SHAFT syndrome revisited.

Wallace aptly described patients with overriding psychological problems and upper extremity complaints as possessing the Shaft syndrome. SHAFT patients studied fell into two categories. The first group inflicted physical harm on themselves, creating factitious injuries. The second group postured their limbs in attitudes that are not explainable anatomically. This latter group is described by Simmons as the clenched fist syndrome. Although patients who had factitious injuries invariably healed with protective casting, 4 patients relapsed. Eight of 14 patients who were employed at the onset of their complaints returned to gainful employment. Some patients received psychological counseling but most lacked sufficient insight to make gainful progress. Reaching a diagnoses was often difficult. At least 5 patients had unwarranted operations. The surgeon needs a high index of suspicion when the history and findings do not match for patients harboring complaints of pain, numbness, stiffness, or inability to use their limb.

Cutaneous scar at anterior hair line in mother and child with associated frontal bone defect in child.

A large frontal bone defect underlying a "V" shaped scar was noted in a newborn male whose mother had an identical "V" shaped scar at the same location in the anterior hairline. Both had hypertelorism and short palpebral fissures. The mother had no radiographic evidence of skull defect and neither mother nor child had other cutaneous or skeletal anomalies. Cranioplasty was performed on the child using the remaining frontal bones with an excellent cosmetic result. Biopsy performed at operation documented scar tissue extending through the dermis and underlain by thickened dura. Mother and child appear to have a variant form of aplasia cutis congenita, an autosomal dominant trait with wide variation in expression.

Chemotaxis of Salmonella typhimurium to amino acids and some sugars.

Patterns of chemotaxis by Salmonella typhimurium strain LT-2 to l-amino acids and to several sugars were quantitated by the Adler capillary procedure. Competition experiments indicated that LT-2 possesses three predominant receptors, or interacting sets of receptors, for amino acids. These were termed the aspartate, serine, and alanine classes, respectively. Studies with strains carrying point and deletion mutations affecting components of the phosphoenolpyruvate: glycose phosphotransferase system (PTS) made unlikely a role in primary reception of d-glucose by the three soluble PTS components, namely HPr, enzyme I, and factor III. A ptsG mutant defective in membrane-bound enzyme IIB' of the high-affinity glucose transport system was shown to exhibit normal chemotaxis providing pleiotropic effects of the mutation were eliminated by its genotypic combination with other pts mutations or, phenotypically, by addition of cyclic AMP and substrate. A correlation was demonstrated between chemotaxis to glucose and activity of the low-affinity glucose transport complex, membrane-bound enzymes IIB:IIA, and an enzyme IIB:IIA mutant was shown to have a preponderant defect in chemotaxis to glucose and mannose. Of four systems capable of galactose transport, only the beta-methylgalactoside transport system was implicated in chemotaxis to galactose. Some properties of a mutant possibly defective in processing of signals for chemotaxis to sugars is described.

Fosfomycin resistance: selection method for internal and extended deletions of the phosphoenolpyruvate:sugar phosphotransferase genes of Salmonella typhimurium.

Selection for resistance to the antibiotic fosfomycin (FOS; L-cis 1,2-epoxypropylphosphonic acid, a structural analogue of phosphoenolpyruvate) was used to isolate mutants carrying internal and extended deletions of varying lengths within the ptsHI operon of Salmonella typhimurium. Strains carrying "tight" ptsI point mutations and all mutants in which some or all of the ptsI gene was deleted were FOS resistant. In contrast, strains carrying ptsH point mutations were sensitive to FOS. Resistance to FOS appeared to result indirectly from catabolite repression of an FOS transport system, probably the sn-glycerol-3-phosphate transport system. Resistant ptsI mutants became sensitive to FOS when grown on D-glucose-6-phosphate, which induces an alternate transport system for FOS, or when grown in the presence of cyclic adenosine 3',5'-monophosphate. A detailed fine-structure map of the pts gene region is presented.