Sjögren's Syndrome with Chronic Pancreatitis, Sclerosing Cholangitis, and Pulmonary Infiltrations

We report a patient with Sjögren's syndrome and multiple gastrointestinal manifestations who successfully responded to therapy with ursodeoxycholic acid. Our patient had sialoadenitis with dry mouth, dry eyes, arthralgia, chronic pancreatitis, sclerosing cholangitis, and pulmonary inflitrations. The first signs of disease were the symptoms of chronic pancreatitis followed by icterus, caused by extrahepatic bile duct obstruction. Sclerosing cholangitis was diagnosed by liver biopsy and endoscopic retrograde cholangiography. Sialoadenitis, causing dry mouth, was verified by buccal biopsy. Pulmonary infiltrations were seen on standard chest x-ray, and also shown by high-resolution computed tomography examination. Obstructive icterus and even pulmonary infiltration responded successfully to treatment with ursodeoxycholic acid.     

The effects of THA on scopolamine and nucleus basalis lesion-induced EEG slowing

The effectiveness of THA (an anticholinesterae) on scopolamine (0.4 mg/kg) and nucleus basalis (NB) lesion-induced change in neocortical spectral electroencephalography (EEG) were investigated. Scopolamine increased the amplitudes of all the spectral components in waking-immobility. In the movement-related EEG spectral values, only the alpha power was increased. THA 7.5 mg/kg, but not THA 3 mg/kg, could reverse scopolamine-induced amplitude change. NB lesioning increased delta and theta amplitudes, but decreased beta amplitude. Delta amplitude was increased during movement recordings in NB-lesioned rats. THA 7.5 mg/kg and pilocarpine 10 mg/kg, but not THA 3 mg/kg, could partially reverse the increase of delta and theta amplitudes induced by NB lesions. However, the beta power decrease could not be restored with cholinomimetics. This study demonstrates that quantitative EEG activity analysis may reflect the THA-induced restoration of the function of the cholinergic nucleus basalis.     

Effect of Vigabatrin on the Electroencephalogram in Rats

Vigabatrin (gamma-vinyl GABA; GVG) is a new antiepileptic drug (AED) that increases the level of the inhibitory transmitter, gamma-aminobutyric acid (GABA) in the brain. We evaluated the effect of GVG on the EEG of normal rats. GVG was administered intraperitoneally (i.p.) at a dose of 100 mg/kg once a day for 12 days. EEG was recorded at baseline, on the fourth day, at the end of the 12-day GVG period and 10 days after discontinuation of GVG. GVG increased the amplitude of delta (1-4 Hz) and theta (4-8 Hz) frequency bands and resulted in slowing of the peak frequency (Fp) and mean frequency (Fm) in both the frontal and occipital cortex, especially during waking-immobility. EEG changes normalized within 10 days after the last GVG injections. The results suggest that a relationship may exist between the EEG changes and increase in GABA levels with GVG.     

The CCR5Delta32 allele is associated with reduced liver inflammation in hepatitis C virus infection.

CCR5Delta32 is a deletion mutation in the chemokine receptor CCR5. Liver inflammatory activity was found to be significantly reduced (P = 0.005) in Jewish Israeli patients infected with the hepatitis C virus (HCV) carrying the CCR5Delta32 allele. The CCR5Delta32 allele does not alter susceptibility to HCV infection; however, it may play a role in the progression and outcome of the disease.     

Raman and UV–vis spectroscopic study of polyaniline membranes containing a bulky cationic additive

Electrically conducting soluble polyaniline (PANI), containing different amounts of a bulky lipophilic cationic additive, tridodecylmethylammonium chloride (TDMACl), was studied by Raman (λ_exc=780 nm) and UV–vis spectroscopy. PANI was made simultaneously electrically conducting and soluble with bis[4-(1,1,3,3-tetramethylbutyl)phenyl]phosphoric acid in dichloromethane. The PANI membranes were prepared by drop casting on glassy carbon or ITO substrates. Raman and UV–vis measurements were carried out in a 0.1 M CaCl₂ solution at potentials between 400 and ?600 mV (vs. SCE) at pH 6, or alternatively at the open circuit potential at pH 10. The results of Raman, UV–vis and cyclic voltammetric measurements confirm that the incorporation of TDMACl into the PANI membrane facilitates the oxidation and reduction of PANI.     

Supracerebellar arachnoid cyst - A rare cause of acquired Chiari I malformation.

Chiari I malformation (CM) associated with a cervico-thoracic syrinx due to supracerebellar arachnoid cyst has not been reported in the literature. We report such a case, managed by fenestration of the arachnoid cyst and foramen magnum decompression (FMD), aiming to reduce the inferiorly directed pressure on the cerebellum and eliminate the craniospinal pressure dissociation respectively. Imaging done post-operatively showed upward displacement of the cerebellar tonsils with a decompressed craniovertebral junction and disappearance of the syrinx.     

Continuous pleural lavage may decrease postoperative morbidity in patients undergoing thoracotomy for stage 2 thoracic empyema.

OBJECTIVE: To assess the impact of postoperative continuous pleural lavage (PCPL) after thoracotomy for the treatment of stage 2 pleural empyema in relation to postoperative length of stay and morbidity. METHODS: Stage 2 pleural empyema was diagnosed with computer tomography. Conservative treatment including antibiotics and pleural aspiration was introduced. 89 patients treated for stage 2 pleural empyema by thoracotomy, pleural discharge evacuation and irrigation after pleural decortication were identified after unsuccessful conservative treatment for 10 days. Whenever pleural discharge remained opaque after operation, PCPL was administered daily through the cranial chest tube and discharge evacuated through the caudal pleural suction (10-15 mmHg) tube. Risk factors related to pleural pus and patient outcome were sought for. RESULTS: Seventy-seven out of 89 patients (86.5%) had clear empyema discharge immediately after pleural decortication and irrigation. Pleural discharge remained opaque despite surgery in 12 out of 89 patients (13.5%) and PCPL was introduced. Presence of a combination of risk factors for pleural empyema, such as dental caries, alcohol abuse or previous inflammatory reaction, was predictive for persistence of opaque pleural discharge after operation (P<0.05). Need for re-thoracotomies (in 11 cases, P=ns) and postoperative deaths (P<0.05) were related with patients who did not have PCPL. The length of the hospital treatment was 20.1+/-3.1 (days+/-SEM) among patients with PCPL and 19.2+/-1.8 without PCPL before possible re-thoracotomy, respectively (P=ns). CONCLUSIONS: Early postoperative (1 day-11 months) mortality was statistically associated with patients having fibrinopurulent empyema but no PCPL. PCPL is a feasible method to clear pleural pus discharge without prolongation of hospitalization and may be recommended after thoracotomy for patients with fibrinopurulent stage 2 empyema.     

The peri‐microvascular edema in hippocampal CA1 area in a rat model of sepsis

Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respiratory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham‐operated and not operated control groups. Significantly more peri‐microvascular edema was found in the hippocampal CA1 area in the septic group. The percentages of the peri‐microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham‐operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics.