Biomedical subjects

C C Lu

Publications and source records attributed to C C Lu.

At least 55 records · Page 3Linked to original sources

PubMed1998

Functional characterization of human N-methyl-D-aspartate subtype 1A/2D receptors.

The human NMDAR2D subunit was cloned, and the pharmacological properties of receptors resulting from injection of transcripts encoding human NMDAR1A and NMDAR2D subunits in Xenopus oocytes were characterized by profiling NMDA receptor agonists and antagonists. We found that glutamate, NMDA, glycine, and D-serine were significantly more potent on hNMDAR1A/2D than on hNMDAR1A/2A or hNMDAR1A/2B. Also, the potencies of NMDA and glycine were higher for hNMDAR1A/2D than for hNMDAR1A/2C. Ifenprodil was more potent at hNMDAR1A/2B than at hNMDAR1A/2D, whereas 5,7-dichlorokynurenate was more potent at hNMDAR1A/2A than at hNMDAR1A/2D. As measured in transiently transfected human embryonic kidney 293 cells, the maximal inward current in the presence of external Mg2 occurred at -40 mV, and full block was not observed at negative potentials. Kinetic measurements revealed that the higher affinity of hNMDAR1A/2D for both glutamate and glycine relative to hNMDAR1A/2A and hNMDA1A/2B can be explained by slower dissociation of each agonist from hNMDAR1A/2D. The hNMDAR1A/2D combination represents a pharmacologically and functionally distinct receptor subtype and may constitute a potentially important target for therapeutic agents active in the human CNS.

Animals↗

PubMed1998

The human N-methyl-D-aspartate receptor 2C subunit: genomic analysis, distribution in human brain, and functional expression.

cDNAs encoding four isoforms of the human NMDA receptor (NMDAR) NMDAR2C (hNR2C-1, -2, -3, and -4) have been isolated and characterized. The overall identity of the deduced amino acid sequences of human and rat NR2C-1 is 89.0%. The sequences of the rat and human carboxyl termini (Gly925-Val1,236) are encoded by different exons and are only 71.5% homologous. In situ hybridization in human brain revealed the expression of the NR2C mRNA in the pontine reticular formation and lack of expression in substantia nigra pars compacta in contrast to the distribution pattern observed previously in rodent brain. The pharmacological properties of hNR1A/2C were determined by measuring agonist-induced inward currents in Xenopus oocytes and compared with those of other human NMDAR subtypes. Glycine, glutamate, and NMDA each discriminated between hNR1A/2C-1 and at least one of hNR1A/2A, hNR1A/2B, or hNR1A/2D subtypes. Among the antagonists tested, CGS 19755 did not significantly discriminate between any of the four subtypes, whereas 5,7-dichlorokynurenic acid distinguished between hNR1A/2C and hNR1A/2D. Immunoblot analysis of membranes isolated from HEK293 cells transiently transfected with cDNAs encoding hNR1A and each of the four NR2C isoforms indicated the formation of heteromeric complexes between hNR1A and all four hNR2C isoforms. HEK293 cells expressing hNR1A/ 2C-3 or hNR1A/2C-4 did not display agonist responses. In contrast, we observed an agonist-induced elevation of intracellular free calcium and whole-cell currents in cells expressing hNR1A/2C-1 or hNR1A/2C-2. There were no detectable differences in the macroscopic biophysical properties of hNR1A/2C-1 or hNR1A/2C-2.

Amino Acid Sequence↗

PubMed1998

Acute effects of thyroid hormones on the production of adrenal cAMP and corticosterone in male rats.

The acute effects of thyroid hormones on glucocorticoid secretion were studied. Venous blood samples were collected from male rats after they received intravenous 3,5,3'-triiodothyronine (T3) or thyroxine (T4). Zona fasciculata-reticularis (ZFR) cells were treated with adrenocorticotropic hormone (ACTH), T3, T4, ACTH plus T3, or ACTH plus T4 at 37 degrees C for 2 h. Corticosterone concentrations in plasma and cell media, and also adenosine 3',5'-cyclic monophosphate (cAMP) production in ZFR cells in the presence of 3-isobutyl-1-methylxanthine, were determined. The effects of thyroid hormones on the activities of steroidogenic enzymes of ZFR cells were measured by the amounts of intermediate steroidal products separated by thin-layer chromatography. Administration of T3 and T4 suppressed the basal and the ACTH-stimulated levels of plasma corticosterone. In ZFR cells, both thyroid hormones inhibited ACTH-stimulated corticosterone secretion, but the basal corticosterone was inhibited only with T3 > 10(-10) M or T4 > 10(-8) M. Likewise, T3 or T4 at 10(-7) M inhibited the basal- and ACTH-stimulated levels of intracellular cAMP. Physiological doses of T3 and T4 decreased the activities of 3 beta-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11 beta-hydroxylase. These results suggest that thyroid hormones counteract ACTH in adrenal steroidogenesis through their inhibition of cAMP production in ZFR cells.

1-Methyl-3-isobutylxanthine↗

PubMed1998

Effects of ovarian steroid hormones and thyroxine on calcitonin secretion in pregnant rats.

In the present study, the roles of ovarian steroid hormones and thyroxine (T4) in regulating the secretion of calcitonin (CT) in pregnant rats were examined. The levels of plasma progesterone, pre- and post-CaCl2 plasma CT, and recovery time of plasma CT and calcium after calcium challenge were greatest in midterm pregnant rats. The levels of basal plasma progesterone, CT, calcium, and recovery time of plasma CT after calcium challenge were less in late pregnant rats, but basal plasma estradiol was highest in late pregnancy. The concentrations of plasma T4 were gradually decreased in rats during pregnancy. Regardless of the presence of estradiol, administration of progesterone in ovariectomized (Ovx) rats resulted in an increase of plasma T4 as well as the basal and calcium-induced secretion of CT. Administration of estradiol alone did not alter the CaCl2-induced levels but decreased the post-CaCl2 levels of plasma calcium in Ovx rats. The basal levels of plasma CT were decreased in Ovx rats treated with T4. These results suggest that the hypercalcitoninemia in midterm pregnant rats is due to an increased secretion of progesterone. Hypocalcitoninemia in late pregnant rats, however, is due in part to lower plasma calcium.

Animals↗

PubMed1998

Age-related differences in the secretion of calcitonin in female rats.

The mechanism that causes hypercalcitonemia in female rats and is associated with aging was investigated. Young (3 mo), adult (8 mo), middle-aged (12 mo), and old (21 mo) rats were infused with CaCl2 and were bled from a jugular catheter after a CaCl2 challenge. To mimic some of the hormonal changes caused by aging, the anterior pituitary (AP)-grafted ovariectomized rats with hyperprolactinemic syndrome were used to mimic the physiological status of aging. The rat thyroid gland was incubated with or without ovine prolactin (oPRL; 40 or 80 ng/ml) at 37 degreesC for 30 min. Old rats possessed the lowest levels of plasma estradiol and progesterone yet had the highest levels of plasma prolactin and calcitonin (CT) compared with young, adult, and middle-aged rats. The basal release of thyroid CT in vitro in thyroid glands gradually increased with age. Compared with cortex (CX)-grafted rats, the AP-grafted rats possessed higher levels of plasma PRL, basal and CaCl2-induced levels of plasma CT, and the release of thyroid CT in thyroid glands. After stimulation with oPRL, the in vitro release of thyroid CT increased in both CX- and AP-grafted rats. These results suggest that the hypersecretion of CT in old rats is due at least in part to hyperprolactinemia.

Aging↗

PubMed1998

Disturbed small intestinal motility in the late rat pregnancy.

We investigated whether various periods of pregnancy might disturb rat gastrointestinal motility. When the proestrus of female rats occurred, they were housed with male rats. Motility studies were conducted on day 7 (first period), day 14 (second) and day 21 (third) of pregnancy, respectively. After the orogastric feeding of radiochromium marker, rats were sacrificed 15 min later. Gastric emptyings of pregnant rats measured at various periods did not differ from the nonpregnant diestrus controls. The geometric center represented intestinal transits in the first, second and third periods of pregnancy and controls were (mean+/-SEM) 4.54+/-0.25, 4.47+/-0.17, 3.61+/-0.27 and 4.98+/-0.13, respectively (p < 0.01) while their plasma progesterone levels were 15.6+/-2.6, 18+/-1.4, 7.1+/-0.5 and 8.6+/-0.4 ng/ml, respectively (p< 0.01). This shows that late pregnancy inhibits small intestinal transit, whereas gastric emptying remains unchanged. Altered progesterone during pregnancy is not a main mediator to disturb intestinal transit.

Animals↗

PubMed1998

Randomized, double-blind, placebo-controlled study of transdermal nicotine patch for smoking cessation.

Smoking cessation is an arduous process because nicotine withdrawal syndrome, which occurs following sudden interruption of nicotine use in long-term smokers, frequently prevents them from giving up the habit. Nicotine supplement systems may relieve smokers' nicotine withdrawal symptoms and, thus, help in the process of abstinence from smoking. The purpose of the present study was to investigate the effectiveness and safety of a 30-mg transdermal nicotine patch in a smoking cessation program for Chinese smokers. In this randomized, double-blind, placebo-controlled study, 30 heavy smokers, who had smoked more than 20 cigarettes per day for more than a year, were treated with 30-mg transdermal nicotine patches, and 32 heavy smokers were given placebo patches during a 6-week smoking cessation program. The clinical characteristics of the two groups were similar. After 6 weeks, the use of the transdermal nicotine patch was associated with markedly reduced nicotine dependence and severity of withdrawal symptoms. Nineteen (63%, 95% confidence interval, CI, 46%-80%) of the smokers treated with the transdermal nicotine patch had successfully quit smoking at the end of the program (6 weeks) and nine (30%, 95% CI 14%-46%) remained abstinent 1 year later. In contrast, only 11 (34%, 95% CI 18%-50%) of the smokers in the placebo group had successfully stopped smoking after 6 weeks, and three remained abstinent 1 year later (9%, 95% CI 0%-19%). However, there was no statistically significant difference between the two groups of smokers after 1 year of follow-up (p = 0.08). Side-effects were minimal and did not affect the efficacy of the skin patch. The results indicate that the transdermal nicotine patch is an effective aid in smoking cessation programs.

Administration, Cutaneous↗

PubMed1997

Interaction between triiodothyronine and ovarian steroid hormones on the regulation of the release of thyrotropin and thyrotropin-releasing hormone in vitro.

In vivo and in vitro experiments were designed to examine [1] the effect of triiodothyronine (T3) and/or ovarian steroids on the spontaneous and thyrotropin-releasing hormone (TRH)-stimulated release of thyrotropin (TSH) by the anterior pituitary gland (AP) in vitro; and [2] the in vivo effects of T3 and ovarian steroids on TRH-release in vitro. In the experiment 1, ovariectomized-thyroidectomized (Ovx-Tx) rats were injected with triiodothyronine (T3, 2 micrograms/kg), estradiol benzoate (EB, 25 micrograms/kg), progesterone (P, 10 mg/kg), T3 plus EB, T3 plus P, EB plus P, or T3 plus EB and P for 6 days before decapitation. The AP was incubated with Locke's medium, challenged with TRH (30 nM), recovered and then with T3 (10 nM) only or with T3+TRH, 30 min for each interval. Mediobasal hypothalami (MBHs) were challenged with high potassium (60 mM) for 30 min. In the experiment 2, the APs of Ovx-Tx rats were enzymatically dispersed and the AP cells were pretreated with or without EB (0-6 nM) for 72 h, and further with T3 (10 nM) for 24 h, followed by an incubation for 30 min with TRH (0-100 nM). The spontaneous and TRH-induced release of TSH in vitro from rat APs, and pituitary TSH content were increased by T3, or T3 plus P as compared with the animals injected with vehicle, or P alone. EB inhibits the effect of T3 on TSH release in vitro. Application of T3 in vitro prevented the release of TSH in response to TRH. EB dose-dependently relieved the inhibitory effect of T3 on TRH-induced TSH release in vitro. TRH release from MBH was increased by EB and inhibited by T3 or P. EB prevented the inhibitory effect of T3 on TRH release. P plus T3 potentiated the stimulatory effects of EB on TRH release. These results suggest that [1] the reduction of the concentration of plasma TSH by T3 is at least in part due to the inhibitory effects of T3 on TRH release from mediobasal hypothalamus, and TSH release in response to TRH, [2] the increased content and release of TSH from rat AP tissue by T3 via an in vivo effect may be involved in a short feedback loop of TSH on TRH release, and [3] ovarian steroid hormones play an inhibitory role in regulating T3 effects on the release of TSH and TRH.

Animals↗

PubMed1997

Pre-emptive analgesia with ketamine, morphine and epidural lidocaine prior to total knee replacement.

PURPOSE: Pre-emptive analgesia can improve postoperative pain management. The purpose of this study was to examine the effectiveness of ketamine as a pre-emptive analgesic as previous studies have shown the involvement of N-methyl-D-Aspartate (NMDA) receptor in neuroplasticity. METHODS: Forty-five ASA 1-2 patients, undergoing unilateral total knee replacement were studied. In the study groups, epidural lidocaine was used as the primary anaesthestic. Patients received ketamine + morphine epidurally 30 min either before (group EB) or after skin incision (group EA). Group G patients received general anaesthesia and ketamine + morphine were given 30 min after skin incision via an epidural catheter used for postoperative pain control. Epidural morphine and ketamine in lidocaine was given to all patients at the end of surgery and every 12 hr for three days for analgesia supplemented with PCA morphine. The time until first PCA trigger, morphine consumption, pain scores, satisfaction scores, and morphine related side effects were recorded at 6, 12, 24, 48 and 72 hr after surgery. RESULTS: Epidural ketamine plus morphine with lidocaine before surgical incision produced better pain relief and patient satisfaction than when given after incision. A longer time to PCA and decreased morphine consumption were observed in group EB than in group G. In group EA, epidural anaesthesia also produced some pre-emptive analgesic effect compared with general anaesthesia shown by decreased morphine consumption. CONCLUSIONS: Administration of ketamine plus morphine with epidural lidocaine anesthesia before surgery provided improved postoperative analgesia compared with general anaesthesia alone or when analgesics were given after skin incision.

Analgesia, Epidural↗

PubMed1997

The role of cyclic AMP production, calcium channel activation and enzyme activities in the inhibition of testosterone secretion by amphetamine.

1. The aim of this study was to investigate the mechanism by which amphetamine exerts its inhibitory effect on testicular interstitial cells of male rats. 2. Administration of amphetamine (10(-12)-10(-6) M) in vitro resulted in a dose-dependent inhibition of both basal and human chorionic gonadotropin (hCG, 0.05 iu ml(-1))-stimulated release of testosterone. 3. Amphetamine (10(-9) M) enhanced the basal and hCG-increased levels of adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in vitro (P<0.05) in rat testicular interstitial cells. 4. Administration of SQ22536, an adenylyl cyclase inhibitor, decreased the basal release (P<0.05) of testosterone in vitro and abolished the inhibitory effect of amphetamine. 5. Nifedipine (10(-6) M) alone decreased the secretion of testosterone (P<0.01) but it failed to modify the inhibitory action of amphetamine (10(-10)-10(-6) M). 6. Amphetamine (10(-10)-10(-6) M) significantly (P<0.05 or P<0.01) decreased the activities of 3beta-hydroxysteroid dehydrogenase (3beta-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography. (t.l.c.). 7. These results suggest that increased cyclic AMP production, decreased Ca2+ channel activity and decreased activities of 3beta-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.

17-Hydroxysteroid Dehydrogenases↗

PubMed1997

Lactate and the effects of exercise on testosterone secretion: evidence for the involvement of a cAMP-mediated mechanism.

The effects of swimming and lactate on the release of testosterone were examined in male rats. During in vivo experiments, male rats were catheterized via the right jugular vein and blood was collected at 0, 10, 15, 30, and 60 min following the exercise, or they were catheterized via the right jugular vein and the left femoral vein and blood was collected at 0, 2, 5, 10, 15, 30, 60, and 120 min after a 10-min infusion at lactate (13 mg.kg-1.min-1). Trunk blood and blood from the testicular vein were also collected after 10 min of swimming or water immersion. In an in vitro experiment, testicular fragments were challenged with lactate (0.01-10 mM) and/or human chorionic gonadotropin (hCG; 0.5 IU.mL-1), and the mediobasal hypothalamus (MBH) was challenged with lactate (8 mM). The post-exercise levels of plasma lactate and testosterone at 10, 15, and 30 min were higher than resting levels. Plasma luteinizing hormone (LH) was increased following 30 min of swimming. Administration of lactate or hCG increased in a dose dependent manner testicular cyclic adenosine 3':5' monophosphate (cAMP) and testosterone release. Plasma testosterone increased after swimming and lactate infusion. Incubation of MBH with lactate increased the gonadotropin-releasing hormone (GnRH) level in the medium. These results suggest that the increased plasma testosterone levels in male rats during exercise is at least partially a result of a direct and LH-independent stimulatory effect of lactate on the secretion of testosterone by increasing testicular cAMP production. Swim-elevated plasma LH may be a result of a rise of GnRH caused by lactate.

Animals↗

PubMed1997

Bronchodilator therapy for chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous group of diseases characterized by cough, sputum production, dyspnoea, airflow limitation and bronchial hyperreactivity. The airflow limitation declines progressively and is irreversible or partially reversible. Bronchodilator therapy is prescribed to relieve the symptoms, reverse airway obstruction and hopefully slow the rate of disease progression and decelerate the decline in pulmonary function. During acute exacerbation, inhalation of beta2-agonists remain the therapy of choice. The usefulness of anticholinergic inhalation in acute attacks is investigated in order to determine if a higher dose and more frequent administration have same benefit as beta2-agonists inhalation. Theophylline is usually given orally as a sustained release formulation for chronic maintenance therapy. Some patients may benefit from theophylline infusion during an acute phase when appropriately used; however, sympathomimetic agents fail to produce adequate bronchodilation. During interim periods of stability, inhalation of ipratropium bromide has increased in popularity as a regular long-term bronchodilator therapy. Although ipratropium and beta2-agonists are equally efficacious when the dosage is adequate enough, a combination of both provides a rapid onset of action of the adrenergic agents and a prolonged action of the anticholinergic. Furthermore, this combination can be given in a reduced dose, thereby avoiding side-effects. Inhalation techniques can influence the efficacy of bronchodilator therapy. For severe dyspnoeic patients or patients with poor technique of co-ordination with metered-dose inhaler (MDI), attachment of a spacer to the MDI or using a nebulizer will overcome these difficulties. Bronchodilator therapy can not prevent the development of COPD or slow down the decline of pulmonary function, other interventions should be included in a comprehensive management programme.

Administration, Inhalation↗

PubMed1997

Gastric emptying and gastrointestinal transit during lactation in rats.

Female sex hormones can influence gastrointestinal function. To understand whether postpartum changes in female sex hormones may affect such function, gastric emptying and gastrointestinal transit were measured in rats on days 1-2, 10, 15, and 21 of lactation, on day 7 postweaning, and at the nonpregnant diestrous stage. Gastric emptying and gastrointestinal transit were assessed in conscious rats 15 min after intragastric instillation of a test meal containing charcoal and (51)Cr. The results showed that gastric emptying was increased throughout the first 2 wk of lactation, with a gradual decrease as lactation proceeded toward weaning, and returned to the level of the virgin rats by 1 wk postweaning. Gastrointestinal transit was greater in the early stage of lactation and was related to gastric emptying (P < 0.001). Increases in gastric emptying and intestinal length were correlated with lactation (P < 0.001) and plasma prolactin levels (P < 0.05) but not with plasma progesterone or estradiol levels. We concluded that the sex steroid hormones associated with lactation do not mediate a change in gastric emptying and gastrointestinal transit during lactation.

Animals↗

PubMed1997

Inhibition of corticosterone secretion by thyroxine in male rats.

The effects of thyroxine (T4) on the secretion of corticosterone both in vivo and in vitro in male rats were studied. Rats were thyroidectomized (Tx) or sham Tx. The Tx rats were subcutaneously with T4 (20 micrograms/kg) or saline once daily for two weeks. In an in vitro experiment, adrenal glands were incubated with ACTH, T4, or ACTH plus T4 in the presence or absence of 0.5 mM 3-isobutyl-1-methylxanthine (IBMX) at 37 degrees C for 60 min. Medium and ether-extracted plasma samples were analyzed for corticosterone by radioimmunoassay (RIA). The accumulation of cyclic adenosine monophosphate (cAMP) in adrenal tissues after incubation with IBMX was measured by RIA. The levels of plasma corticosterone in Tx rats were significantly increased as compared with euthyroid rats. T4 replacement in Tx rats restored plasma corticosterone to euthyroid level. Administration of T4 in vitro resulted in an inhibition of both basal and ACTH-stimulated release of corticosterone. Both basal and ACTH-stimulated generations of cAMP in adrenal tissues were decreased by T4. These results suggest that T4 inhibits the spontaneous and ACTH-stimulated secretion of corticosterone by acting directly at adrenal glands via a decrease in cAMP production.

Adrenal Glands↗

PubMed1997

Diagnostic imaging in the evaluation of constipation in adults.

Acute and chronic constipation are common conditions. In most instances, a thorough history and digital rectal examination provide sufficient information to begin treatment. Occasionally, imaging studies can be useful to confirm the presence of a suspected abnormality. The acute onset of constipation suggests colonic obstruction. Plain abdominal radiographs may be sufficient to determine the level and cause of the obstruction, such as sigmoid or cecal volvulus. Barium enema radiographic examination or colonoscopy may also be useful to detect the cause of obstruction. In patients with chronic constipation, plain abdominal radiographs can be used to show the extent of fecal impaction. Colonic transit time can be assessed on serial abdominal radiographs after the patient has ingested radiopaque markers. Evacuation proctography can be used to diagnose a variety of functional disorders of the rectum and anus, such as rectocele, intussusception and abnormal perineum floor descent.

Acute Disease↗

PubMed1997

Inhibition of bufalin on pituitary and testicular function in rats.

The effects of bufalin on the secretion of testosterone and luteinizing hormone (LH) and the accumulation of testicular adenosine 3':5'-cyclic monophosphate (cAMP) were studied. Male rats were injected with bufalin, human chorionic gonadotropin (hCG), gonadotropin releasing hormone (GnRH), hCG plus bufalin or GnRH plus bufalin via a jugular catheter. Blood samples were collected at several intervals subsequent to the challenge. In the in vitro study, rat testis blocks were incubated with bufalin, hCG or both for 1 h. The anterior pituitary gland was incubated with bufalin, GnRH or both for 30 min. The media were analyzed for testosterone or LH. For studying cAMP accumulation, testicular blocks were incubated for 1 h with the medium containing isobutyl-1-methylxanthine. After incubation, tissues were extracted by ethanol before measuring cAMP concentration. A single intravenous injection of bufalin decreased the basal and hCG-stimulated levels of plasma testosterone. Administration of bufalin in vitro resulted in an inhibition of both basal and hCG-stimulated release of testosterone. Bufalin diminished cAMP accumulation in rat testes. However, the basal levels of plasma and medium LH were not altered by bufalin administration. Likewise, the LH response to GnRH was diminished by bufalin administration, both in vivo and in vitro. These results suggest that the inhibition of testosterone production by bufalin is partly caused by a decrease of testicular cAMP accumulation and LH response to GnRH in rats.

1-Methyl-3-isobutylxanthine↗

PubMed1996

Activation of the hepatitis B virus S promoter by transcription factor NF-Y via a CCAAT element.

The middle and small surface proteins of hepatitis B virus are translated from 5'-heterogeneous transcripts specified by the S promoter. We have generated a series of linker-substitution mutants that encompass the 130 base pairs comprising this promoter and measured the amount of transcripts and protein products synthesized from each mutant. The results confirm our previous finding that a CCAAT element is an important up-stream activating element for this promoter, as mutation of this element leads to a >20-fold decrease in promoter activity. In vitro binding assays showed that the cellular transcription factor NF-Y (CCAAT-binding factor) binds to this element, and expression of a dominant-negative NF-Y subunit in transfected cells specifically reduced surface protein expression from the S promoter via the CCAAT element. In addition, two Sp1 sites also contribute to S promoter activity by a total of approximately 6-fold. Therefore, the S promoter is activated by both NF-Y and Sp1, but more strongly by the former factor.

Base Sequence↗

PubMed1996

Diagnostic imaging in the evaluation of dysphagia.

Evaluation of dysphagia is a challenge commonly encountered by family physicians. Dysphagia may be classified as either the oropharngeal type or the esophageal type and may have a variety of etiologies. Possible causes of oropharyngeal dysphagia include Zenker's diverticulum, pharyngeal carcinoma, pharyngeal webs and strictures, lateral pharyngeal pouches and neuromuscular diseases. Esophageal dysphagia can be caused by esophageal carcinoma, esophageal stricture and webs, achalasia, diffuse esophageal spasm and scleroderma, caustic esophagitis and infectious esophagitis. Studies using different textures of barium allow evaluation of the swallowing mechanism. Static images are obtained to evaluate the integrity of the mucosa.

Algorithms↗