Aim: In the testicular capsulotomized rats, although there was a significant increase in the luteinizing hormone (LH) levels, the secretion of testosterone remained low. In order to clarify the mechanisms of this phenomenon, the binding of endogenous LH to the testes were observed before and after testicular capsulotomy. Methods: Peroxidase-antiperoxidase (PAP) method was used to detect the binding of LH to the testes in rats. Results: An intense positive s taining of LH was found in the Leydig cells of both the normal and sham-operated control testes. However, at 40 d after operation, the LH immunoreactivity was decreased in the Leydig cells of the capsulotomized testis. By d 60, only very weak positive staining could be observed in these cells. Conclusion: A progressive reduction of endogenous LH binding to the testis cccurred in the capsulotomized rat.

AIMTo further clarify the changes occurred in the testicular capsulotomized rats.

METHODSIn testicular capsulotomized and sham-operated rats, the cross sectional area, the nucleus diameter and the number of Leydig cells were morphologically analyzed by the Vidas Image Processing System connected to a microscope.

RESULTSIn the capsulotomized animals, the cross sectional area of Leydig cells was gradually increased from 30 days onwards. There was no obvious change in the nucleus diameter of Leydig cells. However, The Leydig cell number was significantly increased from day 30 onwards.

CONCLUSIONIn rats, testicular capsulotomy may induce hyperplasia/hypertrophy of Leydig cells in the testis.

Animals ; Cell Count ; Cell Nucleus ; Image Processing, Computer-Assisted ; Leydig Cells ; cytology ; Male ; Rats ; Rats, Sprague-Dawley ; Testis ; cytology

People complain about nasal stuffiness after SO2 exposure. This study was to investigate the acute effects of SO2 on nasal vascular and airway resistances in anaesthetized pigs for elucidating the underlying vascular and control mechanisms. Controlled ventilation was passed to the lungs or retrogradely through each nasal cavity. Nasal airway and lower airway pressures were measured to reflect airflow resistance changes. Systemic arterial pressure and nasal arterial flow were measured to calculate nasal vascular resistance. Nasal and pulmonary SO2 challenges were given. At 2 ppm, SO2 decreased systemic blood pressure and nasal vascular resistance but increased nasal airway and lower airway resistances. With increasing level to 8 ppm, SO2 increased systemic arterial pressure, nasal vascular and lower airway resistances but decreased nasal airway resistance. Nasal and pulmonary challenges induced similar responses. Ipsilateral nasal challenge elicited bilateral responses. Ruthenium red abolished the responses to nasal challenges. Bilateral vagosympathectomy eliminated the responses to lung challenges. Hence, SO2 at 2 ppm causes nasal congestion through sensory reflex vasodilatation but at higher levels nasal decongestion through sensory reflex vasoconstriction. Nasal congestion coupled with bronchoconstriction at levels of SO2 below short-term exposure limit (STEL) (≤ 2 ppm) would limit SO2 entering the lungs. Nasal decongestion at levels of SO2 beyond STEL (> 2 ppm) can effectively decrease total airway resistance as concurrent strong bronchoconstriction may impair ventilation.
Administration, Inhalation ; Airway Resistance ; drug effects ; Animals ; Lung ; drug effects ; Nasal Cavity ; drug effects ; Respiration ; Sulfur Dioxide ; pharmacology ; Swine ; Vascular Resistance ; drug effects ; Vasodilation

Serum hepatitis B core-related antigen (HBcrAg) was shown to predict the risk of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients undergoing treatment. We investigated the longitudinal profile of HBcrAg in entecavir (ETV)-treated CHB patients with subsequent HCC develop-ment. We identified HCC cases diagnosed at ≥1 year after ETV initiation. CHB patients without HCC (matched for age, sex, cirrhosis status, baseline hepatitis B virus [HBV] DNA lev-el, and ETV treatment duration) were identified as controls at an HCC:non-HCC ratio of 1:2. Serum samples were retrieved at baseline (ETV initiation) and at 3 and 5 years of ETV therapy for HBcrAg measurement (log IU/mL). In total, 180 patients (60 HCC patients matched with 120 CHB patients without HCC; median age, 56.5 years; 80.6% male; baseline HBV DNA, 5.9 log IU/mL; median follow-up, 6.8 years) were recruited. The median time from ETV initiation to HCC de-velopment was 3.2 years. HBcrAg levels were higher in HCC cases than in controls at all three time points: 5.69 log IU/ mL versus 5.02 log IU/mL (p=0.025), 4.23 log IU/mL versus 3.36 log IU/mL (p=0.007), and 3.86 log IU/mL versus 3.36 log IU/mL (p=0.009), respectively. ETV led to similar rates of decline in HBcrAg from baseline to 3 years in both groups (0.34 log IU/mL/year vs 0.39 log IU/mL/year, p=0.774), al-though the decline from 3 to 5 years was slower in the nonHCC group (0.05 log IU/mL/year) than in the HCC group (0.09log IU/mL/year, p=0.055). ETV time-dependently reduced HBcrAg in HCC and non-HCC patients. HBcrAg interpretation should consider the antiviral treatment duration.

The originally published version of this Article contained an error in the author list: the last and first names of all authors are inverted.

We report a case of unique location of an aneurysm at the atlanto-axial extradural segment of a unilateral aberrant vertebral artery. The MRI vessel wall imaging findings and possible mechanism of aneurysm formation were discussed. A 5 mm extracranial vertebral artery aneurysm located at the interlaminar space between C1 and C2 was diagnosed in a woman presenting with occipital headache. The index vertebral artery ran an aberrant course at the V3 segment, where it entered the dura between C1 and C2 instead of the usual atlanto-occipital space. MR vessel wall imaging showed homogenous wall enhancement of the aneurysm sac. We surmise the anomalous course of the vertebral artery subjected the V3 segment to repeated shearing force secondary to the atlanto-axial rotational neck movement. This led to vessel wall trauma and inflammation, and subsequent aneurysm formation. The aneurysm was successfully treated with endovascular coiling with resolution of symptoms.
Aneurysm* ; Female ; Headache ; Humans ; Inflammation ; Magnetic Resonance Imaging* ; Neck ; Vertebral Artery*

Chronic hepatitis B (CHB) infection leads to clinically heterogeneous disease outcomes. Different viral markers are utilized to monitor treatment effects and predict risk of complications in patients with CHB. Hepatitis B core-related antigen (HBcrAg) is a novel serum composite viral protein whose performance has been proven to be superior to that of existing viral markers. It showed good correlation with intrahepatic covalently closed-circular DNA. Its profile differs drastically in patients in different disease phases, and the level declines with antiviral therapies. HBcrAg may be helpful for predicting hepatocellular carcinoma development and hepatitis B virus (HBV) reactivation in immunosuppressed patients. Another emerging measurable serum marker, HBV RNA, exists in the form of pregenomic RNA-containing virions. Its profile differs between patients in different disease phases in a similar manner to that of HBcrAg. HBV RNA is present in serum at lower levels than HBV DNA in treatment-naive patients by 1–2 logs. In contrast, its level is higher than HBV DNA in patients receiving nucleos(t)ide analogues (NAs). A significant decline in serum RNA was observed in patients receiving novel antiviral therapies, including core protein allosteric modulators and RIG-1/NOD2 agonists. Both HBcrAg and HBV RNA may be helpful for predicting off-therapy sustained virological control in patients who stop long-term NA treatment.
Biomarkers ; Carcinoma, Hepatocellular ; DNA ; Hepatitis B ; Hepatitis B virus ; Hepatitis B, Chronic ; Hepatitis, Chronic ; Humans ; RNA ; Virion