Diagnóstico estratégico para incremento das vendas em uma célula de televendas

Orientador : Simone Regina DidonetTrabalho de Conclusão de Curso (especialização) - Universidade Federal do Paraná, Setor de Ciências Sociais aplicadas, Curso de Especialização MBA em Inteligência de NegóciosInclui referênciasResumo: O presente trabalho de conclusão de curso teve como propósito realizar um diagnóstico estratégico como forma de avaliar o processo de operações , detectando possíveis falhas existentes e propondo melhorias para o incremento dos resultados das vendas em uma célula de televendas. O método de execução envolveu inicialmente uma revisão bibliográfica para atualização de conceitos, normas e procedimentos da área estudada, tais como implantação de telemarketing, venda por telefone, uso de técnicas de venda e o alinhamento estratégico de marketing e de vendas. A coleta de informações aconteceu por meio de escuta e transcrição das ligações recebidas dos consumidores em potencial, no momento da venda, a aplicação de um checklist de procedimentos, análise do benchmarking de concorrentes e a proposição de novos procedimentos para melhorar o desempenho do atendente de telemarketing. Como resultados constatou-se que todas as atendentes não conheciam técnicas de vendas, somente uma das seis atendentes identificava o televendas, só em apenas 7 das 52 ligações (13%) foi feita a pesquisa das necessidades dos consumidores (sondagem), apenas em 11 ligações (21%) foi feita oferta de produto adicional e, finalmente, não era confirmado o selo de vendas tampouco havia frase de encerramento padrão. Conclusão: houve a necessidade de padronizar as técnicas de vendas e realizar novo treinamento e capacitação das atendentes da célula de televendas estudada a fim de melhorar o atendimento, os índices de desempenho e, consequentemente, gerar lucro para a empresa

The Effects of Intravenous Feeding on Tumor Growth : An Autoradiographic Analysis

Effects of parenteral nutrition on tumor growth were examined by using autoradiographic procedures. Growth rate of the Sato\u27s lung cancer inplanted subcutaneously in the back of the rats of malnourished group was significantly lower (2.68±0.82, p<0.001) than that of intravenously alimented group and orally fed group (5.19± 1.50, 5.72±1.69, respectively). Both mitotic index and labeling index of the tumors from malnourished rats were significantly lower compared with orally fed rats, and this tendency was remarkable in the central region of tumor. Labeling index of parenterally fed group was significantly higher than that of orally fed group. Even in the central region of tumor in this group, labeling intensity was not decreased compared with subcapsular region. Percentage of labeled mitoses of the tumors from the intravenously fed animals was lower than orally fed one\u27s. Based on these findings, it is anticipated that parenteral nutrition may increase or maintain the tumor cells being mobilized in the tumor proliferation phase. This point seems to be useful for the anti-tumor chemotherapy

A series of ENU-induced single-base substitutions in a long-range cis-element altering Sonic hedgehog expression in the developing mouse limb bud

AbstractMammal–fish-conserved-sequence 1 (MFCS1) is a highly conserved sequence that acts as a limb-specific cis-acting regulator of Sonic hedgehog (Shh) expression, residing 1 Mb away from the Shh coding sequence in mouse. Using gene-driven screening of an ENU-mutagenized mouse archive, we obtained mice with three new point mutations in MFCS1: M101116, M101117, and M101192. Phenotype analysis revealed that M101116 mice exhibit preaxial polydactyly and ectopic Shh expression at the anterior margin of the limb buds like a previously identified mutant, M100081. In contrast, M101117 and M101192 show no marked abnormalities in limb morphology. Furthermore, transgenic analysis revealed that the M101116 and M100081 sequences drive ectopic reporter gene expression at the anterior margin of the limb bud, in addition to the normal posterior expression. Such ectopic expression was not observed in the embryos carrying a reporter transgene driven by M101117. These results suggest that M101116 and M100081 affect the negative regulatory activity of MFCS1, which suppresses anterior Shh expression in developing limb buds. Thus, this study shows that gene-driven screening for ENU-induced mutations is an effective approach for exploring the function of conserved, noncoding sequences and potential cis-regulatory elements

Impact of Comorbid Hepatic Steatosis on Treatment of Chronic Hepatitis C in Japanese Patients and the Relationship with Genetic Polymorphism of IL28B, PNPLA3 and LDL Receptor

The impact of hepatic steatosis on interferon therapy for patients with chronic hepatitis C (CHC) has been associated with single-nucleotide polymorphisms (SNP) of IL28B, patatin-like phospholipase domain-containing protein 3 (PNPLA3), and low-density lipoprotein (LDL) receptor. Whether this holds true for Japanese patients, however, remains unresolved. The present study prospectively enrolled 226 Japanese patients with CHC, and investigated the impact of hepatic steatosis and its related SNPs, including rs8099917 of IL28B, rs738409 of PNPLA3, and rs14158 of LDL receptor, on outcomes of peg-interferon and ribavirin therapy. In multivariate logistic regression analysis, significant factors affecting the severity of hepatic steatosis were high body mass index and the minor alleles of IL28B SNP (p＝0.020 and 0.039, respectively). The risk alleles of PNPLA3 SNP also showed weak association (p＝0.059). Severe steatosis and the minor alleles of IL28B SNP were significantly associated with null or partial virological response in patients with HCV genotype 1, as were female gender, and low LDL cholesterol (p＝0.049, and ＜0.001, respectively). The SNP genotype of PNPLA3 and LDL receptor did not have a significant impact on therapeutic outcomes. With respect to the SNP sites examined, the SNP of PNPLA3 has a weak association with severe hepatic steatosis, but not with the outcome of interferon therapy

Cryosurgical Hemorrhoidectomy: Technique and Method

The key to gain successful results with cryosurgical hemorrhoidectomy is based on the prevention of prolapse of the edematous tissue after freezing. To prevent the edema, it is important to pull out the hemorrhoid as much as possible during freezing, to freeze only on the rectal side of the anal verge, to avoid freezing the anal verge, and to freeze the hemorrhoids in two or three separate stages when they are large such as the fourth-degree. The anal discomfort and discharge in these patients are related to prolapse of frozen tissue. Cryosurgery is an effective method of treatment for hemorrhoids if care is taken to use the proper techniques

Ultrasonication-based rapid amplification of α-synuclein aggregates in cerebrospinal fluid

Kakuda K., Ikenaka K., Araki K., et al. Ultrasonication-based rapid amplification of α-synuclein aggregates in cerebrospinal fluid. Scientific Reports 9, 6001 (2019); https://doi.org/10.1038/s41598-019-42399-0.α-Synuclein aggregates, a key hallmark of the pathogenesis of Parkinson’s disease, can be amplified by using their seeding activity, and the evaluation of the seeding activity of cerebrospinal fluid (CSF) is reportedly useful for diagnosis. However, conventional shaking-based assays are time-consuming procedures, and the clinical significance of the diversity of seeding activity among patients remains to be clarified. Previously, we reported a high-throughput ultrasonication-induced amyloid fibrillation assay. Here, we adapted this assay to amplify and detect α-synuclein aggregates from CSF, and investigated the correlation between seeding activity and clinical indicators. We confirmed that this assay could detect α-synuclein aggregates prepared in vitro and also aggregates released from cultured cells. The seeding activity of CSF correlated with the levels of α-synuclein oligomers measured by an enzyme-linked immunosorbent assay. Moreover, the seeding activity of CSF from patients with Parkinson’s disease was higher than that of control patients. Notably, the lag time of patients with Parkinson’s disease was significantly correlated with the MIBG heart-to-mediastinum ratio. These findings showed that our ultrasonication-based assay can rapidly amplify misfolded α-synuclein and can evaluate the seeding activity of CSF

Metformin directly binds the alarmin HMGB1 and inhibits its proinflammatory activity

Metformin is the first-line drug in the treatment of type 2 diabetes. In addition to its hypoglycemic effect, metformin has an anti-inflammatory function, but the precise mechanism promoting this activity remains unclear. High mobility group box 1 (HMGB1) is an alarmin that is released from necrotic cells and induces inflammatory responses by its cytokine-like activity and is, therefore, a target of anti-inflammatory therapies. Here we identified HMGB1 as a novel metformin-binding protein by affinity purification using a biotinylated metformin analogue. Metformin directly bound to the C-terminal acidic tail of HMGB1. Both in vitro and in vivo, metformin inhibited inflammatory responses induced by full-length HMGB1 but not by HMGB1 lacking the acidic tail. In an acetaminophen-induced acute liver injury model in which HMGB1 released from injured cells exacerbates the initial injury, metformin effectively reduced liver injury and had no additional inhibitory effects when the extracellular HMGB1 was blocked by anti-HMGB1-neutralizing antibody. In summary, we report for the first time that metformin suppresses inflammation by inhibiting the extracellular activity of HMGB1. Because HMGB1 plays a major role in inflammation, our results suggest possible new ways to manage HMGB1-induced inflammation

RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS

Repulsive guidance molecule A (RGMa) was originally identified as a neuronal growth cone–collapsing factor. Previous reports have demonstrated the multifunctional roles of RGMa mediated by neogenin1. However, the pathogenic involvement of RGMa in amyotrophic lateral sclerosis (ALS) remains unclear. Here, we demonstrated that RGMa concentration was elevated in the cerebrospinal fluid of both patients with ALS and transgenic mice overexpressing the mutant human superoxide dismutase1 (mSOD1 mice). Treatment with humanized anti-RGMa monoclonal antibody ameliorated the clinical symptoms in mSOD1 mice. Histochemical analysis revealed that the anti-RGMa antibody significantly decreased mutant SOD1 protein accumulation in the motor neurons of mSOD1 mice via inhibition of actin depolymerization. In vitro analysis revealed that the anti-RGMa antibody inhibited the cellular uptake of the mutant SOD1 protein, presumably by reinforcing the neuronal actin barrier. Collectively, these data suggest that RGMa leads to the collapse of the neuronal actin barrier and promotes aberrant protein deposition, resulting in exacerbation of the ALS pathology.Shimizu Mikito, Shiraishi Naoyuki, Tada Satoru, et al. RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS. Science Advances 9, 686 (2023); https://doi.org/10.1126/sciadv.adg3193