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At least 253 records · Page 14Linked to original sources
PubMed1998

Expression levels of heat shock factors are not functionally coupled to the rate of expression of heat shock genes.

The expression patterns of two mammalian heat shock factors (HSFs) were analysed in cell systems known to reflect an altered heat shock response. For being able to discriminate between the two closely related factors HSF 1 and HSF 2, specific cDNA sequences were cloned and used to generate antisense RNAs as hybridization probes. In general, in various cell lines expression of the two heat shock factors was clearly different. These expression patterns of the HSF genes were not influenced by retinoic acid-induced differentiation of human NT2 and mouse F9 teratocarcinoma cells. Generally, HSF 2 expression was extremely low, whereas the significantly higher expression of HSF 1 revealed cell specific differences. The highest expression rates of both HSFs were observed in 293 cells. To examine whether these high levels are involved in the constitutive expression of heat shock genes in these cells, we analysed the binding pattern of 293 cell proteins to the heat shock elements (HSEs). As with other cells, HSE-binding activity in 293 cells was only observed after heat shock treatment. This points to an HSE-independent way for high level expression of heat shock genes in these cells.

Animals↗
PubMed1999

A heat shock transcription factor in pea is differentially controlled by heat and virus replication.

Since some heat-inducible genes [heat shock (hs) genes] can be induced by virus infection in pea [e.g. Hsp70; Aranda et al. 1996, Proc. Natl Acad. Sci. USA 93, 15289-15293], we have investigated the effect that heat and virus replication may have on the expression of a heat-shock transcription factor gene (Hsf). We have characterized what appears to be the only member of the Hsf family in pea, PsHsfA. Similar to Hsp70, PsHsfA is heat-inducible in vegetative and embryonic tissues, which is concordant with the presence of heat shock elements (HSEs) and stress responsive elements (STREs) on its promoter sequence. The expression of PsHsfA during virus replication was studied in pea cotyledons and leaves, and compared to that of Hsp70. In situ hybridization experiments showed that whereas Hsp70 is induced, there is no detectable increased accumulation of PsHsfA RNA associated with the replication of pea seed-borne mosaic potyvirus (PSbMV). These experiments indicate that there is a selective control of virus-induced hs gene expression, and suggest that different regulatory pathways control hs gene expression during heat shock and virus replication.

Amino Acid Sequence↗
PubMed1988

Evidence for protection by heat-shock proteins against photoinhibition during heat-shock.

The nuclear-coded 22 kd heat-shock protein (HSP-22) which is transported into the chloroplast and localized in the thylakoids was further characterized and found to be located in the grana lamellae (stacked thylakoids) as an extrinsic protein in the green alga Chlamydomonas reinhardtii. Inhibition of photosynthetic electron flow during heat-shock of Chlamydomonas cells was light-dependent, occurring at low-light intensities (<100 W/m) as compared with photoinhibition at 25 degrees C (>1000 W/m). The site of the damage was localized at the photosystem II (PS II) reaction center. The damage was drastically increased when heat-shock treatment was carried out in the presence of the 80S ribosomal translation inhibitor, cycloheximide (CHI). Pre-incubation of Chlamydomonas cells at 42 degrees C resulted in partial protection against photoinhibition during heat-shock, as compared with cells pre-incubated at 42 degrees C in the presence of CHI which, therefore, did not translate the heat-shock proteins. Analysis of the thylakoid polypeptides' pattern by SDS-PAGE revealed that during heat-shock in the light, thylakoid proteins became aggregated proportionally to the light intensity. Heat-shock in the presence of CHI enhanced the aggregation process which, at low light intensities, was specific to the PS II reaction center D1-protein. The results suggest that the chloroplasts HSPs prevent damage to the PS II reaction center during heat-shock in the light.

Journal Article↗
PubMed1995

Heat-induced bFGF gene expression in the absence of heat shock element correlates with enhanced AP-1 binding activity.

Basic fibroblast growth factor (bFGF) has been shown to be a potent mitogen and a promoter of angiogenesis. It has been hypothesized that the expression of the bFGF gene may be induced by stress of various types. To test that hypothesis, we investigated the expression of the bFGF gene during heat treatment in adriamycin-resistant (MCF-7/ADR) and -sensitive (MCF-7) human breast carcinoma cells. Under normal growth conditions, the bFGF mRNA was detected in MCF-7/ADR cells, while it was not detectable in MCF-7 cells by Northern blot analysis. During heating at 41 degrees C, the level of bFGF mRNA increased in MCF-7/ADR cells and the message became detectable in the MCF-7 cell line. However, after continuous heating at 41 degrees C for 24 h, the bFGF mRNA level decreased to control level in MCF-7/ADR cells. Interestingly, simultaneous treatment with heat and 60 micrograms/ml H-7 (1-(isoquinolinylsulfonyl)-2-methylpiperazine, a potent PKC inhibitor) decreased the level of bFGF mRNA in MCF-7/ADR cells. These results suggest that a protein kinase, likely PKC, is involved in the transcriptional regulation of the heat-enhanced bFGF gene expression in human breast carcinoma cells. Although no heat shock element can be identified in the promoter of the bFGF gene, we observed that the AP-1 binding activity to a TPA responsive element (TRE)-like sequence in the promoter of bFGF gene was enhanced by heat, as tested by mobility shift assay. Antibody developed against the c-Jun and c-Fos proteins inhibited the AP-1 binding activity to TRE. Therefore, the AP-1 complex appears to be responsible for the heat-enhanced binding to the TRE-like motif of the bFGF gene. Furthermore, the increased AP-1 binding activity does not require new protein synthesis but activation of the preexisting c-Jun proteins.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

Lack of integrative control of heat production and heat loss after capsaicin administration.

Body temperature is usually regulated by opposing controls of heat production and heat loss. However, systemic administration of capsaicin activates heat loss and heat production simultaneously. Because capsaicin receptors are located mainly on primary sensory neurons and body temperature is regulated by the central nervous system, we investigated the brain mechanisms involved in these capsaicin-induced thermal responses. For this purpose, we examined the effects of spinalization and decerebration on these responses in artificially ventilated, urethane-anesthetized rats. Cervical spinal transection largely attenuated both responses, showing the critical involvement of the brain. Colonic temperature (Tc) did not change after the capsaicin administration to the spinalized rats. Decerebration between the hypothalamus and midbrain prevented the capsaicin-induced heat loss and enhanced the capsaicin-induced heat production. Consequently, Tc increased without a hypothermic period. The results show that capsaicin activates brainstem-controlled heat production and forebrain-controlled heat loss separately.

Animals↗
PubMed2003

Effect of post-deposition heating temperature and the presence of water vapor during heat treatment on crystallinity of calcium phosphate coatings.

In this study, radiofrequency sputtered calcium phosphate (CaP) coatings were evaluated after 1h post-deposition heat treatment at either 350 degrees C, 400 degrees C, 450 degrees C, 500 degrees C or 600 degrees C in the presence or absence of water vapor. X-ray diffraction analyses indicated the as-sputtered coatings to be amorphous. With different post-deposition heat treatments used, in this study, crystallinity of CaP coatings was observed to be in the range of 0-68%. The 400 degrees C and 450 degrees C heat-treated CaP coatings in the absence of water vapor were poorly crystalline, exhibiting a crystallinity of 2+/-1%. In comparison to heat treatments at 450 degrees C in the absence of water vapor, the presence of water vapor at 450 degrees C heat treatment resulted in a significant increase in coating crystallinity. However, this effect was not observed at higher temperatures. A coating crystallinity of 60-68% was observed for coatings heat treated at 450 degrees C in the presence of water vapor, and at 500 degrees C and 600 degrees C in the presence or absence of water vapor. In addition, increases in the degree of coating crystallinity were observed to be consistent with the increasing number of PO(4) peaks observed as a result of different post-deposition heat treatments. It was concluded that the presence of water vapor at 450 degrees C post-deposition heat treatment significantly affect the crystallinity of CaP coatings, whereas an increase to temperature higher than 450 degrees C and in the presence of water vapor has no significant effect on crystallinity.

Calcium Phosphates↗
PubMed1991

A heat-inducible nuclear factor that binds to the heat-shock element of the human haem oxygenase gene.

Haem oxygenase is a heat-shock protein in several rat tissues, as well as in certain human cells such as Hep3B hepatoma cells. In common with other heat-shock-protein genes, both the human and the rat haem oxygenase genes contain a heat-shock element (HSE) in their promoter regions. In the present study we have identified a factor in nuclear extracts of human Hep3B cells which binds specifically to the HSE of the human haem oxygenase gene. The factor in Hep3B cells was significantly induced within 1 h after heat-shock treatment, and the induction was blocked by treatment of cells with actinomycin D or cycloheximide. The factor was not detected in human HepG2 hepatoma cells, which exhibit the heat-mediated induction of heat-shock protein 70 mRNA, but not that of haem oxygenase mRNA. These findings suggest that the heat-inducible nuclear factor is increased at the level of transcription and that it may activate the human haem oxygenase gene via the HSE after heat treatment.

Base Sequence↗
PubMed1994

The effect of heat on amino acids for growing pigs. 3. The availability of lysine from heat-treated field peas (Pisum sativum cultivar Dundale) determined using the slope-ratio assay.

The effect of heat on the availability of lysine in field peas (Pisum sativum cultivar Dundale) was determined using the slope-ratio assay with growing pigs. The field peas were heated to 110 degrees, 135 degrees, 150 degrees, or 165 degrees for 15 min using a forced-air dehydrator. Lysine availability was significantly depressed (P < 0.05) with the application of heat, even at mild temperatures of 110 degrees. Lysine availability values of 0.96, 0.71, 0.77, 0.56, and 0.47 were determined for the raw peas and peas heated to 110 degrees, 135 degrees, 150 degrees or 165 degrees respectively. The effect of dietary protein level on the ileal digestibility of lysine in raw field peas was determined in a second experiment to estimate true ileal digestibility. Five diets were formulated to contain 85, 105, 125, 145 and 165 g protein/kg. Increasing dietary protein from 85 to 105 g/kg resulted in a significant increase in the estimate of apparent ileal digestibility from 0.84 to 0.93. Comparisons were then able to be drawn between the ileal digestibility, availability and utilization of lysine from raw and heat-treated field peas. The results indicate that unlike ileal digestibility values, estimates of lysine availability are sensitive to heat treatment and are a close reflection of lysine utilization in heated protein concentrates. Thus, lysine availability values would be more suitable for use in diet formulations than ileal digestibility estimates when dealing with heat-processed protein concentrates.

Amino Acids↗
PubMed2001

The effect of heat conditioning of the primary area before and after induction of hyperalgesia by topical/intradermal capsaicin or by controlled heat injury.

The aim of the present study was to test the effect of heat conditioning before and after the induction of hyperalgesia. Three different methods were used for induction of hyperalgesia, topical capsaicin, intradermal capsaicin injection, and a controlled heat injury. The vascular (blood flow and skin temperature) and sensory changes (area of secondary hyperalgesia and ongoing pain) associated with the cutaneous hyperalgesia were compared. Each experiment consisted of two randomized sessions separated by at least 2 days. In one session, pre-conditioning of the skin by heat was performed 30 min before the induction of hyperalgesia using a probe at 45 degrees C for 5 min in the center of the expected primary hyperalgesic area. After the induction of hyperalgesia, heat conditioning was performed twice in the center of the primary hyperalgesic area using a temperature of 2 degrees C above the present individual pain threshold. On the contra-lateral arm, no heat conditioning was applied while hyperalgesia was induced using the same method. This session was evaluated as a control. The pre-conditioning induced an increased skin temperature in the primary area for both topical capsaicin and the controlled heat injury. Post-conditioning caused increased blood flow in the secondary hyperalgesic area for the topical capsaicin method and increased blood flow in the primary hyperalgesic area for the controlled heat injury method. However, conditioning with heat in an attempt to increase the C-fiber input did not have any effect on the ongoing pain ratings and sensory test results in any of the methods. The results of the present study suggest that there is still a need for a better experimental model with more stable allodynia both between sessions and between subjects while at the same time minimizing discomfort to the volunteer.

Administration, Topical↗
PubMed1990

Cell death induced in a murine mastocytoma by 42-47 degrees C heating in vitro: evidence that the form of death changes from apoptosis to necrosis above a critical heat load.

The pathogenesis of heat-induced cell death is controversial. Categorizing the death occurring after various heat loads as either apoptosis or necrosis might help to elucidate this problem, since it has been shown that these two processes differ in their mode of initiation as well as in their morphological and biochemical features. Log-phase cultures of mastocytoma P-815 x 2.1 were heated at temperatures ranging from 42 to 47 degrees C for 30 min. After 42 degrees C heating a slight increase in apoptosis was observed morphologically. However, after heating at 43, 43.5 and 44 degrees C, there was marked enhancement of apoptosis, and electrophoresis of DNA showed characteristic internucleosomal cleavage. With heating at 45 degrees C both apoptosis and necrosis were enhanced, whereas at 46 and 47 degrees C only necrosis was produced. DNA extracted from the 46 and 47 degrees C cultures showed virtually no degradation, which contrasts with the random DNA breakdown observed in necrosis produced by other types of injury; lysosomal enzymes released during heat-induced necrosis may be inactivated at the higher temperatures. It is suggested that apoptosis following heating may be triggered either by a limited increase in cytosolic calcium levels resulting from mild membrane changes or by DNA damage. Necrosis, on the other hand, is likely to be a consequence of severe membrane disruption.

Animals↗
PubMed1987

[Consequences of nutritional and husbandry factors on the heat production of rats and broilers. 2. Effect of environmental temperature on the heat production of fully grown broilers and rats].

In an experiment with broilers (origin Tetra B) and with rats (albino, Wistar line) with 2 animals each, heat production was ascertained by measuring CO2 production and O2 consumption over 20 minutes after their feeding 18 h and 1 h before the beginning of measuring at ambient temperatures of 30, 25, 20, 15 and 10 degrees C. Every variant was followed through over 6 h/d in 12 measuring sections. The feed amount/ánimal and day was adapted to energy maintenance requirement. At the beginning of the experiments the broilers and rats were 14 and 21 weeks old resp. and weighed 2.2 kg and 220 g resp. The variation of the ambient temperature did not influence the heat production of the broilers. In contrast to this, the time of feeding in relation to the beginning of measuring had a distinct effect on heat production. Whereas a heat production of 342 +/- 34 kJ/kg LW0.75.d was ascertained in the postabsorptive state 18 h after the last feed intake, it increased by 11% to 393 +/- 32 kJ/kg LW0.75.d when measuring began 1 h after feeding. The very act of feed intake increased heat production by 75%. Rats showed a distinct increase of heat production caused by a decreasing ambient temperature. In the temperature range of 30-25 degrees C the increase was shallower than in the range of 25-10 degrees C. Per 1 degrees C below 25 degrees C heat production increased by 30 kJ/kg LW0.75.d. The increase was independent of the metabolism level, which was influenced by the feeding variants. The results are discussed in connection with Rubner's theory of heat compensation.

Animal Feed↗
PubMed1990

In vitro comparison of radiofrequency-heated and laser-heated metal probes for angioplasty.

The effects of a metal probe catheter on tissue using radiofrequency (RF) as its energy source is evaluated. The energy dissipation and the temperature increase of this probe was compared with a laser-heated probe. After 15 seconds, the temperature rise of the RF-heated probe at a maximum power setting was 68 degrees C in water and 106 degrees C in plasma. In contrast, the temperature rise of the Nd:YAG laser-heated probe after 10 seconds, 10 watt (W), was 80 degrees C in water and 595 degrees C in plasma. Calorimetric experiments showed that in a 7 to 30 W range of the power setting for the RF generator, only 3.5 to 4.5 W was dissipated at the RF catheter tip. Using axial forces equivalent to 100 g in fatty tissue, the penetration velocity of the RF-heated probe was 0.015 mm/s, with a temperature rise of the tip of 180 degrees C; whereas the velocity of the laser-heated probe was 3.4 mm/s with a temperature rise of the tip of 300 degrees C. These in vitro results suggest that during clinical application, tissue in contact with the front surface of the RF-heated angioplasty probe will be remodeled, whereas with the laser-heated probe tissue will be vaporized circumferentially. The RF-heated probe's risk of vessel wall perforation is probably small.

Electrocoagulation↗
PubMed1997

Heat Denaturation Profiles of Ribulose-1,5-Bisphosphate Carboxylase/Oxygenase (Rubisco) and Rubisco Activase and the Inability of Rubisco Activase to Restore Activity of Heat-Denatured Rubisco.

We compared the heat-denaturation profiles of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) and Rubisco activase and further examined the ability of Rubisco activase to restore the activity of heat-denatured Rubisco originally reported (E. Sanchez de Jimenez, L. Medrano, and E. Martinez-Barajas [1995] Biochemistry 34: 2826-2831). Rubisco was heat-treated in both the carbamylated and uncarbamylated forms and in the presence and absence of 10 mM dithiothreitol (DTT). Both forms were highly resistant to heat denaturation and further protection was gained in the presence of DTT. A 50% loss in total activity occurred after 1 h at 57.5 and 55.2[deg]C for uncarbamylated Rubisco and at 60.2 and 59.6[deg]C for carbamylated Rubisco, in each case with and without DTT, respectively. In contrast, Rubisco activase lost 50% activity after only 5 min at 33[deg]C and the loss in activity was not affected by the presence of Rubisco. When Rubisco, heat-denatured to various extents, was incubated at room temperature with Rubisco activase or bovine serum albumin as a control, Rubisco activase did not have a significant specific ability to restore Rubisco activity. We conclude that Rubisco activase alone does not have the ability to restore the activity of heat-denatured Rubisco and is unlikely to protect or restore Rubisco activity from heat denaturation in vivo because it is more heat-labile than Rubisco.

Journal Article↗
PubMed1986

Biochemical differentiation between enterotoxigenic heat-sensitive and heat-resistant Clostridium perfringens strains.

Some biochemical characteristics of 37 enterotoxigenic Clostridium perfringens strains isolated from human feces, ground beef, and soil samples by heat-selection methods and of two NCTC strains were studied. Two different biochemical patterns closely related to the heat resistance of the strains were found. The strains placed into group 1 were trehalose, inositol, and sorbitol negative and synthesized heat-resistant spores, while those placed into group 2 were trehalose and inositol positive and synthesized heat-sensitive spores. Sorbitol fermentation was variable among the strains of this last group. The strains of group 1 were more cellobiose, melibiose, and salicin fermentative than those of group 2. Only the strains placed into group 2 synthesized toxins of sufficient levels for typing. In spite of having been isolated by mild heat treatment of the specimens, two strains showed the same biochemical and toxigenic characteristics of the strains of group 1. The heating of these two strains did not modify their characteristics. We conclude that enterotoxigenic C. perfringens strains showing the two different toxigenic and biochemical patterns are present in the human gut, ground beef, and, probably, in soil. These strains may be differentiated on the basis of their capacity to produce acid from trehalose, inositol, and sorbitol, heat resistance of the spores and grade of toxigenicity. The heat-selection methods used for isolation of C. perfringens strains from different sources exerted a selection of strains from one or another group, but had no influence on their toxigenic and biochemical properties.

Animals↗
PubMed1987

Postoperative ventilatory and circulatory effects of heating after aortocoronary bypass surgery. Extended rewarming during cardiopulmonary bypass and postoperative radiant heat supply.

Twenty-four patients with stable angina pectoris were studied after aortocoronary bypass surgery with hypothermic cardiopulmonary bypass (CPB). Twelve patients (radiant heat supply group) were rewarmed during CPB to a nasopharyngeal temperature of at least 38 degrees C and a mean rectal temperature of 34.4 degrees C. Postoperatively they received radiant heat supply from a thermal ceiling. In addition, a heating water mattress was used during the end of the operation and heated, humidified inspired gases were administered intra- and postoperatively. The other 12 patients (combination heat supply group) had the rewarming during CPB extended until the rectal temperature exceeded 36 degrees C, but otherwise received the same treatment as the radiant heat supply group. The combination of extended rewarming during CPB and postoperative radiant heat supply significantly reduced oxygen uptake, carbon dioxide production and the required ventilation volumes during early recovery as compared with the values in the radiant heat supply group. The reduced metabolic demands were accompanied by lower cardiac index and oxygen delivery, which, however, were sufficient for adequate tissue perfusion as judged by the similarity in oxygen extraction and arterial base excess values in the two groups. The metabolic demands and ventilatory requirements were reduced to a level at which safe early extubation is possible.

Anesthesia↗
PubMed1999

Physiological responses of horses to a treadmill simulated speed and endurance test in high heat and humidity before and after humid heat acclimation.

To investigate whether horses were able to acclimate to conditions of high temperature and humidity, 5 horses of different breeds were trained for 80 min on 15 consecutive days on a treadmill at 30 degrees C and 80%RH. Training consisted of a combination of long duration low-intensity exercise, medium duration medium intensity exercise and short duration high intensity exercise. Between training sessions the horses were maintained at 11+/-3 degrees C and 74+/-2%RH. Before (PRE-ACC) and after acclimation (POST-ACC) the horses undertook a simulated Competition Exercise Test (CET), designed to represent the Speed and Endurance Test of a 3-day event, at 30 degrees C/80%RH. Maximal oxygen uptake (VO2PEAK) was not changed following acclimation (PRE-ACC 141+/-8 ml/min/kg bwt vs. POST-ACC 145+/-9 ml/min/kg bwt [STPD], P>0.05). Following acclimation, 4 of the 5 horses were able to complete a significantly greater amount of Phase D in the CET (PRE-ACC 6.3+/-0.3 min vs. POST-ACC 7.3+/-0.3 min, P<0.05; target time = 8 min). Resting body temperatures (pulmonary artery [TPA], rectal [TREC] and tail-skin [TTSK] temperatures) were all significantly lower following acclimation. During exercise, metabolic heat production (M) and heat dissipation (HD), for the same exercise duration, were both significantly lower following acclimation (P<0.05), although heat storage (HS) was significantly higher (P<0.05). The higher heat storage following acclimation was associated with a lower TTSK for a given TPA and a decreased total fluid loss (% bodyweight, P<0.05). Plasma volume was not changed following acclimation. The relationship of sweating rate (SR) to TPA or TTSK on either the neck or the gluteal region was not significantly altered by acclimation, although the onset of sweating occurred at a lower TPA or TTSK following acclimation (P<0.05). The horses in the present study showed a number of physiological adaptations to a period of 15 days of exposure to high heat and humidity consistent with a humid heat acclimation response. These changes were mostly similar to those reported to occur in man and other species and were consistent with thermal acclimation and an increased thermotolerance, leading to an improved exercise tolerance. It is concluded that a 15 day period of acclimation is beneficial for horses from cooler and or drier climates, that have to compete in hot humid conditions and that this may redress, to some extent, the decrement in exercise tolerance seen in nonacclimated horses and reduce the risk of heat related disorders, such as heat exhaustion.

Acid-Base Equilibrium↗
PubMed1990

Effect of prior heat shock on heat resistance of Listeria monocytogenes in meat.

The effect of prior heat shock on the thermal resistance of Listeria monocytogenes in meat was investigated. A sausage mix inoculated with approximately 10(7) L. monocytogenes per g was initially subjected to a heat shock temperature of 48 degrees C before being heated at a final test temperature of 62 or 64 degrees C. Although cells heat shocked at 48 degrees C for 30 or 60 min did not show a significant increase in thermotolerance as compared with control cells (non-heat shocked), bacteria heat shocked for 120 min did, showing an average 2.4-fold increase in the D64 degrees C value. Heat-shocked cells shifted to 4 degrees C appeared to maintain their thermotolerance for at least 24 h after heat shock.

Colony Count, Microbial↗
PubMed2001

Effect of water activities of heating and recovery media on apparent heat resistance of Bacillus cereus spores.

Spores of Bacillus cereus were heated and recovered in order to investigate the effect of water activity of media on the estimated heat resistance (i.e., the D value) of spores. The water activity (ranging from 0.9 to 1) of the heating medium was first successively controlled with three solutes (glycerol, glucose, and sucrose), while the water activity of the recovery medium was kept near 1. Reciprocally, the water activity of the heating medium was then kept at 1, while the water activity of the recovery medium was controlled from 0.9 to 1 with the same depressors. Lastly, in a third set of experiments, the heating medium and the recovery medium were adjusted to the same activity. As expected, added depressors caused an increase of the heat resistance of spores with a greater efficiency of sucrose with respect to glycerol and glucose. In contrast, when solutes were added to the recovery medium, under an optimal water activity close to 0.98, a decrease of water activity caused a decrease in the estimated D values. This effect was more pronounced when sucrose was used as a depressor instead of glycerol or glucose. When the heating and the recovery media were adjusted to the same water activity, a balancing effect was observed between the protective influence of the solutes during heat treatment and their negative effect during the recovery of injured cells, so that the overall effect of water activity was reduced, with an optimal value near 0.96. The difference between the efficiency of depressors was also less pronounced. It may then be concluded that the overall protective effect of a decrease in water activity is generally overestimated.

Bacillus cereus↗