Dark gas in the interstellar medium (ISM) is believed to not be detectable either in CO or H i radio emission, but it is detectable by other means including γ rays, dust emission, and extinction traced outside the Galactic plane at |b| > 5• . In these analyses, the 21 cm H i emission is usually assumed to be completely optically thin. We have reanalyzed the H i emission from the whole sky at |b| > 15• by considering temperature stratification in the ISM inferred from the Planck/IRAS analysis of the dust properties. The results indicate that the H i emission is saturated with an optical depth ranging from 0.5 to 3 for 85% of the local H i gas. This optically thick H i is characterized by spin temperature in the range 10 K-60 K, significantly lower than previously postulated in the literature, whereas such low temperature is consistent with emission/absorption measurements of the cool H i toward radio continuum sources. The distribution and the column density of the H i are consistent with those of the dark gas suggested by γ rays, and it is possible that the dark gas in the Galaxy is dominated by optically thick cold H i gas. This result implies that the average density of H i is 2-2.5 times higher than that derived on the optically thin assumption in the local ISM.

We present an analysis of the H i and CO gas in conjunction with the Planck/IRAS submillimeter/far-infrared dust properties toward the most outstanding high latitude clouds MBM 53, 54, The CO emission, dust opacity at 353 GHz (τ 353 ), and dust temperature (T d ) show generally good spatial correspondence. On the other hand, the correspondence between the H i emission and the dust properties is less clear than in CO. The integrated H i intensity W H i and τ 353 show a large scatter with a correlation coefficient of ∼0.6 for a T d range from 16 K to 22 K. We find, however, that W H i and τ 353 show better correlation for smaller ranges of T d every 0.5 K, generally with a correlation coefficient of 0.7-0.9. We set up a hypothesis that the H i gas associated with the highest T d 21.5 K is optically thin, whereas the H i emission is generally optically thick for T d lower than 21.5 K. We have determined a relationship for the optically thin H i gas between atomic hydrogen column density and τ 353 , N H i (cm −2 ) = (1.5 × 10 26 ) • τ 353 , under the assumption that the dust properties are uniform and we have applied this to estimate N H i from τ 353 for the whole cloud. N H i was then used to solve for T s and τ H i over the region. The result shows that the H i is dominated by optically thick gas having a low spin temperature of 20-40 K and a density of 40-160 cm −3 . The H i envelope has a total mass of ∼1.2 × 10 4 M , an order of magnitude larger than that of the CO clouds. The H i envelope properties derived by this method do not rule out a mixture of H i and H 2 in the dark gas, but we present indirect evidence that most of the gas mass is in the atomic state.

Background The signaling mechanisms that regulate the recruitment of bone marrow (BM)-derived cells to the injured heart are not well known. Notch receptors mediate binary cell fate determination and may regulate the function of BM-derived cells. However, it is not known whether Notch1 signaling in BM-derived cells mediates cardiac repair following myocardial injury. Methods and Results Mice with postnatal cardiac-specific deletion of Notch1 exhibit similar infarct size and heart function following ischemic injury as control mice. However, mice with global hemizygous deletion of Notch1 (N1+/−) developed larger infarct size and worsening heart function. When the BM of N1+/− mice were transplanted into wild-type (WT) mice, infarct size and heart function were worsened and neovascularization in the infarct border area was reduced compared to WT mice transplanted with WT BM. In contrast, transplantation of WT BM into N1+/− mice lessened the myocardial injury observed in N1+/− mice. Indeed, hemizygous deletion of Notch1 in BM-derived cells leads to decreased recruitment, proliferation, and survival of mesenchymal stem cells (MSC). Compared to WT MSC, injection of N1+/− MSC into the infarcted heart leads to increased myocardial injury, whereas injection of MSC overexpressing Notch intracellular domain leads to decreased infarct size and improved cardiac function. Conclusions These findings indicate that Notch1 signaling in BM-derived cells is critical for cardiac repair, and suggest that strategies that increase Notch1 signaling in BM-derived MSC could have therapeutic benefits in patients with ischemic heart disease.