PubMed Health⌕ Search

Biomedical subjects

R C Yang

Publications and source records attributed to R C Yang.

At least 19 recordsLinked to original sources
PubMed2006

Lost in publication: Half of all renal practice evidence is published in non-renal journals.

Physicians often scan a select number of journals to keep up to date with practice evidence for patients with kidney conditions. This raises the question of where relevant studies are published. We performed a bibliometric analysis using 195 renal systematic reviews. Each review used a comprehensive method to identify all primary studies for a focused clinical question relevant to patient care. We compiled all the primary studies included in these reviews, and considered where each study was published. Of the 2779 studies, 1351 (49%) were published in the top 20 journals. Predictably, this list included Transplantation Proceedings (5.9% of studies), Kidney International (5.3%), American Journal of Kidney Diseases (4.7%), Nephrology Dialysis Transplantation (4.3%), Transplantation (4.2%), and Journal of the American Society of Nephrology (2.4%). Ten non-renal journals were also on this list, including New England Journal of Medicine (2.4%), Lancet (2.3%), and Diabetes Care (2.2%). The remaining 1428 (51%) studies were published across other 446 journals. When the disciplines of all journals were considered, 59 were classified as renal or transplant journals (42% of articles). Other specialties included general and internal medicine (16%), endocrinology (diabetes) and metabolism (6.5%), surgery (6.2%), cardiovascular diseases (6.1%), pediatrics (4.3%), and radiology (3.3%). About half of all renal practice evidence is published in non-renal journals. Browsing the top journals is important. However, relevant studies are also scattered across a large range of journals that may not be routinely scanned by busy physicians, and keeping up with this literature requires other continuing education strategies.

Evidence-Based Medicine↗
PubMed2006

Proteinuria and reduced kidney function in living kidney donors: A systematic review, meta-analysis, and meta-regression.

We reviewed any study where 10 or more healthy adults donated a kidney, and proteinuria, or glomerular filtration rate (GFR) was assessed at least 1 year later. Bibliographic databases were searched until November 2005. 31 primary authors provided additional information. Forty-eight studies from 27 countries followed a total of 5048 donors. An average of 7 years after donation (range 1-25 years), the average 24 h urine protein was 154 mg/day and the average GFR was 86 ml/min. In eight studies which reported GFR in categories, 12% of donors developed a GFR between 30 and 59 ml/min (range 0-28%), and 0.2% a GFR less than 30 ml/min (range 0-2.2%). In controlled studies urinary protein was higher in donors and became more pronounced with time (three studies totaling 59 controls and 129 donors; controls 83 mg/day, donors 147 mg/day, weighted mean difference 66 mg/day, 95% confidence interval (CI) 24-108). An initial decrement in GFR after donation was not accompanied by accelerated losses over that anticipated with normal aging (six studies totaling 189 controls and 239 donors; controls 96 ml/min, donors 84 ml/min, weighted mean difference 10 ml/min, 95% CI 6-15; difference not associated with time after donation (P=0.2)). Kidney donation results in small increases in urinary protein. An initial decrement in GFR is not followed by accelerated losses over a subsequent 15 years. Future studies will provide better estimates, and identify those donors at least risk of long-term morbidity.

Adolescent↗
PubMed2005

Enhanced growth suppression of Philadephia1 leukemia cells by targeting bcr3/abl2 and VEGF through antisense strategy.

An antisense strategy by targeting both bcr3/abl2 and VEGF was designed to suppress the growth of Philadephia1 leukemia cells in vitro and in vivo in mice. In vitro, although bcr3/abl2 or VEGF antisense oligodeoxyribonucleotides (AS-ODNs) alone was able to inhibit the proliferation of K562 cells, the combination of bcr3/abl2 and VEGF AS-ODNs produced an additive inhibitory effect on the growth of K562 cells and significantly enhanced the sensibility of K562 cells to apoptosis-inducing stimuli including STI571. In vivo, the nude mice xenografted with K562 cells received intratumoral injections of bcr3/abl2 and VEGF AS-ODNs showed a significant reduction in leukemia tumor size and microvessel density and an increase of apoptosis in the tumors when compared to the mice that received an individual agent. These results demonstrate that targeting both bcr3/abl2 and VEGF can result in an additive tumor-suppressive action and may represent an excellent strategy to augment the efficacy of chemotherapy in CML.

Animals↗
PubMed2001

Heat shock pretreatment influences the expression of PKC isoforms during sepsis.

Protein Kinase C (PKC) plays a central role in signal transduction and participates in diverse biological and biochemical functions. PKC dysfunction leads to general immunosuppression that, in turn, increases host susceptibility to infection and sepsis. In our previous study, we demonstrated that the mortality of sepsis is significantly decreased in rats treated with heat shock. It was considered that the modulation of PKC content by previous heat shock might contribute to the resistance to a severe infection. In this study, we attempted to understand the change of various PKC isoforms in the lymphocytes during sepsis and to investigate the role of previous heat shock in influencing PKC expression. Cecal ligation and puncture (CLP) was used as the experimental sepsis model for its biphasic clinical manifestation. Heat shock protein and PKC isoforms were detected by immunochemical study. Ten PKC isoforms (alpha, beta, gamma, delta, epsilon, zeta, theta, iota, lambda, and mu) were detected from peripheral lymphocytes. Results showed that all the PKC isoforms have a declination tendency along with the progression of CLP-induced sepsis, and previous heat shock treatment could prevent the declination of PKC content, particularly the isoforms beta, gamma, and epsilon, during sepsis. We suggest that heat shock response may participate in maintenance of PKC expression and contribute to decrease the severity of systemic infection.

Animals↗
PubMed2001

Hyperthermic pretreatment decreases microvascular protein leakage and attenuates hypotension in anaphylactic shock in rats.

Systemic anaphylaxis is a life-threatening allergic reaction and its pathologic conditions, such as edema, bronchospasm, and hypotension, have been attributed to release of vasoactive mediators. Heat shock protein (HSP) is known to play a protective role in living cells under various stresses. In these studies, we investigated the protective role of heat shock response in anaphylactic shock, focusing on changes of blood pressure (BP) and vascular permeability. Adult sensitized rats were injected intravenously with Evans blue (EB) and challenged with bovine serum albumin (BSA). The rats were treated with whole-body hyperthermia at 41.5 +/- 0.5 degrees for 15 min 24 h before BSA challenge. Vascular protein leakage in tissues was analyzed with the EB technique. The results showed that BSA challenge induced EB extravasation in all sensitized rats. EB values (EB/tissue; microg/g) in heart and lung (112.3 +/- 41 and 244.4 +/- 90.6; mean +/- SD; n = 6) in the nonheated rats were significantly higher than those (33.4 +/- 23.3 and 103.4 +/- 63.9; n = 9) in the heated rats (P < 0.05). The results showed that BSA challenge caused BP to fall drastically in the sensitized rats. BP in the heated rats was significantly higher than BP in the nonheated rats from 4 to 15 min during anaphylactic shock (P < 0.001). Inducible HSP72 appeared overexpressed in heart, lung, and liver tissue in the heated rats tested by Western immunoblotting. The results indicate that reduction of increased protein leakage and attenuation of hypotension may result from induction of HSP by whole-body hyperthermia.

Anaphylaxis↗
PubMed2001

The decrease of PKCalpha is associated with hepatic apoptosis at early and late phases of polymicrobial sepsis.

The present study investigates the relationship between the PKC-alpha and hepatic apoptosis during sepsis. Cecal ligation and puncture- (CLP) induced animal model of polymicrobial sepsis was used, with early and late sepsis referring to those animals sacrificed at 9 and 18 h, respectively, after CLP. The expressions of PKCalpha and Bcl-2 family proteins as well as poly(ADP-ribose) polymerase (PARP) cleavage were quantified to evaluate the possible factors involved in the hepatic cell death during sepsis. The apoptosis of hepatocytes under septic condition or hepatocytes treated with PKCalpha antisense was evaluated by gel electrophoresis and/or flow cytometry after Annexin-V-Fluos and propidium iodide staining. The results indicated that (1) the protein expression of membrane-associated PKCalpha was decreased at early (P < 0.05) and late (P < 0.01) sepsis; (2) the protein expressions of Bcl-2 and Bcl-xL were decreased, whereas Bax expression was increased at late sepsis; (3) the percentage of PARP cleavage was increased at early (P < 0.05) and late (P < 0.01) sepsis; (4) severe DNA fragmentation was observed at late sepsis; (5) the apoptotic cell population was increased at early and late sepsis; and (6) the percentage of apoptotic cell population in PKCalpha antisense-treated cells was significantly higher than that in untreated cells. These results suggest that inactivation of PKCalpha may play an important role in modulating hepatic apoptosis during sepsis and the apoptosis is closely associated with the alterations of Bcl-2 family proteins.

Animals↗
PubMed2001

Prenatal exposure of testosterone prevents SDN-POA neurons of postnatal male rats from apoptosis through NMDA receptor.

The role of N-methyl-D-aspartate (NMDA) receptor in mediating the effect of testosterone exposure prenatally on neuronal apoptosis in the sexual dimorphic nucleus of the preoptic area (SDN-POA) of rats was studied. The endogenous testosterone was diminished by prenatal stress (PNS) or simulated by testosterone exposure (TE) to understand the effect of testosterone on NR(1) (a functional subunit protein of NMDA receptor) expression and neuronal apoptosis. To further study whether the testosterone, after being converted into estradiol, modulates NR(1) expression, 4-androstein-4-ol-3,17-dione (ATD; an aromatase inhibitor) was used to block the conversion of estradiol from testosterone. The expressions of the NR(1) mRNA and NR(1) subunit protein were quantified by RT-PCR and western blotting analysis, respectively. In addition, a noncompetitive antagonist of NMDA receptor, MK-801, was used to find out whether blockage of NMDA receptor affects the naturally occurring apoptosis in SDN-POA. The results showed the following. 1) Expression of perinatal NR(1) subunit protein in the central part of the medial preoptic area of male rats was significantly higher than that of females, especially on postnatal days 1 and 3. 2) The testosterone level of male fetuses on embryonic day 18 was significantly higher than that of females, while the testosterone level of TE females or PNS males was similar to that of intact males or intact females, respectively. 3) The apoptotic incidence of intact male rats was significantly less than that of females, and the apoptosis was stimulated by PNS in male or inhibited by TE in female. 4) The expression of NR(1) subunit protein could be inhibited by PNS or ATD-treatment in male, while stimulated by TE in female. 5) NR(1) mRNA showed no significant difference among intact male, PNS male, ATD-treated male, TE female and intact female rats. 6) The low apoptotic incidence of male rats was significantly increased when NMDA receptor was blocked by MK-801. These results suggest that testosterone, after being converted to estradiol, may prevent the SDN-POA neurons of male rats from apoptosis through enhancing the expression of NR(1) at the posttranscriptional level.

Animals↗
PubMed2001

Superior mesenteric artery syndrome associated with hereditary motor and sensory neuropathy type II--a case report.

A 14-year-old girl with superior mesenteric artery (SMA) syndrome associated with hereditary motor and sensory neuropathy (HMSN) type II is reported. The initial presentations of HMSN type II were developmental delay and gait disturbance at 2 years of age. All deep tendon reflexes were absent. Nerve conduction velocities and left sural nerve biopsy all revealed axonal changes. Recently, she suffered from intermittent bilious vomiting and epigastralgia for 6 months. That caused body weight loss from 40 kg to 28 kg. Abdominal echography showed narrowed superior mesenteric artery angle. Upper gastrointestinal series revealed obstruction of third portion of duodenum. Accordingly, SMA syndrome was diagnosed. To the best of our knowledge, this case is the first report of SMA with HMSN type II in the world. When a child with chronic neurological disease presents with intermittent vomiting, SMA should be considered as a disease entity of differential diagnosis.

Adolescent↗
PubMed2000

Potential protective effect of NF-kappaB activity on the polymicrobial sepsis of rats preconditioning heat shock treatment.

The present study was designed to investigate the role of NF-kappaB in influencing the outcome of sepsis modulated by previous heat shock treatment. Sepsis was induced in rats by cecum ligation and puncture (CLP) method, which manifests two distinct clinical phases: an initial hyperdynamic phase (9 h after CLP, early sepsis) followed by a hypodynamic phase (18 h after CLP, late sepsis). Rats of heated group were treated by whole body hyperthermia 24 h prior to the CLP operation. Lymphocytes were collected during the early and late sepsis phases. The expressions of Hsp72, p65 and I-kappa B were evaluated by Western blot and immunochemical analysis. NF-kappaB activity was detected by EMSA. The results showed that NF-kappaB activation was initiated during early sepsis and apparently suppressed during late stage of sepsis. Previously treated by heat shock, late-sepsis rats emerged with high preservation of p65 expression and NF-kappaB activity, while Hsp72 was over-expressed. In conclusion, down-regulation of NF-kappaB activity during late sepsis could be attenuated by pretreatment of heat shock through the preservation of p65 expression. The results may provide a mechanistic explanation for the improved outcome to polymicrobial sepsis of rats that are preconditioned with heat shock, as well as a novel highlight for therapeutic intervention of severe infection.

Animals↗
PubMed2000

Late diagnosis of Kawasaki disease is associated with haptoglobin phenotype.

BACKGROUND: Kawasaki disease (KD) is an acute febrile illness characterized by multiple clinical and biochemical features of inflammation and the most common complications of coronary artery abnormality (CAA). Haptoglobin (Hp) is an acute-phase protein whose phenotype is known to be involved in coronary artery diseases. In this paper, we report the investigation of the association of Hp phenotype with the formation of CAA in KD. PATIENTS AND METHODS: Forty-seven consecutive patients with clinically diagnosed KD were admitted. Sera were taken before therapy of intravenous immunoglobulins (IVIG) plus aspirin, and levels of serum proteins were measured by a rate immunonephelometer. The echocardiographic criteria for coronary artery abnormality were evaluated during acute or subacute stages. Hp phenotyping was performed by Western immunoblotting. RESULTS: Duration of fever at diagnosis of KD was significantly different between patients with Hp 2-2 (6.4 +/- 1.2 days, n = 25) and with Hp1 allele (Hp 2-1 plus Hp 1-1; 8.8 +/- 3.5 days, n = 22). In contrast, serum levels of Hp between KD patients with Hp2-2 and with Hp1 allele (297 +/- 121 mg dL-1 vs. 330 +/- 101 mg dL-1, respectively) was not significantly different. On the other hand, no patients with Hp 2-2 (0/25) were recognized as having KD in subacute stage. However, 5 out of 20 patients with Hp 2-1 were recognized in subacute stage, and their incidence of CAA was 80.0% (4/5). CONCLUSIONS: Patients with Hp 2-1 have patterns of delayed or incomplete presentation of clinical symptoms. Therefore, the late diagnosis of KD is associated with haptoglobin phenotype.

Acute Disease↗
PubMed2000

Zygotic associations and multilocus statistics in a nonequilibrium diploid population.

The usual approach to characterizing and estimating multilocus associations in a diploid population assumes that the population is in Hardy-Weinberg equilibrium. The purpose of this study is to develop a set of summary statistics that can be used to characterize and estimate the multilocus associations in a nonequilibrium population. The concept of "zygotic associations" is first expanded to facilitate the development. The summary statistics are calculated using the distribution of a random variable, the number of heterozygous loci (K) found in diploid individuals in the population. In particular, the variance of K consists of single-locus and multilocus components with the latter being the sum of zygotic associations between pairs of loci. Simulation results show that the multilocus associations in the variance of K are detectable in a sample of moderate size (> or =30) when the sum of all pairwise zygotic associations is greater than zero and when gene frequency is intermediate. The method presented here is a generalization of the well-known development for the Hardy-Weinberg equilibrium population and thus may be of more general use in elucidating the multilocus organizations in nonequilibrium and equilibrium populations.

Analysis of Variance↗
PubMed2000

Blockage of N-methyl-D-aspartate receptors decreases testosterone levels and enhances postnatal neuronal apoptosis in the preoptic area of male rats.

Sexual dimorphism has been found in the preoptic area of the hypothalamus (POA), a major site of glutamate actions via N-methyl-D-aspartate (NMDA) receptors. The sexually dimorphic nucleus of the preoptic area (SDN-POA) of male rats exhibits about seven-fold greater nuclear volume than that of females. A naturally occurring neonatal neuronal apoptosis, that can be prevented by testosterone, may contribute to this sexual difference in SDN-POA nuclear volume. Since activation of NMDA receptors in the POA induces GnRH secretion, it may be involved in both elevation of serum testosterone and prevention of neuronal death in the SDN-POA. In the present study, protein expression of NMDA receptors in the POA of male and female fetuses was quantified on the day preceding the fetal testosterone peak (embryonic day 16; ED 16). Rats were then distributed in four groups: (1) untreated males, (2) untreated females, (3) males pretreated with MK-801 (a noncompetitive NMDA receptor antagonist), and (4) females pretreated with MK-801. Serum levels of testosterone were estimated on the afternoon of ED 18. Expression of Bcl-2 and Bax, as well as neuronal apoptosis in SDN-POA, were observed on postnatal day 8. The results showed that (1) expression of NMDA receptors in the POA of male fetuses was higher than that of females on ED 16; (2) levels of testosterone were lower in MK-801 pretreated male fetuses than in intact males on ED 18; (3) expression of Bcl-2 in the POA of MK-801 pretreated male rats was significantly less than that of control males; (4) the apoptotic incidence in the SDN-POA of MK-801 pretreated male rats was significantly greater than in control males, while there was no significant difference in apoptotic incidence in the SDN-POA between MK-801 pretreated and intact females. These results suggest that the NMDA receptor is highly expressed in prenatal male fetuses, and that it might play an important role in the elevation of testosterone levels. Moreover, activation of NMDA receptors may protect SDN-POA neurons from naturally occurring neuronal death, by modulating testosterone and/or Bcl-2 expression.

Animals↗
PubMed2000

Attenuation of sepsis-induced apoptosis by heat shock pretreatment in rats.

Apoptosis is a process by which cells undergo a form of non-necrotic cellular suicide. Although it is a programmed process, apoptosis can be induced by various stressors. During sepsis, apoptosis has been regarded as an important cause of cell death in the immune system, leading to unresponsiveness to treatment. This study was designed to investigate how prior heat shock induction can influence the rate of apoptosis in animals that have experienced sepsis. Sprague-Dawley rats were used, and experimental sepsis was induced by cecal ligation and puncture (CLP). Animals in the heated group were anesthetized and received heat shock by whole-body hyperthermia. They were sacrificed 9 h and 18 h after CLP as early and late sepsis, respectively. Apoptosis was evaluated by "DNA ladder" detection in agarose electrophoresis and Tdt-mediated dUTP nick end-labeling (TUNEL) assay. Hsp72 was detected by Western blot analysis. The results showed that the DNA ladder was detected most clearly in the thymus at the late phase of sepsis with time course dependence, while it showed less clearly in heat shock treated animals. Histopathological study by TUNEL assay obtained similar results in the thymus, where the cortex was more susceptible to apoptosis than the medulla. The Western blot analysis showed that the heat shock induced Hsp72 concomitant with an increase in Bcl-2:Bax ratio. In conclusion, heat shock pretreatment prevents rats from sepsis-induced apoptosis that may account for the better outcome of experimental sepsis. An increase in the Bcl-2:Bax ratio may in part explain the molecular mechanism of the effect of heat shock pretreatment.

Animals↗
PubMed2000

Human herpesvirus 6 in hematologic diseases in China.

BACKGROUND AND OBJECTIVE: The prevalence and pathogenic role of human herpesvirus 6 (HHV-6) in various benign and malignant hematologic diseases remain largely unknown. The aim of this study was to search for a possible involvement of HHV-6 in the pathogenesis of hematologic diseases. DESIGN AND METHODS: The presence of HHV-6 DNA sequences was examined by polymerase chain reaction (PCR) in bone marrow mononuclear cells from 241 patients with benign and malignant hematologic diseases in China. Platelet-associated immunoglobulin (PAIg) of 66 idiopathic thrombocytopenic purpura (ITP) patients was measured by competitive enzyme-linked immunosorbent assay. The presence of HHV-6 DNA in sera from 31 ITP patients was examined by PCR. Paired serum samples from 19 ITP patients were analyzed for anti-HHV-6 IgG titers using an indirect immunofluorescence assay. RESULTS: HHV-6 DNA was detected in 41% and 37.5% of ITP and acute leukemia patients respectively, but in only 6.7% of patients with iron deficiency anemia. HHV-6 positivity for ITP patients with excessive PAIgG was significantly higher than in patients with a normal level of PAIgG. HHV-6 DNA was not detected in any of the serum samples from ITP patients. None of the 19 cases of ITP showed a significant increase in anti-HHV-6 antibody titers during the convalescent phase compared with the onset phase. INTERPRETATION AND CONCLUSIONS: Our results indicate that HHV-6 infection might be associated with excessive PAIgG in some cases of ITP, and that the virus persists in a latent state. The pathogenic role of HHV-6 in ITP needs to be confirmed by further investigations.

Acute Disease↗
PubMed1999

Ultrasound effect on level of stress proteins and arthritic histology in experimental arthritis.

OBJECTIVE: To investigate the effect of ultrasound on the levels of stress protein in experimental arthritis and their relation to the therapeutic effects on arthritic cartilage repair. METHODS: Thirty-six rats with similar degree of early arthritis were divided at random into two groups. In group s, 18 rats received sonication; in group c, 18 control rats received sham sonication. The severity of induced arthritis was evaluated from bone scan with technetium-99m. The presence and changes of stress protein were identified from immunostain of SP72 antibody from frozen sections of arthritic cartilage and from electrophoresis of proteins extracted from chondrocytes of arthritic cartilage. The severity index, density of immunostained chondrocytes, and histopathologic changes at various periods were also studied in each group. RESULTS: The density of stress protein was increased markedly in treated rats after sonication and it was closely related to the repair of arthritic cartilage. Once the pathohistology of arthritic cartilage improved, stress protein declined significantly in the follow-up period. CONCLUSION: Therapeutic ultrasound can enhance stress protein production in arthritic chondrocytes. The extragenic production of stress protein was well correlated with the therapeutic effect of ultrasound to preserve chondrocytes and bring about the repair of arthritic cartilage.

Animals↗
PubMed1999

Evidence of multi-step regulation of HSP72 expression in experimental sepsis.

Heat shock proteins (Hsps) are a family of highly conserved proteins induced in response to various stresses. Hsps protect cells against subsequent lethal circumstances. Previous work from our laboratory has indicated that Hsp72 is not induced during experimental sepsis in rats, but the regulation of the induction of Hsp72 synthesis in this disease cascade has not been investigated. In the present study, we evaluated the expression of the hsp72gene, focusing on the activation and DNA-binding ability of heat shock factor 1 (HSF1), hsp mRNA accumulation, and Hsp72 synthesis in animal sepsis models induced by cecal ligation and puncture procedure. The results were compared with those of sham-treated and heat-shocked rats. It was shown that the expression of the hsp72 gene in sepsis was a multi-step process, as previously documented in in vitro studies. Hsp72 synthesis was not induced during sepsis, whereas DNA binding of HSF was detectable, suggesting that the induction of Hsp72 is blocked downstream to HSF-DNA complex formation by the metabolic alteration occurring during sepsis. The dissociation failure of the constitutive heat shock element binding factor (CHBF) from the heat shock element may play an important role in this negative regulation.

Animals↗
PubMed1999

Previous hyperthermic treatment increases mitochondria oxidative enzyme activity and exercise capacity in rats.

The study was designed to investigate the role of hyperthermia in the tolerance of exercise in rats and the possible mechanism was examined. The hyperthermic pretreatment was performed using an electric pad on the anesthesized rats 24 hours before exercise. Rats were exercised passively in a motor-controlled round treadmill in high temperature environment (36-37 degrees C) until exhaustion. The capacity of tolerance was calculated. Lymphocytes and gastrocnemius muscle were collected from both groups. The changes in muscular morphology, mitochondria oxidative enzyme activity and induction of Hsp72 were investigated. The results revealed that experimental rats were more tolerant to exercise at high temperature than the control group; the duration time were 89 +/- 17.8 min and 63.1 +/- 7.3 min, respectively. Hsp72 was induced markedly in the experimental group, both in muscle and lymphocytes, indicating a heat shock response. There was no significant change in morphology of the mitochondria, 24 hours after hyperthermic treatment, as shown by histopathological and electromicroscopic investigation. However, the activity of mitochondrial enzymes increased significantly in experimental group before exercise: 84.6 +/- 6.3 and 345 +/- 15.4 (nmole cytochrome c/min/mg total protein) respectively of NADH-cytochome c reductase and succinate-cytochome c reductase activity in experimental group compared to 58.9 +/- 4.7 and 269.0 +/- 24.0 in control group (p < 0.05, by student t-test). It is concluded that hyperthermic treatment enhances muscular mitochondrial oxidative enzyme activity in rats, and results in increasing tolerance to exercise at high temperature. The heat shock response, most probably the inducible Hsp72, is a crucial factor in this effect.

Adenosine Triphosphate↗