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1 KS and NHL diagnoses during 1996 to 2011 were identified
2 KS and PEL are aggressive KSHV-associated malignancies w
3 KS can develop following organ transplantation through r
4 KS incidence rates per 100000 person-years were 52 in th
5 KS incidence was lower at 12-23 (IRR = 0.47; 95% CI, .23
6 KS is a highly disseminated and vascularized tumor.
7 KS risk was 5 times higher in South African women (aHR,
8 KS risk was lower in girls than in boys (adjusted HR [aH
9 KS spindle cells, the main tumor cells, all contain KSHV
10 KS tumors support both latent and lytic KSHV replication
11 KS was identified by >/= 1 inpatient or >/= 2 outpatient
16 , the reduction in insulin sensitivity after KS-oil supplementation was more marked [27% lower than w
17 R gene frequencies in 250 classic (non-AIDS) KS cases, 280 KSHV-seropositive controls, and 576 KSHV-s
24 way is important in the pathogenesis of AIDS-KS, which could be an attractive therapeutic target for
30 ical characterization of the encoded CPS and KS, and the impact of insertional mutagenesis on virulen
31 phosphate and ent-kaurene synthases (CPS and KS, respectively), which are found within a well-conserv
34 eir potential role in HHV-8 pathogenesis and KS.IMPORTANCE Here we show that HHV-8, a DNA tumor virus
36 d the relationship between cART regimens and KS using multivariable Poisson regression, stratified or
37 urene synthase1 (SrKS1) homologs, SrCPS2 and KS-like (SrKSL), which were specifically expressed in tr
38 nical characteristics, overall survival, and KS progression-free survival were analyzed according to
40 not pathological aggregates, but rather are KS-WNK1-dependent microdomains of the DCT cytosol that m
44 Kgamma were backcrossed into db/+ mice C57BL/KS (>10 generations) to obtain db/db-PI3Kgamma(-/-) mice
45 ation of a protein previously shown to cause KS-like lesions in mice (Rac1), an increase in KS-associ
46 ide Innovations and Technology, Kansas City, KS) designed to protect the head from radiation exposure
47 mmunodeficiency virus (HIV)-negative classic KS cases to plasma from 29 matched controls, using a mul
50 mumax), nitrite half saturation coefficient (KS), oxygen half saturation coefficient (KO), and biomas
51 n both the discovery and validation cohorts, KS was associated with HLA-A*11:01 (adjusted OR for the
53 -out coefficients (or Setschenow constants) (KS [M(-1)]) for 38 diverse neutral compounds in ammonium
54 nowledge about Setschenow salting constants, KS, the exponential dependence of Henry's Law coefficien
59 iofacial, intellectual, and cardiac defects, KS is also characterized by humoral immune deficiency an
62 idence rates and risk factors for developing KS in different periods after starting cART in patients
63 idence rates and risk factors for developing KS up to 90 and 180 days and 1, 2, 5, and 8 years after
65 not associated with the hazard of developing KS in the first year after cART initiation, but was over
66 cell counts increased the risk of developing KS throughout all observation periods after cART initiat
69 erm generally overpredicted the experimental KS, predicted and experimental values were correlated.
70 We screened STAT4 in additional 18 familial KS cases and the variant site from 56 sporadic KS cases
71 L occurred at higher CD4 counts (P < .05 for KS and NHL) and with undetectable HIV RNA (P < .05 for K
75 ion, providing novel therapeutic avenues for KS tumors.IMPORTANCE KSHV is the etiologic agent of Kapo
80 othelial cells (LTC) as a cellular model for KS, we demonstrated that KSHV infection induces Nrf2 con
84 Here we show that keratinocytes derived from KS patients are unable to undergo electrotaxis, and this
85 mine whether consuming Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and B. longum MM-2
86 sitive responses to Stona IB Gel(R), gelatin KS and gelatin RP600, of which the latter two were inclu
87 In this study, we use ketosynthase gene (KS) PCR amplicon sequences (sequence tags) to explore th
88 a simple proof of a theorem: In generalized KS theory (GKS), the band gap of an extended system equa
91 V LSSE and the sudden increases in H K and H KS at 175 K are associated with the spin reorientation
93 V LSSE peak at 75 K is attributed to the H KS and M S (saturation magnetization) whose peaks also o
100 Despite important ART-related declines in KS incidence, men and women in South Africa and men who
102 dlin-1 also failed to rescue electrotaxis in KS cells, indicating that both integrin and lipid bindin
104 ceptor/formyl peptidyl receptor (ALX/FPR) in KS patient tissue sections and in vitro KS and PEL cell
105 -like lesions in mice (Rac1), an increase in KS-associated phenotypes (tube formation in endothelial
106 n of antioxidant genes and genes involved in KS pathogenesis such as the NAD(P)H quinone oxidase 1 (N
109 d find that glyoxal consistently "salts-in" (KS of -0.16, -0.06, -0.065, -0.1 molality(-1), respectiv
111 en who have sex with men remain at increased KS risk, likely due to high human herpesvirus 8 coinfect
112 cally active agents, possess a ketosynthase (KS) domain within each module to catalyze chain elongati
114 from a newly developed coupled ketosynthase (KS)-ketoreductase (KR) assay that established that the d
115 denylation (AD) and polyketide ketosynthase (KS) domain fragments amplified from these microbiomes pr
116 lly, we determined that dysfunction of known KS genes and the genes identified in this study results
123 A close correspondence between the observed KS selectivity and that predicted by phylogenetic analys
126 therwise healthy, received 5 1-g capsules of KS oil or a control (canola oil) for 8 wk and crossed ov
128 of polymicrogyria are not characteristic of KS, and we found only a few previous reports of this ass
132 betic patients contributes to development of KS by promoting KSHV lytic replication and infection.
133 ncogenic activity of KSHV and development of KS, and also suggests a potential of using YAP inhibitor
136 roles of KMT2D and KDM6A in the etiology of KS by using a vertebrate model organism to provide direc
139 t of structures represents a larger group of KS domains from both canonical and AT-less type I PKSs t
141 KMT2D have been identified in a majority of KS patients, a few patients have mutations in KDM6A.
142 n promoting the aggressive manifestations of KS in AIDS patients; however, the pathogenesis underlyin
143 n promoting the aggressive manifestations of KS, the pathogenesis underlying AIDS-KS remains largely
144 dings provide insights into the mechanism of KS selectivity in this important group of PKSs, can serv
151 new insight into the potential treatment of KS and PEL using nature's own anti-inflammatory molecule
154 owever, effects of cART type and duration on KS remain difficult to interpret secondary to KS-associa
160 ed controlled viremia with either persistent KS despite 3 months of antiretroviral therapy (ART) or p
161 ystal structures of seven AT-less type I PKS KS domains that represent various sequence clusters, rev
163 ural diversity within the AT-less type I PKS KS family, and most important, provide a unique opportun
174 nhibitors (BPIs) was associated with reduced KS incidence in the third year of cART (incidence rate r
175 ell counts are essential to further reducing KS incidence worldwide, but additional measures might be
179 32gamma isoforms was observed in HIV-related KS biopsy specimens compared with non-HIV-related KS and
181 unctional interaction between the respective KS-associated genes and their products in zebrafish mode
182 o dietary potassium loading and restriction, KS-WNK1 knockout mice were deficient in these structures
183 ementation with a blend of krill and salmon (KS) oil [which is rich in eicosapentaenoic acid (EPA) an
184 8) is the causative agent of Kaposi sarcoma (KS) and multicentric Castleman disease (MCD), a life-thr
192 V-related, 7 non-HIV-related Kaposi sarcoma (KS), and 7 normal skin tissues (NSTs) of Dutch origin we
193 V) is the causative agent of Kaposi sarcoma (KS), one of the leading cancers in human immunodeficienc
194 virus (KSHV) is the cause of Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a form of Cast
195 ) is the causative agent for Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a subset of mu
196 rstanding of the burden of Kaposi's sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretro
207 is the etiologic agent of Kaposi's sarcoma (KS), a vascular tumor frequently found in immunodeficien
208 ologically associated with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric C
209 rus (KSHV) is the cause of Kaposi's sarcoma (KS), which is the most common AIDS-associated malignancy
218 man herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) and have an important role i
220 cture of the exact multiplicative Kohn-Sham (KS) potential substantially underestimates the fundament
221 pression for the work function in Kohn-Sham (KS) theory is shown to be valid in generalized KS theory
224 between countries using Kolmogorov-Smirnov (KS) tests, Degree Distribution Quantification and Compar
227 s within the Upper Neosho River subdrainage, KS, from June-August 2013 yielded three generalizable ec
228 rmatan sulfate (CS/DS), and keratan sulfate (KS)-mainly novel glycosylation strategies, elongation se
236 -chromosome (45X), and Klinefelter syndrome (KS), where males have an additional X-chromosome (47XXY)
240 l counts (P < .001); 90% of patients with T0 KS who were not receiving cART and 84% of those with T1
243 not receiving cART and 84% of those with T1 KS were treated in accordance with the stage-stratified
244 ART alone; patients with advanced-stage (T1) KS receive cART plus liposomal anthracycline chemotherap
250 0% lower (adjusted OR, 0.6; P = .01) but the KS risk 80% higher with HLA-C group 1 homozygosity (adju
251 the combined cohorts, 0.6; P = .01), but the KS risk was 2-fold higher (adjusted OR, 2.1; P = .002).
253 In contrast, recombinant SEMA3E carrying the KS-associated mutation did not protect GnRH neurons from
255 hose whose counts were <50 cells/microL, the KS risk was halved in South Africa (aHR, 0.53; 95% CI, .
259 Taken together, our studies suggest that the KS pathophysiology overlaps with the RASopathies and pro
269 S remain difficult to interpret secondary to KS-associated immune reconstitution inflammatory syndrom
271 on is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evalu
273 ) in KS patient tissue sections and in vitro KS and PEL cell models offers a novel possibility for tr
275 e activated in KSHV-infected cells in vitro, KS-like mouse tumors and clinical human KS specimens.
281 th complex medical histories consistent with KS in whom next generation sequencing identified the sam
285 issues that are affected in individuals with KS, including craniofacial structures, heart and brain.
288 niparental isodisomy (UPD) in a patient with KS and a de novo, dominant mutation in RAP1B in a second
294 umoral immune defects found in patients with KS with lysine methyltransferase 2D (KMT2D) mutations.
296 Chemical probes capable of reacting with KS (ketosynthase)-bound biosynthetic intermediates were
298 Here, we show that kidney-specific WNK1 (KS-WNK1), a truncated kinase-defective WNK1 isoform that
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