Trends in the Epidemiology of Hepatitis B Virus and Hepatitis C Virus Infections at a Tertiary Care Hospital in East Delhi: A 7-Year Retrospective Analysis

Hepatitis B virus (HBV) and Hepatitis C virus (HCV) infections are major global health problems. In 2009, the national Integrated Disease Surveillance Programme (IDSP) began conducting surveillance across all Indian states for epidemic-prone diseases including viral hepatitis. Hence this retrospective study was conducted to identify trend changes in HBV and HCV epidemiology over a period of 7 years at a tertiary care hospital in Delhi. Enzyme-linked immunoassay result entries for Hepatitis B surface antigen (HBsAg) and Hepatitis C antigen and/or anti-HCV antibody were analyzed. The 7-year seroprevalence of HBV and HCV was found to be 3.084% and 5.381% respectively. The seroprevalence of HBsAg was maximum in 2010. Since then the seroprevalence has shown a small decrease. Government of India has included HBV vaccine in the National Universal Immunization Program in the entire country in 2011-12. We consider the reduction in HBsAg seroprevalence to represent a true fall in HBV transmission due to vaccination and/or public consciousness. In the present study, HCV infection appeared to be more common than HBV infection. During last few years, seroprevalence of HCV also increased, which is possibly attributable to an increase in the population of Delhi and a heavy load of the migrant population. These figures may be important for estimation of the disease burden in this region. The study provides a fine reference for future studies, because of the large number of cases investigated over a long period of 7 years and draws attention to the lacunae in ongoing immunization programs

Deletion of Tsc2 in nociceptors reduces target innervation, ion channel expression, and sensitivity to heat

AbstractThe mechanistic target of rapamycin complex 1 (mTORC1) is known to regulate cellular growth pathways, and its genetic activation is sufficient to enhance regenerative axon growth following injury to the central or peripheral nervous systems. However, excess mTORC1 activation may promote innervation defects, and mTORC1 activity mediates injury-induced hypersensitivity, reducing enthusiasm for the pathway as a therapeutic target. While mTORC1 activity is required for full expression of some pain modalities, the effects of pathway activation on nociceptor phenotypes and sensory behaviors are currently unknown. To address this, we genetically activated mTORC1 in mouse peripheral sensory neurons by conditional deletion of its negative regulator Tuberous Sclerosis Complex 2 (Tsc2). Consistent with the well-known role of mTORC1 in regulating cell size, soma size and axon diameter of C-nociceptors were increased in Tsc2-deleted mice. Glabrous skin and spinal cord innervation by C-fiber neurons were also disrupted. Transcriptional profiling of nociceptors enriched by fluorescence-associated cell sorting (FACS) revealed downregulation of multiple classes of ion channels as well as reduced expression of markers for peptidergic nociceptors in Tsc2-deleted mice. In addition to these changes in innervation and gene expression, Tsc2-deleted mice exhibited reduced noxious heat sensitivity and decreased injury-induced cold hypersensitivity, but normal baseline sensitivity to cold and mechanical stimuli. Together, these data show that excess mTORC1 activity in sensory neurons produces changes in gene expression, neuron morphology and sensory behavior.</jats:p

Graphene Oxide-Based Nanohybrids as Pesticide Biosensors: Latest Developments

Graphene is the most significant two-dimensional nanomaterial with sp2 hybridized carbon atoms in a honeycomb arrangement with an extremely high surface area, excellent electrical properties, high mechanical strength, and advantageous optical properties and is relatively easy to functionalize and mass produce. Various inorganic nanoparticles incorporated with graphene, such as gold, silver, and palladium nanoparticles are brought into sharp focus due to their catalytic, optical, electronic, and quantized charging/discharging properties. Graphene oxide-based nanohybrids are particularly well suited for biosensing applications and catalysis. Consequently, this area of research has grown to represent one of the largest classes within the scope of materials science and is rapidly becoming a key area in nanoscience and nanotechnology offering significant potential in the development of advanced materials in multiple and diverse applications. Here in this present chapter, synthesis, characterization of graphene oxide, and their nanohybrids are discussed thoroughly with their application in the field of pesticide biosensors. This chapter will help in a further understanding of graphene-based nanohybrids as a biosensing platform for their future applications in a sustainable environment

Gpr126/Adgrg6 has Schwann cell autonomous and nonautonomous functions in peripheral nerve injury and repair

Schwann cells (SCs) are essential for proper peripheral nerve development and repair, although the mechanisms regulating these processes are incompletely understood. We previously showed that the adhesion G protein-coupled receptor Gpr126/Adgrg6 is essential for SC development and myelination. Interestingly, the expression of Gpr126 is maintained in adult SCs, suggestive of a function in the mature nerve. We therefore investigated the role of Gpr126 in nerve repair by studying an inducible SC-specific Gpr126 knock-out mouse model. Here, we show that remyelination is severely delayed after nerve-crush injury. Moreover, we also observe noncell-autonomous defects in macrophage recruitment and axon regeneration in injured nerves following loss of Gpr126 in SCs. This work demonstrates that Gpr126 has critical SC-autonomous and SC-nonautonomous functions in remyelination and peripheral nerve repair. SIGNIFICANCE STATEMENT Lack of robust remyelination represents one of the major barriers to recovery of neurological functions in disease or following injury in many disorders of the nervous system. Here we show that the adhesion class G protein-coupled receptor (GPCR) Gpr126/Adgrg6 is required for remyelination, macrophage recruitment, and axon regeneration following nerve injury. At least 30% of all approved drugs target GPCRs; thus, Gpr126 represents an attractive potential target to stimulate repair in myelin disease or following nerve injury

Serotonin 1A receptor-mediated signaling through ERK and PKCα is essential for normal synaptogenesis in neonatal mouse hippocampus

Aberrant expression of the presynaptic serotonin 1A receptor (5-HT1A-R) because of a polymorphism in the 5-HT1A-R gene is associated with severe depression in human, whereas its absence up to postnatal day 21 (P21) in the forebrain of mice results in heightened anxiety in adulthood. These observations collectively indicate that the 5-HT1A-R has a crucial role in brain development. To understand the mechanistic underpinnings of this phenomenon, we used organotypic slice cultures of hippocampi from C57BL6 mice (C57) at P15, which coincides with the peak of neonatal synaptogenesis. Stimulation of the hippocampal 5-HT1A-R caused a dramatic increase in PSD95 expression and dendritic spine and synapse formation through sequential activation of the mitogen-activated protein kinase isozymes Erk1/2 and protein kinase C (PKC). Intrahippocampal infusion of 5-HT1A-R agonists and signaling inhibitors at P15 revealed that the same pathway through PKCα augments PSD95 expression and synaptogenesis in vivo in 24 h in both C57 as well as Swiss Webster mice. Furthermore, intrahippocampal infusion of the antidepressant fluoxetine, a serotonin reuptake inhibitor, also augmented PSD95 expression and synaptogenesis through the same pathway. This increased synaptogenesis was observed even 5 days after treatment. Finally, compared with the wild type, the 5-HT1A-R(−/−) mice harbor significantly less synapses in the hippocampus, but infusion of the PKC-stimulator and Alzheimer drug bryostatin into the 5-HT1A-R(−/−) mice to bypass the non-existent 5-HT1A-R boosted PSD95 expression and synaptogenesis. The elucidated signaling cascade explains how 5-HT1A-R regulates hippocampal sculpting and function, which may determine the affective phenotype of an adult

Co-Infection of HSV in Gonococcal Urethritis Patients

Co-infection with two different pathogens may alter the classical clinical course that manifests infection as single pathogen. In STIs, such co-infection may trigger the reactivation of a latent infection, and syndromic approach may not be insufficient to free the host of the entire gamut of infectivity agents. Present study analyzed appropriate samples for Neisseria gonorrheae and HSV from 200 patients presented to STI clinic. Gonorrhea was detected in 4% and HSV in 5% of patients. 25% of gonorrhea patients had HSV-2 co-infection with an overall 4.5% yield of subclinical HSV cases which would have been missed leading to inappropriate treatment, risk of recurrence and transmission to contacts. Awareness regarding encounter with multiple infections is necessary for effective management

Gpr126 functions in schwann cells to control differentiation and myelination via G-protein activation

The myelin sheath surrounding axons ensures that nerve impulses travel quickly and efficiently, allowing for the proper function of the vertebrate nervous system. We previously showed that the adhesion G-protein-coupled receptor (aGPCR) Gpr126 is essential for peripheral nervous system myelination, although the molecular mechanisms by which Gpr126 functions were incompletely understood. aGPCRs are a significantly understudied protein class, and it was unknown whether Gpr126 couples to G-proteins. Here, we analyze Dhh(Cre);Gpr126(fl/fl) conditional mutants, and show that Gpr126 functions in Schwann cells (SCs) for radial sorting of axons and myelination. Furthermore, we demonstrate that elevation of cAMP levels or protein kinase A activation suppresses myelin defects in Gpr126 mouse mutants and that cAMP levels are reduced in conditional Gpr126 mutant peripheral nerve. Finally, we show that GPR126 directly increases cAMP by coupling to heterotrimeric G-proteins. Together, these data support a model in which Gpr126 functions in SCs for proper development and myelination and provide evidence that these functions are mediated via G-protein-signaling pathways