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1 LAM cells bear mutations in tuberous sclerosis (TSC) gen
2 LAM cells have biallelic loss of either tuberous scleros
3 LAM ELISA had the following sensitivity, specificity, po
4 LAM is a complex heteropolysaccharide synthesized by an
5 LAM is an elegant model of malignancy because biallelic
6 LAM is caused by mutations in the tuberous sclerosis com
7 LAM is caused by mutations in the tuberous sclerosis gen
8 LAM is characterized by neoplastic growth of smooth musc
9 LAM is typically caused by tuberous sclerosis complex 2
10 LAM LFA had a sensitivity of 50% for definite and probab
11 LAM LFA had a sensitivity of 68% for the composite stand
12 LAM LFA had a sensitivity of 75% for definite histopatho
13 LAM LFA in CSF is a useful additional diagnostic tool.
14 LAM lung nodules also produced OPG, as shown by expressi
15 LAM lung nodules showed reactivities to antibodies to tu
16 LAM monoprophylaxis was effective in preventing de novo
17 LAM pathogenic mechanisms mirror those of many forms of
18 LAM patients had significantly higher serum prostaglandi
19 LAM-HTGTS assays are sensitive, reproducible, relatively
20 LAM-HTGTS differs from related approaches because it det
21 Xpert tests improved case finding by 21.6%, LAM testing alone improved it by 13.5%, and dual Xpert t
25 n-Pacific (APAC) (51 cases), Latin American (LAM) (348 cases), European (EU) (750 cases), and North A
31 tion of the arabinose content of both AG and LAM that accompanied the accumulation of DPA in the muta
34 logically slowing the progression of AML and LAM with rapamycin, our understanding of their pathogene
39 nally, we investigated the ability of LM and LAM from C. glutamicum, and C. glutamicumDeltamptC and C
41 l established that the interaction of LM and LAM with TLR2 is a process dependent on the structure of
44 th both tuberous sclerosis complex (TSC) and LAM (TSC-LAM) into induced pluripotent stem cells (iPSC)
45 n used along with rapamycin, might attenuate LAM progression and potentially other TSC-related disord
46 ering RNA-mediated knockdown of GRAIL before LAM treatment abrogated LAM-induced hyporesponsiveness.
49 ibition of human CD4(+) T cell activation by LAM also was associated with increased GRAIL expression.
51 wth factors and matrix remodeling enzymes by LAM cells enables their access to lymphatic channels and
52 zation of L-alpha-lysine to L-beta-lysine by LAM, via the stable allylic anhydroadenosyl radical (anA
53 umor-suppressor genes (TSC1/TSC2) that cause LAM, a multisystem disease characterized by cystic lung
54 ign-appearing spindle and epithelioid cells (LAM cells) that express smooth-muscle and melanocyte-lin
57 alleles that were incapable of complementing LAM production in M. smegmatis were not viable in M. tub
58 as significantly associated with concomitant LAM therapy (adjusted hazard ratio [HR], 4.61; 95% confi
59 as expressed in type II pneumocytes covering LAM nodules and caused AML cell growth and protection fr
61 by the demonstrated sensitivity of cultured LAM cells to complement mediated cytotoxicity via GD3 an
63 oliferation of cells cultured from explanted LAM lungs, and selectively induced migration of LAM cell
66 ogether these results reveal a new model for LAM pathogenesis in which activation of MEK-dependent pa
70 identified in exhaled breath condensate from LAM subjects and was increased by aspirin treatment, ind
72 haMan-based Lipid A mimetics (alpha,alpha-GM-LAM) induced potent activation of NF-kappaB signaling in
77 otein and protease activity were detected in LAM-associated fibroblasts but not the LAM cell line 621
83 itor, Rapamycin, stabilizes lung function in LAM and decreases the volume of renal angiomyolipomas, b
87 ort increased levels of active Src kinase in LAM lungs and in TSC2(-/-) cells, caused by a reduction
89 sizes, infiltrates, and destroys the lung in LAM arises from an unknown source and has an innocent hi
90 We identified Rapamycin-dependent miRNA in LAM patient angiomyolipoma-derived cells using two separ
91 gene expression was 40-fold overexpressed in LAM compared with control lung tissue (P </= 0.0001).
96 antibodies to GD3 may thus be therapeutic in LAM, and enhancement of existing NKT-cell infiltration m
97 andin pathways may have therapeutic value in LAM and TSC-related diseases, and possibly in other cond
101 describing telbivudine (LdT) or lamivudine (LAM) use in late pregnancy for preventing hepatitis B mo
103 itis B patients with preexisting lamivudine (LAM) resistance (LAM-R) undergoing liver transplantation
104 % at month 36 (P < 0.001), while lamivudine (LAM) or emtricitabine (FTC) use remained steady (71.9%)
109 the Determine TB-LAM lateral flow assay (LF-LAM) results among human immunodeficiency virus-infected
111 rabinomannan (LAM) lateral flow assay (LFA), LAM enzyme-linked immunosorbent assay (ELISA), and Xpert
114 IM), lipomannan (LM), and lipoarabinomannan (LAM) are essential components of the cell wall and plasm
117 ed whether mannose-capped lipoarabinomannan (LAM)-induced inhibition of CD4(+) T cell activation resu
119 osis-specific glycolipid, lipoarabinomannan (LAM), a promising urinary biomarker for the detection an
123 iagnostic accuracy of the lipoarabinomannan (LAM) lateral flow assay (LFA), LAM enzyme-linked immunos
127 cs, urine Xpert and urine-lipoarabinomannan (LAM) combined identified 88% of TB blood-culture-positiv
128 of lipomannans (LM) and lipoarabinomannans (LAM) that are abundant components of the multilaminate c
149 rare lung disease, lymphangioleiomyomatosis (LAM), manifests as neoplastic growth of smooth-muscle (S
150 rs that develop in lymphangioleiomyomatosis (LAM) as a consequence of biallelic loss of TSC1 or TSC2
152 d proliferation of lymphangioleiomyomatosis (LAM) cells, abnormal smooth muscle-like cells with mutat
154 omas and pulmonary lymphangioleiomyomatosis (LAM), emerge later, placing adults with undiagnosed TSC
159 ddle of the mannan core is present in mature LAM and allow for an updated working model of the biosyn
160 use truncated alleles were unable to mediate LAM production in Mycobacterium smegmatis and were unabl
162 isease caused by accumulation of metastatic (LAM) cells in the lungs, lymphatics, and the tumor angio
166 60 culture-positive sputa, mixed LAM and non-LAM strains were detected in 4 sputa belonging to 2 (2.8
173 ed tomography of the chest characteristic of LAM, but who have no additional confirmatory features of
175 wall and that the cellular concentration of LAM in M. smegmatis is selectively modulated with the gr
176 ecific questions related to the diagnosis of LAM and management of pneumothoraces in patients with LA
177 tions against making a clinical diagnosis of LAM on the basis of the high-resolution computed tomogra
178 have no additional confirmatory features of LAM (i.e., clinical, radiologic, or serologic), the guid
182 romise the subsequent immunodetectability of LAM, and in 20 min, the tuberculosis biomarker was conce
185 lungs, and selectively induced migration of LAM cells identified by the loss of heterozygosity for T
186 e, we generated a robust human cell model of LAM by reprogramming TSC2 mutation-bearing fibroblasts f
187 ped thus represent a novel cellular model of LAM that can advance our understanding of disease pathog
188 l mechanistic basis for the pathogenicity of LAM cells and they rationalize Src kinase as a novel the
193 nic CD4(+) T cells primed in the presence of LAM also exhibited decreased response upon restimulation
195 -epi-lipoxin-A4 reduced the proliferation of LAM patient-derived cells in a dose-dependent manner.
200 pletes the picture of how the active site of LAM from Clostridium subterminale SB4 "tames" the 5'-dAd
203 remarkable progress in the understanding of LAM and rapid translation of this knowledge to an effect
204 Accumulating evidence supports the view of LAM as a low-grade, destructive, metastasizing neoplasm.
205 st that cathepsin K activity is dependent on LAM cell-fibroblast interactions, and inhibitors of extr
208 beneficial effect when compared with IFN or LAM for CHB on antiviral activity as evidenced by the lo
220 ogically confirmed TB patients, quantitative LAM detection results increased progressively with bacil
221 s, there was no difference in de novo rates: LAM 8% (5 of 62), adefovir 15% (5 of 33), tenofovir 0% (
224 hepatitis B patients with preexisting rt204 LAM-R mutations or virological load refractory to LAM un
225 ughput genome-wide translocation sequencing (LAM-HTGTS) to map hundreds of thousands of RAG-initiated
226 ated high-throughput genome-wide sequencing (LAM-HTGTS) method for the detection of genome-wide 'prey
233 and, like other members of this superfamily, LAM utilizes radical-generating machinery comprising SAM
237 ial lipoarabinomannan in urine (Determine TB LAM), and a molecular assay performed on a sputum sample
239 ccuracy of a urine antigen test Determine TB-LAM Ag (Determine TB-LAM; Alere, Waltham, MA, USA) for s
242 We retrospectively reviewed the Determine TB-LAM lateral flow assay (LF-LAM) results among human immu
246 tigen test Determine TB-LAM Ag (Determine TB-LAM; Alere, Waltham, MA, USA) for screening for HIV-asso
247 and a slightly better effect (P = 0.01) than LAM on the normalization of serum alanine aminotransfera
251 orm lung nodules and it is hypothesized that LAM nodule-derived proteases cause cyst formation and ti
252 lular fractions and spheroplasts showed that LAM and lipomannan (LM) were primarily found in a cell w
253 her, the results presented here suggest that LAM is primarily localized with the mycolic acids in the
254 in spheroplast preparations, suggesting that LAM and LM are primarily associated with the putative ou
258 of these studies significant changes in the LAM/LM content of the cell wall were noted relative to t
262 fer all features that define cancer upon the LAM cell-metabolic reprogramming and proliferative signa
264 sufficiency at the TSC2 locus contributes to LAM pathology, and demonstrated that iPSC reprogramming
265 adulthood, 21 presented with symptoms due to LAM, 19 with renal angiomyolipomas, and 10 with seizures
267 mutations or virological load refractory to LAM undergoing liver transplantation were included, with
270 uberous sclerosis complex (TSC) and LAM (TSC-LAM) into induced pluripotent stem cells (iPSC), followe
277 (3) from 3.5% to 50% (p < 0.001) for urinary LAM ELISA; for urinary LAM strip test, grade 1 and 2 cut
278 < 0.001) for urinary LAM ELISA; for urinary LAM strip test, grade 1 and 2 cut-points performed simil
284 er of positive tests from urine Xpert, urine LAM and MTB-blood-culture correlated with PCs (p < 0.001
286 ned directly from isolated genomic DNA using LAM-PCR and unidirectionally ligated to bridge adapters;
287 omyomatosis (LAM) is a rare disease in which LAM cells and fibroblasts form lung nodules and it is hy
294 rial of sirolimus involving 89 patients with LAM who had moderate lung impairment--a 12-month randomi
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