In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

[Q]: This paper examines the effect of one form of chronic stress--household crowding--on psychological well-being, as measured by multiple inverse indicators of psychological well-being. We rely on data from a large (n = 2017) random sample of households in Bangkok, Thailand, a context that has a higher level and broader range of crowding than typically found in the United States. Objective household crowding is found to be detrimental to psychological well-being, controlling for a number of background characteristics. The effect of objective crowding is mediated by subjective crowding, which has strong, consistent and direct detrimental effects on well-being. There is no evidence of a gender effect. Extended family households are not uncommon in Bangkok, but the effects of objective and subjective crowding are similar in both two- and three-generation households, as well as in one- and multiple-couple households. The argument that subjective crowding is an effect, rather than a cause, of psychological well-being is examined and rejected. The findings suggest that crowding, as a chronic source of stress, constitutes a major threat to psychological well-being. Although the empirical analyses are based on data from one city, we frame the issue of household crowding in a historical and theoretical context in order to suggest in which cultural settings household crowding is most likely to have detrimental effects on psychological well-being.
[A]: Chronic stress and psychological well-being: evidence from Thailand on household crowding.

[Q]: The lower respiratory tract of cigarette smokers contains an increased amount of iron that is predominantly sequestered within alveolar macrophages (AM), but is also present in alveolar epithelial fluid. Extracellular ferritin-bound iron could potentially be released by reductants present in cigarette smoke and catalyze generation of highly reactive hydroxyl radicals capable of causing oxidant injury. To determine whether AM are a source of alveolar extracellular ferritin and iron, we assessed in vitro release of iron, ferritin, and transferrin by AM recovered by bronchoalveolar lavage (BAL) of 27 healthy subjects including nine nonsmokers (NS), nine light smokers (LS), and nine heavy smokers (HS). Release of iron in vitro over 20 h was increased in AM recovered from LS (2.24 +/- 0.21 nmol/10(6) AM/20 h, p < 0.001) and HS (3.11 +/- 0.32 nmol/10(6) AM, p < 0.001) compared with NS (1.28 +/- 0.08 nmol/10(6) AM). Release of ferritin in vitro over 20 h was also increased in AM recovered from LS (71 +/- 24 ng/10(6) AM, p < 0.05) and HS (176 +/- 35 ng/10(6), p < 0.001) compared with NS (18 +/- 3 ng/10(6) AM). AM recovered from 12 smokers (8 HS, 4 LS) contained greater than 10 nmol of iron per 10(6) cells. These iron-loaded AM released a greater percentage of cell ferritin stores in vitro over 4 h (8.4% +/- 1.1, p < 0.01) than did AM from NS (3.2% +/- 0.6). Release of lactate dehydrogenase (LDH) over 4 h was substantially less (2.9% +/- 0.3, p < 0.001) than ferritin release.(ABSTRACT TRUNCATED AT 250 WORDS)
[A]: Increased release of ferritin and iron by iron-loaded alveolar macrophages in cigarette smokers.

[Q]: The outer membrane channel TolC is a key component of multidrug efflux and type I secretion transporters in Escherichia coli. Mutational inactivation of TolC renders cells highly susceptible to antibiotics and leads to defects in secretion of protein toxins. Despite impairment of various transport functions, no growth defects were reported in cells lacking TolC. Unexpectedly, we found that the loss of TolC notably impairs cell division and growth in minimal glucose medium. The TolC-dependent phenotype was further exacerbated by the loss of ygiB and ygiC genes expressed in the same operon as tolC and their homologues yjfM and yjfC located elsewhere on the chromosome. Our results show that this growth deficiency is caused by depletion of the critical metabolite NAD(+) and high NADH/NAD(+) ratios. The increased amounts of PspA and decreased rates of NADH oxidation in Delta tolC membranes indicated stress on the membrane and dissipation of a proton motive force. We conclude that inactivation of TolC triggers metabolic shutdown in E. coli cells grown in minimal glucose medium. The Delta tolC phenotype is partially rescued by YgiBC and YjfMC, which have parallel functions independent from TolC.
[A]:
Metabolic shutdown in Escherichia coli cells lacking the outer membrane channel TolC.