Publications by authors named "Elina Shrestha"

Gram negative bacilli that are carbapenem resistant have emerged and are spreading worldwide. Infections caused by carbapenem resistant isolates posses a significant threat due to their high morbidity and mortality rates. Carbapenemases production by multi-drug resistant pathogens severely restricts treatment choices for illnesses caused by bacteria that are resistant to both carbapenems and majority of β-lactam antibiotics.

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The coronavirus disease 2019 (COVID-19) pandemic has brought attention to the significant risk of thrombotic complications in infected individuals. We present a rare case of a 64-year-old male with COVID-19 who developed bilateral deep vein thrombosis (DVT), pulmonary embolism (PE), and thrombus in the thoracic and abdominal aorta. The patient exhibited common symptoms of COVID-19 and required intensive care unit admission due to respiratory failure.

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Malaria is a parasitic disease that is spread by the bite of an Anopheles mosquito carrying the infection. Microscopic analysis of thick and thin Giemsa-stained smears is the gold standard for diagnosis. If the initial test is negative, but clinical suspicion is high, further smears are required.

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Stauffer's syndrome is a paraneoplastic syndrome that has historically been associated with renal cell carcinoma. It is defined by the anicteric elevation of liver enzymes in the absence of liver metastasis, and the reversibility of clinical and biochemical changes upon treatment of the primary pathology. Here, we discuss the rare presentation of Stauffer's syndrome in a patient with advanced metastatic prostate cancer.

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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is increasingly recognized as an inherited and autosomal dominant arteriopathy of the cerebral vasculature, which is commonly misdiagnosed due to its different modes of presentation. It is characterized by variable manifestations of ischemic episodes, migraine with aura, cognitive deficits, and psychiatric disturbances. CADASIL is caused by a genetic mutation in the  gene, which is present on chromosome 19.

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Todd's paresis or phenomenon (TP) is a focal weakness in a part of the body after a seizure. Seizure is an abrupt change in behavior caused by the cerebral cortex's electrical hyper-synchronization of neuronal networks. After the seizure, there is usually a transition period from the ictal state to the pre-seizure baseline level of awareness and function, referred to as the postictal period.

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Many users of recreational drugs use cocaine and opioids together, often called "speedballing." Hearing loss is a rarely reported adverse effect following recreational drug abuse. Only one case has been reported in history with hearing loss caused by speedballing.

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Pneumomediastinum and subcutaneous emphysema have been reported in COVID-19 around the world except for Nepal. We report a case of a 44-year-old male infected with COVID-19 who developed pneumomediastinum and subcutaneous emphysema during his eighth day of intubation at the hospital. He was managed with remdesivir, antibiotics, mechanical ventilation, steroid, and heparin following which he recovered well.

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BACKGROUND It is unknown if the efficacy of the coronavirus disease-19 (COVID-19) vaccine is affected by the co-administration of other vaccines. The Centers for Disease Control and Prevention (CDC) has shifted their recommendations recently, allowing for the co-administration of the currently available COVID-19 vaccines with other vaccines. This is based on the experience with non-COVID-19 vaccines, where the immunogenicity and adverse event profiles were generally similar when vaccines are administered simultaneously or alone.

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Atherosclerosis and obesity share pathological features including inflammation mediated by innate and adaptive immune cells. LXRα plays a central role in the transcription of inflammatory and metabolic genes. LXRα is modulated by phosphorylation at serine 196 (LXRα pS196), however, the consequences of LXRα pS196 in hematopoietic cell precursors in atherosclerosis and obesity have not been investigated.

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Posttranslational modifications, such as phosphorylation, are a powerful means by which the activity and function of nuclear receptors such as LXRα can be altered. However, despite the established importance of nuclear receptors in maintaining metabolic homeostasis, our understanding of how phosphorylation affects metabolic diseases is limited. The physiological consequences of LXRα phosphorylation have, until recently, been studied only in vitro or nonspecifically in animal models by pharmacologically or genetically altering the enzymes enhancing or inhibiting these modifications.

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Non-alcoholic fatty liver disease (NAFLD) is a very common indication for liver transplantation. How fat-rich diets promote progression from fatty liver to more damaging inflammatory and fibrotic stages is poorly understood. Here, we show that disrupting phosphorylation at Ser196 (S196A) in the liver X receptor alpha (LXRα, NR1H3) retards NAFLD progression in mice on a high-fat-high-cholesterol diet.

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Liver X receptors (LXR) are oxysterol-activated nuclear receptors that play a central role in reverse cholesterol transport through up-regulation of ATP-binding cassette transporters (ABCA1 and ABCG1) that mediate cellular cholesterol efflux. Mouse models of atherosclerosis exhibit reduced atherosclerosis and enhanced regression of established plaques upon LXR activation. However, the coregulatory factors that affect LXR-dependent gene activation in macrophages remain to be elucidated.

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High cholesterol and diabetes are major risk factors for atherosclerosis. Regression of atherosclerosis is mediated in part by the Liver X Receptor (LXR) through the induction of genes involved in cholesterol transport and efflux. In the context of diabetes, regression of atherosclerosis is impaired.

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The success of Mycobacterium tuberculosis (Mtb) as a pathogen rests upon its ability to grow intracellularly in macrophages. Interferon-gamma (IFN-γ) is critical in host defense against Mtb and stimulates macrophage clearance of Mtb through an autophagy pathway. Here we show that the host protein ubiquilin 1 (UBQLN1) promotes IFN-γ-mediated autophagic clearance of Mtb.

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In mouse models of atherosclerosis, normalization of hyperlipidemia promotes macrophage emigration and regression of atherosclerotic plaques in part by liver X receptor (LXR)-mediated induction of the chemokine receptor CCR7. Here we report that LXRα serine 198 (S198) phosphorylation modulates CCR7 expression. Low levels of S198 phosphorylation are observed in plaque macrophages in the regression environment where high levels of CCR7 expression are observed.

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Protein-based vaccines offer safety and cost advantages but require adjuvants to induce immunity. Here we examined the adjuvant capacity of glucopyranosyl lipid A (GLA), a new synthetic non-toxic analogue of lipopolysaccharide. In mice, in comparison with non-formulated LPS and monophosphoryl lipid A, formulated GLA induced higher antibody titers and generated Type 1 T-cell responses to HIV gag-p24 protein in spleen and lymph nodes, which was dependent on TLR4 expression.

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Dendritic cells (DCs), critical antigen-presenting cells for immune control, normally derive from bone marrow precursors distinct from monocytes. It is not yet established if the large reservoir of monocytes can develop into cells with critical features of DCs in vivo. We now show that fully differentiated monocyte-derived DCs (Mo-DCs) develop in mice and DC-SIGN/CD209a marks the cells.

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Protein vaccines for T-cell immunity are not being prioritized because of poor immunogenicity. To overcome this hurdle, proteins are being targeted to maturing dendritic cells (DCs) within monoclonal antibodies (mAbs) to DC receptors. To extend the concept to humans, we immunized human immunoglobulin-expressing mice with human DEC205 (hDEC205) extracellular domain.

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Mouse DC-SIGN CD209a is a type II transmembrane protein, one of a family of C-type lectin genes syntenic and homologous to human DC-SIGN. Current anti-mouse DC-SIGN monoclonal antibodies (MAbs) are unable to react with DC-SIGN in acetone-fixed cells, limiting the chance to visualize DC-SIGN in tissue sections. We first produced rabbit polyclonal PAb-DSCYT14 against a 14-aa peptide in the cytosolic domain of mouse DC-SIGN, and it specifically detected DC-SIGN and not the related lectins, SIGN-R1 and SIGN-R3 expressed in transfected CHO cells.

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