Objectives : This study investigated the effect of Sinseonbulchuidan (SBD-1) on hangover syndrome. We undertook this study to test whether SBD-1 is effective in preventing the signs and symptoms of alcohol-induced hangover. Methods : Fifteen healthy volunteers participated in this double-blind randomized crossover study. All participants received either SBD-1 or indistinguishable placebo capsules before alcohol consumption. The primary outcome measure was the difference in hangover severity scores between SBD-1 and placebo intervention. Secondary outcome measure was the difference in profile of mood states (POMS) between SBD-1 and placebo intervention. Results : After alcohol exposure, the overall symptom scores were significantly decreased in the SBD-1 group compared with those given a placebo. The mean scores for the hangover symptoms were high in the placebo group, and statistical significance was observed in 4 symptom scores (loss of appetite, stomachache, nausea, and total score). There were no differences in the POMS and cognitive performance test results between SBD-1 and placebo intervention. Conclusions : We conclude that the SBD-1 is effective in preventing the signs and symptoms of alcohol-induced hangover. Larger studies are required to confirm these findings.
Introduction: After 17 years since the first production of humidifier disinfectants in Korea, Korea Centers for Disease Control and Prevention (KCDC) announced that the odds ratio of lung injury related with humidifier disinfectant usage was 47.3 (95% confidence interval 6.0-369.7) according to a case-control study with 18 adult cases, including 8 pregnant women at a university hospital in Seoul. Results: From September 2011 to April 2012, one-hundred and seventy four victim cases have been reported to an environmental non-governmental group (NGO). We summarized timetable of humidifier disinfectants accidents, analyzed health outcomes (death, lung or lung and heart transplantation, pulmonary disease) of reported victims, and classified some information for humidifier disinfectants with health outcomes, and government action for this accident. Among the victims, number of death cases are 52 (30.0%), including 26 babies less than 3 years old. Sixty-nine victims come from twenty-seven family with 2 to 4 members per family. About twenty types of humidifier disinfectant products and about 600,000 product items a year have been sold. Fifty-two death cases used 7 different types of disinfectant products, including imported goods and some private brands of well-known supermarkets. KCDC confirmed inhalation toxicity of 6 products through an animal experimental test, and based on this observation recalled disinfectants containing PHMG (polyhexamethylene guanidine) and PGH (Oligo(2-(2-ethoxy)ethoxyethyl guanidinium chloride). Discussions: The use of these biocides involved highly fatal consequences among biologically vulnerable victims, such as pregnant women, several family member victims after semi-acute exposure. This is the first biocide disaster in Korea with non-specific targets, and unknown scale of victims, warranting concerns on use of biocides in the living environment. Conclusions: Special administrative agency for chemical safety and compensation act for environmental health victims are needed to prevent similar problems.
Objective: Nandrolone decanoate (ND) is an anabolic-androgenic steroid frequently used for clinical treatment. However, the inappropriate use of ND results in the reduction of serum testosterone level and sperm production. The suppressive effect of ND on testosterone production has not been investigated in detail. The present study was designed to examine the effect of ND on the expression of steroidogenic enzymes in the rat testis. Methods: Male Sprague Dawley rats at 50 days of age were subcutaneously administrated with either 2 or 10 mg of ND/kg body weight/week for 2 or 12 weeks. The changes of transcript and protein levels of steroidogenic enzymes in the testis were determined by real-time polymerase chain reaction and western blotting analyses, respectively. Moreover, immunohistochemical analysis was employed to determine the changes of immunostaining intensity of these enzymes. The steroidogenic enzymes investigated were steroidogenic acute regulatory protein, cytochrome P450 side chain cleavage enzyme, $17{\alpha}-hydroxylase$, $3{\beta}-hydroxysteroid$ dehydrogenase, and cytochrome P450 aromatase. Results: The treatment of ND resulted in depletion of Leydig cells and sloughing of germ cells in the testis. The ND treatment caused significant expressional decreases of steroidogenic enzymes at transcript and protein levels, and the destructive effects of ND on the testis were more apparent with a higher dose and a longer period of the treatment. Evident reduction of immunostaining intensity present in Leydig cells was clearly detected by the ND treatment. Conclusion: The exposure to ND in young male results not only in histological changes of the testis but also in aberrant gene expression of testicular steroidogenic enzymes, consequently leading into the reduction of testosterone production in the testis and thus likely disruption of spermatogenesis.
Malignant hyperthermia is a catastrophic, hypermetabolic syndrome that arises in susceptible individuals when they are exposed to certain inhalational anesthetics or muscle relaxants. It is characterized by hyperthermia, tachycardia, acidosis, and muscle rigidity. It has been noted that the majority of cases of malignant hyperthermia are fatal unless early diagnosis and treatment are performed. We experienced a 24 year old male Malignant hyperthermia presented for orthognathic surgery under $O_2-N_2O$-sevoflurane anesthesia without succinylcholine. Two half hours after induction, tachycardia developed and was followed by unstable blood pressure and hyperpyrexia. Anesthesia was terminated and vigorous emergency treatment was attempted. The patient was treated by the intravenous administration of dantrolene sodium. The diagnosis of an acute malignant hyperthermia reaction by clinical criteria can be difficult because of the nonspecific nature and variable incidence of many of the clinical signs and laboratory findings. So the malignant hyperthermia clinical grading scale is recommended for use as an aid to the objective definition of this disease. This clinical grading system provides a new and comprehensive clinical case definition for the malignant hyperthermia syndrome. We recently encountered a case of delayed malignant hyperthermia during sevoflurane anesthesia that was successfully treated by the intravenous administration of dantrolene sodium. In conclusion, exposure to sevoflurane should be avoided in patients thought to be susceprible to malignant hyperthermia.
Kim, Jin-Hong;Moon, Yu-Ran;Kim, Jae-Sung;Lee, Min-Hee;Lee, Seung-Sik;Chung, Byung-Yeoup
Korean Journal of Environmental Biology
/
v.26
no.1
/
pp.15-21
/
2008
Ionizing radiation causes many alterations in photosynthetic machineries. However, there is no information about effects of ionizing radiation on the development of photosynthetic machineries in plants. We investigated the greening of etiolated mung bean seedlings after gamma-irradiation of 50 to 300 Gy. The irradiation inhibited seedling growth with great dependence on the radiation dose. In particular, growth of stems was more affected than that of hypocotyls. Irradiated leaves showed inhibition in growth, aberration in morphology, and yellowing in color depending on the radiation dose. Contents of photosynthetic pigments such as chlorophylls and carotenoids were significantly decreased in the irradiated leaves. The apparent electron transport rate for photosynthesis, ETR, was similarly changed depending on the radiation dose. However, the maximal photochemical efficiency of Photosystem II (PSII), Fv/Fm, was little affected by the irradiation. Moreover, the 50-Gy seedlings maintained the control level of light saturating for photosynthesis and showed slightly higher Fv/Fm values in spite of significant decreases in the photosynthetic pigment content and ETR. These results suggest that the inhibition of the overall photosynthetic capacity couldn’t be causally relatqaed with the repression in the initial development of irradiated seedlings and that the overall photosynthetic machineries can develop and work to some extent as a concerted system for photosynthesis even after exposure to acute doses of ionizing radiation.
The incidence and distribution of necrotic and apoptotic neural cells, and activated astrocytes in the brain of rats intoxicated intra peritoneally with diisopropylfluorophosphate were investigated. Pyridostigmine bromide (0.1 mg/kg) and atropine methylnitrate (20 mg/kg) were pretreated intramuscularly 30 min and 10 min, respectively, prior to diisopropylfluorophosphate (4-10 mg/kg) administration. Diisopropylfluorophosphate induced severe limbic seizures, early necrotic and delayed apoptotic brain injuries, and rapid astrocytic responses. The necrosis, which was closely related to seizure intensity, was observed as early as 1 hr after intoxication predominently in hippocampal pyramidal cells, cerebellar Purkinje cells and neurons in pyriform/entorhinal cortices, showing malacia of neurophils. In contrast, apoptosis started to appear 12 hr after intoxication in neurons in thalamus, amygdala and neocortex, and ephendymal cells surrounding the 4th ventricle. Since marked apoptosis was induced in rats exhibiting relatively-low seizure intensity, the degree of necrosis and apoptosis was shifted to each type of injury according to the seizure intensity. Activated astrocytes, observed within 1 hr along the limbic system, were suggested to affect the neural injury patterns by producing high level of nitric oxide. However, the distribution of activated astrocytes was not in parallel with those of necrotic or apoptotic injuries, implying that the astrocytic responses resulted from seizure activity rather than neural injuries. Furthermore, astrocytes in malacic tissues disappeared during the severe limbic seizures. Therefore, it would be one of the cautionary notes on the expression of glial fibrillary acidic protein in astrocytes as a biochemical marker of brain injuries following acute exposure to organophosphates.
Mammalian reproduction is regulated by a feedback circuit of the key reproductive hormones such as GnRH, gonadotropin and sex steroids on the hypothalamic-pituitary-gonadal axis. In particular, the onset of female puberty is triggered by gain of a pulsatile pattern and increment of GnRH secretion from hypothalamus. Previous studies including our own clearly demonstrated that genistein (GS), a phytoestrogenic isoflavone, altered the timing of puberty onset in female rats. However, the brain-specific actions of GS in female rats has not been explored yet. The present study was performed to examine the changes in the activities of GnRH neurons and their neural circuits by GS in female rats. Concerning the drug delivery route, intracerebroventricular (ICV) injection technique was employed to eliminate the unwanted actions on the extrabrain tissues which can be occurred if the testing drug is systemically administered. Adult female rats (PND 100, 210-230 g BW) were anaesthetized, treated with single dose of GS ($3.4{\mu}g$/animal), and sacrificed at 3 hrs post-injection. To determine the transcriptional changes of reproductive hormone-related genes in hypothalamus, total RNAs were extracted and applied to the semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). ICV infusion of GS significantly raised the transcriptional activities of enhanced at puberty1 (EAP-1, p<0.05), glutamic acid decarboxylase (GAD67, p<0.01) which are known to modulate GnRH secretion in the hypothalamus. However, GS infusion could not change the mRNA level of nitric oxide synthase 2 (NOS-2). GS administration significantly increased the mRNA levels of KiSS-1 (p<0.001), GPR54 (p<0.001), and GnRH (p<0.01) in the hypothalami, but decreased the mRNA levels of LH-$\beta$ (p<0.01) and FSH-$\beta$ (p<0.05) in the pituitaries. Taken together, the present study indicated that the acute exposure to GS could directly activate the hypothalamic GnRH modulating system, suggesting the GS's disrupting effects such as the early onset of puberty in immature female rats might be derived from premature activation of key reproduction related genes in hypothalamus-pituitary neuroendocrine circuit.
Objectives Numerous studies have revealed the adverse health effects of acute and chronic exposure to particulate matter less than $10{\mu}m$ in aerodynamic diameter ($PM_{10}$). The aim of the present study was to examine the spatial distribution of $PM_{10}$ concentrations and cardiovascular mortality and to investigate the spatial correlation between $PM_{10}$ and cardiovascular mortality using spatial scan statistic (SaTScan) and a regression model. Methods From 2008 to 2010, the spatial distribution of $PM_{10}$ in the Seoul metropolitan area was examined via kriging. In addition, a group of cardiovascular mortality cases was analyzed using SaTScan-based cluster exploration. Geographically weighted regression (GWR) was applied to investigate the correlation between $PM_{10}$ concentrations and cardiovascular mortality. Results An examination of the regional distribution of the cardiovascular mortality was higher in provincial districts (gu) belonging to Incheon and the northern part of Gyeonggi-do than in other regions. In a comparison of $PM_{10}$ concentrations and mortality cluster (MC) regions, all those belonging to MC 1 and MC 2 were found to belong to particulate matter (PM) 1 and PM 2 with high concentrations of air pollutants. In addition, the GWR showed that $PM_{10}$ has a statistically significant relation to cardiovascular mortality. Conclusions To investigate the relation between air pollution and health impact, spatial analyses can be utilized based on kriging, cluster exploration, and GWR for a more systematic and quantitative analysis. It has been proven that cardiovascular mortality is spatially related to the concentration of $PM_{10}$.
Background: Phenol and alcohol have been used to ablate nerves to treat pain but are not specific for nerves and can damage surrounding soft tissue. Lidocaine at concentrations > 8% injected intrathecal in the animal model has been shown to be neurotoxic. Tests the hypothesis that 10% lidocaine is neurolytic after a peri-neural blockade in an ex vivo experiment on the canine sciatic nerve. Methods: Under ultrasound, one canine sciatic nerve was injected peri-neurally with 10 cc saline and another with 10 cc of 10% lidocaine. After 20 minutes, the sciatic nerve was dissected with gross inspection. A 3 cm segment was excised and preserved in 10% buffered formalin fixative solution. Both samples underwent progressive dehydration and infusion of paraffin after which they were placed on paraffin blocks. The sections were cut at $4{\mu}m$ and stained with hemoxylin and eosin. Microscopic review was performed by a pathologist from Henry Ford Hospital who was blinded to which experimental group each sample was in. Results: The lidocaine injected nerve demonstrated loss of gross architecture on visual inspection while the saline injected nerve did not. No gross changes were seen in the surrounding soft tissue seen in either group. The lidocaine injected sample showed basophilic degeneration with marked cytoplasmic vacuolation in the nerve fibers with separation of individual fibers and endoneurial edema. The saline injected sample showed normal neural tissue. Conclusions: Ten percent lidocaine causes rapid neurolytic changes with ultrasound guided peri-neural injection. The study was limited by only a single nerve being tested with acute exposure.
Cis-diamminedichloroplatinum II (cisplatin), an effective antitumor agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin in the renal proximal tubular transport system, OK cell line was selected as a cell model and $Na^+/H^+$ antiport activity was evaluated during a course of cisplatin treatment. The cells grown to confluence were treated with cisplatin for 1 hour, washed, and incubated for up to 48 hours. At appropriate intervals, cells were examined for $Na^+/H^+$ antiport activity by measuring the recovery of intracellular pH (pHi) after acid loading. Cisplatin of less than 50 ${\mu}M$ induced no significant changes in cell viability in 24 hours, but it decreased the viability markedly after 48 hours. In cells exposed to 50 ${\mu}M$ cisplatin for 24 hours, the $Na^+-dependent$ pHi recovery (i.e., $Na^+/H^+$ antiport) was drastically inhibited with no changes in the $Na^+-independent$ recovery. Kinetic analysis of the $Na^+-dependent$ pHi recovery indicated that the Vmax was reduced, but the apparent Km was not altered. The cellular $Na^+$ and $K^+$ contents determined immediately before the transport measurement appeared to be similar in the control and cisplatin group, thus, the driving force for $Na^+-coupled$ transport was not different. These results indicate that cisplatin exposure impairs the $Na^+/H^+$ antiport capacity in OK cells. It is, therefore, possible that in patients treated with a high dose of cisplatin, proximal tubular mechanism for proton secretion (hence $HCO_3^-$ reabsorption) could be attenuated, leading to a metabolic acidosis (proximal renal tubular acidosis).
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