Collecting and banking human milk: to heat or not to heat?

Data on human breast milk and its handling when fed to babies who cannot be breast-fed were reviewed to determine whether the method of processing and storage affected the properties of the milk. Breast milk is normally contaminated by potential pathogens, which seem to produce no ill effects, but it also contains antimicrobial properties which protect against infection. The evidence suggests that pasteurisation not only eliminates pathogenic bacteria but also damages bacteriostatic mechanisms, so making the milk more susceptible to later contamination. Pasteurisation also affects the nutritional properties of milk. Freezing has little effect on milk proteins, while a study on the effect of refrigeration showed that there was little bacterial growth at temperatures below 8 degrees C. Several years'' experience of feeding donated raw milk to newborn infants has confirmed that it produces no ill effects. These findings suggest that pasteurisation of donated breastmilk is unnecessary, and it is not recommended, while the decision whether or not to freeze the milk may be made on practical grounds. Raw breast milk can be safely stored at 4-6 degrees C for 72 hours.     

From molecular and cellular to integrative heat defense during exposure to chronic heat

Heat acclimation induces adaptive changes that improve the ability to cope with extreme environmental heat. Acclimatory homeostasis is manifested by an expanded dynamic thermoregulatory span (TRS), reflected in the intact organism by a lower temperature threshold (T(sh)) for heat dissipation, and delayed T(sh) for thermal injury. This principle shares common adaptive features with each of the thermoregulatory effectors. In the splanchnic circulation, e.g. the TRS of the thermally induced vasomotor response increases due to greater cardiac output distribution to the splanchnic vasculature, thereby increasing circulatory reserves and delaying thermal injury. During short-term heat acclimation (STHA), accelerated autonomic excitability plays a major role in the control of body temperature. Acclimatory homeostasis, however, is achieved only following long-term heat acclimation (LTHA), and is characterized by increased thermal effector efficiency, namely [effector organ output/autonomic signal] ratio >1. Two acclimatory responses, derived from our data on the acclimating rat model, are discussed: (1) acclimation of the cholinergic-muscarinic signaling for water secretion in the submaxillary gland; and (2) acclimatory mechanisms for increased contractile efficiency in the heart. Our data indicate that increased efficiency upon LTHA develops by reprogramming of gene expression. A reduced thyroid hormone level is responsible for some of the molecular adaptive cascades. Delayed thermal injury observed upon acclimation is due to enhanced cytoprotective mechanisms of which the inducible heat shock protein (HSP) 72 kDa plays a major role. Our data indicate that heat acclimation predisposes the HSP molecular machinery to respond faster and increases the constitutive level of the protein. STHA is the time-window during which most LTHA adaptations are switched on.     

Sensitization to heat by X-rays

1. Paramecium caudatum is sensitized to heat by sublethal dosages of x-rays. Thus if paramecia are irradiated, then exposed to a sublethal dosage of heat they are killed, but if the same heat exposure precedes the same dosage of radiations, they are not. 2. Sensitivity to both heat and x-rays is much greater in paramecia from the log growth phase than in those from the stationary phase of a culture. 3. Recovery from heat sensitization in animals from the stationary phase of a culture is slow, requiring several days. 4. Division is readily retarded and even temporarily inhibited by sublethal dosage of x-rays. Recovery of the division rate is fairly slow requiring several days. 5. Paramecia can be killed by a dosage of 1,200,000 r (of which about one-half reach the animal) units of x-radiation alone. Smaller dosages are not lethal if the paramecia are transferred to fresh medium immediately upon completion of irradiation. 6. The possibility of utilization of heat sensitization in treatment of malignant growths is discussed.     

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T(c)) was 42 degrees C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T(c) 40 degrees C (T40), and 15 min after achieving T(c) 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats (P < 0.05). The duration of survival at T42 degrees C was shortest in the TD+HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T+HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats (P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.     

Body heat balance in man subjected to endogenous and exogenous heat load

The body heat balance, measured by a thermometric method, was investigated in humans subjected to endogenous and exogenous heat load. The purpose of the present study was to test the concept of heat exchange by a servomechanism in human thermoregulation. Two series of experiments were performed on male volunteers. In series I 15 subjects performed physical exercise (50% VO2 max) for 60 min at a constant ambient temperature of 25 degrees C. In series II 16 subjects rested in a climatic chamber where the ambient temperature was elevated over 30 min from 22 to 42 degrees C and kept stable at this level during the subsequent 60 min. It was found that in both series of experiments the sweating rate followed an exponential curve exhibiting an inertial course. Heat was stored in the body mainly at the beginning of experiment. In series I the net body heat load of 125 W/m2 was equalized by sweat evaporation, beginning after 40 min of the exercise. In series II the net body heat load of 80 W/m2 was equalized in the same way, starting after 35 min of the constant high ambient temperature. In both series of experiments the amount of heat stored in the body calculated from the body heat balance was quite close to the amount of heat calculated from the calorimetric equation. It is concluded, that under the present experimental conditions, heat loss from the body by sweat evaporation seems to be a regulated variable in the human thermoregulatory system. The observed increase in rectal temperature may result from an inertial course of the sweating reaction.     

Novel transcriptional responses to heat revealed by turning up the heat at night

Plant Molecular Biology - Genome-wide association study of maize plant architecture using F1 populations can better dissect various genetic effects that can provide precise guidance for genetic...     

Acclimation to heat of the beagle dog

Four beagle dogs showed evidence of heat acclimation (reduced post-exercise heart rate and body temperature) within 10 days of first exposure of one hour a day in a hot environment (38 ± 2°C). One hour of daily exercise (110 m/min, 0% grade) in the heat (as with human subjects) was adequate to produce the effects of heat acclimation. The physiological changes observed were due to heat exposure alone since the work which was done for training (110 m/min, 4% grade) at the control temperature (20 ± 2°C), was reduced in the heat (0% grade).