Circadian rhythm abnormalities in the acute phase of cerebral infarction correlate with poor prognosis in the chronic phase

Background: Late recovery in patients following prolonged coma from carbon monoxide poisoning have been reported, but the probability is unclear. The purpose of this research was to assess the prognosis of patients in prolonged coma after severe carbon monoxide poisoning and related clinical and imaging features. Methods: There were 13 patients who had been in a state of coma for >7 days after acute carbon monoxide poisoning in the retrospective observational study, and demographic data, clinical data, laboratory data, complications, and image data were collected. Outcome was assessed by means of the Glasgow outcome scale after 1 year. The relationship between complications and imaging manifestations and prognosis was also analyzed. Results: One year after severe carbon monoxide poisoning, two patients (15.4%) had died (GOS 1), nine (69.2%) were in a persistent vegetative state (GOS 2), one (7.7%) was moderately disabled (GOS 4), and one (7.7%) achieved a good recovery (GOS 5) with minimal disability. Conclusions: Most patients with prolonged coma after severe carbon monoxide poisoning had a poor prognosis, although the younger patients had a better prognosis. Respiratory failure, hypotension and renal failure during the course of the disease were associated with a poor prognosis. The prognosis of patients with injuries in two sites in early CT was poor. Multiple lesions (≥3) and extensive white matter damage (Fazekas grade (PVH or DWMH) = 3) on MRI of chronic phase were also associated with a poor prognosis.

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Evaluation of Factors Associated With Elevated Levels of Platelet-Derived Microparticles in the Acute Phase of Cerebral Infarction

Clinical and Applied Thrombosis/Hemostasis ◽

10.1177/1076029609338047 ◽

2009 ◽

Vol 16 (1) ◽

pp. 26-32 ◽

Cited By ~ 40

Author(s):

Nagato Kuriyama ◽

Yoshinari Nagakane ◽

Akiko Hosomi ◽

Tomoyuki Ohara ◽

Takashi Kasai ◽

...

Keyword(s):

Cerebral Infarction ◽

Acute Phase ◽

Control Level ◽

Intima Media Thickness ◽

Vascular Lesions ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Large Artery ◽

Vessel Occlusion ◽

Atherosclerotic Lesions

Background: Platelet-derived microparticles (PDMPs) have attracted attention as blood coagulation-promoting, endothelial cell-activating factors. The objective of this study was to determine the parameters associated with elevated PDMP levels and examine their relationship with atherosclerotic lesions of main intracranial and extracranial arteries. Participants and Methods: Participants included a control group (C) of 61 patients with no apparent cerebral vascular lesions and 110 patients with acute-phase cerebral infarction, consisting of a small-vessel occlusion group (S) of 34 patients, a large-artery atherosclerosis group (L) of 41 patients, a cardioembolism group (CE) of 20 patients, and a stroke of undetermined etiology group (U) of 15 patients. Platelet-derived microparticle levels were measured using enzyme-linked immunosorbent assay (ELISA) at the time of admission, and the patients were reclassified into group CP (control level PDMPs), consisting of 70 patients with control PDMP levels, and group HP (high PDMPs), consisting of 40 patients with elevated PDMP levels. All patients underwent cranial magnetic resonance (MR) and carotid ultrasound examinations. Results: Platelet-derived microparticle levels were significantly higher in groups S and L than in group C (P < .01). Concomitant intima-media thickness (IMT; odds ratio [OR] = 1.29, P < .05) and concomitant intracranial stenosis (OR = 3.95, P < .01) were significantly correlated with elevated PDMP levels. Fibrinogen and high-sensitivity CRP levels were significantly higher in group HP than in group CP. Conclusion: Alterations in PDMP levels correlated with the presence of atherothrombotic lesions, and PDMP levels are expected to be useful as a clinical indicator, reflecting the presence of intracranial atherosclerotic lesions in the acute phase of cerebral infarction.

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Abstract 116: Detrimental Role of Toll-Like Receptor 4 in Cardiovirus-Induced Myocarditis

Circulation Research ◽

10.1161/res.111.suppl_1.a116 ◽

2012 ◽

Vol 111 (suppl_1) ◽

Author(s):

Fumitaka Sato ◽

Seiichi Omura ◽

Nicholas E Martinez ◽

Eiichiro Kawai ◽

Ganta V Chaitanya ◽

...

Keyword(s):

Immune Responses ◽

Acute Phase ◽

Viral Entry ◽

Viral Myocarditis ◽

Chronic Phase ◽

Enzyme Linked Immunosorbent Assay ◽

Tlr4 Ligand ◽

Ifn Γ ◽

Deficient Mice

Picornavirus infections have been known as a leading cause of viral myocarditis in humans. Theiler’s murine encephalomyelitis virus (TMEV) belongs to the genus Cardiovirus, the family Picornaviridae and was reported to cause inflammation in the heart in one manuscript, while its pathomechanism is unclear. In viral myocarditis, viral replication in the heart and/or immune responses against virus as well as heart-antigen (autoimmunity) can contribute to the pathogenesis. Toll-like receptors (TLRs) are pattern recognition receptors (PRRs) that are important for recognizing pathogens as well as triggering innate immunity. Among TLRs, TLR4 has been demonstrated to play important roles in virus-mediated pathology: 1) TLR4 can contribute to viral entry in some viruses, 2) TLR4 may mediate tissue damage by anti-virus immune responses (immunopathology), 3) high levels of TLR4 expression were observed in the heart of patients with dilated cardiomyopathy following acute viral myocarditis, and 4) some viruses can bind to lipopolysaccharide (LPS), which is a TLR4 ligand. To determine the role of TLR4 in TMEV-induced myocarditis, we infected male C3H/HeJ (TLR4-deficient) and C3H/HeNtac (control TLR4+) mice with the DA strain of TMEV. We harvested the hearts and spleens on days 6 and 7 (acute phase) or days 63 and 64 (chronic phase) post-infection. Cardiac pathology was evaluated by hematoxylin and eosin staining and production of pro-inflammatory cytokines, interleukin (IL)-17A and interferon (IFN)-γ, from spleen cells was measured by an enzyme-linked immunosorbent assay (ELISA). In both mice, mild myocarditis was observed during the acute phase of TMEV infection. During the chronic phase, both mice developed severe pathology in the heart, including basophilic degeneration and calcification. However, the incidence of myocarditis was higher in control mice than TLR4-deficient mice. IL-17A and IFN-γ production was higher in control mice than in TLR4-deficient mice (control vs. TLR4-deficient mice, acute phase: IL-17A, 196 vs. 146 pg/ml; IFN-γ, 72 vs. 39 ng/ml; chronic phase: IL-17A, 290 vs. 229 pg/ml; IFN- γ, 142 vs. 88 ng/ml). These results suggest that TLR4 may be detrimental in TMEV-induced myocarditis by increasing pro-inflammatory cytokine production.

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Cytokines and T-Lymphocute count in patients in the acute and chronic phases of Bartonella bacilliformis infection in an endemic area in peru: a pilot study

Revista do Instituto de Medicina Tropical de São Paulo ◽

10.1590/s0036-46652011000300006 ◽

2011 ◽

Vol 53 (3) ◽

pp. 149-154 ◽

Cited By ~ 6

Author(s):

Erick Huarcaya ◽

Ivan Best ◽

Juan Rodriguez-Tafur ◽

Ciro Maguiña ◽

Nelson Solórzano ◽

...

Keyword(s):

Pilot Study ◽

Acute Phase ◽

Chronic Phase ◽

Peripheral Tolerance ◽

Bartonella Bacilliformis ◽

Cross Sectional ◽

Bacillary Angiomatosis ◽

Cd8 T Lymphocyte ◽

Ifn Γ ◽

Anti Inflammatory Cytokine

Human Bartonellosis has an acute phase characterized by fever and hemolytic anemia, and a chronic phase with bacillary angiomatosis-like lesions. This cross-sectional pilot study evaluated the immunology patterns using pre- and post-treatment samples in patients with Human Bartonellosis. Patients between five and 60 years of age, from endemic areas in Peru, in the acute or chronic phases were included. In patients in the acute phase of Bartonellosis a state of immune peripheral tolerance should be established for persistence of the infection. Our findings were that elevation of the anti-inflammatory cytokine IL-10 and numeric abnormalities of CD4+ and CD8+ T-Lymphocyte counts correlated significantly with an unfavorable immune state. During the chronic phase, the elevated levels of IFN-γ and IL-4 observed in our series correlated with previous findings of endothelial invasion of B. henselae in animal models.

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Role of kallikrein-kinin system in pathogenesis of bacterial cell wall-induced inflammation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1991.260.2.g213 ◽

1991 ◽

Vol 260 (2) ◽

pp. G213-G219 ◽

Cited By ~ 4

Author(s):

R. A. DeLa Cadena ◽

K. J. Laskin ◽

R. A. Pixley ◽

R. B. Sartor ◽

J. H. Schwab ◽

...

Keyword(s):

Cell Wall ◽

Acute Phase ◽

Bacterial Cell ◽

Chronic Phase ◽

Bacterial Cell Wall ◽

Kinin System ◽

Kallikrein Kinin System ◽

Bacterial Products

The plasma kallikrein-kinin system is activated in Gram-negative sepsis and typhoid fever, two diseases in which bacterial products have been shown to initiate inflammation. Because a single intraperitoneal injection of bacterial cell wall peptidoglycan-polysaccharide polymers from group A steptococci (PG-APS) into a Lewis rat produces a syndrome of relapsing polyarthritis and anemia, we investigated changes in the role of the kallikrein-kinin system in this model of inflammation. Coagulation studies after injection of PG-APS revealed an immediate and persistent decrease in prekallikrein levels. High-molecular-weight kininogen levels decreased significantly during the acute phase and correlated with the severity of arthritis. Factor XI levels were decreased only during the acute phase. Antithrombin III levels remained unchanged, indicating that neither decreased hepatic synthesis nor disseminated intravascular coagulation caused the decreased plasma contact factors. Plasma T-kininogen (an acute phase protein) was significantly elevated during the chronic phase. PG-APS failed to activate the contact system in vitro. Thus the kallikrein-kinin system plays an important role in this experimental model of inflammation, suggesting that activation of this system may play a role in the pathogenesis of inflammatory bowel disease and rheumatoid arthritis in which bacterial products might be etiologically important.

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