rachel Eguia, the study’s lead author, says. But it can’t change so much that it alters its ability to enter cells. +
++Scientists are also keeping their eyes out for a rapid, major mutation event known as recombination. That’s where an individual is infected with two different strains of the virus at the same time, allowing the virus strains to swap parts. These new viruses could then evade the antibodies that targeted their predecessors. Some researchers think that recombination might be how SARS-CoV-2 originated in the first place. +
++“This is all hypothetical in this particular virus, but it happens in other viruses all the time,” Neuman said. +
++Faced with these looming challenges, reducing the transmission of the coronavirus in general is still the best way to protect the fragile progress made in the Covid-19 pandemic so far. Reducing transmissions is also one of the best ways to make sure powerful tools like vaccines remain potent for as long as possible. The fact that multiple Covid-19 vaccines are coming out is not a cause for complacency, and these new variants of SARS-CoV-2 highlight how important it is to remain vigilant. +
++
++Biden called Covid-19 vaccine distribution the “greatest operational challenge we’ve ever faced.” +
++Striking a grim tone in Wilmington, Delaware, President-elect Joe Biden warned that defeating Covid-19 through widespread vaccination will be the “greatest operational challenge we’ve ever faced as a nation.” +
++Biden says he expects “incredible opportunities for our nation in the years ahead,” declaring that the economy is “poised to come back.” However, to get there, Biden newly pledged to invoke the Defense Production Act (DPA) to accelerate private industry manufacturing of protective equipment and vaccines. The president-elect also promised Congress that he would propose another Covid-19 relief package early next year. +
++As Vox’s Alex Ward has explained, the DPA, which President Donald Trump has used to provide some medical equipment, would allow the federal government to require that companies fulfill its orders before they complete any other commercial orders. +
++In early December, Biden announced a goal of 100 million vaccine shots in his first 100 days, but vaccine distribution woes imperil this benchmark. Biden himself threw cold water on this goal in his remarks when he pointed out that the Trump administration’s goal of vaccinating 20 million Americans by the year’s end is extremely unlikely seeing as the United States has only vaccinated “a few million” people so far. +
++Earlier on Tuesday, Vice President-elect Kamala Harris received her first shot of the Moderna vaccine in Washington, DC, on live TV. Biden received the Pfizer/BioNTech vaccine on December 21, also on live TV as part of his bid to increase confidence in the safety of the inoculation. And Vice President Mike Pence received the Pfizer/BioNTech vaccine a few days earlier. +
++Along with his goal of mass vaccinations, Biden also recently pledged two other priorities: universal mask-wearing and reopening the majority of schools within his first 100 days. He reiterated the importance of both of these objectives in this speech, noting that Congress needed to allocate funds to schools so that they can reopen. +
++++Today, I'm announcing key COVID-19 priorities for the first 100 days of my administration:
+— Joe Biden (@JoeBiden) December 8, 2020 +
- Everyone wears a mask
- 100 million vaccinations
- Reopen the majority of schools
With these steps, we can change the course of the disease and change life in America for the better. +
+“It’s not small what we’re asking of you, but we’re in this together,” Biden said, acknowledging the difficulty of asking people to continue social distancing and mask-wearing for several more months. Though Biden’s speech was focused on charting a clear course to defeating the virus, in his self-described best-case scenario — where a million Americans a day are receiving the vaccine — the country could be well into 2021 before coming close to herd immunity. +
++Biden’s remarks come as Covid-19 cases have surged to their highest levels over the holiday season. On December 28, the day before Biden’s address, the United States recorded over 189,000 new cases and almost 1,900 deaths. +
+ ++Vox’s German Lopez analyzes weekly where each state is on Covid-19 cases, infection rates, and test positivity rates based on data from the New York Times and the Census Bureau. As of his most recent pre-holiday update on December 16, not a single state had “fewer than four daily new coronavirus cases per 100,000 people.” Lopez writes that daily case rates are the “most straightforward way to measure whether any place is experiencing a big coronavirus outbreak.” +
++While experts have not definitively traced a surge due to Thanksgiving and Christmas gatherings, expectations are that cases and deaths will spike in the coming weeks. +
++The coronavirus impacted every aspect of people’s lives in 2020. +
++2020 is a year that changed everything. As December draws to a close, Today, Explained is taking a look back at how the coronavirus pandemic impacted every aspect of our lives in the new series You, Me, and Covid-19. +
++Host Sean Rameswaram, along with the Today, Explained team, will examine how the virus changed our relationships to each other and the places we live, how it upended our livelihoods, and how it redefined what we thought of as “normal.” +
++The series includes a special interview with Dr. Anthony Fauci, as well as reporting from Vox reporters Brian Resnick and Haleema Shah. The first episode is out Monday, December 21, with new episodes dropping through December 29, 2020. +
++Subscribe to Today, Explained wherever you listen to podcasts — including Apple Podcasts, Google Podcasts, and Spotify — to automatically get new episodes when they publish. +
++Episode 1, December 21 | Millennials are moving back in with their parents (again), but they are discovering multigenerational living has its perks. A mother and daughter reflect on how the pandemic has brought them closer together, and a professor examines the American stigma of living with your parents. +
++Episode 2, December 22 | First it was SXSW. Then Coachella. Then just about every concert and live show you can imagine. 2020 devastated the music industry and its fans as live performances were canceled or postponed indefinitely because of the pandemic. Vox’s Haleema Shah reports on how, in the wake of economic challenges and struggles to connect with audiences, musicians like DVSN did what artists do best: get creative and find a way through. +
++
++Episode 3, December 23 | The director of the National Institute of Allergy and Infectious Diseases, Dr. Fauci has spent a lot of time in the spotlight recently. In a livestreamed interview with the unofficial human of the year, he told Sean Rameswaram that 85 percent of the US needs to get the Covid-19 vaccine for “true herd immunity.” Fauci also reflects on how this year has impacted him both professionally and personally. +
++
++Episode 4, December 28 | We can’t stop talking about how the coronavirus has changed humanity, but what about the animals? Some of them are dying. Some of them are thriving. Oh, and they started it. Vox’s Brian Resnick and science writer David Quammen explain. +
++
++Episode 5, December 29 | Reflections on how the pandemic and the year’s ensuing politics, economics, and social upheaval changed people’s ways of looking at the world. Featuring a guy who bought a gun, and then bought another; a woman who never wanted kids and then decided to try; someone who had to shut out family over Black Lives Matter; and an incarcerated individual who felt helpless about preventative measures on the inside, and then the outside. +
++
+Cher Amie, Priceless Ruler and Sweet Fragrance shine - Cher Amie, Priceless Ruler and Sweet Fragrance shone when the horses were exercised here on Wednesday (Dec. 30).Outer sand: 800m: Cher Amie (App) 55.
Syed Mushtaq Ali T20 | Sreesanth in Kerala probables list - Sanju Samson will lead the Kerala team. Sachin Baby is his deputy.
New Zealand seal 101-run victory over Pakistan in first Test after tense final day - Pakistan were dismissed for 271, chasing a victory target of 372, with 4.3 overs remaining in the Test at Bay Oval.
India and Australia not to travel to Sydney before January 4: Hockley - Cricket Australia had decided to retain Sydney as the venue for the third Test
Federer and Nadal re-elected to ATP players’ council - The council, as voted by ATP player members, also saw the re-election of Canadian Felix Auger-Aliassime, Australian John Millman, South African Kevin Anderson, Briton Andy Murray and Brazilian Bruno Soares.
Gold smuggling case | Bail plea of suspended IAS officer M. Sivasankar in gold smuggling case dismissed - Mr. Sivasankar was arrested by the Customs on November 24 in connection with the gold smuggling case
2020, a year of turbulence for Congress - Uncertainty over an effective leadership has had an adverse impact both in terms of electoral outcomes and leadership in States
Free, fair elections are not held in Bengal: Dhankhar - West Bengal Governor Jagdeep Dhankhar on Wednesday alleged that free and fair elections are not held in the state, and it his duty to ensure that peo
Farmers' protest | Accept farmers demand as a new year gift, says Congress - Government should not stand on prestige, it says.
Labour surveys to start in March: Minister - Results of four separate surveys for migrant workers, domestic workers, employment generated by professionals, and the transport sector, by October 2021
UK PM promises 'new chapter' ahead of Brexit vote - Parliament is set to back Boris Johnson's EU trade deal, ahead of the UK's exit from the bloc's rules.
Croatia earthquake: Strong aftershocks hit after quake kills seven - The new 4.8 and 4.7 magnitude tremors cause further damage after seven people died on Tuesday.
Alexei Navalny: Russian officials bring new fraud charges - The opposition leader, still recovering in Germany after his poisoning, says the case is fabricated.
Pierre Cardin: French fashion giant dies aged 98 - He helped revolutionise fashion with his futuristic and stylish designs in the 1950s and 60s.
Belarus protests: The demonstrators speaking out in new and creative ways - Faced by a government crackdown, demonstrations over the disputed August election have been forced to evolve.
Protecting great apes from the unknown effects of COVID-19 - People who study and care for 'em take lockdown-style measures to limit transmission risk. - link
WW1984 lassos solid box office return, record downloads for HBO Max - The film will still lose money, but Warner Bros. is fast-tracking a third film - link
Coverage of “wooden satellites” misses the point - Even if it works, the wood will remain in orbit, too. - link
Computer repairman suing Twitter for defamation, seeks $500 million - Claims Twitter's blocking Hunter Biden laptop story amounts to calling him a hacker. - link
Did Columbus find early Caribs in 15th century Caribbean? Jury is still out - Two studies, published 11 months apart, yield conflicting results. - link
+All the DNA matches and there are no dental records +
+ submitted by /u/tsaar21
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+She’s Tolkien in her sleep. +
+ submitted by /u/Po1sonator
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+Walking into the back room, the boy said to the manager, "Some old bastard outside wants to buy half a head of cabbage." +
++As he finished his sentence, he turned around to find that the man had followed and was standing right behind him, so the boy quickly added, "...and this gentleman kindly offered to buy the other half." +
++The manager approved the deal and the man went on his way. +
++Later, the manager said to the boy, "I was impressed with the way you got yourself out of that situation earlier, we like people who can think on their feet here, where are you from son?" +
++"New Zealand, sir." the boy replied. +
++"Why did you leave New Zealand?" the manager asked. +
++The boy said, "Sir, there's nothing but prostitutes and rugby players there." +
++"Is that right?" replied the manager. "My wife is from New Zealand!" +
++"Really?" replied the boy. "Who did she play for?" +
+ submitted by /u/honolulu_oahu_mod
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+After three years, Andy was recognized as one of the best carpenters in the local area. +
++Often he would be given a weekend pass to do odd jobs for the citizens of the community and he always reported back to prison before Sunday night was over. +
++The warden was thinking of remodeling his kitchen and in fact had done much of the work himself. +
++But he lacked the skills to build a set of kitchen cupboards and a large counter top, which he had promised his wife. +
++So he called Andy into his office and asked him to complete the job for him. +
++But, alas, Andy refused. +
++He told the warden, "Gosh, I'd really like to help you but counter fitting is what got me into prison in the first place." +
+ submitted by /u/honolulu_oahu_mod
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+While in Israel, his stepmother died at the hotel. +
++The people there told him: +
++"Sir, if you want to bury her back in the United States, it's going to cost you $5,000 to bring back her corpse. But since she died at the hotel, we can do the funeral here in Israel for free. +
++The man immediately refused and said he would pay the $5,000 fee to do the funeral back home. +
++When in the USA, his wife came up to him and said: +
++"I really love what you just did for my mom. That proves me that you actually loved my mother and you respected her" +
++Man: Babe, are you crazy?! Those Israelis are the same people who buried Jesus and three days later he came back to life. I'm not about to take that risk with your mother. +
+ submitted by /u/MarkyChoco
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