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Based on newly declassified Soviet archives, including secret police reports, Peasant Rebels Under Stalin documents the active history of the vast peasant rebellion against collectivization between 1928-1932. Lynn Viola reveals the manifestation in Stalin's Russia of universal strategies of peasant resistance in what amounted to virtual civil war between state and peasantry.

We studied 16 patients with long-standing irritable bowel syndrome of moderate severity using a controlled, double-blind crossover method. Five sedative-anticholinergic drug combinations and a placebo were tested. The subjective response was assessed with four subjective methods to include an increasing number of response variables. The patients preferred 30 mg phenobarbital plus 8 mg belladonna (P & B) to placebo (P = 0.02). Five of ten patients were helped "some" or "a lot" with placebo, while ten of 15 were helped "some" or "a lot" with P & B (P = 0.07). The ten prominent-symptoms method revealed that subjective symptoms such as nervousness, sleep difficulties, and tiredness were experienced as greater problems than diarrhea. The factor analysis method documented a strong placebo response. Simpler evaluation methods such as drug preference and a five-choice method appear more likely to show a positive drug effect, while the inclusion of a larger number of variables appears to emphasize the placebo portion of the response. These observations may help explain some of the apparent discrepancies between the conclusions of some controlled clinical trials and subsequent clinical experience.

THERAPY for patients with actual or impending hepatic coma has been unsatisfactory in the majority of cases, being hindered by a lack of knowledge regarding the fundamental alterations of metabolic processes that occur in this syndrome of combined liver failure and Central-nervous-system dysfunction. Recently, considerable evidence has accumulated that defective nitrogen metabolism is intimately involved in the genesis of hepatic coma1 2 3 4 5 6 7; such a defect is associated with the diminished removal of ammonia as urea by the liver. Progressive mental changes, deterioration in the state of consciousness, variable neurologic deficit, flapping tremor, fetor hepaticus, elevated blood ammonia and electroencephalographic abnormalities . . .

This work was done to evaluate the effects of hepatic hypoxia and hyperthermia in the dog. Hepatic temperature changes were produced by portal vein perfusion and hypoxia by hepatic arterial inflow occlusion. The extracorporeal circuit consisted of a heat exchanger, plastic tubing, pump, and heating jacket. Blood passed from the femoral artery or jugular vein through the extracorporeal circuit and returned to the portal vein. Forty-two animals were studied. Simple arterial inflow occlusion for 1 hr caused death in three of five animals. Perfusion of the liver with venous blood during hepatic artery occlusion was followed by death in all animals while survival was obtained when arterial blood perfusate was utilized. Death occurred if hepatic temperature exceeded 43 C, with one exception. Portal vein infusion without hepatic anoxia resulted in survival of animals following short periods of hepatic hyperthermia up to 46 C. The greatest increase in serum transaminase and alkaline phosphatase followed hepatic hyperthermia or anoxia, or both. Enzyme values gradually returned to normal within 21 days. It is concluded that hepatic anoxia augments the toxic effect of hepatic hyperthermia. The cause of death was not definitely identified.

SOME patients with hepatic cirrhosis show values for standard thyroid-function tests consistant with hypothyroidism.1 , 2 Whether these patients are actually myxedematous or whether these laboratory values reflect some biochemical aberration connected with disturbed liver function has not been established. Hypothermia, bizarre behavior and slow or absent deep tendon reflexes3 , 4 are several of the similarities between profound myxedema and hepatic precoma. Since metabolic status appears to be more closely related to the concentration of free serum thyroxine than to the concentration of bound hormone5 this study was undertaken to determine the free serum thyroxine in cirrhotic patients with either normal or abnormally . . .

All medical personnel use jargon when conversing about patients. Such jargon can be clarified by questions asked at the moment of discussion. The reader of a discharge summary, however, does not have the option of questioning the author if meanings are ambiguous and vague. Editing discharge summaries is an impossible task--I've tried it and quit, partly from laughing, partly from crying, and mostly because the head record librarian refused to have all the summaries retyped. Save time in the record room by being more concise and clear in your dictation, then use the time you have saved for more rewarding activities. Organize your thoughts, dictate, then go smell the flowers with the recovered time.

GREENSTEIN et al.1 reported on the effectiveness of various agents in preventing experimental amino-acid and ammonia intoxication. Substrates of the urea cycle, most notably arginine, were the most effective materials tested and their protective action required the presence of intact, functioning liver.

SummarySerum arginase activity has been determined in 34 healthy blood donors. A mean value 0.06 ± 0.09 μmole urea formed/ml serum was found with a range of .00 to 0.36 μmole. In sera of 19 patients with proven or suspected liver disease the mean arginase activity was 1.36 with a range of .00 to 6.08 μmoles formed/ml serum under the condition of assay.

IT has been demonstrated that patients with liver disorders are particularly susceptible to ammonia intoxication1. Since ammonia is detoxified by urea synthesis, study of the enzymes of the Krebs–Hensleit cycle in the normal and abnormal liver might provide useful information. Decrease of liver arginase activity in patients suffering from cirrhosis and hepatic coma has been reported by Ugarte, Pino and Valenzuela2. In our study, arginase was crystallized from a ‘normal’ human and a cirrhotic human liver and the catalytic efficiency of the enzymes from the two sources was compared.

A patient presents an array of signs and symptoms which his physician evaluates and analyzes for "diagnostic clues" he hopes will lead him to an understanding of the mechanism of the patient's illness, if not its cause. This diagnostic process followed by each physician should be recognized as one of identifying the patient as being similar to other patients the physician has read about or seen himself. Diagnostic labels derived from such patient study have little importance except as representations of more or less loose association of similar patients about which some statements may be made regarding common mechanisms or causes of illness or regarding therapeutic choice, response and prognosis. 1 Development of a systematic classification of patients into "diagnostic" groups or clusters with similar characteristics is a somewhat different problem and one that must essentially precede the one of identification of the individual patient as belonging to a given

Spironolactone, an aldosterone-antagonist, was administered to 4 adults and 2 children in the treatment of refractory edema of renal origin. The 6 case histories presented show that an excellent response, indicated by loss of edema, was obtained in 5. Three of the adults with azotemia developed hyperkalemia, so that the spironolactone had to be withdrawn. One of these patients showed electrocardiographic signs of hyperkalemia. When spironolactone is used in patients with azotemia observation of serum potassium levels is considered mandatory. The drug does not alter the underlying disease process, but the authors consider it a useful adjunct in the treatment of patients refractory edema of renal origin, especially in children with the nephrotic syndrome.

Excerpt Wegener's granulomatosis, a rare disease of unknown etiology, was first described by Klinger (1) in 1931. Wegener (2), in 1936, reported three additional patients, recognizing the syndrome ...