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J Wilkowski

Publications and source records attributed to J Wilkowski.

6 recordsLinked to original sources
PubMed1997

MCP-1 protects mice in lethal endotoxemia.

The overzealous production of proinflammatory cytokines in sepsis can result in shock, multiorgan dysfunction, and even death. In this study, we assessed the role of monocyte chemoattractant protein-1 (MCP-1) as a mediator of sepsis in endotoxin-challenged mice. Intraperitoneal administration of LPS to CD-1 mice induced a substantial time-dependent increase in MCP-1 in plasma, lung, and liver. The passive immunization of mice with rabbit antimurine MCP-1 antiserum 2 h before endotoxin administration resulted in a striking increase in LPS-induced mortality from 10% in control animals to 65% in anti-MCP-1-treated animals. Importantly, the administration of anti-MCP-1 antibodies to endotoxin-challenged mice resulted in increases in peak TNF-alpha and IL-12 levels, and also in a trend toward decreased serum levels of IL-10. Conversely, the administration of recombinant murine MCP-1 intraperitoneally significantly protected mice from endotoxin-induced lethality, and resulted in an increase in IL-10 levels, a decrease in IL-12 levels, and a trend toward decreased levels of TNF. In conclusion, our findings indicate that MCP-1 is a protective cytokine expressed in murine endotoxemia, and does so by shifting the balance in favor of antiinflammatory cytokine expression in endotoxin-challenged animals.

Animals↗
PubMed1996

Human microtubule-associated protein 1a (MAP1A) gene: genomic organization, cDNA sequence, and developmental- and tissue-specific expression.

Microtubule-associated proteins (MAPs) regulate microtubule stability and play critical roles in neuronal development and the balance between neuronal plasticity and rigidity. MAP1a (HGMW-approved symbol MAP1A) stabilizes microtubules in postnatal axons. We describe human MAP1a's genomic organization and deduced cDNA and amino acid sequences. MAP1a is a single-copy gene spanning 10.5 kb. MAP1a coding sequence is contained in five exons. Translation begins in exon 3. Human MAP1a contains 2805 amino acids (predicted molecular weight 306.5 kDa) and is slightly larger than rat MAP1a (2774 amino acids). Like rat and bovine MAP1a, human MAP1a contains conserved tubulin binding motifs in the amino-terminal region. The carboxy-terminal portion contains a conserved pentadecapeptide that is present in the light chain portion of rat and bovine MAP1a/LC2 polyprotein. We show that human MAP1a gene expression occurs almost exclusively in the brain and that there is approximately 10-fold greater gene expression in adult brain compared to fetal brain. Strong, interspecies conservation between human and rat MAP1a cDNA and amino acid sequences indicates important relationships between MAP1a's function and its primary amino acid sequence.

Adult↗
PubMed1996

Paroxysmal dystonic choreoathetosis: tight linkage to chromosome 2q.

Paroxysmal dystonic choreoathetosis (PDC) is characterized by attacks of involuntary movements that last up to several hours and occur at rest both spontaneously and following caffeine or alcohol consumption. We analyzed a Polish-American kindred with autosomal dominant PDC and identified tight linkage between the disorder and microsatellite markers on chromosome 2q (maximum two-point LOD score 4.77; recombination fraction 0). Our results clearly establish the existence of a locus for autosomal dominant PDC on distal chromosome 2q. The fact that three other paroxysmal neurological disorders (periodic ataxia with myokymia and hypo- and hyperkalemic periodic paralysis) are due to mutation in ion-channel genes raises the possibility that PDC is also due to an ion-channel gene mutation. It is noteworthy that a cluster of sodium-channel genes is located on distal chromosome 2q, near the PDC locus. Identifying the PDC locus on chromosome 2q will facilitate discovery of the PDC gene and enable investigators to determine whether PDC is genetically homogeneous and whether other paroxysmal movement disorders are also genetically linked to the PDC locus.

Athetosis↗
PubMedDate not supplied

[Inhaled nitric oxide in the therapy of acute hypoxemic respiratory failure of newborn].

AIM: To determine the efficiency of inhaled nitric oxide(INO) in term and preterm newborns with acute hypoxemic respiratory failure(AHRF), influence of this therapy on the systemic circulation and efficiency of the therapy in relation to the applied ventilation (conventional or oscillatory (HFOV)). METHODS: Term and preterm ventilated newborns with acute hypoxemic respiratory failure with oxygenation index(OI) >/= 15 were included. The mode of ventilation was not changed before initiation and was continued during INO therapy. Starting dose of INO was 20 parts per million (ppm) and during the last two years it was 1 Oppm. Heart rate, arterial blood pressure, methaemoglobin level, diuresis (in urinary catheterized newborns) were monitored. The efficiency of INO was determined on the ground of 20% decrease of 01. RESULTS: Investigations were performed in 43 term and premature newborns. After initiation of INO there was a statistically significant fall of 01. Therapy was effective in 72.1 % patients. There was no influence of the therapy on the systemic circulation heart rate and medial artery pressure were statistically unchanged. In 16 catheterized newborns statistically essential increase of diuresis was observed. This effect was more distinct in patients in whom INO therapy was effective. INO therapy was more effective in newborns with respiratory distress syndrome, congenital infection and adult respiratory distress syndrome and less effective in newborns with respiratory distress syndrome with congenital infection and meconium aspiration syndrome. There were no essential differences in efficiency of INO between patients ventilated conventionally and oscillatory. CONCLUSIONS: INO improves oxygenation in term and preterm newborns with AHRF. INO does not cause depression of the systemic circulation. The increase of diuresis after initiation of INO seems to be associated with improving of oxygenation of the patients. This observation needs to be confirmed by subsequent investigations. The efficacy of INO therapy depends on the cause of hypoxemic respiratory failure. The synergistic effect of INO and HFOV was not confirmed.

Acute Disease↗