This experiment was designed for the evaluation of the usefulness of enzyme histochemistry in the determination of the lapse of time in brain wound, and also for the establishment of medicolegal 'biological time table' on brain wound. Brain injury was made by contusion and laceration of meninges and brain itself in rats. The results were as follows; 1) By routine histological technique, estimation of the lapse of time in brain wound could be possible 4 hours after the infliction of wound. 2) The earliest change of enzyme activities was recognizable by the decreased activities of ATPase and succinic dehydrogenase 30 minutes after the injury. These decreased enzyme activities were not recovered up to the 4th day after the brain injury. 3) Increased acid phosphatase activity was noticed 1 hour, and beta-glucuronidase, 2 hours after the injury in a mild degree. Both increased activities were pronounced following the lapse of time in brain wound. 4) No significant change was seen in alkaline phosphatase, monoamine oxidase, non-specific esterase and leucine aminopeptidase activities throughout the experimental period up to the 4th day. So the enzyme histochemistry of these enzymes seemed to be little valuable for the study on the timing of wound in brain injury. In the light of these results it appeared that the enzyme histochemistry, in particular of ATPase, succinic dehydrogenase, and acid phosphatase, for the estimation of timing of brain wound not only shortened the histological "lag period" up to 30 minutes after the injury, but also provided a useful information in determining the biological time table following the brain injury.
Acid Phosphatase ; Adenosine Triphosphatases ; Alkaline Phosphatase ; Animals ; Brain Injuries* ; Brain* ; Carboxylesterase ; Contusions ; Glucuronidase ; Histological Techniques ; Lacerations ; Leucyl Aminopeptidase ; Meninges ; Monoamine Oxidase ; Rats ; Succinate Dehydrogenase ; Wounds and Injuries

The importance of the kidney in the development of hypertension was first demonstrated by Goldblatt and his colleagues more than fifty years ago. Many hormones and other regulatory factors have been proposed to play a major role in the development of hypertension. Among these factors angiotensin II (ANG II) is closely involved in renal hypertension development since it directly regulates Na+ reabsorption in the renal proximal tubule. Thus the aim of the present study was to examine signaling pathways of low dose of ANG II on the Na+ uptake of primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. The results were as follows: 1) 10-11 M ANG II has a significant stimulatory effect on growth as compared with control. Alkaline phosphatase exhibited significantly increased activity. However, leucine aminopeptidase and gamma-glutamyl transpeptidase activity were not significant as compared with control. In contrast to 10(-11) ANG II stimulated Na+ uptake (108.03 +/- 2.16% of that of control), 10(-9) M ANG II inhibited (92.42+/-2.23% of that of control). The stimulatory effect of ANG II on Na+ uptake was amiloride-sensitive and inhibited by losartan (ANG II receptor subtype 1 antagonist) and not by PD123319 (ANG II receptor subtype 2 antagonist). 2) Pertussis toxin (PTX) alone inhibited Na+ uptake by 85.52+/-3.52% of that of control. In addition, PTX pretreatment prevented the ANG II-induced stimulation of Na+ uptake. 8-Bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP), forskolin, and isobutylmethylxanthine (IBMX) alone inhibited Na+ uptake by 88.79+/-2.56, 80.63+/-4.38, and 84.47+/-4.74% of that of control, respectively, and prevented the ANG II-induced stimulation of Na+ uptake. However, 10(-11) M ANG II did not stimulate cAMP production. 3) The addition of 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.01 ng/ml) to the PTCs produced significant increase in Na+ uptake (114.43+/-4.05% of that of control). When ANG II and TPA were added together to the PTCs, there was no additive effect on Na+ uptake. Staurosporine alone had no effect on Na+ uptake, but led to a complete inhibition of ANG II- or TPA-induced stimulation of Na+ uptake. ANG II treatment resulted in a 111.83 +/- 4.51% increase in total protein kinase C (PKC) activity. In conclusion, the PTX-sensitive PKC pathway is the main signaling cascade involved in the stimulatory effects of ANG II on Na+ uptake in the PTCs.
8-Bromo Cyclic Adenosine Monophosphate ; Alkaline Phosphatase ; Angiotensin II* ; Angiotensins* ; Colforsin ; gamma-Glutamyltransferase ; Hypertension ; Hypertension, Renal ; Ion Transport* ; Kidney ; Leucyl Aminopeptidase ; Losartan ; Pertussis Toxin ; Protein Kinase C ; Staurosporine

A 60-year-old man presented with a 1-day history of fever, vomiting, and diarrhea. He was diagnosed with severe septic shock on the basis of a body temperature of 38.9degrees C, heart rate of 92/min, respiratory rate of 25/min, WBC count of 22,970/microL, C-reactive protein (CRP) level of 136 mg/L, blood urea nitrogen (BUN) of 34.0 mg/dL, and creatinine of 2.98 mg/dL. On blood culture, Gram-positive cocci were detected in all 6 bottles. Small grayish non-hemolytic colonies were found on blood agar plates after incubation at 37degrees C for 2 days. The isolates were negative for catalase and L-pyrrolidonyl-beta-naphthylamide hydrolysis, and positive for bile-esculin and leucine aminopeptidase activity. The strain was identified as Streptococcus gallolyticus subsp. pasteurianus using Vitek 2 GP II systems. We performed 16S rRNA gene sequencing and detected 100% identity with S. gallolyticus subsp. pasteurianus strain CIP 107122T (1,345/1,345-bp). The patient recovered after receiving ampicillin-sulbactam. This is the first report of phenotypic and genetic identification of S. gallolyticus subsp. pasteurianus causing severe septic shock in a Korean patient.
Agar ; Ampicillin ; Blood Urea Nitrogen ; Body Temperature ; C-Reactive Protein ; Catalase ; Creatinine ; Diarrhea ; Fever ; Genes, rRNA ; Gram-Positive Cocci ; Heart Rate ; Humans ; Hydrolysis ; Leucyl Aminopeptidase ; Middle Aged ; Pyrrolidinones ; Respiratory Rate ; Shock, Septic ; Sprains and Strains ; Streptococcus ; Sulbactam ; Vomiting

AIMTo investigate the effect of adrenalectomy (ADX) on the epididymidis of Sprague-Dawley rats.

METHODSThe histological, biochemical (cholesterol protein, zinc, copper, alkaline and acid phosphatase aryl sulphatase, lactic dehydrogenase and leucine amino peptidase) and hormonal (FSH, LH and testosterone) changes of caput and cauda epididymis in ADX rats were observed.

RESULTSOrgan wet weight, histological studies and morphometric measurements indicated a cellular degeneration in caput and cauda epididymis of ADX rats. Serum testosterone level was significantly lower in ADX than in sham-operated rats, while the serum FSH and LH were below the detection limit of 1 mIU/mL. The enzymatic activity was higher in ADX than in sham-operated rats. Epididymal zinc level increased whereas copper level decreased in ADX rats compared to the sham-operated.

CONCLUSIONAdrenalectomy leads to degeneration of caput and cauda epididymidis epithelial cells as a result of decreased supply of testosterone.

Acid Phosphatase ; metabolism ; Adrenalectomy ; Alkaline Phosphatase ; metabolism ; Animals ; Arylsulfatases ; metabolism ; Cholesterol ; metabolism ; Copper ; metabolism ; Epididymis ; anatomy & histology ; metabolism ; physiology ; Follicle Stimulating Hormone ; blood ; L-Lactate Dehydrogenase ; metabolism ; Leucyl Aminopeptidase ; metabolism ; Luteinizing Hormone ; blood ; Male ; Organ Size ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Testosterone ; blood ; Time Factors ; Zinc ; metabolism