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PubMed1998

Psychophysical study of stinging pain evoked by brief freezing of superficial skin and ensuing short-lasting changes in sensations of cool and cold pain.

Psychophysical methods were used to investigate pain in human subjects elicited by controlled freezing of the skin using a novel vortex thermode. When cooling stimuli delivered with a small thermode (7 mm diameter) exceeded the normal cold pain threshold into the sub-zero temperature range (-5 to -11 degrees C), all subjects reported an intense, sharp stinging pain sensation which occurred suddenly and was readily differentiated from normal cold pain. The onset of this stinging 'freezing' pain was closely correlated with a sudden increase in skin temperature beneath the thermode of 4.77+/-0.86 degrees C (+/-SD) associated with the phase transition of supercooled water to ice. The mean intensity of freezing pain was rated as 1.7 times as intense as cold pain at threshold. Subjects' mean reaction-time latency to signal stinging pain following the onset of phase transition on the volar forearm was 687+/-220 ms, which was slower than that for mechanically evoked impact pain. Freezing pain is suggested to be mediated by A-delta fibers, based on estimates of conduction velocity and on the observation that the freezing pain took on a burning quality of slower onset during an A-fiber pressure block of nerve fibers. We also investigated changes in skin sensation following the freezing stimulus, and found that freezing led to (a) an immediate, significant decrease in the cold pain threshold (to higher temperatures), which recovered to baseline in < 16 min, (b) a concomitant change in the quality of cold pain from dull to burning, (c) a significant, parallel increase in the threshold for the perception of cooling (to lower temperatures) which frequently manifested as a complete loss of cold sensation, and (d) a mild heat pain hyperalgesia which was still present 24 h later. The changes in thermal sensitivity were not accompanied by consistent changes in mechanical sensitivity. These results indicate that a characteristic sharp, stinging pain is reliably evoked abruptly at the phase transition of supercooled skin water to ice The ensuing brief decrease in cold pain threshold with burning quality, coupled with decreased sensitivity to cold, are speculated to reflect a central disinhibition of C-fiber nociceptor input due to reduced cold fiber activity. These effects may be relevant to frostbite, and distinguish themselves from the more pronounced thermal and mechanical hyperalgesia seen following intense freeze lesion of the skin.

Adult↗
PubMed2002

Cold signalling associated with vernalization in Arabidopsis thaliana does not involve CBF1 or abscisic acid.

In genotypes of Arabidopsis that exhibit a winter-annual flowering habit, floral induction in response to extended cold exposure (vernalization) is mediated by repression of the flowering-inhibitor gene FLC. We are interested in identifying components of the cold signal transduction pathway leading to FLC repression. We examined the potential involvement of two factors that are known to play roles in plant cold responses: (1) CBF1, a cold-responsive transcription factor that is involved in activating the cold acclimation response, and (2) the phytohormone abscisic acid (ABA), which has traditionally been associated with plant cold responses. We introduced a transgene driving constitutive expression of CBF1 into a winter-annual genotype of Arabidopsis. In transgenic lines expressing CBF1 mRNA to high levels, FLC mRNA expression was not repressed, and flowering was not accelerated relative to control plants. We also introduced mutations that compromise ABA biosynthesis or sensitivity into a winter-annual genotype and found that the vernalization response was not affected. Finally, we found that presumed increases in ABA levels, as a result of direct application of the hormone or severe water stress, were insufficient to substitute for cold to induce flowering. Taken together, these findings indicate that vernalization involves a pathway that is distinct from cold-response mechanisms involving CBF1, cold-regulated genes under CBF1 control, and ABA.

Journal Article↗
PubMed1994

Waldenström's macroglobulinemia with an IgM paraprotein that is both a cold agglutinin and a cryoglobulin and has a suppressive effect on progenitor cell growth.

BACKGROUND: A patient with Waldenström's macroglobulinemia was admitted to the hospital with fever, leg pain, and dyspnea. The patient had gas gangrene of the left leg that required above-the-knee amputation. Plasmapheresis was instituted to treat hyperviscosity. STUDY DESIGN AND METHODS: The patient's serum contained an IgM-kappa paraprotein, a cryoglobulin, and a cold agglutinin. The serum was studied. RESULTS: The patient's red cells typed as A1, Rh-positive. The direct antiglobulin test was negative. The serum contained a cold agglutinin with anti-Pr cold agglutinin specificity (titer 4096). Maximal thermal range was 30 degrees C. Following dithiothreitol treatment, the cold agglutinin activity disappeared. The serum IgM concentration in the tested sample was 62.3 g per L. The cold agglutinin titer in the supernatant after removal of the cryoglobulin was 256, and the IgM level was 0.31 g per L. Redissolving the cryoglobulin in a equivalent volume of saline resulted in a cold agglutinin titer of 4096 and an IgM level of 68.4 g per L. These results indicate that the cryoglobulin and the cold agglutinin are the same paraprotein. Serum protein electrophoresis using agarose gel and immunofixation of the serum revealed an IgM-kappa monoclonal band. Progenitor cell assays were performed by adding the patient's serum at final concentrations of 0, 1, 5 and 10 percent (vol/vol) to patient's and normal donor's peripheral blood mononuclear cells. Inhibition of burst-forming units-erythroid and colony-forming units-granulocyte/macrophage by the patient's serum was demonstrated. Appropriate controls and the use of the serum of another patient with Waldenström's macroglobulinemia did not suppress progenitor cell growth. The patient's serum inhibited colony formation in a dose-response fashion. CONCLUSION: Reports of cryoprecipitable cold agglutinins are rare. This case is unusual because the IgM-kappa paraprotein was also a cold agglutinin with anti-Pr specificity and erythroid and granulocyte-macrophage progenitor cell-suppressive properties.

Agglutinins↗
PubMed2002

Thyroid cancer yield in patients with Graves' disease selected for surgery on the basis of cold scintiscan defects.

Previous studies have suggested that thyroid nodules found in patients with Graves' disease (GD) have a higher likelihood of being malignant, and that thyroid cancer behaves more aggressively when associated with GD, although both of these assertions remain controversial. The purpose of this study was to assess the frequency of cold scintiscan (SC) defects in patients with GD, and to determine the prevalence of thyroid cancer in such patients. Our secondary objective was to determine if there are any risk factors for developing cold defects by comparing clinical characteristics of both GD patients with cold SC defects and age and gender-matched GD patients without cold defects. We included in this analysis patients with a confirmed diagnosis of GD for whom SC results and adequate follow-up information were available. Clinic records were available in 772 patients with GD. Of these, 325 patients met eligibility criteria. Cold defects were found in 39 of 325 (12.0%) patients. Among these, 22 (56.4%) were referred for surgery, of whom 6 (1.85% of all GD patients, 15.2% of GD patients with cold nodules, 25% of GD patients with palpable nodules, and 27.3% of those undergoing surgery) had papillary thyroid cancer (PTC) in the location corresponding to the SC defect. In 2 PTC patients, no palpable abnormality corresponded to the cold defect found to contain cancer at surgery. One PTC patient was found to have metastatic disease to bone, and 2 additional PTC patients required multiple therapies with radioiodine. Compared to age and gender-matched control patients with GD and without cold SC defects, there were no differences in radioactive iodine uptake (RAIU), goiter size, duration of disease, degree of elevation in microsomal antibody (MA) titers, or thyroid-stimulating immunoglobulin (TSI). We conclude that thyroid scintigraphy is an important preliminary test in the evaluation of patients with GD, and that the prevalence of thyroid cancer in the location corresponding to a focal cold SC defect provides justification for further diagnostic evaluation or surgical management.

Adult↗
PubMed1999

Prevention of cold ischaemia-reperfusion injury by an endothelin receptor antagonist in experimental renal transplantation.

BACKGROUND: Endothelin (ET) is known to play a role in the pathogenesis of warm ischaemic renal damage, however, little is known about its involvement in renal cold ischaemia. This study was designed to investigate the response of ET after kidney cold ischaemia, and to assess the potential protective effect of bosentan, a dual, non-selective ET(A)/ET(B) receptor antagonist, against cold ischaemia reperfusion injury in a rat model of syngeneic renal transplantation. METHODS: Kidneys from Lewis rats were transplanted, either immediately or after 5 h of cold preservation. After 48 h, contralateral nephrectomy was performed. Rats were organized into three groups: Tr-NoISC, no cold ischaemia; Tr-ISC, 5 h cold ischaemia; and Tr-BOS, 5 h cold ischaemia plus bosentan (100 mg/kg/day, from the day before transplantation until the seventh day post-transplantation). On day 7, plasma and tissue immunoreactive ET (irET), as well as ET mRNA tissue expression, were evaluated. Renal function was measured by means of serum creatinine on days 3, 4, 5 and 7, and by creatinine clearance on day 7. Conventional histology was performed. RESULTS: The ischaemic group had significantly higher plasma irET levels than the non-ischaemic group and significantly lower levels than the bosentan group. Tissue irET levels and ET mRNA expression were similar in the ischaemic and bosentan groups and were higher than in the non-ischaemic group. Throughout the follow-up, serum creatinine was significantly higher in the ischaemic group than in the bosentan group. Moreover, creatinine decreased rapidly in the bosentan group after nephrectomy, whereas it continued to increase for 48 h in the ischaemic group. Kidneys from the ischaemic group showed a higher degree of tubular-cell necrosis and epithelial-cell detachment than kidneys from the bosentan group. CONCLUSIONS: We conclude that cold ischaemia and preservation damage induces an increase in renal ET mRNA and irET expression in the reperfusion phase, contributing both to the deterioration of renal function and to tubular necrosis. Bosentan is effective in protecting kidneys from this cold ischaemia reperfusion damage. Non-selective ET(A)/ET(B) receptor antagonists might be potentially useful in clinical renal transplantation.

Animals↗
PubMed2002

Carolina rinse solution minimizes kidney injury and improves graft function and survival after prolonged cold ischemia.

BACKGROUND: Kidney damage caused by cold ischemia-reperfusion injury promotes adverse outcomes after renal transplantation. The purpose of this study was to determine whether Carolina rinse solution (CRS) used at the end of cold ischemic storage decreases kidney injury and improves graft function and survival. METHODS: Inbred male Lewis rats were used as donors and recipients. Left kidneys were removed from donor rats, infused with cold University of Wisconsin solution, and stored for 24, 30, or 48 hr at 0-1 degrees C. Just before implantation, kidneys were flushed with either Ringer's solution or CRS at 35-37 degrees C or were not treated. Kidneys were then transplanted into recipient rats with removal of both native kidneys. RESULTS: Survival and renal function were analyzed over a 14-day postoperative period. Among rats receiving kidneys after 24-hr cold storage, creatinine clearance was 75% greater in rats transplanted with kidneys flushed with CRS compared with Ringer's solution or nontreatment. In animals receiving kidneys after 30-hr cold storage, recipient survival after CRS was significantly higher than with Ringer's solution or without flushing (80% vs. 25% and 17%, respectively). However, CRS failed to prevent renal graft failure after 48 hr of cold storage (14% survival with CRS vs. 0% with Ringer's solution). In separate ex vivo studies, nonviable cell nuclei were labeled by trypan blue after cold preservation and brief warm reperfusion. CRS decreased podocyte and peritubular endothelial cell killing associated with cold ischemia-reperfusion injury. CONCLUSION: Flushing renal explants with warm CRS before implantation diminishes cold ischemia-reperfusion injury and improves the function and survival of transplanted kidneys.

Albuminuria↗
PubMed1993

Cold-Induced Changes in Freezing Tolerance, Protein Phosphorylation, and Gene Expression (Evidence for a Role of Calcium).

The role of Ca2+ in cold-induced changes in protein phosphorylation, gene expression, and development of freezing tolerance has been studied in cell-suspension cultures of a freezing-tolerant cultivar of alfalfa (Medicago sativa spp. falcata cv Anik). Chemical treatments to block Ca2+ channels, antagonize calmodulin action, or inhibit protein kinases markedly inhibited the cellular capacity to develop cold-induced freezing tolerance but had little effect on cell viability. An analysis of phosphoprotein profile by two-dimensional polyacrylamide gel electrophoresis revealed that at low temperature the relative level of phosphorylation of several proteins increased, whereas that of several others decreased. When cold acclimation was carried out in the presence of N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide hydrochloride, an antagonist of calmodulin and Ca2+-dependent protein kinases, or the Ca2+ channel blocker La3+, the cold-induced changes in protein phosphorylation were strongly inhibited, cells lost their capacity to develop freezing tolerance, and accumulation of transcripts of cold acclimation-specific genes was substantially reduced. An inhibitor of protein kinases, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride, had less pronounced effects on the cold-induced protein phosphorylation and caused only a partial inhibition of the cold-induced development of freezing tolerance and accumulation of the transcripts. The level of phosphorylation of one protein, of about 15 kD, increased more than 10-fold at low temperature and showed a strong positive correlation with cold-induced freezing tolerance and gene expression even when the latter were altered with various chemical treatments. These results suggest that Ca2+ and protein phosphorylation, or perhaps a coupling of the two, play an important role during the acquisition of freezing tolerance during cold acclimation.

Journal Article↗
PubMed1989

The vascular "cold patch" is not a prognostic index for headache.

Our previous research has determined that the vascular "cold patch" is a valid diagnostic "marker" and is a persistent constituent of the thermal geography of the external carotid region. It has been suggested by Dalla Volta and Anzola (1988) that the cold patch may be a prognostic index of vascular headache physiology; that is, as headaches improve through the use of vasoactive prophylactic medication, the cold patch would decrease in size or disappear. The purpose of this study is an attempt to replicate these findings. Forty migraine patients were randomly selected, and a thermographic re-examination of the external carotid region (forehead) was conducted. The post-treatment thermogram was then compared to the initial pre-treatment thermogram. Thirty subjects demonstrated an improved condition (IC) and ten subjects a worsened condition (WC). The IC Group exhibited a 73.2% reduction in headache frequency following a mean treatment period of 6.3 months. The WC Group demonstrated a 48.1% increase in headache occurrence at a mean treatment interval of fifteen months. Results demonstrated little thermographic difference between the two conditions. Within the IC Group, 46.7% of subjects exhibited and increase in cold patch size with an improved condition, 40% of cold patches remained stable, 6.7% of cold patches reduced in size, and zero cold patches disappeared with successful treatment. Within the WC Group, 20% of cold patches decreased in size with a worsened condition, 40% increased in size, and 40% remained stable. Chi square analysis determined there was no significant difference in cold patch changes between patients whose headache condition improved or worsened (p less than .70).(ABSTRACT TRUNCATED AT 250 WORDS)

Body Temperature↗
PubMed1997

The effects of glyceryl trinitrate and nicotinic acid ointments during cold exposure.

The aim of the present experimental study was to examine the effects of local application of glyceryl trinitrate and nicotinic acid on the cold-provoked haemodynamic responses, pain and hand dexterity. Ten young healthy volunteers participated in this randomized, cross-over study with three phases at least two days apart. Five cm of 2% glyceryl trinitrate ointment, 10% nicotinic acid ointment or placebo ointment was applied on the back of each subject's both hands 15 min. before the 7 min. cold exposure. Blood pressure and heart rate were measured prior to, during and after the cold exposure. In addition, the effect of cold on hand dexterity was evaluated by the Purdue pegboard test and the subjects assessed the pain in their hands during the cold exposure. Pretreatment with glyceryl trinitrate ointment counteracted the cold-induced haemodynamic response, as evidenced by a significantly (P < 0.05) smaller mean increase in the systolic blood pressure from the baseline compared with placebo. In contrast, the cold-induced increase in the systolic blood pressure observed after pretreatment with nicotinic acid ointment did not differ from placebo. Both glyceryl trinitrate and nicotinic acid alleviated the cold-induced pain, but neither of them prevented the deterioration of hand dexterity. In conclusion, the haemodynamic response provoked by a brief cold exposure could to some extent be counteracted by pretreatment with glyceryl trinitrate ointment, but not with nicotinic acid ointment, compared with placebo.

Administration, Topical↗
PubMed1994

Activation of complement by cold agglutinins.

OBJECTIVE: To review recent reports on the interaction of cold agglutinins with the complement system and its relevance to cold agglutinin disease. DATA SOURCES: Review articles and original papers have been selected for this contribution. SELECTION CRITERIA: The report focuses on experimental data available from in vitro studies as well as clinical findings regarding the mechanisms of cold agglutinin-induced complement activation. RESULTS: Despite the observation that only few cold agglutinins (almost exclusively IgM molecules with anti-I specificity) induce in vitro hemolysis of human red blood cells with human serum (homologous system), the vast majority of these autoantibodies are able to initiate the classical pathway sequence with the fixation of C1 and to a lesser degree of C4. The ability of IgM cold agglutinins to activate, in principle, complement is demonstrated by their hemolytic efficiency in the presence of animal serum as a source of heterologous complement. In addition to the thermal amplitude of cold agglutinin binding, a possible interference with membrane regulatory proteins may render certain cold agglutinins hemolytically active in a homologous system. CONCLUSION: Despite a hemolytic inefficiency, cold agglutinin-induced fixation of early complement components up to C3 leads to an accelerated clearance of red cells from the circulation by hepatic sequestration. However, it is not yet clear, to what degree these cells are eliminated by the reticuloendothelial system or whether they return to the circulation. Dependent on the amount of membrane-bound C3 fragments these cells may even be protected against further cold agglutinin-induced complement attack.

Agglutinins↗
PubMedDate not supplied

Cold knife conization and loop excision for cervical intraepithelial neoplasia.

AIMS AND BACKGROUND: Our aim was to investigate whether loop excision is an acceptable alternative to traditional cold knife conization of the cervix. PATIENTS AND METHODS: 240 with cervical intraepithelial neoplasia (CIN) were randomly assigned to loop excision (n = 120) or cold knife conization (n = 120). Success and complication rates of both methods were analysed. RESULTS: 100% of cold knife conization and 98% of loop excision surgical specimens were positive for dysplasia. The rate of complete resection was 91% in the cold knife and 82% in the loop excision group, but histologic confirmation of residual CIN was obtained in only 2 (1.7%) women after cold knife conization and in 5 (4.2%) after loop excision. Loop excision cones were significantly shallower than those obtained by a cold knife. Secondary surgical procedures due to early hemorrhage were performed in 9 (7.5%) patients treated with cold knife conization and in 8 (6.7%) treated with loop excision. Elevated temperature postoperatively was observed in 16.4% of patients after cold knife conization and in 13.9% after loop excision. There were no other postoperative complications. CONCLUSIONS: The results suggest that cold knife conization and loop excision are comparable and equally effective diagnostic and therapeutic procedures for CIN.

Adult↗
PubMed1978

Transformation of normal follicles into thyrotropin-refractory "cold" follicles in the aging mouse thyroid gland.

Autoradiographs of thyroid glands of aging mice demonstrate the gradual appearance of "cold" follicles which fail to iodinate the intraluminar iodoproteins even after intense exogeneous or endogeneous TSH stimulation. "Cold" follicles first appear at the age of 5 months. They may account for 80% of all thyroid follicles in 13-month-old mice. Morphologically, the "cold" follicles are characterized by a larger than normal colloid volume and a comparatively flat epithelium for any given follicle size. Old thyroids are twice as large as young ones. They contain twice as much normally iodinated thyroglobulin/mg wet weight. The total number of cells per gland remains constant throughout the life time. This is probably also true for the total number of follicles. The iodide pump, as judged by the tissue to serum ratio, remains normal and TSH-responsive. Yet, it is not established whether this is due to a higher activity of the pump in normal follicles or to preservation of inorganic iodide transport in "cold" follicles. Pinocytosis is defective in "cold" follicles and is poorly responsive to TSH stimulation. Furthermore, diffusion of iodocompounds is severely impaired in the colloid of "cold" follicles. It is suggested that the primary defect in the pathogenesis of "cold" follicles in old mice is the gradual failure of endocytosis to respond to normal TSH stimulation. Because exocytosis and iodination would first proceed normally, the follicular lumina would become overdistended up to a point where the apical membrane is functionally impaired. With this sequence of events, "cold" follicles would have impaired iodination while being metabolically as active as hot ones. Thus, several puzzling reports on high metabolic activity of "cold" tissue could possibly be interpreted.

Aging↗
PubMed1980

Comparison of blood flow in the ankle of uninjured subjects during therapeutic applications of heat, cold, and exercise.

Based on clinical evidence, cryokinetics (alternating cold and exercise) is replacing heat modalities as the preferred therapy for rehabilitation of traumatic musculoskeletal injuries in athletes. Theories have been advanced to explain the clinical successes of cryokinetics, but little scientific data have been collected. Strain gauge plethysmography was used to measure blood flow to the ankle of 12 uninjured male subjects. A repeated measures design was utilized with each subject being tested under six experimental conditions: 1) heat packs, 2) cold packs, 3) control, 4) heat-exercise, 5) cold-exercise, 6) control-exercise. Exercise consisted of 5 three-minute bouts (3.5 mph) interspersed with heat, cold, or control throughout a 45-minute period. Non-exercise, heat and cold were administered for 25 minutes each, followed by 20 minutes without treatment. Instantaneous blood flow was measured regularly during non-exercise periods, estimated during exercise, and total flow was computed by integrating over the 45 minute treatment-post treatment period. Total flow (ml flow/100 ml tissue/min) was greater/p. less than .0002) during cold-exercise than during heat treatments. Contrary to some theories, there was neither cold-induced vasodilatation during, nor a reflex vasodilatation following, the 25-minute cold application. These data suggest that during cryokinetics, exercise causes the increased blood flow, and that cold applications function only to allow active motion in a painful joint.

Adult↗
PubMed1998

Cold-induced microtubule disruption and relocalization of membrane proteins in kidney epithelial cells.

Cold preservation of kidneys is commonly used in human transplantation and in vitro studies. However, although disruption of the cytoskeleton by cold has been demonstrated in cultured cells, the effect of cold treatment on intact kidney is poorly understood. In this study, specific antibodies were used to examine the effect of hypothermia on the cytoskeletal network and the trafficking of some membrane proteins in the urinary tubule. Rat kidneys were cut into thin slices (approximately 0.5 mm) that were divided into several groups: (1) some were immediately fixed in paraformaldehyde, sodium periodate, and lysine (PLP); (2) some were stored at 4 degrees C for 15 min or 4 h before being fixed in cold PLP; or (3) after 4 h cold treatment, some slices were rewarmed to 37 degrees C for 15, 30, and 60 min in a physiologic solution, pH 7.4, and were then fixed in warm PLP. Immunofluorescence staining revealed an almost complete disruption of the microtubule network in proximal tubules after 15 min cold treatment, whereas microtubules in other segments were affected after 4 h. A partial recovery of the microtubule network was observed after 60 min rewarming. In contrast, actin filaments seemed to be resistant to cold treatment. gp330, aquaporin-2, H+ ATPase, and the AE1 anion exchanger were all relocated into numerous vesicles that were distributed throughout the cytoplasm after hypothermia followed by rewarming, whereas Na-K-ATPase retained its basolateral localization. The vasopressin-stimulated insertion of aquaporin-2 water channels into the apical membrane was inhibited during the initial rewarming period after cold exposure. Thus, cold preservation of tissues might impair, at least transiently, the polarized membrane expression and function of some transport proteins in renal epithelial cells.

Actins↗
PubMed2000

Cold chain status at immunisation centres in Ethiopia.

BACKGROUND: Child immunisation is among the most cost-effective ways of preventing premature child deaths, and the potency of vaccines, crucial for vaccine efficacy, is dependent on effective management of the cold chain at all levels of vaccine handling. OBJECTIVE: To assess the status of the cold chain at peripheral vaccine stores in Ethiopia. DESIGN: Institution based cross-sectional survey in two rural and one urban administrative areas were included in the study. Sixty seven health institutions providing static vaccination services were included in the study but cold chain system was assessed fully in only sixty four. Data were collected by interviewing health workers and by directly observing the cold chain equipment and records using structured forms. RESULTS: Conditions of the cold chain system were described based on 64 of the 67 centres visited, three were excluded because of non-functioning cold chain. Complete temperature record was observed in 37 (57.8%) of the centres. Thermometer was not available in four (6.3%) and thermometer reading was found to be outside the optimal range in another seven (10.9%) centres. Vaccine storage in the refrigerator was not proper in 47 (73.4%) centres. Majority of the centres had neither trained personnel nor budget for maintenance of the cold chain. CONCLUSION: There is a real danger of vaccines losing their potency at these centres even if they were potent on arrival. Relevant training for those handling the cold chain, improving the maintenance conditions of refrigerators and introduction of cold chain monitoring devises are recommended.

Drug Storage↗
PubMedDate not supplied

Severe cold agglutinin disease and cryoglobulinemia secondary to a monoclonal anti-Pr2 IgM lambda cryoagglutinin.

OBJECTIVE: To present a case of cold agglutinin disease/cryoglobulinemia secondary to a monoclonal anti-Pr2 IgM lambda antibody, and review the literature on the occurrence of this antibody in cold-induced disease and the clinical disease associated with it. METHODS: Cryoantibody characteristics were evaluated by cold precipitation. The antigen specificity of the monoclonal IgM lambda antibody was evaluated using techniques of selective red blood cell absorption. RESULTS: In our patient, we were able to identify an antibody with both cryoglobulinemic and cold agglutinin (cryoagglutinin) properties. This antibody was found to be monoclonal IgM lambda with specificity to the Pr2 antigen on red blood cells. CONCLUSIONS: Monoclonal IgM lambda anti-Pr is a rarely found cold agglutinin antibody. In this report we describe the clinical course of a patient who had this antibody, which not only agglutinated red cells in the cold but also had cryoglobulin properties. The clinical illness of this man was characterized by severe acrocyanosis and digital necrosis with eventual organ necrosis and death. We also review the literature on cold induced disease due to monoclonal anti-Pr IgM lambda antibody. Our patient was found to be unique among the reports reviewed. Our case is the first to report both cold agglutinin and cryoglobulinemic properties with the evaluation of the thermal amplitudes of these activities of the antibody. Also, unlike the lymphoproliferative malignancy observed in the cold agglutinin-associated disease in the other reports, our patient's disease was associated with a monoclonal B-cell expansion on the spectrum between benign monoclonal gammopathy and a low grade lymphoproliferative disorder.

Aged↗
PubMed1964

CYTOLOGICAL RESPONSES OF BROWN FAT TISSUE IN COLD-EXPOSED RATS.

In young adult laboratory rats exposed to cold (6 degrees C) the brown adipose tissue undergoes time-dependent increases in cellularity, vascular supply, and total mass. These changes are largely complete after 16 days in the cold and concurrent generally with the development of a thermoregulatory state not greatly dependent upon shivering. Histologically the brown fat changes from a tissue having both unilocular and multilocular fat cell types to one having almost exclusively the latter. During the first 6 to 12 hours in cold, the multilocular cells lose their lipid vacuoles and decrease in size, but these features are restored to normal by 24 hours. Cell proliferation, as estimated by the DNA synthetic index method (using tritiated thymidine autoradiography), appears in the reticuloendothelial cells of the brown fat at 1 day of cold exposure, becomes maximal at 4 days, and returns to the control level by 16 days. In animals injected with tritiated thymidine on the 3rd day of cold exposure and then maintained for 1 or more additional days in the cold, autoradiographs indicate that new brown fat (multilocular) cells arise by cytogenesis from reticuloendothelial progenitor cells and not by proliferation of existing brown fat cells. Throughout this and subsequent periods, cells of the epididymal white adipose tissue slowly decrease in size. Because a thermogenic role in cold acclimation has been established for the brown fat, the reported changes are regarded as adaptive responses to a cold environment.

Adipose Tissue↗
PubMed2005

Impacts of cold climate on human heat balance, performance and health in circumpolar areas.

In circumpolar areas the climate remains cool or thermoneutral during the majority of the days of the year spite of global warming. Therefore, health consequences related to cold exposure represent also in the future the majority of climate-related adverse health effects. Hot summers may be an exception. At ambient temperatures below +10 - +12 degrees C, humans experience cold stress of varying degree. Man can compensate a 10 degrees C change in ambient temperature by changing metabolic heat production by 30-40 W m(-2) or by wearing an additional/taking off ca. 0.4 clo units (corresponding to one thick clothing layer). Cold ambient temperature may be a risk for human health and cause varying levels of performance limitations. The impacts of cold exposure on health and wellbeing cause a burden to many societies in terms of lowered productivity and higher costs related to health care systems as well as public health planning and management. In order to provide preventive and protective public health actions for cold-induced adverse health effects, it is important to recognize cold related injuries, illnesses and symptoms and their turn-up temperatures, and to identify the most at-risk population subgroups and factors that increase or decrease the health risks posed by cold ambient temperatures. The majority of cold-related harmful health impacts can be prevented or managed by correct preventive and protective actions. Rapid unpredictable changes are more difficult to compensate because of lack of experience (affecting attitude and skills), preparedness (vehicles, garments, supplies, logistics etc.) and/or acclimatization.

Acclimatization↗