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In the article entitled “The Early Growth Response Gene Egr2 (Alias Krox20) Is a Novel Transcriptional Target of Transforming Growth Factor-β that Is Up-Regulated in Systemic Sclerosis and Mediates Profibrotic Responses” (Volume 178, pages 2077–2090 of the May 2011 issue of The American Journal of Pathology), the third author's name was listed incorrectly. The correct name is Swati Bhattacharyya.
In the article entitled “AP-1–Mediated M2 Macrophage Infiltration Underlies IL-1β–but Not VEGF-A–Induced Lymph- and Angiogenesis” (Volume 178, pages 1913–1921 of the April 2011 issue), HLECs were defined incorrectly. The correct expansion for HLECs is human lymphatic endothelial cells. This error occurred in the print article only; the online (HTML and PDF) versions of this article appear correctly.
In the article entitled “NF-κB Inhibition Protects against Tumor-Induced Cardiac Atrophy in Vivo” (Volume 178, pages 1059–1068 of the March 2011 issue), the fourth author's name was listed incorrectly. The correct name is Luge Li.
In the article entitled “Bone Marrow-Derived Progenitor Cells Do Not Contribute to Podocyte Turnover in the Puromycin Aminoglycoside and Renal Ablation Models in Rats” (Volume 178, pages 494–499 of the February 2011 issue), the fourth author's surname was listed incorrectly. The correct surname name is Agustian. In addition, the author affiliation for Jan U. Becker contained errors. The correct author affiliation is Institute of Pathology, Hannover Medical School, Hannover, Germany.
In the article entitled “CD4+ T Cells Sensitized by Vascular Smooth Muscle Induce Vasculitis, and Interferon Gamma Is Critical for the Initiation of Vascular Pathology” (Volume 177, pages 3215–3223 of the December 2010 issue), panel B was inadvertently duplicated as panel C in Figure 1.
Figure 1Vasculitis incidence after transfer of SMC-sensitized lymphocytes is similar in wt and in B cell-deficient (JhD) mice. A–C. Vasculitis incidence scored on H&E sections of lung (each diamond depicts a mouse; horizontal bar is average). Control indicates noninjected mice. A: Adoptive transfer of wt BALB/c lymphocytes previously sensitized by co-culture (wt mL) with syngeneic SMC to wt BALB/c recipient mice; n = 11, P = 0.003 (four experiments). SM are mice injected with primary smooth muscle cultures (106 cells/mouse). Ly are mice injected with isolated naïve spleen lymphocytes (5 × 106 cells/mouse). B: Transfer of sensitized wt BALB/c lymphocytes to RAG-2-deficient mice; n = 7, P = 0.006 (three experiments). C: Transfer of sensitized JhD lymphocytes to JhD mice; n = 12 mice, P = 0.00002 (seven experiments). D: H&E staining of 4-μm paraffin section of lung 7 days after vasculitis induction in JhD mouse, showing blood vessels with granulomatous- like inflammation and infiltration of leukocytes with destruction of vessel wall. L indicates vessel lumen. Scale bar = 20 μm. Original magnification, ×400.
In the article entitled “β-Cell Loss and β-Cell Apoptosis in Human Type 2 Diabetes Are Related to Islet Amyloid Deposition” (Volume 178, pages 2632–2640 of the June 2011 issue), Table 2 contained errors in the definition of NA. The corrected Table 2, which correctly distinguishes between parameters with no data (ND) and those with data not applicable (NA), is shown below.
Table 2Clinicodemographic Characteristics of Individual Subjects
Age (years)/Sex
BMI (kg/m2)
Blood glucose (mmol/L)
Diabetes duration (years)
Diabetes medication
Cause of death
Diabetes group
62/F
30.9
8.53
ND
glyburide, insulin
pulmonary embolism
78/F
28.3
7.67
2
diet
GI hemorrhage
59/M
32.6
7.90
8
insulin
cardiac arrest
59/M
38.4
7.39
ND
insulin
leukemia
69/F
21.2
9.50
ND
metformin
malignancy
81/M
31.4
5.63
ND
glyburide, metformin
aortic dissection
68/M
27.2
11.42
ND
metformin
GI hemorrhage
52/M
26.3
9.07
ND
none
cardiopulmonary failure
61/M
29.7
6.85
14
insulin
respiratory failure
71/F
21.3
9.39
10
glyburide
coronary artery disease
51/F
41.2
11.11
ND
glyburide, insulin
malignancy
62/M
35.9
7.46
ND
insulin in TPN
abdominal hemorrhage
80/F
29.1
8.89
20
acetohexamide,insulin
coronary artery disease
61/M
36.3
8.92
12
diet, glipizide
sepsis
58/M
34.4
8.29
ND
insulin
coronary artery disease
71/M
37.5
6.50
27
insulin
postoperative complications
74/F
36.0
13.17
ND
unknown
aspiration pneumonia
37/M
39.7
7.69
3
unknown
cardiomyopathy
71/F
21.6
ND
12
glyburide
coronary artery disease
70/F
32.8
10.33
ND
oral hypoglycemic, unspecified
abdominal hemorrhage
69/M
21.3
7.06
10
glyburide
coronary artery disease
64/M
22.5
6.47
ND
insulin
sepsis
40/M
41.2
10.17
ND
diet, metformin
postoperative complications
28/M
35.8
7.67
1
metformin
myelodysplastic syndrome
82/M
25.6
17.06
ND
glipizide
sepsis
63/F
38.8
10.50
12
insulin
malignancy
63/M
26.5
7.11
ND
diet
malignancy
68/M
25.0
NA
ND
diet
cardiac arrest
82/M
19.0
7.50
2
diet
sepsis
Control group
87/F
33.0
5.14
NA
NA
valvular heart disease
62/M
23.4
5.58
NA
NA
malignancy
34/M
17.5
5.14
NA
NA
malignancy
63/F
18.7
5.23
NA
NA
malignancy
54/F
49.3
5.94
NA
NA
postoperative complications
82/F
40.9
4.72
NA
NA
perforated duodenal ulcer
61/F
24.3
5.58
NA
NA
abdominal hemorrhage
65/M
20.5
6.31
NA
NA
stroke
21/F
32.2
4.63
NA
NA
pulmonary embolism
64/M
18.7
6.47
NA
NA
malignancy
65/F
40.1
4.79
NA
NA
pulmonary veno-occlusive disease
67/M
24.1
5.12
NA
NA
malignancy
52/M
24.1
5.26
NA
NA
malignancy
77/F
26.3
6.08
NA
NA
sepsis
34/M
28.8
5.44
NA
NA
malignancy
68/F
18.6
4.86
NA
NA
malignancy
89/M
17.8
6.07
NA
NA
malignancy
57/F
19.2
5.87
NA
NA
malignancy
75/M
22.6
4.94
NA
NA
pneumonia
66/F
25.7
5.43
NA
NA
respiratory failure
50/M
28.0
5.50
NA
NA
cardiac failure
45/M
29.8
4.53
NA
NA
cardiac arrest
83/F
19.8
5.15
NA
NA
cardiac arrest
44/F
18.0
5.18
NA
NA
meningitis
20/F
22.8
4.60
NA
NA
pulmonary hypertension
42/F
34.0
5.39
NA
NA
sepsis
88/F
29.2
6.16
NA
NA
respiratory failure
81/M
27.1
5.56
NA
NA
respiratory failure
58/M
24.9
5.44
NA
NA
stroke
19/M
32.7
6.22
NA
NA
malignancy
46/F
28.1
6.47
NA
NA
sepsis
78/F
42.4
3.78
NA
NA
abdominal hemorrhage
75/M
20.9
5.83
NA
NA
malignancy
72/M
34.9
5.56
NA
NA
multiple myeloma
82/M
32.5
6.06
NA
NA
sepsis
94/M
21.9
5.22
NA
NA
sepsis
68/M
24.0
5.17
NA
NA
respiratory failure
60/M
15.9
6.94
NA
NA
respiratory failure
57/M
22.8
5.56
NA
NA
cardiac arrest
F, female; GI, gastrointestinal; M, male; ND, no data; NA, not applicable; TPN, total parenteral nutrition.
A key event in the progression of glomerular disease is podocyte loss that leads to focal and segmental glomerulosclerosis (FSGS). Because adult podocytes are postmitotic cells, podocyte replacement by bone marrow–derived progenitors could prevent podocytopenia and FSGS. This study uses double immunofluorescence for Wilms' tumor-1 and enhanced green fluorescent protein (eGFP) to examine whether an eGFP-positive bone marrow transplant can replace podocytes under normal circumstances and in 3 different rat models of FSGS: puromycin aminoglycoside nephropathy, subtotal nephrectomy, and uninephrectomy.
Cancer cachexia is a severe wasting syndrome characterized by the progressive loss of lean body mass and systemic inflammation. It occurs in approximately 80% of patients with advanced malignancy and is the cause of 20% to 30% of all cancer-related deaths. The mechanism by which striated muscle loss occurs is the tumor release of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. These cytokines interact with their cognate receptors on muscle cells to enhance NF-κB signaling, which then mediates muscle loss and significant cardiac dysfunction.
Although the early growth response-2 (Egr-2, alias Krox20) protein shows structural and functional similarities to Egr-1, these two related early-immediate transcription factors are nonredundant. Egr-2 plays essential roles in peripheral nerve myelination, adipogenesis, and immune tolerance; however, its regulation and role in tissue repair and fibrosis remain poorly understood. We show herein that transforming growth factor (TGF)-β induced a Smad3-dependent sustained stimulation of Egr2 gene expression in normal fibroblasts.
Vascular adhesion protein-1 (VAP-1) contributes to inflammatory and angiogenic diseases, including cancer and age-related macular degeneration. It is expressed in blood vessels and contributes to inflammatory leukocyte recruitment. The cytokines IL-1β and vascular endothelial growth factor A (VEGF-A) modulate angiogenesis, lymphangiogenesis, and leukocyte infiltration. The lymphatic endothelium expresses intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, which facilitate leukocyte transmigration into the lymphatic vessels.
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