Medial brachial fascial compartment syndrome: anatomic basis of neuropathy after transaxillary arteriography

The authors reviewed their experience with 320 transaxillary arteriograms, as well as the English-language literature on neuropathy complicating transaxillary arteriography. Three of their patients had median and ulnar motor and sensory nerve injury, and six others had only sensory involvement. The occurrence or severity of nerve injury did not correlate well with the size or presence of an observable axillary or arm hematoma. Dissection of the axillae and arms of 25 human cadavers revealed a tough medial brachial fascial compartment (MBFC) outside a thin axillary sheath. The median and ulnar nerves were within the MBFC at an arterial puncture site just lateral to the anterior axillary fold. The radial and musculocutaneous nerves exited the MBFC more proximally. The different levels at which the major nerves of the brachial plexus exit the MBFC explain the anatomic distribution of the nerve injuries associated with compression by a hematoma after transaxillary arteriography.     

The autonomic-related cortex: pathology in Alzheimer's disease

Alzheimer's disease (AD) causes progressive deterioration of cognition and behavior. Memory dysfunction is the hallmark, but there are also changes in behavior, emotion and autonomic functions, which cannot be explained simply as a consequence of memory impairment. These observations suggest that the natural disease process of AD involves not only memory-related neural structures, but also specific neural systems related to other behaviors, emotion and autonomic functions. Since recent evidence has indicated a primary role for ventromedial frontal (VMF) cortex in such functions, we examined laminar distribution of neurofibrillary tangles and Alz 50 immunoreactive neurons in subdivisions of VMF cortex in 20 AD patients and seven age- matched controls. The densities of pathological changes were: (i) highest in the posteromedial mesocortical regions, particularly Brodmann's area 25 (A25), posterior orbitofrontal cortex (POF) and anterior insula (AI); (ii) of comparable severity between posteromedial mesocortical regions and most temporal cortices, excluding only the entorhinal cortex and temporal pole; and (iii) located predominantly in layer III and especially layer V. Further analysis demonstrated selective pathology in layer V of A25, POF and AI that would disrupt direct cortico-autonomic projections. This is the first study to detail severe AD pathology in these autonomic-related cortices, which could contribute to the behavioral changes, emotional disturbance and autonomic dysregulation that often accompany AD.      

Hepatitis C virus genotypes in a cohort of Australian blood donors and haemophiliac and liver transplant patients

The aim of the present study was to characterize hepatitis C virus (HCV) genotypes using the INNO-LiPA HCV line probe assay and direct sequencing from three different HCV-RNA-positive (serum) groups: (i) blood donors (n= 59); (ii) haemophiliacs (n= 43); and (iii) patients undergoing liver transplantation (n= 26). Of 128 HCV-RNA-positive samples, 74 (58%) were genotype 1. Of these, 41 were genotype 1a, 32 were genotype 1b and one was genotype 1 indeterminate. Of the remaining 54 samples, seven (5%) were genotype 2a, two (2%) were genotype 2b, 26 (20%) were genotype 3a, three (2%) were genotype 4a, while 16 (12.5%) were of a mixed genotype. There was no significant difference between the three groups with regard to the prevalence of any specific genotype. However, in blood donors and haemophiliac patients there was a statistically significant difference in the occurrence of genotype 3a in patients with elevated alanine aminotransferase (ALT) levels (30.3%) compared with those patients with persistently normal ALT levels (5.6%; P= 0.004; x²) Genotype 3a was also uncommon in liver transplant patients (one of 14) with ‘sporadic’ HCV infection. Genotype 4a was detected only in liver transplant patients. These patients had originated from Egypt (n= 1), Italy (n= 1) and Romania (n= 1).     

Emergence of undifferentiated rat tracheal cell carcinomas, but not squamous cell carcinomas, is associated with a loss of expression of E- cadherin and of gap junction communication

A series of cells representing normal, non-tumorigenic cell lines, as well as differentiating neoplastic and undifferentiated neoplastic rat tracheal epithelial cell populations were evaluated for their ability to establish homologous and/or heterologous cell-cell gap junction communication in culture. Gap junction communication was evaluated by flow cytometric quantitation of the transfer of the fluorescent dye calcein from a donor to a recipient cell population via gap junctions. The data indicate that normal primary cultures of rat tracheal epithelial cells, as well as non-tumorigenic cell lines and squamous cell carcinomas cell populations, retain the ability to establish both homologous and heterologous gap junction communication. In all cases an average of >48% of recipient cells had acquired calcein label during a 5-h interval of co-culture of donor and recipient cells at confluent densities. Cells harvested directly from squamous cell carcinoma tumors exhibited similar levels of cell-cell communication. In contrast, cells giving rise to undifferentiated carcinomas, as well as cells harvested from undifferentiated carcinomas, exhibited very low levels or no homologous or heterologous cell-cell communication. Cell populations exhibiting distinctly different communication phenotypes were evaluated by Northern blot analysis for expression of connexins (Cx 26, 32 and 43) and E-cadherin. Neither communicating nor non-communicating cells expressed connexin 32. Those cell populations, which established functional gap junctions, expressed E-cadherin as well as connexin 26 and/or 43. In contrast, those cell populations that lacked the ability to communicate universally lacked expression of E-cadherin, and a quarter also lacked expression of detectable levels of connexin.