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Background: Postoperative nausea and vomiting is the second most common complaint in the postoperative period after pain. The incidence of postoperative nausea and vomiting was 60-80% in middle ear surgeries in the absence of antiemetic prophylaxis. Because of this high incidence of postoperative nausea and vomiting, we aimed to assess the effect of palonosetron-dexamethasone and ondansetron-dexamethasone combination for the prevention of postoperative nausea and vomiting in patients of middle ear surgery. Methods: Sixty-four patients, scheduled for middle ear surgery, were randomized into two groups to receive the palonosetron-dexamethasone and ondansetron-dexamethasone combination intravenously before induction of anesthesia. Anesthesia technique was standardized in all patients. Postoperatively, the incidences and severity of nausea and vomiting, the requirement of rescue antiemetic, side effects and patient satisfaction score were recorded. Results: Demographics were similar in the study groups. The incidence difference of nausea was statistically significant between groups O and P at a time interval of 2-6 hours only (p = 0.026). The incidence and severity of vomiting were not statistically significant between groups O and P during the whole study period. The overall incidence of postoperative nausea and vomiting (0-24 hours postoperatively) was 37.5% in group O and 9.4% in group P (p = 0.016). Absolute risk reduction with palonosetron-dexamethasone was 28%, the relative risk reduction was 75%, and the number-needed-to-treat was 4. The patient’s satisfaction score was higher in group P than group O (p = 0.016). The frequency of rescue medication was more common in group O than in group P patients (p = 0.026). Conclusion: The combination of palonosetron-dexamethasone is superior to ondansetron-dexamethasone for the prevention of postoperative nausea and vomiting after middle ear surgeries. Resumo Justificativa: Náusea e vômito no pós-operatório é a segunda queixa pós-operatória mais frequente após a dor. Sem profilaxia antiemética, a incidência de náusea e vômito no pós-operatório foi de 60−80% após cirurgia do ouvido médio. Dada a alta incidência relatada de náusea e vômito no pós-operatório, nosso objetivo foi avaliar o efeito da combinação de palonosetrona-dexametasona e ondansetrona-dexametasona na prevenção de náusea e vômito no pós-operatório em pacientes submetidos a cirurgia do ouvido médio. Método: Sessenta e quatro pacientes programados para cirurgia de ouvido médio foram aleatoriamente divididos em dois grupos. Um recebeu a combinação de palonosetrona-dexametasona (grupo P) e o outro ondansetrona-dexametasona (grupo O) por via intravenosa antes da indução anestésica. A técnica anestésica foi padronizada em todos os pacientes. No pós-operatório, foram registradas incidência e gravidade das náuseas e vômitos, necessidade de antiemético de resgate, efeitos colaterais e índice de satisfação dos pacientes. Resultados: As características demográficas foram semelhantes nos grupos estudados. A diferença na incidência de náusea foi estatisticamente significante entre os grupos O e P apenas no intervalo de tempo entre 2 e 6 horas (p = 0,026). A incidência e gravidade de vômito não foram estatisticamente significantes entre os grupos O e P durante todo o período do estudo. A incidência geral de náusea e vômito no pós-operatório (0−24 horas de pós-operatório) foi de 37,5% no grupo O e de 9,4% no grupo P (p = 0,016). A combinação palonosetrona-dexametasona associou-se com redução do risco absoluto de 28%, redução do risco relativo de 75%, e o número necessário para tratar foi 4. O escore de satisfação do paciente foi maior no grupo P (p = 0,016). A frequência da medicação de resgate foi mais comum no grupo O (p = 0,026). Conclusão: A combinação de palonosetrona-dexametasona é superior à ondansetrona-dexametasona na prevenção da náusea e vômito no pós-operatório após cirurgia de ouvido médio.

Resumo Justificativa Nausea e vomito no pos‐operatorio e a segunda queixa pos‐operatoria mais frequente apos a dor. Sem profilaxia antiemetica, a incidencia de nausea e vomito no pos‐operatorio foi de 60−80% apos cirurgia do ouvido medio. Dada a alta incidencia relatada de nausea e vomito no pos‐operatorio, nosso objetivo foi avaliar o efeito da combinacao de palonosetrona‐dexametasona e ondansetrona‐dexametasona na prevencao de nausea e vomito no pos‐operatorio em pacientes submetidos a cirurgia do ouvido medio. Metodo Sessenta e quatro pacientes programados para cirurgia de ouvido medio foram aleatoriamente divididos em dois grupos. Um recebeu a combinacao de palonosetrona‐dexametasona (grupo P) e o outro ondansetrona‐dexametasona (grupo O) por via intravenosa antes da inducao anestesica. A tecnica anestesica foi padronizada em todos os pacientes. No pos‐operatorio, foram registradas incidencia e gravidade das nauseas e vomitos, necessidade de antiemetico de resgate, efeitos colaterais e indice de satisfacao dos pacientes. Resultados As caracteristicas demograficas foram semelhantes nos grupos estudados. A diferenca na incidencia de nausea foi estatisticamente significante entre os grupos O e P apenas no intervalo de tempo entre 2 e 6 horas (p = 0,026). A incidencia e gravidade de vomito nao foram estatisticamente significantes entre os grupos O e P durante todo o periodo do estudo. A incidencia geral de nausea e vomito no pos‐operatorio (0−24 horas de pos‐operatorio) foi de 37,5% no grupo O e de 9,4% no grupo P (p = 0,016). A combinacao palonosetrona‐dexametasona associou‐se com reducao do risco absoluto de 28%, reducao do risco relativo de 75%, e o numero necessario para tratar foi 4. O escore de satisfacao do paciente foi maior no grupo P (p = 0,016). A frequencia da medicacao de resgate foi mais comum no grupo O (p = 0,026). Conclusao A combinacao de palonosetrona‐dexametasona e superior a ondansetrona‐dexametasona na prevencao da nausea e vomito no pos‐operatorio apos cirurgia de ouvido medio.

To test the hypothesis that the cerebrospinal fluid (CSF) could provide a spreading route for pathogenesis of amyotrophic lateral sclerosis (ALS), we have examined the effects of intraventricular infusion during 2 weeks of pooled CSF samples from sporadic ALS patients or control CSF samples into transgenic mice expressing human TDP43WT which do not develop pathological phenotypes. Infusion of ALS-CSF, but not of control CSF, triggered motor and cognitive dysfunction, as well as ALS-like pathological changes including TDP43 proteinopathy, neurofilament disorganization and neuroinflammation. In addition, the neuron-specific translational profiles from peptide analyses of immunoprecipitated ribosomes revealed dysregulation of multiple protein networks in response to ALS-CSF altering cytoskeletal organization, vesicle trafficking, mitochondrial function, and cell metabolism. With normal mice, similar ALS-CSF infusion induced mild motor dysfunction but without significant TDP43 pathology in spinal neurons. We conclude that the CSF from sporadic ALS contains factors that can transmit and disseminate disease including TDP43 proteinopathy into appropriate recipient animal model expressing human TDP43. These findings open new research avenues for the discovery of etiogenic factors for sporadic ALS and for the testing of drugs aiming to neutralize the ALS-CSF toxicity.

Investigations into glial biology have contributed substantially in understanding the physiology and pathology of the nervous system. However, intricacies of the neuron-glial and glial-glial interactions in vivo present significant challenges while delineating the individual cell-type contributions, thus making the in vitro techniques exceedingly relevant to study glial biology. However, obtaining optimal yield along with high purity has been challenging for microglial cultures. Here we present a simple protocol to establish enriched astroglial as well as microglial cultures from the neonatal rat spinal cord. This method results in highly enriched astroglial and microglial cultures with maximal yield.

Surface coatings not only serve as the barrier between the substrate and the adverse operating conditions like wear and corrosion, they also have a decided effect on the thermal performance of the underlying base materials. The present work evaluates the effect of ZrO2, Cr2O3 and TiO2 coating on the thermal properties of the substrate material. Plasma spray technique was adopted for depositing the desired powder particles on the steel plate substrate. The steel plate was heated in a controlled experimental set-up from the coated side while the other side was insulated. K-type thermocouples interfaced with temperature data acquisition system were used to record the time-temperature history of the steel plate. The recorded temperature data was used to analyze the effect of surface coatings on conduction heat transfer across the substrate materials. The results clearly indicate a drastic variation in conduction heat transfer in the underlying steel substrate due to coating. Among the three coating powders, ZrO2 exhibits higher resistance for thermal conduction across the material.

Much of the recent work has given insights into the non-canonical roles of heat shock proteins, strongly indicating a potential avenue for exploring the contribution of these proteins towards the normal physiology as well as various pathological conditions apart from hyperthermia-related stress. In this chapter, the role of intracellular as well as extracellular heat shock proteins in regulating various cellular signalling pathways has been discussed, with an emphasis on the biochemical and functional aspects of signalling in the central nervous system throughout various developmental stages. Further, their influence in regulating various pathological pathways including apoptosis and immune responses has been highlighted concerning different acute and chronic neurological disorders. Finally, the possibility of heat shock proteins as potential neuroprotective targets and the clinical relevance of their intracellular as well as extracellular forms has been explored.

Human trafficking is a multi-layered criminal offence that has plagued India and people in the Odisha (State in the Republic of India) are at an alarming risk of trapped in trafficking. Trafficking takes several forms of exploitation, ranging from forced servitude to commercial sexual exploitation in the state. Owing to its high rural population, Odisha has emerged as a source for trafficking in the last decade. This study analyses the secondary data from various online sources and addresses the major causes which encourages the traffickers to trap more people in the racket of trafficking. It also provides a statistical analysis of the crime in the state with major stakeholder analysis followed by a comparative study of the anti-trafficking model used in the north-eastern states of India. It also addresses the vulnerabilities of the victims who are forced into trafficking and the socio-economic factors that contribute to their vulnerabilities. The article outlines several central and state anti-trafficking legal policies which range from countering trafficking to the successful rehabilitation of the victims. Analysing the several sociological aspects which catalyse the process of trafficking in the community, the study aims to paint a clearer picture of the scenario of trafficking in Odisha whilst recognising the vulnerable people based on the rescue operations made by the state government.

Gynecomastia is an endocrine disorder where the male breast tissue swells and growth in the size abnormally. All men and women have breast glands; however they're no longer significant in males, because they have a tendency to be small and undeveloped. Drugs which include steroids motive 10%-25% of cases of gynecomastia. They throw off the hormonal stability which increases in estrogen (the female sex hormone) and/or a lower in testosterone (the male sex hormone), which reasons the breast tissue to develop. Almost all reasons of gynecomastia may be in a single manner or different much like excess production of the hormone estrogen inside the male frame because of different factors. In this article, we overview the reasons and treatment of gynecomastia.

Background Microglial cell-associated neuroinflammation is considered as a potential contributor to the pathophysiology of sporadic amyotrophic lateral sclerosis. However, the specific role of microglia in the disease pathogenesis remains to be elucidated. Methods We studied the activation profiles of the microglial cultures exposed to the cerebrospinal fluid from these patients which recapitulates the neurodegeneration seen in sporadic amyotrophic lateral sclerosis. This was done by investigating the morphological and functional changes including the expression levels of prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), TNF-α, IL-6, IFN-γ, IL-10, inducible nitric oxide synthase (iNOS), arginase, and trophic factors. We also studied the effect of chitotriosidase, the inflammatory protein found upregulated in the cerebrospinal fluid from amyotrophic lateral sclerosis patients, on these cultures. Results We report that the cerebrospinal fluid from amyotrophic lateral sclerosis patients could induce an early and potent response in the form of microglial activation, skewed primarily towards a pro-inflammatory profile. It was seen in the form of upregulation of the pro-inflammatory cytokines and factors including IL-6, TNF-α, iNOS, COX-2, and PGE2. Concomitantly, a downregulation of beneficial trophic factors and anti-inflammatory markers including VEGF, glial cell line-derived neurotrophic factor, and IFN-γ was seen. In addition, chitotriosidase-1 appeared to act specifically via the microglial cells. Conclusion Our findings demonstrate that the cerebrospinal fluid from amyotrophic lateral sclerosis patients holds enough cues to induce microglial inflammatory processes as an early event, which may contribute to the neurodegeneration seen in the sporadic amyotrophic lateral sclerosis. These findings highlight the dynamic role of microglial cells in the pathogenesis of the disease, thus suggesting the need for a multidimensional and temporally guarded therapeutic approach targeting the inflammatory pathways for its treatment. Electronic supplementary material The online version of this article (10.1186/s12974-017-1028-x) contains supplementary material, which is available to authorized users.

Details of the CSF samples taken for the study. Table S1 describes the age and gender of the subjects, duration of disease, nature of disease progression, symptoms, onset pattern and chit-1 levels. Table S2 provides details about the age and gender matched NALS-CSF samples investigated in the present study. (DOC 41 kb)

Background Non-cell autonomous toxicity is one of the potential mechanisms implicated in the etiopathogenesis of amyotrophic lateral sclerosis (ALS). However, the exact role of glial cells in ALS pathology is yet to be fully understood. In a cellular model recapitulating the pathology of sporadic ALS, we have studied the inflammatory response of astroglia following exposure to the cerebrospinal fluid from ALS patients (ALS-CSF). Methods Various inflammatory markers including pro-inflammatory and anti-inflammatory cytokines, COX-2, PGE-2, trophic factors, glutamate, nitric oxide (NO), and reactive oxygen species (ROS) were analyzed in the rat astroglial cultures exposed to ALS-CSF and compared with the disease control or normal controls. We used immunofluorescence, ELISA, and immunoblotting techniques to investigate the protein expression and real-time PCR to study the messenger RNA (mRNA) expression. Glutamate, NO, and ROS were estimated using appropriate biochemical assays. Further, the effect of conditioned medium from the astroglial cultures exposed to ALS-CSF on NSC-34 motor neuronal cell line was detected using the MTT assay. Statistical analysis was carried out using one-way ANOVA followed by Tukey’s post hoc test, or Student’s t test, as applicable. Results Here, we report that the ALS-CSF enhanced the production and release of inflammatory cytokines IL-6 and TNF-α, as well as COX-2 and PGE-2. Concomitantly, anti-inflammatory cytokine IL-10 and the beneficial trophic factors, namely VEGF and GDNF, were down-regulated. We also found impaired regulation of glutamate, NO, and ROS in the astroglial cultures treated with ALS-CSF. The conditioned medium from the ALS-CSF exposed astroglial cultures induced degeneration in NSC-34 cells. Conclusions Our study demonstrates that the astroglial cells contribute to the neuroinflammation-mediated neurodegeneration in the in vitro model of sporadic ALS. Electronic supplementary material The online version of this article (doi:10.1186/s12974-016-0698-0) contains supplementary material, which is available to authorized users.

Vascular endothelial growth factor (VEGF), the well-known angiogenic factor is both neurotrophic and neuroprotective. Altered VEGF signalling is implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), a fatal degenerative disease of motor neurons. We have shown earlier that VEGF protects NSC-34 motor neuronal cell line, when exposed to cerebrospinal fluid (CSF) from sporadic ALS patients (ALS-CSF). Here, we have investigated the consequences of ALS-CSF and VEGF supplementation on the VEGFR2 receptor and endogenous VEGF expression. ALS-CSF caused significant down-regulation of VEGFR2 as well as the Calbindin-D28K levels, but not endogenous VEGF. Exogenous supplementation restored the depletion of VEGFR2 and Calbindin-D28K with a concomitant up-regulation of endogenous VEGF. The up-regulated caspase 3 in the ALS-CSF group was reinstated to basal levels along with a significant reduction in the number of TUNEL-positive cells. Electron photomicrographs of ALS-CSF-exposed cells divulged presence of cytoplasmic vacuoles alongside severe damage to organelles like mitochondria, endoplasmic reticulum, etc. Substantial recovery of most of the damaged organelles was noted in response to VEGF supplementation. While the enhancement in endogenous VEGF levels highlights the autocrine functions, the up-regulation of VEGFR2 receptor emphasizes the paracrine functions of VEGF in modulating its neuroprotective effect against ALS-CSF. The revival of cellular organellar structure, increased calbindin expression and enhanced survival in response to VEGF supplementation consolidates the opinion that VEGF indeed has a therapeutic potential in sporadic ALS.

Background Potential biomarkers to aid diagnosis and therapy need to be identified for Amyotrophic Lateral Sclerosis, a progressive motor neuronal degenerative disorder. The present study was designed to identify the factor(s) which are differentially expressed in the cerebrospinal fluid (CSF) of patients with sporadic amyotrophic lateral sclerosis (SALS; ALS-CSF), and could be associated with the pathogenesis of this disease. Results Quantitative mass spectrometry of ALS-CSF and control-CSF (from orthopaedic surgical patients undergoing spinal anaesthesia) samples showed upregulation of 31 proteins in the ALS-CSF, amongst which a ten-fold increase in the levels of chitotriosidase-1 (CHIT-1) was seen compared to the controls. A seventeen-fold increase in the CHIT-1 levels was detected by ELISA, while a ten-fold elevated enzyme activity was also observed. Both these results confirmed the finding of LC-MS/MS. CHIT-1 was found to be expressed by the Iba-1 immunopositive microglia. Conclusion Elevated CHIT-1 levels in the ALS-CSF suggest a definitive role for the enzyme in the disease pathogenesis. Its synthesis and release from microglia into the CSF may be an aligned event of neurodegeneration. Thus, high levels of CHIT-1 signify enhanced microglial activity which may exacerbate the process of neurodegeneration. In view of the multifold increase observed in ALS-CSF, it can serve as a potential CSF biomarker for the diagnosis of SALS.