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1 tive intratracheal instillation of liposomal clodronate.
2 y subconjunctival (SC) delivery of liposomal clodronate.
3 gues and the antimacrophage agent, liposomal clodronate.
4 etion of alveolar macrophages with liposomal clodronate.
5 IL17RA(-/-) mice using liposomes loaded with clodronate.
6 y treating B6 mice with liposomes containing clodronate.
7 n after macrophage depletion using liposomal clodronate.
8 hibited by the antiosteolytic bisphosphonate clodronate.
9 travenous injection of liposome-encapsulated clodronate.
10 effects were indistinguishable from those of clodronate.
11 antiresorptive and antimacrophage effects of clodronate.
12 ) group 5 = diabetes + periodontitis + LDD + clodronate.
15 acid (4 mg intravenously every 6 months) or clodronate (1,600 mg/d orally) be considered as adjuvant
16 domly assigned in a 1:1 ratio to either oral clodronate 1600 mg daily for 3 years (n=1662) or placebo
17 igned to take four tablets per day of sodium clodronate (2080 mg) or matching placebo for up to 3 yea
18 ld C57BL/10J mice with liposome-encapsulated clodronate 48 h before 35 min of hepatic ischemia with b
19 ither phosphate-buffered saline (control) or clodronate (a macrophage depleting drug) at 15 weeks pos
20 re-treatment of the recipient with liposomal clodronate, a macrophage depleting agent, with the goal
23 c cells by injection of liposomes containing clodronate abolished diabetes, although inflammation rem
24 M using intracerebroventricular injection of clodronate abrogates the reactive oxygen species product
25 cant benefits for zoledronic acid (ZOL) over clodronate acid (CLO) were seen in the Medical Research
27 owever, treatment with liposome-encapsulated clodronate, an agent that depletes macrophages in vivo,
28 controlled trials assessed the use of sodium clodronate, an oral, first-generation bisphosphonate.
35 evaluate the effect of mono and combined BP clodronate and LDD therapies in reducing gingival levels
36 aims of this study were to determine whether clodronate and liposome-encapsulated clodronate are meta
37 ause there are no direct comparisons between clodronate and pamidronate or zoledronic acid, the super
38 Most studies evaluated zoledronic acid or clodronate, and data are extremely limited for other bis
39 were depleted from mice by administration of clodronate, and their location and phenotype were examin
40 y the positive result of one trial of sodium clodronate, and we found no evidence of a benefit from t
41 x vivo with immunomagnetic beads) metabolize clodronate, and whether rat peritoneal macrophages metab
42 LDD; 4) group 4 = diabetes + periodontitis + clodronate; and 5) group 5 = diabetes + periodontitis +
43 whether clodronate and liposome-encapsulated clodronate are metabolized to adenosine 5'-(beta,gamma-d
44 ronate, risedronate, and lovastatin, but not clodronate, are blocked by geranylgeraniol, a precursor
45 acerebral injection of liposome-encapsulated clodronate at P5 significantly reduced vessel coverage a
46 he intratracheal administration of liposomal clodronate attenuated particulate matter-induced IL-6 pr
47 B6) mice by i.v. administration of liposomal clodronate before allogeneic bone marrow transplantation
48 in the airways were depleted using liposomal clodronate before infection, this resulted in a signific
49 ection of the macrophage-depleting liposomal clodronate before radiotherapy can increase the antitumo
50 acerebral injection of liposome-encapsulated clodronate before transient middle cerebral artery occlu
53 protocol B-34 aims to ascertain whether oral clodronate can improve outcomes in women with primary br
55 gimens and IV zoledronic acid (ZOL) and oral clodronate (CLO) in 1960 patients with newly diagnosed m
56 ence of improvement in overall survival with clodronate compared with placebo (HR 1.12, 0.89-1.42; p=
57 e with metastatic disease from use of sodium clodronate compared with placebo was seen in overall sur
58 ippostrongylus brasiliensis and treated with clodronate-containing liposome to deplete macrophages or
59 capsular sinus CD169-positive macrophages by clodronate-containing liposome was associated with a lac
61 rophages using subconjunctival injections of clodronate-containing liposomes before corneal infection
63 normally developed spleens by treatment with clodronate-containing liposomes demonstrated that these
65 macrophages by intranasal administration of clodronate-containing liposomes in caspase-9 inhibitor-t
68 ed mice and compared tumor development using clodronate-containing liposomes to deplete macrophages i
69 Treatment of PVC-211 MuLV-infected rats with clodronate-containing liposomes, which specifically kill
73 splenic phagocytic APCs by i.v. injection of clodronate- (dichloromethylene diphosphonate) containing
75 ival administration of liposome-encapsulated clodronate efficiently diminished resident ocular surfac
76 al macrophages with the macrophagicidal drug clodronate eliminated the latex beads' protective effect
79 hamsters were treated, intratracheally, with clodronate-encapsulated liposomes or control liposomes a
83 s or older on study entry showed benefits of clodronate for recurrence-free interval (0.75, 0.57-0.99
86 tion was noted in 23 of 1612 patients in the clodronate group and 12 of 1623 patients in the placebo
89 not differ between groups (286 events in the clodronate group vs 312 in the placebo group; hazard rat
91 at a first-generation bisphosphonate, sodium clodronate, improves overall survival in men with metast
93 e infiltration by systemic administration of clodronate-incorporated liposomes fails to suppress LSI-
97 Interestingly, macrophage depletion with clodronate inhibited the development of colitis, while t
99 re generated by the combination of liposomal clodronate injection, irradiation, and BM transplantatio
100 lled trials is modest but supports that oral clodronate, intravenous pamidronate, and intravenous zol
101 ted CCR2 chimeric mice by the combination of clodronate, irradiation, and bone marrow (BM) transplant
103 hese results provide proof-of-principle that clodronate is effective at sparing the number of donor B
105 somiasis with macrophage-depleting liposomal clodronate (LC) to define how macrophages mediate bladde
107 in the induction of LPC proliferation using clodronate liposome deletion of Kupffer cells and adopti
115 phages, through subconjunctival injection of clodronate liposome, attenuated lissamine green staining
118 ost-AAI rAMs was studied in vivo by means of clodronate liposome-mediated depletion, adoptive transfe
119 ndent of lymphoid tissues but dependent on a clodronate liposome-sensitive population of liver-reside
120 AFIA mice had reduced CD68(+) cells, whereas clodronate liposome-treated mice had increased CD68(+) a
121 tion of these infiltrating macrophages using clodronate-liposome administration shows a significant r
125 rophage depletion was achieved by daily i.v. clodronate liposomes (-1 day to +3 days) during AngII in
127 onducted to determine whether treatment with clodronate liposomes (CL(2)MDP-lip), which cause depleti
128 nvestigate this, we depleted phagocytes with clodronate liposomes (CL) in vivo through systemic deliv
129 Moreover, depletion of SCS macrophages using clodronate liposomes abolished NK cell accumulation and
130 In addition, the treatment of rats with clodronate liposomes depleted KCs and led to increased s
132 ction, we depleted them by the inhalation of clodronate liposomes in an established mouse model of re
137 pletion of alveolar macrophages with inhaled clodronate liposomes reduced both NK and T cell numbers
140 phage depletion in wild-type (WT) mice using clodronate liposomes resulted in impaired muscle regener
141 using splenectomized mice or treatment with clodronate liposomes suggested that macrophages in the s
142 apoE-/- mice before and after treatment with clodronate liposomes to deplete tissue macrophages, comp
143 effects were mitigated in mice treated with clodronate liposomes to reduce circulating monocytes and
144 peritoneal macrophages were depleted (using clodronate liposomes) from PD-1(-/-) mice, the animals'
145 epletion of macrophages in the cornea (using clodronate liposomes) prior to injury significantly inhi
146 rone mice SNF(1) mice that were treated with clodronate liposomes, but not mice treated with vehicle,
147 is in vivo, induced by the administration of clodronate liposomes, can exacerbate the autoimmune phen
149 s were not affected following treatment with clodronate liposomes, immunization of CCR2(-/-) mice, or
155 significantly elevated in mice treated with clodronate-liposomes at 3 and 5 days p.i., while IL-10 l
158 Both groups of inbred mice treated with clodronate-liposomes compared with PBS-liposomes (contro
160 inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathologi
161 this monocytic cell population, using either clodronate-liposomes or gadolinium chloride, prevented p
162 and selective depletion of macrophages with clodronate-liposomes protects hearts against allograft r
166 cterial plate counts in B6 mice treated with clodronate-liposomes were unchanged at 3 days and were h
167 methylene diphosphonate (Cl2MDP-liposomes or clodronate-liposomes) before priming mice with vesicular
170 xpansion was abrogated by prior injection of clodronate-loaded liposomes, indicating a role for subca
171 phoma depletion by CD20 mAb in vivo, whereas clodronate-mediated depletion of macrophages eliminated
175 iven to patients with primary breast cancer, clodronate might reduce the subsequent incidence of bone
177 rrence of nonosseous metastases was similar (clodronate, n = 112; placebo, n = 128; P =.257), but the
178 uction in the occurrence of bone metastases (clodronate, n = 12; placebo, n = 28; HR, 0.44; 95% CI, 0
179 reduction in occurrence of bone metastases (clodronate, n = 63; placebo, n = 80; hazards ratio [HR],
180 re was a significant reduction in mortality (clodronate, n = 98; placebo, n = 129; P =.047) during th
182 tiinflammatory and antiresorptive effects of clodronate on macrophages and osteoclasts in vivo occur
183 ravenously with either liposome-encapsulated clodronate or empty liposomes prior to and after OBX or
184 phage depletion agent (liposome-encapsulated clodronate) or with a neutrophil depletion agent (cyclop
188 epletion of splenic macrophages by liposomal clodronate protects against PIFA-induced chemoresistance
190 se changes, whereas depleting monocytes with clodronate resulted in a modest partial inhibition.
192 r bisphosphonates, including pamidronate and clodronate, seem to be ineffective in this setting.
193 was associated with an increase in levels of clodronate-sensitive, phagocytic SiglecF(low) alveolar m
194 rom the fetal cerebral cortex with liposomal clodronate significantly increased the number of neural
195 reating mice with i.v. liposome-encapsulated clodronate, significantly attenuated perfusate cytokine
196 ocyte ablation were used: systemic liposomal clodronate (sLC), inducible depletion using CD11b diphth
201 first time the use of liposome-encapsulated clodronate to selectively deplete macrophages during the
203 fa, Il-1beta, Il-10, Cxcl1, and iNos, in the clodronate-treated H. bilis-infected Rag2(-/-) mice comp
206 tic cells were more numerous in MAFIA versus clodronate-treated mice and flow cytometric analyses of
207 f macrophages in the OE of both sham and OBX clodronate-treated mice were significantly reduced compa
208 When compared with vehicle-treated controls, clodronate-treated non-lupus-prone DBF(1) mice developed
209 caspase-3 in the OE and olfactory nerves of clodronate-treated OBX mice compared to liposome-treated
212 , 1.32+/-0.41 mm(3) in liposome-encapsulated clodronate-treated versus 3.04+/-0.72 mm(3) in saline-tr
216 ion of monocytes or macrophages by liposomal clodronate treatment or genetic deficiency of macrophage
221 By depleting macrophages using liposomal clodronate, we found that alveolarization defects were s
223 iposomes containing the macrophagicidal drug clodronate were used to deplete conjunctival macrophages
224 t-generation bisphosphonates (etidronate and clodronate) were not suitable for long-term treatment an
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