A type of polycystic ovary resembling some aspects of human polycystic ovarian syndrome (PCOS) can be induced in the rat with a single injection of long-acting estradiol valerate. Among several theories behind the development of polycystic ovaries (PCO), the involvement of the sympathetic nervous system draws much attention, and herbal medicine is known to relieve the abnormal symptoms of PCO. Two herbal formulas, Changbudodam-Tang (cang fu dao tan tang) and Yongdamsagan-Tang (long dan xie gan tang), were used in the present study. The administration of herbal medicine was done every other day for 60 days. The morphological changes of ovaries from herbal medicine treatment were compared to those from an oil-treated control group and an estradiol valerate-injected group. This study also examined the possible hypothesis of neurogenic participation in terms of nerve growth factor (NGF) in the pathology of ovarian dysfunction. The nerve growth factor was analyzed in the central nervous system and ovaries by immunohistochemistry. The main findings of the present study were: (1) PCO were fully developed in rats with a single intramuscular injection of estradiol valerate, (2) PCO resulted in the expression of NGF in the ovaries and the brain tissues, and (3) herbal medicine administration significantly decreased the elevated NGF staining in the ovaries without affecting the brain tissues significantly.

Polycystic ovary syndrome (PCOS) remains one of the most common causes of anovulation in women of reproductive age. There is some evidence that nerve growth factor (NGF) is involved in the pathogenesis of PCOS. Therefore, seeking the pathogenesis of PCOS is important for controlling fertility. In traditional Oriental Medicine, acupuncture has been used for the function of ovaries. The present study was designed to determine whether electro-acupuncture (EA) could affect experimentally induced polycystic ovary (PCO) in the rat. The two acupoints Sp-6 and E-128 were stimulated to test for efficacy in the protein expression of NGF. Polycystic ovaries were induced by a single injection of estradiol valerate (4 mg i.m.). During the experimental period of 8 weeks, some of the rats were treated with EA twice weekly; this group was compared with a vehicle-treated control group and an estradiol-injected group not subjected to EA. At day 60, the protein expression of NGF was examined by immunohistochemistry in the ovaries, the adrenal glands and some parts of the brain. The estradiol treatment induced a clear PCO appearance, and was associated with a robust increase in NGF expression in the ovaries, the adrenal glands and the brain. EA treatment partly reversed the NGF abundance, particularly in the ovaries, but not in the brain. Our data show that EA affects the NGF involvement in ovarian dysfunction.

This study was designed to examine the therapeutic effect of honeybee (Apis mellifera L.) venom in piglets with bacterial diarrhea Comparison between bee venom- and drug-treated groups was our main concern in the present study. Preweaning piglets were assigned to treated and non-treated control groups. In the treated group, 47 piglets were acupunctured with the worker honeybee once a day for three consecutive days. Two acupoints, GV-1 (Jiao-chao) and ST-25 (Hai-men), were selected for apitherapy. In the control group, 44 piglets were intramuscularly injected with a standard dose of a known antibacterial drug, colistin sulfate (300,000 IU/kg of body weight), and an antidiarrheal drug (berberine, 2 ml/kg) once a day for three consecutive days. At post-treatment, 90.9% of the control piglets and 93.6% of piglets in the treated group recovered from bacterial diarrhea. Bee acupuncture therapy did not show any side effects such as allergy, intoxication, hemorrhage or infection. It is concluded that bee venom therapy was effective in controlling bacterial diarrhea in preweaning piglets.

It is possible from these data that BALB/c mice have different susceptibilities to different doses of OVA regulated by pulmonary TH1 and TH2 type cytokines, independent of splenic TH1 and TH2 type cytokines production. These results also indicate that administration of Asian pear pectin-sol in presensitized mice suppresses allergic asthmatic reaction.

Vibrio vulnificus is a halophilic estuarine bacterium which causes fatal septicemia and necrotizing wound infections, especially in patients with hepatic disease, heavy alcohol drinking habits and hemochromatosis. V. vulnificus septicemia is characterized by rapid and fulminant progression, and results in a high mortality rate of over 50%. 1) Several bacterial components have been suggested to be virulence factors of V. vulnificus.2,3) Of these, an extracellular hemolysin or cytolysin (VvhA) and an extracellular protease (VvpE) have been the most extensively studied factors. VvhA, the most potent exotoxin, kills mice and shows a variety of biological activities including hemolysis or cytolysis, apoptosis, vasodilatation, and so on. [4][5][6][7][8] In animal studies, the injection of purified VvhA reproduces the same pathological manifestations of septicemia as caused by the injection of live bacteria. 4,9,10) VvpE also exhibits a host of biological activities including dermonecrosis, edema, and ulceration, and increased vascular permeability. [11][12][13][14] However, the pathogenetic significance of both VvhA and VvpE has been brought into serious doubt by mouse-lethality studies of VvhA-and/or VvpE-deficient mutants. [15][16][17] The inactivation of vvhA gene does not affect the mouse-lethality. This raises the possibility that only very small amounts of VvhA may be produced in vivo, 18,19) and the produced VvhA may be rapidly inactivated by host factors such as cholesterol and bacterial factors such as VvpE. 5,16,[20][21][22] Therefore, in order to evidently determine the pathogenetic roles of VvhA, further detailed studies regarding the in vitro and in vivo production and inactivation of VvhA are necessary.Physiologically, VvhA is produced in the early growth phase, and becomes abruptly inactivated in the late growth phase with the concomitant production of VvpE. Accordingly, it has been classically believed that the inactivation of VvhA is attributable to the destruction of VvhA by VvpE. 9)Recently, it has also been reported that the activity of VvhA in the culture supernatant of a VvpE-deficient mutant was twice that of the wild-type strain, and persisted for a much longer period, suggesting that VvhA might be a substrate of VvpE.16) However, direct evidence for the destruction of VvhA by VvpE has never been presented. From the standpoint of evolution, some doubt also exists as to whether VvhA is destroyed by VvpE or other proteases. In addition, if VvpE or other proteases can destroy and inactivate VvhA, the routine functional assay measuring hemolytic activity using red blood cells (RBC) may not reflect the actual production of VvhA. In this study, therefore, we attempted to obtain direct evidence for the inactivation of VvhA in the late growth phase. Surprisingly, we observed that the inactivation of VvhA was due to the novel oligomerization of VvhA by unknown mechanism, but not to the destruction of VvhA by VvpE. MATERIALS AND METHODSMedia, Bacterial Strains, Plasmids, and Primers 2.5% NaCl-Heart Infus...