Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HS”

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 559 records · Page 31Linked to original sources
PubMed2004

Surgical implications of anatomical landmarks on the lateral surface of the mastoid bone.

The aim of this study was to examine the relationships of the surgical landmarks on the lateral surface of the mastoid bone with the landmarks in a deeper location. Simple mastoidectomy was carried out without drilling over the linea temporalis inferior (LTI) on 20 adult temporal bones. The suprameatal spine, i.e., Henle spine (HS), variants were noted. Morphometric measurements were performed between these surgical landmarks, and their variations with pneumatization or HS types were evaluated. Three types of HS were identified: triangular, crest, absent. The HS-lateral semicircular canal distance was 15 mm on average and longer in bones with a triangular HS than a crest type HS (16.4 vs. 14.3 mm). The LTI was found to be located on average 4.7 mm inferior to the middle fossa dural plate (MFD). The LTI-MFD distance had a tendency to be longer in bones without an HS than with a crest type of HS (5.9 vs. 3.9 mm). Chorda tympani emerged from the facial nerve at the stylomastoid foramen in five specimens (25%). This anatomical organization was not correlated with the type of HS. Korner's septum (KS) was identified in nine bones (45%). It was present in eight of 16 (50%) bones with good pneumatization. No tendency for the existence of KS was found for any specific type of HS. This study confirms that the mastoid antrum is located 15 mm deep to the lateral surface of the mastoid bone. It should be expected to be longer in bones with a triangular HS. In addition, the MFD is located on average 5 mm above the LTI, which could be useful information for beginners or inexperienced surgeons. The ear surgeon should anticipate that the MFD might be longer in bones without an HS.

Adult↗
PubMed2005

Transiently enhanced LPS-induced fever following hyperthermic stress in rabbits.

Hyperthermia has been shown to induce an enhanced febrile response to the bacterial-derived endotoxin lipopolysaccharide (LPS). The aim of the present study was to test the hypothesis that the enhanced LPS-induced fever seen in heat stressed (HS) animals is caused by leakage of intestinal bacterial LPS into the circulation. Male rabbits were rendered transiently hyperthermic (a maximum rectal temperature of 43 degrees C) and divided into three groups. They were then allowed to recover in a room at 24 degrees C for 1, 2 or 3 days post-HS. One day after injection with LPS, the post-HS rabbits exhibited significantly higher fevers than the controls, though this was not seen in rabbits at either 2 or 3 days post-HS. The plasma levels of endogenous LPS were significantly increased during the HS as compared to those seen in normothermic rabbits prior to HS. LPS fevers were not induced in these animals. One day post-HS, rabbits that had been pretreated with oral antibiotics exhibited significantly attenuated LPS levels. When challenged with human recombinant interleukin-1beta instead of LPS, the 1-day post-HS rabbits did not respond with enhanced fevers. The plasma levels of TNFalpha increased similarly during LPS-induced fevers in both the control and 1-day post-HS rabbits, while the plasma levels of corticosterone and the osmolality of the 1-day post-HS rabbits showed no significant differences to those seen prior to the HS. These results suggest that the enhanced fever in the 1-day post-HS rabbits is LPS specific, and may be caused by increased leakage of intestinal endotoxin into blood circulation.

Animals↗
PubMed1986

A solid-phase substrate of heparanase: its application to assay of human melanoma for heparan sulfate degradative activity.

We found a tumor metastasis-associated heparan sulfate (HS)-degrading endoglycosidase in melanoma cells that is a unique endo-beta-glucuronidase (heparanase) capable of specifically cleaving HS at intrachain sites (M. Nakajima, T. Irimura, N. DiFerrante, and G. L. Nicolson, 1984, J. Biol. Chem. 259, 2283-2290). To perform rapid and microscale quantitative assays of heparanase we developed a solid-phase HS substrate by crosslinking radiolabeled HS onto agarose gel beads using one covalent linkage. The HS from bovine lung was partially N-desulfated and labeled with [14C]acetic anhydride. Free HS amino groups were completely acetylated, and reducing terminal saccharides were reductively aminated. The HS derivatives with amino groups at their reducing termini were coupled to amino-reactive agarose beads. Incubation of the solid-phase HS substrates with B16 melanoma cell extracts in the presence of D-saccharic acid 1,4-lactone (a potent exo-beta-glucuronidase inhibitor) resulted in the time- and dose-dependent release of [14C]HS fragments. Human melanoma cell lines were tested for HS-degrading endoglycosidase using the newly developed solid-phase HS substrates. The human malignant melanoma cells tested had high levels of HS-degrading activity that were comparable to those of highly metastatic murine B16-F10 melanoma cells.

Glucuronidase↗
PubMed1992

Effects of MgCl2 on the release and recycling of heparan sulfate proteoglycans in a rat parathyroid cell line.

Divalent cations, such as Mg2+, Ba2+, and Co2+, are known to mimic the effects of Ca2+ in parathyroid cells, but it is not clear whether the mechanism of their action is the same as that of Ca2+. We have shown that extracellular Ca2+ concentration ([Ca2+]e) regulates the distribution and recycling of cell-surface heparan sulfate (HS) proteoglycans in a rat parathyroid cell line; at normal to high [Ca2+]e (e.g., 2 mM) HS proteoglycans are primarily localized intracellularly, while at low [Ca2+]e (0.05 mM) they are translocated to the cell surface and rapidly recycle (Takeuchi, Y., Sakaguchi, K., Yanagishita, M., Aurbach, G. D., and Hascall, V. C., 1990, J. Biol. Chem. 265, 13661-13668). We now show that a high concentration of Mg2+ (8 mM) reduces the amount of recycling HS proteoglycans in low [Ca2+]e. However, the primary effects of high Ca2+ and high Mg2+ on the recycling HS proteoglycans are different. High [Ca2+]e causes translocation of HS proteoglycans to intracellular compartments, while high Mg2+ stimulates cleavage of their core proteins and subsequent shedding of HS proteoglycans into the medium, thereby depleting the recycling molecules. However, high Mg2+ does not induce shedding of HS proteoglycans in high [Ca2+]e. The effects of Ba2+ and Co2+ were similar to those of Mg2+, but Sr2+ showed no significant effects on HS proteoglycan translocation. Otherwise, 8 mM Mg2+ did not alter biosynthesis or intracellular catabolism of HS proteoglycans. These observations suggest that the recycling of HS proteoglycans in parathyroid cells is sensitive only to [Ca2+]e, whereas several other divalent cations can deplete the recycling HS proteoglycans by a distinctly different mechanism. Thus, the mechanism by which Ca2+ regulates the amounts of the recycling HS proteoglycans may be more physiological and play a functional role in parathyroid cells.

Animals↗
PubMed1990

Two different proteoheparan sulfate species are synthesized by bovine corneal endothelial cells.

Cultured bovine corneal endothelial cells were labeled with either [35S]sulfate or a combination of [3H]glucosamine and [35S]methionine. The medium proteoheparan sulfate (HS-PG) and cell-associated HS-PG were isolated and identified as heparan sulfate-containing proteoglycans by the susceptibility of their glycosaminoglycan component to specific enzymatic and chemical degradation. The native medium HS-PG has an apparent Mr of about 300,000 and an Mr of its protein core of 64,000, while the native cell-associated HS-PG had a lower molecular weight (approx. 100,000) and an Mr of its protein core of 33,000. The protein core of both HS-PG types consisted of a single polypeptide chain. After beta-elimination reaction of the native HS-PGs the resulting heparan sulfate side chains of medium HS-PG had an Mr of about 60,000, and those of cell-associated HS-PG an Mr of about 30,000. The different molecular parameters of medium HS-PG and cell-associated HS-PG refer to different functional roles. The medium HS-PG secreted by the endothelial cells is regarded as a metabolic precursor of the Descemet's membrane, while the cell-associated HS-PG might represent a cell membrane-integrated proteoglycan.

Animals↗
PubMed1978

Comparison of absorption and metabolism of beta-sitosterol and beta-sitostanol in rats.

The fates of [4-14C]beta-sitosterol ([14C]S) and [4-14C]beta-sitostanol ([14C]HS) were compared after after oral or intravenous administration to rats. Excretion into feces of oral [14C]HS was significantly higher than that of [14C]S. More than 97% of [14C]HS and 88% of [14CS]S were recovered in the feces within 7 days. Thus, deposition of [14C]HS was negligible in the tissues that were examined. Turnover in serum of [14C]HS which was injected intravenously appeared to be more rapid than that of [14C]S; [14C]HS was excreted as neutral steroids at a rate more than twice that of [14C]S. The rate of excretion of [3H]cholesterol was slightly greater when HS was administered simultaneously. The liver contained significantly less radioactivity after [14C]HS than after [14C]S administration. More [14C]HS than [14C]S was present in esterified form in serum and liver. The ratio of sterol in very low density lipoprotein to that in high density lipoprotein was less for HS or S than for endogenous cholesterol; this was particularly marked with HS. These results suggest that HS would be a more effective hypocholesterolemic agent than S.

Administration, Oral↗
PubMed1989

Airway responsiveness to methacholine after inhalation of nebulized hypertonic saline in bronchial asthma.

To assess whether the changes in airway methacholine (Meth) responsiveness induced by an initial hypertonic challenge determine the response to a subsequent hypertonic provocation, 11 subjects with asthma had bronchial challenges with 3.6% hypertonic saline (HS) and Meth in a dose-dependent manner and in random order. Challenges consisted of (1) an HS challenge (HS1) followed 1 hour later by a second HS challenge (HS2), (2) a Meth challenge alone (Meth1), and (3) an HS challenge followed 1 hour later by a Meth challenge (Meth2). The dose of HS that produced a 35% fall in SGaw (PD35) in HS1 was 69 L (geometric mean), and the PD35 in HS2 was 107 L (p = 0.02). Refractory index (PD35 HS2/PD35 HS1) ranged from 0.7 to 5.0. After HS challenge, airway responsiveness to Meth increased, and the Meth PD35 fell from 0.26 mumol to 0.11 mumol (geometric mean, p = 0.004). There was an inverse linear correlation between the refractory index and increases in Meth sensitivity (PD35 Meth1/PD35 Meth2) (r = -0.66; p = 0.027). After an initial HS challenge, the ratio of PD35 HS to PD35 Meth increased in all subjects, indicating that all subjects had become less responsive to HS compared to Meth, irrespective of their refractory index. We suggest that an initial HS challenge induces protective mechanisms toward a subsequent HS challenge in all individuals. The degree of increase in Meth responsiveness elicited by the initial provocation is a major factor in determining the airway response to a subsequent HS challenge.

Administration, Inhalation↗
PubMed1995

The pathogenic role of the NMDA receptor in hyperthermia-induced seizures in developing rats.

Hyperthermia-induced seizures (HS) in rats have been used as a model of febrile seizures. Activation of the N-methyl-D-aspartate (NMDA) receptor by increased extracellular glutamate (Glu) in the cortex during hyperthermia may be involved in the induction of HS and HS kindling. To confirm this hypothesis, the effects of a potent blocker of the NMDA receptor, MK-801, on the threshold and pattern of HS were evaluated. The threshold temperatures for rats given 0.1 (low dose) and 0.5 (high dose) mg/kg MK-801 (i.p.) for the first time were 41.6 degrees C (39.7-42) (median, range) and 42.0 (41.2-42.0), respectively, which were significantly higher than the 40.5 (39.4-41.2) for rats without MK-801 administration (P < 0.01). The recurrent occurrence of HS suppressed the increase in the threshold temperature with age, and changed the seizure from partial to generalized seizures (HS kindling), whereas these effects of recurrent HS on the threshold and pattern of HS were inhibited by the high dose (0.5 mg/kg) of MK-801. MK-801 blocks HS and HS kindling. The activation of the NMDA receptor during hyperthermia plays an important role in the induction of HS and HS kindling.

Age Factors↗
PubMed2005

The effects of noxious heat, auditory stimulation, a cognitive task, and time on task on pain perception and performance accuracy in healthy volunteers: a new experimental model.

The effects of cognitive and competing sensory processing tasks on pain perception and as a function of time are only partially understood. To study these effects, we compared the simultaneous effects of noxious heat stimulation (HS), auditory stimulation (AS) (sinusoidally modulated speech-like signal, SMSLS), and a cognitive task (CT) (rate change detection of the SMSLS) on pain perception and task performance over repeated experimental runs. Sixty healthy paid volunteers were randomly assigned to four groups, one exposed to AS while performing the CT, one to HS (46 degrees C/6 min), one to AS and HS, and one to AS and HS while performing the CT. Each group performed the experimental run four times, each run for 6 min. Immediately after each run, the subjects rated pain intensity using a VAS (0-100). Two-way RM-ANOVA for analyzing pain intensities among the three heat pain groups demonstrated significant differences of VAS ratings (F(2,179) = 4.57, P = 0.019), being highest in the HS group (55 +/- 0.7SEM), followed by the AS+HS (39 +/- 6.8) and AS + HS + CT (33 +/- 0.7) groups. Post-hoc analyses revealed that group HS differed significantly from group AS + HS + CT and from group AS + HS (P < 0.05, SNK), whereas group AS+HS did not differ significantly from group AS + HS + CT. Neither pain rating, nor rate of errors on the CT varied significantly across runs. These findings point to a significant influence of competing passive sensory processing on pain perception, with the cognitive task not necessarily adding to the perception of pain. Advantages and shortcomings of the present experimental model for future pain studies are discussed.

Acoustic Stimulation↗
PubMed1999

Heparan sulfate chains with antimitogenic properties arise from mesangial cell-surface proteoglycans.

Heparan sulfate (HS) chains accumulate in both the medium and the cell layer of mesangial cell cultures. When given in fresh medium to quiescent cultures at naturally occurring concentrations, they suppress entry into the cell cycle and progression to DNA synthesis. We have attempted to identify the proteoglycan (PG) source of the antimitogenic HS chains from mesangial cell layers (HS(c)) and medium (HS(c)). When cells were labeled for 16 hours with [35S]sulfate, 25% of the label was found in intracellular HS chains and 5% in extracellular HSPGs. Cell-surface HSPGs accounted for the remaining 70% of the label associated with cell-layer HS and were released by either trypsin or 2% Triton X-100. About 20% of this cell-surface fraction was released by treatment with phosphatidylinositol-specific phospholipase C (PI-PLC), and probably represents glypican-like PG; glypican mRNA was present in the cells. The remainder of this fraction could be incorporated into liposomes, indicating the presence of hydrophobic transmembrane regions suggestive of syndecans. Upon purification and deglycosylation, an antiserum to rat liver HSPGs that reacts primarily with syndecan-2 showed a strong signal corresponding to this protein and three weaker bands that may represent additional syndecans. mRNAs for syndecan-1, -2, and -4 were present in the cultures. Syndecan-1 and -2 mRNAs were increased 30 minutes after stimulation of quiescent rat mesangial cells (RMCs) with serum. Heparin, HS(c), and HS(m) all prevented this increase. Syndecan-4 mRNA was not affected by serum, heparin, or HS. In pulse-chase experiments, the amount of 35S appearing in the cellular protein-free HS fraction was accounted for almost entirely by cell-surface PGs, as matrix-associated label was a minor contribution at the end of the pulse-labeling. The appearance of [35S]HS in cell extracts was unaffected by phospholipase C treatment, indicating that turnover of the newly labeled syndecan fraction is the source of the antimitogenic HS chains.

Animals↗
PubMed2002

Extending the golden hour of hemorrhagic shock tolerance with oxygen plus hypothermia in awake rats. An exploratory study.

In a previous study of volume-controlled hemorrhagic shock (HS) in awake rats, without fluid resuscitation, either breathing of 100% oxygen or moderate hypothermia while breathing air, increased survival time. We hypothesized that combining oxygen and hypothermia can maximally extend the "golden hour" of HS from which resuscitation can be successful in terms of survival rate. Rats were prepared under light general anesthesia, breathing spontaneously via face mask, and then awakened for 2 h. Then, 3.25 ml arterial blood/100 g were withdrawn over 20 min. At the end of HS of 30, 60, 90 or 180 min duration, the shed blood was reinfused. Breathing was spontaneous. Survival endpoint was 24 h or earlier death. HS of 30 or 60 min was used for preliminary experiments; HS of 90 or 180 min for 35 definitive experiments. Control groups A-1 and B-1 had normothermia (rectal temperature 37.5 degrees C) and were breathing air. Treatment groups A-2 and B-2 had total body surface cooling during HS to rectal temperature 32 degrees C and were breathing 100% O(2). Arterial pressure during HS was higher in the hypothermia-O(2) groups. With HS of 90 min, in the normothermia-air group A-1 (n=10), none of the 10 rats survived to 3 h; while in the hypothermia-O(2) group A-2 (n=5), all rats survived to 24 h (P<0.001). With HS of 180 min, in the normothermia-air group B-1 (n=10), three of 10 rats survived to 3 h and 24 h (hypotension during HS in these three survivors was less severe than in the non-survivors); and in the hypothermia-O(2) group B-2 (n=10) all 10 rats survived to 24 h (P<0.003). We conclude that moderate hypothermia (32 degrees C) plus 100% oxygen inhalation during volume-controlled HS in awake rats mitigates hypotension and increases the chance of survival. It enables survival even after 3 h of moderate HS.

Animals↗
PubMed2002

Pancreatic tumor growth is regulated by the balance between positive and negative modulators of angiogenesis.

There is increasing evidence for the implication of tumor-derived angiogenic and anti-angiogenic factors in controlling tumor growth in vivo. In this study, we documented the production of inhibitors of angiogenesis by pancreatic cancer cells and examined how changes in the balance between pro- and anti-angiogenic factors regulate tumor growth in vivo. The human pancreatic cancer cell line Hs-776T (HS-W) produces slow-growing tumors in SCID mice. Cells of a variant form (HS-R) of Hs-776T produced faster-growing tumors compared to HS-W. Characterization of HS-W and HS-R cells in vitro showed similar proliferation rates and production of the angiogenic factors vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). Analyzes of anti-angiogenic factors showed comparable levels of angiostatin and thrombospondin 1 and 2, but endostatin was only detected in conditioned media of HS-W cells and was absent in HS-R. Cell proliferation was similar in both tumor types in vivo, whereas HS-W tumors demonstrated increased apoptosis with a high percentage of apoptotic endothelial cells (EC). Subsequently, VEGF was over-expressed in Hs-776T cells (HS-VF), resulting in rapidly growing tumors and lowering tumor and EC apoptosis. Collectively, our study confirms that tumor growth is dependent on its ability to increase the angiogenic stimulus or to reduce the amounts of endogenous anti-angiogenic factors.

Animals↗
PubMed1999

Heat stress produces an early phase of protection against oxidative damage in human muscle.

BACKGROUND: It has been rarely reported that heat stress induces an early phase of protection against oxidative damage, whereas a delayed phase of protection is shown in heat stress. To explore the early effect of heat stress against oxidative damage, we evaluated the changes in contractility, lipid peroxidation, and ultrastructure induced by hydrogen peroxide (H2O2) with or without heat stress (HS) in human skeleton muscle. METHODS: Thirty-two muscle samples were obtained from the vastus lateralis muscle of 7 subjects. These specimens were divided into three groups based on form of treatment: HS (n = 13), non HS (n = 14), and control group (n = 5). The control group was performed under identical conditions without H2O2. Specimens in the HS group were incubated at 42 degrees C for 20 min, while those in the non-HS and control groups were maintained at 37 degrees C. RESULTS: The control group showed no significant change in contractile force. Although contractile force significantly decreased 30 min after H2O2 administration in both the HS and non-HS groups, only the HS group showed apparent recovery of contractile force 60 min after H2O2 administration. Lipid peroxidation was lower in the HS group than in the non-HS group. Ultrastructural examination revealed less mitochondrial damage in the HS group compared with the non-HS group. CONCLUSION: We found that human skeleton muscle escaped cellular damage induced by H2O2 in the early phase after heat stress. These data suggest evidence for an early effect of heat stress against ischemia/reperfusion injury in human muscle.

Adult↗
PubMed1997

Heparanase and a synthetic peptide of heparan sulfate-interacting protein recognize common sites on cell surface and extracellular matrix heparan sulfate.

Heparanase is an endo-beta-D-glucuronidase that degrades the glycosaminoglycan chains of heparan sulfate (HS) proteoglycans at specific sites. Elevated levels of heparanase are associated with the metastatic potential of melanoma and other types of tumor cells. We previously reported heparanase degradation of cell surface HS subpopulations of the human adenocarcinoma cell line RL95. In the present study, heparanase activity was examined on RL95 cell surface HS subpopulations in the presence of a synthetic peptide (CRPKAKAKAKAKDQTK) of heparin/heparan sulfate-interacting protein (HIP; Liu, S., Smith, S. E., Julian, J., Rohde, L. H., Karin, N. J., and Carson, D. D. (1996) J. Biol. Chem. 271, 11817-11823). Heparanase digestion generated HS fragments from cell surface- or extracellular matrix-derived HS of approximately 25 and 9 kDa, respectively. In contrast, HS of various size classes isolated from proteoglycans secreted or released by RL95 and endothelial cells in culture were not susceptible to heparanase digestion. Incubation of heparanase-containing melanoma cellular extracts or partially purified heparanase preparations with cell surface- or ECM-derived HS and HIP peptide, but not a scrambled sequence of this peptide or other HS-binding proteins present in ECM, completely inhibited heparanase action. Conversely, predigestion of cell surface HS with either heparanase-containing cellular extracts or with secreted or partially purified heparanase destroyed binding to HIP peptide. Preincubation of HS with HIP peptide prevented subsequent heparanase digestion. Collectively, these data demonstrate that HIP peptide and heparanase recognize specific, common motifs within HS chains at cell surfaces and in ECM and may mutually modulate HS-dependent activities.

Amino Acid Sequence↗
PubMed2006

Distribution of C-reactive protein and its relation to arterial hypertension in a country representing a high-risk region for cardiovascular diseases.

AIMS: The high-sensitivity C-reactive protein (hs-CRP) measurement is recommended by ESC/ESH Guidelines 2003 in patients with arterial hypertension. The aim of this study was to assess distribution of hs-CRP in Poland, a country representing a high-risk region for CVD. METHODS AND RESULTS: In 2002, the cross-sectional survey NATPOL PLUS was performed in a representative sample of adults in Poland aged 18-94 years. The questionnaire, anthropometrical and blood pressure measurements, glycaemia, lipidogram and hs-CRP were performed in 2333 respondents. The results of hs-CRP > 10 mg/l were excluded from analysis. Mean hs-CRP was 2.03+/-2.14 mg/l (2.13+/-2.12 mg/l in women vs 1.91+/-2.16 mg/l in men; p < 0.05). Hs-CRP > or = 1 mg/l was observed in 58% of women and in 52% of men (p < 0.05). In hypertensives (> or =140/90 mmHg or treatment: women 30% vs men 29%, ns.), hs-CRP > or = 1 mg/l was found in 74% of women, and in 63% of men. The transformed values of hs-CRP [-1/[hs-CRP](1/2)] were higher in hypertensive patients than in normotensives (-0.94 vs -1.05; p < 0.01). CONCLUSION: (i) The increased level of hs-CRP was found in more than half of adults in Poland. (ii) The hs-CRP is higher in hypertensive patients than in normotensives. (iii) In view of the given results, routine measurements of hs-CRP in hypertensive patients in a country like Poland should be reconsidered.

Adolescent↗
PubMed1995

CD44 isoforms containing exon V3 are responsible for the presentation of heparin-binding growth factor.

Glycosaminoglycan-modified isoforms of CD44 have been implicated in growth factor presentation at sites of inflammation. In the present study we show that COS cell transfectants expressing CD44 isoforms containing the alternatively spliced exon V3 are modified with heparan sulfate (HS). Binding studies with three HS-binding growth factors, basic-fibroblast growth factor (b-FGF), heparin binding-epidermal growth factor (HB-EGF), and amphiregulin, showed that the HS-modified CD44 isoforms are able to bind to b-FGF and HB-EGF, but not AR. b-FGF and HB-EGF binding to HS-modified CD44 was eliminated by pretreating the protein with heparitinase or by blocking with free heparin. HS-modified CD44 immunoprecipitated from keratinocytes, which express a CD44 isoform containing V3, also bound to b-FGF. We examined whether HS-modified CD44 isoforms were expressed by activated endothelial cells where they might present HS-binding growth factors to leukocytes during an inflammatory response. PCR and antibody-binding studies showed that activated cultured endothelial cells only express the CD44H isoform which does not contain any of the variably spliced exons including V3. Immunohistological studies with antibodies directed to CD44 extracellular domains encoded by the variably spliced exons showed that vascular endothelial cells in inflamed skin tissue sections do not express CD44 spliced variants. Keratinocytes, monocytes, and dendritic cells in the same specimens were found to express variably spliced CD44. 35SO4(-2)-labeling experiments demonstrated that activated cultured endothelial cells do not express detectable levels of chondroitin sulfate or HS-modified CD44. Our results suggest that one of the functions of CD44 isoforms expressing V3 is to bind and present a subset of HS-binding proteins. Furthermore, it is probable that HS-modified CD44 is involved in the presentation of HS-binding proteins by keratinocytes in inflamed skin. However, our data suggests that CD44 is not likely to be the proteoglycan principally involved in presenting HS-binding growth factors to leukocytes on the vascular cell wall.

Alternative Splicing↗
PubMed2004

A survey on high-concentration-capability headspace sampling techniques in the analysis of flavors and fragrances.

This survey critically discusses high-concentration-capacity (HCC) headspace (HS) techniques applied to sample the volatile fraction of matrices of interest in the flavors and fragrance fields. In particular, the advantages, limits, and fields of application of HS solid-phase microextraction (SPME), high-capacity HS sorptive extraction (HSSE) and HS solid-phase dynamic extraction (SPDE) are evaluated. These techniques are discussed in view of the peculiar characteristic of HCC-HS techniques, from the standpoint that these techniques are a bridge between static (S-HS) and dynamic HS (D-HS) because they are as simple, fast, easy to automate, and reliable as S-HS, yet afford analyte concentration factors comparable to those of D-HS. Moreover, the different degree of their development is a consequence of the different times in which they were introduced into the market, because the potential of HS-SPME is now well known, having been introduced approximately 12 years ago, but that of HSSE has still to be fully explored, and HS-SPDE still has to be investigated because it is very recent.

Data Collection↗
PubMed1990

Induction of the heat shock response in rats modulates heart rate, creatine kinase and protein synthesis after a subsequent hyperthermic treatment.

STUDY OBJECTIVE - The aim of the study was to examine the effect of prior induction of the heat shock response on heat shock protein synthesis and physiological variables relevant to the shock response. DESIGN - Synthesis of heat shock protein (SP71, molecular mass 71,000) was induced in rats by 15 min hyperthermia (42 degrees C). Protein synthesis, heart rate, blood pressure and creatine kinase activity were determined in comparison with controls (no heat shock) and a group receiving two heat shock treatments 24 h apart (prior induction group). SUBJECTS - 24 male Sprague-Dawley rats (125-150 g) were used, divided into three groups: controls (n = 4), heat shock X 1 (HS, n = 11), heat shock X 2 (2 X HS, n = 9). Heat shock was induced under anaesthesia on a heating pad. MEASUREMENTS and RESULTS - Blood pressure and heart rate were measured at the beginning of the hyperthermia period, when body temperature first reached 42 degrees C (t = 0 min) and at the end of the hyperthermia treatment (t = 15 min). At t = 0 min systolic blood pressure and heart rate were increased compared to the control values in both HS and 2 X HS groups. At t = 15 min heart rate in the HS group was increased to 554 (SEM21) beats.min-1 v control 465(19) (p less than 0.05). In the 2 X HS group, heart rate of 494(14) beats.min-1 at t = 15 min was not significantly different from control. At t = 15 min, creatine kinase values in the hyperthermia treatment groups were not different from control. However at 2.5 h after hyperthermic treatment plasma creatine kinase was increased in the HS group to 481(83) mU.ml-1 (n = 6) v 223(20) in controls, but was not increased in the 2 X HS group [178(64), n = 4]. Rats were radiolabelled for 2 h with 1.0 mCi of [35S]-methionine 30 min after hyperthermic treatment in HS group and 30 min after the second hyperthermic treatment in 2 X HS group. Following the 2 X HS treatment, synthesis of SP71, though increased above control values, was lower than in the HS group. CONCLUSIONS - The reduction in heart rate, plasma creatine kinase and synthesis of SP71 following a second hyperthermic exposure could be caused by a protective influence of the first exposure.

Animals↗