Anthelmintics
Mebendazole
Antinematodal Agents
Albendazole
Echinococcus
Sulfoxides
Giardia
2-Pyridinylmethylsulfinylbenzimidazoles
Omeprazole
Tubulin
Drug Resistance
Blocking angiotensin II ameliorates proteinuria and glomerular lesions in progressive mesangioproliferative glomerulonephritis. (1/3157)
BACKGROUND: The renin-angiotensin system is thought to be involved in the progression of glomerulonephritis (GN) into end-stage renal failure (ESRF) because of the observed renoprotective effects of angiotensin-converting enzyme inhibitors (ACEIs). However, ACEIs have pharmacological effects other than ACE inhibition that may help lower blood pressure and preserve glomerular structure. We previously reported a new animal model of progressive glomerulosclerosis induced by a single intravenous injection of an anti-Thy-1 monoclonal antibody, MoAb 1-22-3, in uninephrectomized rats. Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta (TGF-beta) and extracellular matrix components. METHODS: We studied the effect of an ACEI (cilazapril) and an Ang II type 1 receptor antagonist (candesartan) on the clinical features and morphological lesions in the rat model previously reported. After 10 weeks of treatment with equihypotensive doses of cilazapril, cilazapril plus Hoe 140 (a bradykinin receptor B2 antagonist), candesartan, and hydralazine, we examined systolic blood pressure, urinary protein excretion, creatinine clearance, the glomerulosclerosis index, and the tubulointerstitial lesion index. We performed a semiquantitative evaluation of glomerular immunostaining for TGF-beta and collagen types I and III by immunofluorescence study and of these cortical mRNA levels by Northern blot analysis. RESULTS: Untreated rats developed massive proteinuria, renal dysfunction, and severe glomerular and tubulointerstitial injury, whereas uninephrectomized control rats did not. There was a significant increase in the levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III in untreated rats. Cilazapril and candesartan prevented massive proteinuria, increased creatinine clearance, and ameliorated glomerular and tubulointerstitial injury. These drugs also reduced levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III. Hoe 140 failed to blunt the renoprotective effect of cilazapril. Hydralazine did not exhibit a renoprotective effect. CONCLUSION: These results indicate that ACEIs prevent the progression to ESRF by modulating the effects of Ang II via Ang II type 1 receptor on the production of TGF-beta and collagen types I and III, as well as on intrarenal hemodynamics, but not by either increasing bradykinin activity or reducing blood pressure in this rat model of mesangial proliferative GN. (+info)Mibefradil (Ro 40-5967) inhibits several Ca2+ and K+ currents in human fusion-competent myoblasts. (2/3157)
1. The effect of mibefradil (Ro 40-5967), an inhibitor of T-type Ca2+ current (I(Ca)(T)), on myoblast fusion and on several voltage-gated currents expressed by fusion-competent myoblasts was examined. 2. At a concentration of 5 microM, mibefradil decreases myoblast fusion by 57%. At this concentration, the peak amplitudes of I(Ca)(T) and L-type Ca2+ current (I(Ca)(L)) measured in fusion-competent myoblasts are reduced by 95 and 80%, respectively. The IC50 of mibefradil for I(Ca)(T) and I(Ca)(L) are 0.7 and 2 microM, respectively. 3. At low concentrations, mibefradil increased the amplitude of I(Ca)(L) with respect to control. 4. Mibefradil blocked three voltage-gated K+ currents expressed by human fusion-competent myoblasts: a delayed rectifier K+ current, an ether-a-go-go K+ current, and an inward rectifier K+ current, with a respective IC50 of 0.3, 0.7 and 5.6 microM. 5. It is concluded that mibefradil can interfere with myoblast fusion, a mechanism fundamental to muscle growth and repair, and that the interpretation of the effect of mibefradil in a given system should take into account the action of this drug on ionic currents other than Ca2+ currents. (+info)Binding of Cob(II)alamin to the adenosylcobalamin-dependent ribonucleotide reductase from Lactobacillus leichmannii. Identification of dimethylbenzimidazole as the axial ligand. (3/3157)
The ribonucleoside triphosphate reductase (RTPR) from Lactobacillus leichmannii catalyzes the reduction of nucleoside 5'-triphosphates to 2'-deoxynucleoside 5'-triphosphates and uses coenzyme B12, adenosylcobalamin (AdoCbl), as a cofactor. Use of a mechanism-based inhibitor, 2'-deoxy-2'-methylenecytidine 5'-triphosphate, and isotopically labeled RTPR and AdoCbl in conjunction with EPR spectroscopy has allowed identification of the lower axial ligand of cob(II)alamin when bound to RTPR. In common with the AdoCbl-dependent enzymes catalyzing irreversible heteroatom migrations and in contrast to the enzymes catalyzing reversible carbon skeleton rearrangements, the dimethylbenzimidazole moiety of the cofactor is not displaced by a protein histidine upon binding to RTPR. (+info)Resetting of exaggerated tubuloglomerular feedback activity in acutely volume-expanded young SHR. (4/3157)
One purpose of the present study was to evaluate the ability of 7-wk-old spontaneously hypertensive rats (SHR) to reset tubuloglomerular feedback (TGF) activity in response to acute volume expansion (VE). Second, we evaluated the contribution of ANG II, via its action on AT1 receptors, to TGF control of glomerular function during VE. TGF was assessed by micropuncture methods and proximal tubular stop-flow pressure (SFP) determinations in SHR, Wistar-Kyoto rats (WKY), and Sprague-Dawley rats (SD). During euvolemia SHR exhibited enhanced TGF activity. In the same animals acute VE was achieved by infusion of saline (5 ml. h-1. 100 g body wt-1). VE led to resetting of TGF in all three strains. Maximal SFP responses, elicited by a 30-40 nl/min loop of Henle perfusion rate, decreased from 19 to 12 mmHg in SHR and, on average, from 11 to 5 mmHg in WKY and SD (P < 0.001). Tubular flow rate producing a half-maximal response (turning point) shifted to higher flow rates during VE, from 12 to 14 nl/min in SHR and from 15 to 19 nl/min in WKY. Administration of the AT1 receptor blocker candesartan (0.05 mg/kg iv) during sustained VE decreased TGF-mediated reductions in SFP in SHR and slightly increased the turning point in WKY. Nevertheless, other parameters of TGF activity were unaffected by AT1 receptor blockade. In conclusion, young SHR possess the ability to reset TGF activity in response to VE to a degree similar to compensatory adjustments in WKY. However, TGF remains enhanced in SHR during VE. ANG II and its action on AT1 receptors are in part responsible for the exaggerated SFP responses in young SHR during VE. (+info)Effect of 5-HT4 receptor stimulation on the pacemaker current I(f) in human isolated atrial myocytes. (5/3157)
OBJECTIVE: 5-HT4 receptors are present in human atrial cells and their stimulation has been implicated in the genesis of atrial arrhythmias including atrial fibrillation. An I(f)-like current has been recorded in human atrial myocytes, where it is modulated by beta-adrenergic stimulation. In the present study, we investigated the effect of serotonin (5-hydroxytryptamine, 5-HT) on I(f) electrophysiological properties, in order to get an insight into the possible contribution of I(f) to the arrhythmogenic action of 5-HT in human atria. METHODS: Human atrial myocytes were isolated by enzymatic digestion from samples of atrial appendage of patients undergoing coeffective cardiac surgery. Patch-clamped cells were superfused with a modified Tyrode's solution in order to amplify I(f) and reduce overlapping currents. RESULTS AND CONCLUSIONS: A time-dependent, cesium-sensitive increasing inward current, that we had previously described having the electrophysiological properties of the pacemaker current I(f), was elicited by negative steps (-60 to -130 mV) from a holding potential of -40 mV. Boltzmann fit of control activation curves gave a midpoint (V1/2) of -88.9 +/- 2.6 mV (n = 14). 5-HT (1 microM) consistently caused a positive shift of V1/2 of 11.0 +/- 2.0 mV (n = 8, p < 0.001) of the activation curve toward less negative potentials, thus increasing the amount of current activated by clamp steps near the physiological maximum diastolic potential of these cells. The effect was dose-dependent, the EC50 being 0.14 microM. Maximum current amplitude was not changed by 5-HT. 5-HT did not increase I(f) amplitude when the current was maximally activated by cAMP perfused into the cell. The selective 5-HT4 antagonists, DAU 6285 (10 microM) and GR 125487 (1 microM), completely prevented the effect of 5-HT on I(f). The shift of V1/2 caused by 1 microM 5-HT in the presence of DAU 6285 or GR 125487 was 0.3 +/- 1 mV (n = 6) and 1.0 +/- 0.6 mV (n = 5), respectively (p < 0.01 versus 5-HT alone). The effect of 5-HT4 receptor blockade was specific, since neither DAU 6285 nor GR 125487 prevented the effect of 1 microM isoprenaline on I(f). Thus, 5-HT4 stimulation increases I(f) in human atrial myocytes; this effect may contribute to the arrhythmogenic action of 5-HT in human atrium. (+info)Differential effects of pinacidil, cromakalim, and NS 1619 on electrically evoked contractions in rat vas deferens. (6/3157)
AIM: To compare the inhibitory action of electrically evoked contractions of rat epididymal vas deferens by pinacidil (Pin), cromakalim (Cro), and NS 1619. METHODS: Monophasic contractions were evoked by electric field stimulation in rat isolated epididymal half of vas deferens. RESULTS: Newly developed ATP-sensitive K+ channel openers, Pin and Cro, concentration-dependently reduced the electrically evoked (0.3 Hz, 1 ms pulse duration, 60 V) contractions and glibenclamide but not charybdotoxin antagonized the inhibitory effects of both agents. Pin shifted the concentration-response curve for norepinephrine to the right with reducing the magnitude of the maximum contraction in a glibenclamide-sensitive fashion. The large-conductance Ca(2+)-activated K+ channel opener, NS 1619, inhibited the electrically evoked contractions in a concentration-dependent manner. Charybdotoxin (100 nmol.L-1) partially reduced the effect of NS 1619 but glibenclamide (10 mumol.L-1) showed no effect. None of these 3 agents affected the basal tension. CONCLUSION: Both ATP-sensitive and Ca(2+)-activated K+ channels presented in vas deferens smooth muscles involved in regulation of muscle contractility. (+info)Development of nuclear transfer and parthenogenetic rabbit embryos activated with inositol 1,4,5-trisphosphate. (7/3157)
The present study was carried out to evaluate the effects of different activation protocols, enucleation methods, and culture media on the development of parthenogenetic and nuclear transfer (NT) rabbit embryos. Electroporation of 25 mM inositol 1,4, 5-trisphosphate (IP3) in calcium- and magnesium-free PBS immediately induced a single intracellular calcium transient in 6 out of 14 metaphase II-stage rabbit oocytes evaluated during a 10-min recording period. The percentage of oocytes treated with IP3 followed by 6-dimethylaminopurine (IP3 + DMAP) that cleaved (83.9%) and reached the blastocyst stage (50%) was significantly higher (p < 0.05) than those activated with multiple pulses (61.6% and 30.1%, respectively) or treated with ionomycin + DMAP (52.9% and 5.7%, respectively). Development of IP3 + DMAP-activated rabbit oocytes and in vivo-fertilized zygotes in different culture media was studied. Development of activated oocytes to the blastocyst stage in Earle's balanced salt solution (EBSS) supplemented with MEM nonessential amino acids, basal medium Eagle amino acids, 1 mM L-glutamine, 0.4 mM sodium pyruvate, and 10% fetal bovine serum (FBS) (EBSS-complete) (40.6%) was significantly higher (p < 0.05) than those that developed in either Dulbecco's Modified Eagle's medium (DMEM)/RPMI + 10% FBS (15.5%) or CR1aa + 10% FBS (4%) medium. In addition, 100% of in vivo-fertilized rabbit zygotes developed to the blastocyst stage in EBSS-complete. A third set of experiments was carried out to study the efficiency of blind versus stained (Hoechst 33342) enucleation of oocytes. Twenty-nine of 48 blind enucleated and IP3 + DMAP-activated oocytes cleaved (60.4%), and 15 (31.2%) subsequently reached the blastocyst stage, whereas 9 of 52 oocytes enucleated using epifluorescence (17.3%) cleaved, and none of these reached the blastocyst stage. When the above parameters that yielded the highest blastocysts were combined in an NT experiment using adult rabbit fibroblast nuclei, 72.2% (39 of 54) of the fused nuclear transplant embryos cleaved and 29.6% (16 of 54) reached the blastocyst stage. (+info)Serial changes in sarcoplasmic reticulum gene expression in volume-overloaded cardiac hypertrophy in the rat: effect of an angiotensin II receptor antagonist. (8/3157)
This study was designed to clarify whether gene expression in the cardiac sarcoplasmic reticulum [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, ryanodine receptor and calsequestrin] changes in accordance with left ventricular functional alterations in the volume-overloaded heart. Further, the effect of the angiotensin II type 1 receptor antagonist, TCV-116, on the expression of these genes was also evaluated. Left ventricular fractional shortening was significantly increased at 7 days, had returned to control levels at 21 days, and had significantly decreased at 35 days after the shunt operation, compared with sham-operated rats. The level of SERCA mRNA was significantly decreased at both 21 days and 35 days after the shunt operation. The levels of ryanodine receptor and phospholamban mRNAs were significantly decreased at 35 days in shunt-operated rats. The decrease in the SERCA mRNA level preceded the development of cardiac dysfunction. The levels of SERCA and ryanodine receptor mRNAs were correlated positively with left ventricular fractional shortening (r=0.73, P<0.0001 and r=0.61, P<0.01 respectively). Attenuation of the decrease in left ventricular fractional shortening occurred on treatment with TCV-116. After the treatment with TCV-116, the levels of SERCA and phospholamban mRNAs were restored to the respective values in sham-operated rats. Ryanodine receptor mRNA levels remained unchanged after treatment with TCV-116. These results indicate that the down-regulation of SERCA and ryanodine receptor mRNA levels may be related to cardiac dysfunction in the volume-overloaded heart. In addition, treatment with an angiotensin II receptor antagonist may restore the altered sarcoplasmic reticulum mRNA levels to control levels, and this may result in attenuation of the functional impairment in the volume-overloaded heart. (+info)Benzimidazoles are a class of heterocyclic compounds containing a benzene fused to a imidazole ring. They have a wide range of pharmacological activities and are used in the treatment of various diseases. Some of the benzimidazoles are used as antiparasitics, such as albendazole and mebendazole, which are effective against a variety of worm infestations. Other benzimidazoles have antifungal properties, such as thiabendazole and fuberidazole, and are used to treat fungal infections. Additionally, some benzimidazoles have been found to have anti-cancer properties and are being investigated for their potential use in cancer therapy.
Anthelmintics are a type of medication used to treat infections caused by parasitic worms, also known as helminths. These medications work by either stunting the growth of the worms, paralyzing them, or killing them outright, allowing the body to expel the worms through normal bodily functions. Anthelmintics are commonly used to treat infections caused by roundworms, tapeworms, flukeworms, and hookworms. Examples of anthelmintic drugs include albendazole, mebendazole, praziquantel, and ivermectin.
Mebendazole is a medication used to treat various types of worm infections, such as roundworm, whipworm, hookworm, and threadworm. It belongs to a class of drugs called anthelmintics, which work by preventing the worms from absorbing nutrients, leading to their eventual death and elimination from the body.
Mebendazole is available in various forms, including tablets, chewable tablets, and suspensions. It is usually taken as a single dose or for several days, depending on the type and severity of the infection being treated.
It's important to note that mebendazole is not effective against all types of worm infections, so it should only be used under the guidance and supervision of a healthcare professional. Additionally, while taking mebendazole, it's recommended to maintain good hygiene practices, such as washing hands frequently and avoiding contaminated food or water, to prevent reinfection.
Antinematodal agents are a type of medication used to treat infections caused by nematodes, which are also known as roundworms. These agents work by either killing the parasitic worms or preventing them from reproducing. Some examples of antinematodal agents include albendazole, ivermectin, and mebendazole. These medications are used to treat a variety of nematode infections, such as ascariasis, hookworm infection, and strongyloidiasis. It is important to note that the use of antinematodal agents should be under the guidance of a healthcare professional, as they can have side effects and may interact with other medications.
Albendazole is an antiparasitic medication used to treat a variety of parasitic infections, including neurocysticercosis (a tapeworm infection that affects the brain), hydatid disease (a parasitic infection that can affect various organs), and other types of worm infestations such as pinworm, roundworm, hookworm, and whipworm infections.
Albendazole works by inhibiting the polymerization of beta-tubulin, a protein found in the microtubules of parasitic cells, which disrupts the parasite's ability to maintain its shape and move. This leads to the death of the parasite and elimination of the infection.
Albendazole is available in oral form and is typically taken two to three times a day with meals for several days or weeks, depending on the type and severity of the infection being treated. Common side effects of albendazole include nausea, vomiting, diarrhea, abdominal pain, and headache. Rare but serious side effects may include liver damage, bone marrow suppression, and neurological problems.
It is important to note that albendazole should only be used under the supervision of a healthcare provider, as it can have serious side effects and interactions with other medications. Additionally, it is not effective against all types of parasitic infections, so proper diagnosis is essential before starting treatment.
'Echinococcus' is a genus of tapeworms that can cause serious infections known as echinococcosis in humans and other animals. The most common species that infect humans are Echinococcus granulosus and Echinococcus multilocularis.
Echinococcus granulosus typically causes cystic echinococcosis, also known as hydatid disease, which affects the liver, lungs, or other organs. The tapeworm's eggs are passed in the feces of infected animals, such as dogs or sheep, and can be ingested by humans, leading to the development of cysts in various organs.
Echinococcus multilocularis typically causes alveolar echinococcosis, a more severe and invasive form of the disease that affects the liver and can spread to other organs. This species has a complex life cycle involving small mammals as intermediate hosts and canids (such as foxes or dogs) as definitive hosts.
Human infections with Echinococcus are rare but can lead to severe health complications if left untreated. Preventive measures include proper hygiene, avoiding contact with infected animals, and cooking meat thoroughly before consumption.
Sulfoxides are organic compounds characterized by the functional group consisting of a sulfur atom bonded to two oxygen atoms and a carbon atom. The general structure is R-S(=O)O-R', where R and R' represent alkyl or aryl groups. They are often formed by the oxidation of sulfides, which contain a sulfur atom bonded to two carbon atoms. Sulfoxides have a trigonal pyramidal geometry at the sulfur atom due to the presence of two electron-withdrawing oxygen atoms. They exhibit properties of both polar and nonpolar compounds, making them useful as solvents and intermediates in organic synthesis.
Antiprotozoal agents are a type of medication used to treat protozoal infections, which are infections caused by microscopic single-celled organisms called protozoa. These agents work by either killing the protozoa or inhibiting their growth and reproduction. They can be administered through various routes, including oral, topical, and intravenous, depending on the type of infection and the severity of the illness.
Examples of antiprotozoal agents include:
* Metronidazole, tinidazole, and nitazoxanide for treating infections caused by Giardia lamblia and Entamoeba histolytica.
* Atovaquone, clindamycin, and pyrimethamine-sulfadoxine for treating malaria caused by Plasmodium falciparum or other Plasmodium species.
* Pentamidine and suramin for treating African trypanosomiasis (sleeping sickness) caused by Trypanosoma brucei gambiense or T. b. rhodesiense.
* Nitroimidazoles, such as benznidazole and nifurtimox, for treating Chagas disease caused by Trypanosoma cruzi.
* Sodium stibogluconate and paromomycin for treating leishmaniasis caused by Leishmania species.
Antiprotozoal agents can have side effects, ranging from mild to severe, depending on the drug and the individual patient's response. It is essential to follow the prescribing physician's instructions carefully when taking these medications and report any adverse reactions promptly.
Giardia is a genus of microscopic parasitic flagellates that cause giardiasis, a type of diarrheal disease. The most common species to infect humans is Giardia intestinalis (also known as Giardia lamblia or Giardia duodenalis). These microscopic parasites are found worldwide, particularly in areas with poor sanitation and unsafe water.
Giardia exists in two forms: the trophozoite, which is the actively feeding form that multiplies in the small intestine, and the cyst, which is the infective stage that is passed in feces and can survive outside the body for long periods under appropriate conditions. Infection occurs when a person ingests contaminated water or food, or comes into direct contact with an infected person's feces.
Once inside the body, the cysts transform into trophozoites, which attach to the lining of the small intestine and disrupt the normal function of the digestive system, leading to symptoms such as diarrhea, stomach cramps, nausea, dehydration, and weight loss. In some cases, giardiasis can cause long-term health problems, particularly in children, including malnutrition and developmental delays.
Preventing the spread of Giardia involves maintaining good hygiene practices, such as washing hands thoroughly after using the toilet or changing diapers, avoiding contaminated water sources, and practicing safe food handling and preparation. In cases where infection occurs, medication is usually effective in treating the illness.
2-Pyridinylmethylsulfinylbenzimidazoles is a class of chemical compounds that have both a pyridinylmethylsulfinyl group and a benzimidazole ring in their structure. Pyridinylmethylsulfinyl refers to a functional group consisting of a sulfinyl group (-S(=O)-) attached to a methyl group (-CH2-) that is, in turn, attached to a pyridine ring. Benzimidazoles are heterocyclic compounds containing a fused benzene and imidazole ring.
These types of compounds have been studied for their potential biological activity, including anti-inflammatory, antiviral, and antitumor properties. However, it's important to note that medical definitions typically refer to specific substances or classes of substances that have established clinical use or are under investigation for therapeutic purposes. As such, 2-Pyridinylmethylsulfinylbenzimidazoles do not have a recognized medical definition in this sense.
Omeprazole is defined as a proton pump inhibitor (PPI) used in the treatment of gastroesophageal reflux disease (GERD), gastric ulcers, and other conditions where reducing stomach acid is desired. It works by blocking the action of the proton pumps in the stomach, which are responsible for producing stomach acid. By inhibiting these pumps, omeprazole reduces the amount of acid produced in the stomach, providing relief from symptoms such as heartburn and pain caused by excess stomach acid.
It is available in various forms, including tablets, capsules, and oral suspension, and is typically taken once or twice a day, depending on the condition being treated. As with any medication, omeprazole should be used under the guidance of a healthcare professional, and its potential side effects and interactions with other medications should be carefully considered before use.
Tubulin is a type of protein that forms microtubules, which are hollow cylindrical structures involved in the cell's cytoskeleton. These structures play important roles in various cellular processes, including maintaining cell shape, cell division, and intracellular transport. There are two main types of tubulin proteins: alpha-tubulin and beta-tubulin. They polymerize to form heterodimers, which then assemble into microtubules. The assembly and disassembly of microtubules are dynamic processes that are regulated by various factors, including GTP hydrolysis, motor proteins, and microtubule-associated proteins (MAPs). Tubulin is an essential component of the eukaryotic cell and has been a target for anti-cancer drugs such as taxanes and vinca alkaloids.
Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.
Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.
The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.
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