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1.
Management Dynamics ; 21(1):1-6, 2021.
Article in English | ProQuest Central | ID: covidwho-2285623

ABSTRACT

In August 2021, nearly 200 million people globally were believed to have had Covid-19 since the first case was reported in China in late 2019. The reported global death toll topped 4.26 million even as the World Health Organisation (WHO) expressed grave concern over the coronavirus, its mutations and the ever growing list of symptoms. The Covid-19 pandemic has rightly been regarded as the worst disaster befalling the global social and economic landscape in the last almost 100 years. Whilst previous natural or manmade disasters viz. earthquakes, floods, epidemics and World War I/II were largely confined to a continent or two, the magnitude of coronavirus contagion is still unfolding for mankind. The pandemic, which quickly spread far and wide due to an interconnected world, faster travel modes and voluminous international trade, has impacted every facet of life and society, business being no exception. During these troubled times, the conventional mass media of newspapers, periodicals and news channels were at the forefront of informing the public about the outbreak and the aftermath of the pandemic, which is believed to have originated from a discreet lab in Wuhan, China. The media has been tirelessly disseminating news about Covid-19, lockdown, restrictions on trade and movement, the development of vaccines, probe into its genesis, collaboration between nations, vaccination process et al. The media has dextrously been highlighting the radical shift in the pre-Covid norms of society as also business, trade and industry. The crystallisation of new normal taking shape in these domains has lucidly been narrated and presented by the mass media for the general public.Ironically, while the media resiliently dispensed a yeoman's service to the community by informing and educating on the crisis, it also underwent an irreversible metamorphosis itself! Beyond the noble purpose of serving as a vital pillar of democracy, a news organisation is intrinsically a business or a non-profit entity, as the case may be according to its constitution, for sustenance and growth. It also follows the standard principles that power the biggest of the global corporations to the more modest trading or industrial units locally. With the entire value and supply chains of the industrial and commercial world getting disrupted, thus bringing about a sudden shift in the conventional processes and the work hierarchies, the media could no longer afford the luxury of a status quo.

3.
biorxiv; 2022.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2022.04.07.487556

ABSTRACT

Pathogenic infections cause thymic atrophy, perturb thymic-T cell development and alter immunological response. Previous studies reported dysregulated T cell function and lymphopenia in coronavirus disease-19 (COVID-19) patients. However, immune-pathological changes, in the thymus, post severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection have not been elucidated. Here, we report SARS-CoV-2 infects thymocytes, depletes CD4+CD8+ (double positive DP) T cell population associated with an increased apoptosis of thymocytes, which leads to severe thymic atrophy in K18-hACE2-Tg mice. CD44+CD25- T cells were found to be enriched in infected thymus, indicating an early arrest in the T cell developmental pathway. Further, Interferon gamma was crucial for thymic atrophy, as anti-IFN{gamma}; antibody neutralization rescued the loss of thymic involution. Therapeutic use of remdesivir (prototype anti-viral drug) was also able to rescue thymic atrophy. While Omicron variant of SARS-CoV2 caused marginal thymic atrophy, delta variant of SARS-CoV-2 exhibited most profound thymic atrophy characterized by severely depleted DP T cells. Recently characterized broadly SARS-CoV-2 neutralizing monoclonal antibody P4A2 was able to rescue thymic atrophy and restore thymic developmental pathway of T cells. Together, we provide the first report of SARS-CoV-2 associated thymic atrophy resulting from impaired T cell developmental pathway and also explains dysregulated T cell function in COVID-19.


Subject(s)
Lymphoma, T-Cell , Coronavirus Infections , Severe Acute Respiratory Syndrome , Chronobiology Disorders , COVID-19 , Atrophy , Lymphopenia
4.
Archives of Disease in Childhood ; 106(Suppl 1):A42-A43, 2021.
Article in English | ProQuest Central | ID: covidwho-1443380

ABSTRACT

BackgroundFacio-brachial dystonic seizures (FBDS), which affects the ipsilateral face and arm, is a disorder in the watershed between epilepsy and movement disorders, and a transitional presentation of limbic encephalitis.It is rarely described in children.ObjectivesWe present an unusual case of presumed autoimmune encephalitis - with the only positive investigations being Anti-TPO antibodies and COVID-19 antibodies.Methods17-month-old male presenting with the following different, progressive event types:1) Clusters of focal motor seizures described as head and eyes deviating to the left and occasionally associated with stiffening of the upper limbs/entire body2) Focal dyscognitive seizures described as staring episodes associated with increased aggression then unresponsiveness with eyes deviating upwards to the right3) Clusters of facio-brachial dystonic seizures described as right eyelid and facial twitching with posturing upward movement of ipsilateral armThese events were associated with developmental regression mainly involving speech/language and behaviour change.This was preceded by upper respiratory tract symptoms 1-week prior.ResultsThis was associated with resistance to conventional AED’s (carbamazepine, phenytoin, clonazepam) but response to immunosuppression (steroids and IVIG).Initial EEG showed diffuse background slowing and independent right and left temporal sharp waves. This improved post immunomodulation.MRI brain was normal. CSF studies were normal (CSF acellular, protein 31 mg/dL)Autoimmune encephalitis panel by IIFT (NMDA, AMPA1, AMPA2, GLUR1/GLUR2, CASPR2, DPPX, LGI1, GABARB1/B2) negativeAnti-TPO Ab 72.1 (elevated), anti-thyroglobulin Ab and thyroglobulin negative (post methylprednsiolone pulse x2)COVID-19 IgM Ab 1.416, IgG 0.229;SARS-CoV-2 Nasopharygeal swab negativeHe was treated as presumed autoimmune/limbic encephalitis initially with steroids, followed by IVIG. Seizure frequency improved significantly 1-week post IVIG, however mild improvement in the developmental regression and altered behaviour. He continues on a tapering prednisolone dose over the next 4 months.ConclusionsThis case highlights the association of facio-brachial dystonic seizures and limbic encephalitis in a child.We have considered whether this can be attributed to Hashimoto’s encephalopathy as a post-inflammatory neurological manifestation of SARS-CoV-2.

5.
Indian Journal of Chest Diseases and Allied Sciences ; 62(4):179-191, 2020.
Article in English | CAB Abstracts | ID: covidwho-1235587

ABSTRACT

This report is the first expert panel report on the management of post-COVID-19 patients from India. The report contains high risk groups, post-COVID-19 patient management at primary care level, general principles of medical management of post-COVID-19 in primary care settings, management of post-COVID-19 symptoms in primary care settings, recommendations for inclusion and exclusion into the Pulmonary Rehabilitation Programme, post-COVID-19 patient management at tertiary care level, post-COVID-19 complete assessment and management, and respiratory disease-specific conditions requiring expert opinion and further research.

6.
ssrn; 2021.
Preprint in English | PREPRINT-SSRN | ID: ppzbmed-10.2139.ssrn.3802514

ABSTRACT

Background & Aims: A procoagulant state with pulmonary micro-thrombosis has been described in COVID-19, which contributes to pathophysiology of respiratory failure along with diffuse alveolar damage. Cytokine storm and systemic inflammation in COVID-19 generates endogenous heparinoids from the endothelium which leads to secondary organ failures. We prospectively studied the dynamic association of the coagulation abnormalities with respiratory failure and mortality in patients with COVID-19.Methods: We did a prospective observational study in adults aged between 18-80 years with COVID 19 pneumonia requiring intensive care (ICU) admissions in a tertiary care hospital in North India. All patients received standard medical therapy based on best available evidence. Patients were categorized based on the oxygen support therapy into low flow, high flow and invasive ventilation groups. In patients considered to be at risk of thromboembolic or bleeding phenomena, paired coagulation tests were performed at days 1 and 3 with, Sonoclot ® (glass beaded and heparinase-treated). All patients were consecutively followed for inflammatory markers, ventilator requirements and survival. Activated clotting time (ACT) <110s and peak amplitude > 75 units were used as the cut-off for hypercoagulable state. The heparin like effect (HLE) was considered by a correction of ≥ 40 s in hACT (heparinized treated ACT). The trial is registered with ClinicalTrials.gov (NCT04668404).Results: A total of 2324 patients with COVID-19 were screened from August 2020 to November 2020. Two hundred and fifteen patients requiring ICU admission were assessed and 74 patients with a median age of 54(42-67) years were enrolled. A procoagulant profile was seen in 45.5%, 32.4% and 20.7% in low-flow, high-flow, and invasive ventilation. Paired Sonoclot ® assays in 33 patients demonstrated HLE in 17 (51.5%) and 20 (62.5%) at days 1 and 3 respectively. In multivariate analysis, the presence of HLE (HR 1.02; CI 1.08-1.6; p < 0.05), C-reactive protein (HR 1.2; CI 1.1-1.4; p=0.014)] and platelet function (HR 0.9; CI 0.7-1.1 p < 0.05) predicted mortality. The presence of HLE at day 1 predicted the need for invasive ventilation (HR 1.4; CI 1.01-1.5; p <0.05). An ACT > 131 s, clot rate < 27.5 units/min and CRP > 96.7 mg/l at admission predicted mortality.Conclusions: HLE contributes to hypocoagulable effect, need for invasive ventilation and mortality in patients with COVID-19.Trial Registration: The trial is registered with ClinicalTrials.gov (NCT04668404).Funding Statement: NoneDeclaration of Interests: NoneEthics Approval Statement: Ethical clearance was obtained from the Institutional Review Board (PGI/IEC/2020/000997 dated 24 August 2020)


Subject(s)
Thromboembolism , Depressive Disorder , Pneumonia , Blood Coagulation Disorders, Inherited , COVID-19 , Inflammation , Respiratory Insufficiency
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