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BACKGROUND: The diffusion of information and communication technologies (ICTs) in type 1 diabetes (T1D) management has generated a debate on the ways in which ICTs can support the patient-provider relationship. Several studies have focused on text messages. Most of the literature proposes quantitative analysis of the impact of text messaging on the clinical conditions of patients and/or their satisfaction with the technology, while the qualitative studies have focused mainly on patients' perceptions about strengths and weaknesses of this technology. OBJECTIVE: In contrast to past studies, we adopted a qualitative approach for the in-depth examination of patient-health care professionals' interactions in text messaging. METHODS: The study focused on the use of the Trento Cartella Clinica del Cittadino Diabetes System (TreC-DS), a digital platform with a built-in messaging system, in two diabetes centers, integrating message analysis with interviews with patients and health care professionals. Each center focused on a specific patient profile: the first one focused on pregnant women with T1D and the second one focused on adult patients with poorly controlled diabetes. RESULTS: The main results of the study were as follows: (1) Health care professionals and patients perceived the messaging system as useful for sharing information (ie, pregnant women for prescriptions and adults with poorly controlled diabetes for advice); (2) The content and communication styles of the two centers differed: in the case of pregnant women, interactions via text messaging were markedly prescriptive, while in the case of adult patients with poorly controlled diabetes, they were conceived as open dialogues; and (3) Conversations were initiated mainly by professionals; in the cases considered, it was mainly the diabetes center that decided whether a messaging conversation was needed. CONCLUSIONS: The results show how the features of interactions of text messaging changed based on the patient profiles in two different centers. In addition, in both diabetes centers that were involved, the system seems to have laid a foundation for a closer relationship between patients and health care professionals.
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Over the last 15 years, we have seen a huge expansion of the development of drugs directed against biomolecular targets within breast cancer cells. The over-expression of certain receptors (ER, PgR, HER-2, VEGF-R), as well as alteration of several intracellular signal transduction pathways (the PI3K-AKT-mTOR pathway, MEK-MAPK pathway, loss of PTEN, etc ...) has a great impact on the likelihood of recurrence and progression of the disease, influencing the natural history of breast cancer. The recent biomolecular classification of breast cancer (Luminal A / B, HER2- driven, Basal Like) allowed finally to identify specific treatments against molecular target to associate or not to traditional chemotherapy, and to use in relation to the prognosis of the disease. In the following paragraphs, we will set out the major targeted drug that have received indications in breast cancer, both in the localized and in advanced disease, referring to the specific target (hormonal receptors, HER2, VEGF, m-TOR, PARP etc ...).
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Antineoplásicos/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/metabolismo , Terapia de Alvo Molecular , Proteínas de Neoplasias/antagonistas & inibidores , Neoplasias da Mama/patologia , Feminino , Humanos , Medicina de Precisão , PrognósticoRESUMO
Improvements in the care of kidney transplant recipients and advances in immunosuppressive therapy have reduced the incidence of graft rejection. As a result, other types of kidney transplant complications, such as surgical, urologic, parenchymal, and vascular complications, have become more common. Although vascular complications account for only 5-10 % of all post-transplant complications, they are a frequent cause of graft loss. Ultrasonography, both in B-mode and with Doppler ultrasound, is a fundamental tool in the differential diagnosis of renal allograft dysfunction. Doppler ultrasound is highly specific in cases of transplanted renal artery stenosis, pseudoaneurysms, arteriovenous fistulas, and thrombosis with complete or partial artery or vein occlusion. A single measurements of color Doppler indexes display high diagnostic accuracy and in particular cases are more useful during the post-transplantation follow-up period. More recent techniques, such as contrast-enhanced ultrasound, undoubtedly increase the accuracy of ultrasonography in the diagnosis of vascular complications involving the transplanted kidney.
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Kidney transplantation is the treatment of choice for end-stage renal disease, given the better quality of life of transplanted patients when compared to patients on maintenance dialysis. In spite of surgical improvements and new immunosuppressive regimens, part of the transplanted grafts still develop chronic dysfunction. Ultrasonography, both in B-mode and with Doppler ultrasound, is an important diagnostic tool in case of clinical conditions which might impair kidney function. Even though ultrasonography is considered fundamental in the diagnosis of vascular and surgical complications of the transplanted kidney, its role is not fully understood in case of parenchymal complications of the graft. The specificity of Doppler ultrasound is low both in case of acute complications such as acute tubular necrosis, drug toxicity and acute rejection, and in case of chronic conditions such as chronic allograft nephropathy. Single determinations of resistance indices present low diagnostic accuracy, which is higher in case of successive measurements performed during the follow-up of the graft. Modern techniques including tissue pulsatility index, maximal fractional area and contrast-enhanced ultrasound increase the diagnostic power of ultrasonography in case of parenchymal complications of the transplanted kidney.
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Nefropatias/diagnóstico por imagem , Nefropatias/etiologia , Transplante de Rim/efeitos adversos , Transplante de Rim/diagnóstico por imagem , Ultrassonografia Doppler em Cores , Doença Aguda , Doença Crônica , Rejeição de Enxerto/diagnóstico por imagem , Humanos , Necrose Tubular Aguda/diagnóstico por imagem , Necrose Tubular Aguda/etiologiaRESUMO
Kaposi's sarcoma is a highly vascularized mesenchymal neoplasm arising with multiple lesions of the skin. Endogenous cannabinoids have been shown to inhibit proliferation of a wide spectrum of tumor cells. We studied the effects of cannabinoids on human Kaposi's sarcoma cell proliferation in vitro. To do so, we first investigated the presence of the cannabinoid receptors CB(1) and CB(2) mRNAs in the human Kaposi's sarcoma cell line KS-IMM by RT-PCR and, subsequently, the effects of the mixed CB(1)/CB(2) agonist WIN-55,212-2 (WIN) on cell proliferation in vitro. WIN showed antimitogenic effects on Kaposi's sarcoma cells. Western blot analysis of Kaposi's sarcoma lysates suggested that WIN treatment induced activation of both caspase-3 and -6, as well as increased phosphorylation of the stress kinase p38 and JNK, along with transient phosphorylation of ERK(1/2). To better characterize the involvement of each single CB receptor in cannabinoid-induced cell death, we incubated Kaposi's sarcoma cells with different selective cannabinoid receptor agonists, respectively ACEA (CB(1)) and JWH-133 (CB(2)). None of the agonists was able to induce KS-IMM cell apoptosis. Moreover, we co-incubated Kaposi's sarcoma cells with WIN-55,212-2 and either the CB(1) receptor antagonist AM251, the CB(2) receptor antagonist AM630, or a combination of both substances. The CB(2) receptor antagonist AM630 was able to significantly increase survival of Kaposi's sarcoma cells treated with WIN. In view of the antiproliferative effects of cannabinoids on KS-IMM cells, one could envision the cannabinoid system as a potential target for pharmacological treatment of Kaposi's sarcoma.
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Benzoxazinas/farmacologia , Morfolinas/farmacologia , Naftalenos/farmacologia , Receptor CB1 de Canabinoide/agonistas , Receptor CB2 de Canabinoide/agonistas , Sarcoma de Kaposi/patologia , Animais , Antineoplásicos/farmacologia , Canabinoides/farmacologia , Caspases/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Feminino , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Gravidez , Receptor CB1 de Canabinoide/antagonistas & inibidores , Receptor CB1 de Canabinoide/genética , Receptor CB2 de Canabinoide/antagonistas & inibidores , Receptor CB2 de Canabinoide/genética , Sarcoma de Kaposi/genética , Sarcoma de Kaposi/metabolismo , Especificidade por SubstratoRESUMO
Epidemiological and experimental studies have provided evidence that human papillomavirus (HPV) infection is a main player in the development of uterine cervical neoplasms. Migration of cancer cells from the origin tissue to surrounding or distant organs is essential for tumor progression. Many studies of tumor invasion and metastases have focused on the degradation of the extracellular matrix where matrix metalloproteinases (MMPs) play a central role. Two of these enzymes, MMP-2 and MMP-9, have been correlated with the processes of tumor cell invasion and metastasis in human cancers, including uterine neoplasms. It has been shown that the up-regulation of MMPs is associated with progression of cervical uterine neoplasms. This review describes the current understanding of MMP-2 and MMP-9 expression and activity in pre-cancer and cancer lesions of cervical uterine, which may open new strategies for diagnostic and therapeutic interventions.
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Carcinoma/diagnóstico , Carcinoma/patologia , Colo do Útero/metabolismo , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Neoplasias do Colo do Útero/diagnóstico , Neoplasias do Colo do Útero/patologia , Proliferação de Células , Progressão da Doença , Feminino , Humanos , Inflamação , Modelos Biológicos , Invasividade Neoplásica , Fases de Leitura Aberta , Prognóstico , Regulação para CimaRESUMO
Renal interstitial fibrosis is a major complication of cisplatin treatment, due to the increased accumulation of extracellular matrix (ECM) proteins whose remodeling is important for the development of normal tissues; indeed, its malfunction might play a role in the etiology of various diseases. Biopharmacological evaluations suggest that L-carnitine can prevent cardiac metabolic damage caused by doxorubicin, as well as can inhibit cisplatin-induced injury in the kidney and in the small intestine, without any interference with the drug's antitumoral properties. Since the glomerular basement membrane and the mesangial matrix constitute the ECM of the renal glomerulus, we examined the localization and expression of MMP-9 and TIMP-3 in normal rat kidney and the changes in their expression over a period of time by treatment with cisplatin, with and without L-carnitine. MMP-9 immunoreaction in cisplatin-treated rat kidney tissue suggests an involution of the basal membrane, an alteration of ECM components and low glomerular function, due to the increased thickness of the mesangium. Our results suggest that the matrix remodeling by MMP-9 and TIMP-3, in the later stages, can play an important role in the development of glomerular sclerosis and interstitial fibrosis after cisplatin treatment. It can also be postulated that L-carnitine protects from cisplatin injury, by modulating the relationship between MMP-9 and TIMP-3.
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Carnitina/farmacologia , Cisplatino/toxicidade , Nefropatias/prevenção & controle , Complexo Vitamínico B/farmacologia , Animais , Antineoplásicos/toxicidade , Mesângio Glomerular/enzimologia , Imuno-Histoquímica , Rim/efeitos dos fármacos , Rim/patologia , Nefropatias/induzido quimicamente , Nefropatias/patologia , Masculino , Metaloproteinase 9 da Matriz/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Inibidor Tecidual de Metaloproteinase-3/efeitos dos fármacosRESUMO
Breast cancer is the most common malignancy among women. It is frequently treated with chemotherapy and hormone therapy. More recently, however, 'targeted therapy' has emerged as an important approach to cancer therapy. Targeted therapy works by interfering with a specific molecular target, though inter-individual variability in drug response often causes treatment failure. Anticancer agents inhibit breast cancer progression by several different mechanisms. The Ras/Raf/MEK/ERK signal transduction pathway regulates cell cycle progression and apoptosis in diverse cell types. Alterations in this pathway are often associated with human cancer, including breast cancer. Understanding breast cancer biology is useful for the identification of appropriate anticancer drugs. This review describes the effect of gene alterations on breast cancer development. In addition, it shows how each anticancer drug used to treat breast cancer may block aberrant cell proliferation. Finally, the mechanisms of resistance to therapy are also discussed.
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Endometrial carcinoma (EC) and colorectal cancer (CRC) are closely linked in a well-documented, predominantly inherited cancer syndrome known as hereditary non-polyposis colorectal cancer (HNPCC). Epidemiological studies report that women with EC have a 1.5- to 3-fold increased risk of developing CRC. However, this elevated risk could be the consequence of genetic confounding. In order to plan a proper CRC prevention program, we sought to verify and quantify this risk, first estimating it in 697 women with EC who received treatment and follow-up in one health care district between 1986 and 2000. The standardised incidence ratio (SIR), which compares observed with expected cases of CRC in the general population, was calculated. Multiple logistic regression analysis was used to estimate the odds ratio and 95% confidence interval of a dependent variable, second primary CRC, as a function of clinical and pathological features. Multiple primary tumours were observed in 6.7% of the patients, with CRC being the second most frequently occurring type of cancer. The estimated overall risk for CRC was slightly higher than that observed in the general population, but was nonetheless not statistically significant. Multivariate analysis revealed a family history of CRC to be a risk factor for developing the disease as a second primary cancer. A BMI ≤25 and the pathological spectrum of EC were clinical and pathological features associated with CRC development, but were without statistical significance. MSH2 and MLH1 mutational screening confirmed genetic involvement in most of the CRCs observed in the cohort. Overall, the data show that women with EC have a CRC risk similar to that of the general population, and should therefore be screened on the basis of risk factors for CRC.
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AIM: With the rationale that amyloid beta (AB) is toxic to the retina, we here assessed the role of TRAIL, a mediator of AB toxicity and related signal transduction, in a rat model. We also attempted to demonstrate possible protective effects of sigma 1 receptor agonists in these processes. METHODS: AB and the sigma 1 receptor agonist Pre-084 were injected intravitreally in the anaesthetised rat. In additional experiments, the sigma 1 receptor antagonist BD1047 was administered to assess specificity of the effects of Pre-084. Western blot analysis was performed on retinas to evaluate the expression of TRAIL and TRAIL receptors in the retina, as well as of Bax and phosphorylated JNK following the different treatments. Lactic dehydrogenase (LDH) levels were measured as a cytotoxicity marker. RESULTS: All TRAIL receptors were expressed in rat retinas. Intravitreal injection of AB in rat eyes induced overexpression of TRAIL and the proapoptotic protein Bax, as well as phosphorylation of JNK. All these effects of AB were abrogated by pretreatment with the sigma(1) receptor agonist Pre-084. CONCLUSIONS: It is likely that TRAIL is a mediator of AB effects on the retina. In light of their specific inhibitory effects upon TRAIL expression, it is plausible to hypothesise that sigma(1) receptor agonists could represent potential pharmacological tools for restraining AB related retinal damage.