Job Security and Labour Market Flexibility

This paper discusses the desirability of government-legislated job security. Job security may be beneficial to employed workers, but it can also impose a cost on unemployed workers by lowering labour market turnover and thereby increasing the average duration of unemployment spells. This externality can lead to self-reinforcing behaviour between workers at different firms: If most workers in the economy have job security then turnover will be low and the duration of unemployment following a layoff is likely to be high. As a result, other workers will also desire job security. Even in the absence of legislation, therefore, the externality may result in more job security being provided than is socially desirable.

Employment Adjustment versus Hours Adjustment: Is Job Security Desirable?

Firms can adjust to shocks by laying off and hiring workers or by adjusting the hours worked by each worker. Adjustment of hours provides job security for employed workers. Adjustment of employment generates higher labor market turnover and, thus, better job prospects for the unemployed. Since high turnover lowers the expected cost of being laid off by reducing the expected duration of unemployment, there is a strategic complementarity between firms in the provision of job security. This gives the possibility of multiple equilibria with different amounts of turnover. Copyright 1995 by The London School of Economics and Political Science.

Is There Compelling Evidence against Increasing Returns to Matching in the Labour Market?

Matching models of the labour market have been of particular interest in macroeconomics where the notion of 'thick-market' externalities can lead to multiple equilibria. This has led to some recent interest in constructing empirical estimates of labor-market matching functions. This paper argues that existing estimates do not provide compelling evidence against the hypothesis of increasing returns in matching. The assumption made in several studies, that the relevant pool of job searchers is proportional to the stock of unemployment, is a potentially important source of downward bias in returns-to-scale estimates. We show the source of this bias theoretically and illustrate its magnitude by estimating Canadian aggregate and regional labour-market matching functions over the period 1978-88. This evidence suggests significant increasing returns to labor-market matching.

Evidence that encoded shRNA did not influence HCT-116 clonal cell growth <i>in vivo</i>.

<p>(A) Distribution of the 4,109 unique barcodes retrieved most abundantly from the three xenograft tumors (marked with red vertical lines) across the entire shRNA population distribution in the shRNA library. (B) Detection of a large fraction of the most abundant barcodes from the three xenograft tumors (marked in red) in the shRNA population most toxic to HCT-116 upon Doxycycline induction <i>in vitro</i> for 15 days (measured by a negative Log2 ratio of mean read counts for individual shRNA at Day 15 following Doxycycline to mean read counts at Day 0).</p

Barcode recovery rate in Athymic Nude xenograft experiments.

<p>Barcode recovery rate in Athymic Nude xenograft experiments.</p

Evidence for clonal dominance: comparison of the distributions of HCT-116 barcoded clones and cells by clone size category <i>in vitro</i> and <i>in vivo</i><b>.</b>

<p>For each graph, the number of independent clones (blue bars) or the total aggregate number of cells (orange bars) is plotted for each clone size category across the X axis. (A) Distribution of HCT-116 barcodes <i>in vitro</i>: 80% of the barcodes (clones) were identified in categories “128–255” to “2048–4095”, indicating that 80% of the cells divided between 7 and 12 times; 95% of the cells were identified in categories “128–255” to “2048–4095”, indicating that 95% of the cells belong to clones derived from 80% of the originally transduced cells, which divided between 7 and 12 times. Scale for number of cells was adjusted 500 fold to allow side by side comparisons of clone numbers and cell numbers. (B) Distribution of HCT-116 barcodes <i>in </i><i>vivo</i>: 75% of the barcodes are found in categories “missing” to “2–3”, indicating that they either didn’t survive at all, didn’t divide, or divided no more than once and represented only 1% of the retrieved tagged cells. However, only 6% of the bar-codes were located in categories “64–127” to “16384–32767”, indicating that they divided between 6 and 14 times; 95% of the cells accrued in categories “64–127” to “16384–32767”, indicating that 95% of the tagged cells are derived from 6% of the initially barcoded clones that divided the most. Scale for number of cells was adjusted 25 fold to allow side by side comparisons of clone numbers and cell numbers.</p

Evidence that encoded shRNA are not induced in the absence of Doxycycline <i>in vitro.</i>

<p>(A) A lentiviral library containing 27,500 unique barcodes was used to transduce HCT-116 cells at a MOI of 0.3. After 72 hours, of puromycin selection, cells were continuously passaged for 15 days in the absence of Doxycycline. Day 0 and Day 15 cell aliquots were obtained and total DNA from both time points were subjected to the barcode high-throughput sequencing retrieval procedure. (B) Correlation plot for Day 15 measurement against Day 0. shRNA barcode reads for all samples from all time points were first normalized to 2×10⁷ reads. Values for triplicate samples were averaged. At Day 15, strong repression of shRNA expression in the absence of Doxycycline is evident in the correlations with the Day 0 reference. Plot of log10 mean normalized reads for Day 0 against Day 15 (Pearson correlation: R = 0.99).</p

Barcode recovery rate from HCT-116 cells in NSG mice and <i>in vitro</i>.

<p>Barcode recovery rate from HCT-116 cells in NSG mice and <i>in vitro</i>.</p