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Herten plus

Category: Blood Pressure

Description

Hydrochlorothiazide is used for treating high blood pressure.

Active Ingredient:

Hydrochlorothiazide (Herten plus) as known as: Acesistem, Acortiz, Acuren, Adelphan, Aldoril, Altace hct, Amiloretic, Ampril hd, Angiozide, Aquazide, Aratan-d, Belsar plus, Benalapril plus, Benazeplus, Berlipril, Beta-turfa, Bifril plus, Bifrizide, Bihasal, Bisobeta comp, Bisocombin, Bisohexal plus, Bisolich comp, Bisoplus, Bisostad plus, Bitensil diu, Blopress plus, Bpzide, Briazide, Bumeftyl, Byol, Capto-corax comp, Capto-isis plus, Captobeta comp, Captogamma hct, Captosol comp, Cardace comp, Cesplon plus, Cibadrex, Cilazil, Clorana, Co aprovel, Co diovan forte, Co renitec, Co-amilozide, Co-enac hexal, Co-enalapril, Co-enatec, Co-epril, Co-inhibace, Co-lisinopril, Co-lisinostad, Co-mepril, Co-quinapril, Co-renistad, Co-renitec, Co-reniten, Coepratenz plus, Comilorid-mepha, Concor plus, Condiuren, Cordinate plus, Corodil comp, Corodin d, Corvo hct, Cosaar, Coteveten, Crinoretic, Dehydratin, Dehydratin neo, Di-ertride, Di-eudrin, Dichlotride, Diclotride, Dilabar diu, Disalunil, Disothiazide, Disys plus, Ditenside, Dithiazide, Diu venostasin, Diunorm, Diur, Diurace, Diuretidin, Diuretikum verla, Do-hydro, Dociteren, Drenol, Duopril, Duradiuret, Dynacil comp, Dynorm plus, Dytenzide, Dytide, Ednyt hct, Elektra, Elpradil hct, Emconcor comp, Emcoretic, Emestar plus, Enacecor, Enacomi, Enahexal comp, Enala-q comp, Enalagamma hct, Enalich comp, Enap-co, Enaplus, Enulid 15, Epratenz, Epratenzide plus, Epril plus, Eprosartan, Eprotan, Esidrex, Esidrix, Femipres plus, Fempress plus, Fosicard plus, Fosicomb, Fosicombi, Fosicomp, Fosinopril, Fosinorm comp, Fositens plus, Fozide, Foziretic, Futuran plus, Gamathiazid, Gentipress, Gliotenzide, Herten plus, Hexal-lisinopril, Hexazide, Hidroclorotiazida, Hidroronol, Hidrosaluretil, Hidrotiadol, Hiperlex plus, Hipoartel plus, Hydra-zide, Hydrene, Hydrex, Hydrodiuril, Hydromet, Hydrozide, Hypodehydra, Hypothiazid, Inderide, Inhibace, Inibace plus, Initiss plus, Inocar plus, Iperton, Irtan plus, Isoptin rr plus, Ixia plus, Kalpress plus, Konveril plus, Labodrex, Lidaltrin diu, Linatil comp, Lisi tad hct, Lisi-puren comp, Lisibeta comp, Lisigamma hct, Lisihexal comp, Lisiplus, Lisoretic, Lispirl, Lodoz, Logroton retard, Loortan plus, Loren-press, Lorzaar, Losapot-h, Losar-q comp, Losar-tevacomp, Losargamma hct, Losarplus al, Losartas ht, Losatan hz, Losatrix comp, Losavik-h, Lotrial d, Maxsoten, Medozide, Mencord plus, Meramyl hct, Meto-succinat hct, Metobeta comp, Metodura comp, Metohexal comp, Metostad comp, Microzide, Miten plus, Modrex, Monoplus, Monopril, Monozide, Navixen plus, Nefrix, Neo lotan plus, Neoprex, Neotensin diu, Nephral, Newtolide, Nolarmin, Normolose-h, Nu-triazide, Olina, Olinapril h, Olmax-h, Openvas plus, Oretic, Pantemon, Parapres plus, Pharmapress co, Pressitan plus, Prestole, Pritor plus, Propra, Quinaplus, Quinaretic, Quiril comp, Ramasar hct, Rasilez hct, Regulaten plus, Renacor, Renapril plus, Renezide, Renil hct, Reniten plus, Rethizid, Ridaq, Rofucal, Sarilen plus, Sarteg hct, Sectrazide, Selokomb, Synerpril, Tandiur, Tekturna hct, Tevafos, Tevanap, Tevetec, Teveten plus, Tevetens plus, Tiaren, Tiazid, Timolide, Tri-thiazid, Triamizide, Triampur, Triamtereen, Triamteril, Triastad hct, Triatec comp, Triniton, Tritace comp, Tritace hct, Turfa, Uniretic, Urirex k, Vaseretic, Votum plus, Wytens, Zaprace-d, Zapto-co, Ziak, Zofenil diu, Zofenil plus, Zofenilduo, Zok-zid, Zopranol diu, Zoprazide

StateMaster - Encyclopedia: Parkinson plus syndrome

Encyclopedia > Parkinson plus syndrome

Parkinson-plus syndromes are a group of diseases featuring the classical features of Parkinson's disease (tremor; rigidity; akinesia/bradykinesia; postural instability) with additional features that distinguish them from simple idiopathic Parkinson's disease.


The Parkinson-plus syndromes and their additional features are:

It is said by neurologists that patients presenting with falls early in the course of a Parkinsonian illness are more likely to have a Parkinson-plus syndrome than idiopathic Parkinson's disease. Multiple System Atrophy (MSA) is a rare and always terminal degenerative neurological disorder characterized by a combination of Parkinsonism, cerebellar or corticospinal signs, pyramidal signs, and autonomic dysfunction. Ataxia (from Greek ataxiā, meaning failure to put in order) is unsteady and clumsy motion of the limbs or trunk due to a failure of the fine coordination of muscle movements. This is about the polyhedron. Anatomy and Physiology of the A.N.S. In contrast to the voluntary nervous system, the involuntary or autonomic nervous system is responsible for homeostasis, maintaining a relatively constant internal environment by controlling such involuntary functions as digestion, respiration, and metabolism, and by modulating energy needed to cope with stressful. Shy-Drager syndrome (named after Dr. Milton Shy and Dr. Glenn Drager, who identified this syndrome in 1960) is a rare, progressively degenerative disease of the autonomic nervous system. Stridor is a high pitched sound heard on inspiration that is indicative of airway obstruction. Progressive Supranuclear Palsy (or the Steele-Richardson-Olszewski syndrome) is a rare congenital disorder involving the gradual deterioration and death of selected neurons in the brain. Apraxia is a neurological disorder characterized by loss of the ability to execute or carry out learned (familiar) movements, despite having the desire and the physical ability to perform the movements. Myoclonus is brief, involuntary twitching of a muscle or a group of muscles. Dementia with Lewy bodies is the second most frequent cause of hospitalization for dementia, after Alzheimers disease.


The Parkinson-plus syndromes are usually more rapidly progressive and less likely to respond to anti-parkinsonian medication than Parkinson's disease. However, the additional features of the diseases may respond to medications not used in Parkinson's disease.

Other articles

Four Diseases Frontline Plus Can Keep At Bay

Four Diseases Frontline Plus Can Keep At Bay

All pet owners know it: Fleas and ticks are a big pain. Some pet owners resort to Frontline Plus, others turn to Comfortis, but all pet owners owe it to their animals to provide their pets with some type of flea and tick medication.

However, if you need a little extra incentive, consider the fact that fleas and ticks are capable of far more than just gnawing on a few ankles. Don't procrastinate when it comes to renewing your Frontline Plus supply; there are some very serious diseases that pet owners can contract from their pets' fleas and ticks. Here are four of them.

1. The Plague
That's right, the plague as in the Plague. The Black Death, which killed between a third and a half of Europe's entire human population in the 13th and 14th centuries, is transmitted by infected fleas. Although it's incredibly rare for Bubonic Plague to strike in the United States, it does occasionally happen. When it does, the disease usually originates from a flea infested dog or cat. Even today, with a cure for Plague, one out of seven people who contract it still die. Those who survive become seriously ill and are usually hospitalized before recovering.

2. Lyme Disease
"Lyme disease" may not trigger the same negative knee-jerk reaction that the words "Bubonic Plague" do, but Lyme disease is all-too common and very serious. As Lyme disease progresses, its victims develop heart problems, chronic fatigue, and Alzheimer's-like symptoms.
Lyme disease is spread primarily by deer ticks. If you're the type of dog owner who lives near a wooded area or likes to hike in the woods with your dog, it wouldn't be too hard for your dog to pick up an infected tick and transfer it to you.

3. Cat Scratch Disease
Cat scratch disease, more commonly known as "cat scratch fever," occurs when an infected cat bites or scratches a human. Initial symptoms include a mild infection, swollen lymph nodes, and flu-like symptoms.

Although it's rare, serious side-effects can result from cat scratch fever. People with compromised immune systems, for example, can develop dangerous liver and spleen problems from the fever. Likewise, a meningitis-like disease can also arise as a result of a serious case of cat scratch fever.
While cat scratch disease is transmitted from cat-to-human rather than from flea-to-human, the infected cat initially picks up the bacteria from fleas. Kittens are especially likely to carry the bacteria, making it very easy for them to pass the disease along to their human families.

4. Rocky Mountain Spotted Fever
Rocky Mountain spotted fever, like Lyme disease, is spread by infected ticks. One to two weeks after a tick bite, those infected with this disease experience fever, vomiting, severe headaches, muscle pain, and lack of appetite. After these initial symptoms, the rashes and joint pain set in.

This disease is quite dangerous, frequently requiring hospitalization. Severe cases may interfere with the victim's respiratory system, nervous system, or renal system. After a serious case of the disease, victims face long-term health problems, including partial paralysis, loss of bladder control,Frontline Plus and language disorders.

These four diseases represent just a handful of dangerous diseases that pet owners can contract as a result of their pets' fleas and ticks. Luckily, pet meds can help to keep pets flea and tick free. Pet medications may be purchased at retail stores, veterinary offices, or online from discount pet medication sites.

Do you have a story about catching any kind of illness from your dog's or cat's fleas and ticks? If so, share it in the comment section below.

End-Stage Kidney Disease: Causes, Symptoms, Prevention

End-Stage Kidney Disease What Is End-Stage Kidney Disease?

Chronic kidney disease is a condition in which your kidneys lose function over time. A diagnosis of end-stage kidney disease means that you’re in the final stage of chronic kidney disease and your kidneys are not functioning well enough to meet the needs of daily life. Your kidneys are responsible for filtering waste and excess water from your blood in the form of urine.

End-stage kidney disease is also referred to as end-stage renal disease (ESRD). If you have ESRD, your kidneys are functioning below 10 percent of their normal function. This may mean that your kidneys are barely functioning or not functioning at all. Kidney disease is usually progressive. Chronic kidney disease typically doesn’t reach the end stage until 10 to 20 years after you’re diagnosed. ESRD may also develop slowly.

What Causes End-Stage Kidney Disease?

Many types of kidney diseases attack the nephrons, which are the tiny units in the kidneys that do the filtering. This results in your blood not being filtered properly and eventually leads to ESRD.

Diabetes and high blood pressure, or hypertension, are the two most common causes of ESRD. If you have diabetes, your body can’t break down glucose, or sugar, correctly and glucose levels remain high in your blood. High levels of glucose in your blood damage your nephrons.

If you have hypertension, the increased pressure that’s forced upon the small vessels in your kidneys leads to damage. This damage prevents your blood vessels from performing their blood-filtering duties.

Who Is at Risk for End-Stage Kidney Disease?

The two main groups at risk for ESRD are people with diabetes and those with hypertension. You are also more likely to develop the condition if you have relatives with the disease.

Your risk of developing ESRD also rises when you have any type of kidney disease or condition, including:

  • polycystic kidney disease
  • Alport syndrome
  • interstitial nephritis
  • pyelonephritis
  • certain autoimmune conditions, such as lupus
What Are the Symptoms of End-Stage Kidney Disease?

You may experience a wide range of symptoms. Common symptoms include:

  • a decrease in how much you urinate
  • an inability to urinate
  • fatigue
  • a general ill feeling
  • headaches
  • unexplained weight loss
  • a loss of appetite
  • nausea and vomiting
  • dry skin and itching
  • changes in skin color
  • bone pain
  • confusion and difficulty concentrating

Other symptoms may include:

  • bruising easily
  • frequent nosebleeds
  • numbness in your hands and feet
  • bad breath
  • excessive thirst
  • frequent hiccups
  • absence of menstrual cycles
  • sleeping problems such as obstructive sleep apnea and restless leg syndrome (RLS)
  • low libido or impotence
  • swelling, or edema, especially in your legs and hands
How Is End-Stage Kidney Disease Diagnosed?

Your doctor will diagnose ESRD through a physical examination and tests to check your kidney function. Kidney function tests your doctor may use include the following:

  • A urinalysis is used to check for protein and blood in your urine. These are signs that your kidney isn’t processing waste properly.
  • A serum creatinine test is used to check whether creatinine, a waste product your kidney filters out of your body, is building up in your blood.
  • Blood urea nitrogen is used to check how much nitrogen is in your blood.
  • The estimated glomerular filtration rate (GFR) estimates how well your kidneys are filtering waste.
How Is End-Stage Kidney Disease Treated?

The two treatments for ESRD are dialysis or a kidney transplant.

Dialysis

You have two options when you undergo dialysis.

One option is hemodialysis, which is a process that uses a machine to process your blood. It then filters out the waste using a solution and places the clean blood back into your body. This treatment method is usually used three times per week. It takes three to four hours each time.

Your doctor may also prescribe peritoneal dialysis, which involves placing a solution into your abdomen that’s later removed using a catheter.

Kidney Transplant

Kidney transplant surgery involves removing your diseased kidneys and replacing them with a donated organ. One healthy kidney is all you need. This means that donors are often living because they can donate one and continue to function normally. According to the National Kidney Foundation. more than 17,000 kidney transplants were done in the United States in 2014.

Other Management Techniques

People with diabetes and those with hypertension should control their conditions in order to prevent ESRD. Both conditions benefit from drug therapy using angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).

A diet low in sodium, potassium, and other electrolytes may be needed, along with fluid restrictions. Caloric intake may need to be increased, and protein consumption may need to decrease.

Complications of End-Stage Kidney Disease

Possible complications of ESRD include the following:

  • skin infections from itching and dry skin
  • hepatitis B
  • hepatitis C
  • liver failure
  • heart and blood vessel problems
  • a fluid buildup around your lungs
  • hyperparathyroidism
  • an increased risk of infections
  • malnutrition
  • nerve damage
  • joint, bone, and muscle pain
  • anemia
  • stomach and intestinal bleeding
  • brain dysfunction and dementia
  • abnormal electrolyte levels
  • blood glucose level changes
  • seizures
  • a weakening of your bones
  • joint disorders
  • fractures
Long-Term Outlook

Advancements in treatments allow people with ESRD to live much longer than ever before. Treatment is crucial because without dialysis or a kidney transplant, ESRD can be life-threatening. The outcome of your treatment depends on you and your condition.

Preventing End-Stage Kidney Disease

In some cases, ESRD isn’t preventable. However, you should keep your blood glucose levels and your blood pressure under control. You should always call a doctor if you have any ESRD symptoms. Early detection and treatment can delay or prevent the disease from progressing.

Medical Advisor Journals, Kyle J

(Preview) Most common diseases of 50 plus - Diseases of Central Nervous system - Free radical causes of Parkinson's disease

By Kyle J. Norton
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Diseases of Central Nervous system

About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability, severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people.
II. Causes of dementia
B. Free radical causes of dementia
B.2. Parkinson's disease
1. Free radicals and Parkinson's disease

Patients with Parkinson's disease have low levels of polyunsaturated fat in the substania nigra(44)(45) than other part of the brain, but higher levels of lipid peroxidation as indication of higher levels of malonaldehyde(44). Also patients with the disease found to contain waste pigments of lipofusion(46) and other polymers in the neurons(47) where dopamine is most active.


2. Aging and Parkinson's disease
According to Julius-Maximilians-University, physiological aging and OS-dependent aggregation of proteins, accompanied with environment toxins(49) are found to associated to the progression of the disease(48).

3. Antioxidants and Parkinson's disease
Antioxidants play an vital role for patients with Parkinson's disease.
a. Superoxide dismutase
Researcher found that the progression of the disease may be associated with the decrease levels of superoxide dismutase, a antioxidant enzyme(50). According to University of Thessaloniki, Patients with advanced Parkinson' diseases showed a statistically significant decrease of SOD activity in whole blood and in red blood cells(51).

b. NADH ubiquinone reductase
Levels of NADH ubiquinone reductase is decreased in the substania nigra(52) in patients with PD, leaded to neurons apoptosis, but this can be treated with antioxidants Acetyl-L-carnitine (53) and alpha lipoic acid(54).

c. Uric acid
People with a high blood level of the natural antioxidant uric acid have a lower risk of developing Parkinson's disease(55) than do people with lower levels(56), but high levels of uric acid increases the risk of kidney diseases(57) and gout(58).

d. Glutathione
Glutathoine showed to deactivate the harmful product HNE of lipid peroxidation(59).

Andréa Albright Featured on Health and Fitness Jan. 2015: Lose Weight and Keep Them Off Forever


Wanna a Perfect Body Like Andréa Albright(Fat Gene Herself) Featured on Health and Fitness Jan. 2015. She will Personally Coach You How to Get There the easy way. Endorsed by Michael Beckwith, star of The Secret and Julie Achterhoff with Weightrater.com 4 out of 5 stars rating.f

Click the link below to view or download the complete study

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Parkinson plus syndrome

Parkinson plus syndrome

Parkinson plus syndrome

Parkinson-plus syndromes are a group of diseases featuring the classical features of Parkinson's disease (tremor; rigidity; akinesia/bradykinesia; postural instability) with additional features that distinguish them from simple idiopathic Parkinson's disease.

The Parkinson-plus syndromes and their additional features are:

* Multiple system atrophy (MSA)
**cerebellar ataxia
** pyramidal weakness
** autonomic failure (previously known as Shy-Drager syndrome )
**nocturnal stridor
* Progressive supranuclear palsy (PSP)
**supranuclear palsy of eye movements (failure of voluntary vertical eye movements, especially downward gazing)
** pseudo-bulbar palsy
**dementia
* Corticobasal degeneration (CBD)
**cognitive impairment, often including some form of aphasia and/or apraxia. and eventually developing to a full dementia
** myoclonus
* Dementia with Lewy bodies (DLB)
**early cognitive impairment
**hallucinations
* Olivopontocerebellar atrophy (OPCA)
** ataxia
** dysarthria

It is said by neurologists that patients presenting with falls early in the course of a Parkinsonian illness are more likely to have a Parkinson-plus syndrome than idiopathic Parkinson's disease.

The Parkinson-plus syndromes are usually more rapidly progressive and less likely to respond to anti-parkinsonian medication than Parkinson's disease. However, the additional features of the diseases may respond to medications not used in Parkinson's disease.

Wikimedia Foundation. 2010 .

Look at other dictionaries:

Parkinson plus — Illustration der Parkinson Krankheit von Sir William Richard Gowers aus A Manual of Diseases of the Nervous System (Handbuch für Krankheiten des Nervensystems) von 1886 Die Parkinson Krankheit bzw. Morbus Parkinson (weitere Synonyme:… … Deutsch Wikipedia

Parkinson'sche Krankheit — Illustration der Parkinson Krankheit von Sir William Richard Gowers aus A Manual of Diseases of the Nervous System (Handbuch für Krankheiten des Nervensystems) von 1886 Die Parkinson Krankheit bzw. Morbus Parkinson (weitere Synonyme:… … Deutsch Wikipedia

Parkinson-Krankheit — Klassifikation nach ICD 10 G20 Primäres Parkinson Syndrom … Deutsch Wikipedia

Parkinson-Syndrom — Illustration der Parkinson Krankheit von Sir William Richard Gowers aus A Manual of Diseases of the Nervous System (Handbuch für Krankheiten des Nervensystems) von 1886 Die Parkinson Krankheit bzw. Morbus Parkinson (weitere Synonyme:… … Deutsch Wikipedia

Parkinson's disease — Parkinson s redirects here. For other uses, see Parkinson s (disambiguation). Parkinson s disease Classification and external resources … Wikipedia

Syndrome de wolff-parkinson-white — Pour les articles homonymes, voir WPW. Nom du symptôme/signe : Syndrome de Wolff Parkinson White Code CIM 10 : I45.6 Décrit en 1930 par les Docteurs Wolff … Wikipédia en Français

Syndrome de Wolff-Parkinson-White — Pour les articles homonymes, voir WPW. Syndrome de Wolff Parkinson White Classification et ressources externes Décrit en 1930 par les Docteurs Wolff, Parkinson et White[1], le syndrome de Wolff Parkinson Whit … Wikipédia en Français

parkinson — [ parkinsɔn ] n. m. • 1974; de maladie de Parkinson 1876, du nom d un médecin angl. (1755 1824) ♦ Méd. Maladie dégénérative de certains noyaux gris centraux du cerveau, caractérisée par des tremblements lents (surtout des mains) et une raideur… … Encyclopédie Universelle

Syndrome post-commotionnel — Classification et ressources externes CIM 10 F07.2 CIM 9 310.2 eMedicine … Wikipédia en Français

Syndrome de Wittmaack-Ekbom — Syndrome des jambes sans repos Le syndrome des jambes sans repos se caractérise par le besoin impérieux de bouger les membres inférieurs. Lorsqu il est d origine iatrogène, ce syndrome se nomme akathisie voire tasikinésie. Dans le cas d un… … Wikipédia en Français

Article Page

Computer-aided diagnosis of plus disease via measurement of vessel thickness in retinal fundus images of preterm infants
  • Faraz Oloumi a
  • Rangaraj M. Rangayyan a,.
  • Paola Casti b
  • Anna L. Ells c,a
  • a Department of Electrical and Computer Engineering, Schulich School of Engineering, University of Calgary, Calgary, AB, Canada T2N 1N4
  • b Department of Electronics Engineering, University of Rome Tor Vergata, 00133 Rome, Italy
  • c Division of Ophthalmology, Department of Surgery, Alberta Children׳s Hospital, Calgary, AB, Canada T3B 6A8

Received 9 June 2015. Accepted 10 September 2015. Available online 25 September 2015.

Highlights

We present techniques for measurement of the width of the major temporal arcade.

Gabor filters and morphological image processing methods are applied.

The methods can detect plus disease and retinopathy of prematurity.

Area under the receiver operating characteristic curve of 0.76 obtained.

Abstract

Changes in the characteristics of retinal vessels such as width and tortuosity can be signs of the presence of several diseases such retinopathy of prematurity (ROP) and diabetic retinopathy. Plus disease is an indicator of ROP which requires treatment and is signified by an increase in posterior venular width. In this work, we present image processing techniques for the detection, segmentation, tracking, and measurement of the width of the major temporal arcade (MTA), which is the thickest venular branch in the retina. Several image processing techniques have been employed, including the use of Gabor filters to detect the MTA, morphological image processing to obtain its skeleton, Canny׳s method to detect and select MTA vessel-edge candidates, least-squares fitting to interpolate the MTA edges, and geometrical procedures to measure the width of the MTA. The results, obtained using 110 retinal fundus images of preterm infants, indicate a statistically highly significant difference in MTA width of normal cases as compared to cases with plus disease . The results provide good accuracy in computer-aided diagnosis (CAD) of plus disease with an area under the receiver operating characteristic curve of 0.76. The proposed methods may be used in CAD of plus disease and timely treatment of ROP in a clinical or teleophthalmological setting.

Keywords
  • Computer-aided diagnosis
  • Gabor filters
  • Plus disease
  • Retinal blood vessels
  • Retinal fundus images
  • Retinopathy of prematurity
  • Temporal arcade
  • Vessel width

Fig. 1. Fig. 2. Fig. 3. Fig. 4. Fig. 5. Fig. 6.

Table 2. Fig. 7.

Management of patients with Alzheimer s disease plus cerebrovascular disease: 12 month treatment with galantamine - Kent Academic Repository

Management of patients with Alzheimer's disease plus cerebrovascular disease: 12 month treatment with galantamine

Bullock, Roger A. and Erkinjuntti, Timo and Lilienfeld, Sean (2004) Management of patients with Alzheimer's disease plus cerebrovascular disease: 12 month treatment with galantamine. Dementia and Geriatric Cognitive Disorders, 17 (1-2). pp. 29-34. ISSN 1420-8008. (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)

The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided. (Contact us about this Publication )

Abstract

We evaluated the long-term cognitive effects and safety of galantamine 24 mg/day in patients with Alzheimer's disease plus cerebrovascular disease ( AD + CVD or mixed dementia). Subgroup analysis was performed of patients with AD + CVD who participated in a 6-month, multicenter, randomized, double-blind, parallel-group study and a 6-month, open-label, active-treatment extension. Method: Two hundred and eighty-five patients with AD + CVD were randomized to receive either placebo (n = 97) or galantamine 24 mg/day (n = 188) for 6 months. Two hundred and thirty-eight (84%) patients continued with the open-label phase of the study ( 86 from the placebo group, 152 from the galantamine group) and were treated with galantamine 24 mg/day. The primary efficacy measure was cognitive performance as assessed using the eleven-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog/11). Standard safety evaluations and adverse-event monitoring were performed throughout the 12-month study period. Patients with AD + CVD treated with galantamine experienced statistically and clinically significant improvement in cognition at month 6 ( mean change in ADAS-cog/11 score -1.1; p less than or equal to 0.05 vs. baseline) and maintained their cognitive function for the entire 12-month study (mean change in ADAS-cog/11 score + 0.1). In contrast, the cognitive function deteriorated among those in the placebo group (mean change in ADAS-cog/11 at month 6 + 2.0; p less than or equal to 0.001 vs. baseline). Patients with AD + CVD who were switched from placebo to galantamine for the open-label phase of the trial did show improvement in cognitive function; however, they never attained the same cognitive level as patients who had been treated with galantamine for the entire 12 months [mean (+/- SE) ADAS-cog/11 scores in the placebo/galantamine group 25.7 +/- 1.32 and 24.2 +/- 1.57 at months 6 and 12, respectively, and in the galantamine/galantamine group 21.5 +/- 0.87 and 22.2 +/- 1.06 at months 6 and 12, respectively]. The results of this subgroup analysis indicate that galantamine is effective for long-term maintenance of the cognitive function in patients with AD + CVD and is safe and well tolerated in this patient population.

Orchid Diseases

Microfungus or Virus or Mites? We've heard this malady described as all three.

Symptoms: In the order of appearance, the leaves display yellow chlorotic spots, then more defined yellow spotting that can grow into elongated yellow streaking, then pitting, and finally large areas of grayish tissue collapse. It can be confused with mesophyllic cell collapse caused by watering with cold water, although cold damage weathers to dark rather than light sunken spots in phals. Paph infections weather to darkish sunken spots. Cattleya may have small black spots on the leaves.

From Bob Gordon Culture of the Phalaenopsis Orchid. "sometimes a condition prevails that is caused by a systemic infection of microfungi. As there are literally hundreds of these, the symptoms vary from plant to plant. Some of the more common are a spotty, ill-defined chlorosis; a streaky chlorosis beginning at the edge of the leaf where it looks as if the leaf edge had been burned with a match or candle; a red-brown coloration appearing at the apical third or half of the lower leaves followed by a dehydrated and senescent (old) appearance and also mesophyll tissue collapse where deep pitting becomes apparent on the surface of the leaves. This latter condition can also be caused by cold water and by virus infections. However, in the latter instance, the pitting is usually dark-brown to black in appearance rather than the white to light fawn caused by fungi."

Treatment: If you believe it is broad mites, spray with a miticide (labeled for Tarsonemidae family mites) at the first sign of chlorotic spotting. If you believe it is a microfungus, follow the recommendations from Alan Koch of Gold Country Orchids: spray first with Banrot plus Aliette, then Cleary's plus Subdue, then Banrot plus Subdue. These sprays / drenches should be 7 days apart in summer and 10 to 14 days apart in winter, all at label strength. The combination of fungicides results in a synergistic effect. Follow all label instructions and wear protective equipment.

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