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PubMed2004

AAA ATPase p97/valosin-containing protein interacts with gp78, a ubiquitin ligase for endoplasmic reticulum-associated degradation.

Endoplasmic reticulum-associated degradation (ERAD) is a protein quality control mechanism that eliminates unwanted proteins from the endoplasmic reticulum (ER) through a ubiquitin-dependent proteasomal degradation pathway. gp78 is a previously described ER membrane-anchored ubiquitin ligase (E3) involved in ubiquitination of ER proteins. AAA ATPase (ATPase associated with various cellular activities) p97/valosin-containing protein (VCP) subsequently dislodges the ubiquitinated proteins from the ER and chaperones them to the cytosol, where they undergo proteasomal degradation. We now report that gp78 physically interacts with p97/VCP and enhances p97/VCP-polyubiquitin association. The enhanced association correlates with decreases in ER stress-induced accumulation of polyubiquitinated proteins. This effect is abolished when the p97/VCP-interacting domain of gp78 is removed. Further, using ERAD substrate CD3delta, gp78 consistently enhances p97/VCP-CD3delta binding and facilitates CD3delta degradation. Moreover, inhibition of endogenous gp78 expression by RNA interference markedly increases the levels of total polyubiquitinated proteins, including CD3delta, and abrogates VCP-CD3delta interactions. The gp78 mutant with deletion of its p97/VCP-interacting domain fails to increase CD3delta degradation and leads to accumulation of polyubiquitinated CD3delta, suggesting a failure in delivering ubiquitinated CD3delta for degradation. These data suggest that gp78-p97/VCP interaction may represent one way of coupling ubiquitination with retrotranslocation and degradation of ERAD substrates.

Adenosine Triphosphatases↗

PubMed2004

Comparison of systemic and mucosal delivery of 2 canarypox virus vaccines expressing either HIV-1 genes or the gene for rabies virus G protein.

BACKGROUND: Since the primary routes of human immunodeficiency type 1 (HIV-1) infection are across mucosal barriers, a randomized trial of canarypox virus-based vectors was conducted in 84 individuals, with delivery of vaccine by mucosal routes, and was accompanied by a detailed analysis of humoral, cellular, and mucosal immune responses. METHODS: Over the course of 6 months, HIV-1-specific (vCP 205) and rabies (vCP 65) canarypox virus vectors were delivered systemically and/or mucosally into the nose, mouth, vagina, or rectum in a 4-dose schedule, followed by 2 doses of HIV-1 MN recombinant glycoprotein (rgp) 120 or subunit rabies vaccine administered by the intramuscular route. RESULTS: Administration of vaccine and collection of samples were well tolerated. Serum IgG HIV-1-specific antibodies to rgp120 were rarely seen after either systemic or mucosal delivery of canarypox virus vaccine. In contrast, serum IgG rabies and canarypox antibodies were detected in all individuals after systemic, but rarely after mucosal, delivery of vaccine. Suggestions of mucosal recognition of HIV-1 antigen included a cytotoxic T lymphocyte response in 4 of 8 individuals after administration of vaccine by the intrarectal route and a limited immunoglobulin A response at the same site. CONCLUSIONS: Each of the routes of vaccine administration was feasible in the context of a phase 1 study with motivated individuals. However, with the doses and routes of administration used, canarypox virus was not an effective mucosal immunogen.

AIDS Vaccines↗

PubMed2003

Vaccinia virus complement control protein increases early bacterial clearance during experimental peritonitis.

BACKGROUND: Complement is one of the first immunological pathways activated in peritonitis. It functions to initiate and augment the innate immune response. Complement activation has also been shown to contribute to multiple organ failure after sepsis. Vaccinia virus complement control protein (VCP) is an immunomodulatory protein encoded by vaccinia virus and binds complement components C3b and C4b of the complement cascade to inhibit both the classical and alternative pathways of complement activation. This study investigates the effect of complement inhibition by recombinant (r) VCP on bacterial clearance after cecal ligation and puncture (CLP). METHODS: Swiss Webster mice were intravenously given either 20 mg/kg rVCP in 0.2 mL of normal saline, or 0.2 mL of normal saline alone, at the time of CLP. After 4 and 18 h, samples of peritoneal washout, blood, liver, and lung were collected for bacteriology, myeloperoxidase (MPO) assay for neutrophil accumulation, differential cell counts, and interleukin (IL)12 ELISA. Statistical analysis was by Mann-Whitney U test for bacteriology, and analysis of variance (ANOVA) for MPO and IL-12 concentrations. RESULTS: Aerobic and anaerobic bacterial levels were significantly lower at 4 h after treatment with rVCP (p < 0.05) in peritoneal lavage, blood, and liver compared with controls. There were no differences in bacterial levels at 18 h. There were no differences in myeloperoxidase concentrations or in the differential cell counts between the groups at either 4 or 18 h after CLP. IL-12 concentrations in serum or peritoneal washout were also not different. CONCLUSIONS: rVCP enhances early bacterial clearance in mice after CLP, although not through neutrophil recruitment, as MPO concentrations and cell counts were not different. rVCP may, however, increase neutrophil function potentially by prevention of accumulation of complement factors that inhibit leukocytes. Further studies will be needed to elucidate this pathway.

Animals↗

PubMed1998

Tyrosine phosphorylation regulates cell cycle-dependent nuclear localization of Cdc48p.

Cdc48p from Saccharomyces cerevisiae and its highly conserved mammalian homologue VCP (valosin-containing protein) are ATPases with essential functions in cell division and homotypic fusion of endoplasmic reticulum vesicles. Both are mainly attached to the endoplasmic reticulum, but relocalize in a cell cycle-dependent manner: Cdc48p enters the nucleus during late G1; VCP aggregates at the centrosome during mitosis. The nuclear import signal sequence of Cdc48p was localized near the amino terminus and its function demonstrated by mutagenesis. The nuclear import is regulated by a cell cycle-dependent phosphorylation of a tyrosine residue near the carboxy terminus. Two-hybrid studies indicate that the phosphorylation results in a conformational change of the protein, exposing the nuclear import signal sequence previously masked by a stretch of acidic residues.

Adenosine Triphosphatases↗

PubMed2003

DNA damage modulates nucleolar interaction of the Werner protein with the AAA ATPase p97/VCP.

We report a novel nucleolar interaction between the AAA ATPase p97/VCP and the Werner protein (WRNp), a member of the RecQ helicase family. p97/VCP mediates several important cellular functions in eucaryotic cells, including membrane fusion of the endoplasmic reticulum and Golgi and ubiquitin-dependent protein degradation. Mutations in the WRN gene cause Werner syndrome, a genetic disorder characterized by premature onset of aging symptoms, a higher incidence of cancer, and a high susceptibility to DNA damage caused by topoisomerase inhibitors. We observed that both WRNp and valosin-containing protein (VCP) were present in the nucleoplasm and in nucleolar foci in mammalian cells and that WRNp and p97/VCP physically interacted in the nucleoli. Importantly, the nucleolar WRNp/VCP complex was dissociated by treatment with camptothecin, an inhibitor of topoisomerase I, whereas other WRNp-associated protein complexes, such as WRNp/Ku 80, were not dissociated by this drug. Because WRN syndrome cells are sensitive to topoisomerase inhibitors, these observations suggest that the VCP/WRNp interaction plays an important role in WRN biology. We propose a novel role for VCP in the DNA damage response pathway through modulation of WRNp availability.

Adenosine Triphosphatases↗

PubMed2004

Interaction of U-box-type ubiquitin-protein ligases (E3s) with molecular chaperones.

Members of the U-box family of proteins constitute a class of ubiquitin-protein ligases (E3s) distinct from the HECT-type and RING finger-containing E3 families. Two representative mammalian U-box proteins, UFD2a and CHIP, interact with the molecular chaperones VCP and either Hsp90 or Hsc70, respectively, and are implicated in the degradation of damaged proteins. We have now investigated the roles of mammalian U-box proteins by performing a comprehensive screen for molecules that interact with these proteins in the yeast two-hybrid system. All mammalian U-box proteins tested were found to interact with molecular chaperones or cochaperones, including Hsp90, Hsp70, DnaJc7, EKN1, CRN, and VCP. These observations suggest that the function of U box-type E3s is to mediate the degradation of unfolded or misfolded proteins in conjunction with molecular chaperones as receptors that recognize such abnormal proteins.

Amino Acid Sequence↗

PubMed2006

Sensitization of pelvic nerve afferents and mast cell infiltration in the urinary bladder following chronic colonic irritation is mediated by neuropeptides.

Irritable bowel syndrome and interstitial cystitis frequently overlap. We have shown that acute colitis sensitizes urinary bladder afferents to both mechanical and chemical stimuli and that chronic colitis similarly produces neurogenic cystitis. We hypothesize that chronic irritation of the colon releases neuropeptides from bladder afferents, leading to receptor sensitization and neurogenic inflammation. Female Sprague-Dawley rats received intrarectal trinitrobenzenesulfonic acid (TNBS) or vehicle 3 days following either systemic capsaicin (CP) pretreatment or vehicle. Ten days later, action potentials of single-unit pelvic C-fiber afferents with receptive fields in the bladder were recorded under urethane anesthesia during graded bladder distensions (UBD) or intravesical capsaicin (vCP) administration. In controls, UBD increased bladder afferent firing in proportion to intravesical pressure. At intravesical pressures of 30 mmHg and above, the percent increase in afferent firing was significantly accentuated following TNBS compared with controls (1,222 +/- 176 vs. 624 +/- 54%, P < 0.01). The response to vCP was also enhanced (4,126 +/- 775 vs. 1,979 +/- 438%, P < 0.01). Systemic depletion of neuropeptides from sensory nerves abolished these effects. Histological examination of the bladders revealed an increase in mast cell density in TNBS-treated animals compared with controls (18.02 +/- 1.25 vs. 3.11 +/- 0.27 mast cells/x100 field, P < 0.01). This effect was significantly ameliorated with CP (10.25 +/- 0.95, P < 0.5 vs. TNBS-treated animals). In summary, chronic colonic irritation in the rat sensitizes urinary bladder afferents to noxious stimuli and causes mast cell infiltration in the bladder. Depletion of neuropeptides from sensory afferents diminishes these effects, suggesting they play an important role.

Anesthesia↗

PubMed1985

Centrally administered naloxone blocks reflex natriuresis after acute unilateral nephrectomy.

Acute unilateral nephrectomy (AUN) leads to a natriuresis and kaliuresis by the remaining kidney through reflex mechanisms involving opiate receptors. To determine whether the opiate receptors mediating these responses are located in the central nervous system, we carried out AUN in anesthetized rats undergoing continuous ventriculocisternal perfusion (VCP) with artificial cerebrospinal fluid (CSF). AUN caused large increases in both Na (UNaV) and K (UKV) excretion without changes in glomerular filtration rate or arterial blood pressure. When the opiate receptor antagonist naloxone was added to the perfusate to achieve a perfusion rate of 32 micrograms X kg-1 X h-1, AUN failed to increase either UNaV or UKV by the remaining kidney. This dose of naloxone, however, was without effect when infused intravenously. Addition of thyrotropin-releasing hormone (TRH) to the artificial CSF to achieve a VCP rate of 50 micrograms X kg-1 X h-1 also blocked the expected increase in UNaV and UKV by the remaining kidney after AUN. Infusion of TRH intravenously at the same rate did not interfere with the postnephrectomy natriuresis or kaliuresis. Higher intravenous infusion rates of TRH (1 and 2 mg X kg-1h-1) prevented the postnephrectomy natriuresis without affecting the kaliuresis. These results indicate that the effect of naloxone to block the reflex natriuresis and kaliuresis after AUN resides largely in the central nervous system. The blockade by naloxone of the postnephrectomy natriuresis is duplicated by centrally administered TRH, providing another example of the interaction of this hormone with the endogenous opioid system. Large intravenous infusions of TRH also block the postnephrectomy natriuresis but not the kaliuresis.

Animals↗

PubMed1989

CSF acidosis augments ventilation through cholinergic mechanisms.

Ventilation is influenced by the acid-base status of the brain extracellular fluids (ECF). CO2 may affect ventilation independent of changes in H+. Whether the acidic condition directly alters neuronal firing or indirectly alters neuronal firing through changes in endogenous neurotransmitters remains unclear. In this work, ventriculocisternal perfusion (VCP) was used in anesthetized (pentobarbital sodium, 30 mg/kg) spontaneously breathing dogs to study the ventilatory effects of acetylcholine (ACh), eucapnic acidic (pH approximately 7.0) cerebrospinal fluid (CSF), and hypercapnic acidic (pH approximately 7.1) CSF in the absence and presence of atropine (ATR). Each animal served as its own control. Base line was defined during VCP with control mock CSF (pH approximately 7.4). With ATR (4.8 mM) there was an insignificant downward trend in minute ventilation (VE). ACh (6.6 mM) increased VE 53% (n = 12, P less than 0.01), eucapnic acidic CSF increased VE 41% (n = 12, P less than 0.01), and hypercapnic acidic CSF increased VE 47% (n = 6, P less than 0.01). These positive effects on ventilation were not seen in the presence of ATR. This suggests that acidic brain ECF activates ventilatory neurons through muscarinic cholinergic mechanisms. Higher concentrations of ACh increased ventilation in a concentration-dependent manner. Higher concentrations of ATR decreased ventilation progressively, resulting in apnea. The results suggest that ACh plays a significant role in the central augmentation of ventilation when the brain ECF is made acidic by either increasing CSF PCO2 or decreasing CSF bicarbonate.

Acetylcholine↗

PubMed2024

Stool Protein Mass Spectrometry Identifies Biomarkers for Early Detection of Diffuse-type Gastric Cancer.

There is a high unmet need for early detection approaches for diffuse gastric cancer (DGC). We examined whether the stool proteome of mouse models of gastric cancer (GC) and individuals with hereditary diffuse gastric cancer (HDGC) have utility as biomarkers for early detection. Proteomic mass spectrometry of the stool of a genetically engineered mouse model driven by oncogenic KrasG12D and loss of p53 and Cdh1 in gastric parietal cells [known as Triple Conditional (TCON) mice] identified differentially abundant proteins compared with littermate controls. Immunoblot assays validated a panel of proteins, including actinin alpha 4 (ACTN4), N-acylsphingosine amidohydrolase 2 (ASAH2), dipeptidyl peptidase 4 (DPP4), and valosin-containing protein (VCP), as enriched in TCON stool compared with littermate control stool. Immunofluorescence analysis of these proteins in TCON stomach sections revealed increased protein expression compared with littermate controls. Proteomic mass spectrometry of stool obtained from patients with HDGC with CDH1 mutations identified increased expression of ASAH2, DPP4, VCP, lactotransferrin (LTF), and tropomyosin-2 relative to stool from healthy sex- and age-matched donors. Chemical inhibition of ASAH2 using C6 urea ceramide was toxic to GC cell lines and GC patient-derived organoids. This toxicity was reversed by adding downstream products of the S1P synthesis pathway, which suggested a dependency on ASAH2 activity in GC. An exploratory analysis of the HDGC stool microbiome identified features that correlated with patient tumors. Herein, we provide evidence supporting the potential of analyzing stool biomarkers for the early detection of DGC. Prevention Relevance: This study highlights a novel panel of stool protein biomarkers that correlate with the presence of DGC and has potential use as early detection to improve clinical outcomes.

Feces↗

PubMed2002

Videocapillaroscopic findings in the microcirculation of the psoriatic plaque.

BACKGROUND: Videocapillaroscopy (VCP) is a method to study the morphology and dynamics of microcirculation, but information about capillaroscopic features of the psoriatic plaque is limited. OBJECTIVE: To investigate the distribution, morphology and density of capillaries in lesional and perilesional skin of the psoriatic plaque. METHODS: VCP of a well-delimited plaque of the trunk, arms or legs in 15 consecutive patients with untreated, chronic plaque psoriasis was performed. RESULTS: In the lesional skin, capillaries were tortuous and dilated, homogeneously appearing as 'bushy'. In the perilesional skin, capillary loops seemed to be on a parallel course with respect to the skin surface, with their apex directed towards the marginal zone. The number of capillary loops per area unit was statistically increased in perilesional compared to lesional skin. CONCLUSION: According to the morphology, distribution and density of capillary loops, two different angiogenetic patterns were found in lesional and perilesional skin.

Adult↗

PubMed2005

Curcumin inhibits the classical and the alternate pathways of complement activation.

Curcumin (Cur), the golden yellow phenolic compound in turmeric, is well studied for its medicinal properties. In the current investigation, Cur dissolved using sodium hydroxide solution (CurNa) was tested for in vitro complement inhibitory activity and compared with rosmarinic acid (RA) and quercetin (Qur) dissolved using sodium hydroxide (RANa and QurNa, respectively) and the vaccinia virus complement control protein (VCP). The comparative study indicated that CurNa inhibited the classical complement pathway dose dependently (IC50 = 404 microM). CurNa was more active than RANa, but less active than QurNa. VCP was about 2,212, 2,786, and 4,520 times more active than QurNa, CurNa, and RANa, respectively. Further study revealed that CurNa dose dependently inhibited zymosan-induced activation of the alternate pathway of complement activation.

Analysis of Variance↗

PubMed1994

Effect of mannitol on cerebrospinal fluid dynamics and brain tissue edema.

Mannitol is used widely to decrease intracranial pressure (ICP); however, the mechanism by which this effect occurs is unclear. This study was designed to examine the effects of mannitol on cerebrospinal fluid (CSF) formation rate (Vf), resistance to reabsorption of CSF (Ra), and brain tissue water content (BTWC). Eighteen New Zealand White rabbits were allocated into one of three groups and studied at baseline and at two sequential doses of 20% mannitol: 0.75 g/kg followed by 4.4 mg.kg-1.min-1, and 2.0 g/kg (1.25 g/kg added to the initial dose of 0.75 g/kg) followed by 8.6 mg.kg-1.min-1. In Group 1, closed ventriculocisternal perfusion (VCP) was performed to determine changes in ICP due to mannitol. In Group 2, the increase in CSF osmolality due to mannitol was determined. In Group 3, mock CSF was used for open VCP to determine Vf and Ra. At the conclusion of each study, brain tissue samples were taken for determination of BTWC. Mannitol increased CSF and plasma osmolality. Ra was increased by 104% with the low dose of mannitol and not significantly changed by the high dose. Mannitol decreased BTWC, Vf (by 49% with the high dose), ICP, and hematocrit. The authors conclude that two of the mechanisms contributing to decreased ICP with mannitol are: 1) decreased CSF volume as indicated by decreased Vf, and 2) decreased brain tissue volume as indicated by decreased BTWC.

Animals↗

PubMed2000

Human cell exposure assays of Bacillus thuringiensis commercial insecticides: production of Bacillus cereus-like cytolytic effects from outgrowth of spores.

Most contemporary bioinsecticides are derived from scaled-up cultures of Bacillus thuringiensis subspecies israelensis (Bti) and kurstaki (Btk), whose particulate fractions contain mostly B. thuringiensis spores (> 10(12)/L) and proteinaceous aggregates, including crystal-like parasporal inclusion bodies (PIB). Based on concerns over relatedness to B. cereus-group pathogens, we conducted extensive testing of B. thuringiensis (BT) products and their subfractions using seven human cell types. The Bti/Btk products generated nonspecific cytotoxicities involving loss in bioreduction, cell rounding, blebbing and detachment, degradation of immunodetectable proteins, and cytolysis. Their threshold dose (Dt approximately equal.5 times 10(-14)% BT product/target cell) equated to a single spore and a target cell half-life (tLD(50)) of approximately 16 hr. At Dts > 10(4), the tLD(50) rapidly shifted to < 4 hr; with antibiotic present, no component, including PIB-related [delta]-endotoxins, was cytolytic up to an equivalent of approximately 10(9 )Dt. The cytolytic agent(s) within the Bti/Btk-vegetative cell exoprotein (VCP) pool is an early spore outgrowth product identical to that of B. cereus and acting possibly by arresting protein synthesis. No cytolytic effects were seen with VCP from B. subtilis and Escherichia coli. These data, including recent epidemiologic work indicate that spore-containing BT products have an inherent capacity to lyse human cells in free and interactive forms and may also act as immune sensitizers. To critically impact at the whole body level, the exposure outcome would have to be an uncontrolled infection arising from intake of Btk/Bti spores. For humans, such a condition would be rare, arising possibly in equally rare exposure scenarios involving large doses of spores and individuals with weak or impaired microbe-clearance capacities and/or immune response systems.

Bacillus cereus↗

PubMed2006

Contribution of genetic factors to the pathogenesis of Paget's disease of bone and related disorders.

Paget's disease of bone (PDB) is a common condition with a strong genetic component that is characterized by focal increases in bone turnover, leading to bone deformity, pathological fractures, and various other complications. Several rare disorders have also been described that show phenotypic overlap with PDB. Genome-wide searches have identified several susceptibility loci for PDB and PDB-like disorders, and mutations that cause these disorders have now been identified in four genes, all of which are involved in the RANK-NF-kappaB signaling pathway. Mutations in SQSTM1, which encodes an important scaffold protein in this pathway, have been found to be a common cause of classical PDB. Thus far, all disease-causing mutations in SQSTM1 affect the ubiquitin-associated (UBA) domain of the gene product and cause loss of ubiquitin binding. The rare PDB-like disorders of familial expansile osteolysis, early-onset familial PDB, and expansile skeletal hyperphosphatasia are caused by duplication mutations in exon 1 of the TNFRSF11A gene, which encodes the RANK receptor. This gene does not seem to be involved in the pathogenesis of classical PDB. Inactivating mutations in the TNFRSF11B gene, which encodes osteoprotegerin, cause juvenile PDB, and TNFRSF11B polymorphisms seem to increase the risk of classical PDB. The rare syndrome of hereditary inclusion body myopathy, PDB, and frontotemporal dementia (IBMPFD) is caused by mutations in the VCP gene, which is involved in regulating I-kappaB degradation by the proteasome. The disease-causing mutations in VCP cluster in and around a domain involved in ubiquitin binding. Whereas SQSTM1 has emerged as an important gene for classical PDB, most kindreds with familial PDB do not carry SQSTM1 mutations, indicating that additional genes for PDB remain to be discovered. In light of the molecular defects that have been identified thus far, it seems likely that these genes will also be involved in the RANK-NF-kappaB signaling pathway or its interactions with the ubiquitin-proteasome system.

Genetic Predisposition to Disease↗

PubMed1999

Microvascular fluid filtration capacity (Kf) assessed with cumulative small venous pressure steps and with various degrees of tilt.

UNLABELLED: Orthostatic dysregulation is a frequent phenomenon in pilots experiencing extreme G forces and after prolonged exposures to microgravity in cosmonauts. We used non-invasive venous congestion plethysmography (VCP) to study microcirculatory changes and the ability to activate peripheral and centrally mediated protective mechanisms during various degrees of tilt, which we used as an orthostatic challenge. METHOD: The study, which was approved by the local ethical committee of the Institute of Biomedical Problems, was performed on six healthy 20 - 26 years old male volunteers. We applied 6 - 8 cumulative small venous congestion pressure steps (8 mmHg) to the thigh and determined the fluid filtration capacity (Kf), the linear relationship between cuff pressure (Pcuff) and measured fluid filtration (Jv). We then measured the fluid filtration (Jv) response to varying cumulative degrees of tilt, starting at 0 degrees followed by head down -8 degrees -15 degrees, -30 degrees -15 degrees, -8 degrees, 0 degrees, and then head up 15 degrees, 30 degrees, 70 degrees, 30 degrees, 15 degrees and 0 degrees. Each tilt stage was sustained for 15 minutes. The change in hydrostatic load, at the level of the strain gauge, was determined by measuring the difference in vertical height between the right atrium and mid calf at the level of the gauge. Limb arterial blood flow was measured and lung function tests were performed before and after the small cumulative pressure step protocol, as well as at the end of each tilt step. RESULTS: No significant changes in blood pressure (BP) and heart rate (HR) occurred during the cumulative pressure step protocol. However, an increase in HR was observed during the tilt, but only reached significance at 30 degrees and 70 degrees. The mean Kf value measured with small cumulative pressure steps was 3.25 +/- 0.5 (10(-3) ml.100 ml tissue(-1) mmHg(-1) = KfU), which was significantly (p < 0.005) higher than the value obtained using tilt to increase the hydrostatic load (0.98 +/- 0.2 KfU). One subject had an unchanged Kf value and experienced vaso - vagal syncope following the imposition of 70 degrees tilt, with a heart rate < 35 / min and a systolic blood pressure of 60 mmHg. The measurement of blood flow in the limb showed no significant change during the tilt procedure. The lung function measurements revealed, that only expiratory reserve volume (ERV) did significantly increase during 35 degrees and 70 degrees head up tilt. All other parameters were unchanged. We suggest that the differences in these Kf values can be explained by the activation of both central and peripheral mediated changes in pre- capillary resistance in response to the tilt. We suspect, that the vaso - vagal syncope, experienced by one subject, reflected his inability to activate these protective reflex mechanisms, a situation that could be exacerbated by sub-clinical venous insufficiency. We believe that these results show that VCP is a useful tool for the determination of intolerance to orthostatic stress.

Adult↗

PubMedDate not supplied

[Value of the electrocardiogram to predict the pattern of left ventricular contraction in ischemic cardiopathy].

A correlative electrocardiographic and ventriculographic study was performed in a series of 100 patients with clinical and electrocardiographic diagnosis of ischemic heart disease. The analysis was focused on the possibility of predicting ventricular contraction pattern (VCP) disturbances, through electrocardiographic signs of coronary insufficiency. Two main groups were separated on the basis of the presence of necrosis. There were 66 cases with necrosis, and 34 without it. The type of VCP was calssified in accordance with the criterion of Herman et al. in: asyneresis, akinesis and dyskininesis. The degree of coronary narrowing was arbitrarily evalued as less than 50%, between 50 and 75%, and over 75% of the lumen.

Coronary Disease↗

PubMed1992

[Comparative assessment of various programs of plasmapheresis in the combined treatment of patients with rheumatoid arthritis].

Therapeutic efficacy of various plasmapheresis (PA) programmes was comparatively studied in 92 patients with rheumatoid arthritis. PA performed as a placebo (the control group) confirmed the efficacy of PA in the patients with rheumatoid arthritis. The choice of a particular regimen of the procedure depended on the health status of the patient. The programme of PA with the elimination of one volume of the circulating plasma (VCP) turned to be the most effective in the patients with highly active course of the disease while the procedures with the elimination of 1/2 and 1/4 VCP should be used in those with moderate or minimal activity of the disease. The assessment of the therapeutic response should be based on the clinical data, ESR and the contents of circulating immune complexes--the most dynamic laboratory tests.

Adult↗