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1 he cellular basis of immune dysregulation in bacterial sepsis.
2 ts obtained for neonates suspected of having bacterial sepsis.
3  patients or experimental animals undergoing bacterial sepsis.
4 ected neutropenic rats against gram-negative bacterial sepsis.
5  treat patients with potential gram-negative bacterial sepsis.
6 ing SYK as a potential therapeutic target in bacterial sepsis.
7  complex were translationally altered during bacterial sepsis.
8 e coreceptor, B-Klotho (KLB), is required in bacterial sepsis.
9 and mortality of patients with Gram-negative bacterial sepsis.
10 found hypoferremia which may protect against bacterial sepsis.
11 ggestive of a shared genetic architecture of bacterial sepsis.
12 ent for patients with peritonitis-associated bacterial sepsis.
13 time and ultimately were similar to presumed bacterial sepsis.
14 haviour reversed the increased resistance to bacterial sepsis.
15 rriage, skin and soft tissue infections, and bacterial sepsis.
16 te its prior training and validation only in bacterial sepsis.
17 opathic (27%), similar to our prior study in bacterial sepsis.
18 y of illness in a cohort of 40 patients with bacterial sepsis.
19 rithms to conduct surveillance for viral and bacterial sepsis.
20 testing of immune-inflammatory resilience to bacterial sepsis.
21  was sensitive enough to detect and identify bacterial sepsis.
22 ponse in 113 internal medicine patients with bacterial sepsis.
23 l killing, we determined the role of DJ-1 in bacterial sepsis.
24  system, similar to those reported in severe bacterial sepsis.
25  reveals a potential avenue for treatment in bacterial sepsis.
26 may prove a promising treatment strategy for bacterial sepsis.
27 tritional supplementation was detrimental in bacterial sepsis.
28  cause of the high mortality associated with bacterial sepsis.
29 ti-organ failure contributes to mortality in bacterial sepsis.
30 ere unable to mount trained immunity against bacterial sepsis.
31  inflammation and greater than 2.0 ng/ml for bacterial sepsis.
32 moniae are a frequent cause of Gram-negative bacterial sepsis.
33  critical role in the pathogenesis of severe bacterial sepsis.
34 is a key event in neonatal susceptibility to bacterial sepsis.
35  produce IL-10 is a risk factor for neonatal bacterial sepsis.
36 ection and died from fulminant gram-positive bacterial sepsis.
37 ng cause of human soft tissue infections and bacterial sepsis.
38 tective early innate immune responses during bacterial sepsis.
39 s in the early innate immune response during bacterial sepsis.
40 he cytokine storm caused by TLR agonists and bacterial sepsis.
41 identify patients at high risk of developing bacterial sepsis.
42 vival benefit in both experimental models of bacterial sepsis.
43 , compromised wound integrity, and increased bacterial sepsis.
44 id bacterial identification in patients with bacterial sepsis.
45  endotoxin but has not been evaluated during bacterial sepsis.
46 ial cell death associated with Gram-negative bacterial sepsis.
47 een shown to be essential in protection from bacterial sepsis.
48 everity of necrotizing enterocolitis, and/or bacterial sepsis.
49 d that this reactivation can be triggered by bacterial sepsis.
50 a bacterial pathogen and predisposes mice to bacterial sepsis.
51 onents that function coordinately to prevent bacterial sepsis.
52           Neonates are at increased risk for bacterial sepsis.
53 t, if not all, of the events associated with bacterial sepsis.
54 ol patients and patients dying from systemic bacterial sepsis.
55 by macrophages which occurs in Gram-negative bacterial sepsis.
56  lung, and resembles the clinical picture of bacterial sepsis.
57  involvement in the inflammatory response to bacterial sepsis.
58 TNFalpha results in many of the hallmarks of bacterial sepsis.
59  of the association between this variant and bacterial sepsis.
60 mortality was higher (68%) for patients with bacterial sepsis.
61            One patient died of pneumonia and bacterial sepsis 1 year after therapy discontinuation an
62             By contrast, in a mouse model of bacterial sepsis after intraperitoneal inoculation of GA
63                          Transfusion-related bacterial sepsis, although infrequent, is a serious and
64 d hypotension (both resolved), and 1 died of bacterial sepsis and acute respiratory distress syndrome
65 uent and associated with the cooccurrence of bacterial sepsis and clinically significant pneumothorax
66 ociated with an increased risk of nosocomial bacterial sepsis and coagulase negative staphylococcal i
67 s were also detected in patient cohorts with bacterial sepsis and coronavirus disease.
68  developed progressive pulmonary failure and bacterial sepsis and died.
69 dmission to the intensive care unit, notably bacterial sepsis and enterocolitis.
70 nclude that dantrolene decreases survival in bacterial sepsis and has no effect on survival in endoto
71 al. investigate the renal translatome during bacterial sepsis and identify the global shutdown of ren
72                  Despite extensive research, bacterial sepsis and its associated systemic inflammatio
73 tion induced by endotoxin is a key factor in bacterial sepsis and many other human diseases.
74 e dysfunction and prognosis in patients with bacterial sepsis and may prove to be useful prognostic m
75  Streptococcus (GBS) is the leading cause of bacterial sepsis and meningitis among neonates.
76 ptococcus agalactiae is the leading cause of bacterial sepsis and meningitis among newborns.
77  B Streptococcus (GBS) is a leading cause of bacterial sepsis and meningitis in newborns.
78 scherichia coli is a major cause of neonatal bacterial sepsis and meningitis.
79 g, including increased incidence of neonatal bacterial sepsis and necrotizing enterocolitis.
80                There was a smaller impact on bacterial sepsis and pneumonia, and an increase observed
81 or interaction can drive the pathogenesis of bacterial sepsis and provide molecular insights into the
82                                              Bacterial sepsis and severe COVID-19 share similar clini
83  in coordinating complex immune responses to bacterial sepsis and suggests that future strategies for
84 theless, the exact status of NK cells during bacterial sepsis and their capacity directly to respond
85 D14(+) monocyte state, MS1, in patients with bacterial sepsis and validated expansion of this cell su
86  systemic inflammatory response syndromes in bacterial sepsis and viral haemorrhagic fevers, and anti
87  including malaria, dengue fever, influenza, bacterial sepsis, and severe acute respiratory syndrome
88 hen using reverse cancer-then-sepsis models, bacterial sepsis applied to mice with cancer conversely
89 he inhibition of TNF-alpha production during bacterial sepsis are critical in attenuating adverse hos
90 ren and, in particular, the distinction from bacterial sepsis are imprecise.
91                        Immunosuppression and bacterial sepsis are thought to stimulate reactivation o
92     Studies that define natural responses to bacterial sepsis assumed new relevance after the lethal
93                      Males are more prone to bacterial sepsis, but some studies suggest females may h
94 Our recent work has shown that polymicrobial bacterial sepsis can trigger reactivation of latent muri
95                                       In the bacterial sepsis cases with a later cognitive assessment
96                                              Bacterial sepsis caused significant maldistribution of i
97                                Gram-negative bacterial sepsis commonly causes organ dysfunction and d
98 d cohort of previously healthy children with bacterial sepsis detected variants of uncertain signific
99 efore therapy, another died with concomitant bacterial sepsis during induction therapy.
100 udy was to test whether a previously defined bacterial sepsis endotypes classifier recapitulates the
101 BMI; kg/m2) and risk of early-onset neonatal bacterial sepsis (EOS).
102                                       In the bacterial sepsis group, GFAP was elevated in cases diagn
103 tween cytokine gene polymorphisms and severe bacterial sepsis, have reached conflicting conclusions.
104 nduction course complicated by Gram-negative bacterial sepsis, her counts recovered by day 32, and bo
105 biased by unmeasured confounding from severe bacterial sepsis, immunity, and duration of illness.
106            Using a well-established model of bacterial sepsis in Drosophila melanogaster, we found th
107 dotoxin in the pathogenesis of Gram-negative bacterial sepsis in preclinical investigations and numer
108 GBS) infections are the most common cause of bacterial sepsis in the immediate newborn period.
109  The current standard of care for evaluating bacterial sepsis in the newborn is performing blood cult
110 the role of the endothelial selectins during bacterial sepsis in vivo, Streptococcus pneumoniae (1-10
111 or were admitted to a PICU with a COSBI (ie, bacterial sepsis, including meningitis, purpura fulminan
112                                              Bacterial sepsis involves a complex interaction between
113 gta1 function in mice enhances resistance to bacterial sepsis, irrespectively of a-Gal-specific immun
114                                              Bacterial sepsis is a major cause of neonatal morbidity
115                       Transfusion-associated bacterial sepsis is a persistent problem in transfusion
116                                              Bacterial sepsis is a serious life-threatening condition
117           Thus, the benefit of B-1a cells in bacterial sepsis is mediated by CREB and the identificat
118      An important site of cellular damage in bacterial sepsis is mitochondrial DNA (mtDNA), which we
119 to transfusion-related acute lung injury and bacterial sepsis is not suspected, the correct diagnosis
120                The morbidity associated with bacterial sepsis is the result of host immune responses
121                          Under conditions of bacterial sepsis, large amounts of NO are produced, caus
122                                       Severe bacterial sepsis leads to a proinflammatory condition th
123                                              Bacterial sepsis leads to heterogenous populations of ci
124 y immune responses and oxidant stress during bacterial sepsis {lsqb;i.e., cecal ligation and puncture
125 feature of several disease states, including bacterial sepsis, malaria, and sickle cell disease.
126 hypothesize that MCMV reactivation following bacterial sepsis may be caused by inflammatory mediators
127 odels have provided clues to whether and how bacterial sepsis may impact malignant tumor growth.
128             Procalcitonin (PCT), a marker of bacterial sepsis, may also act as a mediator of the infl
129                   Thus, during Gram-negative bacterial sepsis Mkp-1 not only plays a critical role in
130 , a dopamine agonist, mitigates lethality in bacterial sepsis mouse models.
131 ts died in complete remission as a result of bacterial sepsis (n = 2), chronic GVHD and fungal infect
132 uncomplicated malaria (n = 91), or suspected bacterial sepsis (n = 56), as well as healthy participan
133 idered possibly related to momelotinib], and bacterial sepsis [n=1]); and four patients (8%) receivin
134      Transient neutropenia/thrombocytopenia, bacterial sepsis, neurotoxicity, stomatitis, and hospita
135 rate that the detrimental immune response to bacterial sepsis occurs via TLR9 stimulation.
136                                       Severe bacterial sepsis often leads to a systemic procoagulant
137      We found that plasma from patients with bacterial sepsis or COVID-19 induced myelopoiesis in HSP
138 g enterocolitis, bronchopulmonary dysplasia, bacterial sepsis, or administration of inotrope or vasop
139 gs contributes to poor health outcomes among bacterial sepsis patients and the spread of antimicrobia
140 reptococcus agalactiae, the leading cause of bacterial sepsis, pneumonia, and meningitis in neonates
141                             In Gram-negative bacterial sepsis, production of excess pro-inflammatory
142 apy or as a single agent in animal models of bacterial sepsis, rats were implanted intraperitoneally
143 virus infection but - similar to findings in bacterial sepsis - reduction of inflammation, rather tha
144  The roles of miRNAs in host defense against bacterial sepsis remain unclear.
145 bal progress in reducing neonatal mortality, bacterial sepsis remains a major cause of neonatal death
146        Identifying patients at high risk for bacterial sepsis remains an important clinical challenge
147 hreatening infectious event of polymicrobial bacterial sepsis reported 2 months after the final chemo
148 he SVRI was lower in patients with suspected bacterial sepsis than in those with severe malaria, afte
149 tensive research into the mechanisms driving bacterial sepsis, the target molecules controlling vascu
150 enectomy are considered at increased risk of bacterial sepsis, they typically receive vaccination, ed
151 f commonly encountered diseases ranging from bacterial sepsis to sterile syndromes such as major trau
152 arly antibiotics are considered critical for bacterial sepsis treatment, although the benefit of this
153                                              Bacterial sepsis triggers robust activation of the compl
154 ignificant amounts of these cytokines during bacterial sepsis via Toll-like receptor 4 (TLR4)/MyD88 s
155 entially life-threatening disorders, such as bacterial sepsis, viral infection, and necrotizing enter
156                 Crude mortality for presumed bacterial sepsis was 4451 of 30 604 patients (14.5%) and
157                                     Presumed bacterial sepsis was defined by modified US Centers for
158 tion in 10 premature infants with documented bacterial sepsis was then followed for 2 to 12 weeks aft
159                       Using a mouse model of bacterial sepsis, we found that the numbers of B-1a cell
160            Given the fitness cost imposed by bacterial sepsis, we infer that the observed reduction i
161 ality for SARS-CoV-2-associated and presumed bacterial sepsis were assessed using negative binomial a
162                            Similarities with bacterial sepsis were observed; however, few studies spe
163  have suggested that empirical treatment for bacterial sepsis with antianaerobic antibiotics (eg, pip
164 influenza, other seasonal coronaviruses, and bacterial sepsis), with paradoxical down-regulation of s
165 sis, and 30 604 patients (7.1%) had presumed bacterial sepsis without SARS-CoV-2 infection.
166 kdrop, of the 8 million deaths per year from bacterial sepsis worldwide, over 3 million are from trea

 
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