Biomedical subjects

S Takeo

Publications and source records attributed to S Takeo.

At least 19 recordsLinked to original sources

PubMed2006

Inhibitor of vascular endothelial growth factor receptor tyrosine kinase attenuates cellular proliferation and differentiation to mature neurons in the hippocampal dentate gyrus after transient forebrain ischemia in the adult rat.

Neurogenesis in the adult hippocampal dentate gyrus is promoted by transient forebrain ischemia. The mechanism responsible for this ischemia-induced neurogenesis, however, remains to be determined. It has been suggested that there may be a close relationship between neurogenesis and the expression of vascular endothelial growth factor, an angiogenic factor. The purpose of the present study was to examine the relationship between vascular endothelial growth factor and cell proliferation in the dentate gyrus after transient forebrain ischemia. The mRNA expression of vascular endothelial growth factor was increased in the dentate gyrus on day 1 after ischemia. Immunohistochemical analysis on day 9 after ischemia, when a significant increase in cell proliferation was seen, showed that the cerebral vessel space in the subgranular zone of the dentate gyrus had not been affected by the ischemia. Neither were the vascular densities on days 1 and 3 after ischemia altered compared with those of non-operated naïve control rats. Furthermore, the distance from the center of the proliferative cells to the nearest cerebral vessel of ischemic rats was comparable to that of the sham-operated rats. We demonstrated that transient forebrain ischemia-induced cell proliferation and differentiation to mature neurons in the hippocampal dentate gyrus was attenuated by the i.c.v. administration of a vascular endothelial growth factor receptor tyrosine kinase inhibitor. These results suggest that vascular endothelial growth factor receptor at the early period of reperfusion may contribute to neurogenesis rather than to angiogenesis in the hippocampal dentate gyrus.

Animals↗

PubMed2004

Dieulafoy's lesion of the esophagus correctly diagnosed and successfully treated by the endoscopic injection of N-butyl-2-cyanoacrylate.

Dieulafoy's lesion is an arterial malformation in the subumucosal layer of the gastrointestinal tract that can cause massive bleeding. The esophagus is not a common location for this lesion. We present here a first report of Dieulafoy's lesion of the esophagus correctly diagnosed and successfully treated by the endoscopic injection of N-butyl-2-cyanoacrylate.

Aged↗

PubMed2004

Infant schistosomiasis in Ghana: a survey in an irrigation community.

We used a rapid, visually read, field applicable monoclonal antibody (MoAb)-dipstick assay for specific diagnosis of urinary schistosomiasis together with microscopy to determine the prevalence of infant schistosomiasis in a community in the Awutu-Efutu Senya District in the Central Region of Ghana. The study group consisted of 97 infants (51 males and 46 females) aged 2 months to 5 years. A total of 75 of 97 (77.3%) subjects submitted stool samples; none had Schistosoma mansoni. Three individuals (3.1%) had hookworms but there were no other intestinal helminths. The urinary schistosomiasis prevalence by MoAb-dipstick (30%) was higher (P < 0.05) than that estimated by microscopy (11.2%). However, three of nine (33.3%) microscopically confirmed cases tested MoAb-dipstick positive after pre-treatment of the urine specimen with heat. The youngest infant to be found infected with S. haematobium microscopically was 4 months old. Fifteen of 71 S. haematobium egg negative individuals tested dipstick positive, giving a dipstick specificity of 78.9% as compared with microscopy as gold standard test. The relative sensitivity of the dipstick was 100%.

Antibodies, Monoclonal↗

PubMed2003

Matrix metalloproteinase-7 and matrix metalloproteinase-9 are associated with unfavourable prognosis in superficial oesophageal cancer.

If oesophageal carcinoma is detected in the superficial stage, the prognosis is better than for advanced oesophageal carcinoma. But the factors which predict the prognosis and treatment policy remain unclear. Matrix metalloproteinase-7 (MMP-7) and matrix metalloproteinase-9 (MMP-9) have been reported to have close associations with tumour invasion and metastasis. In this study, we retrospectively studied the relations between MMP-7 and MMP-9 expression in immunohistochemistry, clinicopathologic factors, and prognosis in 55 superficial oesophageal carcinomas. MMP-7 and MMP-9 expression occurred in 23.6% and 47.3% of the patients, respectively. MMP-7 expression was significantly correlated with the presence of nodal metastasis (P=0.004). MMP-9 expression was significantly correlated with the depth of tumour invasion (P=0.004), lymphatic permeation (P=0.001), nodal metastasis (P=0.049), and pathologic differentiation grade (P=0.003). By the log-rank test, MMP-7 expression and MMP-9 expression on the invasive front were related to the prognosis. In multivariate analysis, MMP-9 expression on the invasive front was an independent prognostic indicator. The combined expression of MMP-7 and MMP-9 may be a good marker for the degree of malignancy of oesophageal cancer and for the presence of lymphatic metastasis.

Adenocarcinoma↗

PubMed2002

Impairment of cerebral cAMP-mediated signal transduction system and of spatial memory function after microsphere embolism in rats.

The transcription factor cAMP-responsive element binding protein (CREB) has been implicated in synaptic plasticity and memory. The purpose of the present study was to characterize alterations in the cAMP/protein kinase A (PKA)/CREB system after sustained cerebral ischemia. Sustained cerebral ischemia was induced by injection of 900 microspheres (48 microm in diameter) into the right (ipsilateral) hemisphere of rats. Alterations in the CREB, PKA, and cAMP levels in the cerebral cortex and hippocampus were examined up to 7 days after microsphere embolism. Immunoblotting analysis showed a decrease in the immunoreactivity of phosphorylated CREB (pCREB) in the ipsilateral hemisphere on the third day after microsphere embolism, whereas that of the total CREB was not altered. An electrophoretic gel mobility shift assay showed a decrease in the cAMP response element (CRE)-DNA binding activity of CREB in the ischemic region on the third day after the microsphere embolism. Cytosolic PKA C beta in the ipsilateral hemisphere was selectively decreased on the first day after the microsphere embolism, whereas the levels of another catalytic subunit, C alpha, and a regulatory subunit, RII alpha, were not altered. Immunoreactivity of the PKA catalytic subunit C alpha in the nucleus of the ipsilateral hemisphere was decreased on the third day after the embolism. The decreases in the pCREB, CRE-DNA binding activity, and PKA C alpha and C beta levels lasted at least up to 7 days after the operation. A decrease in the cAMP content was also seen in the ipsilateral hemisphere throughout the experiment. Furthermore, microsphere embolized rats showed prolongation of the escape latency in the water maze task determined on the seventh to ninth day after the operation. Our results suggest that sustained cerebral ischemia may impair the phosphorylation and CRE-DNA binding activity of CREB and that these effects may be one of the possible causes for learning and memory dysfunction.

Animals↗

PubMed2001

Thymidine phosphorylase activity in nonsmall cell lung carcinoma tissues.

BACKGROUND: This is the first study on the quantitative assessment of thymidine phosphorylase (TP) activity in patients with nonsmall lung carcinoma. TP is identical to the platelet-derived endothelial cell growth factor with its angiogenic activity. Thus, it is believed that TP activity in tumor tissues plays an important role in disease progression. METHODS: Using a sandwich enzyme immunoassay, the TP activity in lung carcinoma tissues was measured quantitatively in 39 patients with primary lung carcinoma who underwent pulmonary lobectomy between July 1999 and May 2000. RESULTS: The mean value of TP activity in tumor tissues was significantly higher than the level in normal lung tissues (226 U/mg protein vs. 46 U/mg protein, respectively; P < 0.0001). TP activity in normal lung tissues was high in male patients (male vs. female, respectively: 56.1 U/mg protein vs. 29.3 U/mg protein; P = 0.001) and in heavy smokers (Brinkmann index [BI] > or = 600 [57.9 U/mg protein] vs. BI < 600 [31.7 U/mg protein]; P = 0.001). Conversely, the TP activity in tumor tissues was correlated with neither gender nor smoking status. Although there was no difference in the TP activity among histologic types, well-differentiated tumors exhibited a significantly lower level of TP activity compared with the activity in both moderately and poorly differentiated tumors. However, the TP activity in tumor tissues was not correlated with disease progression. CONCLUSIONS: High TP activity in tumor tissues from patients with primary lung carcinoma did not reflect the malignant potential of the disease.

Adult↗

PubMed2001

Examination of oncogene amplification by genomic DNA microarray in hepatocellular carcinomas: comparison with comparative genomic hybridization analysis.

To identify amplified oncogenes involved in hepatocellular carcinomas (HCC), we applied a genomic DNA microarray spotted with 57 oncogenes to 20 HCCs. Aberrations in DNA copy number also were analyzed by comparative genomic hybridization (CGH) using an aliquot of DNA samples. In 5 of 20 HCCs, only 6 oncogenes (CCND1, FGF3/FGF4, SAS/CDK4, TERC, MET, and MYC) were amplified, whereas in the remaining 15 tumors no oncogenes were amplified. A comparison of DNA microarray and conventional CGH analyses showed that, although 5 of 6 amplified oncogenes shown by microarray were located in chromosomal regions shown by CGH to have increased DNA copy numbers, not all genes located in such chromosomal regions were affected. One of the amplified oncogenes (SAS/CDK4) was found in a chromosomal region that was undetected by CGH. We, therefore, conclude that amplification of the oncogenes examined in this series is not directly implicated in hepatocellular carcinogenesis.

Adult↗

PubMed2001

Long-term treatment with neutral endopeptidase inhibitor improves cardiac function and reduces natriuretic peptides in rats with chronic heart failure.

OBJECTIVE: Increased secretion of atrial and brain natriuretic peptide (ANP and BNP) from hearts is known to exhibit favorable effects in patients and animals with heart failure, and inhibition of neutral endopeptidase (NEP), an enzyme that degrades ANP and BNP, may further increase these peptide levels. However, it is still unknown whether such elevation of the ANP and BNP may offer a therapeutic benefit to the progression of chronic heart failure (CHF). We examined the effects of ONO-9902, a novel NEP inhibitor, on changes in hemodynamic parameters, NEP activity and neurohumoral factors in rats with CHF induced by left coronary artery ligation (CAL). METHODS: Male Wistar rats (220-240 g) were subjected to induction of acute myocardial infarction by CAL. Rats were orally treated with ONO-9902 (300 mg/kg/day) from the 1st to 6th week after the operation. Hemodynamic and/or biochemical assessments were performed at the 1st and 6th weeks after the operation. RESULTS: A single administration of ONO-9902 inhibited the plasma and kidney NEP activities and thereby further augmented the elevation of plasma ANP concentration in rats with CAL at the 1st week after the operation. In rats with CAL at the 6th week after the operation, the left ventricular end-diastolic pressure (LVEDP) increased and cardiac output index (COI) decreased as compared with those of sham-operated rats. These changes were accompanied by marked increases in the plasma ANP, BNP and endothelin-1 (ET-1). Chronic treatment with ONO-9902 attenuated the increase in LVEDP and the decrease in COI. These changes were associated with a decrease in plasma ANP, BNP and ET-1 concentrations. CONCLUSIONS: The results suggest that chronic treatment with NEP inhibitor improves depressed cardiac function in rats with CHF. ONO-9902 may offer a new and possible therapeutic approach in patients with CHF.

Analgesics, Non-Narcotic↗

PubMed2001

Activated astrocytes with glycogen accumulation in ischemic penumbra during the early stage of brain infarction: immunohistochemical and electron microscopic studies.

Brain infarction was induced in rats by injection of microspheres through the right internal carotid artery, and structural changes in the astrocytes were observed during the early period following the infarction. Necrotic foci, varying in size and shape, were found in the right hemisphere. After immunohistochemical staining for GFAP, GFAP-positive astrocytes in the perinecrotic area known as the ischemic penumbra had distinctly increased in number and size with elongation of cytoplasmic processes 3 days after infarction. Electron microscopic observation revealed that glycogen granules had markedly accumulated in the cytoplasm of astrocytes located in the ischemic penumbra 3 and 5 days after infarction. Seven days after infarction, however, the glycogen granules disappeared from the astrocytes. Intermediate filaments increasingly appeared in the protoplasmic astrocytes after 3 days and were abundant in the activated and hypertrophied astrocytes after 7 days. As a result of our present study, we conclude that: (1) the function of glucose uptake from blood vessels was not impaired in the astrocytes under hypoxic conditions; (2) the astrocytes actively ingested blood glucose through the endothelial cells and accumulated it as glycogen for activation of their functions, and the cell volume increased under hypoxic conditions; (3) the depression of energy metabolism and the decrease in the uptake of energy sources in the nerve cells promoted glycogen accumulation in the astrocytes under hypoxic conditions; (4) intermediate filaments (GFAP filaments) increased in number, coincident with the activation and enlargement of the astrocytes; and (5) protoplasmic astrocytes were transformed into fibrous astrocytes in the ischemic penumbra of the brain infarction.

Animals↗

PubMed2001

Myocardial heat shock proteins during the development of heart failure.

When cardiomyocytes are exposed to stresses, production of heat shock proteins (HSPs) in the cells is enhanced. Such increase in cellular HSP production is considered to bring about tolerance against stress-induced cell damage. The exact role of the cellular HSPs remains unclear. In the present study, HSPs in the viable left ventricular myocardium were determined during the development of heart failure following coronary artery ligation (CAL). The rats after CAL showed symptoms of chronic heart failure (CHF) at the 8th week, but not at the 1st and 2nd weeks. Myocardial HSP27, which may bind to cytoskeletal protein, at the 1st, 2nd, and 8th weeks after CAL was approximately 180, 160, and 125% of the control, respectively. Myocardial HSP60, one of mitochondrial proteins, at the 8th week increased to 140% of the control, whereas those at the 1st and 2nd weeks did not change. Myocardial HSP72, an inducible form of HSP70 family, at the 1st week after CAL increased to 180% of the control, whereas that at the 2nd or 8th week was similar to control. Myocardial heat shock constitutive protein 73 (HSC73), a constitutively expressed form of HSP70 family, and HSP90, which may bind to steroid hormone receptor and actin fiber, of CAL rats did not alter throughout the experiment. These findings show that diverse changes in the production of myocardial HSPs occur during the development of heart failure. Only the increase in myocardial HSP60 production was associated with the development of CHF.

Animals↗

PubMed2001

Video-assisted extended thymectomy in patients with thymoma by lifting the sternum.

We present use of minimally invasive video thoracoscopic surgery to perform complete extended thymectomy in patients with thymoma. These procedures were performed using a sternum-elevating method that provides a wide field of vision between the sternum and heart. Indications for this method are Masaoka Stage I, II and some Stage III (invasion to the lung and pericardium). This new method may be useful from the standpoint of minimal access, rapid recovery, less pain, and good cosmetic results.

Adult↗

PubMed2001

Characterization of cardiac myocyte and tissue beta-adrenergic signal transduction in rats with heart failure.

OBJECTIVE: The cellular basis of alterations in beta-adrenergic signal transduction in rats with chronic heart failure (CHF) remains unclear. The aim of the present study was to examine this signal transduction system in isolated ventricular cardiomyocytes of rats with CHF. We focused on changes in the levels of stimulatory (Gs) and inhibitory G-proteins (Gi). METHODS: CHF was induced in male Wistar rats by coronary artery ligation (CAL). Hemodynamic and biochemical parameters were measured 8 weeks after CAL. Alterations in contractile function and Ca(2+) transients via beta-adrenergic receptor signaling of cardiomyocytes isolated from rats with CHF were characterized by simultaneous measurements of cell shortening and fura-2 fluorescence intensity. RESULTS: Coronary artery-ligated rats showed symptoms of CHF, such as decreased contractile function, increased left ventricular volume, decreased chamber stiffness, and about 40% infarct formation of the left ventricle, by 8 weeks after surgery. The contractile function and Ca(2+) dynamics of cardiomyocytes from the rats with CHF remained normal under basal conditions. Only cardiac cell length was increased. The responses of peak shortening, fura-2 fluorescence ratio amplitude, and cAMP content to beta-adrenoceptor stimulation were reduced in cardiomyocytes of the rats with CHF, whereas direct stimulation of adenylate cyclase did not affect the response of these variables. Cardiomyocyte Gsalpha protein was decreased, whereas no changes in Gialpha proteins were seen in these cells. Increases in tissue Gsalpha and Gialpha proteins in the scar zone were detected. The results on tissue levels of collagen and G-proteins in the viable left ventricle appeared to depend on the presence of nonmyocytes. CONCLUSIONS: The results suggest that impaired contractile function of cardiomyocytes is unlikely to account for global LV contractile dysfunction, and that down-regulation of beta-adrenoceptors occurs in cardiomyocytes per se. The difference in changes of G-protein between the cardiomyocyte and myocardial tissue suggests an appreciable contribution of nonmyocytes to myocardial G-protein levels.

Animals↗

PubMed2001

Isolation of mitochondria from Plasmodium falciparum showing dihydroorotate dependent respiration.

Using N2 cavitation, we established a protocol to prepare the active mitochondria from Plasmodium falciparum showing a higher succinate dehydrogenase activity than previously reported and a dihydroorotate-dependent respiration. The fact that fumarate partially inhibited the dihydroorotate dependent respiration suggests that complex II (succinate-ubiquinone reductase/quinol-fumarate reductase) in the erythrocytic stage cells of P. falciparum functions as a quinol-fumarate reductase.

Animals↗

PubMed2001

Effects of ACE inhibition and angiotensin II type 1 receptor blockade on cardiac function and G proteins in rats with chronic heart failure.

1. Inhibition of the renin-angiotensin system (RAS) improves symptoms and prognosis in heart failure. The experimental basis for these benefits remains unclear. We examined the effects of inhibition of ACE or blockade of angiotensin II type 1 (AT1) receptor on the haemodynamics, cardiac G-proteins, and collagen synthesis of rats with coronary artery ligation (CAL), a model in which chronic heart failure (CHF) is induced. 2. Rats were orally treated with the ACE inhibitor trandolapril (3 mg kg(-1) day(-1)) or the AT1 receptor blocker L-158809 (1 mg kg(-1) day(-1)) from the 2nd to 8th week after CAL. CAL resulted in decreases in the left ventricular systolic pressure and its positive and negative dP/dt, an increase in the left ventricular end-diastolic pressure, and the rightward shift of the left ventricular pressure-volume curve. Long-term treatment with either drug improved these signs of CHF to a similar degree. 3. Cardiac Gsalpha and Gqalpha protein levels decreased, whereas the level of Gialpha protein increased in the animals with CHF. Long-term treatment with trandolapril or L-158809 attenuated the increase in the level of cardiac Gialpha protein of the animals with CHF without affecting Gsalpha and Gqalpha protein levels. Cardiac collagen content of the failing heart increased, whose increase was blocked by treatment with either drug. 4. Exogenous angiotensin I stimulated collagen synthesis in cultured cardiac fibroblasts, whose stimulation was attenuated by either drug. 5. These results suggest that blockade of the RAS, at either the receptor level or the synthetic enzyme level, may attenuate the cardiac fibrosis that occurs after CAL and thus affect the remodelling of the failing heart.

Angiotensin I↗

PubMed2001

Effect of long-term treatment with trandolapril on Hsp72 and Hsp73 induction of the failing heart following myocardial infarction.

1. The effect of long-term treatment of rats with chronic heart failure (CHF) following acute myocardial infarction with trandolapril, an angiotensin I-converting enzyme (ACE) inhibitor, on heat shock-induced Hsp72 and Hsp73 production was examined. 2. Acute myocardial infarction was induced by coronary artery ligation (CAL). The animals with CAL showed symptoms of CHF at the 8th week after the operation. The hearts isolated from animals with CAL at the 2nd and 8th week after surgery were subjected to hyperthermia at 42 degrees C for 15 min followed by 6-h perfusion (hyperthermia/6-h perfusion). 3. In the hearts isolated from the animals at the 2nd week, an approximate 20% decline in the rate pressure product (RPP) was seen after hyperthermia/6-h perfusion, which was similar to that in non-operated controls. In contrast, a significant reduction in the RPP after hyperthermia/6-h perfusion was seen in the hearts of rats with CHF. These hearts did not increase Hsp72 and Hsp73 production after hyperthermia. The decline in RPP was associated with failure in the production of myocardial Hsp72 and Hsp73. 4. When rats with CAL were treated with 3 mg kg(-1) day(-1) trandolapril from the 2nd to 8th week after the operation, the decline in RPP of the failing heart after hyperthermia was similar to that of the sham-operated rats. The induction of myocardial Hsp72 and Hsp73 production of the coronary artery-ligated rats after hyperthermia was reversed by treatment with trandolapril. 5. These findings suggest that the preserved ability to induce Hsp72 and Hsp73 production in the heart with CAL by trandolapril treatment may be attributed to the increased tolerance against heat stress-induced deterioration of myocardial contractile function.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2001

Protective effect of heat shock protein 72 on contractile function of perfused failing heart.

The contribution of heat shock protein 72 (HSP72) to the protection of cardiac function was examined in rats with chronic heat failure (CHF) following coronary artery ligation (CAL). The CAL animals revealed functional deterioration without low cardiac output 2 wk after CAL and with low cardiac output 8 wk after CAL, suggesting that CHF had developed by 8 wk after CAL. The hearts isolated from animals 2 and 8 wk after CAL (2-wk CAL heart and 8-wk CAL heart, respectively) were subjected to hyperthermia (at 42 degrees C) for 15 min, followed by 6-h perfusion (hyperthermia/6-h perfusion). The 2-wk CAL heart showed a 19.0 +/- 3.9% decline in the rate- pressure product (RPP) after hyperthermia/6-h perfusion, similar to the nonoperated control (19.8 +/- 2.9% decline). The production of myocardial HSP72 increased in the 2-wk CAL heart in response to hyperthermia (412.7 +/- 29.5% of each prehyperthermia value). The 8-wk CAL heart showed a reduction in the RPP (45.2 +/- 4.3% decline) after hyperthermia/6-h perfusion, associated with blunting of the production of HSP72 (68.9 +/- 22.6% increase, respectively). The results suggest that functional deterioration of the isolated failing heart may be attributed to a reduction in the production of myocardial HSP72.

Animals↗

PubMed2001

Characterization of microsphere embolism-induced impairment of learning and memory function and the cholinergic system.

The impairments of learning and memory function and of the cholinergic system were examined in rats with microsphere embolism. Microsphere embolism was induced by injection of 900 microspheres with a diameter of 48 microm into the right internal carotid artery. The retention latency of a passive avoidance test was shortened and the escape latency of a water maze test was prolonged, when the animals were tested on the 5th to 10th day after the embolism, suggesting learning and memory dysfunction. Cholinergic parameters of the striatum and hippocampus, such as acetylcholine (ACh) content (67 and 60% decrease, respectively), choline acetyltransferase (ChAT) activity (45 and 56% decrease, respectively), and Bmax of muscarinic acetylcholine M1-receptor (43 and 37% decrease, respectively), were reduced on the 11th day after the embolism, suggesting attenuation of ACh synthesis and a decrease in the number of muscarinic acetylcholine M1-receptors mainly in the striatum and hippocampus. Areas not stained with triphenyltetrazolium chloride, an indication of infarction, were detected mainly in the striatum and hippocampus and partly in the frontal cortex on the 11th day after the embolism. The results suggest that an animal with microsphere embolism may be a good ischemic model with relatively sustained impairments of learning and memory function and of the striatal and hippocampal cholinergic system.

Animals↗

PubMed2000

Succinate dehydrogenase in Plasmodium falciparum mitochondria: molecular characterization of the SDHA and SDHB genes for the catalytic subunits, the flavoprotein (Fp) and iron-sulfur (Ip) subunits.

Mitochondria of malaria parasites generate a membrane potential through an electron transport system that is a possible target of primaquine and a new anti-malarial drug, atovaquone. However, little information is available for conclusive understanding of the respiratory chain in Plasmodium mitochondria. In the present study, we cloned and characterized from Plasmodium falciparum the genes for the catalytic subunits, SDHA for the flavoprotein (Fp) and SDHB for iron-sulfur protein (Ip), of succinate-ubiquinone oxidoreductase (complex II), which is a marker enzyme for mitochondria and links the TCA cycle and respiratory chain directly. Each of the two genes contains a single open reading frame (ORF), which are located on different chromosomes, 1860 nucleotides on chromosome 10 for SDHA and 963 nucleotides on chromosome 12 for SDHB. The expression of these genes in asynchronous erythrocytic stage cells was confirmed by observation of 3.3 and 2.4 kb transcripts from the SDHA and SDHB genes, respectively. The SDHA and SDHB genes encode proteins of 620 (Fp) and 321 (Ip) amino acids with molecular masses of 69.2 and 37.8 kDa, respectively. A mitochondrial presequence essential for the import of mitochondrial proteins encoded by nuclear DNA, as well as almost all the conserved amino acids indispensable for substrate binding and the catalytic reaction were found in these peptides, indicating the functional importance of this enzyme in the parasite. Interestingly, a P. falciparum-specific insertion and a unicellular organism-specific deletion were found in the amino acid sequence of Fp. This is the first report of the primary structure of the protozoan succinate dehydrogenase.

Amino Acid Sequence↗