Biomedical subjects

K Fukuda

Publications and source records attributed to K Fukuda.

At least 289 records · Page 16Linked to original sources

PubMed1998

Evaluation of left atrial filling using systolic pulmonary venous flow velocity measurements in patients with atrial fibrillation.

BACKGROUND: The pattern of pulmonary venous flow velocity is useful for understanding the hemodynamic relationship between the left atrium and left ventricle in patients with a variety of diseases, and the systolic flow wave, in particular, is considered a clinically important parameter that reflects left atrial filling. HYPOTHESIS: The study was undertaken to determine whether systolic pulmonary venous flow velocity patterns can be used to evaluate left atrial filling in patients with atrial fibrillation. METHODS: We performed transesophageal pulsed Doppler echocardiography and cardiac catheterization in 34 patients with chronic atrial fibrillation (10 with hypertrophic cardiomyopathy, 5 with dilated cardiomyopathy, 7 with previous myocardial infarction, and 12 with isolated atrial fibrillation) and 15 normal controls in sinus rhythm. RESULTS: Mean pulmonary capillary wedge pressure, V-wave height in the pulmonary capillary wedge pressure curve, and left ventricular end-diastolic pressure were significantly higher in the hypertrophic cardiomyopathy and dilated failing heart (previous myocardial infarction and dilated cardiomyopathy) groups than in the isolated atrial fibrillation and normal groups. The peak velocity and time-velocity integral of the systolic pulmonary venous flow velocity, and percent left atrial emptying fraction were significantly lower in the dilated failing heart group than in the isolated atrial fibrillation, hypertrophic cardiomyopathy, and normal groups. The peak velocity and time-velocity integral of the systolic pulmonary venous flow velocity, percent left atrial emptying fraction, and V-wave height were comparatively constant when the preceding R-R intervals were relatively stable in the isolated atrial fibrillation group and in 4 of the 10 patients with hypertrophic cardiomyopathy. However, changes in these variables correlated with the preceding R-R interval in all patients with dilated failing hearts and in 6 of the 10 patients with hypertrophic cardiomyopathy. CONCLUSION: Transesophageal pulsed Doppler echocardiographic measurements of systolic pulmonary venous flow velocity are valid indicators of left atrial filling in patients with atrial fibrillation.

Adult↗

PubMed1998

Assessment of abnormal left atrial relaxation by transesophageal pulsed Doppler echocardiography of pulmonary venous flow velocity.

BACKGROUND: Several studies on left ventricular relaxation have been undertaken in the past; however, left atrial (LA) relaxation has not been fully evaluated. HYPOTHESIS: The purpose of this study was to assess abnormalities in LA relaxation by evaluating pulmonary venous flow velocity and interatrial septal motion using transesophageal echocardiography. METHODS: The subjects were 56 untreated patients in sinus rhythm, including 25 with previous myocardial infarction, 9 with hypertrophic cardiomyopathy, 11 with dilated cardiomyopathy, as well as 11 with chest pain syndrome as controls. Peak first systolic velocity (PVS1), peak atrial systolic velocity (PVA), and their time-velocity integrals (PVS1-I and PVA-I, respectively) were calculated from the pulmonary venous flow velocity. RESULTS: The PVS1 and PVS1-I correlated negatively with the maximum LA dimension and mean pulmonary capillary wedge pressure, and correlated positively with the amplitude of the interatrial septal motion during LA relaxation and percent fractional LA relaxation. The PVA and PVA-I did not correlate with the mean pulmonary capillary wedge pressure. There was a weak positive correlation between PVA and PVS1, and a close positive correlation between the ratio of PVA to PVS1 and mean pulmonary capillary wedge pressure. Multiple regression analysis indicated that the PVS1 was most closely related to percent fractional LA relaxation, followed by mean pulmonary capillary wedge pressure. CONCLUSION: The PVS1 determined from the pulmonary venous flow velocity is closely related to parameters of LA relaxation which may be determined by transesophageal M-mode echocardiography, and the ratio of PVA to PVS1 is useful for noninvasive evaluation of LA pressure.

Adult↗

PubMed1998

Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction.

The authors previously reported that transforming growth factor beta1 (TGF-beta1) induces apoptosis in McA-RH7777 (7777) and McA-RH8994 (8994) rat hepatoma cell lines. Although these cell lines exhibit different responses to glucocorticoid treatment in various cellular functions and gene expression, dexamethasone (DEX) inhibited spontaneous and TGF-beta1-induced apoptosis in both. Analysis of analogous hormones in TGF-beta1-induced apoptosis in 8994 cells suggested the inhibitory effect to be glucocorticoid-specific. By cell-cycle analysis and DNA fragmentation assay using sodium butyrate, a G1-arrest-inducing reagent, regulation of apoptosis by TGF-beta1 and DEX was shown independent of the cell cycle. For elucidation of the mechanisms of anti-apoptotic action of DEX, the effects of various chemical probes on this apoptosis model were examined, and various reagents known to exhibit anti-apoptotic activity in other experimental systems were found to be ineffective. The effect of TGF-beta1 and DEX on cellular amounts of several apoptosis-related proteins, members of the Bcl-2 family, Bcl-2, Bcl-xL, Bcl-xS, Bad, and Bax was also examined. DEX drastically increased Bcl-xL in both cell lines irrespective of the presence of TGF-beta1. Bcl-2 and Bcl-xS proteins were not detected, and Bax and Bad content did not change by treatment with TGF-beta1 or DEX. Progesterone (Prog), a partial antagonist for glucocorticoid receptor, inhibited the effects of DEX on apoptosis and Bcl-xL expression in 8994 cells. Thus, Bcl-xL induction by DEX would appear closely associated with its inhibitory effect on spontaneous and TGF-beta1-induced apoptosis in the hepatoma cell lines.

Animals↗

PubMed1998

Characteristics of patients with hepatitis C virus with and without GB virus C/hepatitis G virus co-infection and efficacy of interferon alfa.

GB virus C/hepatitis G virus (GBV-C/HGV) infection seems to be common among patients with hepatitis C virus (HCV) infection. We studied retrospectively the proportions of patients with GBV-C/HGV RNA and antibodies to the GBV-C/HGV second envelope protein (anti-E2) among 149 subjects with chronic hepatitis C who had received interferon alfa. The clinical characteristics of patients with GBV-C/HGV RNA or anti-E2 were examined, as was the efficacy of the treatment. Stored serum specimens were tested for GBV-C/HGV RNA by the reverse transcription polymerase chain reaction and for anti-E2 by an enzyme-linked immunosorbent assay. Of the 149 patients before therapy, 8 (5%) had GBV-C/HGV RNA only, 72 (48%) had anti-E2 only, and 4 (3%) had both. The mean age of patients with GBV-C/HGV RNA (some with anti-E2) was significantly less than that of patients with anti-E2 only. Results of laboratory and histological evaluations were not different depending on the presence of GBV-C/HGV RNA or anti-E2. The GBV-C/HGV RNA titer decreased during therapy in all 12 patients with GBV-C/HGV RNA; only 4, with a low titer before therapy and with anti-E2 detected at some time, had sustained clearance of GBV-C/HGV. Our results suggested that half of the patients with chronic hepatitis C had been exposed to GBV-C/HGV, but in almost all, the virus had been cleared; also, even chronic GBV-C/HGV infection did not affect the severity of the disease arising from HCV. Interferon alfa treatment was sometimes effective against GBV-C/HGV, and anti-E2 may be associated with clearance of GBV-C/HGV.

Adult↗

PubMed1998

Altered regulation of Src tyrosine kinase by transforming growth factor beta1 in a human hepatoma cell line.

Transforming growth factor betas (TGF-betas) are the potent growth inhibitors for various cell types. Certain transformed cells, however, show poor response to TGF-beta-induced growth inhibition, which contributes to their uncontrolled proliferation. Recently, we have reported that TGF-beta1 induces degradation of activated Src tyrosine kinase in rat fibroblasts. To elucidate the alteration in TGF-beta signaling pathway in tumor cells that cannot respond to the cytokine, we compared the effects of TGF-beta1 on Src kinase in two human hepatoma cell lines, TGF-beta1-insensitive Mahlavu cells and TGF-beta1-sensitive HepG2 cells. TGF-beta1 decreased Src kinase activity in HepG2 cells, but increased cellular Src levels and Src kinase activity in Mahlavu cells. Co-incubation of Mahlavu cells with TGF-beta1 and 12-O-tetradecanoyl phorbol 13-acetate (TPA) decreased Src protein levels and Src kinase activity, inducing TGF-beta1 sensitivity. TGF-beta1 induced tyrosine dephosphorylation of Ras guanosine triphosphatase-activating protein (Ras-GAP) and Ras inactivation in HepG2 cells, but induced Ras-GAP phosphorylation and Ras activation in Mahlavu cells. The Src kinase inhibitor abolished the increase of Src kinase activity in TGF-beta1-treated Mahlavu cells, and induced TGF-beta1 sensitivity. These findings suggest that regulation of Src kinase by TGF-beta1 is altered in Mahlavu cells. The altered regulation of Src may contribute to TGF-beta1 insensitivity in this cell line, at least in part through activation of Ras.

Animals↗

PubMed1998

Prognostic significance of progesterone receptor immunohistochemistry in endometrial carcinoma.

OBJECTIVE: The aim of this study was to evaluate the prognostic significance of steroid hormone receptors in endometrial carcinoma using immunohistochemical staining for progesterone receptor (PR) and estrogen receptor (ER). METHODS: We evaluated the correlation between PR/ER immunohistochemistry and age, clinical stage, tumor grade, myometrial tumor invasion, and disease-free survival in a series of 92 cases of endometrioid adenocarcinoma. RESULTS: Fifty (54.4%) endometrial carcinomas were PR-positive and 44 (47.8%) were ER-positive. PR immunohistochemistry of endometrial carcinoma was statistically correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage (I, II vs III, IV, P = 0.001), FIGO grade (G1 vs G2 vs G3, P = 0.007), the depth of myometrial tumor invasion (< or = 1/2 vs > 1/2, P = 0.006), and disease-free survival (living vs dead, P = 0.0025). In contrast, ER immunohistochemistry had significant correlations with the depth of myometrial tumor invasion (P = 0.026) and disease-free survival (P = 0.032). Multivariate analysis of PR/ER immunohistochemistry, stage, grade, and myometrial invasion showed that the PR immunohistochemistry was a significant prognostic factor for survival (P = 0.026). CONCLUSION: PR/ER immunohistochemistry was significantly related to survival and PR immunohistochemistry appeared to be the most reliable means for predicting survival in endometrioid adenocarcinoma of the endometrium, independent of other clinicopathological parameters.

Adult↗

PubMed1998

Neoadjuvant chemotherapy with mitomycin C, etoposide, and cisplatin for adenocarcinoma of the cervix.

Between May 1990 and February 1995, 16 patients with adenocarcinoma or adenosquamous carcinoma of the uterine cervix were prescribed neoadjuvant chemotherapy consisting of cisplatin (50 mg/m2) on day 1, mitomycin C (10 mg/m2) on day 1, and etoposide (100 mg/m2) on days 1, 3, and 5 (MEP). In 2 patients stage was IB1, 5 were in stage IB2, 1 was in stage IIA, 5 were in stage IIB, 2 were in stage IIIB, and one was in stage IVB. A median of three courses of chemotherapy was given (range two to five). Of the 16 patients, 3 had a complete response and 5 had a partial response (response rate, 50%). Following termination of this chemotherapy, 12 patients with stage I or stage II carcinoma underwent radical hysterectomy. Three were given adjuvant radiotherapy because of positive pelvic nodes. One stage IIB patient, 1 stage IIIB patient and 1 stage IVB patient underwent standard radiotherapy and 1 stage IIIB patient underwent chemotherapy with another regimen because MEP therapy was without effect. Histopathological examinations revealed that changes as a result of the chemotherapy correlated well with clinical responses. Moderate or marked pathological changes occurred in 3 with a clinically complete response. The mean survival period of responders was 47.5 months while that of nonresponders was 28.3 months. Side effects of chemotherapy with MEP were within acceptable limits. The dose-limiting toxicity was myelosuppression and for only 1 patient the dose was reduced because of thrombocytopenia. Our preliminary study indicates that this chemotherapy regimen is effective for subjects with adenocarcinoma of the cervix. A prospective cooperative group trial on this regimen is ongoing.

Adenocarcinoma↗

PubMed1998

Angiotensin II potentiates DNA synthesis in AT-1 transformed cardiomyocytes.

Angiotensin II has been shown to be mitogenic in various cell types. In cultured neonatal cardiomyocytes, we have demonstrated that angiotensin II causes hypertrophy, not hyperplasia. However, fetal or neonatal cardiomyocytes exhibit limited proliferation in primary culture, and are mitotically less potent. In order to determine whether angiotensin II is simply a hypertrophic or hyperplastic growth factor for mitotically-potent cardiomyocytes, we analysed [3H]-thymidine uptake and cell cycle-regulated gene expression using SV40 large T-transformed AT-1 cardiomyocytes. Angiotensin II, alone and in combination with other growth factors, increased [3H]-thymidine uptake in a dose-dependent manner. The mRNA expression of G1 cyclins (Cyclin C, D1, D2, D3) and histone H1-kinase activity by CDK2 increased 6 h after angiotensin II stimulation. Western blot analysis revealed cyclin B1 expression after 18 h , which peaked at 30 h. Histone H1-kinase activity by cdc2 was also increased by angiotensin II, and peaked at 24-36 h, indicating that these changes were cell cycle dependent. Double immunofluorescent photography showed that AT-1 cells incorporated BrdU, and expressed cdc2 by angiotensin II stimulation. [3H]-thymidine and BrdU uptake were blocked by losartan, but not by PD123319. In contrast with neonatal cardiomyocytes, angiotensin II potentiated DNA synthesis and induced cell cycle regulated gene expression in AT-1 cardiomyocytes, and this activity was mediated by the angiotensin II type-1 receptor.

Angiotensin II↗

PubMed1998

Involvement of gp130-mediated signaling in pressure overload-induced activation of the JAK/STAT pathway in rodent heart.

Previously, we showed that the JAK/STAT pathway was activated in pressure-overloaded rat heart, and that angiotensin II was partially involved in this activation. The present study was designed to investigate whether gp130-mediated signaling is involved in this activation, and if so, which interleukin (IL)-6 family cytokine is involved. Pressure overload was produced by ligation of the abdominal aorta of Wistar rats or ICR mice. IP-Western blot was performed to detect tyrosine phosphorylation of STATs, gp130, and the association of gp130 with JAK kinases. The serum concentration of IL-6 was measured by enzyme-linked immunosorbent assay. Expression of IL-6, IL-11, leukemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), oncostatin M (OSM), and cardiotrophin-1 (CT-1) mRNA was quantitated. After pressure overload, rapid phosphorylation of STAT1 and STAT3 was observed at 5 min, STAT1 was rephosphorylated at 60 min, and intense phosphorylation of STAT3 was observed at 60 min. Both the phosphorylation of gp130 and the association of gp130 with JAK1 and JAK2 were increased after pressure overload. IL-6 was significantly increased by two-fold in the pressure-overloaded rats. Only CT-1 mRNA expression could be detected by Northern blot, and it increased after pressure overload. Reverse transcription-polymerase chain reaction revealed that IL-6 mRNA expression was increased 9.5-fold. IL-11, LIF, CNTF, and OSM expression were unaffected by pressure overload. These results suggested that gp130-mediated signaling was involved in the pressure overload-induced activation of the JAK/STAT pathway, and that IL-6 and CT-1 might be involved in this activation.

Animals↗

PubMed1998

Protein kinase C modulates the synthesis of nitric oxide by osteoblasts.

To determine the involvement of protein kinase C (PKC) in nitric oxide (NO) synthesis of osteoblast, a combination of proinflammatory cytokines (tumor necrosis factor-alpha, interferon-gamma, bacterial lipopolysaccharide) were added on rat osteoblast-like cells. Results show that these cytokines clearly enhanced the synthesis of NO. The activation of PKC with phorbol ester also resulted in the stimulation of NO synthesis in these cells. These cytokines activated PKC and increased the levels of intracellular Ca2+. In addition, the cytokine-induced synthesis of NO was blocked by PKC inhibitors. Findings suggest the involvement of PKC in the synthesis of NO by rat osteoblasts.

Animals↗

PubMed1998

Simulation by stereographic processing of computed tomography for transtrochanteric rotation osteotomy in necrosis of the femoral head.

The transtrochanteric rotation osteotomy described by Sugioka will preserve the femoral head in patients with avascular necrosis of the femoral head, but there is controversy about the clinical results. We developed a simulation system for rotation osteotomy, based on stereographic processing through computed tomography, the object being to determine the indication for this procedure and the degree of rotation required. This method makes it possible to determine the degree of rotation needed to displace the necrotic areas from the weightbearing zone; the need for a varus osteotomy can also be assessed. Our clinical results improved when we used this method. CT stereographic drawings in patients with avascular necrosis of the femoral head are useful for assessing the necrotic area.

Adult↗

PubMed1998

Infrahyoid spread of deep neck abscess: anatomical consideration.

The aim of this study was to determine the pathway of infrahyoid extension of the oropharyngeal abscess considering the anatomy of the fascial spaces by cross-sectional imaging. CT scans and MR images were retrospectively reviewed in ten patients with known infrahyoid extension of oropharyngeal abscesses (eight with acute tonsillitis, two with acute phlegmonous oropharyngitis). In seven of eight patients tonsillar abscesses descended along the deep cervical fascia converging on the hyoid bone and further accumulated in the anterior cervical space through which extension to the mediastinum took place in four patients. In seven patients the abscesses involved the retropharyngeal space at the infrahyoid neck. In two of these seven patients the abscesses directly extended down into the upper mediastinum through the retropharyngeal space. In one patients of the seven mediastinal spread of an abscess occurred through the posterior cervical space, not through the retropharyngeal space. Cross-sectional imaging is valuable in the evaluation of deep neck abscesses and the pathway of spread. The anterior cervical space in the infrahyoid neck is important for mediastinal extension of pharyngeal abscesses.

Abscess↗

PubMed1998

Middle-term results of anatomic medullary locking total hip arthroplasty.

We report the results of cementless, anatomic, medullary locking hip prosthesis application in our first consecutive series. We used the so-called Asian size of prosthesis with proportionally smaller stem sizes in both diameter and length. Forty-seven stems and sockets were analyzed with a mean follow-up of 69 months. The mean Merle d'Aubigné hip scores were 8 points preoperatively and 16 points at the final follow-up. Radiologically, the stems showed excellent stability without loosening. Stress shielding around the stems did occur in most cases but did not progress. Preoperative bone quality influenced the extent of stress shielding evaluated at the final follow-up: higher stress shielding was noted in poorer quality bones at the time of operation. There were problems with the sockets. The shallow socket and impingement at the protruded rim seemed to cause a high incidence of dislocation (13%). Massive polyethylene wear occurred in 5 sockets. These sockets were 48 and 46 mm in diameter with 26 mm heads. In conclusion, the stems of the anatomic medullary locking hip prostheses used in Japan showed satisfactory stability even in poor quality bones, but there were problems with the polyethylene liners. Our solution was to use larger sockets with 22 mm heads.

Aged↗

PubMed1998

Tyrosine kinase inhibitors suppress N-type and T-type Ca2+ channel currents in NG108-15 cells.

Modulation of Ca2+ channel activity by protein kinases constitutes one of the major mechanisms regulating neuronal functions. Here, we explored the possible modulation of neuronal Ca2+ channels by protein tyrosine kinases (PTKs). To this end, the effects of PTK inhibitors on whole-cell Ba2+ currents (IBa) through voltage-gated Ca2+ channels were analysed in differentiated NG108-15 neuroblastoma x glioma hybrid cells. Genistein suppressed IBa in a concentration-dependent fashion (IC50 = 22 microM). Although daidzein, an analogue of genistein that is devoid of PTK inhibitory activity, also suppressed IBa, we estimated that specific PTK inhibition by genistein reduced IBa amplitude by 30%. In addition, lavendustin A (20 microM) and herbimycin A (20 microM), two other distinct PTK inhibitors, depressed IBa by 22% and 20%, respectively. Genistein suppressed N-type and T-type currents, sparing L-type current, and its effect was independent of G protein activation. The results suggest that the activity of neuronal Ca2+ channels can be modulated by PTKs, opening the possibility that some of the functions of PTKs in the nervous system are mediated by Ca2+ channel modulation.

Animals↗

PubMed1998

Telomerase activation in cervical neoplasia.

OBJECTIVE: To examine the critical point at which telomerase activation occurs in the course of cervical carcinogenesis. METHODS: Telomeric repeat assay protocol was used to measure telomerase activity in cell samples obtained from 155 Japanese women with various cervical conditions: normal cytology (n = 62), cervical intraepithelial neoplasia (CIN) (n = 63), and invasive squamous cell carcinoma (n = 30). RESULTS: Telomerase activity was detected in five (8%) women with normal cytology, in 26 (41%) patients with CIN (26% of patients with CIN I, 35% with CIN II, and 68% with CIN III), and in 29 (97%) patients with invasive carcinoma. Telomerase activation was significantly more frequent in CIN than in normal cervices (P < .001), and the positive rate in CIN III was significantly higher than that in CIN I (P < .01) and CIN II (P < .05). Furthermore, telomerase activation was significantly more frequent in invasive carcinoma than in CIN III (P < .01). CONCLUSION: Our findings suggest that telomerase activation is a relatively early event in cervical carcinogenesis and correlates well with grade of cervical lesion.

Adult↗

PubMed1998

Factors related to degradation of articular cartilage in osteoarthritis: a review.

OBJECTIVES: Osteoarthritis (OA) is a common joint deterioration initiated by multiple factors. To better understand related factors in the development of this disease, we focused on the mechanical stress loaded on articular cartilage. MATERIALS AND METHODS: The anterior cruciate ligaments of rabbit knee joints were transected, and expression of protein kinase C (PKC) examined immunohistochemically. The PKC activator 12-o-tetradecanoyl-phorbol-13-acetate (TPA) was then administered intraarticularly. To determine the involvement of gas mediators, a cartilage defect was made on the medical femoral condyle of rabbit knee joints. Hydrostatic pressure was loaded on the cartilage taken from the surrounding defects, and levels of superoxide anion and nitric oxide (NO) were measured. Bovine chondrocytes were subjected to cyclic mechanical stretch using a Flexercell Strain Instrument. Proteoglycan synthesis and PKC activity were measured. Expression of matrix metalloproteinase (MMP)-3 and tissue inhibitor of metalloproteinase (TIMP)-1 in articular cartilages obtained from OA patients were examined using Northern blots. RESULTS: Chondrocytes from experimentally induced OA were stained positively with anti-alpha-PKC antibody. Intraarticular administration of TPA prevented the development of OA changes. Cyclic tensile stretch loaded on chondrocytes decreased proteoglycan synthesis and PKC activity. Thus, PKC is involved in the stress-mediated degradation of articular cartilage. Cartilage defects led to degradation of surrounding cartilage and to enhanced superoxide anion and NO synthesis. We also noted increased and decreased expressions of MMP-3 and TIMP-1 mRNA in human OA cartilage, respectively. CONCLUSION: PKC, gas mediators (superoxide anion, NO), and proteinases are all involved in OA.

Animals↗

PubMed1998

Effect of adrenomedullin on ion transport and muscle contraction in rat distal colon.

We have investigated the effects of adrenomedullin (AM) on mucosal ion transport using the Ussing method and smooth muscle contraction using the Magnus method in rat. Our results indicate that AM increases Isc (short-circuit current) for Cl- secretion (100 nM:170.0 +/- 41.2%, 1 microM:193.8 +/- 45.5%, 100% Isc:28.2 +/- 3.1 microA/cm2) with an initial small decrease of Isc, inhibiting Na+ absorption. Tetrodotoxin (TTX) inhibits the Isc response elicited by AM (86%). In addition, AM relaxes potassium-induced contraction (10 nM:11.1 +/- 8.51%, 100 nM:33.4 +/- 12.7%, 100% contraction: 1.8 +/- 0.22 g), and TTX inhibits the response elicited by AM (90%). We conclude that AM modulates water and ion transport as well as bowel movement, mainly through the colonic nervous system.

Adrenomedullin↗

PubMed1998

Influenza.

Influenza viruses are unique in their ability to cause recurrent epidemics and truly global pandemics during which acute febrile respiratory disease occurs explosively in all age groups. Epidemics of varying severity occur almost annually in temperate climates and are punctuated by the much less frequent but more dramatic occurrence of pandemic influenza. Increases in hospitalization and death often accompany widespread morbidity during influenza epidemics and pandemics. Influenza pandemics also threaten to disrupt other essential and nonessential services through high absenteeism, with high economic losses resulting. The medical impact and disruptive effects of epidemics and pandemics clearly justify careful global monitoring of influenza and strenuous efforts to prevent this emerging and reemerging disease.

Antigens, Viral↗