Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CAMPS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed1979

The role of the ATP--adenylate cyclase--cAMP system and its pharmacological regulation in the development of gastric hypersecretion and ulceration.

The role and pharmacological regulation of the ATP-adenylate-cyclase--cAMP system were studied in the mucosa of the gastric fundus, and in the forestomach, of pylorus-ligated rats to elucidate the development of gastric hypersecretion and ulceration. (1) cAMP content of the tissue of the fundus mucosa and of the forestomach decreased before the significant increase of gastric H+ output and ulcer development; (2) the gastric H+ outputs depended on the breakdown of ATP in the fundus mucosa; (3) the gastric H+ secretion was inhibited in a dose-dependent way by theophylline, epinephrine and cimetidine; (4) the inhibition of gastric H+ secretion by epinephrine , theophylline or epinephrine plus theophylline associated with a significant increase in the mucosal cAMP of the gastric fundus (5) the significant increase in gastric H+ secretion due to histamine associated with a significant decrease in fundic mucosal cAMP; (6) the gastric H+ secretion could be inhibited dose-dependently by ADP, AMP, cyclic 2', 3'-AMP and cAMP; (7) the inhibition of gastric H+ secretion by cimetidine developed without and with histamine application in pylorus-ligated rats; (8) the histamine on gastric H+ secretion could not be stimulated further with theophylline (9) no significant correlation was found between the mucosal cAMP level and the gastric H+ secretion and/or between the decrease of mucosal cAMP content and gastric H+ secretion. It has been concluded that in pylorus-ligated rats (1) the gastric H+ secretion is an ATP-dependent process; (2) the cAMP system has an inhibitory effect as regards the development of gastric hypersecretion and of ulceration; (3) histamine and cimetidine show no close correlation with the cAMP system; (4) an extracellular and intracellular feed-back mechanism system exists between th ATP-membrane-bound ATPase-ADP and the ATP--adenylate cyclase--cAMP systems in the background of the development of gastric hypersecretion and ulceration.

Adenosine Diphosphate↗
PubMed1987

[Effect of cAMP modifiers on the cytotoxic activity of macrophages].

The effects of various cAMP modifiers on the changes in the intracellular cAMP level and on the coupling of the cAMP system with realization of macrophage cytotoxicity depending on their functional activity were studied. Nonactivated and activated by E. coli polysaccharides peritoneal macrophages of BALB/c mice and macrophage-like cells of J744 mice were incubated in the presence of cAMP modifiers and further assayed for cytolytic and cytostatic activities. Cells of tetraploid strain of Ehrlich carcinoma G10 were used as target cells. Among other modifiers only dibutyryl-cAMP caused a steady increase of the intracellular nucleotide content, whereas methylisobutylxanthine and isoproterenol in combination with methylisobutylxanthine caused only a temporary increase of the cAMP level. Isoproterenol did not induce any appreciable changes in the intracellular cAMP level. All modifiers under study suppressed the cytotoxic activity of macrophages irrespective of the nature of changes in the intracellular cAMP content. It was assumed that cAMP accomplishes a triggering function in the regulation of the cytotoxic activity of macrophages and that the cAMP system is universal in the regulation of cytotoxicity at various functional states of macrophages.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Regulation of differentiation of the BC3H1 muscle cell line through cAMP-dependent and -independent pathways.

Serum mitogens, fibroblast growth factor (FGF), and type beta transforming growth factor (TGF-beta) suppress differentiation of the mouse muscle cell line BC3H1; however, the signal transduction pathways whereby these growth factors exert their effects on this system are unknown. The goal of this study was to determine whether the program for differentiation of BC3H1 cells was susceptible to negative regulation by signaling pathways involving cAMP or protein kinase C and whether these intracellular effectors participate in the mechanism by which growth factors prevent establishment of the myogenic phenotype. Exposure of BC3H1 cells to dibutyryl cAMP, 8-bromo-cAMP, or compounds that stimulate adenylate cyclase, i.e. forskolin, prostaglandin E1, and cholera toxin, prevented up-regulation of muscle-specific gene products following growth arrest in mitogen-deficient medium. Conversely, addition of cAMP to differentiated BC3H1 myocytes caused down-regulation of muscle-specific mRNAs. In contrast to the ability of cAMP to block differentiation, chronic exposure to O-tetradecanoylphorbol-13-acetate, the potent activator of protein kinase C, exhibited no apparent effects on expression of muscle-specific gene products. The proto-oncogenes c-myc and c-fos were up-regulated rapidly by cAMP in a manner similar to that observed previously by serum, FGF, and TGF-beta. However, these growth factors failed to increase intracellular cAMP levels, and they did not induce ornithine decarboxylase, which was subject to positive regulation by cAMP and O-tetradecanoyl-13-acetate. Together, these data indicate that differentiation of BC3H1 cells is subject to negative regulation through a cAMP-dependent pathway and that serum mitogens, FGF, and TGF-beta inhibit differentiation through a mechanism independent of cAMP or protein kinase C.

1-Methyl-3-isobutylxanthine↗
PubMed1989

[Effect of cyclic nucleotides (cAMP) on experimental HSV-I keratitis].

The authors report an experimental study on the effect of cAMP on HSV-I keratitis. Rabbit corneas developed typical dendritic keratitis on the 3rd day after inoculation of HSV-I. On the 9th day, the cAMP level in plasma significantly decreased from 174.9 +/- 20.2 to 52.1 +/- 18.2 pmol/ml, while the cGMP level increased. The cAMP level in aqueous humour also decreased, with an increase in cGMP level increased. The cAMP level in aqueous humour also decreased, with an increase in cGMP level. cAMP was used subconjunctivally for treatment of HSV-I keratitis. 48 hours after injection, the cAMP level in aqueous humour markedly rose from 11.1 +/- 2.0 to 35.6 +/- 12.9 pmol/ml and 6 days later to 65.0 +/- 30.9 pmol/ml, with concurrent decrease in cGMP level, and the ratio of cAMP/cGMP increased from 1.6 +/- 0.6 to 15.3 +/- 4.6. In the group of treatment by acyclovir, the level of cAMP in aqueous humour increased by 9.5 times after 3 days of treatment, with no remarkable effect on the cGMP level. These results showed that cAMP was equally effective as ACV in treatment of experimental HSV 1 keratitis. The antiviral action of cAMP was discussed and the pharmacological effect of cAMP approached.

Acyclovir↗
PubMed1984

Characterization and localization of cAMP-dependent protein kinases in rat caudal epididymal sperm.

We have studied the subcellular localization of type I and type II cAMP-dependent protein kinases in rat caudal epididymal sperm. Our studies indicated that a large fraction of the cAMP-binding activity (approximately 60%), as well as a significant portion of the catalytic activity (approximately 40%), remained associated with insoluble material after the plasma membrane was extracted with 1% Triton X-100. Only 15% of the cAMP-binding activity in sperm was membrane bound. To explore the possibility of a surface location for the membrane-associated cAMP-binding proteins, whole sperm were subjected to proteolysis. Sperm treated with alpha-chymotrypsin lost cAMP-binding activity in cytoplasmic, detergent-soluble, and detergent-resistant fractions. These results demonstrate that alpha-chymotrypsin had access to intracellular locations and to all of the cAMP-binding proteins in sperm. Photoaffinity labeling studies using 8-azido-[32P]cAMP suggest that the regulatory subunit (R) present in the membrane was predominantly RI, while the major species present in the cytoplasm and on detergent-resistant structures was RII. Detergent-resistant sperm structures could be depleted of endogenous catalytic activity by the addition of cAMP, and cAMP-dependent kinase activity could be subsequently regained by the addition of bovine heart catalytic subunits. Separation of head and tailpieces showed that the detergent-resistant regulatory subunits were almost exclusively located on the tailpiece. This finding is consistent with the involvement of cAMP-dependent protein kinases in sperm motility.

Adenosine Monophosphate↗
PubMed1995

[Calcium ion effects on cAMP system in cultured chick ciliary epithelial cells].

I investigated stimulation of cyclic adenosine 3': 5'-monophosphate (cAMP) production by vasoactive intestinal peptide (VIP), isoproterenol (ISO), sodium fluoride (NaF), and forskolin (FSK) in cultured chick embryo ciliary epithelium (CE). In order to clarify the influence of intracellular calcium ions on cAMP production when CE was activated by cAMP activating agents, I also studied the effects of calcium ionophore (A23187) on VIP, ISO NaF, and FSK stimulated cAMP production. After stimulation with VIP, ISO, NaF, and FSK, a concentration dependent increase in cAMP level was observed. Addition of A23187 activated VIP and ISO stimulated cAMP production. However, A23187 had no effect on the cAMP level when CE was stimulated by NaF and FSK. The activating effect of A23187 was inhibited by calcium/calmodulin-dependent protein kinase inhibitor (W-7). I speculate that calcium ions have different effects on receptor-mediated cAMP pathway and non-receptor-mediated cAMP pathway, and that calcium ions modulate the cAMP pathway through the calcium/calmodulin-dependent protein kinase.

Animals↗
PubMed1993

cAMP analogs prevent activation-induced apoptosis of T cell hybridomas.

Activation of T cell hybridomas through their TCR leads to secretion of IL-2, inhibition of proliferation, and apoptosis. The identification of various inhibitors that prevent activation-induced T cell death (AICD) has helped identify several essential events in apoptosis. For example, inhibition of AICD by dexamethasone indicates a connection between these two programmed death pathways. In this study, we have investigated the interaction between the cAMP signal transduction pathway and the activation- or glucocorticoid-induced cell death. cAMP induced DNA fragmentation in thymocytes. T cell hybridomas displayed different sensitivity to cAMP. Regardless of its cAMP sensitivity, programmed cell death promoted by anti-CD3 or Ag in hybridoma was prevented by the presence of cAMP analogs. In contrast, cAMP had no effect on glucocorticoid-induced T cell death. The inhibitory effect of cAMP on AICD was unlikely to be due to quenching of T cell activation signals, because cAMP added 1 h after T cell activation could still prevent cell death. In addition, the increased binding of AP-1, NF-AT, and NF-kappa B during T cell activation was not significantly affected by cAMP. The presence of the inhibitory cAMP-mediated signals, together with the glucocorticoid-induced pathway, suggest there are at least two distinct mechanisms regulating AICD in immature lymphocytes.

Amino Acid Sequence↗
PubMed1994

Conditional activation of cAMP signal transduction by protein kinase C. The effect of phorbol esters on adenylyl cyclase in permeabilized and intact cells.

To understand the convergence of cAMP and protein kinase C signal transduction, adenylyl cyclase isozyme identification and biochemical studies were performed on the HT4 neural cell line. In HT4 cells, basal cAMP production by adenylyl cyclase types I and VI were unaffected by phorbol esters, nor did phorbol esters have any effect on forskolin-induced cAMP production. However, phorbol esters synergistically increased cAMP production when adrenaline receptors were simultaneously activated, indicating a conditional activation of cAMP production by phorbol esters. A permeabilized cell preparation was used to analyze the mechanism by which phorbol esters were affecting cAMP production. This preparation enables G-proteins to be activated directly by GTP gamma S or bacterial toxins. In the permeabilized cell preparation, phorbol esters enhanced cAMP produced by GTP gamma S-activated G-protein. A stimulatory G-protein pathway may be involved since phorbol esters synergistically increased cAMP production by cholera toxin, yet had no effect on that produced by pertussis toxin. In this cell culture model, phorbol esters stimulate cAMP production only when some component of the cAMP cascade is simultaneously activated. Moreover, the pattern of modulation suggests that protein kinase C acts on an activated component of the second messenger system, such as the G-protein or the coupling of the G-protein with adenylyl cyclase, and not on the resting state of the protein components.

Adenylyl Cyclases↗
PubMed1993

Activation of metabotropic glutamate receptors increases cAMP accumulation in hippocampus by potentiating responses to endogenous adenosine.

Metabotropic glutamate receptors (mGluRs) are coupled to effector systems through GTP-binding proteins (G-proteins) and appear to mediate slow synaptic responses in the CNS. Although mGluR-mediated increases in phosphoinositide hydrolysis have been well characterized, other mechanisms for signal transduction employed by mGluRs are poorly understood. We recently reported that the selective mGluR agonist 1-aminocyclopentane-1 S,3R-dicarboxylic acid (1S,3R-ACPD) increases cAMP accumulation in rat hippocampal slices. We have now investigated the mechanisms involved in this response. A number of G-protein-linked receptors that are not directly coupled to adenylate cyclase increase cAMP accumulation by potentiating cAMP responses to other agonists. Furthermore, previous studies suggest that glutamate increases cAMP accumulation by a mechanism that is dependent upon the presence of endogenous adenosine. Therefore, we tested the hypothesis that 1S,3R-ACPD-stimulated increases in cAMP accumulation in rat hippocampal slices are dependent upon the presence of endogenous adenosine and are mediated by an mGluR that potentiates cAMP responses to other agonists. We found that adenosine deaminase abolished 1S,3R-ACPD-stimulated cAMP accumulation whereas the adenosine uptake blocker dipyridamole enhanced this response. Additionally, adenosine receptor antagonists blocked mGluR-mediated increases in cAMP accumulation with potencies that were highly correlated with their potencies at A2 adenosine receptors. Furthermore, we performed a series of studies that suggest that 1S,3R-ACPD activates an mGluR subtype that potentiates responses to agonists of other receptors that are coupled to adenylate cyclase and that 1S,3R-ACPD-stimulated increases in cAMP accumulation in hippocampal slices are mediated by potentiation of the cAMP response to low levels of endogenous adenosine that are continuously present extracellularly.

Adenosine↗
PubMed1996

The inhibitory effect of angiotensin II on stimulus-induced release of cAMP is augmented in the genetically hypertensive rat kidney.

In the present study, with isolated perfused kidneys, we evaluated whether angiotensin II (Ang II) inhibits stimulus-induced release of adenosine 3',5'-cyclic monophosphate (cAMP) and whether this effect is augmented in spontaneously hypertensive rats (SHR). The basal release of cAMP (in venous effluent) in the presence of captopril (1 mumol/l) and a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (10 mumol/l), was significantly (P < .05) higher in the SHR (n = 20) than in Wistar-Kyoto (WKY) kidneys (n = 18) although perfusion pressures were not significantly different in the two strains. Isoproterenol infusions (ISO; 0.3, 1 and 3 mumol/l) significantly and similarly increased cAMP release in both WKY (n = 5; P < .01) and SHR (n = 6; P < .01) kidneys. A time-related attenuation of the cAMP response to ISO in both strains was observed in these experiments. In control experiments, Ang II (3 and 10 ng/min), by itself, did not significantly alter basal cAMP release in either strain but raised perfusion pressure in both SHR and WKY kidneys. In a separate set of experiments, Ang II significantly (3 ng/min: P < .05; 10 ng/min: P < .01) inhibited ISO-induced increases in release of cAMP from SHR kidneys (n = 8), whereas cAMP release in response to ISO in WKY kidneys (n = 8) was not affected by Ang II (3 and 10 ng/min). In the same experiments, ISO produced small but significant decreases in perfusion pressure in WKY (P < .01) but not in SHR. These data clearly and directly demonstrate that ISO-induced increases in cAMP in the renal vasculature are similar in SHR and WKY rats; however, Ang II exerts a much greater negative influence on the ISO-induced increases in cAMP levels in the renal vasculature of SHR. The augmented inhibition of stimulus-induced cAMP release may be associated with an increased renovascular responsiveness to Ang II in SHR.

Angiotensin II↗
PubMed1996

cAMP levels increased by activation of metabotropic glutamate receptors correlate with visual plasticity.

We have investigated the cAMP level increased by stimulation of metabotropic glutamate receptors (mGluRs) in cat visual cortex during development. The cAMP level increases activated by the general mGluR agonist (1S,3R)-1-amino-1,3-cyclopentane-dicarboxylic acid (ACPD) were closely correlated with the critical period for ocular dominance plasticity in both light- and dark-reared animals. Activation of either group I or group II mGluRs increased the cAMP level. Group II mGluR activation also reduced the forskolin-stimulated cAMP increase. The correlation was emulated by a mixture of groups I, II, and III mGluR agonists but not by agonists applied singly; therefore, the correlation is attributable to activation of multiple groups of mGluRs. The cAMP level increased by the mixture was greater than the sum of the increases produced by the agonists applied singly (super-additive effect), suggesting an interaction between the G-proteins and/or second messengers controlled by these mGluRs. The basal cAMP level also correlated closely with the critical period until shortly after the peak of the critical period. Therefore, the major factor that contributes to the correlation between the ACPD-stimulated cAMP increase and the peak of the critical period is the basal level of cAMP: the activation of multiple mGluRs amplifies the basal cAMP. We suggest that both basal activity of cAMP production and activation of mGluRs may be important in plasticity in the visual cortex.

Animal Husbandry↗
PubMed1998

Therapy for X-adrenoleukodystrophy: normalization of very long chain fatty acids and inhibition of induction of cytokines by cAMP.

X-adrenoleukodystrophy (X-ALD) is an inherited fatty acid metabolic disorder with secondary manifestation of neuroinflammatory disease process. We report that compounds (forskolin, 8-bromo cAMP, and rolipram) that increase cAMP and activate protein kinase A (PKA) were found to stimulate the peroxisomal beta-oxidation of lignoceric acid (C24:0) whereas compounds (H-89 and myristoylated PKI) that decrease cAMP and PKA activity inhibited the peroxisomal beta-oxidation of lignoceric acid in cultured skin fibroblasts from X-ALD patients. Consistent with the stimulation of beta-oxidation of lignoceric acid, activators of PKA normalized the level of very long chain fatty acids (VLCFA) in X-ALD cultured skin fibroblasts. This normalization of VLCFA in X-ALD cells with forskolin, 8-Br cAMP or with rolipram, an inhibitor of cAMP phosphodiesterase, was realized independent of expression of mRNA or protein of the ALD gene, suggesting that cAMP derivatives can correct the metabolic defect in X-ALD fibroblasts without involving the candidate gene for the disease. Because astrocytes and microglia in demyelinating lesions of X-ALD brain express proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta), we examined the effect of cAMP derivatives or rolipram on lipopolysaccharide-stimulated rat primary astrocytes and microglia and found that cAMP derivatives and rolipram inhibited the induction of TNF-alpha and IL-1beta in both astrocytes and microglia. The ability of cAMP derivatives and rolipram to block the induction of TNF-alpha and IL-1beta in astrocytes and microglia and to normalize the fatty acid pathogen in skin fibroblasts of x-adrenoleukodystrophy (X-ALD) clearly identify cAMP analogs or rolipram as candidates for potential therapy for X-ALD patients.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

cAMP-mediated regulation of neurotrophin-induced collapse of nerve growth cones.

Neurotrophins are known to promote the survival, differentiation, and neurite outgrowth of developing neurons. Here we report that acutely applied brain-derived neurotrophic factor (BDNF) induces rapid growth cone collapse and neurite retraction of embryonic Xenopus spinal neurons in culture. The collapsing effect of BDNF depends on the activation of Trk receptor tyrosine kinase, requires an influx of extracellular Ca2+, and is regulated by cAMP-dependent activity. Elevation of intracellular cAMP levels ([cAMP]i) by forskolin or (Sp)-cAMP completely blocked the collapsing effect, whereas inhibition of protein kinase A (PKA) by (Rp)-cAMP potentiated the collapsing action. BDNF-induced growth cone collapse was only observed in 6 hr cultures but not in 24 hr cultures. However, inhibition of PKA by (Rp)-cAMP restored the collapsing response of these "old" neurons in 24 hr cultures, suggesting that embryonic Xenopus spinal neurons may upregulate their endogenous cAMP-dependent activity during development in culture, leading to the blockade of their collapsing response to BDNF. Taken together, our results suggest the presence of cross-talk between Ca2+- and cAMP-signaling pathways involved in the collapsing action of neurotrophins, in which the cAMP-pathway regulates the Ca2+-mediated signal transduction required for BDNF-induced collapse. By modulating the cAMP-dependent activity through the intrinsic programming or interaction with other factors present in the environment, a neuron thus could respond to the same extracellular factors with different morphological and cellular changes at different stages during development.

Actins↗
PubMed1998

Modulation by angiotensin II of isoproterenol-induced cAMP production in preglomerular microvascular smooth muscle cells from normotensive and genetically hypertensive rats.

The objectives of the present study were to determine whether angiotensin II (Ang II) modifies beta-adrenoceptor-induced cAMP production in preglomerular microvascular smooth muscle cells (PMVSMCs), to determine whether the Ang II/beta-adrenoceptor interaction on cAMP production differs in PMVSMCs from normotensive Wistar-Kyoto (WKY) rats vs. PMVSMCs from spontaneously hypertensive rats (SHR), and to elucidate the mechanism of Ang II/beta-adrenoceptor interactions on cAMP production in PMVSMCs. In cultured PMVSMCs, isoproterenol increased cAMP levels and this effect was markedly enhanced by Ang II. The Ang II enhancement of isoproterenol-induced cAMP was significantly greater in SHR PMVSMCs compared with WKY PMVSMCs. Neither inhibition of calcineurin with FK506, inhibition of calcium-calmodulin with W-7 and calmidazolium, nor inhibition of Gi proteins with pertussis toxin attenuated Ang II enhancement of isoproterenol-induced cAMP in PMVSMCs from either SHR or WKY rats. Moreover, the effect of Ang II on isoproterenol-induced cAMP was not mimicked by alpha-2 adrenoceptor stimulation. In contrast, chelation of intracellular calcium with BAPTA-AM attenuated, increasing intracellular calcium with A23187 augmented, and inhibition of protein kinase C with either calphostin C or chelerythrine chloride abolished Ang II enhancement of isoproterenol-induced cAMP. We conclude that in cultured PMVSMCs Ang II enhances the cAMP response to beta-adrenoceptor agonists via a mechanism that involves coincident activation of adenylyl cyclase by stimulatory G proteins and protein kinase C. Thus, protein kinase C-mediated activation of adenylyl cyclase may attenuate Ang II-induced vasoconstriction in the renal microcirculation by raising the intracellular levels of cAMP, and this mechanism may be augmented in genetic hypertension.

Angiotensin II↗
PubMed2006

Psychosocial impacts of a camping experience for children with cancer and their siblings.

BACKGROUND: We conducted a prospective two-group evaluation of pediatric cancer patients and their siblings regarding experiences and affective changes resulting from a 1-week summer camp experience. METHODS: The patients and siblings were assessed prior to camp (Baseline), at the end of camp (Follow-up 1), and again 4-6 months later (Follow-up 2). Assessments included standardized tests for depressive affects, social competency, and a measure of pleasure and participation in camp activities. RESULTS: Sixty-six children were assessed, including 31 (47%) patients and 35 (53%) siblings. Ages ranged from 7 to 17 years. Of the patient campers 19 (61%) had leukemia or lymphoma and 12 (39%) had solid tumors. Results showed marked changes in affective symptoms for patient campers over time (improvements), not shown by sibling campers. For patient campers these affective changes were not present immediately after camp, but were quite significant when measured 4-6 months later. Both patient and sibling campers reflected the same positive memories and pleasure in camp activities over time. For neither group did memories or pleasure fade over time. The camping experience did not have differential impacts on first time versus returning campers. Twelve campers (18% of sample) indicated suicidal ideation on the measure of depressive affects. They did well at camp and presented no special management issues. CONCLUSION: Expectations appear substantially different for patient versus sibling campers. The camping experience appeared to impact these groups differently, with patient campers impacted in ways not experienced by sibling campers.

Adolescent↗
PubMedDate not supplied

Summer camps for diabetic children in Beijing of China.

The first summer camp for diabetic children was held in 1984 in Beijing. Since then we have held summer camp every year, the last summer camp was the fifth camp in 1988. The purpose of summer camps for diabetic children are to train the patients and increase the skills of diabetics self-control practice. The recreation activities are also important for their good communication and psychological adaptation. The campers of camps were 28-35 diabetic children, totally 154 participants consisting of 73 boys and 81 girls. Most of the children were 10-14 years old. The staffs include pediatricians, nurses and others. The ratio of campers with staffs were 2.7-3.2. The session of the camps were always of five days length. The characters of activities in camps were all the arrangements must be for diabetic children, included planning diet, insuring the urine sugar exam, insulin injection before each meal, and give some lectures for training the managed skills of diabetes, meanwhile the recreation programs and exercise were also a consisting portion of activations. The summer camps were beneficial for diabetic children. They learned many useful techniques of diabetes and their capacity of life adaptation were increased, and the self-confidence enhanced their future daily life.

Adolescent↗
PubMedDate not supplied

Changes in perceived health of children with congenital heart disease after attending a special sports camp.

Sports camps for children with cardiac anomalies have existed for many years. However, no formal evaluation of the benefits of attending such camps has been undertaken heretofore. We assessed potential changes in the self-perceived health of children with congenital heart disease who attended a special sports camp. Thirty-one children with cardiac anomalies attended a 3-day multisports camp. Sixteen children, all of whom were 10 years or older, literate, and Dutch- or French-speaking, completed the Child Health Questionnaire (CHQ-CF87) before and after attending the camp. The scores of the children were compared with those of healthy peers by calculating mean standardized differences. After attendance at the sports camp, the children achieved significant improvements in the self-perception of their physical functioning, role functioning due to emotional problems, role functioning due to behavioral problems, mental health, and general behavior. The children's self-esteem and general behavior after the camp were significantly better than that of their healthy counterparts. We conclude that children with congenital heart disease who participate in activities at special sports camps may reap benefits in terms of their subjective health status. Although further research is needed, we recommend the participation in sport activities by children with heart defects, and more specifically their participation in sports camps.

Adolescent↗
PubMed2005

[Medicine in the concentration camps of the Third Reich].

Between 1942 and 1944 millions of prisoners were subjected to forced labor in concentration camps throughout the Third Reich, all the while being the victims of a systematic and "scientific" extermination policy. Though the policy was directed mainly against Jews, it was implemented against other "inferior races" as well. The prisoners, stripped of all rights, experienced constant humiliation, uncertain survival and terror. The harsh living condition, characterized by crowding, absent sanitation and poor personal hygiene led to considerable morbidity, mainly due to injuries, infectious diseases and famine, and to high mortality rates. Medical care in the camps was the responsibility of the S.S. Each camp had a chief S.S. physician accompanied by a number of assistants and orderlies. There was also a parallel system of "prisoner-physicians." There was a chief prisoner-physician in every camp, and each block was assigned a "block doctor" who was responsible for sanitation, the removal of corpses, setting up the sick- call and authorizing sick leave. Work teams were accompanied by "mobile doctors" (Streckenpfleger), who dispensed first aid for work injuries. Prisoner-physicians were also charged with disinfecting the blocks and maintaining hygienic conditions in the camp. Every camp had one or more blocks, called "Reviers", that were used for treatment and hospitalization. In the larger camps a number of blocks were designated to function as a sort of hospital (Krankenbau). At times one camp out of a group of camps would be set aside as quarantine, primarily for patients with infectious diseases. Officially, the "Revier" was the responsibility of an S.S. physicians', assisted by a chief prisoner-physician, his assistants and, at times, nurses. But in actuality the Reviers were managed by prisoners (Capos) who did not have medical training but were authorized to make decisions in medical matters such as operations and, on occasion, even performed them. The Reviers suffered from shortage of everything: beds, manpower, diagnostic and therapeutic means, sterile supplies and drugs for anaesthesia. Crowding was the rule, and each cot was occupied simultaneously by several patients regardless of their condition or the nature of their disease. Life-saving procedures could not be performed and surgery, if done, was usually without anaesthesia. Mortality was high, and the Revier was commonly perceived by the prisoners as a place of death, not of healing. Occasionally there were visits, or inspections, by the S.S. physicians. The main purpose of those visits was "selection". Patients with no chance of recovery were sent to their death and the others were returned to work in spite of their condition. The prisoner-physicians made every effort to prevent this "selection" in various ways. They were often punished or even executed for their efforts.

Concentration Camps↗