147.Wolkowitz OM, Pickar D: Benzodiazepines in the treatment of schizophrenia: a review and reappraisal. J Psychiatry 1991; 148: 714-726 [B] 148.Hekimian LJ, Friedhoff AJ: A controlled study of placebo, chlordiazepoxide, and chlorpromazine with 30 male schizophrenic patients. Dis Nerv Syst 1967; 28: 675-678 [A] 149.Altamura AC, Mauri MC, Mantero M, Brunetti M: Clonazepam haloperidol combination therapy in schizophrenia: a double-blind study. Acta Psychiatr Scand 1987; 76: 702-706 [A] 150.Csernansky JG, Riney SJ, Lombarozo L, Overall JE, Hollister LE: Double-blind comparison of alprazolam, diazepam and placebo for the treatment of negative schizophrenic symptoms. Arch Gen Psychiatry 1988; 45: 655-659 [A] 151.Salzman C, Solomon D, Miyawaki E, Glassman R, Rood L, Flowers E, Thayer S: Parenteral lorazepam versus parenteral haloperidol for the control of psychotic disruptive behavior. J Clin Psychiatry 1991; 52: 177-180 [A, B] 152 Elroy SL, Keck PE, Pope HG Jr: Sodium valproate: its use in primary psychiatric disorders. J Clin Psychopharmacol 1987; 7: 16-24 [D] 153.Neppe VM: Carbamazepine as adjunctive treatment in nonepileptic chronic inpatients with EEG temporal lobe abnormalities. J Clin Psychiatry 1983; 44: 326-331 [A] 154.Luchins D: Carbamazepine in violent non-epileptic schizophrenics. Psychopharmacol Bull 1987; 20: 569-571 [B] 155.Okuma T, Yamashita I, Takahashi R, Itoh H, Otsuki S, Watanabe S, Sarai K, Hazama H, Inanaga K: A double-blind study of adjunctive carbamazepine versus placebo on excited states of schizophrenic and schizoaffective disorders. Acta Psychiatr Scand 1989; 80: 250-259 [A] 156.Jann MW, Ereshefsky L, Saklad SR, Seidel DR, Davis CM, Burch NR, Bowden CL: Effect of carbamazepine on plasma haloperidol levels. J Clin Psychopharmacol 1985; 5: 106-109 [B] 157.Fast DK, Jones BD, Kusalic M, Erickson M: Effect of carbamazepine on neuroleptic plasma levels and efficacy letter ; . J Psychiatry 1986; 143: 117118 [B] 158.Raitasuo V, Lehtovaara R, Huttunen MO: Carbamazepine and plasma levels of clozapine letter ; . J Psychiatry 1993; 150: 169 [B] 159.Ishizaki T, Chiba K, Saito M, Kobayashi K, Iizuka R: The effects of neuroleptics haloperidol and chlorpromazine ; on the pharmacokinetics of valproic acid in schizophrenic patients. J Clin Psychopharmacol 1984; 4: 254-261 [B] 160 eedman R, Kirch D, Bell J, Adler LE, Pecevich M, Pachtman E, Denver P: Clonidine treatment of schizophrenia: double-blind comparison to placebo and neuroleptic drugs. Acta Psychiatr Scand 1982; 65: 35-49 [A] 161.Pickar D, Wolkowitz OM, Doran AR, Labarca R, Roy A, Breier A, Narang PK: Clinical and biochemical effects of verapamil administration to schizophrenic patients. Arch Gen Psychiatry 1987; 44: 113-118 [B] 162.van Kammen DP, Peters JL, van Kammen WB, Rosen J, Yao JK, McAdam D, Linnoila M: Clonidine treatment of schizophrenia: can we predict treatment response? Psychiatry Res 1989; 27: 297-311 [C].
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Table 1. Chemical structure and target specificity of oligonucleotides tested as antimalarial agents Chemical structure and target specificity Name Sequence PSI 5'-TAA AAA GAA TAT GAT CTT CAT-3' Oligodeoxynucleotide phosphorotbioate complementary in sequence to the first 21 nucleotides of the ORF from the start codon of P195 PSII 5'-AGC AAC TGA GCC ACC TGA-3' Oligodeoxynucleotide phosphorothioate complementary in sequence to the 18 nucleotide sequences in P195 coding for the first two tripeptide repeats PNII 5'-AGC AAC TGA GCC ACC TGA-3' Oligodeoxynucleotide phosphomorpholidate complementary in sequence to the same sequence in P195 as PSH1 POII 5'-AGC AAC TGA GCC ACC TGA-3' Oligodeoxynucleotide phosphodiester internucleoside bond ; complementary in sequence to the same sequence in P195 as PSII PSIII 5'-GTC GCA GAC TTG TTC CAT CAT-3' Oligodeoxynucleotide phosphorothioate having a sequence complementary to the first 21 nucleotides of the ORF of P. falciparum DHFR-TS gene starting with the start codon PSNIII 5'-GTC GCA GAC TTG TTC CAT CAT-3' Oligodeoxynucleotide phosphorothioate with the last 3' phosphodiester bond being a phosphorbutylamidate for the inhibition of exonuclease activity, having the same sequence as PSIII RI 5'-CTT GGC AGC TGC GCG TGA CAT-3' Oligodeoxynucleotide phosphorothioate of mismatched sequence in which the 3'- end is complementary to the 5'-AUG-3' translation start codon RUI 5'-AAA AAT ATT TAT TTT CTA A-3' Oligodeoxynucleotide phosphorothioate of mismatched sequence RIII 5'-CGC GGC GGC CCG CGG CGC CGG-3' Oligodeoxynucleotide phosphorothioate of mismatched sequence ORF, open reading frame and
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The form of Gary Smith and Paul Jaep and I thoroughly recommend that you look at their website : yeast-candida-infections-uk . They are in the process of trying to culture bacteria that have already been through a human's gut, remove the pathogens if present ; and turn them into a bio-available culture. At present, this is very much in the formative stages but watch this space! What was clear from the day's conference is that the gut flora is extremely stable and difficult to change. Therefore if one is going to take probiotics, they have to be taken long term. The second important thing I learned is that many preparations on the market are ineffective. Those found to be most effective are those milk ferments and live yoghurts where the product is freshly made. It is not really surprising. Keeping bacteria alive is difficult and it is not surprising that they do not survive dehydration and storage at room temperature. So your best chance of eating live viable bacteria is to buy live yoghurts or drinks. These can be easily grown at home, just as one would make home made yoghurt. If you cannot grow easily from a culture, then it suggests that the culture is not active, so this is a good test of what is and is not viable. I have tried to culture on milk and soya from dried extracts with very poor success rates suggesting that the dried extracts are not terribly viable. In the interim, the best you can do is grow your own probiotics since this is a cheap and effective way of sorting the situation out as follows: The idea here is to take a substrate on which to grow the bugs and to which one is not allergic and make your own culture. This means one can swallow high dose probiotics, which are alive and kicking so much better able to colonise the gut ; and they can be eaten regularly throughout the day very cheaply and deliciously. It also means that on what ever you grow the culture, the sugar is fermented out of it and so this provides a good low glycaemic index food. This inhibits fermentation by yeasts. Furthermore, probiotics convert sugars and starches in the gut into short chain fatty acids, which are the preferred fuel for mitochondria. Therefore, anyone with a tendency to hypoglycaemia will find their symptoms greatly reduced. Even for normally healthy people probiotics will stabilise blood sugar levels and reduce risk of obesity, diabetes, Syndrome X, heart disease, PCOS, cancer and all those problems arising from a hypoglycaemic tendency. Indeed, this idea of using fermented foods is very popular in many human societies and is associated with long and good health! The sort of problems I expect to see in people with abnormal gut flora result clinically from the fermentation of sugars and starches by yeasts, which form alcohol and wind. They are: Gut symptoms - irritable bowel syndrome alternating constipation or diarrhoea, wind gas, pain ; , stools like pellets, foul smelling offensive wind, indigestion, poor digestion, constipation; Tendency to low blood sugar with carbohydrate craving; Tendency to "candida" problems such as thrush, skin yeast infections; Tendency to develop allergies to foods; Leaky gut positive PEG test ; . In theory any probiotics on the market can be used to start the culture going but in practice many of the dried preparations are inactive. You could try starting with plain live yoghurt, but the bacteria in yoghurt may be chosen for its ability to make tasty yoghurt rather than what is good for your gut! One of my patients swears by kefir thekefirshop ; . I can supply individual sachets of kefir if you have problems finding a source. Please, email your request to my dispensing team on judy doctormyhill or phone the office. I have been growing Kefir and it goes well at room temperature. I dairy allergic so I use soya milk but it also grows on rice milk or coconut milk and who knows what else! Start off with one litre of soya milk in a jug, add the Kefir sachet and within 55.
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Clinical Studies1-4 The efficacy of intramuscular olanzapine for injection for the treatment of agitation was established in 3 short-term 24 hours of IM treatment ; double-blind, placebo-controlled trials in agitated inpatients from two diagnostic groups: schizophrenia and Bipolar I Disorder manic or mixed episodes ; . Each of the trials included a single active comparator treatment arm of either haloperidol injection schizophrenia studies ; or lorazepam injection bipolar mania study ; . Patients enrolled in the trials needed to be: 1 ; judged by the clinical investigators as clinically agitated and clinically appropriate candidates for treatment with intramuscular medication, and 2 ; exhibiting a level of agitation that met or exceeded a threshold score of 14 on the five items comprising the Positive and Negative Syndrome Scale Excited Component PANSS-EC ; , i.e. poor impulse control, tension, hostility, uncooperativeness and excitement items, with at least one individual item score 4 using a 1-7 scoring system 1 absent, 4 moderate, 7 extreme ; . In the studies, the mean baseline PANSS-EC score was 18.4, with scores ranging from 13 to 32 out of a maximum score of 35 ; , thus suggesting predominantly moderate levels of agitation with some patients experiencing mild or severe levels of agitation. All patients provided written consent after the procedures had been fully explained. The primary efficacy measure used for assessing agitation in these trials was the change from baseline in the PANSS-EC at 2 hours post-injection. There were three secondary measures of agitation: Agitated Behavior Scale ABS, a validated 14-item scale that has been used in the emergency department setting for monitoring agitation levels Agitation-Calmness Evaluation Scale ACES, single-item 9-point scale developed by Eli Lilly and Company to assess the degree of sedation associated with reduction in agitation; 1 marked agitation, 2 moderate agitation, 3 mild agitation, 4 normal, 5 mild calmness, 6 moderate calmness, 7 marked calmness, 8 deep sleep, 9 unarousable and the 11-item Young-Mania Rating Scale YMRS, for agitation severity ; . To assess general psychopathology, they employed the PANSS-derived Brief Psychiatric Rating Scale BPRS ; and the Clinical Global ImpressionsSeverity of Illness CGI-S ; scale. The BPRS was also used to assess positive symptoms. Patients could receive up to three injections during the 24 hour IM treatment periods; however, patients could not receive the second injection until after the initial 2 hour period when the primary efficacy measure was assessed, and the third no earlier than 2 to 4 hours after the second injection. There were no treatment group differences regarding baseline demographics or illness in any of the studies. All studies prohibited the use of central nervous system and prophylactic anticholinergic agents. The first two studies comparing Zyprexa to haloperidol and placebo allowed use of BZDs after the second or third injections. Anticholinergic medication was permitted for the treatment of newly emergent extrapyramidal symptoms. In the third study comparing Zyprexa to lorazepam and placebo, only lithium or valproate were permitted as concomitant treatment, as long as patients were already receiving them before entry; however initiation nor dosage adjustments were permitted at any time during the study. The results of the trials are on the following page.
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