Correlation of Point of Care Ultrasound (POCUS) Guided Pupillary Assessment Parameter with Glasgow Coma Scale in Patients with Altered Mental Status- A Cross Sectional Study.

Earlier studies have proved deteriorating Glasgow Coma Scale (GCS) as a marker of raised intracranial pressure (ICP). Low GCS is associated with abnormal pupillary parameters. Currently, many studies have proved that ultrasound provides a feasible and objective assessment of pupillary light reflex.

Full Outline of Unresponsiveness Score versus Glasgow Coma Scale in Predicting Clinical Outcomes in Altered Mental Status.

Introduction: Full outline of unresponsiveness (FOUR) score has advantages over Glasgow Coma Scale (GCS); as it can be used in intubated patients and provides greater neurological details. It has been studied mainly in the trauma and neuroscience setting. Our primary objective was to compare the FOUR versus GCS score as predictors of mortality at 30 days and poor functional outcome at 3 months among nontrauma patients in the emergency department (ED).

Feasibility of USG-Guided Objective Initial Assessment of Pupillary Size and Pupillary Reflexes Versus Clinical Examination in Patients With Altered Mental Status: A Cross-Sectional Study.

Background: Pupillary assessment is an important part of the neurological assessment which provides vital information in critically ill patients. However, clinical pupillary assessment is subjective. The ultrasound-guided pupillary examination is objective.

Fluorescence microscopy-based sensitive method to quantify dopaminergic neurodegeneration in a model of Parkinson's disease.

Death of dopaminergic (DAergic) neurons in the of the human brain is the characteristic pathological feature of Parkinson's disease (PD). On exposure to neurotoxicants, too exhibits mobility defects and diminished levels of brain dopamine. In the fly model of sporadic PD, our laboratory has demonstrated that there is no loss of DAergic neuronal number, however, a significant reduction in fluorescence intensity (FI) of secondary antibodies that target the primary antibody-anti-tyrosine hydroxylase (TH).

Adult health and transition stage-specific rotenone-mediated model of Parkinson's disease: Impact on late-onset neurodegenerative disease models.

Parkinson's disease (PD) affects almost 1% of the population worldwide over the age of 50 years. Exposure to environmental toxins like paraquat and rotenone is a risk factor for sporadic PD which constitutes 95% of total cases. Herbicide rotenone has been shown to cause Parkinsonian symptoms in multiple animal models.

MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways.

Mutations in BLM in Bloom Syndrome patients predispose them to multiple types of cancers. Here we report that BLM is recruited in a biphasic manner to annotated DSBs. BLM recruitment is dependent on the presence of NBS1, MRE11 and ATM.

Mitochondrial functions of RECQL4 are required for the prevention of aerobic glycolysis-dependent cell invasion.

Germline mutations in RECQL4 helicase are associated with Rothmund-Thomson syndrome, which is characterized by a predisposition to cancer. RECQL4 localizes to the mitochondria, where it acts as an accessory factor during mitochondrial DNA replication. To understand the specific mitochondrial functions of RECQL4, we created isogenic cell lines, in which the mitochondrial localization of the helicase was either retained or abolished.

Nonsyndromic Synchronous Multifocal Central Giant Cell Granulomas of the Maxillofacial Region: Report of a Case.

Central giant cell granuloma (CGCG) is a benign proliferation of fibroblasts and multinucleated giant cells that almost exclusively occurs in the jaws. It commonly occurs in young adults showing a female predilection in the anterior mandible. Multifocal CGCGs in maxillofacial region are very rare and suggestive of systemic diseases such as hyperparathyroidism, an inherited syndrome such as Noonan-like multiple giant cell lesion syndrome or other disorders.

Enhancement of c-Myc degradation by BLM helicase leads to delayed tumor initiation.

The spectrum of tumors that arise owing to the overexpression of c-Myc and loss of BLM is very similar. Hence, it was hypothesized that the presence of BLM negatively regulates c-Myc functions. By using multiple isogenic cell lines, we observed that the decrease of endogenous c-Myc levels that occurs in the presence of BLM is reversed when the cells are treated with proteasome inhibitors, indicating that BLM enhances c-Myc turnover.

Ubiquitin-dependent recruitment of the Bloom syndrome helicase upon replication stress is required to suppress homologous recombination.

Limiting the levels of homologous recombination (HR) that occur at sites of DNA damage is a major role of BLM helicase. However, very little is known about the mechanisms dictating its relocalization to these sites. Here, we demonstrate that the ubiquitin/SUMO-dependent DNA damage response (UbS-DDR), controlled by the E3 ligases RNF8/RNF168, triggers BLM recruitment to sites of replication fork stalling via ubiquitylation in the N-terminal region of BLM and subsequent BLM binding to the ubiquitin-interacting motifs of RAP80.

Chk1-dependent constitutive phosphorylation of BLM helicase at serine 646 decreases after DNA damage.

BLM helicase, the protein mutated in Bloom syndrome, is involved in signal transduction cascades after DNA damage. BLM is phosphorylated on multiple residues by different kinases either after stress induction or during mitosis. Here, we have provided evidence that both Chk1 and Chk2 phosphorylated the NH(2)-terminal 660 amino acids of BLM.

BLM helicase stimulates the ATPase and chromatin-remodeling activities of RAD54.

Mutation of BLM helicase results in the autosomal recessive disorder Bloom syndrome (BS). Patients with BS exhibit hyper-recombination and are prone to almost all forms of cancer. BLM can exhibit its anti-recombinogenic function either by dissolution of double Holliday junctions or by disruption of RAD51 nucleofilaments.