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1 ling mediates cisplatin-induced anorexia and body weight loss.
2 ppress disease, as it is manifested by total body weight loss.
3 est systemic toxicity as reflected in animal body weight loss.
4 ays postimplantation, with negligible animal body weight loss.
5 and body weight gain or decreased intake and body weight loss.
6 week) was determined by efficacy and minimal body weight loss.
7 otor performance, accompanied by progressive body weight loss.
8 severity, as assessed by striatal volume and body weight loss.
9  the humane endpoint, which was due to rapid body weight loss.
10 ted viral infection-induced liver injury and body weight loss.
11 icacy but worsened survival due to excessive body weight loss.
12  of cisplatin-induced malaise, anorexia, and body weight loss.
13  improves glucose tolerance independently of body weight loss.
14 sistant to chemotherapy-induced anorexia and body weight loss.
15 orticosterone, reduction of food intake, and body weight loss.
16 id extractable Ba were linearly related to % body weight loss.
17 ase parasite burden, but it had no effect on body weight loss.
18 le TNBC xenograft models without significant body weight loss.
19 on with no observed toxicities as defined by body weight loss.
20 duction in 24 h food intake with concomitant body weight loss.
21 toxicity was assessed in rats as measured by body weight loss.
22 ts, rather, treated mice suffered tremendous body weight loss.
23 eated with mP-PTX had no obvious ascites and body-weight loss.
24 r of therapy and maintained a 20.1% +/- 3.5% body weight loss (54.6% +/- 12.0% of EWL).
25  performance quartiles when comparing excess body weight loss (67.2% vs 68.5%; P = .86) at 1 year.
26        Women who achieved a > or =50% excess body weight loss after surgery were asked to complete th
27 ften surpass the expected improvement due to body weight loss alone.
28 d whether food restriction in the absence of body weight loss alters drug reward sensitivity.
29 l or control treatment that (1) RYGB-induced body weight loss and (2) the satiating efficacy of endog
30  IL-1 of corticosterone and IL-6, and causes body weight loss and B cell hyperplasia with serum IgG a
31 ving the disease activity index and reducing body weight loss and colonic tissue damage.
32 reatment-induced toxicity was quantified via body weight loss and complete blood count.
33 tiated early after lethal infection hampered body weight loss and completely protected mice from leth
34  in knockout mice does not protect them from body weight loss and death upon infection with H3N2 infl
35                                          The body weight loss and disease activity scores for TregPMA
36 ment delayed the onset of motor symptoms and body weight loss and extended the survival of HD mice.
37 he lowest severity of infection, assessed by body weight loss and food intake.
38 al disease, including its vicious cycle with body weight loss and heavier infection with malnutrition
39                             PINTA745 reduced body weight loss and improved body weight recovery after
40  Paroxetine attenuated motor dysfunction and body weight loss and improved glucose metabolism in the
41       The CaM-fragment significantly reduced body weight loss and improved motor function as indicate
42 farction, respectively, along with decreased body weight loss and improved neurological function as c
43 dy-treated group by week 9, with significant body weight loss and increased bacterial load in the lun
44 (P<0.05) reduction of neurological deficits, body weight loss and infarct volume (22.8+/-2.1%) withou
45 resulted in a reduction in infection-induced body weight loss and inflammation and significantly incr
46 -/-) mice developed dramatically exacerbated body weight loss and intestinal pathology, but they surp
47  also been found to reduce radiation-induced body weight loss and lethality in mouse models.
48 , where GcgR activation failed to induce the body weight loss and lipid metabolism changes observed i
49 ined locomotor impairment in the open field, body weight loss and metabolic alterations measured by i
50 d and lung pathology, in addition to reduced body weight loss and mortality.
51 ng the AM depletion phase caused significant body weight loss and mortality.
52 tor (+)-JQ1 protects tumor-bearing mice from body weight loss and muscle and adipose tissue wasting.
53 taxis, reduce lung virus titers, and prevent body weight loss and pulmonary inflammation.
54 its ability to inhibit dexamethasone-induced body weight loss and systemic hypertension in rats.
55 gnificant weight loss (60% percent of excess body weight loss) and resolution (83%) of T2DM.
56 trated by undetectable viral titers, lack of body weight loss, and a significant reduction in the lev
57 O mice causes suppression of food intake and body weight loss, and decreased food intake is primarily
58 replication in the lungs, prevented dramatic body weight loss, and increased survival rates of mice i
59 th antibiotics reduced microorganism growth, body weight loss, and mortality but had no effect on ves
60 reatment with adelmidrol decreased diarrhea, body weight loss, and myeloperoxidase activity.
61                              Infarct volume, body weight loss, and neurological deficit were measured
62 treatment resulted in decreased food intake, body weight loss, and reduced adiposity at doses that pr
63  observed that IL-22 induces thymic atrophy, body weight loss, and renal proximal tubule metabolic ac
64 perative complications, percentage of excess body weight loss, and time to return to activities of da
65                                       Severe body weight loss as high as 20-25% was observed which wa
66 ge heart rate, plasma lactate concentration, body weight loss as well as post-game sprint performance
67                                       Excess body weight loss at 1 year was 13% lower for SG (60%) th
68                                       Excess body weight loss at 1 year; resolution of medical comorb
69           Cox regression showed that percent body weight loss at 24 hours predicted death by 48 hours
70                                              Body weight loss at 6 weeks and 3 months postoperatively
71                              The mean excess body weight loss at time of second biopsy was 59% +/- 22
72 s a multifactorial syndrome characterized by body weight loss, atrophy of adipose tissue (AT) and sys
73   Again, these effects were not secondary to body weight loss, because food restricted rats had the s
74         The 1.2% ARG HD group showed reduced body weight loss, better motor functioning, and fewer ch
75 ificant differences in the percent of excess body weight loss between the 2 groups at the 3-year foll
76 tory of complicated delivery, percent excess body weight loss, BMI, type of weight loss procedure and
77 uine herpesvirus 1 (EHV-1) displayed reduced body weight loss but had higher pulmonary viral loads.
78 w flutters, head shakes, diarrhea, and total body weight loss), but did not elicit any cannabimimetic
79 acy and reduced toxicity as measured by mean body weight loss (BWL) in vivo [body weight loss of 7.7
80 s against cancer-induced cardiac atrophy and body weight loss by signaling through its receptor.
81 ut altering LPS-induced sickness measured by body weight loss, decreased motor activity, and reduced
82 ermates that was evaluated by survival rate, body weight loss, diarrhea and fecal blood score, and hi
83 cancer-related death that causes progressive body weight loss due to depletion of skeletal muscle mas
84 diabetic rats restored euglycemia, minimized body weight loss due to food restriction, substantially
85 s, decrease in BMI, and percentage of excess body weight loss (% EBWL) after surgery.
86  IL-1 and IL-6 in mediating the anorexic and body weight loss effects of GLP-1 receptor activation.
87 cted the bone marrow cells and prevented the body weight loss from the effect of irradiation, and fac
88       Mice expressing mutant huntingtin show body weight loss, have motor function deficits, and die
89 ira, which was followed by urinary shedding, body weight loss, hypothermia, and colonization of the k
90     We found that 4b significantly prevented body weight loss, improved several parameters of motor f
91 ation developed symptoms of cachexia such as body weight loss in a time- and dose-dependent manner.
92 de attenuates cisplatin-induced anorexia and body weight loss in addition to pica, demonstrating that
93 2a (YSH6000) resulted in diarrhea and severe body weight loss in adult B6 mice.
94 ury, and elevated levels are associated with body weight loss in numerous chronic human diseases.
95 d 73% of tumor growth delay without apparent body weight loss in the murine CT26 syngeneic model, aft
96 s) vs 15.9% excess weight loss (6.0% initial body weight loss) in the sham group.
97  biological activity attenuated anorexia and body weight loss induced by central exendin-4 administra
98 rtin receptors 3/4 reversed the anorexia and body weight loss induced by TLR2 activation.
99          During prolonged cold, however, the body weight loss is attenuated, caused by adaptive mecha
100 ant to Lm infection, with significantly less body weight loss, less Lm burden in liver and spleen, an
101 rapeutic agent-induced toxicities, including body weight loss, lethality, neurotoxicity, and hematoto
102  not differ between the injection sites, but body weight loss measured 24 h after lateral-i.c.v. inje
103 ypes than the original BACHD mice, including body weight loss, movement deficits, robust striatal neu
104 velop a progressive disease characterized by body weight loss, muscle weakness, brain atrophy, and mo
105 xia models induced a more rapid and profound body weight loss of 15.4%.
106 ble for a subset and suggested median excess body weight loss of 31%-61%.
107 ured by mean body weight loss (BWL) in vivo [body weight loss of 7.7 +/- 4% vs. 18 +/- 5% for Dtxl-NP
108 on than free DOX without causing significant body weight loss or cardiotoxicity.
109 ated suppression of FGF21 was independent of body weight loss or improved hepatic insulin sensitivity
110 rmittent or daily schedule in the absence of body weight loss or Notch-related toxicities.
111  in HD mice accelerated the time of onset of body weight loss (P<0.05) and motor impairments (P<0.05)
112 sion of Fah-positive hepatocytes rescued the body weight loss phenotype.
113                      FL118 induced favorable body-weight-loss profiles (temporary and reversible) and
114              Compared to young mice, delayed body weight-loss recovery and a lag in polycythemic resp
115 ns attenuated cisplatin-induced anorexia and body weight loss significantly.
116 ns attenuated cisplatin-induced anorexia and body weight loss significantly.
117 in supplementation occurred after an initial body weight loss similar to what we previously reported
118 stration from 5 to 11 weeks of age prevented body weight loss, skeletal muscle atrophy, muscle weakne
119 OMP, CpG, and alum showed significantly less body weight loss than the corresponding control mice imm
120 t physiological mechanisms to defend against body weight loss, they have only weak physiological mech
121 unds evaluated in the model, CpG-ODN reduced body weight loss (to <6% on days 3-7 after challenge), r
122 y fourth day) to induce an approximately 15% body weight loss, upon which they were randomized to con
123 4% excess weight loss (9.2% of their initial body weight loss) vs 15.9% excess weight loss (6.0% init
124                         At week 16, the mean body weight loss was 15.4 kg (95% CI, 12.3-18.5 kg; P <
125                                              Body weight loss was doubled in knockout (28%) and wa-1
126             RSV-induced clinical illness and body weight loss were also reduced by BHA treatment, whi
127                          However, anemia and body weight loss were partially prevented, tissue cell a
128 n1a(Pax8/LC1)) that exhibit hyperkalemia and body weight loss when kept on a regular-salt diet, thus
129 eductions in tumor burden with minimal total body weight loss when treated with L-377, 202.
130 o mice, the 11SB17 strain causes only slight body weight loss, whereas 11SB23 produces acute and leth
131 duces dextran sulfate sodium colitis-induced body weight loss, which is accompanied by reduced expres
132 ents with advanced cancers and causes severe body weight loss, with rapid depletion of skeletal muscl
133  as that dose that produces a maximum 12-15% body weight loss within 2 weeks after a single i.v. inje
134  PACAP dose-dependently induced anorexia and body weight loss without affecting locomotor activity.

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