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Viral load responses to HAART is an independent predictor of a new AIDS event in late stage HIV infected patients: prospective cohort study
Powel Kazanjian, Wei Wei, Morton Brown, Tejal Gandhi, Kamal Amin
Journal of Translational Medicine , 2005, DOI: 10.1186/1479-5876-3-40
Abstract: A cohort of patients with pre-therapy CD4 < 200/mm3 who had CD4 and VL measurements for > one year after receiving HAART at a university clinic were prospectively enrolled. Cox proportional multivariate regression model was used to determine whether CD4 and VL responses were independently associated with new AE.The patient (N = 214) mean baseline CD4 = 92/mm3, VL = 219,000 c/mL and follow-up duration 42.3 months (range 13–72 months). A new AE occurred in 56 patients; CD4 cell count response to HAART that remained < 200/mm3 throughout the study period was a significant risk factor for new AE (RR = 9.7–12.5; p < 0.001). Similarly, VL responses that remained > 5,000 c/mL during this period was also a significant risk factor (RR = 6.7–12.8; p = 0.001) that was independent of CD4 response adjusted for <> 200/mm3.Maintaining adequate long-term virologic responses to HAART provides a clinical benefit independent of CD4 responses.Despite an overall decline in AIDS-associated illnesses since the introduction of HAART [1,2], some patients receiving combination antiretrovirals remain at risk for developing new AIDS events (AE) [3,4]. Those who have a pre-treatment CD4 cell count < 200/mm3 [5-9] or have insufficient CD4 cell responses to HAART [6] are at risk for progressing to AIDS or dying while receiving therapy. Persistent viremia [10], independent of insufficient CD4 cell count responses [13-16], has also been shown to be a predictor of disease progression. These studies, however, have differed in regards to the VL that they identify as being predictive of disease progression-- > 1,000 c/mL [10], > 7,000 c/mL [13], or > 20,000 c/mL [11]. Furthermore, although these studies have linked short virologic markers in response to HAART with a successful clinical outcome [11-14], the importance of sustaining immunologic and virologic responses to HAART over a more prolonged time period remains to be addressed.It is important to evaluate whether maintaining adequate responses to lo
Mycobacterium avium complex immune reconstitution inflammatory syndrome: Long term outcomes
James Riddell, Daniel R Kaul, Petros C Karakousis, Joel E Gallant, Jennifer Mitty, Powel H Kazanjian
Journal of Translational Medicine , 2007, DOI: 10.1186/1479-5876-5-50
Abstract: Cases of MAC IRIS were retrospectively identified at four HIV clinics (Michigan, Maryland, Rhode Island, and Indiana) from 1996–2004. Patients were included if they were initially diagnosed with AIDS and found to have evidence of focal MAC infection documented by tissue culture or PCR after initiating HAART, and at least 6 months of follow up.Among the 20 patients included, the mean age was 40 years, mean CD4 cell count was 24/mm3 at pretreatment baseline and 100/mm3 at time of MAC IRIS diagnosis. Sites of disease included lymph nodes (15 patients [8 peripheral, 8 abdominal and 1 peripheral and abdominal]), gastrointestinal tract (7) and liver (3). Sixteen patients (80%) responded to treatment and were disease free after a mean of 17.4 months of therapy for MAC IRIS; IRIS therapy was withdrawn in 6 without relapse. Four patients (non-responder group) had persistent or relapsing disease despite 27 months of ongoing MAC IRIS treatment. At the time of resolution or last follow-up, the mean CD4 cell count and viral load was 143/mm3 and 7,000 c/mL for responders, and 65/mm3 and 17,000 c/mL for non-responders, respectively. Most patients with peripheral adenopathy were responders (7/8; 88%); many with abdominal adenopathy (4/8; 50%) were nonresponders.The majority of patients with MAC IRIS eventually responded to treatment. Our sample size was not adequate to perform statistical analysis, but there was a tendency towards adequate CD4 response to HAART and peripheral rather than intraabdominal adenopathy among responders.Focal manifestations of Mycobacterium avium complex (MAC) may occur in AIDS patients with severe immune suppression after starting HAART [1,2]. This is thought to be the result of specific cell mediated immune response to MAC antigens associated with highly active antiretroviral therapy (HAART). The syndrome, referred to as the immune reconstitution inflammatory syndrome (IRIS), most often occurs within 3 months of initiating HAART, but may also occur year
Actividades biológicas del extracto acuoso de la esponja Aplysina lacunosa (Porifera: Aplysinidae)
Kazanjian,Arda; Fari?as,Milagros;
Revista de Biología Tropical , 2006,
Abstract: biological activity of an aqueons extract of the sponge aplysina lacunosa (porifera: aplysinidae). the aqueous extract and protein precipitate of aplysina lacunosa (pallas, 1776) were studied to assess their hemagglutinating, hemolysing, antibacterial, and antifungal activities. specimens of the marine sponge were collected in el morro de tigüitigüe, santa fe, sucre state, venezuela. the active protein was separated by molecular exclusion chromatography and its molar mass estimated by sds-page electrophoresis. the sponge a. lacunosa has a protein with a molar mass of about 43 000 daltons which is capable of agglutinating human erythrocytes of the blood groups a, b, and o in a strong and unspecific mode. the assayed samples did not evidence any hemolysing activity. as for the antibacterial assay, only the aqueous extract was able to inhibit the growth of enterococcus faecalis, bacillus cereus, escherichia coli, and salmonella enteritidis, with inhibition halos of 24, 20, 24, and 22 mm, respectively. none of the samples exhibited antifungal activity. the chemical analysis of the aqueous extract revealed the presence of several secondary metabolites. it is presumed that its hemagglutinating activity is mediated by agglutinative proteins. the antibacterial activity could be attributed to the presence of saponins, alkaloids, tannins, and polyphenols, which are highly antimicrobial compounds. poriferans are a rich source of bioactive compounds that can be used in the development of new drugs potentially useful in medicine. rev. biol. trop. 54 (suppl. 3): 189-200. epub 2007 jan. 15.
Actividades biológicas del extracto acuoso de la esponja Aplysina lacunosa (Porifera: Aplysinidae)
Arda Kazanjian,Milagros Fari?as
Revista de Biología Tropical , 2006,
Abstract: Evaluamos el extracto acuoso y precipitado de proteínas de Aplysina lacunosa, en relación con su actividad hemaglutinante, hemolizante, antibacteriana y antimicótica. Los ejemplares de la esponja marina fueron recolectados en el Morro de Tigüitigüe, Santa Fe, Estado Sucre, Venezuela. La proteína activa fue separada por cromatografía de exclusión molecular; y su masa molar fue estimada por electroforesis SDS-PAGE. La esponja A. lacunosa posee una proteína con masa molar aproximada de 4.000 Daltons capaz de aglutinar fuertemente y de manera inespecífica los eritrocitos humanos de los grupos sanguíneos A, B y O. No se observó actividad hemolizante por parte de las muestras ensayadas. únicamente el extracto acuoso fue capaz de inhibir el crecimiento de Enterococcus faecalis, Bacillus cereus, Escherichia coli y Salmonella enteritidis con halos de inhibición de 24, 20, 24, 22 mm, respectivamente; ninguna de las muestras exhibió actividad antifúngica. El análisis químico del extracto acuoso reveló la presencia de diversos metabolitos secundarios. Se presume que la actividad hemaglutinante se deba a la presencia de proteínas aglutinantes. La actividad antibacteriana podría atribuirse a la presencia de saponinas, alcaloides, taninos y polifenoles, compuestos altamente antimicrobianos. Los poríferos constituyen una fuente rica de compuestos bioactivos que pueden ser utilizados para el desarrollo de nuevos fármacos. Biological activity of an aqueons extract of the sponge Aplysina lacunosa (Porifera: Aplysinidae). The aqueous extract and protein precipitate of Aplysina lacunosa (Pallas, 1776) were studied to assess their hemagglutinating, hemolysing, antibacterial, and antifungal activities. Specimens of the marine sponge were collected in El Morro de Tigüitigüe, Santa Fe, Sucre state, Venezuela. The active protein was separated by molecular exclusion chromatography and its molar mass estimated by SDS-PAGE electrophoresis. The sponge A. lacunosa has a protein with a molar mass of about 43 000 Daltons which is capable of agglutinating human erythrocytes of the blood groups A, B, and O in a strong and unspecific mode. The assayed samples did not evidence any hemolysing activity. As for the antibacterial assay, only the aqueous extract was able to inhibit the growth of Enterococcus faecalis, Bacillus cereus, Escherichia coli, and Salmonella enteritidis, with inhibition halos of 24, 20, 24, and 22 mm, respectively. None of the samples exhibited antifungal activity. The chemical analysis of the aqueous extract revealed the presence of several secondary metabolites. It i
The origins of estrogen receptor alpha-positive and estrogen receptor alpha-negative human breast cancer
D Craig Allred, Powel Brown, Daniel Medina
Breast Cancer Research , 2004, DOI: 10.1186/bcr938
Abstract: Invasive breast cancers (IBCs) can be divided into two subtypes based on whether or not the tumor cells express estrogen receptor alpha (ER) in their nuclei. The ER status is important because, when circulating estrogen binds ER, it stimulates cell division and tumor growth [1]. Many strategies have been developed over the years to inhibit this estrogen-induced mitogenic pathway. Numerous previous studies have shown that these so-called hormonal therapies significantly prolong life, although they rarely cure patients with ER-positive IBCs, where the mitogenic pathway is intact, but that they are ineffective in ER-negative disease, where the pathway is inactive [1]. More recent studies suggest that hormonal therapies can also delay or prevent the development of IBC in high-risk women, primarily by reducing ER-positive disease, although longer follow-up may show a benefit in ER-negative disease as well [2].Despite their usefulness, current hormonal therapies are still imperfect and improving them will depend on gaining a better understanding of the cellular and molecular mechanisms responsible for determining whether ER is expressed and how it is regulated during the evolution of IBCs. There are probably several mechanisms and, although none are understood at a fundamental level, several clinical, pathological, and experimental observations provide food for thought for future research in this area [3].All IBCs appear to evolve over long periods of time from premalignant breast lesions, which in turn appear to evolve from normal epithelial cells lining terminal duct lobular units (TDLUs) [4]. Understanding ER and growth in IBCs may benefit from, or even depend on, a similar understanding of their precursors, especially normal cells. Since estrogen, presumably mediated through ER, appears necessary to stimulate mitosis and populate the TDLU with normal epithelial cells, one might postulate that all epithelial cells or their ancestors must express ER at some time during
Advances in breast cancer treatment and prevention: preclinical studies on aromatase inhibitors and new selective estrogen receptor modulators (SERMs)
Rachel Schiff, Gary C Chamness, Powel H Brown
Breast Cancer Research , 2003, DOI: 10.1186/bcr626
Abstract: Hormonal (endocrine) therapy (HT) is one of the most effective treatments for breast cancer in the adjuvant, the metastatic, and the prevention settings. For more than two decades, the anti-estrogen tamoxifen has been the HT of choice for all stages of ER-positive breast cancer [1], and tamoxifen is still the only approved agent, in the United States, to reduce the risk of breast cancer in high-risk women. Tamoxifen is a prototype of a class of drugs called selective estrogen-receptor (ER) modulators (SERMs), which exhibit anti-estrogen effects in the breast but possess estrogen-like activity in other tissues such as bone and blood [1]. This inherent mixed agonist/antagonist nature of tamoxifen is probably responsible for the two major limits of its successful therapeutic promise, i.e. tumor resistance, de novo or acquired, seen in many patients, and its adverse effects in other tissues. Developments over the past two decades have led to potentially more effective, less toxic, and safer HT agents that are currently being implemented into the management of breast cancer, or soon will be. This, in turn, brings the challenge of determining the optimal use of these new drugs, either in combination or in sequence, questions that are currently under investigation in key preclinical models and clinical trials. Two recently reported preclinical studies – one by Long and colleagues [2] that demonstrates the efficacy of anti-estrogens as second-line therapy in breast tumors failing aromatase inhibitor (AI) therapy, and one by Suh and colleagues [3] that shows high synergism between arzoxifene and the new rexinoid LG 100268 in treatment and prevention – make significant contributions in this area and are discussed.Estrogen deprivation was suggested long ago as one of the most efficient strategies to block ER action [4]. After menopause, estrogen deprivation is most specifically achieved using inhibitors that block the conversion of adrenal androgens to estrogens by the enzyme
Tumor-suppressor activity of RRIG1 in breast cancer
Guihong Zhang, Abenaa Brewster, Baoxiang Guan, Zhen Fan, Powel H Brown, Xiao-Chun Xu
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-32
Abstract: Immunohistochemistry was used to detect RRIG1 expression in breast tissue specimens. Gene transfection was used to restore or knock down RRIG1 expression in breast cancer cell lines for analysis of cell viability, colony formation, and migration/invasion potential. Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression. The RhoA activation assay was used to assess RRIG1-induced inhibition of RhoA activity.The immunohistochemical data showed that RRIG1 expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues. RRIG1 expression was inversely correlated with lymph node metastasis of breast cancer but was not associated with the status of hormone receptors, such as estrogen receptor, progesterone receptor, or HER2. Furthermore, restoration of RRIG1 expression inhibited proliferation, colony formation, migration, and invasion of breast cancer cells. Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity. In contrast, knockdown of RRIG1 expression promoted breast cancer cell proliferation, colony formation, migration, and invasion potential.The data from the current study indicated that RRIG1 expression was reduced or lost in breast cancer and that restoration of RRIG1 expression suppressed breast cancer cell growth and invasion capacity. Future studies will determine the underlying molecular mechanisms and define RRIG1 as a tumor-suppressor gene in breast cancer.Breast cancer is the leading cause of cancer-related death in women between 35 and 45 years of age and remains the second-leading cause of cancer-related death among all women in the United States [1]. Despite success in screening for early stages of breast cancer and remarkable improvement in treatment outcomes, many women still develop metastatic disease and ultimately die [2-4]. Efforts for ultimate elimination of this diseas
Hormone-induced protection of mammary tumorigenesis in genetically engineered mouse models
Lakshmanaswamy Rajkumar, Frances S Kittrell, Raphael C Guzman, Powel H Brown, Satyabrata Nandi, Daniel Medina
Breast Cancer Research , 2007, DOI: 10.1186/bcr1645
Abstract: Two mouse models, the p53-null mammary epithelial transplant and the c-neu mouse, were exposed to estrogen and progesterone for 2 and 3 weeks, respectively, and followed for development of mammary tumors.In the p53-null mammary transplant model, a 2-week exposure to estrogen and progesterone during the immediate post-pubertal stage (2 to 4 weeks after transplantation) of mammary development decreased mammary tumorigenesis by 70 to 88%. At 45 weeks after transplantation, analysis of whole mounts of the mammary outgrowths demonstrated the presence of premalignant hyperplasias in both control and hormone-treated glands, indicating that the hormone treatment strongly affects the rate of premalignant progression. One possible mechanism for the decrease in mammary tumorigenesis may be an altered proliferation activity as the bromodeoxyuridine labeling index was decreased by 85% in the mammary glands of hormone-treated mice. The same short-term exposure administered to mature mice at a time of premalignant development also decreased mammary tumorigenesis by 60%. A role for stroma and/or systemic mediated changes induced by the short-term hormone (estrogen/progesterone) treatment was demonstrated by an experiment in which the p53-null mammary epithelial cells were transplanted into the cleared mammary fat pads of previously treated mice. In such mice, the tumor-producing capabilities of the mammary cells were also decreased by 60% compared with the same cells transplanted into unexposed mice. In the second set of experiments using the activated Her-2/neu transgenic mouse model, short-term estradiol or estradiol plus progesterone treatment decreased mammary tumor incidence by 67% and 63%, and tumor multiplicity by 91% and 88%, respectively. The growth rate of tumors arising in the hormone-treated activated Her-2/neu mice was significantly lower than tumors arising in non-hormone treated mice.Because these experiments were performed in model systems that mimic many essential
园艺学报 , 2003,
Abstract: 概述了细胞壁蛋白质膨胀素(expansin)的发现、作用机制、基因家族、功能和研究现状。重点论述了膨胀素在果实完熟中的作用及其与细胞壁酶之间的相互关系,提出了利用转基因技术调节果实完熟和软化的新策略。关键词:中图分类号:
A moderate elevation of circulating levels of IGF-I does not alter ErbB2 induced mammary tumorigenesis
Robert K Dearth, Isere Kuiatse, Yu-Fen Wang, Lan Liao, Susan G Hilsenbeck, Powel H Brown, Jianming Xu, Adrian V Lee
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-377
Abstract: We crossed heterozygous TTR-IGF-I mice with heterozygous MMTV-ErbB2 mice to generate 4 different genotypes: TTR-IGF-I/MMTV-ErbB2 (bigenic), TTR-IGF-I only, MMTV-ErbB2 only, and wild type (wt). Virgin females were palpated twice a week and harvested when tumors reached 1000 mm3. For study of normal development, blood and tissue were harvested at 4, 6 and 9 weeks of age in TTR-IGF-I and wt mice.TTR-IGF-I and TTR-IGF-I/ErbB2 bigenic mice showed a moderate 35% increase in circulating total IGF-I compared to ErbB2 and wt control mice. Elevation of circulating IGF-I had no effect upon pubertal mammary gland development. The transgenic increase in IGF-I alone wasn't sufficient to initiate mammary tumorigenesis. Elevated circulating IGF-I had no effect upon ErbB2-induced mammary tumorigenesis or metastasis, with median time to tumor formation being 30 wks and 33 wks in TTR-IGF-I/ErbB2 bigenic and ErbB2 mice respectively (p = 0.65). Levels of IGF-I in lysates from ErbB2/TTR-IGF-I tumors compared to ErbB2 was elevated in a similar manner to the circulating IGF-I, however, there was no effect on the rate of tumor growth (p = 0.23). There were no morphological differences in tumor type (solid adenocarcinomas) between bigenic and ErbB2 mammary glands.Using the first transgenic animal model to elevate circulating levels of IGF-I to those comparable to women at increased risk of breast cancer, we showed that moderately high levels of systemic IGF-I have no effect on pubertal mammary gland development, initiating mammary tumorigenesis or promoting ErbB2 driven mammary carcinogenesis. Our work suggests that ErbB2-induced mammary tumorigenesis is independent of the normal variation in circulating levels of IGF-I.IGF-I has the characteristics of both a circulating hormone and a tissue growth factor. While numerous studies have focused on the autocrine and/or paracrine ability of IGF-I to regulate mammary gland development and tumorigenesis [1], only a few have focused on the role of c
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