Physiological differences between individuals can significantly affect human thermal response to the environment. In practice, most thermal models use a single set of physiological data to represent an average person. We have developed a model to translate descriptive data about an individual into a set of physiological parameters which may be used in thermal models. We have incorporated these parameters into a model of human thermoregulation and comfort, which may be used to predict variations in thermal response between individuals. This paper presents this model and examples of its use in thermal simulation. r 2001 Elsevier Science Ltd. All rights reserved.

Some HVAC systems save energy by creating stratified air temperature distributions in which the occupied lower regions are cooler and the upper regions warmer. Comfort standards prescribe a 3°C limit to vertical stratification, independent of where the mean temperature is relative to the comfort zone. This paper evaluates thermal comfort in stratified environments using a model developed to predict local thermal sensation and comfort. The results indicate that near the center of the comfort zone, acceptable stratification is up to 7ºC, considerably larger than the 3°C limit imposed by standards. As the mean temperature moves from the center of the comfort zone, the acceptable stratification becomes smaller. At the lower and upper ends of the comfort zone, even a small amount of stratification causes cool feet or warm head discomfort. We briefly explore the potential of using local air motion to reduce local discomfort in highly stratified conditions.

The surface temperatures of radiant floor and ceiling systems should depend on the ambient air temperature, yet the surface temperature limits specified by current standards do not vary with air temperature. In addition, the limits for ceiling temperature are specified in terms of radiant temperature asymmetry, which is difficult to convert into surface temperatures. This paper provides graphs that allow designers to directly determine, for a representative room geometry, the acceptable range of floor- and ceiling surface temperatures as a function of air temperatures.

The graphs were generated using the Berkeley Thermal Comfort Model (BCM). Acceptable and optimal floor or ceiling temperatures were found for a range of air temperatures for normal office work activity level (1.2 met). Acceptability was defined as the absence of whole-body discomfort. Depending on the air temperature, the acceptable floor temperature range is 15-40ºC, wider than that specified in ASHRAE Standard 55 and ISO 7730 (19-29°C). The upper limit of 40ºC is based on avoiding discomfort through skin contact, supported by several studies showing that people are comfortable with floor temperatures near 40ºC. The 15ºC lower limit was chosen to avoid local foot discomfort as reported in a laboratory study. The acceptable ceiling temperature range is 10-50ºC, also wider than in Standard 55 and ISO 7730 (radiant asymmetry <5ºC for a warm ceiling, and <14ºC for a cool ceiling). The maximum temperature of 50ºC was chosen as a reasonable water temperature available from heat reclamation, and it was felt that temperatures below 10ºC were unlikely to be used in any climate because of the risk of moisture condensation on surfaces. The model simulation results were compared with published laboratory experiments on radiant floors and ceilings. The results are in generally good agreement, given a number of uncertainties in reproducing the laboratory conditions and matching a variety of different comfort voting scales.

Activation of the transcription factor nuclear factor-kappaB (NF-kappaB) is one of the important responses of cells to an external stress such as ionizing radiation. We studied radiation-induced NF-kappaB activation in vivo in male BALB/c mice. After the mice were exposed to 8.5 Gy total-body gamma irradiation, the spleen, mesenteric lymph nodes, thymus, liver, lung, colon, brain and bone marrow were harvested 1, 2.5, 5, 10 and 20 h postirradiation. NF-kappaB DNA-binding activity was analyzed in the nuclear protein extracts by a gel shift assay. When compared to the levels in untreated control mice, radiation induced activation of NF-kappaB in spleen, mesenteric lymph nodes and bone marrow but not in the other tissues examined. In contrast, an i.p. injection of a lethal dose (3 mg/kg) of lipopolysaccharide also increased activity of NF-kappaB in the liver and lung. The gel supershift assay with Nfkb1, Rela and/or Rel antibodies revealed that the specific molecular forms of NF-kappaB activated by radiation in the spleen were Nfkb1 homodimers and Nfkb1/Rela heterodimers. In mesenteric lymph nodes, the heterodimerized Rel/Rela NF-kappaB was also activated. In bone marrow, an NF-kappaB-like binding factor was induced that may be Nfkb1/Rela- and Rel/Rela-like heterodimers, but it exhibited a higher mobility than Nfkb1 homodimers. These results indicate that in vivo, ionizing radiation induces NF-kappaB activation that varies in both tissue distribution and moleoular composition.

Anyone who has ever sat near a cold window on a winter day or in direct sunlight on a hot day recognizes that windows can cause thermal discomfort. In spite of this broad recognition there is no standard method to quantify the extent of such discomfort. The purpose of this study was to: 1. Review the literature to identify relevant work relating to windows and thermal comfort. 2. Develop an improved understanding of the impact of windows on thermal comfort and to propose an analytical method for evaluating this impact. The method could form the basis for a future NFRC window comfort rating method that could be used by both designers and consumers.

To investigate the cellular origin of ionizing radiation (IR)-induced NF-kappaB activation in vivo and the role of NF-kappaB in IR-induced lymphocyte apoptosis.

NF-kappaB activities were analysed by gel shift/supershift assay in isolated murine T- and B-cells, macrophages (MPhi) and tissues from normal and T- and B-cell-deficient Rag1 mice with or without exposure to IR. IR-induced lymphocyte apoptosis was determined by analysis of 3,3'-dihexyloxacarbocyanine iodide (DiOC(6)) uptake, annexin-V staining and the sub-G0/1 population, or by TUNEL assay.

The results showed that IR activated NF-kappaB in lymphocytes, including both T- and B-cells, but failed to do so in MPhi. Furthermore, T- and B-cell-deficient Rag1 mice exposed to IR exhibited a significant reduction in NF-kappaB activation as compared with normal mice. Although NF-kappaB1 (p50) gene knockout or NF-kappaB decoy oligonucleotide treatment specifically inhibited IR-induced lymphocyte NF-kappaB activation, they had no significant effect on IR-induced lymphocyte apoptosis.

This finding suggests that lymphocytes are the main cellular origin of IR-induced NF-kappaB activation in vivo. However, NF-kappaB activation has no significant effect on IR-induced lymphocyte apoptosis.

To investigate the role of the NF-kappaB1 (p50) gene in ionizing radiation (IR)-induced NF-kappaB activation and TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA expression in vivo.

NF-kappaB activation was analysed by the gel shift/supershift assay and the levels of TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA were measured using RNase protection assay (RPA). Various tissues from BALB/c, B6,129P-Nfkb1 (NF-kappaB1 or p50 gene knockout, p50(-/-)) and B6,129PF2 (wild-type, p50(+/+)) mice were analysed before or after exposure to a lethal dose (8.5 Gy) of total-body gamma-irradiation.

Exposure of BALB/c mice to total-body IR selectively activated NF-kappaB in the spleen, mesenteric lymph nodes (LN) and bone marrow (BM). Gel supershift assay using polyclonal antibodies against NF-kappaB p50, p65 or c-Rel protein revealed that the NF-kappaB p50 subunit is a critical component of the NF-kappaB complexes activated by IR in vivo. Discretely augmented TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA expression was found in the spleen, LN and BM after BALB/c mice received IR. However, mice lacking the p50 gene (p50(-/-)) showed a significant reduction in IR-induced activation of NF-kappaB and increases in TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA expression, as compared with that of wild-type mice (p50(+/+)).

The NF-kappaB p50 subunit is a critical component of the NF-kappaB complexes activated by IR and it plays an important role in mediating IR-induced TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA expression in vivo.